Traumatic Brain Injury (Severe TBI)

Populations and Risk Factors

• Young adults aged 15–24 have the highest incidence — motor vehicle accidents are the leading mechanism in this group
• Elderly adults aged 65+ are the second peak — falls are the primary mechanism; anticoagulant use increases hemorrhagic severity
• Males are affected approximately 2:1 over females across all age groups
• Military personnel — blast injuries produce a unique mechanism of diffuse injury from pressure wave transmission through the cranium; often compounded by polytrauma
• Athletes in contact sports (football, hockey, boxing, rugby) — repeated subconcussive impacts produce cumulative damage leading to chronic traumatic encephalopathy (CTE), a progressive tauopathy distinct from single-event TBI
• Pre-existing conditions that increase severity: coagulopathy, prior TBI (second-impact syndrome risk), substance use at time of injury, advanced age with brain atrophy (greater coup-contrecoup displacement)

Causes and Pathophysiology

Primary Injury

The primary injury occurs at the moment of impact and represents mechanical damage that is complete and irreversible within seconds.

• Coup-contrecoup injury: The brain, suspended in cerebrospinal fluid within the skull, decelerates against the interior surface at the point of impact (coup) and then rebounds against the opposite side (contrecoup). This produces bilateral cortical contusions — the frontal and temporal poles are most vulnerable because the anterior and middle cranial fossae have irregular, ridged bony surfaces that lacerate brain tissue during impact. Clinically, this explains why frontal lobe executive dysfunction and temporal lobe memory impairment are so common even when the primary impact is occipital or parietal.
• Diffuse axonal injury (DAI): Rotational acceleration-deceleration forces shear axons at gray-white matter junctions, the corpus callosum, and the brainstem. DAI is the most common cause of prolonged unconsciousness and vegetative state after TBI. Unlike focal contusion, DAI produces widespread disconnection of neural networks — this is why severe TBI presentations are diffuse, bilateral, and difficult to predict from injury mechanism alone. DAI damage continues for hours to days after the initial injury as severed axons undergo Wallerian degeneration.
• Intracranial hemorrhage: Three types, each with different clinical significance:
• Epidural hematoma: arterial bleeding between the dura and skull (middle meningeal artery); rapid expansion; classically presents with a lucid interval followed by rapid deterioration — a neurosurgical emergency
• Subdural hematoma: venous bleeding between the dura and arachnoid; slower expansion; more common in the elderly where brain atrophy stretches bridging veins
• Subarachnoid hemorrhage: bleeding into the subarachnoid space; produces severe headache, meningeal irritation, and vasospasm risk

Secondary Injury

Secondary injury evolves over hours to weeks after the primary event. Unlike primary injury, secondary injury is partially preventable and treatable — this is why acute medical management focuses on preventing secondary damage.

• Cerebral edema and increased intracranial pressure (ICP): Cytotoxic and vasogenic edema increase brain volume within the rigid skull. Once ICP exceeds cerebral perfusion pressure, ischemia compounds the original damage. Sustained elevated ICP causes herniation — displacement of brain tissue through the tentorium or foramen magnum — which is the primary cause of death in severe TBI.
• Excitotoxicity: Damaged neurons release excessive glutamate, overstimulating NMDA receptors and causing calcium influx, mitochondrial failure, and neuronal death in surrounding tissue. This expands the zone of damage beyond the original mechanical injury.
• Inflammatory cascade: Microglial activation and blood-brain barrier breakdown produce neuroinflammation that persists for months to years after injury. Chronic neuroinflammation is now recognized as a driver of progressive neurodegeneration after TBI and contributes to the development of CTE.
• Ischemia: Combination of edema, vasospasm, and impaired autoregulation produces secondary ischemic infarction in tissue that survived the primary impact.

Upper Motor Neuron Damage and Spasticity

• UMN damage in TBI follows the same pathophysiological mechanism as stroke — loss of cortical inhibition over spinal motor neuron pools releases the stretch reflex, producing velocity-dependent hypertonia (spasticity). However, TBI spasticity differs from stroke spasticity in distribution: stroke typically produces a unilateral hemispheric pattern (contralateral hemiplegia), while TBI often produces bilateral or quadriplegic spasticity because DAI and bilateral contusions damage both hemispheres.
• Spastic posturing patterns depend on the severity and level of damage:
• Decorticate posturing: damage above the red nucleus — upper extremities flexed, adducted, internally rotated; lower extremities extended — indicates cortical damage with intact brainstem
• Decerebrate posturing: damage at or below the red nucleus — all four extremities extended, internally rotated — indicates brainstem damage and carries a worse prognosis
• Chronic spasticity: over months, the initial posturing resolves into persistent hypertonic patterns that produce contracture if not managed — hip adductors, knee flexors, plantarflexors, elbow flexors, wrist flexors, and finger flexors are most commonly affected

Heterotopic Ossification (HO)

• Abnormal formation of mature lamellar bone within soft tissue, most commonly periarticular (around joints). Occurs in 10–20% of severe TBI patients, significantly higher than in other neurological conditions. The mechanism is not fully understood but involves dysregulated osteoblastic activity triggered by the combination of immobilization, neurological injury, and local inflammation.
• Most common sites: hip (most frequent), elbow, shoulder, knee
• Clinical significance for MT: HO presents as a warm, firm, non-mobile mass near a joint with progressively decreasing ROM. It is NOT a soft tissue lesion — massage, stretching, and mobilization of HO areas can cause fracture, hemorrhage, or acceleration of bone formation. HO areas are a local contraindication.

