para>Interactions of physical, cognitive, and behavioral sequelae interfere with new learning. Effects of early TBI may not become apparent until later. � �
ETIOLOGY AND PATHOPHYSIOLOGY
- Falls and motor vehicle accidents are the most common causes.
- Violence-related TBI is increasing (10% of all cases).
- Sports and recreation injuries (especially in teenagers and young adults)
- Cortical contusions due to coup-contrecoup injuries. Although axonal rupture from shear and tensile forces can occur at the time of severe head injury, milder degrees of axonal damage play a role in mTBI.
- Disruption of axonal neurofilament organization impairs axonal transport, leading to axonal swelling, Wallerian degeneration, and transection.
- Release of excitatory neurotransmitters acetylcholine, glutamate, and aspartate and generation of free radicals may contribute to secondary injury.
RISK FACTORS
- High risk: male, age 15 to 34 years
- Moderate risk <5 years and >60 years
- Lower socioeconomic status (head injury)
GENERAL PREVENTION
Improved safety standards and programs to minimize injury from vehicular-related events (motor vehicle, motorcycle, bicycle, pedestrian), falls, violence, sports, and recreation provide best prevention against TBI. � �
This includes car seat safety, seatbelt use, helmet use, trip hazards (senior living), balance activities (seniors), safety gates, and playground safety regulations. � �
COMMONLY ASSOCIATED CONDITIONS
- Psychosis
- Depression
- Chronic headaches
- Suicide attempts
- Substance abuse
- Attention deficit disorder
DIAGNOSIS
HISTORY
- Most neurologic complications appear within days following injury; long-term sequelae include seizures, headache, hydrocephalus, visual defects, neuroendocrine abnormalities, and movement and sleep disorders.
- Cognitive consequences: memory impairment, difficulties in attention and concentration, language deficits, visual perception problems, poor problem solving, difficulty with reasoning, insight, judgment, and information processing
- Behavioral problems: altered social responses, verbal and physical aggression, agitation, learning difficulties, diminished self-awareness, altered sexual functioning, impulsivity, social disinhibition
- Psychological consequences: mood disorders, personality changes, altered emotional control, depression, anxiety
- Sleep disruption
- Fatigue; visual tracking disturbances and altered coordination
- Social consequences: increased risk of suicide, divorce, unemployment, economic strain, alcohol/substance abuse
- Comprehensive review of patient medication list
PHYSICAL EXAM
TBI severity (mild, moderate, severe) is classified based on the Glasgow Coma Scale, a point-scoring system based on verbal response, eye opening response, and motor response to voice or pain following an injury. Physical exam should include assessment of vital signs and a complete neurologic examination including a thorough cognitive assessment. Other systems should be examined based on individual patient complains. The DoD/VA Clinical Practice Guideline provides a useful table to guide targeted physical examination based on patient presentation (1)[A]. � �
DIFFERENTIAL DIAGNOSIS
- Chronic pain is common following TBI, and the specific diagnosis can be challenging given comorbid cognitive, language, and behavioral deficits.
- Dysautonomia: tachypnea, hypertension, painful posturing/contractions, diaphoresis
- Neuropathic pain: burning, shock-like, or pins and needles; allodynia/hyperpathia; three most common: complex regional pain syndrome, central pain syndrome, and peripheral neuropathy
- Headache: posttraumatic headache, hydrocephalus, increased intracranial pressure
- Myofascial pain syndrome
- Chronic infection; depression; hypothyroidism; hydrocephalus; intracerebral hemorrhage; seizures; fractures; tracheal stricture; pain; alcohol, drugs, polypharmacy, and/or CNS depressant use; anxiety; chronic fatigue syndrome
DIAGNOSTIC TESTS & INTERPRETATION
- Complete metabolic profile, thyroid-stimulating hormone, complete blood count; drug screen
- Evoked potentials (auditory, visual, somatosensory)
- Behavioral assessment, neuropsychologic testing, vocational assessment
- Cognitive test for orientation and arousal; use Western Neuro Sensory Stimulation Profile or Galveston Orientation and Amnesia Test.
- CT is preferred for urgent neuroanatomic imaging. MRI shows greater detail and can identify axonal injury and better predict long-term outcomes.
