How the NPTE Works and How to Think Like the Exam

The physical therapist licensing exam does not reward the student who memorized the most facts; it rewards the student who can read a short clinical story, see what the patient needs right now, and choose the safest, most effective next step. That is a learnable skill. This chapter explains how the exam is built, how its questions are written, the clinical models its authors think in, and a study plan that turns review time into points.

Section 1The structure of the licensing exam

What the exam is and who it serves

The National Physical Therapy Examination (NPTE) is the entry level licensing exam for physical therapists in the United States. It is developed and administered by the Federation of State Boards of Physical Therapy, an organization of the state licensing boards, and every state uses it as one requirement for licensure. A separate exam exists for physical therapist assistants. The purpose of a licensing exam is public protection: it asks whether a new graduate can practice safely and effectively at entry level. That purpose explains its personality. Questions favor safety, common conditions, sound clinical reasoning and the core of practice over rare trivia, and most questions put you in the role of a therapist making a decision about a real patient.

Passing the NPTE is necessary but not sufficient for a license. States also set their own requirements, which may include a jurisprudence exam on the state practice act, a background check and proof of graduation from an accredited program. Rules on registration, eligibility, scheduling, attempt limits and accommodations change, so the only reliable source is the current official candidate handbook. Read it early, because some steps (state approval of eligibility, accommodation requests) take weeks.

The testing experience

The NPTE is a computer based, multiple choice exam delivered at secure testing centers. It is long: the day is divided into several timed sections with a scheduled break, and most candidates describe it as an endurance event as much as a knowledge test. Each item is a stem followed by four options, and you choose the single best answer. There is no penalty for guessing, so you should never leave an item blank. Within a section you can flag items and return to them; once a section closes, you cannot go back. You will see a short tutorial before the first section, and the clock does not stop for breaks taken inside a section.

Most items are scenario items: a vignette with age, setting, diagnosis and findings that asks what to do or what a finding means. A minority are direct recall items. Media items add an image, graph, ECG strip, radiograph or short video (a gait pattern, a transfer) to interpret, and some items share a scenario but are scored independently.

Scored and pretest items

Not every item counts. A portion of each form is made up of pretest items: new questions being tried out so their statistics can be checked before they ever count toward a score. Pretest items look exactly like scored items and are mixed in among them, so you cannot tell which is which. The practical lesson is important for your nerves. When you meet a question that seems strange, ambiguous or far outside what you studied, it may well be a pretest item that will be discarded. Make your best choice, flag it if time allows, and move on without letting it shake your confidence.

Scaled scores

Different forms of the exam contain different items, and some forms are slightly harder than others. To be fair, raw scores are converted to a scaled score so that a given scaled score represents the same level of ability on every form. The NPTE reports scores on a scale of 200 to 800, and the passing standard is a scaled score of 600. Because of equating, the number of items you must answer correctly to reach 600 varies a little from form to form, which is why nobody can honestly tell you a fixed percentage to aim for. The passing standard is set by a criterion referenced process: expert panels judge how a minimally competent entry level therapist would perform. You are not competing with the other candidates on your test day.

The content outline: systems and nonsystems

The exam is built from a published content outline, a blueprint that sets how many items come from each area. Its organization is two dimensional. One dimension is content: the body systems and the nonsystems areas. The other is the clinical task being tested.

Musculoskeletal and neuromuscular content together account for about half of the exam, which is why they receive the largest share of this book. Cardiovascular and pulmonary is the next largest system. The smaller systems still matter, because each item is worth the same; a candidate who skips integumentary or lymphatic review gives away points that are often easier to earn than difficult neurology items. Exact weights change when the outline is revised (it is updated periodically from a practice analysis survey of working therapists), so download the current version from the official source.

The clinical tasks

The second dimension is what you are asked to do with the content. The outline groups this into broad clinical tasks:

• Examination: history, systems review and tests and measures. Questions ask which test to choose, how to perform it, or what a result shows.
• Evaluation, differential diagnosis and prognosis: interpreting findings, identifying the likely condition or the movement system problem, recognizing when the problem is outside physical therapy, and predicting outcome.
• Intervention: choosing, dosing, progressing and modifying treatment, including exercise, functional training, manual therapy, modalities, devices, education and discharge planning.
• Foundational sciences: anatomy, physiology, pathology, pharmacology and exercise science that underpin the decisions above.

A single condition can be tested in all of these ways. Take a rotator cuff repair: one item asks which test detects a full thickness tear (examination), another asks what a weak lag sign means for prognosis (evaluation), and a third asks when active elevation may begin (intervention). As you study each condition later in this book, rehearse it across every task.

What the exam writers value

Items are written and reviewed by practicing clinicians and educators and anchored to entry level practice and current evidence. The same values recur: safety first (stability, red flags, precautions), function and the patient's goals over isolated impairments, current guidelines as the default answer, the least restrictive option that keeps the patient safe, and practice within scope, with appropriate delegation and referral.

Section 2Reading a physical therapy question

The three things every stem tells you

Before you look at the options, read the stem and find three things. Experienced test takers do this almost automatically; at first you should do it deliberately.

1. The patient. Age, diagnosis, time since onset or surgery, comorbidities, medications, vital signs and current function. Every detail was put there for a reason, and the most important details are often the quiet ones: "two days after," "takes warfarin," "lives alone," "type 1 diabetes."
2. The setting. Intensive care unit, acute hospital floor, inpatient rehabilitation facility, skilled nursing facility, home, outpatient clinic or school. The setting changes what is safe, what is realistic and what the goal of the visit is.
3. The task. What exactly is being asked: the first action, the best intervention, the most likely diagnosis, the expected finding, the appropriate referral, the correct documentation, the parameter of a modality. Underline it mentally, then answer that question and not a different one.

A useful habit is to read the last sentence of the stem first, so you know the task, and then read the whole stem with that task in mind. In long vignettes this keeps you from drowning in details that do not bear on the question.

Keywords that change the answer

Small words carry big weight. Item writers use a consistent vocabulary, and misreading one word is the most common source of avoidable error.

Predict, then compare

Form an answer in your head before reading the options. If it is there, it is probably right, though you should still check the others; if it is not, reread the stem for the clue you missed. Prediction protects you from the most persuasive distractors.

The anatomy of a distractor

Wrong options are not random. They are built to catch predictable mistakes, and once you recognize the types you eliminate them faster.

• True but irrelevant. The statement is correct medicine but does not answer this task. A stem asking for the first action after a fall may offer an excellent strengthening exercise; true, useful, not first.
• Right action, wrong time. Correct for a later phase (resisted exercise two days after a tendon repair) or an earlier one (passive range of motion only, when the patient is ready for strengthening).
• Right idea, wrong patient. Appropriate for a different diagnosis or setting, such as a home exercise program for a patient in the ICU.
• Overreach. An action outside physical therapist scope (adjusting a medication dose, ordering imaging where not permitted, diagnosing a medical disease) or outside entry level competence.
• Absolutes and extremes. "Always," "never," "complete bed rest," "discontinue all exercise." Real practice rarely works in absolutes, so these options are usually wrong unless they describe a true contraindication.
• Passive or modality heavy choices when the patient needs active, functional work. Modalities are adjuncts; they are rarely the best answer when an active intervention is available.

When two options remain, ask: which one is more specific to the problem described, which one is more functional, which one comes earlier in the logical sequence, and which one is safer? Usually one of these questions breaks the tie.

Priority and safety logic

Many items are really ranking problems. When the stem describes a patient who could be harmed, the hierarchy below almost always decides the answer.

When a stem reports a change in status (new confusion, sudden pain, calf swelling, falling oxygen saturation) or gives abnormal values, the answer usually involves stopping or modifying the activity and assessing or reporting, not pushing on with the plan.

Common traps

Do not add information the stem does not give, and do not change a reasoned answer without a specific clue. Avoid the impressive specialist technique when a standard, well supported one fits entry level practice. Let the setting shape the answer, and never treat numbers as decoration: a Berg score of 38, an ankle brachial index of 0.6 or a platelet count of 15,000 each changes the answer.

Section 3The patient and client management model and the ICF

Why the model matters on the exam

Physical therapy practice in the United States is organized around the patient and client management model: a cycle of examination, evaluation, diagnosis, prognosis, intervention and outcomes. Many exam items are really asking "which step are we in?" An option can be the right action in the wrong step. If a question asks what the therapist should do when a patient arrives for the first visit, the answer lies in examination; if it asks what to conclude from the findings, it lies in evaluation; if it asks how long recovery will take, it lies in prognosis. Recognizing the step narrows the options immediately.

The steps one by one

Examination has three parts. The history collects demographics, the chief complaint, onset and course, past medical and surgical history, medications, social history, living environment, prior and current function and the patient's goals. The systems review is a brief screen of the cardiovascular and pulmonary (heart rate, respiratory rate, blood pressure, edema), integumentary (skin integrity, color, scar), musculoskeletal (gross symmetry, strength, range, height and weight) and neuromuscular (gross coordinated movement such as balance, gait and transfers) systems, plus communication, affect, cognition, language and learning style. Its purpose is to find problems that need further testing or referral. Tests and measures are the specific, chosen procedures (goniometry, manual muscle testing, special tests, balance scales, gait speed) used to confirm or refute hypotheses.

Evaluation is the thinking step: a dynamic process of making clinical judgments from the examination data. It weighs the severity, chronicity, stability and complexity of the problem and leads to a diagnosis. Evaluation is also where the therapist decides whether the problem belongs in physical therapy at all.

Diagnosis in physical therapy labels the problem at the level of the movement system and function. It is not a substitute for a medical diagnosis; a therapist may describe "impaired joint mobility and motor function associated with a shoulder disorder," while the physician's diagnosis is "adhesive capsulitis." Physical therapists do diagnose within their scope, and in direct access settings they also screen for conditions that need medical diagnosis.

Prognosis is the predicted optimal level of improvement and the time needed to reach it. It is written into the plan of care, which includes the goals, the expected frequency and duration of visits, the interventions planned and the discharge plan. Good goals are functional and measurable; a common framework names the Audience, Behavior, Condition, Degree and expected time ("Patient will ambulate 150 feet on level surfaces with a single point cane and supervision within 2 weeks").

Intervention is broader than procedures. It includes coordination, communication and documentation (case management, communication with the team, discharge planning), patient and client instruction (education of the patient, family and caregivers), and procedural interventions (therapeutic exercise, functional training, manual therapy, airway clearance, integumentary repair, devices and equipment, modalities).

Outcomes are the results of care, measured with valid instruments: change in impairments, activity, participation, risk reduction, patient satisfaction and quality of life. Outcomes justify continuing care and support the discharge decision. Reexamination occurs throughout care to judge progress and modify the plan. Discharge occurs when goals are met; discontinuation occurs when care ends before goals are met (the patient declines, the condition changes, or further benefit is not expected).

The International Classification of Functioning, Disability and Health

The ICF, published by the World Health Organization, is the framework that physical therapy uses to describe health and disability. It replaced older, linear disablement models (pathology leading to impairment, then functional limitation, then disability). The ICF is biopsychosocial: function and disability result from an interaction between a health condition and contextual factors, and the arrows run in both directions.

• Health condition: the disease, disorder, injury or state (stroke, total hip arthroplasty, pregnancy).
• Body functions and structures: physiological functions and anatomical parts. Problems here are impairments (decreased knee flexion range, weakness of hip abductors, impaired sensation, reduced vital capacity).
• Activity: the execution of a task by the individual. Problems are activity limitations (cannot climb stairs, needs assistance for bed to chair transfer, walks slowly).
• Participation: involvement in a life situation. Problems are participation restrictions (cannot return to work as a mail carrier, cannot attend church, cannot care for grandchildren).
• Environmental factors: the physical, social and attitudinal environment (stairs at home, supportive spouse, insurance coverage, workplace accommodations). They can be facilitators or barriers.
• Personal factors: features of the individual that are not part of the health condition (age, coping style, education, motivation, fear of movement).

Using the ICF in clinical reasoning

The ICF is not just vocabulary. It guides goal setting and outcome selection. Long term goals should be written at the activity and participation levels because those are what matter to patients and payers; impairment goals support them. Outcome measures can also be mapped: goniometry and dynamometry measure impairments, the Timed Up and Go and 6 minute walk test measure activity, and many self report questionnaires capture activity and participation. When a stem asks which goal is "most appropriate" for a plan of care, the functional, measurable, patient centered goal tied to the patient's stated priority is usually the answer.

Section 4Clinical decision rules and setting differences

Screening for referral: treat, treat and refer, or refer

Every examination ends with one of three decisions. The therapist can treat (the problem is within physical therapy and no concerning findings exist), treat and refer or consult (physical therapy is appropriate, but another finding needs a provider's attention, such as elevated blood pressure in a patient with knee pain), or refer without treating (the presentation suggests a medical condition that must be addressed first). Some situations are emergencies and call for immediate activation of emergency services rather than a routine referral.

Screening uses the whole history. Classic red flags include a history of cancer, unexplained weight loss, constant pain unchanged by position or rest, night pain that wakes the patient and does not ease, fever or chills, recent infection or immunosuppression, progressive neurological deficit, bowel or bladder changes, saddle anesthesia, pain out of proportion to the injury, and symptoms that do not follow a musculoskeletal pattern (for example, shoulder pain that increases with exertion and eases with rest, which could be cardiac). Yellow flags are psychosocial factors (fear avoidance, catastrophizing, depression, job dissatisfaction) that predict a slower recovery; they do not call for referral by themselves but do change how you treat.

Clinical prediction and decision rules

A clinical prediction rule (also called a clinical decision rule) combines a small set of findings to estimate the probability of a diagnosis, the need for imaging, or the likelihood of responding to a treatment. Rules are judged by their validation: a rule that has only been derived in one sample is weaker than one that has been validated in new patients and tested for impact. The exam expects you to know the major rules and how to apply them.

On the Wells DVT score, the commonly used two level version calls DVT likely at a score of 2 or more and unlikely at 1 or less. A patient with a likely score should not be exercised or treated with manual techniques to that limb until medically cleared; the physician will typically order a D-dimer or duplex ultrasound. Homans sign is no longer considered a reliable test and should not be used to rule DVT in or out.

The settings of practice

The same diagnosis looks different in each setting, and the exam expects you to know what is realistic and safe where the patient is. The table summarizes the defining features; detailed payer rules vary and change, so learn the principles rather than memorizing billing codes.

Acute care specifics that recur on the exam

In the hospital, review the chart before every session: orders (activity, weight bearing, precautions), vital sign trends, laboratory values and the nursing report, looking for a reason not to treat today, such as new fever, an acute hemoglobin drop, a very low platelet count, new chest pain, an unstable arrhythmia or a dangerous glucose level (Chapter 8 gives the values). Patients with arterial or central lines, chest tubes, urinary catheters or nasogastric tubes can usually be mobilized; plan the route of the lines and protect them during transfers.

Discharge recommendation is a classic acute care item. Consider the patient's current function, prior level of function, expected trajectory, tolerance for intensity, caregiver support and the home environment. A patient who needs moderate assistance, can tolerate several hours of therapy and has a good prognosis after a stroke fits inpatient rehabilitation; a frail patient who needs similar help but tolerates only short sessions fits skilled nursing; a patient who is safe with supervision and has help at home may go home with home health services if homebound, or with outpatient therapy if not.

Scope, direct access and supervision

Each state's practice act defines what physical therapists may do and how. Across the country, patients may now see a physical therapist without a physician referral (direct access), but many states attach provisions such as a time limit or visit limit after which a referral or physician involvement is required, and some payers require referral for payment even where the law does not. Medicare does not require a physician referral to begin evaluation, but it does require a plan of care certified by a physician or other allowed practitioner. Know the principle, and on the exam assume that a therapist practicing under direct access carries the full responsibility to screen for conditions requiring medical care.

Supervision of support personnel is tested often. The physical therapist performs the initial examination and evaluation, establishes the diagnosis, prognosis and plan of care, performs reexaminations, and writes the discharge summary; these cannot be delegated. The physical therapist assistant may provide selected interventions within the plan of care, adjust interventions within the plan (progressing repetitions or resistance as the plan allows), collect data and document progress, but may not perform evaluations, change the plan of care or discharge the patient. The PT decides what to delegate based on the patient's stability and complexity and the assistant's competence. Aides and technicians are not licensed; they perform nonskilled tasks (preparing the treatment area, assisting with transfers under direct supervision) and may not provide skilled interventions independently. Supervision levels (general, direct, direct personal) vary by state and payer.

Section 5A study plan that works

How memory works, and why cramming fails

Two findings from learning science should shape your plan. The first is the spacing effect: material reviewed several times with gaps between reviews is remembered far longer than the same material studied in one block. Each time you return to a topic just as it begins to fade, the memory is rebuilt more durably. The second is the testing effect (retrieval practice): trying to recall information, as in answering questions or flashcards, strengthens memory more than rereading or highlighting. Rereading creates a feeling of familiarity that is easily mistaken for knowledge; retrieval shows you what you can actually produce under pressure.

A third principle, interleaving, matters for an exam that mixes topics. Practicing mixed sets (a stroke item, then a knee item, then a lab value item) is harder than practicing one topic at a time, but it trains the skill the exam actually demands: recognizing what kind of problem you face. Blocked practice is fine when you first learn a topic; interleaved practice should dominate the final weeks.

Building the calendar

Most candidates do best with a structured plan of about 8 to 12 weeks of dedicated review after graduation, adjusted for their starting point and other obligations. A plan that is realistic and followed beats an ambitious plan abandoned in week three. A practical structure:

1. Baseline (week 1). Take a full length, timed practice exam under realistic conditions. The score matters less than the profile: which systems and which tasks are weakest.
2. Content building (weeks 2 to 7). Work through the systems in order of weight and weakness, starting with musculoskeletal and neuromuscular. For each topic: read the chapter, make or use flashcards, then do a mixed question set the same day and a review set two to three days later.
3. Integration (weeks 8 to 10). Shift to mixed, timed question blocks and a second full length practice exam. Revisit weak topics identified by miss analysis.
4. Final phase (last 7 to 10 days). A final full length exam about a week before test day, then light, targeted review of high-yield tables (special tests, lab values, nerve lesions, modality parameters). No new major topics in the last two days.

Analyzing your misses

Doing questions without studying the misses wastes most of their value. Keep a miss log with the topic, the type of error and the fix. Classifying errors shows patterns that rereading never would.

For every missed question, write one sentence explaining why the right answer is right and one explaining why your answer was wrong. Also review a sample of questions you answered correctly but guessed; a lucky guess is a hidden knowledge gap.

Pacing on test day

Work out your per item time budget from the current handbook's section length and time limit, and set checkpoints (for example, where you should be at the quarter, half and three quarter marks of each section). A comfortable target leaves a few minutes at the end of each section for flagged items. Hard items should get a reasoned choice and a flag, not an open ended struggle. Answer every item before time expires, because there is no penalty for guessing.

Confirm the test center, travel time, identification and room rules days ahead, sleep well, and plan a familiar breakfast and a snack for the break.

Test anxiety

Some anxiety improves performance; too much narrows attention and blocks retrieval. Well supported strategies include simulation (at least two full length timed practice exams, including the break), slow breathing with a longer exhale to reduce sympathetic arousal, reappraisal of arousal as readiness rather than danger, brief expressive writing about worries before the test, and a reset routine after a hard item (breathe out, relax the shoulders, read the next stem fresh).

Candidates who have a diagnosed condition that affects testing may request testing accommodations through the official process, which requires documentation and time. Start early. If anxiety is severe or longstanding, a counselor or physician can help, and that help is a sign of good judgment, not weakness.

Using this book's companion exams and flashcards

Each chapter of this book ends with ten "Check yourself" questions; treat them as a first retrieval pass on the day you read the chapter, and revisit them a few days later. The companion practice exams and flashcard decks on the same site are built to match the chapters. Use them this way:

Use flashcards for facts that must be automatic (nerve roots, special test positives, lab ranges, modality parameters), reviewing only the cards due each day; topic sets in tutor mode during content building; mixed timed exams in exam mode during integration, followed by miss analysis; and the glossary tables as a quick self test with the right column covered.

Words worth knowing

Musculoskeletal Foundations: Tissue, Kinesiology and the Spine

Every orthopedic decision on the exam, from how soon a repaired tendon can be loaded to which way to glide a stiff joint and whether a patient with neck pain needs imaging, rests on a few foundations: how tissues heal, how joints move, and how to examine the spine without missing something dangerous. This chapter builds those foundations and then applies them to the cervical, thoracic, lumbar and sacroiliac regions, where clinical prediction rules, classification systems and safety screening are tested heavily.