Chronic Traumatic Encephalopathy (CTE)

• CTE is a distinct neurodegenerative disease caused by the cumulative effect of repeated subconcussive and concussive impacts over years. It is not a direct complication of a single severe TBI but represents a separate pathological process.
• Pathologically characterized by perivascular accumulation of hyperphosphorylated tau protein in neurons and astrocytes at the depths of cortical sulci — a pattern unique to CTE and distinct from Alzheimer's disease tau distribution.
• Currently can only be definitively diagnosed post-mortem. Clinically suspected in athletes and military personnel with progressive cognitive decline, behavioral changes (aggression, impulsivity, depression, suicidality), and motor impairment years after exposure to repetitive head impacts.

Signs and Symptoms

By Severity (Glasgow Coma Scale)

Motor Deficits

• Hemiplegia or hemiparesis: when damage is predominantly unilateral (focal contusion to one hemisphere) — identical presentation to stroke; contralateral to the lesion
• Quadriplegia or quadriparesis: when damage is bilateral or involves the brainstem — DAI commonly produces this pattern; spasticity may be asymmetric even when bilateral
• Ataxia: cerebellar or brainstem damage produces coordination deficits — intention tremor, dysmetria, dysdiadochokinesia, wide-based gait; may coexist with spasticity
• Dystonia: sustained involuntary muscle contractions producing abnormal postures — more common in TBI than in stroke due to basal ganglia vulnerability to shearing forces

Cognitive Deficits

• Processing speed: the most consistently impaired cognitive domain after severe TBI — slowed information processing affects all other cognitive functions
• Memory: anterograde amnesia (difficulty forming new memories) is more common than retrograde; hippocampal damage from medial temporal lobe contusions
• Executive function: frontal lobe vulnerability in coup-contrecoup produces deficits in planning, judgment, impulse control, and cognitive flexibility — this is the deficit most likely to affect treatment compliance and informed consent
• Attention: sustained and divided attention are impaired; client may lose focus during treatment or be unable to follow multi-step instructions

Behavioral and Emotional Changes

• Disinhibition: frontal lobe damage removes social behavioral filters — inappropriate comments, impulsive actions, lack of awareness of social boundaries
• Aggression and irritability: may be unprovoked and disproportionate to stimulus; the MT must understand this as a neurological symptom, not a personal threat
• Emotional lability: rapid, unpredictable shifts between emotional states — crying, laughing, or anger without proportionate stimulus (pseudobulbar affect)
• Apathy and reduced motivation: damage to frontal-subcortical circuits reduces initiation of behavior — client may appear uncooperative when actually neurologically unable to initiate responses

Post-Traumatic Epilepsy

• Seizures occurring more than 7 days after TBI (late seizures) — risk is highest in the first 2 years but remains elevated lifelong
• Risk factors: penetrating injury, cortical contusion, intracranial hemorrhage, depressed skull fracture
• Clinical significance for MT: a client with post-traumatic epilepsy may have a seizure during treatment. The MT must know seizure first-aid protocols and have a plan in place before treatment begins.

Autonomic Dysfunction

• Paroxysmal sympathetic hyperactivity (PSH): episodes of tachycardia, hypertension, diaphoresis, hyperthermia, and extensor posturing — occurs in the subacute phase; triggered by stimulation including therapeutic touch
• Dysautonomia: chronic autonomic dysregulation affecting heart rate variability, blood pressure regulation, thermoregulation, and gastrointestinal motility
• Clinical significance: autonomic instability may cause unpredictable physiological responses during treatment — monitor vital signs and be prepared for diaphoresis, flushing, or sudden changes in tone

Assessment Profile

Subjective Presentation

• Chief complaint: Varies enormously by injury severity and chronicity — chronic-phase clients typically present with stiffness, reduced mobility, pain from spastic muscle groups, difficulty with daily activities (dressing, transfers, mobility), headaches, and fatigue; history will include the mechanism of injury (MVA, fall, assault, blast), duration of unconsciousness, and the rehabilitation trajectory; a caregiver often provides the history rather than the client
• Pain quality: Spasticity-related deep muscular aching and cramping in chronically hypertonic groups; headache (post-traumatic headache — tension-type or migraine-like); neuropathic pain in areas of sensory disturbance (burning, shooting, dysesthetic); pain at HO sites is deep and activity-limiting
• Onset: Acute traumatic event with a clearly defined date; motor and cognitive deficits are maximal in the early phase and improve over months to years through neuroplasticity and rehabilitation, but significant residual deficits persist in severe TBI; the client seen in MT practice is typically months to years post-injury in the chronic rehabilitation phase
• Aggravating factors: Sustained positions that load spastic muscles (prolonged sitting increases hip flexor and hamstring spasticity); fatigue (neurological, not muscular — worsens all deficits); overstimulation (noise, bright lights, complex environments); rapid passive movement (invokes stretch reflex and increases spasticity)
• Easing factors: Slow, rhythmic movement; warmth to spastic muscles (unlike MS, heat is generally well-tolerated unless seizure threshold is a concern); rest; reduced environmental stimulation; established routine (cognitive predictability reduces agitation)
• Red flags: New or worsening neurological signs weeks to months after injury — may indicate chronic subdural hematoma, hydrocephalus, or delayed hemorrhage; emergency referral. New-onset seizures — medical evaluation required. Sudden severe headache with altered consciousness — potential ventriculoperitoneal shunt malfunction in clients with shunts; emergency referral; do not treat.

