Traumatic Brain Injury Rehabilitation

o Contusions- can also be produced by contact but most commonly caused by acceleration/deceleration; typically located in the inferior frontal and anterior temporal lobes regardless of point of contact.

o Diffuse axonal injury- refers to widespread stretching of axons caused by rotation of brain around its axis; caused by acceleration/deceleration

o Multiple petechial hemorrhages- caused by acceleration/deceleration

o Cranial nerve injuries- caused by acceleration/deceleration

Secondary Injury- caused by the primary mechanism

o Intracranial hemorrhages- epidural, subdural, intracerebral

o Brain swelling- vasogenic or cytogenic edema

o Hypoxia

o Excitotoxicity- neuronal damage caused by higher than normal concentration of excitatory neurotransmitters released by injured neurons

o Production of free radical molecules

Assessment Techniques and Prognosis

Glasgow Coma Scale- it has been repeatedly demonstrated that the depth and duration of unconsciousness, as indexed by GCS score, is the single most powerful predictor of outcome from TBI.

o Disadvantages:

§ can be unscorable during early acute care phase because of chemical paralysis or sedation, SCI, facial injury, sedation or intubation

§ can be affected by intoxication

§ unscorable at younger ages

§ unscorable in patients who do not understand the examiner's language

Severity of TBI- is reflected by lowest postresuscitation GCS score (usually at the ER)

o Mild Brain Injury- GCS at ER 13-15; no objective signs of brain injury on neurologic exam or CT of the brain; usually with good long-term prognosis

o Moderate Brain Injury- GCS at ER 9-12; many with moderate TBI will have permanent impairments and disabilities but some will make good recovery with only mild persisting impairments

o Severe brain Injury - GCS at ER 3- 8; usually with permanent neuropsychological impairment and functional disabilities

	Patient's response	Score
Eye opening	Spontaneously	4
	When spoken to	3
	Painful stimulation	2
	Do not open	1
Motor	Follows commands	6
	Localizing movements to pain	5
	Withdraws to pain	4
	Flexor (decorticate) posturing to pain	3
	Extensor (decerebrate) posturing to pain	2
	No motor response to pain	1
Verbal	Oriented to place and date	5
	Converses but disoriented	4
	Utters inappropriate words, not conversing	3
	Incomprehensible nonverbal sounds	2
	Not vocalizing	1

Neuroimaging of TBI

o CT - technique of choice for neuroimaging of TBI during the acute care stage because of its sensitivity to the presence of blood, edema, facial and skull fractures and most other intracranial injuries requiring medical treatment

§ Normal CT findings have best prognosis; CT findings of acute SDH, ICH and massive bilateral hemispheric swelling have worst prognosis.

o MRI- more sensitive than CT to nonhemorrhagic shear injuries and to contusions in certain areas such as the inferior frontal region and brainstem which are located near bony surfaces that produce artifacts on CT.

§ More useful during the rehabilitation phase since MRI is more helpful in explaining patients' neurologic and neuropsychologic deficits.

o Single photon emission CT (SPECT)- could have important role in evaluating unconscious or mild TBI patients.

Neurophysiological Evaluations

o EEG

o Evoked potentials

§ bilateral absence of waves N20 to P22 in SSEP of comatose patients is a strong predictor of failure to recover consciousness.

§ Absence of wave V or other components of the BAEP is also predictor of poor outcome.

§ Normal BAEP was not a valid predictor of good outcome.

Neuropsychological Testing

o Major tool used to evaluate cognitive functions in brain-injured patients.

o Disadvantages: time needed for testing, requirement of good patient motivation and limited testability of many low-level patients.

Neurobehavioral Recovery from TBI- almost all spontaneous recovery from brain injury is complete by 1 year or at most 2 years.