Section 1Tissue healing and loading

The three overlapping phases

Soft tissue healing after injury or surgery proceeds through three overlapping phases. Their timelines vary with tissue type, blood supply, age, nutrition, smoking, diabetes and medications such as systemic corticosteroids, so the numbers below are typical ranges, not rules. What the exam tests is the biology of each phase and the type of loading that fits it.

The inflammatory phase begins immediately and lasts roughly the first 3 to 7 days. Vasoconstriction and clotting stop bleeding; then vasodilation and increased permeability bring plasma proteins and white cells to the area. Neutrophils arrive first, followed by macrophages, which clear debris and release growth factors that drive the next phase. The cardinal signs are redness, heat, swelling, pain and loss of function. Clinically, pain is felt before end range, at rest or with any stress. The goals are to protect the tissue, control edema and pain, and maintain motion in neighboring regions. Complete rest is not the goal; gentle, pain free movement within protected limits reduces stiffness and supports circulation.

The proliferative phase (also called repair or fibroplasia) overlaps inflammation and runs from about day 3 to about week 3 to 6. Fibroblasts lay down type III collagen, a thin, weak, randomly arranged collagen, along with new capillaries (angiogenesis) and granulation tissue. Wound contraction by myofibroblasts draws the edges together. The new tissue is fragile, and tensile strength is low. Controlled, low load stress now begins to orient the new fibers; too much load disrupts them and restarts inflammation.

The remodeling phase (maturation) begins at about week 3 and continues for months to more than a year. Type III collagen is gradually replaced by stronger type I collagen, fibers align along lines of stress, cross links form and the scar shrinks and strengthens. Even after a year, a ligament or tendon scar typically regains only a portion of its original tensile strength. Progressive loading, specific to the demands the patient will face, is the stimulus that drives this alignment.

Mechanical behavior: the stress strain curve

Connective tissues are viscoelastic: their response depends on how fast and how long they are loaded. On a stress strain (load deformation) curve for tendon or ligament, the first segment is the toe region, where crimped collagen fibers straighten with little force. The elastic (linear) region follows; deformation is proportional to load and fully recoverable when the load is removed. Beyond the yield point lies the plastic region, in which some fibers fail and deformation is permanent (a clinical sprain or strain). At the ultimate failure point the tissue ruptures. The slope of the elastic region is the stiffness (Young modulus).

Two viscoelastic properties are used in treatment. Creep is continued elongation under a constant load over time; it is why a low load, long duration stretch is more effective than a brief forceful one at producing lasting length change. Stress relaxation is the decline in internal force when tissue is held at a constant length; it is the principle behind serial casting and static progressive splinting. Tissues are also stiffer when loaded quickly, and warm tissue deforms more readily than cold tissue, which is why heat combined with prolonged stretch is effective.

How specific tissues respond

Bone healing

Fracture healing follows its own phases. In indirect (secondary) healing, typical of fractures treated with casts or flexible fixation, a hematoma and inflammation form in the first days, a soft callus of fibrocartilage bridges the gap over the next few weeks, a hard callus of woven bone replaces it (often visible on radiographs by 4 to 8 weeks), and remodeling into lamellar bone continues for months to years. Rigid fixation allows direct (primary) healing without callus. Fracture timelines and weight bearing status are covered in Chapter 4.

Wolff law states that bone adapts its density and architecture to the loads placed on it: bone is laid down where stress is applied and resorbed where it is absent. This explains osteoporosis with bed rest or spinal cord injury and the use of weight bearing and impact exercise to build bone. Davis law is the soft tissue counterpart: soft tissues remodel according to the demands placed on them, lengthening under sustained tension and shortening when kept slack. A patient whose knee is kept flexed in bed develops shortened hamstrings and posterior capsule; prolonged low load positioning can reverse it.

Protected motion and progressive loading

Modern rehabilitation favors protected early motion over immobilization whenever the repair allows. Controlled motion reduces adhesions, maintains cartilage nutrition, limits atrophy and helps align new collagen. Protection means respecting the limits the surgeon or the tissue sets: range limits (for example, after a rotator cuff repair), load limits (weight bearing status), speed (slow before fast), and direction (avoiding the motion that stresses the repair). Within those limits, loading is progressed by one variable at a time, guided by the patient's response during and over the 24 hours after a session. Pain that is mild, settles quickly and does not increase the next morning is generally acceptable; pain that lingers, increasing swelling, or loss of motion means the load was too much.

Section 2Kinesiology essentials

Planes, axes and the language of motion

Motion is described from anatomical position: standing, facing forward, arms at the sides with palms forward. Each plane of motion has a perpendicular axis around which the motion occurs.

Open and closed kinetic chain

In an open kinetic chain (OKC) exercise the distal segment moves freely in space (a seated knee extension, a biceps curl). In a closed kinetic chain (CKC) exercise the distal segment is fixed against a surface and the proximal segments move over it (a squat, a push up, a step up). The distinction matters for joint loading and for which muscles work.

Open chain knee extension pulls the tibia anteriorly in the last 30 to 40 degrees, straining the ACL, so early ACL rehab favors closed chain work and limits open chain extension to a protected arc.

Arthrokinematics and the convex concave rule

Osteokinematics describes the movement of the bones (flexion, abduction). Arthrokinematics describes what the joint surfaces do: roll (new points on one surface meet new points on the other, like a tire rolling), glide or slide (one point on one surface contacts new points on the other, like a skidding tire), and spin (rotation around a fixed point, like the radial head in pronation). Most joints combine roll and glide.

The convex concave rule predicts the direction of glide. When a convex surface moves on a fixed concave surface, it rolls in the direction of the bone's movement but glides in the opposite direction. When a concave surface moves on a fixed convex surface, roll and glide occur in the same direction as the bone movement. Joint mobilization uses this rule: to restore a lost motion, the therapist glides the moving bone in the direction its surface should glide.

Close packed, loose packed and capsular patterns

In the close packed position the joint surfaces are maximally congruent and the capsule and ligaments are taut, so the joint is most stable and least able to be mobilized; it is also the position in which joints are typically injured by high loads and in which stability tests are often done. In the loose packed (resting) position the capsule is most lax, and joint play is greatest, so it is where mobilization usually begins. A capsular pattern is the characteristic proportional loss of motion when the whole capsule is involved (arthritis, adhesive capsulitis); a noncapsular pattern suggests a more local problem such as a ligament adhesion, internal derangement or extra-articular lesion.

Length tension, force velocity and insufficiency

The force a muscle can produce depends on its length. Active tension is greatest near resting length, where actin and myosin overlap optimally; at short lengths the filaments crowd and overlap, and at long lengths few cross bridges can form. Passive tension from connective tissue and the protein titin rises as the muscle is stretched beyond resting length. Total tension is the sum, which is why a muscle on stretch can still resist strongly even as its active force falls.

Active insufficiency occurs when a muscle that crosses two or more joints is shortened across all of them at once and cannot generate enough force to complete the motion: the hamstrings cannot fully flex the knee when the hip is already extended, and the finger flexors make a weak fist when the wrist is flexed. Passive insufficiency occurs when a two joint muscle is lengthened across both joints and its passive tension stops motion at the other end: tight hamstrings limit hip flexion when the knee is extended (the basis of the straight leg raise for hamstring length), and the rectus femoris limits knee flexion when the hip is extended (the Ely test). Tenodesis uses passive insufficiency deliberately: in a person with C6 tetraplegia, active wrist extension pulls the finger flexors taut and closes the hand for grasp, which is why finger flexors are not stretched over an extended wrist in these patients.

The force velocity relationship states that concentric force falls as shortening speed rises, isometric force is intermediate, and eccentric force exceeds isometric and rises with lengthening speed up to a plateau. Eccentric work therefore produces the highest forces at the lowest metabolic cost, and it is also the type most associated with delayed onset muscle soreness.

Muscle actions and roles

A concentric contraction shortens the muscle while it produces force; an eccentric contraction lengthens it under load (the quadriceps controlling descent into a squat or down stairs); an isometric contraction produces force without a change in length. Isokinetic exercise holds velocity constant with a machine that matches resistance to the force produced. A force couple is two or more muscles pulling in different directions to produce rotation: the upper trapezius, lower trapezius and serratus anterior upwardly rotate the scapula, and the deltoid and rotator cuff together elevate the arm while keeping the humeral head centered.

Levers and torque

Torque equals force multiplied by the perpendicular distance from the axis to the line of force (the moment arm). Muscle torque must overcome resistance torque, which is why the same weight feels heavier when held at arm's length and why a long lever arm is used to progress resistance (straight arm versus bent arm raises). The mechanical advantage is the ratio of the force arm to the resistance arm; a value above 1 favors force, below 1 favors speed and range of motion.

Section 3Examination of the cervical and thoracic spine

Screening first

Neck pain is usually benign and mechanical, but the cervical spine sits next to the spinal cord, the vertebral and carotid arteries and the upper airway, so the exam weights screening heavily. Before any test that loads the neck, the therapist screens for fracture (after trauma), upper cervical ligamentous instability, cervical arterial dysfunction, cervical myelopathy, and nonmusculoskeletal sources such as cancer, infection and cardiac referral.

Upper cervical ligament integrity tests include the Sharp-Purser test (with the head slightly flexed, the examiner stabilizes C2 and glides the head posteriorly; a clunk or reduction of symptoms suggests atlantoaxial instability from transverse ligament laxity) and the alar ligament stress test (side bending or rotating the head while palpating the C2 spinous process, which should move immediately). Screening for cervical arterial dysfunction is now framed as a clinical reasoning process built on history and risk factors; positional tests such as sustained end range rotation have poor accuracy and should not be relied on alone.

Imaging after trauma: the Canadian C-spine rule

The Canadian C-spine rule decides whether an alert (Glasgow Coma Scale 15), stable adult trauma patient needs cervical radiographs. It is highly sensitive, so a patient who clears it has a very low probability of a clinically important injury.

Nerve root levels

Remember that cervical roots exit above the vertebra of the same number (the C6 root exits between C5 and C6), and C8 exits between C7 and T1. A C5 to C6 disc herniation therefore affects the C6 root. The C7 root is the most commonly involved in radiculopathy, followed by C6.

Cervical radiculopathy versus myelopathy

Cervical radiculopathy is compression or irritation of a nerve root, usually in the intervertebral foramen by a disc herniation in younger adults or by uncovertebral and facet osteophytes in older adults. It causes unilateral arm pain in a dermatomal pattern, paresthesia, and lower motor neuron signs in that root's distribution: myotomal weakness and a diminished reflex. Resting the hand on the head often eases symptoms (shoulder abduction sign).

The Wainner test item cluster diagnoses cervical radiculopathy with four tests: a positive Spurling test (extension, side bending and gentle compression toward the symptomatic side reproduces arm symptoms), a positive distraction test (lifting the head relieves symptoms), a positive upper limb tension test A (median nerve bias: scapular depression, shoulder abduction, forearm supination, wrist and finger extension, shoulder external rotation, elbow extension, then contralateral cervical side bending), and cervical rotation toward the involved side of less than 60 degrees. Three of four positive gives a moderate shift toward the diagnosis, and all four positive a large one (positive likelihood ratio about 30). The upper limb tension test A is the most sensitive single test, so a negative result helps rule radiculopathy out, while Spurling is the most specific and helps rule it in.

Cervical myelopathy is compression of the spinal cord itself, usually by degenerative spondylosis narrowing the central canal in people over 50. It causes upper motor neuron signs below the level: bilateral hand numbness and clumsiness (difficulty with buttons and handwriting), a broad based, unsteady gait, hyperreflexia, clonus, a positive Hoffmann sign (flicking the middle finger distal phalanx causes thumb and index flexion), a positive Babinski sign, an inverted supinator sign (tapping the brachioradialis tendon produces finger flexion instead of the expected response) and sometimes the Lhermitte sign (neck flexion sends an electric sensation down the spine). A five item cluster (gait deviation, positive Hoffmann, inverted supinator sign, positive Babinski, age over 45) helps: one or fewer positive makes myelopathy unlikely, three or more makes it very likely. Myelopathy is a contraindication to cervical manipulation and needs medical referral.

Neck pain classification and other conditions

Current neck pain practice guidelines classify patients by the dominant impairment: neck pain with mobility deficits (treated with thoracic and cervical mobilization or manipulation and exercise), neck pain with movement coordination impairments (commonly after whiplash; education, active exercise, deep neck flexor training), neck pain with headaches (cervicogenic headache; manual therapy and exercise) and neck pain with radiating pain (radiculopathy; mechanical intermittent traction combined with exercise, neural mobilization). A six item prediction rule for thoracic manipulation in neck pain (recent onset under 30 days, no symptoms below the shoulder, looking up not painful, low fear avoidance, reduced upper thoracic kyphosis, cervical extension under 30 degrees) was not well supported in later validation, but thoracic manipulation remains a reasonable option for mechanical neck pain.

Cervicogenic headache is unilateral, starts in the neck, is provoked by neck postures and shows reduced C1 to C2 rotation on the flexion rotation test.

Whiplash associated disorders follow acceleration and deceleration injury and are graded by the Quebec Task Force system.

Thoracic outlet syndrome is compression of the brachial plexus (neurogenic, by far the most common), subclavian vein or subclavian artery at the interscalene triangle, the costoclavicular space or beneath the pectoralis minor. Neurogenic symptoms most often follow the lower trunk (C8, T1: medial forearm and ulnar hand). The Adson test (head extended and rotated toward the tested side with a deep breath while the radial pulse is monitored) targets the scalenes, the costoclavicular (military brace) test the space between clavicle and first rib, the Wright hyperabduction test the pectoralis minor, and the Roos elevated arm stress test (arms at 90 degrees abduction and external rotation, opening and closing the hands for 3 minutes) reproduces symptoms. Pulse changes occur in many healthy people, so reproduction of symptoms is more meaningful than pulse loss.

In the thoracic spine, think first of visceral referral: cardiac (left chest, arm, jaw, interscapular), gallbladder (right scapula), kidney (flank), aortic dissection (tearing interscapular pain). Minimal trauma in an older adult suggests an osteoporotic compression fracture; a young adult with morning stiffness over 30 minutes that improves with exercise and reduced chest expansion suggests ankylosing spondylitis.

Section 4Examination and management of the lumbar spine and sacroiliac region

Red flags in low back pain

Most low back pain is nonspecific and has a favorable course, and imaging is not recommended in the absence of red flags. The examination therefore begins by excluding the small number of serious causes.

Screen psychosocial risk as well (for example with the STarT Back tool, which stratifies risk of persistent disability), and track outcomes with the Oswestry Disability Index.

Lumbar radiculopathy and neural tension tests

Lumbar roots exit below the pedicle of the vertebra of the same number (the L4 root exits between L4 and L5). Because the common posterolateral disc herniation hits the root that is traversing the disc on its way down, an L4 to L5 posterolateral herniation compresses the L5 root and an L5 to S1 herniation compresses S1. A less common far lateral herniation at L4 to L5 catches the exiting L4 root.

The straight leg raise is positive when it reproduces radicular leg pain between about 30 and 70 degrees; it is sensitive for disc related radiculopathy, so a negative test helps rule it out. The crossed straight leg raise (raising the uninvolved leg reproduces pain in the involved leg) is specific and helps rule it in. The slump test adds trunk and neck flexion; release of neck flexion that eases symptoms confirms neural tension. The prone knee bend (femoral nerve tension) tests the L2 to L4 roots.

Treatment based classification

The treatment based classification (TBC) system sorts patients with low back pain into subgroups that respond to different treatments. The classic version, still widely tested, has four categories.

A shortened two item version of the manipulation rule (symptoms under 16 days and no symptoms below the knee) is also used. The prone instability test is done with the patient prone, trunk on the table and feet on the floor; posterior to anterior pressure provokes pain, and the test is positive when the pain disappears as the patient lifts the legs and contracts the back extensors. The updated TBC reframes care by goal: symptom modulation for highly irritable patients, movement control for those with moderate irritability and motor control deficits, and functional optimization for low irritability patients ready for full loading.

Centralization is the movement of referred symptoms from distal to proximal toward the spine during repeated movements or sustained positions. It is a strong good prognostic sign. Peripheralization, symptoms spreading distally, means that direction should be avoided for now. Pain in the back may increase as leg symptoms centralize; that is still a good response.

Stenosis and spondylolisthesis

Lumbar spinal stenosis narrows the central canal or lateral recesses, usually through disc degeneration, facet hypertrophy and ligamentum flavum thickening in older adults. It produces neurogenic claudication: buttock and leg pain, numbness or heaviness with standing and walking that eases with sitting or flexion (flexion widens the canal and foramina). Patients lean forward on a shopping cart. Helpful findings include age over about 48, bilateral symptoms, leg pain worse than back pain, pain while walking or standing and relief with sitting. A two stage treadmill test separates stenosis from other causes: symptoms begin sooner when walking level than walking on an incline (the incline flexes the trunk).

Management emphasizes flexion based exercise, manual therapy to the spine and hips, cycling or body weight supported treadmill walking, and conditioning; surgery is considered for progressive deficits or failed conservative care.

Spondylolysis is a defect (often a stress fracture) of the pars interarticularis, most often at L5, common in adolescent athletes who repeatedly extend and rotate (gymnastics, diving, football linemen, cricket bowlers). An oblique radiograph shows a "collar on the Scotty dog." Spondylolisthesis is the forward slip of one vertebra on the one below. Isthmic spondylolisthesis follows bilateral pars defects, usually L5 on S1 in younger people; degenerative spondylolisthesis occurs with intact pars from facet arthritis, usually L4 on L5 in older women. The Meyerding grade describes slip as a percentage of the vertebral body width below: grade I up to 25 percent, II 26 to 50, III 51 to 75, IV 76 to 100, and V (spondyloptosis) beyond 100 percent. A palpable step off may be felt. Treatment avoids end range extension early, emphasizes trunk stabilization and hamstring flexibility, and may include bracing and activity modification for an acute pars fracture in an adolescent.

The sacroiliac joint

Sacroiliac pain is felt over the posterior superior iliac spine and buttock, typically below L5, and can refer to the thigh. Single SI tests are unreliable, so the exam expects the Laslett provocation cluster:

• Distraction: supine, posterolateral pressure on both anterior superior iliac spines gaps the front of the joints.
• Thigh thrust: supine with the hip flexed to 90 degrees, a posterior force along the femur shears the SI joint.
• Compression: side lying, downward force on the iliac crest.
• Sacral thrust: prone, posterior to anterior force on the sacrum.
• Gaenslen test: one hip flexed to the chest while the other leg drops off the table into extension, tested on both sides.

Two of the first four positive, or three or more of all tests, supports SI joint pain; all negative makes it unlikely. The cluster works best once a discogenic source has been excluded (no centralization).

Section 5Manual therapy and therapeutic exercise for the spine

Joint mobilization grades

Joint mobilization is a passive, skilled movement of a joint at a speed the patient can stop. The two grading systems the exam uses describe where in the available range the movement occurs and how large it is.

Oscillations run at about one to three per second for 30 to 60 seconds and are repeated. Begin in the resting position for irritable joints, glide according to the convex concave rule or distract perpendicular to the treatment plane, and stabilize the proximal segment.

Effects are both mechanical (stretching capsule, restoring glide) and neurophysiological (spinal and descending pain inhibition, reduced guarding), which is why a thoracic thrust can ease neck pain.

Thrust manipulation: indications, contraindications and precautions

Thrust manipulation (Maitland grade V) is a high velocity, low amplitude movement, often accompanied by an audible cavitation (which is not required for benefit). It has good evidence for acute low back pain in patients who fit the prediction rule, for mechanical neck pain (particularly thoracic thrust) and for cervicogenic headache. The decision to thrust is a risk benefit judgment; rare but serious adverse events, especially with cervical thrust, make screening essential.

Motor control training

People with recurrent low back pain often show delayed activation of the transversus abdominis and atrophy or poor activation of the lumbar multifidus, and people with neck pain show poor endurance of the deep neck flexors (longus colli and longus capitis) with overactivity of the sternocleidomastoid and anterior scalenes. Motor control training first teaches isolated activation of the deep muscles, then integrates it into posture and function.