Initial Tests (lab, imaging)
As needed for suspected metabolic complications � �
- Bone scan: heterotopic ossification
- Video fluoroscopic swallowing study
- EEG: to evaluate subclinical seizure activity; limited predictive value in the setting of acute TBI
Test Interpretation
Evidence of microscopic axonal injury, axon retraction bulbs, and microglial clusters � �
TREATMENT
GENERAL MEASURES
- Typically requires an integrative, multidisciplinary approach to care; goal is to restore maximal independent function.
- Treat individual patients based on individual symptoms and individual presentations. Early intervention and treatment improves outcomes (1)[A].
- Reduce sedatives.
- Rehabilitative practices: Rehabilitative programs should be interdisciplinary, comprehensive, and include cognitive and behavioral assessment and intervention.
- Nonpharmacologic treatment often preferred in chronic care for TBI patients.
- Headaches: sleep hygiene, physical therapy, relaxation, meditation
- Insomnia: sleep hygiene
- Visual disturbances: sunglasses, light desensitization
MEDICATION
- Tailor medical therapy to individual patient symptoms.
- Psychostimulants may affect speed of cognitive processing, mood, and behavior; may also improve memory, attention, concentration, and mental processing. Rule out sleep disorder before use.
- Methylphenidate: max of 20 mg twice daily; dextroamphetamine 5 to 40 mg/day divided QD " �TID (1,2)[C]
- Modafinil use is controversial. Start 100 mg/day to max of 400 mg/day in split daily dosage (3)[B].
- Amantadine 100 to 400 mg/day
- Antidepressants
- Minimize the use of antipsychotics and benzodiazepines because they worsen cognition.
- � �-Blockers have the best evidence for efficacy in agitation/aggression (4)[A].
- Antidepressants (selective serotonin reuptake inhibitors) may help agitation/aggression (5)[B].
- Citalopram 10 mg/day for 1 week, then 20 mg/day; max is 80 mg/day.
- Sertraline 25 mg/day increase 25 mg/week to max of 200 mg/day (1)[C]
- Sleep agents
- Zolpidem 5 mg at night; max of 10 mg
- Epilepsy: American Academy of Physical Medicine and Rehabilitation does not recommend prophylactic AEDs for preventing late (>7 days post-TBI) posttraumatic seizures.
- Spasticity: Be aware of potential negative consequences of all agents:
- Use baclofen, diazepam, clonidine, tizanidine, and gabapentin; botulinum toxin injections for focal spasticity; dantrolene sodium and intrathecal baclofen may be considered (6)[C].
- Neurogenic bladder: oxybutynin 2.5 mg TID
- May increase to 5 mg QID if bladder pressures low and/or postvoid residuals low
- Bowel routine: high-fiber diet, stool softener such as docusate sodium (daily) combined with or without a stimulant laxative; use of suppositories may be needed.
- Heterotopic ossification: indomethacin 25 to 50 mg TID. If severe, progressive, or history of GI ulceration, then etidronate (Didronel) 20 mg/kg/day for 2 weeks then 10 mg/kg/day for 10 weeks or alendronate 20 mg/day.
- Neurobehavioral problems: Psychostimulants are inconsistently effective in treatment of inattention and apathy. High-dose � �-blockers are inconsistently effective for treatment of agitation and aggression, and anticonvulsants and antidepressants are inconsistently effective in treatment of agitation and aggression with an affective disorder. Rivastigmine showed promising results when used at least 12 months after TBI in a subgroup of patients with moderate to severe memory deficits (7)[C].
- Precautions: Medications may have significant adverse effects in persons with TBI and can impede rehabilitation progress.
- Insomnia: nonpharmacologic interventions (relaxation, cognitive-behavioral therapy, sleep hygiene education), pharmacologic interventions (zopiclone, lorazepam, melatonin, tricyclic antidepressants) (8)[C]
- Eliminate unnecessary chronic medications that could exacerbate patient symptoms
ISSUES FOR REFERRAL
- Refer to multidisciplinary rehabilitation programs.
- Suicide attempts and ideation are more prevalent in people with TBI.
COMPLEMENTARY & ALTERNATIVE MEDICINE
- Cognitive exercises (including computer-assisted strategies), compensatory devices (memory books, paging systems), psychotherapy, behavior modification, vocational rehabilitation, school rehabilitation, nutritional support, music and art therapy, therapeutic recreation
- Hyperbaric oxygen therapy cannot be routinely recommended for patients with TBI because of few trials, methodologic shortcomings, and poor reporting.
