Stroke (Cerebrovascular Accident)

Populations and Risk Factors

• Age is the strongest non-modifiable risk factor; risk doubles each decade after age 55; however, stroke can occur at any age including pediatric populations
• Men have a slightly higher overall incidence, but women have higher lifetime risk and higher mortality, partly due to longer life expectancy and higher rates of atrial fibrillation in older women
• Hypertension is the single most important modifiable risk factor — present in approximately 70% of stroke cases; sustained elevated blood pressure damages arterial endothelium and accelerates atherosclerosis
• Atrial fibrillation increases ischemic stroke risk approximately 5-fold due to cardiac embolism from mural thrombus formation in the fibrillating atrium
• Diabetes mellitus accelerates atherosclerosis and increases stroke risk 2–4 times; also worsens outcomes post-stroke
• Smoking doubles stroke risk through endothelial damage, increased coagulability, and accelerated atherosclerosis
• Transient ischemic attack (TIA) — a temporary focal neurological deficit lasting less than 24 hours with complete resolution — is the most important warning sign; approximately 10–15% of TIA patients will have a full stroke within 90 days, with the highest risk in the first 48 hours
• Carotid artery stenosis (atherosclerotic narrowing) — especially relevant for MTs because the carotid bifurcation lies within the anterior triangle of the neck, a region requiring precaution during cervical treatment
• Obesity, sedentary lifestyle, excessive alcohol use, and oral contraceptive use (especially combined with smoking) are additional modifiable risk factors

Causes and Pathophysiology

Ischemic Stroke (87% of Cases)

• Thrombotic stroke: atherosclerotic plaque in a cerebral or carotid artery narrows the lumen progressively; a thrombus forms on the plaque surface and occludes the artery. Most common in the middle cerebral artery (MCA) territory, producing contralateral face and upper extremity deficits. Thrombotic strokes often have a stuttering onset with symptoms that fluctuate before completing.
• Embolic stroke: a clot or debris forms elsewhere — most commonly the left atrium in atrial fibrillation, or a carotid plaque — and travels to lodge in a cerebral artery. Onset is typically sudden and maximal at presentation. The MCA is the most common destination because it is the direct continuation of the internal carotid artery.
• Ischemic penumbra: the tissue immediately surrounding the infarct core receives marginal collateral blood supply. This penumbra is functionally impaired but not yet dead — it is the target of acute medical intervention (thrombolysis, thrombectomy). If blood flow is restored within the therapeutic window (typically 4.5 hours for IV thrombolysis), penumbral tissue can recover. If not, the penumbra converts to infarct, expanding the area of permanent damage.

Hemorrhagic Stroke (13% of Cases)

• Intracerebral hemorrhage: rupture of a small penetrating artery within the brain parenchyma, most commonly from chronic hypertensive damage to small vessel walls (Charcot-Bouchard microaneurysms). Blood accumulates as a hematoma, compressing surrounding tissue and increasing intracranial pressure. Onset is typically during activity, with rapid deterioration and severe headache ("the worst headache of my life" when subarachnoid).
• Subarachnoid hemorrhage (SAH): rupture of an arterial aneurysm (often at the circle of Willis) into the subarachnoid space. Presents with sudden thunderclap headache, neck stiffness, photophobia, and rapid loss of consciousness. This is a neurosurgical emergency with high mortality.

Upper Motor Neuron Damage — Why Spasticity Develops

• Stroke damages upper motor neurons (UMNs) in the motor cortex and corticospinal tract. The UMN normally exerts inhibitory control over spinal motor neuron pools (lower motor neurons). When UMN input is lost, LMNs become disinhibited, leading to excessive alpha motor neuron firing.
• Flaccid stage (acute/shock phase): immediately after stroke, the affected side is flaccid — loss of all voluntary motor control with decreased tone and absent reflexes. This represents neural shock (diaschisis), during which the nervous system has not yet reorganized. Duration varies from days to weeks.
• Spastic stage (chronic phase): as neural shock resolves, spinal reflexes emerge unopposed by cortical inhibition. Muscle spindle sensitivity increases without UMN dampening, producing velocity-dependent hypertonia (spasticity). Deep tendon reflexes become hyperactive (3+ to 4+), clonus may develop at the ankle, and Babinski sign becomes positive (great toe dorsiflexion with fanning of lesser toes on plantar stimulation).
• Synergy patterns: disinhibited spinal circuits do not produce isolated voluntary movements — they produce mass movement patterns called synergies. The patient cannot flex the elbow without simultaneously flexing the wrist, fingers, and shoulder:
• Flexor synergy (upper extremity): scapular retraction and elevation, shoulder abduction and external rotation, elbow flexion, forearm supination, wrist and finger flexion — the classic hemiplegic arm posture
• Extensor synergy (lower extremity): hip extension, adduction, and internal rotation, knee extension, ankle plantarflexion and inversion — produces the stiff-leg gait pattern
• Shoulder subluxation: loss of deltoid and rotator cuff tone in the flaccid stage allows the weight of the arm to distract the humeral head inferiorly from the glenoid fossa. The supraspinatus (which normally maintains superior approximation of the GH joint) cannot provide its tonic support. A palpable gap appears inferior to the acromion. As spasticity develops, the internal rotators and adductors shorten, but the subluxation may persist, predisposing to adhesive capsulitis and shoulder-hand syndrome.