• Abdominal drawing in maneuver: gently draw the lower abdomen in without moving the spine or holding the breath; a pressure biofeedback unit under the abdomen in prone (starting near 70 mmHg) should drop a few mmHg with a correct contraction.
• Multifidus: palpated contraction in prone or side lying, progressed to quadruped arm and leg lifts (bird dog).
• Craniocervical flexion test and training: supine with a pressure unit under the neck inflated to 20 mmHg, the patient nods to raise the pressure in steps of 2 mmHg up to 30 mmHg, holding each for 10 seconds without superficial muscle substitution.
• Progression: supine bridges, side planks, curl ups (the classic "big three" emphasize trunk endurance with low spinal load), then standing, lifting, and sport or work specific tasks with a neutral spine.

General exercise works about as well as specific motor control training for many with chronic low back pain; progressive, functional active exercise is the key.

McKenzie principles

Mechanical Diagnosis and Therapy, developed by Robin McKenzie, uses repeated movements and sustained positions to classify spinal pain into three mechanical syndromes.

The typical extension progression for a posterior derangement is prone lying, prone on elbows, prone press ups, then standing extension. A lateral shift (the trunk displaced away from the painful side in most cases) is corrected before extension. When extension peripheralizes symptoms, it stops; flexion or lateral movements are explored instead.

Return to function

Current guidelines recommend staying active, reassuring education (including pain neuroscience education for persistent pain), exercise, and manual therapy combined with exercise; passive modalities and rest are not primary care. For fear of movement, graded activity (quota based increases regardless of pain) and graded exposure (gradual confrontation of feared movements) reduce disability, and work conditioning or hardening prepares the return to work.

Words worth knowing

Musculoskeletal: The Upper Extremity

The upper extremity questions on the NPTE rarely ask you to name a muscle; they hand you a patient with a painful arc, a weak grip or a numb ring finger and ask what is wrong, what to test next and what is safe to do this week. Shoulder pathology, postoperative protocols, elbow and hand injuries and peripheral nerve lesions form a large and predictable block of the musculoskeletal content. This chapter organizes that block around the decisions you will make on the exam and in clinic.

Section 1The shoulder complex

Joints and the scapulohumeral rhythm

The shoulder complex is four articulations working as one unit: the glenohumeral joint, the sternoclavicular joint, the acromioclavicular joint and the functional scapulothoracic articulation. The glenohumeral joint is a ball and socket with a shallow glenoid that covers only about a quarter to a third of the humeral head; the labrum deepens it, and the capsule, glenohumeral ligaments and rotator cuff supply the rest of its stability. That trade of bony stability for mobility is the reason the shoulder dislocates more than any other large joint and the reason rotator cuff function matters so much.

Full elevation of the arm (about 180 degrees) is shared between the glenohumeral joint and the scapula. The classic teaching ratio is 2:1: about 120 degrees of glenohumeral motion and 60 degrees of scapular upward rotation. The ratio is not constant through the range; in the first 30 degrees or so of abduction (the setting phase) the scapula moves little and variably, and most scapular contribution comes later. The clavicle elevates about 30 to 40 degrees at the sternoclavicular joint and rotates posteriorly about its long axis, which allows the scapula to finish upward rotation. If the clavicle cannot rotate (for example after acromioclavicular fusion), elevation is limited to roughly 110 to 120 degrees.

Two arthrokinematic rules drive many questions. The humeral head is convex moving on a concave glenoid, so the head glides opposite to the direction the shaft moves: during abduction the head rolls up and glides inferiorly; during flexion and internal rotation it glides posteriorly; during extension and external rotation it glides anteriorly. To gain abduction you therefore mobilize the humerus inferiorly; to gain external rotation, the traditional rule says anterior glide, although several studies show posterior glides also improve external rotation in adhesive capsulitis. Full elevation also requires external rotation of the humerus so the greater tubercle clears the acromion.

Force couples and scapular dyskinesis

Scapular upward rotation is produced by a force couple of the upper trapezius, lower trapezius and serratus anterior. The serratus also holds the medial border against the thorax and posteriorly tilts the scapula. At the glenohumeral joint the deltoid pulls the humerus upward, and the rotator cuff (especially infraspinatus, teres minor and subscapularis) compresses and depresses the head so the deltoid produces rotation rather than superior translation. When the cuff is weak or torn, the deltoid shears the head toward the acromion and the subacromial space narrows.

Scapular dyskinesis is any altered position or motion of the scapula: prominence of the medial border, early or excessive shrugging, or poor control on lowering. True winging of the medial border at rest or during a wall push up suggests long thoracic nerve palsy (serratus anterior); lateral winging with a depressed, laterally displaced scapula suggests spinal accessory nerve injury (trapezius), often after posterior triangle surgery. Dyskinesis from weakness or tightness (tight pectoralis minor, weak lower trapezius and serratus) is far more common than nerve palsy and responds to targeted exercise.

Subacromial pain and rotator cuff disease

The older term impingement described compression of the supraspinatus tendon and subacromial bursa between the humeral head and the coracoacromial arch. Current practice increasingly uses subacromial pain syndrome or rotator cuff related shoulder pain, because most of the problem is a tendinopathy driven by load and age rather than mechanical pinching. The exam may still use the Neer stages, so know them: stage I, edema and hemorrhage, typically under 25 years, reversible; stage II, fibrosis and tendinitis, about 25 to 40 years; stage III, bone spurs and tendon rupture, over 40 years.

External impingement is classified as primary (structural narrowing: hooked type III acromion, acromioclavicular osteophytes) or secondary (functional narrowing from instability, cuff weakness, scapular dyskinesis or posterior capsule tightness). Internal impingement is a different entity: in the throwing athlete in abduction and external rotation, the articular side of the posterior supraspinatus and infraspinatus is pinched between the greater tuberosity and the posterosuperior glenoid and labrum. Throwers often show glenohumeral internal rotation deficit (GIRD), a loss of internal rotation of 20 degrees or more compared with the other side (or a loss of total arc), linked to posterior capsule tightness; the sleeper stretch and cross body stretch are the usual treatments.

Typical findings of rotator cuff related pain: lateral shoulder or upper arm pain (deltoid region), worse with overhead reaching and lying on the side, a painful arc between about 60 and 120 degrees, pain and possible weakness on resisted abduction and external rotation, and full or near full passive motion. Passive motion that is well preserved separates cuff disease from adhesive capsulitis.

Full thickness tears increase with age; many are asymptomatic in people over 60. The supraspinatus is torn most often. A large tear produces weakness and the inability to hold the arm raised (positive drop arm test), external rotation lag sign and hornblower sign (teres minor). An acute tear in a younger person after trauma, or an acute traumatic tear with marked weakness in any age, warrants early surgical referral; degenerative tears in older adults are first managed with exercise, which many patients do as well with as with surgery.

Conservative management of cuff related pain emphasizes progressive loading of the cuff and scapular muscles: isometrics for pain relief early, then isotonic external rotation, scaption below shoulder height, rows, serratus punch and lower trapezius work, progressing to overhead and functional loading. Add posterior capsule stretching when internal rotation is limited, thoracic mobility and education on load management. Subacromial decompression surgery has not been shown to beat exercise for most patients.

Shoulder instability

Instability ranges from subtle subluxation to frank dislocation. A useful classic split is TUBS (traumatic, unidirectional, Bankart lesion, often requires surgery) versus AMBRI (atraumatic, multidirectional, bilateral, treated with rehabilitation, and inferior capsular shift if rehab fails). About 95 percent of dislocations are anterior, from a force on the abducted and externally rotated arm. Associated lesions: a Bankart lesion (avulsion of the anteroinferior labrum and inferior glenohumeral ligament, sometimes with a bony fragment) and a Hill Sachs lesion (impaction fracture of the posterolateral humeral head against the glenoid rim). The axillary nerve is the nerve most often injured with anterior dislocation and proximal humerus fracture: check deltoid strength and sensation over the lateral shoulder (the regimental badge area). Posterior dislocation is associated with seizures and electric shock; the arm is held in internal rotation and cannot be externally rotated.

Recurrence after a first anterior dislocation is very high in young athletes (often quoted as well over half under age 20 to 25) and much lower in older adults, in whom an associated cuff tear is more common. SLAP lesions (superior labrum anterior to posterior) cause deep pain and clicking in throwers.

Adhesive capsulitis

Adhesive capsulitis (frozen shoulder) is inflammation followed by fibrosis of the glenohumeral capsule, producing painful, progressive loss of both active and passive motion in a capsular pattern: external rotation lost most, then abduction, then internal rotation (some sources list flexion with internal rotation; external rotation is always first). It is most common in people aged 40 to 65, in women, and strongly associated with diabetes mellitus (and thyroid disease); diabetic cases tend to be more severe and prolonged. The course is often described in stages: freezing (painful, pain dominant, motion beginning to decrease), frozen (stiffness dominant, pain easing), and thawing (gradual return of motion), lasting a year or more in total.

Management follows tissue irritability. In the high irritability stage use pain relieving modalities, gentle low grade mobilization (grades I and II), pendulums and pain free active assisted range; an intra articular corticosteroid injection combined with mobility exercise gives faster short term improvement and is recommended by the clinical practice guideline. As irritability falls, progress to sustained end range stretching and grade III and IV mobilization.

Special tests of the shoulder

No single shoulder test is diagnostic. Clusters work better: for a full thickness supraspinatus tear, a painful arc plus a positive drop arm test plus weakness in external rotation raises the probability considerably; for subacromial pain, a combination of Hawkins Kennedy, painful arc and infraspinatus weakness performs well. Use apprehension and relocation together for anterior instability.

Section 2Shoulder surgery and rehabilitation

Principles that apply to every shoulder protocol

Postoperative shoulder rehabilitation is governed by three questions: what tissue was repaired or replaced, what motion or load stresses that tissue, and how long that tissue needs before it tolerates the stress. Tendon to bone healing after rotator cuff repair takes roughly 12 weeks to reach useful strength and continues to mature for months; labral and capsular repairs need about 6 weeks of protection; a subscapularis tenotomy or peel during arthroplasty must be protected from stretch and active load for about 6 weeks. When a stem gives a protocol, follow it; when it does not, apply the tissue logic.

Progression between phases should be criterion based as well as time based. Typical criteria: pain controlled at rest and with the current exercises, passive range targets reached, no signs of a failed repair (sudden loss of active motion, a new pop with weakness), adequate strength (often expressed as a percentage of the uninvolved side) and normal scapular control before overhead or plyometric loading.

Rotator cuff repair

The repaired supraspinatus is under tension when the arm is adducted and is stressed most by active elevation and by passive motion beyond what the surgeon allows. Retear rates rise with age, tear size, fatty infiltration of the muscle, smoking and diabetes, and most retears happen in the first 3 to 6 months. Larger repairs and poorer tissue are progressed more slowly.

Stabilization procedures

An arthroscopic Bankart repair reattaches the anteroinferior labrum and capsule to the glenoid rim. The tissue at risk is stretched by external rotation combined with abduction and by extension. Typical restrictions: sling for about 4 to 6 weeks; external rotation limited (often to about 30 degrees at the side in the first weeks, progressing gradually); no combined abduction and external rotation (the apprehension position) for about 6 weeks or longer; no extension behind the body. Isometrics and scapular work begin early; strengthening progresses from about 6 to 12 weeks; contact and overhead sport usually waits 4 to 6 months. A Latarjet procedure (transfer of the coracoid with the conjoined tendon to the anterior glenoid) is used for glenoid bone loss and recurrent instability; it protects the subscapularis and the bone block. Posterior stabilization reverses the logic: avoid internal rotation, horizontal adduction and flexion with internal rotation (posterior capsule stress).

A SLAP repair protects the biceps anchor: avoid resisted elbow flexion and forearm supination and avoid loaded biceps activity for about 6 weeks; limit external rotation in abduction early, because the peel back mechanism stresses the superior labrum. A biceps tenodesis also avoids resisted elbow flexion and supination for about 6 weeks.

Total shoulder arthroplasty

An anatomic total shoulder arthroplasty replaces the humeral head and resurfaces the glenoid. It requires a functioning rotator cuff and is used for glenohumeral osteoarthritis with an intact cuff. The deltopectoral approach detaches the subscapularis (tenotomy, peel or lesser tuberosity osteotomy), so the main early precautions protect that repair: limit passive external rotation (often to about 30 degrees, per surgeon) for about 6 weeks, no active internal rotation or resisted internal rotation for about 6 weeks, no lifting heavier than a cup of coffee, no supporting body weight with the hand (such as pushing up from a chair). The operated arm is typically supported so the elbow sits slightly forward of the trunk when lying supine, avoiding extension. Subscapularis failure produces weakness in internal rotation, a positive lift off or belly press and anterior instability.

A hemiarthroplasty replaces only the humeral head (for some fractures or when the glenoid cannot be resurfaced). After fracture fixation or hemiarthroplasty, tuberosity healing is the main concern, so active motion often waits until the tuberosities have united.

Reverse total shoulder arthroplasty

A reverse total shoulder arthroplasty (rTSA) puts a ball (the glenosphere) on the glenoid and a socket on the humerus. This moves the center of rotation medially and inferiorly, lengthening the deltoid lever arm and tensioning the deltoid so that it can elevate the arm without a rotator cuff. It is indicated for cuff tear arthropathy, massive irreparable cuff tears with pseudoparalysis, complex proximal humerus fractures in older adults and failed previous arthroplasty. Because rehabilitation depends on the deltoid, the emphasis is on deltoid and scapular strengthening; strengthening the absent cuff is not the goal, and full external and internal rotation are often not achievable.

The key risk is dislocation, which typically occurs with the arm in extension, adduction and internal rotation together, the position used to reach behind the back to tuck in a shirt or perform toileting hygiene, or to push up from a chair with the arm behind the body. Classic early precautions (about 12 weeks): no combined shoulder extension, adduction and internal rotation; no reaching behind the back; no extension past neutral (keep the elbow in front of the trunk, using a pillow under the elbow in supine); no supporting body weight with the operated arm; no lifting more than a light object. The acromion takes much more deltoid load after rTSA, so new acute pain over the acromion with loss of elevation suggests an acromial stress fracture.

Section 3The elbow and forearm

Lateral and medial epicondylalgia

Lateral epicondylalgia (tennis elbow) is a degenerative tendinopathy of the common extensor origin, chiefly the extensor carpi radialis brevis. Histology shows disorganized collagen and new vessels rather than inflammatory cells, which is why the terms tendinopathy or epicondylalgia are preferred to epicondylitis. It peaks between 35 and 55 years and is linked to repetitive gripping and wrist extension, in manual work more than in tennis. Findings: pain at or just distal to the lateral epicondyle, pain with resisted wrist extension and resisted middle finger extension, pain with passive wrist flexion with the elbow extended, and reduced pain free grip strength (the most useful outcome measure). Cozen test (resisted wrist extension with a fist) and Mill test (passive stretch into wrist flexion, pronation and elbow extension) reproduce pain.

Management: load modification, progressive tendon loading (isometrics for pain, then eccentric and concentric wrist extensor strengthening), a counterforce brace placed distal to the painful area, manual therapy including mobilization with movement of the elbow, and attention to cervical and thoracic contributions. Corticosteroid injection gives good short term relief but worse outcomes and more recurrence at one year than physical therapy or waiting, a classic exam point.

Medial epicondylalgia (golfer's elbow) affects the common flexor and pronator origin (pronator teres and flexor carpi radialis). Pain is reproduced by resisted wrist flexion and pronation and by passive wrist extension with elbow extension. It is often accompanied by ulnar neuropathy at the elbow, so always check ulnar nerve sensation and intrinsic strength.

Ulnar collateral ligament injury

The ulnar collateral ligament (UCL), especially its anterior bundle, is the primary restraint to valgus stress between about 20 and 120 degrees of elbow flexion. During the late cocking and early acceleration phases of throwing, huge valgus torque stretches the UCL, compresses the lateral radiocapitellar joint and shears the posteromedial olecranon (the valgus extension overload pattern). Overhead throwers present with medial elbow pain during throwing, loss of velocity and sometimes ulnar paresthesia. Tests: valgus stress test at about 20 to 30 degrees of flexion, milking maneuver and the moving valgus stress test (pain between about 70 and 120 degrees of flexion as the elbow is extended under valgus load). Partial tears are rehabilitated; complete tears in throwers who wish to return are often reconstructed with a tendon graft (commonly palmaris longus). After UCL reconstruction, valgus stress is avoided for months, a hinged brace is used early, and an interval throwing program usually begins around 4 months, with return to competitive pitching often taking 12 months or more. In young throwers the same forces cause medial epicondyle apophysitis (Little League elbow); pitch count limits and rest are the main prevention.

Fractures and dislocations around the elbow

The elbow stiffens quickly, so early protected motion matters, and its neurovascular structures are vulnerable. Know these patterns:

• Supracondylar humerus fracture: the most common elbow fracture in children, from a fall on an outstretched hand with the elbow hyperextended. Risks: brachial artery injury, anterior interosseous nerve palsy (most common nerve injury; cannot make the OK sign), and Volkmann ischemic contracture from compartment syndrome of the forearm flexors. Pain with passive finger extension, increasing pain out of proportion and tense forearm swelling are emergencies.
• Radial head fracture: the most common elbow fracture in adults, from a fall on an outstretched hand. Nondisplaced fractures are treated with brief sling use and early active motion within days. Look for associated injuries: the Essex Lopresti lesion (radial head fracture with interosseous membrane disruption and distal radioulnar joint injury).
• Olecranon fracture: from a direct fall on the elbow; displaced fractures need fixation because the triceps pulls the fragment proximally. Avoid resisted elbow extension until healed.
• Elbow dislocation: usually posterior, the second most commonly dislocated major joint in adults. The terrible triad is posterior dislocation with radial head and coronoid fractures. Stable reductions are moved early in a hinged brace; loss of extension is the commonest long term problem.
• Monteggia (proximal ulna fracture with radial head dislocation; posterior interosseous nerve at risk) and Galeazzi (distal radius shaft fracture with distal radioulnar joint dislocation) fracture dislocations.

Heterotopic ossification and myositis ossificans of the brachialis are risks after elbow trauma, especially if the elbow is forcefully stretched. Avoid aggressive passive stretching after elbow trauma; use active motion, gentle low load prolonged stretch and static progressive orthoses instead.

Nerve entrapments around the elbow

Three nerves cross the elbow, and each has typical entrapment sites. Recognizing the motor and sensory pattern localizes the lesion.

Section 4The wrist and hand

Carpal tunnel syndrome

Carpal tunnel syndrome (CTS) is compression of the median nerve beneath the transverse carpal ligament, the most common entrapment neuropathy. Risk factors include female sex, pregnancy, diabetes, hypothyroidism, rheumatoid arthritis, obesity and repetitive forceful wrist flexion with vibration. Symptoms: numbness and tingling in the thumb, index, middle and radial half of the ring finger, worse at night and relieved by shaking the hand (the flick sign); clumsiness; in advanced cases thenar atrophy and weakness of abductor pollicis brevis and opponens pollicis. The palmar cutaneous branch leaves the median nerve proximal to the tunnel, so sensation over the thenar eminence is spared in CTS (thenar numbness suggests a more proximal lesion).

Tests include Phalen (sustained wrist flexion for up to 60 seconds reproduces symptoms), Tinel at the carpal tunnel, and the carpal compression test (Durkan), which is among the more sensitive. Nerve conduction studies show prolonged distal latency of the median nerve. Conservative care, recommended by the clinical practice guideline for mild to moderate cases: a neutral wrist orthosis worn at night, education to avoid sustained end range wrist positions, nerve and tendon gliding, and possibly corticosteroid injection. Thenar atrophy or persistent sensory loss warrants surgical referral for carpal tunnel release, after which scar management, gentle motion and gradual grip strengthening follow; pillar pain at the base of the palm is common for weeks.

De Quervain tenosynovitis and other tendinopathies

De Quervain tenosynovitis is thickening of the tendon sheath of the first dorsal compartment, containing the abductor pollicis longus and extensor pollicis brevis, at the radial styloid. It is common in new parents lifting infants, in middle aged women and with repetitive thumb use. Finkelstein test (examiner deviates the wrist ulnarly while the thumb is held flexed) and the more specific Eichhoff variant (patient grasps the thumb in a fist before ulnar deviation) reproduce pain over the radial styloid; the WHAT test (wrist hyperflexion and abduction of the thumb) is also described. Treatment: a thumb spica orthosis that leaves the interphalangeal joint free, activity modification, and corticosteroid injection, which is often effective. Distinguish it from intersection syndrome (pain and crepitus about 4 to 6 cm proximal to the wrist where the first compartment crosses the second, often in rowers) and from first carpometacarpal osteoarthritis (positive grind test at the thumb base).

