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.

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