Residency · Residency · Physical Medicine & Rehabilitation
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.
For the intern
At 3am, immediately address changes in vital signs or neurological status. If you see sudden tachycardia, hypertension, and diaphoresis, think Paroxysmal Sympathetic Hyperactivity (PSH)—check for pain, bladder distension, or constipation first before reaching for medications. New seizure activity requires urgent evaluation and ensuring the patient has been on prophylaxis if within 7 days of injury. Declining mental status warrants checking serum sodium and considering hydrocephalus with CT imaging. Most other issues—therapy scheduling adjustments, family meetings, outpatient referrals, neuroendocrine screening—can wait until morning rounds when the full team is available.
Common pitfalls
- Treating PSH episodes with medications before identifying and removing noxious stimuli. Always check for full bladder, constipation, pain, or uncomfortable positioning first. These triggers are more common than you think.
- Continuing seizure prophylaxis beyond 7 days. Evidence supports only 7 days of prophylaxis. Longer duration doesn't prevent late seizures and adds unnecessary cognitive side effects, particularly with phenytoin.
- Attributing fatigue, mood changes, or cognitive slowing solely to TBI. Screen thyroid, cortisol, and growth hormone at appropriate intervals—pituitary dysfunction affects 20-50% of patients and mimics TBI sequelae.
- Aggressive range-of-motion exercises through suspected heterotopic ossification. Gentle ROM is appropriate, but forceful manipulation can worsen HO formation. If you see warmth, swelling, and decreased ROM, order imaging before pushing harder in therapy.
Make it stick (one 80-word vignette)
You're pre-rounding on Mr. Jones, a 35-year-old with severe traumatic brain injury (TBI) who was admitted for inpatient rehabilitation. He's suddenly agitated, diaphoretic, tachycardic, and posturing. Your first thought is "sympathetic storming," but you remember the lecture. You quickly check his Foley catheter, which is kinked and full. After unkinking it, Mr. Jones calms down, and his vitals normalize. You've just avoided unnecessary medication and addressed a direct cause of his paroxysmal sympathetic hyperactivity (PSH).
If you remember one thing
Always rule out and address noxious stimuli first when managing suspected paroxysmal sympathetic hyperactivity (PSH) in traumatic brain injury (TBI) patients, as this is often the most effective intervention. Remember that post-traumatic amnesia (PTA) duration is a more robust predictor of long-term functional outcome than the initial Glasgow Coma Scale (GCS) score.
