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.

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