Hemiplegia

Populations and Risk Factors

• Adults over 65 are most commonly affected when hemiplegia results from stroke; males have a slightly higher stroke incidence than females
• Younger populations affected when the cause is traumatic brain injury (peak incidence 15–30 years, predominantly male 3:1), brain tumor, or MS
• Cerebral palsy produces hemiplegia present from birth or early infancy — spastic hemiplegia is the most common CP subtype
• Hypertension, diabetes, atrial fibrillation, smoking, and hyperlipidemia increase stroke risk (the most common etiology)
• Prior TIA (transient ischemic attack) is a strong predictor of future stroke with hemiplegic consequences
• Left hemisphere lesions produce right hemiplegia with potential aphasia; right hemisphere lesions produce left hemiplegia with potential hemineglect — the side and cognitive accompaniments depend on lesion location, not the condition itself

Causes and Pathophysiology

UMN Lesion Mechanism

• Hemiplegia results from damage to the corticospinal (pyramidal) tract at or above the level of the brainstem. The corticospinal tract carries voluntary motor commands from the motor cortex to the spinal cord alpha motor neurons. Because approximately 85% of corticospinal fibers decussate (cross) at the pyramidal decussation in the medulla, a lesion in one cerebral hemisphere produces contralateral (opposite-side) motor loss.
• The lesion also disrupts descending inhibitory pathways that normally modulate spinal reflex arcs. When this inhibition is removed, the spinal reflexes become disinhibited — the physiological basis for the transition from flaccidity to spasticity.

Flaccid-to-Spastic Transition

• Acute phase (neural shock/flaccid stage): Immediately after the lesion, the affected side is flaccid — limp, areflexic, and without voluntary movement. This reflects the sudden loss of all descending input to the spinal motor neurons, including both excitatory and inhibitory pathways. The spinal cord is functionally "silenced."
• Spastic phase (weeks to months): As spinal shock resolves, the spinal reflex arcs recover function — but without the cortical inhibition that normally regulates them. The stretch reflex becomes hyperactive: muscle spindle afferents now trigger exaggerated motor responses because the descending dampening signals are absent. This produces velocity-dependent spasticity (resistance to passive stretch that increases with speed), hyperreflexia, clonus, and a positive Babinski sign.
• Clasp-knife phenomenon: In established spasticity, rapid passive stretch of a muscle initially meets high resistance (hyperactive stretch reflex) that then suddenly gives way — like closing a jackknife. This occurs because Golgi tendon organ inhibition eventually overcomes the stretch reflex, but only at high tension. Clinically, the therapist feels strong resistance followed by a sudden "release."
• Why this matters for palpation: The velocity-dependent nature of spastic hypertonia means slow passive movement meets less resistance than rapid movement. This is the physiological basis for using slow, sustained techniques rather than rapid mobilization.

Synergy Patterns

• As voluntary control partially returns, it does not return muscle-by-muscle. Instead, groups of muscles activate together in fixed patterns called synergies — reflecting the dominance of subcortical and spinal motor circuits over individual cortical control.
• Upper extremity flexor synergy: shoulder elevation and adduction, external rotation, elbow flexion, forearm supination, wrist and finger flexion. The arm pulls into a characteristic "guarded" posture — elbow bent, wrist curled, fist clenched.
• Lower extremity extensor synergy: hip extension, adduction, and internal rotation; knee extension; ankle plantarflexion and inversion. The leg becomes a rigid pillar — functional for weight-bearing but not for normal gait.
• Why synergies matter clinically: The therapist cannot stretch one component of a synergy in isolation without understanding that the entire pattern will resist. Attempting to extend the elbow against flexor synergy, for example, may provoke increased shoulder elevation and wrist flexion as the entire pattern co-activates.

Brunnstrom Stages of Recovery

• Signe Brunnstrom described six stages of motor recovery following UMN damage, representing increasing dissociation from synergy patterns:
• Stage 1: Flaccidity — no voluntary movement
• Stage 2: Spasticity developing; synergies beginning to appear; minimal voluntary movement
• Stage 3: Spasticity peaks; voluntary movement only within synergy patterns
• Stage 4: Spasticity begins to decrease; some movement outside synergy patterns becomes possible
• Stage 5: Synergy patterns largely overcome; near-normal voluntary movement with some residual clumsiness
• Stage 6: Individual joint movements are normal; coordination restored
• Many patients plateau at Stage 3 or 4. The stage determines which muscles can be isolated during assessment and treatment — Stage 3 patients cannot produce isolated movements, only synergy-linked patterns.