Signs and Symptoms

Acute Stroke (Emergency Recognition)

• FAST assessment: Face drooping (unilateral facial weakness), Arm drift (one arm drifts downward when both are raised), Speech difficulty (slurred or incomprehensible), Time to call emergency services — this is a screening tool for bystanders and healthcare providers; a positive FAST is a medical emergency
• Sudden onset of contralateral hemiparesis or hemiplegia
• Sudden severe headache with no known cause (especially hemorrhagic)
• Sudden confusion, trouble speaking or understanding speech
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking, dizziness, loss of balance or coordination

Flaccid Stage (Days to Weeks Post-Stroke)

• Complete loss of voluntary movement on the affected side (hemiplegia)
• Flaccid tone — affected limbs feel heavy and limp
• Absent or diminished deep tendon reflexes on the affected side
• Loss of postural control — unable to sit unsupported
• Shoulder subluxation risk is highest during this stage
• Dysphagia (swallowing difficulty) — risk of aspiration pneumonia
• Bladder dysfunction — urinary retention or incontinence

Spastic Stage (Weeks to Months Post-Stroke, Persists Chronically)

• Spasticity develops in characteristic UMN patterns — flexor synergy dominates the upper extremity (arm held flexed across chest), extensor synergy dominates the lower extremity (leg held stiff in extension)
• Hyperreflexia (exaggerated DTRs, 3+ to 4+) and positive Babinski sign
• Clonus — rhythmic involuntary oscillation, most commonly at the ankle with rapid dorsiflexion
• Progressive contracture risk — chronically spastic muscles shorten over time, particularly shoulder adductors/internal rotators, elbow flexors, wrist and finger flexors, ankle plantarflexors
• Hemiplegic gait — circumduction pattern: the spastic extended leg swings outward in a semicircle because the patient cannot flex the hip and knee normally to clear the foot; plantarflexion contracture produces a foot-slapping or toe-drag pattern
• Compensatory overload on the unaffected side — the sound limb performs double duty for all transfers, gait, and ADLs, leading to overuse strain in the contralateral shoulder, hip, and trunk muscles

Cognitive and Communication Deficits

• Broca's aphasia (expressive): left frontal lobe damage; the patient understands speech but cannot produce fluent language — speech is effortful, halting, and telegraphic; comprehension preserved; frustration common
• Wernicke's aphasia (receptive): left temporal lobe damage; the patient speaks fluently but content is nonsensical; cannot understand spoken or written language; the patient may be unaware of the deficit
• Hemispatial neglect (unilateral neglect): typically right parietal lobe damage; the patient fails to attend to or perceive stimuli on the contralateral (left) side — they may eat food from only one side of the plate, shave one side of the face, or fail to notice the therapist approaching from the neglected side; this is not a visual field defect but an attentional deficit
• Cognitive impairment: impaired memory, attention, executive function, and visuospatial processing; vascular dementia may develop with repeated or extensive infarcts
• Emotional lability: uncontrolled crying or laughing disproportionate to the stimulus; the patient may be unable to suppress emotional expression — this is neurological, not psychological

Assessment Profile

Subjective Presentation

• Chief complaint: variable depending on stage and time since stroke — chronic-stage patients typically report stiffness and tightness on the affected side, difficulty using the arm or hand, balance problems, pain in the hemiplegic shoulder, or compensatory pain on the unaffected side; history is often provided partly or entirely by a caregiver, especially if the patient has aphasia or cognitive impairment
• Pain quality: spastic-origin deep muscular aching and cramping in affected-side muscles; hemiplegic shoulder pain — may be sharp with movement (subluxation, impingement) or deep and constant (capsular contracture); neuropathic pain — burning, shooting, or tingling in the affected limbs (central post-stroke pain syndrome affects approximately 8% of survivors)
• Onset: sudden onset of the original stroke event (now historical); the physical effects being assessed develop over weeks to months post-stroke; note time since stroke (acute vs. subacute vs. chronic) and current rehabilitation status
• Aggravating factors: rapid passive movement of spastic limbs (triggers stretch reflex, increases spasticity); prolonged static positioning (increases stiffness and contracture); cold environments may increase spasticity in some patients; emotional stress and fatigue worsen spastic tone
• Easing factors: slow, rhythmic passive movement reduces spastic tone temporarily; warmth may decrease tone (but check for sensory deficits before applying heat); positioning with the affected arm supported reduces hemiplegic shoulder pain; rest reduces compensatory overload pain on the unaffected side
• Red flags: Any new sudden-onset neurological deficit — facial droop, arm weakness, speech change — indicates possible new stroke or TIA; emergency referral; do not treat. Progressive worsening of existing deficits beyond the expected recovery trajectory → medical referral for reassessment. New onset of seizures post-stroke → medical referral.