Summary of Acute Prognostic Factors

	Poorer	Better
GCS Score	<7	>7
CT	Large blood clot; massive bihemispheric swelling	Normal
Age	Extremes of age	Youth
Pupillary light reflex	Pupils remain dilated	Pupils contract
Doll's eye sign	Impaired	Intact
Caloric testing with ice water	Eyes do not deviate	Eyes deviate to irrigated side
Response to noxious stimuli	Decerebrate rigidity	Localizes
SSEP	Deficient	Normal
Length of coma	>4 weeks
PTA length	>2 weeks	<2 weeks
ETOH	+	-
Drugs	+	-
Socioeconomic/Educational status	low
Previous TBI	+	-
CKBB level	Elevated
Blood sugar	Elevated
Thyroid hormone level	Elevated

Rehabilitation of Unconscious Patients

Rule out possibility that unconsciousness is due to artifacts of examination techniques or due to reversible medical factors (e.g. sedating drugs, systemic illness, malnourishment, etc.).

Coma/Unconsciousness

o Caused by disruption of input to surface brain structures from deeper structures that subserve arousal and wakefulness (through disconnection of ascending fiber pathways due to DAI, or by compression of brainstem or diencephalic structures due to mass effects of supratentorial lesions.

o TBI recovery sequence is consistent with "centripetal model of injury", which predicts that functions that are subserved by deeper structures such as sleep-wake cycles, should recover earlier than functions subserved by surface brain structures, such as memory.

Predictors of Recovery of Consciousness:

o Age- best in children and adults under 40 years old.

o Duration of unconsciousness- probability of regaining consciousness by 1 yr. post injury was 36% in patients unconscious at 3 months post injury; 21% in those remaining unconscious at 6 months post injury.

Pharmacologic Management- most promising intervention to directly increase arousal and facilitate recovery of consciousness. Some of agents used:

o stimulants: methylphenidate, dextroamphetamine

o antiparkinsonian drugs: bromocriptine, amantadine

Post-traumatic Amnesia and Agitation

Post-traumatic Amnesia- period of disorientation and confusion following TBI

o Patient's ability to learn new information is minimal or non-existent.

o After emerging from PTA, patients have a permanent memory gap for the entire period of the PTA and coma as well as for events that occurred during a shorter period leading up to the moment of injury (retrograde amnesia).

o Galveston Orientation and Amnesia Test (GOAT) is a standard technique for assessing PTA. GOAT Score range from 0-100, with score of 75 or better defined as normal. End of PTA is defined as the date when the patient scores 75 or higher on the GOAT for 2 consecutive days.

o In general duration of PTA is usually 3x as long as duration of unconsciousness.

o Management:

§ During PTA: Reorient patients (Post place, date, daily schedules in patient's room), avoid overstimulation and unpleasant emotional interactions with family or staff.

§ After PTA: Neuropsych eval for long-term prognosis and treatment planning, community outings, behavioral management techniques, psychiatric medications for mood disorder., family education

Agitation- includes cognitive confusion, extreme emotional lability, motor overactivity and physical or verbal aggression.

o Risk factors may include severe cognitive deficits and frontal lobe damage.

o Management:

§ Need to rule out possible causes of agitation: electrolyte imbalance, malnutrition, seizure activity, sleep disturbance or hydrocephalus, drugs.

§ Once medical cause of agitation is ruled out, first line of intervention is environmental management. Goal is to lower level of stimulation and cognitive complexity in the patient's immediate surrounding.

§ Pharmacologic intervention may be necessary if patient is still dangerous despite environmental interventions.

Medical Problems Following TBI- a lot of medical problems (i.e. fractures peripheral nerve injuries, etc.) not detected/documented prior to rehabilitation transfer.

Neurologic Complications

Post-traumatic Epilepsy (PTE)- occurs in 5% of TBI patients who are hospitalized.