Observation

• Local inspection: Muscle atrophy in paretic limbs from disuse; may have surgical scars (craniotomy, tracheostomy, gastrostomy); assistive devices (wheelchair, walker, AFO, wrist splint, head support); possible visible cranial deformity from decompressive craniectomy or cranioplasty; HO may be visible as swelling near affected joints
• Posture: Depends on the pattern of damage — unilateral damage produces hemiplegic posture (flexed upper extremity, extended lower extremity on the affected side); bilateral damage produces more complex patterns including trunk asymmetry, forward head posture, thoracic kyphosis from wheelchair positioning, and pelvic obliquity; compensatory overload patterns develop in functional limbs
• Gait: Spastic gait (circumduction, scissoring) if ambulatory; ataxic gait (wide-based, uncoordinated) with cerebellar involvement; many severe TBI clients are wheelchair-dependent; those who are ambulatory may use assistive devices and demonstrate combined spastic-ataxic patterns

Palpation

• Tone: Spastic hypertonia (UMN pattern) — velocity-dependent increased resistance to passive movement; bilateral distribution is more common than in stroke; classic spastic groupings: elbow flexors (biceps, brachialis, brachioradialis), wrist and finger flexors (flexor carpi radialis, FDS/FDP), hip adductors (adductor longus/brevis/magnus), knee flexors (hamstrings), plantarflexors (gastrocnemius, soleus); may be asymmetric even when bilateral; spastic muscles palpate as rigid, boardlike, and poorly extensible; clonus may be present at the ankle (rapid dorsiflexion triggers repetitive plantarflexion beats) or wrist
• Tenderness: Tender trigger points in chronically spastic muscles from sustained contraction and ischemia; periarticular tenderness at HO sites — palpate for warm, firm, non-mobile masses near the hip, elbow, shoulder, and knee; if found, these are bone, not soft tissue — local contraindication to massage, mobilization, and stretching; compensatory overload tenderness in functional limbs and cervical muscles from effort of movement against spasticity; clients with sensory impairment may not report tenderness accurately — bilateral comparison is essential
• Temperature: HO sites may feel warm due to metabolic activity and local inflammation — warmth with firm mass near a joint is a clinical indicator; affected limbs may be cooler from reduced activity and impaired sympathetic regulation; insensate areas must be identified before any thermal modality application — do not apply heat to areas where the client cannot report temperature sensation
• Tissue quality: Disuse atrophy in paretic muscles — soft, wasted, reduced bulk; spastic muscles are hypertonic but may also develop secondary fibrotic changes over months to years of sustained contraction; fascial mobility severely reduced in chronically immobile segments; edema in dependent limbs from immobility and impaired autonomic regulation; skin may be fragile in areas of prolonged immobility or pressure

Motion Assessment

• AROM: Severely limited in affected limbs — spasticity, weakness, and impaired motor planning all contribute; bilateral involvement produces greater functional limitation than the unilateral pattern of stroke; AROM may vary significantly session to session depending on fatigue, medication timing, and spasticity fluctuation; voluntary movement may be present but poorly coordinated (ataxic component) or very slow (motor planning deficit)
• PROM / end-feel: Velocity-dependent resistance defines the spastic contribution — slow passive movement achieves significantly greater range than rapid movement; end-feel varies by chronicity: early chronic phase shows elastic-muscular end-feel from spasticity alone; late chronic phase may show firm/leathery end-feel from contracture (capsular and myostatic); at HO sites, end-feel is bony/hard — this is an absolute stop point; do not attempt to push through a bony end-feel near a joint; PROM substantially exceeds AROM in most cases (the motor deficit is neural, not structural, until contracture develops)
• Resisted testing: UMN-pattern weakness — broad, not myotomal; confounded by spasticity (co-contraction), fatigue, cognitive deficits (may not understand instructions), and motor planning impairment; resisted testing may be unreliable in severe TBI — PROM and observation are more clinically useful for the MT

Special Test Cluster

The SOT cluster for severe TBI is oriented toward monitoring neurological status and differentiating UMN from LMN pathology rather than confirming the diagnosis (which is established by history and imaging). These tests track the client's baseline and detect changes that require medical referral.

UMN vs. LMN reminder — critical for TBI assessment:

Differential Assessment