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Neuropsychiatric Sequelae of Traumatic Brain Injury

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Neuropsychiatric Sequelae of Traumatic Brain Injury Neuropsychiatric Sequelae of Traumatic Brain Injury Jeffrey Nicholl, M.D.,1 and W. Curt LaFrance, Jr., M.D., M.P.H.2 ABSTRACT The prevalence of traumatic brain injury (TBI) is increasing, particularly in the population of veterans. Many times, the motor and sensory consequences of TBI are addressed, but the post-TBI neuropsychiatric sequelae, which may be as, or even more devastating than the motor and sensory deficits, are left unattended. Cognitive, mood, anxiety, thought, impulse, and substance disorders, and a variety of personality disorders can be seen following TBI. The neuropsychiatric sequelae of TBI not only interfere with day-to-day function, but can severely impede rehabilitation efforts. To date, there have been few large-scale studies looking at the effectiveness of the various treatment modalities, including psychotherapeutic and pharmacological interventions. KEYWORDS: Traumatic brain injury, concussion, neuropsychiatric sequelae, cognitive disorders, mood disorders, treatment EPIDEMIOLOGY AND ETIOLOGY elderly. Recurrent head injury is common in patients with Traumatic brain injury (TBI) is defined as traumatically a history of alcohol abuse and individuals playing contact induced physiological disruption of the brain, and sports.3 The estimated annual cost of TBI in the United is occurring with increasing frequency. The incidence States is $60 billion for treatment and lost productivity. is 506 per 100,000 people.1 Traumatic brain injury is As significant as the epidemiology of TBI is, the being seen more often, particularly in patients injured in prevalence of post-TBI syndromes is significant and war. Many of the veterans with TBI whose other injuries includes post-traumatic stress disorder (PTSD), depres- would have been fatal in previous wars are now surviving sion, mania, and aggression.4 Post-TBI post-traumatic because of improved protective gear.2 The peak inci- stress disorder occurs in up to 27%, including patients dence is between the ages of 15 and 24 and older than with no clear recall of the event.5,6 Post-TBI depression the age of 64 years. Males are affected twice as often as has an incidence of 15 to 33% and prevalence of 18 to females. In the civilian population, alcohol is involved in 42%.7 Post-TBI mania occurs in <10% of patients with more than half the cases of TBI. People from lower TBI.8 Post-TBI aggression (agitation, disinhibition, This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. socioeconomic groups are significantly more likely to be personality changes) occurs in variable frequencies de- affected by TBI. Motor vehicle accidents (MVAs), par- pending on criteria, ranging from 20 to 49%.9,10 ticularly motorcycle accidents, account for the most Although delusions and auditory hallucinations are frequent civilian cause of TBI. Falls are the next most common in the acute post-traumatic state, post-TBI common cause of head injury, with a high rate in the psychosis occurs in <10% of the TBI population.11,12 1Department of Psychiatry and Neurology, Tulane University School 3, Providence, RI 02903 (e-mail: [email protected]). of Medicine, New Orleans, Louisiana; 2Division of Neuropsychiatry Psychiatry for Neurologists; Guest Editor, Randolph B. Schiffer, and Behavioral Neurology, Brown Medical School/Rhode Island M.D. Hospital, Providence, Rhode Island. Semin Neurol 2009;29:247–255. Copyright # 2009 by Thieme Address for correspondence and reprint requests: W. Curt Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, LaFrance, Jr., M.D., M.P.H., Director of Neuropsychiatry and USA. Tel: +1(212) 584-4662. Behavioral Neurology, Rhode Island Hospital, 593 Eddy Street, Potter DOI 10.1055/s-0029-1223878. ISSN 0271-8235. 247 248 SEMINARS IN NEUROLOGY/VOLUME 29, NUMBER 3 2009 Table 1 Glasgow Coma Scale Scores Table 3 Prevalence and Prognostic Indicators for Traumatic Brain Injury14 Eyes Open spontaneously ¼ 4 Severity Percentage Glasgow Coma in Patients Admitted Open to verbal stimuli ¼ 3 Scale Score to Hospital (%) Mortality (%) Open to pain ¼ 2 Do not open ¼ 1 Mild (13–15) 80 0 Verbal Moderate (9–12) 10 10 Spontaneous speech, oriented ¼ 5 Severe ( <9) 10 60 Spontaneous speech, disoriented ¼ 4 Nonsense speech ¼ 3 Sounds ¼ 2 No speech at all ¼ 1 Because the brainstem is fixed to the base of Motor the skull, it turns as the skull does, but the cerebrum Spontaneous movement ¼ 6 does not. This causes axonal shearing injuries in the Localizes pain ¼ 5 long white matter tracts in the parasagittal areas, the Withdraws from pain ¼ 4 corpus callosum, and the upper brainstem. This injury Decorticate posturing ¼ 3 may range from neurapraxia, with focal