Trigger finger is a flexor tendon catching at the A1 pulley, common in diabetes.

Wrist fractures and instability

After a distal radius fracture, the cast or orthosis is typically worn about 6 weeks. During that time, active motion of the fingers, elbow and shoulder prevents stiffness and swelling. After immobilization, active and active assisted wrist and forearm motion progress to strengthening. Monitor for complex regional pain syndrome: burning pain out of proportion, swelling, color and temperature change, and hypersensitivity. Early recognition, desensitization, graded motor imagery and active use are key.

Tendon injuries and flexor zones

The flexor tendon zones guide prognosis and protocols. Zone II, between the A1 pulley at the distal palmar crease and the insertion of flexor digitorum superficialis at the middle phalanx, contains both flexor tendons inside a tight fibro osseous sheath, so adhesions form easily. It was historically called no man's land. Zone I lies distal to the FDS insertion (FDP only; a jersey finger is an avulsion of FDP, most often of the ring finger, when a grabbing finger is forcibly extended). Zone III is the palm, zone IV the carpal tunnel and zone V the wrist and forearm.

After flexor tendon repair, the hand is placed in a dorsal blocking orthosis with the wrist in slight flexion (or neutral), MCP joints flexed about 50 to 70 degrees and interphalangeal joints extended against the orthosis. The aim is to permit tendon gliding without tension on the repair. Classic early protocols: passive flexion with active extension within the orthosis (Duran style passive motion; Kleinert style rubber band traction) or early active motion (place and hold or controlled active flexion), now favored for strong multistrand repairs. Avoid active gripping, passive extension of the wrist and fingers together and resisted flexion for about 6 to 8 weeks; light resistance usually begins around 8 weeks and full strengthening around 12 weeks. A repaired tendon is weakest around days 5 to 21, when rupture risk peaks.

Extensor injuries: a mallet finger is disruption of the terminal extensor tendon at the distal phalanx (zone I) and is treated with continuous DIP extension splinting for about 6 to 8 weeks with the PIP free; any flexion of the DIP during that time restarts the clock. A rupture of the central slip (zone III) allows the lateral bands to slip volarly and leads to a boutonniere deformity; it is splinted with the PIP in extension and the DIP free to flex actively.

Deformities

Splinting principles

Orthoses immobilize (rest inflamed or repaired tissue), mobilize (apply low load prolonged stress to lengthen tissue, as with dynamic or static progressive designs) or restrict motion. The safe position or intrinsic plus position for immobilizing the hand is wrist in about 20 to 30 degrees of extension, MCP joints in 70 to 90 degrees of flexion and IP joints in full extension, which keeps the MCP collateral ligaments and the IP volar plates at length so the hand does not stiffen. A resting hand orthosis in a functional position is used for rheumatoid arthritis flares. Check every orthosis for pressure points over bony prominences, especially in insensate skin, and teach a wearing schedule and skin checks.

Section 5Peripheral nerve injuries of the upper limb

The brachial plexus

The brachial plexus forms from the ventral rami of C5 to T1 and is organized as roots, trunks, divisions, cords and terminal branches (a common memory aid is "Read That Darn Cadaver Book"). C5 and C6 join as the upper trunk, C7 continues as the middle trunk, and C8 and T1 form the lower trunk. Each trunk splits into anterior and posterior divisions. The three posterior divisions form the posterior cord (axillary and radial nerves), the anterior divisions of the upper and middle trunks form the lateral cord (musculocutaneous nerve and the lateral root of the median nerve), and the anterior division of the lower trunk forms the medial cord (ulnar nerve and the medial root of the median nerve). Branches from the roots include the dorsal scapular (C5, rhomboids) and long thoracic (C5 to C7, serratus anterior); from the upper trunk the suprascapular nerve (supraspinatus and infraspinatus).

Erb palsy (upper trunk, C5 and C6) results from forced separation of the head and shoulder (birth with shoulder dystocia, motorcycle falls). The deltoid, cuff, biceps and brachialis are weak, producing the waiter's tip posture. Klumpke palsy (lower trunk, C8 and T1) results from traction on the abducted arm (grabbing a branch while falling, breech birth). It weakens the intrinsic hand muscles and long finger flexors and may include Horner syndrome (ptosis, miosis, anhidrosis) if T1 sympathetic fibers are injured, which also suggests a root avulsion with a poor prognosis. Thoracic outlet syndrome most commonly compresses the lower trunk, giving ulnar side symptoms; provocative tests (Adson, Roos elevated arm stress test, Wright hyperabduction) have poor specificity.

Radial, median and ulnar nerve lesions

Froment sign: when pinching paper between thumb and index finger, the thumb IP joint flexes because flexor pollicis longus (median) substitutes for a weak adductor pollicis (ulnar). Wartenberg sign: the little finger rests abducted from weak third palmar interosseous. The ulnar paradox: a more proximal ulnar lesion produces less clawing because FDP to the ring and little fingers is also paralyzed, so the IP joints are not pulled into flexion. The same logic applies to median lesions; a high median lesion causes the benediction posture on attempting a fist, while a low median lesion leaves finger flexion intact.

Seddon classification, recovery and testing

After axonal injury the distal segment undergoes Wallerian degeneration. Regeneration proceeds at roughly 1 mm per day, so a lesion 30 cm above a muscle needs about 10 months to reach it; motor end plates degenerate if reinnervation takes much beyond 12 to 18 months, so proximal lesions recover less. An advancing Tinel sign along the nerve tracks regrowth. Needle EMG should be delayed about 3 weeks after injury, because fibrillation potentials and positive sharp waves take that long to appear. Sensory recovery typically returns in sequence: pain and temperature, then touch, then moving two point discrimination, then static two point discrimination. Test with Semmes Weinstein monofilaments (the 4.31 filament marks the threshold of normal light touch on the hand in common teaching, and inability to feel 6.65 means loss of protective sensation) and two point discrimination (normal fingertip static value about 6 mm or less).

Rehabilitation during recovery: protect anesthetic skin with visual checks and education (burns and pressure injury are the main hazards), maintain passive range and prevent contracture with orthoses (a wrist cock up orthosis or dynamic extension orthosis for radial palsy, a thumb web spacer for median palsy, an anticlaw MCP blocking orthosis for ulnar palsy), avoid overstretching denervated muscle, begin active assisted and then resisted exercise as muscle reinnervates, and use desensitization and sensory reeducation.

Words worth knowing

Musculoskeletal: The Lower Extremity and Gait

Most of what a physical therapist does for the lower extremity comes down to one question: can this patient bear weight and walk safely, and if not, why not? The NPTE tests that question through hip and knee arthroplasty precautions, ligament and meniscus injuries, ankle sprains, the gait cycle and its deviations, and weight bearing orders after fracture. This chapter ties the tissue, the protocol and the gait pattern together so you can reason from findings to the safest correct answer.

Section 1The hip

Hip osteoarthritis

The hip is a deep ball and socket joint whose stability comes mainly from bone, the labrum and strong capsular ligaments (iliofemoral, pubofemoral and ischiofemoral, all tightening in extension). Osteoarthritis of the hip is a disease of the whole joint: cartilage loss, subchondral sclerosis, osteophytes and capsular thickening. The classic presentation is groin or anterior thigh pain (sometimes referred to the knee), morning stiffness lasting less than an hour, pain with weight bearing and a capsular pattern of loss: internal rotation and flexion most, then abduction, with extension also limited. The hip clinical practice guideline lists features that support the diagnosis in adults over 50: moderate anterior or lateral hip pain with weight bearing, morning stiffness under an hour, and hip internal rotation and flexion each limited by more than 15 degrees compared with the other side.

Evidence based treatment includes patient education and weight management, manual therapy (mobilization and manipulation) for short term pain relief and motion, flexibility and strengthening (especially hip abductors, extensors and quadriceps), functional and balance training and an assistive device when needed. A cane is held in the hand opposite the painful hip: it moves with the involved leg and reduces the abductor force needed on the stance side, lowering joint reaction force. Carrying a load in the hand on the same side as the painful hip also reduces abductor demand, whereas carrying it on the opposite side increases it.

Femoroacetabular impingement and labral tears

Femoroacetabular impingement (FAI) is abnormal contact between the femoral head neck junction and the acetabular rim. A cam lesion is an aspherical bump at the femoral head neck junction, more common in young athletic men; it is jammed into the acetabulum in flexion and internal rotation, shearing the cartilage and labrum. A pincer lesion is acetabular overcoverage (retroversion or a deep socket), more common in middle aged women, where the rim crushes the labrum. Mixed forms are common. Patients report groin pain with prolonged sitting, deep squatting, pivoting and getting in and out of a car. The FADIR test (flexion, adduction, internal rotation) is very sensitive, so a negative test helps rule out intra articular pathology, but it is not specific.

A labral tear causes groin pain with mechanical symptoms (clicking, catching, locking), often with a C sign (the patient cups the lateral hip with thumb and fingers). Most occur in the anterosuperior labrum. Initial treatment is activity modification, avoiding end range flexion and rotation under load, core and hip strengthening and movement retraining. After arthroscopic labral repair or osteoplasty, typical precautions are protected weight bearing (often flat foot or partial weight bearing for 2 to 4 weeks), limits on flexion (often to about 90 degrees) and on external rotation and extension early (to protect the capsule), and avoidance of active straight leg raising and loaded hip flexion, which irritate the iliopsoas.

Lateral hip pain and other conditions

Greater trochanteric pain syndrome (gluteal tendinopathy, with or without trochanteric bursitis) causes lateral hip pain worse lying on the side, climbing stairs and standing on one leg. Single leg stance held for 30 seconds reproducing lateral hip pain is a useful test. Avoid compressive positions (crossing legs, hip adduction stretches such as the iliotibial band stretch) and progress isometric and then isotonic abductor loading. Remember hip conditions in children and adolescents: Legg Calve Perthes disease (avascular necrosis of the femoral head, boys about 4 to 8 years, painless limp), slipped capital femoral epiphysis (obese adolescents, often boys about 10 to 16, knee or groin pain, obligatory external rotation with hip flexion; a non weight bearing emergency referral) and developmental dysplasia (Ortolani and Barlow tests in infants).

Hip fractures

Hip fractures in older adults usually follow a fall from standing height in a person with osteoporosis. The leg is classically shortened and externally rotated. Location determines treatment because of the blood supply to the femoral head, which comes mainly from the medial circumflex femoral artery through retinacular vessels along the neck:

• Femoral neck (intracapsular) fractures can disrupt this supply, leading to avascular necrosis and nonunion. Displaced neck fractures in older adults are usually treated with hemiarthroplasty or total hip arthroplasty; nondisplaced ones with screws.
• Intertrochanteric and subtrochanteric (extracapsular) fractures have good blood supply and are fixed with a sliding hip screw or intramedullary nail.

Modern fixation and arthroplasty generally allow weight bearing as tolerated immediately, and early mobilization (within 24 to 48 hours) reduces complications such as pneumonia, pressure injury, deep vein thrombosis and delirium. Mortality within a year is high, and many patients do not return to prior function, so balance training, strengthening and fall prevention are core goals. If a hemiarthroplasty was done through a posterior approach, posterior hip precautions apply.

Total hip arthroplasty and precautions by approach

The precautions after total hip arthroplasty (THA) follow the capsule and muscles that were cut, because those positions are the ones that let the femoral head lever out of the socket. Many surgeons now relax or drop precautions, especially with the anterior approach, so the surgeon's orders always come first; on the exam, apply the classic set for the stated approach.

Early rehabilitation after THA: ankle pumps, quadriceps and gluteal sets, heel slides within precautions, bed mobility and transfers using adaptive equipment (reacher, sock aid, long handled shoe horn), gait training with a walker progressing to a cane, and stair training (up with the good, down with the bad: the uninvolved leg leads going up, the involved leg and assistive device lead going down). Most cemented and modern cementless implants allow weight bearing as tolerated. Watch for DVT (calf pain, swelling, warmth; the Wells criteria guide referral), dislocation (sudden pain, a shortened and rotated limb, inability to bear weight), infection and leg length discrepancy.

Section 2The knee

Ligament injuries

The anterior cruciate ligament (ACL) resists anterior translation of the tibia on the femur and rotational loads. Most tears are noncontact: deceleration, cutting or landing with the knee near extension, valgus collapse and tibial rotation. Patients report a pop, rapid swelling (hemarthrosis within hours) and giving way. Women have a higher risk, linked to landing mechanics, neuromuscular control and other factors; injury prevention programs that train landing, cutting and hamstring strength reduce ACL injuries. The unhappy triad classically combines ACL, MCL and medial meniscus tears, although lateral meniscus tears are actually more common with acute ACL injury.

The posterior cruciate ligament (PCL) resists posterior tibial translation; it is torn by a fall on a flexed knee with the foot plantarflexed or a dashboard injury. Isolated PCL tears are usually managed nonoperatively with quadriceps emphasis, since the quadriceps pulls the tibia anteriorly; avoid isolated resisted hamstring work early because it pulls the tibia posteriorly. The medial collateral ligament (MCL) resists valgus stress and is injured by a blow to the lateral knee; most isolated MCL tears heal well with a hinged brace and early motion. The lateral collateral ligament resists varus and is often injured with the posterolateral corner, which may need surgery.

Meniscus injuries

The menisci deepen the tibial plateau, spread load and assist stability. The medial meniscus is attached to the MCL and joint capsule, less mobile, and injured more often; the lateral meniscus is more mobile. Only the outer third (the red zone) has a good blood supply, so peripheral tears can be repaired while inner (white zone) tears are usually trimmed. Patients report twisting on a loaded, flexed knee, delayed swelling (over 24 hours), joint line pain and mechanical symptoms (locking, catching). A truly locked knee that cannot extend suggests a displaced bucket handle tear and needs prompt surgical referral. Degenerative tears in middle aged and older adults respond to exercise as well as to arthroscopic partial meniscectomy in most trials. After partial meniscectomy, weight bearing as tolerated and rapid progression are usual. After meniscus repair, protect the repair: limited weight bearing or a brace locked in extension for weight bearing (often about 4 to 6 weeks), limited flexion (often to 90 degrees), and no deep squatting or loaded flexion beyond 90 for about 3 to 4 months.

Patellofemoral pain

Patellofemoral pain is diffuse anterior knee pain around or behind the patella, worse with squatting, stairs (especially descending), running and prolonged sitting (the movie sign). It is common in adolescents and young adults, especially women. Contributing factors include weak hip abductors and external rotators (allowing dynamic knee valgus and femoral internal rotation under the patella), quadriceps weakness, reduced flexibility and excessive load. The Q angle (the angle between a line from the ASIS to the center of the patella and a line from the center of the patella to the tibial tubercle) averages about 13 degrees in men and 18 degrees in women; a larger angle increases lateral pull. The clinical practice guideline supports combined hip and knee strengthening as the core intervention, plus patellar taping and foot orthoses for short term relief, and education on load management. Squat and step exercises are often started in a pain free arc (open chain knee extension is gentler on the patellofemoral joint from 90 to 45 degrees and closed chain exercise from 0 to 45 degrees).

Related conditions: patellar tendinopathy (jumper's knee, pain at the inferior pole with jumping, treated with progressive isometric and heavy slow resistance or eccentric decline squats), Osgood Schlatter disease (tibial tubercle apophysitis in adolescents), iliotibial band syndrome (lateral knee pain in runners, often near 30 degrees of flexion), and patellar dislocation (usually lateral, in young women, often with a medial patellofemoral ligament tear).

ACL reconstruction rehabilitation

Common grafts are bone patellar tendon bone (strong bony fixation, more anterior knee pain and kneeling pain), hamstring tendon (less anterior knee pain, avoid aggressive hamstring loading for about 6 to 8 weeks) and quadriceps tendon. Grafts go through ligamentization: they are weakest about 6 to 12 weeks after surgery as the graft revascularizes, so although the patient feels well, the graft is vulnerable. Accelerated protocols are standard: immediate weight bearing as tolerated (if no meniscus repair), early full extension (loss of extension is the most troublesome complication; a cyclops lesion or arthrofibrosis may be the cause), quadriceps activation with neuromuscular electrical stimulation, and closed chain exercise early.

Open chain knee extension stresses the ACL graft most between about 0 and 45 degrees (the quadriceps pulls the tibia forward near extension), so it is commonly restricted early to 90 to 45 degrees; closed chain exercise in roughly 0 to 60 degrees produces low graft strain because of hamstring cocontraction and compression. Running usually begins around 3 months once there is no effusion, full motion and adequate strength. Return to sport is generally considered no earlier than about 9 months, when a battery of criteria is met: quadriceps and hamstring limb symmetry index of 90 percent or more, hop test symmetry of 90 percent or more (single, triple, crossover and timed hops), full motion, no effusion and psychological readiness. Returning before 9 months and with poor strength symmetry substantially increases reinjury risk.

Total knee arthroplasty

Total knee arthroplasty (TKA) relieves pain in advanced knee osteoarthritis. Goals after surgery: early mobilization (often the day of surgery), weight bearing as tolerated, quadriceps activation, control of swelling, and range of motion targets of full extension and at least about 90 degrees of flexion early (about 105 to 115 for stairs and rising from low chairs, about 110 for many daily tasks). Extension loss is functionally worst, so avoid a pillow under the knee; place a towel roll under the ankle instead. Quadriceps strength is markedly reduced after TKA, and early progressive strengthening plus neuromuscular electrical stimulation improves quadriceps strength and function (supported by the guideline). Continuous passive motion adds little and is not recommended routinely. Watch for DVT, infection, wound problems and arthrofibrosis; a patient who has not reached about 90 degrees by 6 to 12 weeks may be referred for manipulation under anesthesia.

Section 3The ankle and foot

Ankle sprains and the Ottawa rules

The lateral ankle sprain is the most common sports injury. The mechanism is inversion and plantarflexion, and the ligaments fail in sequence: the anterior talofibular ligament (ATFL, weakest and most often torn, taut in plantarflexion), then the calcaneofibular ligament (CFL), and rarely the posterior talofibular ligament. Grade I is a stretch without laxity, grade II a partial tear with some laxity, grade III a complete tear with gross laxity and marked swelling. The anterior drawer test (ATFL) and the talar tilt (inversion) test (CFL) assess laxity. Management: protection and optimal loading early, a semirigid or lace up brace for moderate to severe sprains (better than a cast), early weight bearing, range of motion, then progressive strengthening (evertors and dorsiflexors), and balance and proprioceptive training, which reduces recurrence. Up to a third or more develop chronic ankle instability.

A high ankle sprain injures the distal tibiofibular syndesmosis (anterior inferior tibiofibular ligament) by forced external rotation and dorsiflexion. It causes pain above the ankle, a positive squeeze test (compressing tibia and fibula at midcalf produces distal pain) and external rotation (Kleiger) test, and takes roughly twice as long to recover as a lateral sprain. A medial (deltoid) sprain from eversion is uncommon and often accompanies a fibular fracture.

The Ottawa ankle rules decide when x rays are needed after acute ankle trauma, with sensitivity near 100 percent for fracture. An ankle series is needed if there is pain in the malleolar zone plus any of: bone tenderness along the distal 6 cm of the posterior edge or tip of the lateral malleolus, bone tenderness along the distal 6 cm of the posterior edge or tip of the medial malleolus, or inability to bear weight both immediately and in the emergency department (four steps). A foot series is needed if there is pain in the midfoot zone plus bone tenderness at the base of the fifth metatarsal or the navicular, or inability to bear weight for four steps.

Achilles disorders

Achilles tendinopathy is either midportion (2 to 6 cm above the insertion, the area of poorest blood supply) or insertional. Risk factors include increased training load, older age, obesity, fluoroquinolone antibiotics and reduced calf strength. Morning stiffness and pain that warms up with activity are typical. The guideline supports progressive tendon loading: the eccentric heel drop program (Alfredson) or heavy slow resistance for midportion tendinopathy. For insertional tendinopathy, avoid dropping the heel below the step (dorsiflexion compresses the tendon against the calcaneus), so eccentrics are performed to floor level only. Heel lifts can reduce symptoms short term.