ONGOING CARE
PATIENT MONITORING
Patients make slow, steady gains; review medical status monthly. � �
DIET
Ensure adequate hydration and nutrition. � �
PATIENT EDUCATION
- Brain Injury Information Network: http://www.braininjurynetwork.org/
- Brain Injury Association of America: www.biausa.org
- www.cdc.gov/traumaticbraininjury/
PROGNOSIS
- Most rapid return of function occurs during first 2 years, but some improve slowly for 5 to 10 years.
- Highly variable (80% of individuals with severe injuries become independent in dressing and self-care at 1 year)
- Negative prognostic factors
- Age >40 years old
- Abnormal pupillary responses or extraocular eye movements
- Prolonged coma
- Abnormal evoked potentials
- Accurate prediction of return to work is not feasible, with rates in the 12 " �70% range.
- The Oxford Handicap Scale at hospital discharge is a good tool to predict disability at 6 months.
COMPLICATIONS
Major affective disorder (depression, psychosis) in up to 50% of patients, family and caregiver burnout, substance abuse, social isolation, dental caries, osteoporosis, aspiration pneumonia, pressure ulcers, dysphagia, esophagitis, bladder incontinence, contractures/spasticity � �
REFERENCES
11 Management of Concussion/mTBI Working Group. VA/DoD clinical practice guideline for management of concussion/mild traumatic brain injury. J Rehabil Res Dev. 2009;46(6):CP1 " �CP68.22 Siddall � �OM. Use of methylphenidate in traumatic brain injury. Ann Pharmacother. 2005;39(7 " �8):1309 " �1313.33 Jha � �A, Weintraub � �A, Allshouse � �A, et al. A randomized trial of modafinil for the treatment of fatigue and excessive daytime sleepiness in individuals with chronic traumatic brain injury. J Head Trauma Rehabil. 2008;23(1):52 " �63.44 Fleminger � �S. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev. 2003;(1):CD003299.55 Deb � �S, Crownshaw � �T. The role of pharmacotherapy in the management of behaviour disorders in traumatic brain injury patients. Brain Inj. 2004;18(1):1 " �31.66 Zafonte � �R, Elovic � �EP, Lombard � �L. Acute care management of post-TBI spasticity. J Head Trauma Rehab. 2004;19(2):89 " �100.77 Silver � �J, Koumaras � �B, Chen � �M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748 " �755.88 Zeitzer � �JM, Friedman � �L, O 'Hara � �R. Insomnia in the context of traumatic brain injury. J Rehabil Res Dev. 2009;46(6):827 " �836.
ADDITIONAL READING
Quinlan � �JD, Guaron � �MR, Deschere � �BR, et al. Care of the returning veteran. Am Fam Physician. 2010;82(1):43 " �49. � �
CODES
ICD10
- S06.0X0S Concussion without loss of consciousness, sequela
- S06.9X9S Unsp intracranial injury w LOC of unsp duration, sequela
- S06.0X1S Concussion w LOC of 30 minutes or less, sequela
- S06.0X2S Concussion w loss of consciousness of 31-59 min, sequela
- S06.0X3S Concussion w LOC of 1-5 hrs 59 min, sequela
- S06.0X4S Concussion w LOC of 6 hours to 24 hours, sequela
ICD9
- 850.0 Concussion with no loss of consciousness
- 850.9 Concussion, unspecified
- 850.11 Concussion, with loss of consciousness of 30 minutes or less
- 850.12 Concussion, with loss of consciousness from 31 to 59 minutes
- 850.2 Concussion with moderate loss of consciousness
- 850.3 Concussion with prolonged loss of consciousness and return to pre-existing conscious level
- 850.5 Concussion with loss of consciousness of unspecified duration
SNOMED
- Concussion injury of brain (disorder)
- concussion with no loss of consciousness (disorder)
- concussion with loss of consciousness (disorder)
- concussion with less than 1 hour loss of consciousness (disorder)
- Concussion with more than 24 hours loss of consciousness and return to pre-existing conscious level (disorder)
- concussion with 1-24 hours loss of consciousness (disorder)
CLINICAL PEARLS
- TBI can cause chronic neurologic and nonneurologic manifestations.
- Treatment involves a comprehensive multi- and interdisciplinary team.
- Prevention of TBI is more effective than treatment.