Observation

• Local inspection: hemiplegic posture — affected upper extremity held in flexor synergy pattern (shoulder adducted and internally rotated, elbow flexed, forearm pronated, wrist and fingers flexed); affected lower extremity in extensor synergy (hip extended and adducted, knee extended, ankle plantarflexed and inverted); muscle atrophy in chronically immobile or flaccid muscles; palpable gap inferior to acromion in shoulder subluxation; edema in dependent affected limb from reduced mobility and impaired venous return
• Posture: lateral trunk flexion toward the affected side (from trunk weakness); elevated and protracted shoulder on the unaffected side (compensatory); weight bearing shifted entirely to the unaffected leg; affected foot often in equinovarus from plantarflexor and invertor spasticity
• Gait: hemiplegic circumduction gait — the affected leg swings outward in a semicircle with hip hiking on the affected side because the spastic extended leg cannot flex to clear the ground; foot slap or toe drag from ankle plantarflexion contracture; absent or reduced arm swing on the affected side; slow cadence with prolonged stance phase on the unaffected leg; may use assistive device (cane on the unaffected side, AFO on the affected ankle)

Palpation

• Tone: UMN spastic hypertonia on the affected side — velocity-dependent increased resistance to passive movement; distinct from the constant resistance of muscle guarding or the lead-pipe rigidity of Parkinson's; most affected muscles are elbow flexors (biceps, brachialis, brachioradialis), wrist and finger flexors, shoulder internal rotators and adductors (pectoralis major, subscapularis, latissimus dorsi), hip adductors, and ankle plantarflexors (gastrocnemius, soleus); in the flaccid stage (less commonly seen by MTs), the affected side feels limp and heavy with no muscle activation; clonus may be elicitable at the ankle with rapid dorsiflexion — if present, avoid rapid passive movement in that direction
• Tenderness: hemiplegic shoulder tenderness — inferior GH joint line (subluxation), bicipital groove (long head of biceps under tension), supraspinous fossa (atrophied or stretched supraspinatus); trigger points in chronically spastic muscles from sustained contraction and ischemia — particularly biceps, upper trapezius (compensatory on both sides), forearm flexor mass, calf muscles; referred path tenderness is not dermatomal in stroke — pain patterns follow the spastic muscle groups and their referral patterns rather than a specific nerve root distribution; compensatory overload tenderness on the unaffected side — contralateral shoulder (rotator cuff overuse from one-armed ADLs), contralateral hip (weight-bearing overload), lumbar paraspinals (asymmetric gait loading)
• Temperature: affected limbs may be cooler from reduced active movement and impaired sympathetic regulation; warmth does not indicate inflammation in the chronic stage — it may reflect local circulatory changes; critical: assess sensation before applying any thermal modality — insensate areas cannot provide feedback about burns; heat to areas of diminished sensation is contraindicated
• Tissue quality: spastic muscles palpate as hypertonic, taut, and poorly extensible with reduced fascial glide; chronically immobile muscles develop fibrotic changes and reduced elasticity; flaccid muscles (if still present) feel soft and atrophic with reduced bulk; edema in dependent limbs — pitting edema may be present in the affected hand, ankle, and foot; periarticular thickening around the hemiplegic shoulder if early adhesive capsulitis is developing

Motion Assessment

• AROM: severely restricted on the affected side — movements are dominated by synergy patterns rather than isolated voluntary control; the patient attempting to flex the elbow will simultaneously flex the wrist and fingers and elevate the shoulder (flexor synergy); AROM on the unaffected side may be limited by compensatory overuse (particularly the shoulder and hip); AROM is far less than PROM in spastic muscles, and the difference is diagnostically significant — it reflects neural control deficits rather than structural restriction
• PROM / end-feel: slow passive movement through spastic muscles meets elastic-muscular resistance that decreases with sustained hold (spasticity reduces with slow, sustained stretch); rapid passive movement meets increased resistance (velocity-dependent — defining characteristic of spasticity vs. rigidity); end-feel varies by structure — muscular-elastic in spastic muscles; may be firm/leathery if contracture has developed (capsular shortening); empty end-feel at the hemiplegic shoulder if pain prevents reaching the anatomical barrier; GH joint PROM should be compared to the unaffected side to document baseline available range
• Resisted testing: UMN-pattern weakness — broad distribution affecting the entire hemiplegic side rather than specific myotomes; weakness is most pronounced in the anti-gravity muscles (UE extensors, LE flexors) while spasticity dominates the gravity-dependent muscles (UE flexors, LE extensors); resisted testing may be confounded by spasticity, synergy overflow, and impaired voluntary motor control; the unaffected side should be tested for compensatory overuse strain

Special Test Cluster

UMN vs. LMN distinction — essential for stroke assessment:

| Feature | UMN (stroke, MS, cord compression) | LMN (disc herniation, peripheral neuropathy) | |––––-|––––––––––––––––––-|––––––––––––––––––––––-| | Tone | Increased (spasticity) | Decreased (flaccidity) | | Reflexes | Hyperreflexia, clonus | Hyporeflexia or absent | | Babinski | Positive | Negative | | Weakness distribution | Broad — limb or body half | Specific — dermatomal or peripheral nerve | | Atrophy | Late, from disuse | Early, from denervation |

Differential Diagnoses