Achilles rupture occurs with sudden push off or landing, usually in middle aged recreational athletes ("I felt like I was kicked"). Findings: a palpable gap, weak plantarflexion (other plantarflexors still work, so active plantarflexion can be present), and a positive Thompson test (squeezing the calf produces no plantarflexion). Both operative and nonoperative care, when paired with early functional rehabilitation in a boot with heel wedges, produce similar rerupture rates. Protect from dorsiflexion past neutral for about 8 to 12 weeks and from forceful stretching for months.

Plantar heel pain

Plantar fasciitis (plantar heel pain) causes pain at the medial calcaneal tubercle that is worst with the first steps in the morning or after rest and eases with walking, then returns after prolonged standing. Risk factors include limited ankle dorsiflexion, high body mass index and prolonged standing. The windlass test (passive great toe extension in standing reproduces pain) is specific. Guideline supported interventions: manual therapy, plantar fascia specific and calf stretching, taping, prefabricated or custom foot orthoses for short term relief, night splints holding the ankle in dorsiflexion for patients with morning pain, education and strengthening. Distinguish tarsal tunnel syndrome (tibial nerve under the flexor retinaculum, burning and numbness in the sole, positive Tinel behind the medial malleolus) and a calcaneal stress fracture (positive squeeze test of the calcaneus, often in runners).

Foot fractures

Foot posture and mechanics

The subtalar joint produces the triplanar motions of pronation (in open chain: eversion, abduction and dorsiflexion) and supination (inversion, adduction and plantarflexion). In closed chain the calcaneus everts while the talus adducts and plantarflexes, and the tibia rotates internally with pronation. During gait the foot pronates from initial contact through loading response to absorb shock and adapt to the ground, as the transverse tarsal joint axes become parallel and the midfoot unlocks. It then supinates from midstance through terminal stance, and the axes converge so the foot becomes a rigid lever for push off. The windlass mechanism assists: extension of the toes at heel off tightens the plantar fascia, raising the arch and inverting the calcaneus.

A pes planus (flat, overpronated) foot is flexible if the arch reappears when non weight bearing or on toe rise, and rigid if not (consider tarsal coalition). Excess pronation is associated with medial tibial stress syndrome, posterior tibial tendon dysfunction, patellofemoral pain and plantar heel pain. Posterior tibial tendon dysfunction is the commonest cause of acquired flatfoot in adults; signs include the too many toes sign from behind and inability to perform a single leg heel raise. A pes cavus (high arched, supinated) foot is rigid and poor at shock absorption, linked to lateral ankle sprains, stress fractures and neurologic disease (Charcot Marie Tooth). Other forefoot terms: hallux valgus (bunion, lateral deviation of the great toe), hallux rigidus (first MTP arthritis limiting extension, which needs about 60 degrees or more for normal push off), Morton neuroma (third web space interdigital neuroma) and claw and hammer toes.

Section 4Normal and pathological gait

Phases and terminology

One gait cycle (a stride) runs from initial contact of one foot to the next initial contact of the same foot. It is divided into stance (about 60 percent) and swing (about 40 percent). A step is from initial contact of one foot to initial contact of the other, so one stride contains two steps. Double limb support occurs twice per cycle, each about 10 percent at normal speed (roughly 20 percent in all); as walking speed increases, double support shrinks, and running has no double support but a flight phase instead. Older adults and people with impaired balance walk with longer double support.

Two vocabularies appear on the exam. The Rancho Los Amigos terms are preferred: initial contact, loading response, midstance, terminal stance, preswing, initial swing, midswing and terminal swing. The traditional terms are heel strike, foot flat, midstance, heel off, toe off, acceleration, midswing and deceleration. They do not line up perfectly; for example traditional heel off begins terminal stance, and traditional toe off ends preswing.

Spatiotemporal values

Joint angles and muscle activity

Muscles in stance mostly work eccentrically to absorb and control motion; propulsion comes from the plantarflexors in terminal stance and the hip flexors in preswing and initial swing. Knowing which muscle is active in which phase lets you predict the deviation produced by its weakness.

Range needed for normal walking, commonly taught: about 30 degrees hip flexion and 10 degrees apparent hyperextension, about 60 degrees knee flexion, about 10 degrees ankle dorsiflexion and 20 degrees plantarflexion, and about 60 degrees or more first MTP extension. Stairs need more knee flexion (about 90 to 105) and rising from a standard chair about 90 to 105 degrees of knee and hip flexion.

Common gait deviations and their causes

Section 5Fractures, weight bearing and orthopedic special populations

Fracture healing

Bone heals by two routes. Secondary (indirect) healing with callus occurs when there is some motion at the fracture, as with casting, intramedullary nails or external fixation. Primary (direct) healing without visible callus occurs with rigid compression plating, where osteons cross the fracture directly. Secondary healing passes through overlapping stages.

Factors that delay healing: smoking, diabetes, poor nutrition, older age, NSAIDs in some studies, corticosteroids, infection, poor blood supply (scaphoid, femoral neck, talus, fifth metatarsal Jones zone, distal tibia), excessive motion and open fractures. A delayed union is slower than expected; a nonunion has stopped healing (often after about 6 to 9 months). Malunion heals in a poor position. Watch after any fracture for compartment syndrome (pain out of proportion and with passive stretch), fat embolism (after long bone fractures, typically 24 to 72 hours: confusion, dyspnea, petechiae), DVT and pulmonary embolism, and complex regional pain syndrome. Exercise prescription during immobilization keeps the joints above and below moving and maintains strength in the rest of the body.

Weight bearing status

Weight bearing orders come from the surgeon and depend on fixation stability more than on the fracture alone. Most hip fractures and arthroplasties allow weight bearing as tolerated; intra articular fractures (tibial plateau, pilon, calcaneus), unstable ankle fractures and many osteotomies require non weight bearing or touch down weight bearing for about 6 to 12 weeks. Patients poorly judge partial weight bearing, so teach it with a scale and recheck. If a patient cannot maintain a NWB restriction safely, a wheelchair may be the safer mobility choice. For gait patterns: three point gait (device and involved limb together) for a restricted limb; two point and four point gaits (reciprocal, with each crutch moving with the opposite limb) for bilateral weakness; swing to and swing through for bilateral lower extremity paralysis. On stairs with crutches, go up with the good limb first and down with the crutches and involved limb first.

Osteoporosis

Osteoporosis is low bone mass with microarchitectural deterioration. The World Health Organization defines it by DXA T score (comparison with young adult peak bone mass): normal T score at or above negative 1.0; osteopenia (low bone mass) between negative 1.0 and negative 2.5; osteoporosis at or below negative 2.5; severe osteoporosis at or below negative 2.5 with a fragility fracture. Z scores compare with age matched peers and are used in children and premenopausal adults. Common fragility fractures: vertebral compression (often thoracic, causing kyphosis and height loss), distal radius (Colles) and hip.

Exercise for bone health combines progressive resistance training, impact or weight bearing activity as tolerated, balance training and posture work (back extensor strengthening reduces vertebral fracture risk). For people with osteoporosis, avoid loaded spinal flexion (sit ups, toe touches, deep forward bending with rotation, some yoga poses) and sudden twisting, which raise vertebral compression fracture risk. Teach hip hinge lifting, home fall prevention and adequate calcium and vitamin D. Pain with mild trauma or a sudden onset of thoracic pain in an older adult with osteoporosis suggests a compression fracture and needs medical evaluation.

Rheumatoid arthritis

Rheumatoid arthritis (RA) is a systemic autoimmune inflammatory arthritis of the synovium. Contrast it with osteoarthritis:

During an acute flare (warm, swollen, painful joints), use rest, splinting in a functional position, gentle active or active assisted range of motion (one or two repetitions to maintain motion), isometrics and joint protection; avoid vigorous stretching and resisted exercise through inflamed joints. Between flares, use aerobic exercise, low load strengthening, joint protection and energy conservation. Long term corticosteroid use causes osteoporosis and skin fragility. Atlantoaxial instability from transverse ligament laxity is a serious risk: avoid cervical manipulation and end range upper cervical flexion, and report symptoms such as occipital headache, dizziness, bilateral paresthesia or gait change as possible cord compression.

Amputation level overview

Lower limb amputations in adults are mostly due to vascular disease and diabetes; trauma and tumor are the main causes in younger people. Energy cost of walking rises as the level becomes more proximal, and bilateral and transfemoral amputees often need more help.

Preprosthetic care: residual limb shaping with figure of eight elastic wrapping (tighter distally, diagonal turns, no circular turns that form a tourniquet) or a shrinker, positioning to prevent contractures, strengthening (especially hip extensors and abductors), desensitization, skin inspection of both limbs (the remaining foot is at high risk in diabetes), cardiovascular training and transfer and wheelchair training. Phantom limb sensation is nearly universal and harmless; phantom pain responds to mirror therapy, graded motor imagery and desensitization. A rigid removable dressing protects transtibial limbs and limits edema.

Words worth knowing

Neuromuscular Foundations: Neuroanatomy, Examination and Motor Control

Every neurologic question on the licensing exam is really a localization problem followed by a management problem: where is the lesion, what will the patient be able to do, and what is the safest, most effective intervention? This chapter builds the foundation for the neuromuscular half of the exam: the anatomy that predicts deficits, the examination that confirms them, the motor learning science that shapes treatment, the balance tests with their cutoffs, and the interventions with the strongest evidence.

Section 1Neuroanatomy that the exam tests

The exam asks you to read a vignette, recognize the pattern of deficits and connect it to a structure and a blood supply. For each system, ask what it normally does and what a patient looks like when it fails.

The cerebral cortex

Each hemisphere has four lobes on its lateral surface (frontal, parietal, temporal and occipital) plus the limbic lobe and insula, which lie deep or medial. The central sulcus separates the frontal lobe (motor planning and execution) from the parietal lobe (sensation and spatial processing). The lateral (Sylvian) fissure separates the frontal and parietal lobes above from the temporal lobe below.

The primary motor cortex (precentral gyrus, Brodmann area 4) contains the cell bodies of many upper motor neurons. Its body map, the motor homunculus, places the leg and foot on the medial surface of the hemisphere inside the longitudinal fissure, and the trunk, arm, hand and face progressively more lateral, with the face just above the lateral fissure. That layout explains why anterior cerebral artery strokes cause leg greater than arm weakness and middle cerebral artery strokes cause face and arm greater than leg weakness.

The premotor cortex and supplementary motor area plan and sequence movement and set up anticipatory postural adjustments; lesions cause apraxia and poor initiation. The prefrontal cortex governs executive function, so frontal damage brings impulsivity, perseveration and poor insight, which matter more for safety than strength. The dominant hemisphere (left in almost all right handed and most left handed people) holds the language areas. The nondominant (usually right) inferior parietal lobule governs spatial attention, so damage there produces unilateral neglect and anosognosia. The limbic system links emotion, motivation and memory, which is why lability and memory loss are common after brain injury. Figure 5.1 maps the main areas.

The long tracts and where they cross

Three tracts answer most lateralization questions. The rule is simple: find where the tract crosses, and the side of the deficit flips at that level.

• Lateral corticospinal tract (voluntary movement). Upper motor neurons leave the motor cortex, pass through the corona radiata and the posterior limb of the internal capsule, descend through the cerebral peduncle and the basis pontis, and form the medullary pyramids. About 85 to 90 percent of fibers cross at the pyramidal decussation in the caudal medulla and descend in the lateral funiculus to synapse on anterior horn cells. The uncrossed remainder forms the anterior corticospinal tract, which mainly controls axial and proximal muscles. A lesion above the decussation gives contralateral weakness; a lesion in the cord gives ipsilateral weakness below the level.
• Dorsal column medial lemniscus (DCML: discriminative touch, vibration, proprioception, two point discrimination). First order neurons enter the cord and ascend ipsilaterally in the fasciculus gracilis (lower body, medial) and fasciculus cuneatus (upper body above about T6, lateral). They synapse in the nucleus gracilis and cuneatus of the medulla; second order fibers cross as the internal arcuate fibers and ascend as the medial lemniscus to the ventral posterolateral (VPL) nucleus of the thalamus, then to the postcentral gyrus. Cord lesions cause ipsilateral loss; lesions above the medulla cause contralateral loss.
• Spinothalamic tract (anterolateral system: pain, temperature, crude touch). First order fibers synapse in the dorsal horn; second order fibers cross in the anterior white commissure within one or two segments and ascend in the anterolateral cord to the VPL thalamus. A cord lesion therefore causes contralateral pain and temperature loss beginning one to two segments below the lesion.

The spinocerebellar tracts carry unconscious proprioception to the ipsilateral cerebellum. The reticulospinal and vestibulospinal tracts control posture and tone; loss of cortical inhibition over them contributes to spasticity and antigravity posturing after brain injury.

Cerebellum

The cerebellum compares intended with actual movement and corrects errors in timing, force and direction; it does not cause weakness. Midline lesions (vermis, flocculonodular lobe) cause truncal ataxia, wide based gait and nystagmus; lateral hemisphere lesions cause limb dysmetria, intention tremor and dysdiadochokinesia. Because the cerebellar output crosses once and the corticospinal tract crosses again, cerebellar lesions produce signs on the same side as the lesion. Other features are hypotonia, a positive rebound phenomenon, scanning or ataxic dysarthria, and a gait that does not improve much with vision (contrast with sensory ataxia).

Basal ganglia

The basal ganglia (caudate and putamen, which form the striatum; globus pallidus; subthalamic nucleus; substantia nigra) select desired movements and suppress unwanted ones through a loop with the cortex and thalamus. In the simplified model, the direct pathway facilitates movement and the indirect pathway inhibits it. Dopamine from the substantia nigra pars compacta excites the direct pathway (D1 receptors) and inhibits the indirect pathway (D2 receptors), so its net effect is to promote movement. Loss of dopamine in Parkinson disease produces a hypokinetic disorder: bradykinesia, rigidity, resting tremor and postural instability. Degeneration of the caudate in Huntington disease and a lesion of the subthalamic nucleus (contralateral hemiballismus) produce hyperkinetic disorders. External cues help because automatic, internally cued movement is impaired.

Brainstem and cranial nerves

The brainstem (midbrain, pons, medulla) contains the cranial nerve nuclei, all of the long tracts, the reticular activating system for arousal, and centers for breathing, heart rate and blood pressure. A brainstem lesion is suggested by crossed findings: an ipsilateral cranial nerve deficit with contralateral weakness or sensory loss in the body, often with vertigo, diplopia, dysarthria, dysphagia or ataxia. Cranial nerves III and IV are in the midbrain; V, VI, VII and VIII in the pons; IX, X, XI (in part) and XII in the medulla.

Blood supply

The brain is supplied by two paired systems that join at the base in the circle of Willis. The anterior circulation comes from the internal carotid arteries, which give the anterior cerebral artery (medial frontal and parietal lobes: leg and foot area, bladder control, frontal executive areas) and the middle cerebral artery (lateral convexity: face and arm motor and sensory areas, language areas in the dominant hemisphere, spatial attention in the nondominant hemisphere, and through lenticulostriate branches the internal capsule and basal ganglia). The posterior circulation comes from the vertebral arteries, which join as the basilar artery to supply the brainstem and cerebellum and end as the two posterior cerebral arteries (occipital lobe, inferior temporal lobe, thalamus). Communicating arteries allow collateral flow. Chapter 6 matches each artery to its stroke syndrome.

Section 2The neurologic examination

The neurologic examination localizes the problem, separates upper from lower motor neuron involvement, sets a baseline and catches findings that need referral. Begin with a systems review: arousal, orientation, ability to follow commands, communication, vital signs and red flags. A patient who cannot follow commands cannot give valid sensory or strength results.

Sensory examination

Sensation is tested in three groups. Superficial (exteroceptive) sensation includes pain (sharp versus dull with a safety pin or broken tongue depressor), temperature (warm and cold test tubes), light touch (cotton ball or fingertip) and pressure. Deep (proprioceptive) sensation includes proprioception (static joint position sense), kinesthesia (awareness of movement) and vibration (128 Hz tuning fork over a bony prominence). Combined cortical sensation includes stereognosis (identifying an object by touch), graphesthesia (recognizing numbers traced on the skin), two point discrimination, tactile localization, barognosis (weight) and recognition of texture, and bilateral simultaneous stimulation (extinction, a sign of neglect).

Technique rules: demonstrate with vision, then occlude vision; apply stimuli randomly and at irregular intervals; compare sides; and test superficial before deep and cortical sensation, because cortical tests mean little if primary sensation is absent. Pain and temperature test the anterolateral system; vibration and proprioception test the dorsal columns. In diabetes, inability to feel the 5.07 (10 gram) monofilament means loss of protective sensation. Patterns localize: dermatomal (root), named nerve field, stocking and glove (polyneuropathy), a trunk sensory level (cord), or one whole side including the face (contralateral thalamus, capsule or cortex).

Reflexes

Deep tendon reflexes (muscle stretch reflexes) test a monosynaptic arc: muscle spindle, Ia afferent, the spinal segment, the alpha motor neuron and the muscle. Descending pathways normally damp the arc. A lower motor neuron or sensory lesion breaks the arc and reduces the reflex; an upper motor neuron lesion removes inhibition and exaggerates it. Use reinforcement (Jendrassik maneuver) before calling a reflex absent.

Tone and spasticity

Tone is the resistance of a relaxed muscle to passive stretch. Spasticity is a velocity dependent increase in resistance to passive stretch caused by hyperexcitable stretch reflexes after an upper motor neuron lesion; it may show a clasp knife response (high resistance that suddenly gives way). It favors upper extremity flexors and lower extremity extensors. Rigidity is increased resistance that is not velocity dependent and is present in both agonist and antagonist; lead pipe rigidity is uniform through the range and cogwheel rigidity is ratchety (tremor superimposed on rigidity), typical of Parkinson disease. Hypotonia or flaccidity follows lower motor neuron or cerebellar lesions and the early shock phase of stroke and spinal cord injury. Decorticate (arms flexed, legs extended) and decerebrate (all four extremities extended) posturing are described in Chapter 6.

Spasticity is graded with the Modified Ashworth Scale (MAS), testing with the patient relaxed and supine and moving the limb through the range in about one second. The Modified Tardieu Scale compares the catch angle at fast stretch (R1) with slow passive range (R2); a large gap suggests a reflex component, a small gap suggests contracture.

Coordination

Coordination tests separate cerebellar, sensory and basal ganglia problems. Nonequilibrium tests are done sitting or lying: finger to nose, finger to therapist's finger, heel to shin, rapid alternating movements such as pronation and supination (inability is dysdiadochokinesia), finger tapping and foot tapping, drawing a circle, and the rebound test (the limb overshoots when resistance is suddenly released). Observe for dysmetria (overshoot or undershoot), intention tremor (increasing as the target nears, cerebellar), resting tremor (decreasing with movement, basal ganglia) and decomposition of movement. Test with eyes open and then closed: a sensory ataxia worsens dramatically without vision, whereas cerebellar ataxia changes little. Equilibrium tests are done standing and walking: the Romberg test (feet together, eyes open then closed; positive if balance is maintained with eyes open but lost with eyes closed, indicating a proprioceptive or vestibular problem, not cerebellar), the sharpened (tandem) Romberg, single limb stance, tandem walking and walking with sudden stops and turns.

Upper versus lower motor neuron signs

A stroke and a peroneal nerve palsy can both cause foot drop, but the stroke patient has a brisk ankle jerk, clonus and plantarflexor spasticity, while the palsy patient has a flaccid foot, anterior compartment atrophy and a nerve pattern of sensory loss. A spinal cord injury gives LMN signs at the injured level and UMN signs below it once spinal shock resolves. ALS mixes both in the same limb.

Cranial nerve screening and other components

Cranial nerve screening (table in Section 1) focuses on findings that change management: visual field loss, nystagmus and eye movement problems, facial weakness pattern, and dysphagia signs such as a wet voice or coughing with swallowing, which call for speech language pathology referral and aspiration precautions. The full examination also covers cognition, communication, perception, motor function, balance and gait.

Section 3Motor control and motor learning

Motor control is the ability to regulate the mechanisms essential to movement: posture, stability and the coordination of muscles across joints. Motor learning is a set of internal processes, associated with practice or experience, that produce a relatively permanent change in the capability for skilled movement. The difference matters on the exam. Performance is what you see during practice, and it can be inflated by guidance and frequent feedback or depressed by fatigue. Learning is inferred from retention (performance after a rest period without practice) and transfer (performance of a related task or in a new setting). Conditions that depress in-session performance often produce better learning.