demyelina- Decerebrate posturing ¼ 2 tion, to axonotmesis with complete severing of the No movement at all ¼ 1 axon. The severity of the injury to the axons deter- mines whether there will eventually be resumption of function. The prognosis following TBI is related to Secondary (delayed, nonmechanical) postinjury the initial Glasgow Coma Scale (GCS) score13,14 factors include excitotoxic amino acid release, including (Tables 1–3). glutamate. Oxidant injury from free radical release may result in secondary injury. Secondary causes of injury following the immediate head injury include physiolog- PATHOPHYSIOLOGY ical and pathological responses, such as alterations in The neuropathophysiology of TBI can be divided into cerebral blood flow and cerebral perfusion pressure. biomechanical, biochemical, and biomolecular mecha- Reperfusion injury may result. Seizures may occur, along nisms. The acute injury results from primary (mechan- with centrally mediated systemic effects, which may ical) physical disruption of the brain. Head injuries are include shock, electrolyte imbalances, and hypothermia. divided into open, where there is a breach of the skull by Hypoxia, brain edema, increased intracranial pressure, fracture or penetrating injury, and closed, when the hemorrhage, ischemia, and infection (with open head cranium is intact. Because of the brain’s environment— injuries) may occur. floating in the cerebrospinal fluid (CSF) in the cra- nium—sudden acceleration, deceleration, or torsion in- juries can cause the brain to strike the skull, causing COURSE OF ILLNESS: ACUTE, SUBACUTE, injury. There are two basic types of brain injury: (1) AND LONG TERM direct trauma to the brain, causing contusions, hemor- rhages, and lacerations; and (2) diffuse axonal injury, Acute Phase: Emergency Management from stretch injuries to the deep white matter. Coup/ Emergency management in the acute phase of TBI contrecoup injuries occur when the brain is injured by a includes GCS classification, documenting clinical find- torsion injury of the head in which opposite sites in the ings, monitoring fluid balance, and maintaining airway This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. brain are injured; for example, the left frontal and right and oxygenation. Pharmacological, surgical, and invasive parieto-occipital areas. The most commonly injured interventions are also part of acute TBI management; areas of the brain are the anterior poles of the frontal however, the emergency care of TBI is beyond the scope and temporal lobes, where they abut bony ridges of the of this article and is not discussed. skull. Table 2 Severity Grading of Traumatic Brain Injury Subacute Phase: Post-Traumatic Delirium Glasgow Coma Loss of Consciousness and Amnesia Scale Score (time) In the subacute phase, during the period immediately following regaining consciousness following a TBI, Mild 13–15 Less than 30 min patients go through a state during which they are Moderate 9–12 30 min to 1 wk delirious and of which they are amnestic. Risk factors Severe <9 More than 1 wk for more severe and more prolonged delirium include NEUROPSYCHIATRIC SEQUELAE OF TRAUMATIC BRAIN INJURY/NICHOLL, LAFRANCE 249 older age,15 hypoalbuminemia,16 and prior neurological affected by TBI. A commonly overlooked area in TBI is abnormalities.17 As with delirium of other causes, there the effect on relationships and sexual functioning. Fam- may be a fluctuating course with episodes of hyper- and ily, friends, work, and community of faith may be hypoactivity. Patients with this condition demonstrate estranged due to new frustrations or behaviors or bol- disorientation and impaired attention. Often they have a stered as supports after TBI. disrupted sleep-wake cycle, sleeping during the day and Common issues related to symptoms include waking at night. The period of amnesia often outlasts behavioral outbursts, emotional adjustments, cognitive the period of clear delirium. The duration of post- deficits, and physical concerns. The link between ability traumatic delirium varies with the number of lesions to adjust to TBI and the capacity to do so is complicated seen on computed tomography (CT) scan and fluid by a major factor. In addition to having to adjust to attenuated inversion recovery (FLAIR) sequence mag- dysregulation in behavior, emotions, thinking, and phys- netic resonance imaging (MRI).18 Magnetic resonance ical challenges, persons with TBI must make these spectroscopy (MRS) shows decreased N-acetylaspartate adjustments with a brain that processes information and increased choline, which is due to the loss of neurons poorly. A person with limited coping skills may become and increased glial cells.19 frustrated with his or her mood variability or with limb Treatment of the delirium includes treatment of weakness,
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