# Moderate-to-Severe TBI: Inpatient Rehabilitation Principles

## Overview
Moderate TBI: GCS 9-12; Severe TBI: GCS 3-8. Inpatient rehabilitation facility (IRF) admission criteria: medical stability, ability to participate in 3 hours of therapy/day, need for physician-directed rehabilitation. Multidisciplinary team: physiatrist, PT, OT, SLP, neuropsychology, nursing, social work, case management. Early rehabilitation consultation (within 48-72 hours of injury) improves outcomes.

## Medical Complications in Acute TBI Rehabilitation

### Paroxysmal Sympathetic Hyperactivity (PSH)
Previously termed "sympathetic storming," "dysautonomia," or "diencephalic seizures". Characterized by tachycardia, hypertension, tachypnea, diaphoresis, hyperthermia, and posturing. Occurs in 15-33% of severe TBI patients. Diagnosis using the PSH Assessment Measure (PSH-AM).

Triggered by noxious stimuli (pain, constipation, bladder distension, repositioning). Management hierarchy: Remove noxious stimuli first. Beta-blockers (propranolol) for sympathetic dampening.

Bromocriptine (dopamine agonist). Gabapentin for central modulation. Benzodiazepines (short-term). Intrathecal baclofen in refractory cases. Opioids for analgesia if pain-triggered. Avoid cooling blankets (mask fever workup).

### Post-Traumatic Seizures
Early seizures: within 7 days of injury (incidence ~10-15%). Late seizures: beyond 7 days (risk 10-25% depending on severity). Risk factors: penetrating injury, cortical contusion, subdural hematoma, depressed skull fracture, prolonged unconsciousness. Prophylaxis with levetiracetam or phenytoin for first 7 days only (AAN guideline).

No evidence supporting prophylaxis beyond 7 days. Preferred anti-seizure medications in TBI: levetiracetam (less cognitive impact). Avoid phenytoin long-term (cognitive impairment, drug interactions).

<image>Algorithm for post-traumatic seizure prophylaxis and management in TBI rehabilitation</image>

### Hydrocephalus
Post-traumatic hydrocephalus occurs in 0.7-29% of severe TBI. Types: communicating (most common post-TBI) vs. obstructive. Signs: declining neurological status, plateau in recovery, new urinary incontinence, gait changes. Diagnosis: serial CT imaging, lumbar puncture with high-volume tap test. Treatment: ventriculoperitoneal (VP) shunt placement. Monitor for shunt complications during rehabilitation.

### Heterotopic Ossification (HO)
Incidence 10-20% in severe TBI. Most common locations: hip > elbow > shoulder > knee. Early signs: warmth, swelling, decreased ROM, pain with movement. Diagnosis: triple-phase bone scan (most sensitive early), ultrasound, alkaline phosphatase (nonspecific).

Prophylaxis: indomethacin, ROM exercises (gentle, not forceful). Treatment: NSAIDs, bisphosphonates, surgical excision when mature. Continue ROM through diagnosis to prevent ankylosis.

### Neuroendocrine Dysfunction
Pituitary dysfunction occurs in 20-50% of moderate-severe TBI. Acute phase: SIADH, cerebral salt wasting, diabetes insipidus. Chronic phase: growth hormone deficiency (most common), hypogonadism, hypothyroidism, adrenal insufficiency. Screening recommended at 3-6 months and 12 months post-injury.

Symptoms may mimic TBI sequelae (fatigue, cognitive slowing, mood changes). Growth hormone deficiency can impair rehabilitation participation and outcomes.

<image>Neuroendocrine complications following traumatic brain injury with pituitary anatomy</image>

## Therapy Programming

### Physical Therapy Focus Areas
Balance and vestibular rehabilitation. Progressive mobility (bed mobility, transfers, ambulation). Strength and endurance training. Aerobic conditioning (when medically appropriate). Orthotic assessment and training.

### Occupational Therapy Focus Areas
ADL retraining (grooming, dressing, bathing, feeding). Upper extremity motor recovery. Visual-perceptual skills. Cognitive rehabilitation through functional tasks. Home modification planning.

### Speech-Language Pathology
Cognitive-communication assessment and treatment. Swallow evaluation (instrumental with MBSS or FEES as needed). Voice and speech production. Augmentative and alternative communication (AAC). Social communication skills.

## Pharmacologic Considerations
Amantadine: only medication with Level 1 evidence for improving recovery from disorders of consciousness in TBI. Methylphenidate: may improve attention and processing speed. Avoid: typical antipsychotics, benzodiazepines, phenytoin (impair neuroplasticity). Melatonin for sleep-wake cycle regulation. SSRIs for mood disorders (after acute phase).

<image>Medications to avoid and prefer during TBI rehabilitation with mechanisms of action</image>

## Family Education and Discharge Planning
Structured family training throughout rehabilitation stay. Education on behavioral and cognitive changes. Safety awareness (supervision needs, driving restrictions, fall prevention). Community reintegration planning.

Return-to-work/school assessment. Connection to brain injury support organizations (Brain Injury Association of America). Long-term follow-up planning: neuropsychology, physiatry, neuroendocrine screening.

## Prognostication
Avoid early definitive prognostication (neuroplasticity continues for months to years). Duration of post-traumatic amnesia (PTA) is strongest predictor of functional outcome. PTA < 1 week: good recovery expected. PTA 1-4 weeks: moderate disability likely.

PTA > 4 weeks: severe disability likely. Galveston Orientation and Amnesia Test (GOAT) to track PTA resolution. Age, pre-injury function, and injury severity interact to determine outcome.

## Clinical Pearls
Always check for and treat noxious stimuli before pharmacologically managing PSH episodes. Monitor serum sodium closely in the acute phase - both hypo- and hypernatremia are common and dangerous. PTA duration is a better functional outcome predictor than initial GCS score. Screen for pituitary dysfunction if rehabilitation plateau occurs without clear explanation. Amantadine is the only drug with Class I evidence for improving consciousness in severe TBI (dosing: 100 mg BID, titrate to 200 mg BID).

<image>Rancho Los Amigos Levels of Cognitive Functioning Scale with corresponding rehabilitation strategies</image>

## References
- Giacino JT, et al. Practice guideline update: Disorders of consciousness. Neurology. 2018;91(10):450-460.
- Pinto SM, et al. Paroxysmal sympathetic hyperactivity after traumatic brain injury. J Neurotrauma. 2022;39(1-2):5-14.
- Temkin NR. Risk factors for posttraumatic seizures in adults. Epilepsia. 2003;44(Suppl 10):18-20.
- Tanriverdi F, et al. Pituitary dysfunction after traumatic brain injury. Nat Rev Endocrinol. 2015;11(2):77-88.
- Cifu DX, et al. Braddom's Physical Medicine and Rehabilitation. 6th ed. Elsevier; 2020.