Theories of motor control

Older reflex and hierarchical theories (cortex in charge, reflexes released when higher control is lost) underlie the neurofacilitation approaches. The current systems and dynamic systems theories hold that movement emerges from the interaction of the individual, the task and the environment, and that changing a control parameter such as speed can shift the pattern (walking becomes running). So train functional tasks in meaningful environments and manipulate task constraints, rather than expecting normalized tone alone to restore function. Open loop control runs a preprogrammed command without feedback (fast, ballistic movements); closed loop control uses ongoing sensory feedback to correct movement (slow, accurate tasks and early learning).

Stages of motor learning

Gentile's two stage model starts with getting the idea of the movement, then moves to fixation (refining one consistent pattern for closed skills in a stable environment) or diversification (building adaptable patterns for open skills in a changing environment). Progressing from closed to open tasks, and from body stability to transport with manipulation, is a principled way to advance a program.

Practice schedules

The contextual interference effect explains why random practice beats blocked practice for learning. Switching tasks forces the learner to reconstruct the action plan on each trial and to compare tasks, which is effortful and lowers performance during the session but strengthens memory for each skill. Blocked practice lets the learner repeat the same plan from working memory, which looks good in the session and fades by the next visit.

Feedback

Intrinsic feedback comes from the learner's own senses (proprioception, vision, vestibular input). Extrinsic (augmented) feedback comes from an outside source: the therapist, a mirror, a video or a biofeedback device. Extrinsic feedback is described along several dimensions.

• Knowledge of results (KR) is information about the outcome of the movement ("you walked 30 meters," "the cup reached the shelf"). Knowledge of performance (KP) is information about the movement pattern itself ("you kept your knee straight at heel strike"). KP is especially useful when a patient reaches the goal using an abnormal pattern; KR is enough when the outcome tells the learner what went wrong.
• Concurrent feedback (during the movement) aids performance but breeds dependence; terminal feedback comes after. A short delay while the learner estimates their own error improves retention.
• Frequency. Feedback after every trial helps early acquisition but weakens retention (the guidance hypothesis). Better learning follows faded feedback (high frequency early, decreasing later), bandwidth feedback (given only when error exceeds a set range), summary feedback (after a set of trials, summarizing all) and average feedback (the mean of a set of trials).
• Focus of attention. An external focus on the effect of the movement ("push the floor away") generally produces better learning than an internal focus on body parts ("straighten your knee").

Principles of experience dependent neuroplasticity

Recovery after a lesion combines spontaneous recovery (resolving edema, reperfusion of the penumbra, reversal of diaschisis) and experience dependent plasticity (synaptogenesis, sprouting, unmasking of latent pathways, cortical map reorganization). Regaining the original pattern is restitution; reaching the goal another way is compensation. A widely cited synthesis lists ten principles.

Learned nonuse is a classic illustration of interference and of use it or lose it: after a stroke, early failed attempts to use the affected arm are punished, successful use of the other arm is rewarded, and the patient stops trying the affected arm even after motor capacity returns.

Section 4Balance and fall risk

Balance (postural control) is the ability to keep the body's center of mass over its base of support. It has a static component (holding a posture), a dynamic component (controlling the center of mass during movement), a reactive component (recovering from an unexpected perturbation) and an anticipatory component (preparing the body before a voluntary movement, such as activating the trunk before reaching).

The systems model of balance

Balance emerges from interacting systems, any of which can be the limiting factor: sensory input (somatosensory input dominates on a firm surface in good light; vision reports head position relative to the surroundings; vestibular input reports head position relative to gravity and resolves conflicts when the other two are inaccurate), central integration that reweights inputs, motor output (ankle and hip strength, ankle dorsiflexion range, timing of responses), cognition (attention and dual tasking) and biomechanics (base of support and limits of stability).

Postural strategies

Sensory organization testing

The Sensory Organization Test (SOT), performed on computerized dynamic posturography, measures sway under six conditions that systematically remove or distort visual and somatosensory input. Sway referencing means the platform or visual surround tilts in step with the patient's sway, so the input is present but inaccurate. The modified Clinical Test of Sensory Interaction in Balance (mCTSIB) is the clinical version: the patient stands for 30 seconds on a firm surface with eyes open, firm with eyes closed, foam with eyes open, and foam with eyes closed. Standing on foam degrades somatosensory input; closing the eyes removes vision.

Standardized balance and fall risk tests

Choose a test that matches the patient's level and the question being asked. Cutoffs vary by study; these are the values usually taught for community dwelling older adults.

Gait speed as a vital sign

Comfortable gait speed, usually measured with the 10 Meter Walk Test over the middle 6 meters to exclude acceleration and deceleration, is fast, reliable and predictive of falls, hospitalization, discharge destination and survival. Classic categories from stroke research: below 0.4 m/s suggests a household ambulator, 0.4 to 0.8 m/s a limited community ambulator, and above 0.8 m/s a community ambulator. A speed below about 1.0 m/s in older adults flags increased risk of adverse outcomes, and crossing a street safely at a timed signal typically requires about 1.2 m/s or more. A change of about 0.1 m/s is commonly cited as a meaningful change.

Fall risk factors and prevention

Falls are multifactorial. Intrinsic risk factors include a history of falls (the strongest single predictor), lower extremity weakness, gait and balance impairment, visual impairment, peripheral neuropathy, cognitive impairment, depression, orthostatic hypotension, urinary urgency and incontinence, foot problems, and fear of falling. Medications are a major modifiable factor: psychoactive drugs (sedatives, hypnotics, antidepressants, antipsychotics), antihypertensives, opioids, and polypharmacy (often defined as four or more medications). Extrinsic factors include poor lighting, loose rugs, clutter, lack of grab bars, unsafe footwear and stairs without rails.

Prevention follows a screen, assess, intervene sequence: ask about falls in the past year, unsteadiness and fear of falling; assess gait, strength, balance, orthostatic blood pressure, vision, feet and home hazards, and request a medication review by the prescriber. The most effective single intervention is progressive, challenging balance exercise, about three hours per week over months, usually with strengthening (structured home programs and tai chi both reduce falls). Add home modification, footwear, vision correction, management of orthostatic hypotension and vitamin D for those who are deficient. Walking alone, without balance challenge, does not reliably prevent falls.

Section 5Neurologic outcome measures and interventions

Patients improve the tasks they practice, with enough repetitions, at enough intensity, in a meaningful context. The exam expects you to match outcome measures to questions and to know who is eligible for the highest evidence interventions and how they are dosed.

Choosing outcome measures

Classify measures by the ICF: body function (Fugl-Meyer, Modified Ashworth), activity (10 Meter Walk Test, Berg, ARAT, FIM) and participation (community mobility). Include at least one activity measure, because functional goals are written at that level. The minimal detectable change exceeds measurement error; the minimal clinically important difference is the smallest change patients perceive as meaningful.

Task specific training

Task specific (task oriented) training means practicing whole, functional tasks (or meaningful parts of them) in a realistic context, with many repetitions, progressive difficulty and feedback. Examples include repeated sit to stand from different seat heights, reaching for objects of different sizes at different distances, and stepping practice over and around obstacles. It exploits specificity. Strengthening still helps when weakness limits the task, and progressive resistance training after stroke does not worsen spasticity.

Walking recovery: intensity and stepping practice

The clinical practice guideline on improving locomotor function in chronic (more than six months) stroke, spinal cord injury and brain injury recommends moderate to high intensity walking training as the core intervention: large amounts of stepping practice at about 60 to 80 percent of heart rate reserve or 70 to 85 percent of age predicted maximum heart rate, or a rating of perceived exertion of roughly 15 to 17 on the 6 to 20 scale. Train on a treadmill or overground with variable tasks (speeds, slopes, surfaces, obstacles). Balance training without walking, seated exercise and robotic gait training should not replace stepping practice when walking is the goal. Beta blockers blunt heart rate, so use perceived exertion in those patients.

Body weight supported treadmill training (BWSTT) unloads part of body weight with a harness so patients who cannot yet walk independently can step safely and repetitively. Start with no more than about 30 to 40 percent support, reduce it as loading improves, and progress speed toward normal. A large trial in subacute stroke found BWSTT no better than an equal dose of progressive home exercise: the active ingredient is the amount and intensity of stepping, not the device.

Constraint induced movement therapy

Constraint induced movement therapy (CIMT) reverses learned nonuse by restraining the less affected upper extremity and intensively training the more affected one. The traditional protocol has three components: restraint of the less affected hand in a mitt for about 90 percent of waking hours; intensive training of the more affected arm for about six hours per day for two weeks using shaping (tasks progressed in small steps, with immediate feedback on improvement) and repetitive task practice; and a transfer package of behavioral strategies (daily activity log, home practice, problem solving) to carry use into daily life. Modified CIMT (mCIMT) uses shorter daily training (for example, a few hours) over more weeks with restraint for part of the day and is more practical in most settings.

Eligibility is essential: the classic minimum motor criteria are at least 20 degrees of active wrist extension and 10 degrees of active extension at the thumb and at least two fingers (metacarpophalangeal and interphalangeal joints). Patients also need safe balance while wearing the mitt and enough cognition to participate. Very high dose CIMT in the first days after stroke has not shown added benefit.

Electrical stimulation in neurologic rehabilitation

Neuromuscular electrical stimulation (NMES) produces muscle contraction by depolarizing the motor nerve. When the contraction is timed to accomplish a functional task (dorsiflexion during swing, grasp and release, cycling) it is called functional electrical stimulation (FES). Common uses are listed below.

• Foot drop (stroke, MS, incomplete SCI): a peroneal nerve stimulator triggered by a heel switch or tilt sensor fires the dorsiflexors during swing; outcomes are similar to an AFO, but it needs an intact peripheral nerve.
• Shoulder subluxation after stroke: stimulate the supraspinatus and posterior deltoid, ideally early in the flaccid stage.
• Hand recovery: wrist and finger extensor stimulation with task practice; EMG triggered stimulation adds a volitional component.
• FES cycling after SCI: preserves muscle and fitness; watch for autonomic dysreflexia at T6 and above.

Contraindications to electrical stimulation include a demand type cardiac pacemaker or implanted defibrillator (avoid stimulation near it and generally avoid stimulation in these patients unless cleared), placement over the carotid sinus or anterior neck, over a known or suspected deep vein thrombosis or thrombophlebitis, over the trunk or pelvis during pregnancy, over an area of active or suspected malignancy, and over the eyes. Precautions include impaired sensation, inability to communicate discomfort, cardiac disease, seizure disorder, open wounds or damaged skin, and patients at risk of autonomic dysreflexia. Check the skin before and after each session.

Other options include mirror therapy (a visual illusion of the affected limb moving normally), mental practice, robotic and virtual reality devices that add repetitions, and bilateral arm training for patients who do not meet CIMT criteria. Older facilitation approaches such as NDT and PNF have not proven superior to task specific training.

Words worth knowing

Neuromuscular: Stroke, Brain Injury and Spinal Cord Injury

Stroke, traumatic brain injury and spinal cord injury fill a large share of neurologic questions on the licensing exam, and they share one theme: the location of the lesion predicts the deficits, the prognosis and the dangers. This chapter teaches you to read a stroke syndrome from its artery, stage motor recovery, manage the agitated patient with brain injury, classify a spinal cord injury and predict function from its level, and recognize the medical emergencies, such as autonomic dysreflexia, that you must act on immediately.

Section 1Stroke syndromes by artery

A stroke (cerebrovascular accident) is the sudden onset of a focal neurologic deficit from interrupted blood flow lasting more than 24 hours or showing infarction on imaging. About 85 to 87 percent are ischemic (thrombotic, embolic often from atrial fibrillation, or small vessel lacunar disease). The rest are hemorrhagic: intracerebral hemorrhage, usually from chronic hypertension, and subarachnoid hemorrhage, usually from a ruptured aneurysm and announced by a sudden "worst headache of my life." A transient ischemic attack (TIA) is a temporary episode without infarction; it is a warning, and about one in ten patients has a stroke within the following weeks to months, so new or recurring symptoms require emergency referral. The public warning sign BE FAST covers balance loss, eye (vision) changes, face drooping, arm weakness, speech difficulty and time to call emergency services. Major modifiable risk factors are hypertension (the most important), atrial fibrillation, diabetes, smoking, hyperlipidemia, obesity and physical inactivity.

Arterial syndromes

Each artery supplies a predictable territory (Chapter 5), so each stroke produces a predictable cluster. Deficits from hemispheric strokes appear on the side of the body opposite the lesion. The hemisphere matters as much as the artery: a dominant (usually left) hemisphere lesion causes language deficits; a nondominant (usually right) lesion causes neglect and visuospatial problems.

Aphasia

Aphasia is an acquired disorder of language, distinct from dysarthria (a motor speech disorder of articulation with intact language). Classify aphasia with three questions: is speech fluent, is comprehension intact, and can the patient repeat?

Communication strategies: for Broca aphasia, ask yes or no questions, allow time, and offer gestures or picture boards. For Wernicke aphasia, use short, simple sentences with demonstration and gestures, and do not rely on the patient's verbal report of understanding.

Neglect and pusher syndrome

Unilateral spatial neglect is failure to attend to the side of space and body opposite the lesion, most often left neglect after a right parietal stroke. It differs from hemianopia: a patient with hemianopia alone knows the field is missing and turns the head to compensate, while a patient with neglect does not. Neglect is tested with line bisection, cancellation tasks and copying drawings, and it predicts poor function and falls. Treatment includes visual scanning training, anchoring cues on the neglected side, prism adaptation, mirror therapy and trunk rotation toward the neglected side. Early on, place the call light and key items on the intact side for safety while training attention toward the neglected side during therapy.

Pusher syndrome (contraversive pushing) is a disorder of perceived body verticality, usually from a lesion of the posterolateral thalamus. The patient perceives upright as tilted toward the less affected side, so they actively push with the less affected arm and leg toward the hemiparetic side and resist any attempt to correct the posture toward midline, which causes falls toward the weak side. It is more common with right hemisphere lesions and often coexists with neglect. Treatment uses vision, which is intact: show the patient vertical references (a door frame, the therapist's body, a mirror), have them reach toward objects on the less affected side so that weight shifts over the midline, and seat or stand them with the less affected side next to a wall so that pushing is futile. Avoid pulling the patient upright against their push; that increases resistance. The prognosis for resolution within months is good.

Section 2Stroke recovery and rehabilitation

Most motor recovery after stroke occurs in the first three months, with the steepest gains in the first weeks, but meaningful improvement continues for many months and responds to training even years later. Recovery tends to proceed from proximal to distal and from mass patterns to isolated movement. Early return of some voluntary movement, particularly finger extension and shoulder abduction in the first days, predicts good upper extremity recovery; a flaccid arm with no movement at four weeks predicts poor recovery of hand function.

Brunnstrom stages and synergies

After an upper motor neuron lesion, voluntary movement often first returns within stereotyped mass patterns called synergies, in which the patient cannot move one joint without the others in the pattern. Brunnstrom described the sequence of recovery in stages; patients may stop at any stage.

The typical resting posture of the hemiplegic arm (shoulder adducted and internally rotated, elbow flexed, forearm pronated, wrist and fingers flexed) mixes the strongest components of both synergies; the leg is typically held in extension synergy (hip adduction, knee extension, plantarflexion and inversion), which supports standing but causes toe drag and circumduction in swing.

Positioning and the hemiplegic shoulder

Positioning aims to prevent contracture, pressure injury and shoulder injury, and to give sensory input to the affected side. In supine, support the affected shoulder on a pillow with the scapula protracted and the arm slightly abducted and externally rotated, elbow extended, wrist neutral; keep the hip and knee in neutral with a small towel under the hip to limit external rotation. Side lying on the affected side is encouraged for sensory input and elongation of the trunk, with the shoulder protracted forward so the patient does not lie on the point of the shoulder. In sitting, support the affected arm on a lap tray or armrest trough. Turn every two hours in bed when the patient cannot reposition.

Hemiplegic shoulder pain affects many survivors and has several causes: inferior glenohumeral subluxation (in the flaccid stage the rotator cuff and deltoid no longer hold the humeral head, and gravity pulls it down; palpate a gap below the acromion), rotator cuff and biceps tendon injury, adhesive capsulitis, spasticity of the internal rotators and adductors, complex regional pain syndrome (shoulder hand syndrome with a painful, swollen, discolored hand), and impingement from raising the arm overhead without scapular upward rotation and humeral external rotation. Prevention is the best treatment:

• Never pull on the affected arm during transfers or bed mobility; teach caregivers to move the patient through the trunk.
• Support the arm in sitting (lap tray, arm trough) and when standing or walking; a sling may be used for standing and walking in the flaccid stage but should not be worn constantly because it holds the arm in adduction and internal rotation.
• Perform range of motion with scapular mobilization and external rotation before elevation; avoid overhead pulleys, which cause impingement and pain.
• Use NMES to the supraspinatus and posterior deltoid to reduce subluxation, and strapping (taping) to reduce pain.

Gait training after stroke

Common deviations reflect the stance and swing problems of the paretic leg. Treatment combines high intensity stepping practice (Chapter 5), strengthening, orthoses and, when needed, an assistive device.

A hemi walker or quad cane gives more stability than a straight cane for patients with poor balance and one functional upper extremity; any cane is held in the hand opposite the weak leg.

Acute care precautions

In the acute phase, protect the brain's perfusion. For ischemic stroke treated with intravenous thrombolysis (alteplase or tenecteplase), blood pressure is kept below 180/105 mmHg for 24 hours afterward, and therapy is usually delayed or limited during that first day while bleeding risk is highest; watch for signs of hemorrhage (new headache, declining consciousness, worsening deficit) and bleeding from puncture sites. For ischemic stroke without thrombolysis, permissive hypertension up to about 220/120 mmHg is commonly allowed in the first 24 to 48 hours to maintain flow to the penumbra. In hemorrhagic stroke, blood pressure is lowered (a systolic target around 140 mmHg is common), so a rising pressure is a reason to stop. Facility protocols vary; follow the physician's specific parameters.

Mobilization should begin once the patient is medically stable, typically within the first days. A large trial found that very early, high dose mobilization within the first 24 hours produced worse outcomes than usual care, so current guidelines advise against high dose mobilization in the first day while supporting short, frequent sessions afterward. Monitor for orthostatic hypotension, cardiac arrhythmias (atrial fibrillation is common), dysphagia and aspiration (keep the head of bed elevated and follow the swallowing plan), deep vein thrombosis, and new or worsening neurologic signs, which require stopping and notifying the team immediately.

Section 3Traumatic brain injury

Traumatic brain injury (TBI) results from an external force: falls (most common overall, especially in older adults and young children), motor vehicle crashes, assaults, sports and blast. Primary injury occurs at impact: contusions, often in a coup and contrecoup pattern at the frontal and temporal poles; hematomas; and diffuse axonal injury from shearing during acceleration and rotation, which causes prolonged coma with few focal signs. Secondary injury develops over hours to days from hypoxia, hypotension, cerebral edema, raised intracranial pressure, seizures and infection; much of acute medical care aims to prevent it.

An epidural hematoma (usually a torn middle meningeal artery with a temporal fracture) classically causes a brief loss of consciousness, a lucid interval, then rapid deterioration. A subdural hematoma (torn bridging veins) may be acute or chronic; chronic subdural hematoma in older adults and people on anticoagulants presents with gradual confusion, headache or new falls days to weeks after minor trauma, and is a reason to refer an older patient whose cognition declines after a fall.

Severity scales

The total ranges from 3 to 15. Severity is classified as mild 13 to 15, moderate 9 to 12 and severe 3 to 8 (a score of 8 or less generally means coma and the need to protect the airway). Duration of loss of consciousness and of post traumatic amnesia (PTA, the period of confusion and inability to form new memories after injury) also grade severity; PTA longer than about a day suggests at least moderate injury and longer than a week severe injury, and PTA duration is one of the best predictors of long term outcome. Decorticate posturing (arms flexed, legs extended) reflects a lesion above the red nucleus in the midbrain; decerebrate posturing (all four limbs extended, arms pronated) reflects a brainstem lesion below the red nucleus and carries a worse prognosis.