Risk factors: depressed skull fractures, acute intracranial hematomas, seizures during the first week; other risk factors are dural tears, foreign bodies, focal signs, PTA > 24 hrs.
Using phenytoin beyond the first week following brain injury does not prevent development of late PTE.
Carbamazepine is drug of choice for management of PTE; Disadvantages are occurrence of bone marrow suppression (monitor WBC count, keep >4000/mm³, short half-life (requires TID dosing which might decrease compliance inpatients with memory impairment)

Post-traumatic Hydrocephalus (PTH)- relatively uncommon (1%- 8%)

High risk in patients with subarachnoid hemorrhage.
If with high suspicion, perform serial monthly CT
Management: Shunting beneficial if pressure>180 mm H2O or if ventricles progressively increasing in size and in those with clinical features of NPH

Musculoskeletal Complications

71%-82% of patients with TBI has associated extracranial injuries, especially those who sustain their injury from MVA, pedestrian-automobile accidents

Cranial Nerve Damage

Most commonly involved in decreasing frequency: CN VII (9%), CN III (6%); least frequently injured are CN's IX and XI.

Heterotopic Ossification

Incidence range from 11% to 76%; 10-20% have functionally significant HO
Risk factors: spasticity, unconsciousness>2 weeks, long-bone fractures, and decreased ROM
Management:

pharmacologic- Etidronate 20 mg/kg/day for 3 months, then 10 mg/kg/day for 3-6 months; NSAIDS (indomethacin, naproxen)
non-pharmacologic- ROM exercises
surgical removal if clinically indicated is done once HO has matured

Spasticity

Management:

non-pharmacologic- physical modalities (heat, cold), stretching, splinting, casting (including inhibitory casting), proper positioning, FES, vibration relaxation techniques, biofeedback, motor re-education
pharmacologic: chemical neurolysis utilizing nerve blocks and motor point blocks, botox; dantrolene sodium has least cognitive and sedating effects.

Thrombophlebitis

More frequent in paralyzed limbs.

Respiratory Complications

One of most common complications of TBI is respiratory failure followed by radiographically defined pneumonitis- associated with longer LOS in both acute care and rehabilitation

Gastrointestinal Complications

Nutritional Status
GI Bleeding

H2 antagonists may cause cognitive and behavioral disturbances and should be withdrawn once risk of GI Bleed has passed.

Swallowing Disorders

Incidence of dysphagia in patients with TBI coming to acute rehab facilities is about 27%.
Videofluoroscopy is gold standard for evaluating patients with dysphagia.
Thin liquids are to be avoided in acute neurosurgical setting, since they are typically the most difficult to handle from a swallowing perspective.

Bowel Incontinence

Genitourinary Problems

Neurogenic bladder rare after TBI- if it happens, usually due to uninhibited detrussor hyperreflexia

Dermatologic Complications
Endocrine Complications

Most common in acute care setting is SIADH, resulting in oversecretion of ADH which result in hyponatremia. Managed with fluid restriction initially, if needed may use urea and NaCl. Diabetes Insipidus (DI) rare after TBI
Other endocrine disorders that can occur after TBI include anterior hypopituitarism, thyroid dysfunction and sexual dysfunction.

Autonomic Disturbances

Hypertension- can result from high intracranial pressure and catecholamine release and focal brain injuries near the hypothalamus; manage with beta-blocker (propranolol) during hyperdynamic state.
Hypotension- usually orthostatic but may also result from hypopituitarism.
Temperature Instability

Central fever may result from injury to the anterior hypothalamus, from general decerebration and drugs.
Hypothermia may result from lesions in the posterior hypothalamus, myxedema, and barbiturates.

Rehabilitation of Mild TBI

Postconcussion Syndrome- constellation of symptoms reported by mild TBI patients: dizziness, headache, cognitive impairment, irritability, disturbed sleep.

Colorado Medical Society Guidelines for Management of Concussion in Sports

Grade	1^st	2^nd	3^rd
I- Confusion w/o amnesia, No LOC	20 minutes	1 week	1 month
II- Confusion w/ amnesia, NO LOC	1 week	1 month	Terminate season
III- LOC	1 month	Terminate season

Sources:

Physical Medicine & Rehabilitation. Braddom RL, editor

Rehabilitation Medicine: Principles and Practice. DeLisa JA, editor

PM&R Secrets. O'Young B, editor

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