Contracture Development

• Muscles held in shortened positions by persistent synergy patterns gradually develop structural shortening. Sarcomeres are lost from the muscle; collagen deposition increases in the muscle and surrounding fascia; the joint capsule adapts to the restricted range. Over months, what began as dynamic spasticity becomes fixed contracture — the tissue itself is physically shorter and cannot be restored to full length even under anesthesia.
• The most vulnerable muscles: elbow flexors (biceps, brachialis), wrist/finger flexors, ankle plantarflexors (gastrocnemius/soleus), and hip adductors.
• Why this matters for treatment: Early and consistent PROM is the primary defense against contracture. Once contracture is established, the tissue is structurally altered and the therapeutic goal shifts from restoration to maintenance of remaining range.

Shoulder Subluxation

• The glenohumeral joint depends on muscular support (supraspinatus, deltoid, rotator cuff) to maintain the humeral head in the glenoid fossa. In the flaccid stage, these muscles lose tone completely, and the weight of the unsupported arm pulls the humeral head inferiorly. A palpable gap (sulcus) develops between the acromion and the humeral head.
• Subluxation may persist or worsen as spasticity develops if the returning tone is unevenly distributed — internal rotators and adductors overpower the external rotators and abductors, pulling the humeral head into a mechanically disadvantaged position.
• Subluxation creates a cycle of pain, immobility, and further muscle atrophy. It also predisposes to adhesive capsulitis and complex regional pain syndrome (CRPS/shoulder-hand syndrome).

Signs and Symptoms

Flaccid Stage (Brunnstrom Stages 1–2)

• Complete loss of voluntary movement on the affected side
• Hypotonia — limbs feel heavy, limp, without resistance to passive movement
• Areflexia or hyporeflexia — deep tendon reflexes absent or diminished
• Shoulder subluxation developing as deltoid and rotator cuff lose tone
• Loss of protective reflexes — the limb does not withdraw from noxious stimuli
• Sensation may be impaired depending on lesion extent — touch, proprioception, temperature, and pain perception may all be reduced

Spastic Stage (Brunnstrom Stages 3–4)

• Velocity-dependent spasticity — resistance to passive movement increases with speed
• Hyperreflexia — exaggerated deep tendon reflexes (3+ to 4+)
• Clonus — rhythmic, involuntary oscillation at a joint (most common at the ankle) when a sustained stretch is applied
• Positive Babinski sign — great toe dorsiflexion with fanning of the lesser toes on plantar stimulation
• Flexor synergy posture in the upper extremity — shoulder elevated/adducted, elbow flexed, wrist and fingers flexed
• Extensor synergy posture in the lower extremity — hip extended/adducted, knee extended, ankle plantarflexed/inverted
• Circumduction gait — because the spastic lower extremity cannot flex at the hip or knee during swing phase, the patient swings the entire leg laterally in a semicircle to advance it; foot drop (inability to dorsiflex) requires the arc to clear the ground
• Pronator drift — when the patient holds both arms forward with palms up and eyes closed, the affected arm pronates and drifts downward, indicating UMN weakness
• Hemineglect (with right hemisphere lesions) — the patient fails to attend to stimuli on the affected (left) side; may be unaware of the left arm, fail to dress the left side, or ignore food on the left half of the plate

Recovery Stage (Brunnstrom Stages 5–6)

• Spasticity decreasing; voluntary movement outside synergy patterns returning
• Isolated joint movements becoming possible
• Gait improving but residual asymmetry common — reduced arm swing, persistent foot drop, or mild circumduction
• Fine motor coordination often remains impaired even with good gross motor recovery
• Many patients plateau at Stage 3–4 and do not reach full recovery

Assessment Profile

Subjective Presentation

• Chief complaint: "I can't use my [right/left] side" — difficulty with dressing, feeding, walking, or self-care on the affected side; may report arm "stuck" in a bent position; may describe leg as "stiff" or "dragging"; affected side may be described as "dead" (flaccid stage) or "tight and pulling" (spastic stage)
• Pain quality: deep aching in spastic muscles from sustained contraction; sharp shoulder pain from subluxation or developing adhesive capsulitis; neuropathic burning or dysesthesia in some patients depending on lesion extent; pain reports may be unreliable due to sensory impairment
• Onset: sudden onset in stroke (the most common history); gradual onset in brain tumor or MS; present from birth/early development in cerebral palsy; linked to a specific traumatic event in TBI; the patient or caregiver can usually identify the causative event clearly
• Aggravating factors: rapid movements provoke increased spasticity and clonus; cold environments may increase tone in some patients; fatigue and emotional stress worsen motor control; attempting movements against synergy patterns increases co-contraction
• Easing factors: slow, sustained positioning reduces spastic tone; warmth (in non-MS etiologies) may reduce tone temporarily; resting the affected limb in an anti-spasticity position (UE: shoulder abducted, elbow extended, wrist neutral, fingers open; LE: hip neutral, knee slightly flexed, ankle neutral)
• Red flags: sudden worsening of neurological status, new-onset seizure, severe headache with altered consciousness, or signs of a new stroke (sudden facial droop, speech changes, contralateral weakness) → emergency referral; do not treat; signs of DVT in the immobile lower extremity (unilateral swelling, warmth, calf tenderness) → urgent medical referral