Rancho Los Amigos levels of cognitive functioning

Behavior management and medical precautions

The patient at Rancho level IV is confused and agitated because of the injury, not by choice. Management principles: keep the environment calm, quiet and low in stimulation (one person speaking, television off); use consistent staff and a consistent daily schedule; give short, simple instructions; offer limited choices; keep sessions short and change activities often; allow safe movement (an enclosed or floor level bed, supervised walking) rather than restraints, which increase agitation; do not argue with confabulation, but gently redirect; and stay calm and step back if the patient becomes aggressive. Overlearned, automatic tasks such as walking or folding towels are better than new learning at this stage.

In the acute phase, intracranial pressure (ICP) is normally about 5 to 15 mmHg, and sustained values above about 20 mmHg require treatment. Cerebral perfusion pressure (CPP) equals mean arterial pressure minus ICP, with a target of about 60 to 70 mmHg. Activities that raise ICP include the Valsalva maneuver, isometric exercise, coughing, neck flexion or rotation that obstructs venous drainage, hip flexion beyond 90 degrees, the head down position and noxious stimulation. Keep the head of the bed at about 30 degrees with the head in midline, and stop activity and notify the nurse if ICP rises and stays elevated. Other complications include seizures, heterotopic ossification (common in TBI as well as SCI), spasticity, dysphagia, and endocrine and sleep disturbances.

Concussion and return to play

A concussion is a mild traumatic brain injury caused by a direct or transmitted force to the head that produces a rapid onset of transient neurologic dysfunction, usually without structural injury on standard imaging. Loss of consciousness is not required. Symptoms include headache, dizziness, nausea, light and noise sensitivity, feeling slowed or "in a fog," poor concentration, irritability and sleep disturbance. Signs on the sideline include balance problems, confusion, blank stare and amnesia. Any athlete suspected of a concussion is removed from play and is not returned the same day.

Red flags requiring emergency transfer: worsening or severe headache, repeated vomiting, seizure, deteriorating consciousness, increasing confusion or agitation, weakness or numbness in the limbs, double vision, slurred speech, unequal pupils, and severe neck pain or tenderness (suspect cervical injury and immobilize). Second impact syndrome, rapid and often fatal brain swelling after a second blow before recovery from the first, is the main reason for conservative return.

Current consensus favors a short period of relative rest (about 24 to 48 hours), followed by gradual return of light activity that does not more than mildly worsen symptoms. Early subsymptom threshold aerobic exercise speeds recovery; exercise tolerance can be determined with a graded treadmill test and the training heart rate set below the level that provokes symptoms. Return to learn (school or work) proceeds first, with academic accommodations as needed. Most adults recover within about two weeks and most children within about four weeks; symptoms beyond that warrant a multidisciplinary evaluation, often including vestibular, oculomotor and cervical spine assessment.

Section 4Spinal cord injury

Traumatic spinal cord injury (SCI) most often follows motor vehicle crashes and falls (falls dominate in older adults), followed by violence and sports such as diving. Injuries cluster at the mobile cervical spine (especially C5 and C6) and the thoracolumbar junction. Tetraplegia means impairment of the cervical segments, affecting the arms, trunk, legs and pelvic organs; paraplegia means impairment of thoracic, lumbar or sacral segments, sparing the arms. Immediately after injury, spinal shock causes flaccid paralysis, areflexia and loss of autonomic function below the lesion; it usually resolves over days to weeks, signaled by the return of reflexes such as the bulbocavernosus reflex, after which spasticity and hyperreflexia appear below an upper motor neuron level.

Classifying the injury

The International Standards for Neurological Classification of SCI (the ASIA examination) test 10 key muscles on each side (graded 0 to 5) and 28 key sensory points on each side for light touch and pin prick (0 absent, 1 altered, 2 normal), plus an anorectal examination. Useful sensory landmarks: C4 over the acromioclavicular joint, C5 lateral antecubital fossa, C6 thumb, C7 middle finger, C8 little finger, T1 medial antecubital fossa, T4 nipple line, T10 umbilicus, L1 inguinal area, L3 medial femoral condyle, L4 medial malleolus, L5 dorsum of the foot at the third metatarsophalangeal joint, S1 lateral heel, and S4 to S5 perianal area.

The motor level is the lowest key muscle with a grade of at least 3, provided all key muscles above it are 5. The sensory level is the lowest dermatome with normal light touch and pin prick. The neurological level of injury is the most caudal segment with normal sensory and antigravity motor function on both sides. An injury is complete when there is no sacral sparing: no sensation at S4 to S5, no deep anal pressure and no voluntary anal contraction. In a complete injury, partially preserved segments below the level form the zone of partial preservation.

Incomplete cord syndromes

Functional expectations by level

Expected outcomes for a complete injury at each level, assuming no complications, guide goals, equipment and discharge planning. Incomplete injuries often exceed them.

Tenodesis is the passive finger flexion that occurs when the wrist is actively extended (and finger opening when the wrist flexes), because the long finger flexors are slightly shortened over the wrist. It provides a functional grasp for C6 and C7 injuries. To preserve it, never stretch the finger flexors with the wrist extended: range the fingers with the wrist flexed and the wrist with the fingers flexed. For long sitting, which is needed for dressing and bed mobility, hamstring length of about 100 to 110 degrees of straight leg raise is required, but avoid overstretching the low back extensors, which provide passive trunk stability.

Section 5Medical complications of SCI and neurologic injury

Many complications after spinal cord and brain injury are preventable, and some are emergencies that a therapist may be the first to see. The exam rewards fast recognition and the correct first action.

Autonomic dysreflexia

Autonomic dysreflexia (AD) is a potentially life threatening rise in blood pressure in people with injuries at T6 and above. A noxious stimulus below the lesion triggers a massive sympathetic reflex through the intact cord below the injury, causing vasoconstriction in the large splanchnic vascular bed. Baroreceptors detect the hypertension and the brain responds with vagal slowing of the heart and attempts at vasodilation, but the descending inhibitory signals cannot pass the injury, so the pressure keeps rising. Above the lesion, the body shows the brain's response; below it, the body shows the sympathetic storm.

• Triggers: bladder distension or a blocked or kinked catheter (most common), bowel distension or impaction, pressure injury, tight clothing or leg bag straps, ingrown toenail, sunburn, sexual activity, menstruation and labor, fractures and other painful stimuli.
• Signs: systolic pressure 20 to 40 mmHg above the person's baseline (often baseline is low, around 90 to 110 systolic, so 140 may already be dangerous), pounding headache, flushing and sweating above the lesion, nasal congestion, blurred vision, anxiety, bradycardia (sometimes), and pale, cool skin with goosebumps below the lesion.
• Management: sit the patient upright and lower the legs (orthostatic pooling lowers pressure), loosen clothing, binders and straps, check the bladder and catheter for kinks or blockage, check for bowel distension and other triggers, monitor blood pressure every 2 to 5 minutes, and call for medical help. If the pressure remains high (commonly a systolic of 150 mmHg or more) after removing the trigger, medication is given by the medical team. Never lay the patient flat.

Orthostatic hypotension

Orthostatic hypotension is a fall in systolic pressure of at least 20 mmHg or in diastolic pressure of at least 10 mmHg within three minutes of moving upright. It is common after SCI above T6 (loss of sympathetic vasoconstriction and of the muscle pump), and after prolonged bed rest, stroke and TBI. Symptoms include lightheadedness, blurred vision, nausea, yawning and loss of consciousness. Prevent it with gradual elevation (head of bed, then reclining wheelchair, then tilt table), compression stockings, an abdominal binder, adequate hydration, and medications such as midodrine prescribed by the physician. If symptoms occur, recline the patient or tilt the wheelchair back and elevate the legs. Note the contrast with AD: in hypotension, lie back and raise the legs; in AD, sit up and lower them.

Heterotopic ossification

Heterotopic ossification (HO) is the formation of bone in soft tissue around joints, typically 1 to 6 months after SCI or TBI. It occurs below the level of SCI, most often at the hip, then the knee; after TBI it also affects the shoulder and elbow. Early signs are warmth, swelling, erythema and decreasing range of motion, sometimes with fever; serum alkaline phosphatase rises and a bone scan detects it early. Because it mimics deep vein thrombosis and cellulitis, a swollen warm leg needs medical evaluation, including Doppler ultrasound, before therapy continues. Management includes medications (bisphosphonates such as etidronate, or NSAIDs) and gentle range of motion within the pain free range to maintain function; avoid forceful stretching, which may worsen the process. Surgical excision is considered after the bone matures.

Pressure injury

Loss of sensation, immobility, moisture, poor nutrition and spasticity make pressure injuries a lifelong risk after SCI. The usual sites are the ischial tuberosities (sitting), sacrum and coccyx (supine and semireclined), heels, trochanters and the occiput. Prevention: turn at least every 2 hours in bed; perform wheelchair pressure relief every 15 to 30 minutes for about 1 to 2 minutes (push ups, side leans or forward leans, or power tilt of at least about 30 to 45 degrees); use pressure redistributing cushions and mattresses; inspect the skin twice daily with a mirror; manage moisture; and optimize protein and calorie intake. Push ups are less effective than forward and side leans and stress the shoulders.

Spasticity management

Spasticity after SCI, stroke, TBI and MS is not always harmful: extensor tone can assist standing and transfers, and muscle activity helps maintain bulk and venous return. Treat it when it interferes with function, hygiene, positioning, sleep or skin, or causes pain or contracture. A sudden increase in spasticity is a warning sign of a new noxious stimulus, such as a urinary tract infection, pressure injury, ingrown toenail or fracture, and should prompt a search for the cause.

Other complications

• Deep vein thrombosis and pulmonary embolism: highest risk in the first weeks to months after SCI; prevention with anticoagulants and compression. Suspect DVT with unilateral calf or thigh swelling, warmth or pain (often painless when sensation is absent); hold the session and notify the physician. Patients can generally be mobilized once therapeutically anticoagulated, per the physician's orders.
• Respiratory: the diaphragm is innervated by C3 to C5; injuries at C5 and above reduce vital capacity, and the loss of abdominal and intercostal muscles impairs cough in tetraplegia and high paraplegia. Train assisted (quad) coughing, diaphragmatic and glossopharyngeal breathing and inspiratory muscle training, and use an abdominal binder. Avoid manual abdominal thrusts after recent abdominal surgery or with an inferior vena cava filter. Pneumonia is a leading cause of death after SCI.
• Thermoregulation: above T6, impaired sweating and vasomotor control make patients vulnerable to hyperthermia and hypothermia; dress appropriately and avoid exercise in heat.
• Bladder and bowel: injuries above the sacral cord produce a reflexive (spastic, UMN) bladder and bowel; conus and cauda equina injuries produce areflexic (flaccid, LMN) organs. Intermittent catheterization and a scheduled bowel program reduce infections and AD triggers.
• Bone loss: rapid osteoporosis below the lesion raises fracture risk, often at the distal femur and proximal tibia during transfers or stretching; use gentle technique.
• Shoulder pain from years of transfers and wheelchair propulsion in paraplegia: teach efficient long, smooth push strokes, level transfers when possible and rotator cuff and scapular strengthening.

Words worth knowing

Neuromuscular: Progressive, Peripheral and Vestibular Disorders

Progressive neurologic disease asks the physical therapist not only how to restore function, but how to protect it, pace it and plan for the losses ahead. The exam leans on these conditions because the right answer depends on the diagnosis: avoiding overwork weakness in Guillain Barre syndrome, cooling the patient with multiple sclerosis, timing exercise to the levodopa dose, or choosing the maneuver for the involved canal.

Section 1Parkinson disease and movement disorders

What goes wrong in the basal ganglia

Parkinson disease (PD) is a progressive neurodegenerative disorder in which dopamine producing neurons of the substantia nigra pars compacta die, and the surviving neurons contain clumps of alpha synuclein called Lewy bodies. By the time motor signs appear, more than half the nigral neurons are often lost. Dopamine normally facilitates the direct pathway of the basal ganglia and inhibits the indirect pathway, which brakes movement. Without it, the internal globus pallidus overinhibits the thalamus, so movement becomes small (hypokinesia), slow (bradykinesia), hard to start (akinesia), and shrinks as it is repeated.

Typical onset is after age 60, men are affected slightly more often than women, and signs begin on one side. Nonmotor features often come first: loss of smell, constipation, REM sleep behavior disorder, depression, orthostatic hypotension, fatigue and, later, dementia.

The cardinal signs

The four classic motor signs are remembered as TRAP:

• Tremor at rest: a 4 to 6 Hz "pill rolling" tremor of the thumb and fingers that is present at rest, lessens with voluntary movement, worsens with stress, and disappears in sleep. About a quarter of patients never develop it.
• Rigidity: increased resistance to passive movement that is the same in both directions and does not depend on velocity. Smooth resistance is lead pipe rigidity; when tremor is superimposed the resistance catches and releases in a ratchet pattern called cogwheel rigidity. This is the key contrast with spasticity, which is velocity dependent and usually greater in one direction.
• Akinesia and bradykinesia: poverty and slowness of movement, including reduced blinking, a masked face (hypomimia), soft speech (hypophonia), small handwriting (micrographia), reduced arm swing and difficulty turning in bed.
• Postural instability: impaired righting and protective reactions, especially backward (retropulsion). It appears later in the disease, responds poorly to levodopa, and is a major cause of falls.

Posture becomes flexed, extension and rotation range are lost, and kyphosis lowers vital capacity. Dysphagia raises the risk of aspiration pneumonia, a leading cause of death in late PD.

Parkinsonian gait and freezing

The gait is slow with a short step length, reduced foot clearance, decreased hip and knee excursion, reduced or absent arm swing, a narrow base and en bloc turning (the head, trunk and pelvis turn as one unit, with many small steps). Festination is an involuntary acceleration of progressively shorter steps as the center of mass falls ahead of the feet; the patient appears to chase the center of mass. Freezing of gait is a brief, episodic inability to step despite the intention to walk, as if the feet were glued to the floor. It is provoked by starting to walk, turning, passing through doorways or narrow spaces, approaching a destination, dual tasking and stress, and it is strongly associated with falls.

Medications and timing therapy

Carbidopa levodopa is the most effective drug; carbidopa blocks peripheral conversion of levodopa so more reaches the brain and nausea is reduced. Dopamine agonists, MAO B inhibitors and COMT inhibitors supplement it. After several years many patients develop motor fluctuations: a wearing off of benefit before the next dose, unpredictable on off switching, and peak dose dyskinesias, which are involuntary writhing or choreiform movements caused by too much dopamine effect, not by the disease itself. Watch for orthostatic hypotension, hallucinations and confusion.

Schedule therapy during the on period, typically about 45 to 60 minutes after a dose, when mobility is best and learning is easiest. Record the time of the last dose; a patient who varies from week to week may simply arrive at a different point in the dose cycle.

Examination and outcome measures

The disease specific scale is the Movement Disorder Society Unified Parkinson Disease Rating Scale (MDS-UPDRS), whose part III is the motor examination. Recommended measures include the Mini BESTest, Berg Balance Scale, Timed Up and Go (with a dual task), Five Times Sit to Stand, gait speed and the Six Minute Walk Test. In the pull test (shoulders pulled briskly backward), more than two backward steps or needing to be caught is abnormal. Always measure orthostatic blood pressure: a drop of 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing defines orthostatic hypotension.

Intervention principles

Exercise improves fitness, gait, balance, strength and quality of life at every stage. The PD clinical practice guideline strongly supports aerobic exercise (including moderate to high intensity, roughly 60 to 85 percent of heart rate reserve), resistance training, balance training, and external cueing for gait.

• Amplitude based training (for example the LSVT BIG approach and its speech counterpart LSVT LOUD) uses high effort, large amplitude, whole body movements repeated intensively (classically four sessions a week for four weeks) with recalibration of the patient's sense of normal size. Patients perceive their small movements as normal; the training teaches them that "big" feels exaggerated but looks normal.
• External cueing bypasses the defective internal timing of the basal ganglia by using cortical and cerebellar circuits. Visual cues include transverse lines or tape on the floor at the desired step length and laser lines projected from a walker or shoe. Auditory cues include a metronome or music set near or slightly above the comfortable cadence. Attentional cues ask the patient to think "big step" or to step over an imagined line. Somatosensory cues include rhythmic tapping.
• Freezing strategies: stop, stand tall, shift weight side to side, then step big over a real or imagined line; turn in a wide arc rather than pivoting; count steps aloud; avoid carrying objects while walking through doorways.
• Flexibility and posture: spinal extension and rotation, hip extension, and pectoral, hamstring and hip flexor length.
• Treadmill and dual task training once single task walking is safe; movement strategy training breaks complex tasks into conscious steps in advanced disease.

Other movement disorders

Section 2Multiple sclerosis, ALS and other progressive diseases

Multiple sclerosis: mechanism and presentation

Multiple sclerosis (MS) is an immune mediated inflammatory disease of the central nervous system in which T cells and B cells attack myelin and oligodendrocytes, leaving plaques of demyelination and, over time, axonal loss. Because only the CNS is affected, peripheral nerves and the neuromuscular junction are spared. Lesions are scattered in time and space (periventricular white matter, optic nerves, brainstem, cerebellum, cervical cord). Onset is usually at 20 to 40 years, women are affected two to three times as often, and risk rises with distance from the equator, low vitamin D, smoking and prior Epstein Barr virus infection.

Symptoms include:

• Fatigue, the most common and often most disabling symptom, frequently worse in the afternoon.
• Sensory changes: numbness, tingling, a band like feeling around the trunk, and Lhermitte sign (an electric sensation down the spine and limbs with neck flexion, a sign of cervical cord involvement).
• Optic neuritis (painful unilateral vision loss, often the first event) and internuclear ophthalmoplegia.
• Motor: weakness and spasticity with upper motor neuron signs, typically in the legs.
• Cerebellar: ataxia, intention tremor, dysmetria, scanning speech and nystagmus (the classic Charcot triad is nystagmus, intention tremor and scanning speech).
• Heat sensitivity: the Uhthoff phenomenon is a temporary worsening of symptoms when core temperature rises (exercise, hot weather, a hot bath, fever). Heat slows conduction in demyelinated axons; it resolves with cooling.

Clinical courses

The older label progressive relapsing MS is now folded into primary progressive disease described as active. Disability is commonly graded with the Expanded Disability Status Scale (EDSS, 0 to 10 in half steps). Anchor points worth knowing: 4.0 means fully ambulatory without aid for about 500 meters; 6.0 means a unilateral assistive device is needed to walk about 100 meters; 6.5 means bilateral assistance; 7.0 means essentially restricted to a wheelchair; 10 is death due to MS.

Examination and intervention in MS

Useful measures include the Timed 25 Foot Walk, the Six Minute Walk Test (speed falling in later minutes shows motor fatigability), the 12 item MS Walking Scale, the Modified Fatigue Impact Scale, the Berg Balance Scale and the Modified Ashworth Scale.

Exercise is safe and beneficial in MS and does not trigger relapses. Current guidance supports moderate intensity aerobic exercise (for example about 30 minutes at moderate intensity two or three times a week, built up gradually) and resistance training two or three times a week, plus balance training, flexibility and task specific gait training. Practical precautions:

• Prevent overheating: exercise in a cool, air conditioned room, early in the day, with fans, cooling vests, cold drinks and pre cooling. Aquatic therapy should use cool water, generally below about 84 to 85 degrees Fahrenheit (about 29 degrees Celsius); avoid hot tubs and warm therapy pools.
• Use interval training and rest breaks; schedule sessions in the morning when fatigue is lowest.
• Do not exercise vigorously during an acute relapse, especially while receiving high dose corticosteroids; shift to positioning, gentle ROM and maintaining function, then resume a graded program as the relapse settles.
• Manage spasticity with daily stretching and positioning; leg spasticity sometimes aids standing, so treat it when it interferes.

Energy conservation is taught explicitly, often as the four Ps: plan the day and week, pace activities with rest before fatigue sets in, prioritize what truly matters, and position the body and the environment for efficiency (sitting to dress, keeping items within reach).

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive degeneration of both upper motor neurons (motor cortex and corticospinal tracts) and lower motor neurons (anterior horn cells and motor cranial nerve nuclei). About 10 percent of cases are familial; onset is usually in the late 50s to 60s. The patient shows a mixed picture: weakness, atrophy, fasciculations and cramps (lower motor neuron) together with spasticity, hyperreflexia and a Babinski sign (upper motor neuron), often in the same limb. Onset is usually asymmetric in a hand or foot; bulbar onset (dysarthria, dysphagia, tongue fasciculations) carries a worse prognosis.

ALS characteristically spares sensation, eye movements, and bowel and bladder control, and most patients keep their cognition, although a minority develop frontotemporal dementia. Median survival is about three to five years from symptom onset, and death is usually from respiratory failure. Riluzole and edaravone modestly slow progression.

Physical therapy goals follow the stage and the prognosis:

• Early (mild weakness): moderate, submaximal aerobic and resistance exercise without exhaustion, only for muscles with at least antigravity strength. Weaker muscles may suffer overwork; fatigue lasting over about 30 minutes, or weakness the next day, means the dose was too high.
• Middle (some limbs severely weak): ROM and stretching, energy conservation, orthoses (ankle foot orthosis, cervical collar, wrist hand orthoses) and assistive devices.
• Late (dependent): positioning, skin protection, airway clearance, caregiver training, hospital bed, lift, and a tilt in space power wheelchair with head support.

Anticipate equipment: start the power wheelchair evaluation months before it is needed, with controls adaptable to future hand weakness. Monitor respiratory function: forced vital capacity below about 50 percent of predicted, orthopnea, morning headaches or disturbed sleep signal the need to discuss noninvasive ventilation. Teach assisted cough and breathing strategies.

Section 3Peripheral neuropathies and neuromuscular disease

Localizing weakness along the motor unit

A motor unit is one lower motor neuron and all the muscle fibers it supplies. Disease can strike the cell body (anterior horn cell), the axon or its myelin (peripheral nerve), the synapse (neuromuscular junction), or the muscle fiber itself. Each site leaves a recognizable fingerprint, and identifying the site is often the first step to the right answer.

Guillain Barre syndrome

Guillain Barre syndrome (GBS) is an acute immune mediated polyneuropathy, most often the demyelinating form (acute inflammatory demyelinating polyradiculoneuropathy). About two thirds of patients report a respiratory or gastrointestinal infection one to four weeks earlier; Campylobacter jejuni is the classic trigger.

• Presentation: rapidly progressive, relatively symmetric weakness that usually starts in the legs and ascends, with distal paresthesias, back or limb pain, and areflexia. Cranial nerves (especially bilateral facial weakness) and respiratory muscles may be involved.
• Autonomic instability: fluctuating blood pressure, arrhythmias, tachycardia or bradycardia, and orthostatic hypotension.
• Course: weakness peaks within four weeks, plateaus, then recovers over months in a descending order. Most patients walk independently within a year; about 20 percent keep significant disability.
• Diagnosis: high cerebrospinal fluid protein with a normal cell count (albuminocytologic dissociation) and slowed nerve conduction.
• Treatment: intravenous immunoglobulin or plasma exchange, which shorten the course when given early. Corticosteroids are not effective.

About a quarter of patients need mechanical ventilation. Monitor vital capacity: a falling value (below about 20 mL/kg is a commonly cited threshold for intubation), weak cough, and difficulty counting to 20 in one breath are warnings. In the acute phase, the therapist focuses on positioning, gentle passive and active assisted ROM, splinting to prevent contracture (for example resting ankle splints), pressure injury prevention, chest physical therapy and airway clearance, and gradual tilt to upright with blood pressure monitoring.

In recovery, exercise must avoid overwork of reinnervating muscles. Use low intensity, low repetition, frequently rested exercise and progress slowly, watching for increased weakness, cramping or prolonged fatigue in the following 24 hours. Chronic inflammatory demyelinating polyneuropathy (CIDP) progresses for more than eight weeks and, unlike GBS, responds to corticosteroids.

Diabetic and other polyneuropathies

Diabetic peripheral neuropathy is the most common neuropathy in developed countries. The usual form is a distal symmetric sensorimotor polyneuropathy that begins in the toes and spreads proximally in a stocking and glove distribution, because the longest axons fail first. Small fiber loss causes burning pain; large fiber loss causes loss of vibration and proprioception, reduced ankle reflexes and a positive Romberg test. Intrinsic foot weakness produces claw toes. Autonomic neuropathy causes dry, cracked skin, orthostatic hypotension, resting tachycardia and a blunted heart rate response to exercise.

The key screening test is the 5.07 (10 gram) Semmes Weinstein monofilament: inability to feel it at tested plantar sites indicates loss of protective sensation and a high risk of ulceration. Combine it with vibration testing (128 Hz tuning fork), ankle reflexes and a foot inspection. Management includes daily foot inspection, depth shoes and insoles, never walking barefoot, balance training, and exercise with glucose monitoring. Weight bearing exercise is acceptable with proper footwear if there is no active ulcer; choose non weight bearing exercise (cycling, swimming) when an ulcer or acute Charcot foot is present. Because autonomic neuropathy blunts the heart rate response, use RPE rather than target heart rate.

A warm, red, swollen foot with intact skin in a person with neuropathy should be treated as an acute Charcot neuroarthropathy until proven otherwise; it needs immediate offloading (total contact cast) and referral, not exercise.

Post polio syndrome

Poliomyelitis destroys anterior horn cells; surviving neurons sprout to adopt orphaned muscle fibers, creating giant motor units. Decades later (typically 15 or more years after the acute illness), these overextended units begin to fail. Post polio syndrome presents with new weakness, often in previously affected muscles, unusual fatigue, muscle and joint pain, cold intolerance, and sometimes new breathing or swallowing problems. Management centers on pacing: nonfatiguing, submaximal exercise with frequent rests, energy conservation, weight control, and lightweight orthoses and devices to unload overused muscles.

Myasthenia gravis and Lambert Eaton syndrome

Myasthenia gravis (MG) is an autoimmune disease in which antibodies attack the postsynaptic acetylcholine receptors at the neuromuscular junction (some patients have antibodies against MuSK instead). Fewer functional receptors means each nerve impulse has less safety margin, so strength fades with repeated use. Hallmarks are fatigable weakness that worsens through the day and with activity and improves with rest, ptosis and diplopia (ocular muscles are involved in most patients and are often first), bulbar weakness (dysarthria, dysphagia, a nasal voice, difficulty chewing), and proximal limb and neck extensor weakness. Sensation and reflexes are normal. Thymus abnormalities are common, and thymectomy is part of treatment.

Treatment includes acetylcholinesterase inhibitors (pyridostigmine), corticosteroids and other immunosuppressants, and IVIG or plasma exchange for crises. Two emergencies matter:

• Myasthenic crisis: respiratory and bulbar failure, often triggered by infection, surgery or drugs such as aminoglycosides.
• Cholinergic crisis: weakness from excess anticholinesterase drug, with salivation, sweating, diarrhea, small pupils and bradycardia.

For therapy, schedule exercise when the medication is at peak effect (commonly about one to two hours after a pyridostigmine dose) and when fatigue is low (often the morning). Use short bouts with rest, avoid exhaustion and heat, and monitor breathing and swallowing; moderate exercise is safe in stable MG.

Lambert Eaton myasthenic syndrome is an autoimmune attack on presynaptic voltage gated calcium channels, so less acetylcholine is released. Strength and reflexes briefly improve with repeated effort (facilitation), the weakness is proximal and in the legs, autonomic symptoms such as dry mouth are common, and about half the cases are associated with small cell lung cancer. A patient with new proximal weakness, dry mouth and a smoking history needs referral to look for a tumor.

Muscular dystrophies

In Duchenne muscular dystrophy, the absence of dystrophin leaves the membrane fragile, so contraction, especially eccentric, tears fibers that are replaced by fat and connective tissue. Creatine kinase is markedly elevated. The Gowers sign (climbing up the thighs to stand) reflects hip extensor weakness. Plan ahead:

• Prevent contractures: daily stretching of heel cords, hamstrings, hip flexors and iliotibial bands, night resting ankle foot orthoses, and standing programs.
• Exercise: submaximal swimming, cycling and play; avoid eccentric work and exhaustion. Muscle pain or dark urine after exercise signals overwork.
• Mobility, spine and breathing: knee ankle foot orthoses may prolong standing; then a power wheelchair with postural support. Monitor scoliosis, teach assisted cough, and support cardiac and vital capacity monitoring.

Section 4Vestibular disorders

The vestibular system in brief

Each inner ear contains three semicircular canals (anterior, posterior and horizontal) that sense angular acceleration, and two otolith organs (utricle and saccule) that sense linear acceleration and head tilt relative to gravity. The utricle contains calcium carbonate crystals called otoconia. The canals work in push pull pairs: turning the head right excites the right horizontal canal. Vestibular signals drive the vestibulo ocular reflex (VOR), which moves the eyes opposite to the head to keep images stable on the retina, and the vestibulospinal reflexes, which keep the body upright. A mismatch between the two sides produces vertigo (an illusion of movement) and nystagmus, a rhythmic eye movement with a slow drift and a fast corrective beat. Nystagmus is named by the direction of its fast phase.

Benign paroxysmal positional vertigo

Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo. Otoconia dislodge from the utricle and move into a semicircular canal. In canalithiasis, the debris floats freely in the canal and drags the endolymph when the head moves into the plane of that canal, causing brief vertigo with a short latency. In cupulolithiasis, debris sticks to the cupula and makes it gravity sensitive, causing vertigo and nystagmus that persist as long as the head stays in the provoking position.

Spells of spinning vertigo last seconds and are triggered by rolling in bed, lying down or looking up; hearing and the neurologic examination are normal.

• Posterior canal BPPV is by far the most common (roughly 80 to 90 percent), because the posterior canal is the lowest part of the labyrinth when upright and supine.
• Horizontal (lateral) canal BPPV accounts for most of the rest.
• Anterior canal BPPV is rare.

Positional tests and treatment by canal

The Dix-Hallpike test examines the posterior (and anterior) canal. The patient sits long sitting on the table, the head is rotated 45 degrees toward the side being tested, and the patient is brought quickly back to supine with the neck extended about 20 degrees over the end of the table. The examiner watches the eyes for 30 to 60 seconds. Posterior canal canalithiasis produces upbeating and torsional nystagmus (top of the eye beating toward the down, affected ear) after a few seconds of latency, lasting under 60 seconds and fatiguing with repetition. The side-lying test is an alternative when neck extension is unsafe.

The supine roll test examines the horizontal canal: with the patient supine and the head flexed about 30 degrees, the head is rotated quickly about 90 degrees to each side. Horizontal canal BPPV produces horizontal nystagmus on both sides.

• Geotropic nystagmus (beating toward the ground on each side) indicates canalithiasis; the side with the stronger nystagmus and symptoms is the affected side.
• Apogeotropic nystagmus (beating away from the ground) indicates cupulolithiasis (or debris near the cupula); the side with the weaker response is usually the affected side.

The Epley canalith repositioning maneuver for right posterior canal BPPV proceeds through four positions, holding each until the nystagmus stops (generally at least 30 seconds to a minute): (1) from sitting, head turned 45 degrees to the right, recline into the right Dix-Hallpike position; (2) turn the head 90 degrees to the left so it is 45 degrees to the left, keeping the neck extended; (3) roll the body onto the left side while turning the head another 90 degrees so the face points toward the floor; (4) return to sitting with the head slightly flexed. The goal is to move the otoconia around the canal and out into the utricle. One or two maneuvers resolve the problem in most patients. Post maneuver restrictions are no longer routinely recommended; Brandt-Daroff exercises are a less effective home option.

Unilateral vestibular hypofunction

Sudden loss of function in one labyrinth or vestibular nerve creates a large imbalance between the two sides. Vestibular neuritis (inflammation of the vestibular nerve, presumed viral) presents with acute, continuous, severe vertigo lasting days, nausea and vomiting, imbalance (veering toward the affected side), and spontaneous horizontal torsional nystagmus beating away from the affected ear. The nystagmus follows Alexander's law (stronger when gazing in the direction of the fast phase) and is suppressed by visual fixation. Hearing is normal. Labyrinthitis produces the same picture plus hearing loss. Vestibular schwannoma (acoustic neuroma) causes slowly progressive one sided hearing loss, tinnitus and imbalance.

The head impulse test (head thrust) checks the VOR: the examiner turns the patient's head quickly through a small angle while the patient looks at the examiner's nose. With a normal VOR the eyes stay on target. With hypofunction, turning toward the affected side produces a corrective saccade back to the target. Also measure dynamic visual acuity (losing more than two lines with head movement is abnormal), the Dizziness Handicap Inventory and the Functional Gait Assessment.

Recovery depends on central compensation, which is driven by error signals created by moving the head. Vestibular suppressants help in the first days but slow compensation if continued. Vestibular rehabilitation uses four types of exercise:

• Adaptation (gaze stabilization): VOR times 1 (the target stays still and the head moves side to side or up and down while keeping the target in focus) and VOR times 2 (head and target move in opposite directions, a harder task). Progress speed, duration, background and posture while the target stays clear.
• Habituation: repeated, graded exposure to movements or visual environments that provoke mild symptoms, so the brain learns to reduce its response. Best for motion provoked dizziness and visual motion sensitivity.
• Substitution: using vision and somatosensation, or eye movements and saccades, to replace lost vestibular input; most important with bilateral loss.
• Balance and gait training with varied surfaces, vision and head turns.

The vestibular rehabilitation clinical practice guideline recommends gaze stabilization exercises for both acute and chronic hypofunction, with a typical minimum dose of about three times per day totaling at least 12 minutes per day in acute and subacute cases, and three to five times per day totaling about 20 minutes per day in chronic cases, plus about 20 minutes per day of balance and gait exercise. A mild, short lived increase in symptoms during exercise is expected.

Bilateral vestibular hypofunction

Loss on both sides, most often from aminoglycoside ototoxicity (gentamicin), causes oscillopsia (the visual world bounces with head movement and walking), marked imbalance, especially in the dark or on uneven ground, and a high fall risk. Vertigo is usually absent because the loss is symmetric. The head impulse test is abnormal in both directions. Rehabilitation emphasizes gaze stabilization, substitution with vision and somatosensation, balance training, night lights and often a cane. Recovery is slower and less complete, and the guideline dose is higher (about three to five times per day totaling 20 to 40 minutes per day).

Meniere disease

Meniere disease (endolymphatic hydrops) produces episodic attacks of vertigo lasting about 20 minutes to 12 hours, with fluctuating low frequency sensorineural hearing loss, tinnitus and aural fullness in the affected ear. Management is medical (low sodium diet, diuretics, procedures). Vestibular rehabilitation does not help during attacks but helps once the deficit is stable.

Central versus peripheral signs

Not every dizzy patient has an ear problem. A stroke in the brainstem or cerebellum can mimic vestibular neuritis. In a patient with acute continuous vertigo and nystagmus, the bedside HINTS examination (head impulse, nystagmus, test of skew) is more sensitive for stroke than early MRI when performed by a trained examiner. A normal head impulse in an acutely vertiginous patient is a worrying sign, because the peripheral VOR is intact and the lesion is probably central.

Section 5Cerebellar, cranial nerve and other neurologic conditions

Bell palsy

Bell palsy is an acute, idiopathic, unilateral lower motor neuron paralysis of the facial nerve (cranial nerve VII), thought to result from swelling of the nerve in the facial canal, often linked to herpes simplex reactivation, and more common in pregnancy and diabetes. Weakness develops over hours to about three days and involves the entire half of the face: the patient cannot wrinkle the forehead, close the eye completely, smile symmetrically or puff the cheek. There may also be loss of taste on the anterior two thirds of the tongue, hyperacusis (stapedius paralysis) and pain behind the ear.

The key distinction is from a central (upper motor neuron) facial palsy, such as after a stroke. The upper face receives corticobulbar input from both hemispheres, so a unilateral cortical lesion weakens only the lower face on the opposite side and spares the forehead. A lower motor neuron lesion (Bell palsy) affects the upper and lower face on the same side.

Most patients recover: about 70 percent fully, and as many as 85 percent or more show improvement within three weeks. Incomplete paralysis at onset, early improvement and younger age predict a good outcome. Oral corticosteroids started within 72 hours improve recovery; antivirals may be added in severe cases. The House Brackmann scale grades facial function from I (normal) to VI (total paralysis).

Physical therapy priorities:

• Protect the eye: incomplete closure (lagophthalmos) and reduced tearing risk corneal drying and ulceration. Teach artificial tears by day, lubricating ointment and taping or a moisture chamber at night, and sunglasses outdoors.
• Facial neuromuscular retraining: slow, small, symmetric, isolated movements in front of a mirror (mirror biofeedback), gentle massage and stretching of the affected side, and functional tasks (eating, drinking, speaking).
• Avoid mass action: forceful, maximal grimacing and gross exercises can encourage synkinesis, the unwanted linked movements (for example the eye closing when the patient smiles) that follow aberrant regeneration. Teach the patient to suppress synkinesis by moving gently and in isolation.
• Electrical stimulation is not recommended routinely for Bell palsy, because evidence is weak and there is concern that it may promote synkinesis.
• Refer if there is no improvement by three to four months, or if weakness is bilateral, progressive or joined by other cranial nerve signs.

Other cranial nerve conditions

Cerebellar ataxia

The cerebellum compares intended with actual movement and corrects errors. Damage (stroke, tumor, MS, alcohol, hereditary ataxias) produces ataxia, poorly scaled and timed movement. Cerebellar signs appear on the same side as the lesion, because the pathways cross twice. A lesion of the midline vermis produces truncal ataxia, a wide based staggering gait and titubation (head and trunk oscillation); a lesion of a cerebellar hemisphere produces limb ataxia on the same side.

Unlike sensory ataxia from dorsal column or large fiber neuropathy, cerebellar ataxia is not much worse with the eyes closed, so the Romberg test is typically negative or only mildly worse; a markedly positive Romberg points to proprioceptive loss. The Scale for the Assessment and Rating of Ataxia (SARA) is the disease specific measure.

The best supported intervention is intensive, task oriented balance and coordination training with a progressively narrower base, perturbations and varied gait. Classic approaches include Frenkel exercises (slow, repetitive, visually guided movements progressing from lying to sitting to standing) and PNF techniques such as rhythmic stabilization and alternating isometrics to build proximal stability. Light weights may damp tremor during a task but do not train lasting control. Practice must be high in volume; gains fade if training stops.

Huntington disease

Huntington disease (HD) is an autosomal dominant neurodegenerative disease caused by an expanded CAG trinucleotide repeat in the huntingtin gene on chromosome 4. Each child of an affected parent has a 50 percent risk, and longer repeats cause earlier onset. Neurons of the caudate and putamen (striatum) degenerate, reducing the brake on movement and producing excessive involuntary movement. Onset is typically between 30 and 50 years, and the disease progresses over roughly 15 to 20 years to death, often from aspiration pneumonia or complications of falls.

The classic triad is:

• Motor: chorea (brief, irregular, flowing, dance like involuntary movements), impaired voluntary movement and saccades, motor impersistence (inability to sustain a grip or tongue protrusion), dysarthria, dysphagia, and a wide based, irregular gait with sudden lurches. Late in the disease chorea often lessens and rigidity, bradykinesia and dystonia dominate. Juvenile onset (Westphal variant) presents with rigidity rather than chorea.
• Cognitive: executive dysfunction, slowed processing and eventually dementia.
• Psychiatric: depression, irritability, apathy, impulsivity, obsessive behavior and an elevated suicide risk.

Therapy moves from aerobic, strength, balance and fall prevention work early, to devices, home safety and caregiver training in the middle stage, to seating, padding, positioning and skin and respiratory care late. Chorea is treated with tetrabenazine, which can worsen depression. Keep instructions simple and routine, and screen for depression and suicidal thoughts.

Vertigo and dizziness red flags

Most dizziness is benign, but some presentations demand immediate referral. Before cervical manual therapy or positional testing, screen for cervical artery dysfunction with the familiar mnemonic of the 5 Ds and 3 Ns: dizziness, diplopia, dysarthria, dysphagia, drop attacks, and nausea, numbness, nystagmus, plus ataxia of gait.

Distinguish vertigo (a spinning or moving illusion, usually vestibular) from presyncope (lightheadedness, near fainting, usually cardiovascular or orthostatic) and disequilibrium (imbalance without a head sensation, often from neuropathy, cerebellar or multisensory loss).

Words worth knowing

Cardiovascular and Pulmonary Foundations: Physiology, Examination and Monitoring

Every exercise prescription is a request for more oxygen, and the heart, lungs and blood decide whether the body can meet it. On the licensing exam, cardiovascular and pulmonary questions rarely ask for physiology for its own sake: they ask whether a patient is safe to treat, when to stop, and what a number or rhythm means for the session in front of you. This chapter builds the physiology, monitoring, ECG, auscultation, imaging, pulmonary function, blood gas and laboratory knowledge that lets you answer those questions with confidence.