Observation

• Local inspection: visible muscle atrophy on the affected side (disuse); edema in dependent extremities from reduced mobility; shoulder sulcus sign (visible gap between acromion and humeral head in subluxation); wrist and hand held in flexion posture; assistive devices (sling, AFO, cane, wheelchair)
• Posture: hemiplegic posture — affected UE held in flexor synergy (shoulder adducted/internally rotated, elbow flexed, wrist/fingers flexed); affected LE in extensor synergy (hip extended/adducted, knee extended, ankle plantarflexed); trunk may laterally flex toward the affected side; head may be rotated away from the affected side (especially with hemineglect); weight-bearing shifted to the unaffected side
• Gait: circumduction gait is the hallmark — the spastic, extended LE is swung laterally in a semicircle because hip and knee flexion during swing phase is lost to extensor synergy; foot drop produces foot slap or toe-catching; reduced arm swing on the affected side; compensatory hip hiking on the affected side; trunk lateral lean toward the unaffected side during stance phase on the affected leg; reduced cadence and step length

Palpation

• Tone: Velocity-dependent spastic hypertonia on the affected side with clasp-knife response in established spasticity. Muscles most affected: biceps/brachialis, wrist/finger flexors, hip adductors, gastrocnemius/soleus. Contralateral (unaffected) side shows compensatory hypertonia from overuse — particularly upper trapezius, cervical extensors, lumbar erectors, and weight-bearing hip stabilizers. Flaccid stage: affected side has no resistance to passive movement. Assess tone bilaterally to document the asymmetry.
• Tenderness: trigger points in chronically spastic muscles (biceps, forearm flexors, hip adductors, calf); compensatory overload tenderness on the unaffected side (upper trapezius, lumbar paraspinals, hip abductors); shoulder joint line tenderness in subluxation; sensation is often impaired on the affected side — the patient may not report tenderness accurately; absence of reported tenderness does not mean absence of pathology
• Temperature: affected limbs may be cooler due to reduced active movement and potentially altered sympathetic regulation; warm hydrotherapy is NOT contraindicated in hemiplegia (unless the etiology is MS, in which case Uhthoff's applies — clarify the underlying cause before applying heat); acute inflammatory warmth around the shoulder may indicate developing adhesive capsulitis or CRPS
• Tissue quality: Affected side — spastic muscles palpate as hypertonic, boardlike, and poorly extensible. Flaccid muscles feel soft and atrophied. Fascial mobility reduced in chronically immobile segments. Early contracture detectable as reduced tissue extensibility at end-range. Joint play restricted at the shoulder (especially inferior glide in subluxation). Unaffected side — muscles may feel ropy and hypertonic from compensatory overuse.

Motion Assessment

• AROM: severely reduced or absent on the affected side depending on Brunnstrom stage; Stage 1–2: no voluntary AROM; Stage 3: AROM only within synergy patterns (cannot isolate individual joint movements); Stage 4+: increasing ability to move outside synergies; test both synergy-linked and isolated movements to determine stage; unaffected side may also show restricted AROM from compensatory postural patterns (cervical rotation toward affected side, trunk lateral flexion)
• PROM / end-feel: in the spastic stage, PROM meets velocity-dependent resistance — slow passive movement achieves significantly more range than rapid movement; end-feel is elastic/muscular (spasticity) in earlier stages, progressing to hard/inelastic (contracture) as structural shortening develops; PROM significantly exceeds AROM — the difference represents the neurological deficit (not a tissue barrier); in the flaccid stage, PROM is full and unrestricted with a soft/empty end-feel; shoulder PROM may reveal crepitus or hard end-feel if adhesive capsulitis is developing secondary to subluxation
• Resisted testing: largely non-applicable in the traditional sense — the patient cannot voluntarily activate individual muscles against resistance in Stages 1–3; pronator drift test is the most informative resisted screen: arms held forward, palms up, eyes closed — the affected arm pronates and drifts downward, confirming UMN weakness; in later stages (4+), test grip strength and individual muscle groups to document recovery; compare bilaterally

Special Test Cluster

Stage-specific testing note: In the flaccid stage (Brunnstrom 1–2), Babinski and DTRs may be absent or diminished (neural shock). Their emergence during recovery confirms the transition to the spastic phase and UMN disinhibition. Serial assessment over time is more informative than a single session.

Differential Assessment