Neuropsychiatric Aspects of Traumatic Brain Injury

Psychiatric TimesPsychiatric Times Vol 23 No 4
Volume 23
Issue 4

Each year, more than 2 million individuals in the United States sustain a traumatic brain injury. Increased vigilance for previously undiagnosed or incidental TBIs in general mental health populations may lead to more effective clinical management.

Special Report: Neuropsychiatry

Each year, more than 2 million individuals in the United States sustain a traumatic brain injury (TBI), leading to more than 500,000 hospital admissions and 80,000 survivors with persistent neurologic disabilities. The population at highest risk for TBI is in the 15- to 24-year age range, with a male-to-female ratio of approximately 3:2. The most common causes of TBI include motor vehicle accidents, falls, assaults, and sporting accidents. In patients older than 65, the most common cause is a fall.1

Risk factors for TBI include substance abuse and psychiatric conditions associated with impulsive behaviors, such as bipolar disorder, cluster B personality disorders, and attention-deficit/ hyperactivity disorder (ADHD). These pre-injury psychiatric conditions are associated with high-risk behaviors that can lead to TBI. More than 50% of TBIs involve alcohol intoxication, and 30% to 60% of patients are intoxicated at the time of injury.2

TBI involves the application of force to the brain that results in structural or metabolic alterations manifested by altered consciousness or focal neurologic deficits of varying severity and duration. An initial score on the Glasgow Coma Scale of 13 to 15 constitutes a mild TBI, while a score of 9 to 12 represents moderate TBI, and a score below 9 is severe TBI. Mild TBI accounts for about 80% of all cases, with moderate and severe cases each being responsible for 10%.

The American Congress of Rehabilitation Medicine has further refined the definition of mild TBI, stating that it is any traumatically induced disruption of brain function with limited loss of consciousness (30 minutes or less) or post-traumatic amnesia for less than 24 hours (Table).3 Given the fact that most TBIs are mild, clinicians may encounter orbitofrontal and anterior temporal cortex tend to be selectively damaged.4 Additional diffuse axonal injury (DAI) occurs at the white-gray matter junction and in connecting pathways throughout the brain.5 Often undetectable through structural neuroimaging methods such as CT and MRI, DAI results from shearing forces applied to the brain during rapid acceleration and deceleration of the head.

These acceleration-deceleration mechanics do not require the blunt force impact that occurs when a moving head strikes a stationary object or vice versa. They can also occur through rotational mechanics, such as whiplash injuries. Thus, the absence of external stigmata of injury or structural neuroimaging abnormalities does not rule out the presence of a TBI. It is these mild TBIs that while leaving few, if any, lasting neurologic or cognitive sequelae, may lead to disruptive psychiatric syndromes that are far from mild.

Secondary injuries from edema or hemorrhage result from increased intracranial pressure in severe trauma. However, TBI may also activate intracellular processes involving excitatory amino acids that lead to cell death.6 This process is initiated within hours of injury, although the cascade of events that ultimately cause cell death may take days or weeks. The precise mechanism that mediates excitotoxic cell death is not understood, but it is possible that prolonged excitation of neurons may secondarily cause intracellular metabolic disruption. While clinical trials of excitatory amino acid antagonists have been disappointing,7 these studies have targeted a more severely injured population. The clinical manifestation of this process in mild TBI may be the progressive emergence of neuropsychiatric symptoms over several days or weeks following injury.8

Cognitive deficits

Given the reliance of higher cognitive functions on distributed rather than focal processing, DAI tends to profoundly affect the executive cognitive functions even in the absence of neurologic or focal cortical deficits. Acquired deficits in attention, concentration, and vigilance may resemble those of ADHD, although the postinjury onset or worsening of these deficits helps clarify the cause. Deficits in executive cognitive functioning may particularly affect persons in occupations that are highly dependent on rapid decision making and the complex use of information.

In uncontrolled studies, the cholinesterase inhibitor donepezil (Aricept) has demonstrated some beneficial effects on TBI-related memory deficit.9 The psychostimulants have demonstrated efficacy in improving attention, concentration, and vigilance, but patients should be monitored for increased irritability.10 Clinicians must also take into consideration these acquired cognitive deficits when providing instructions and education to patients, who may be easily overwhelmed by the information exchange.

Aggression and impulsivity

Patients who sustain multiple head injuries over time appear to demonstrate increased irritability with each subsequent injury, particularly when the injuries are associated with loss of consciousness.11 Premorbid risk factors for aggression include a history of impulsive aggression,12 arrest, and substance abuse.13 Aggression is also frequently encountered in post-TBI mania, which occurs in 7% to 9% of patients independent of severity of injury, cognitive impairment, or physical disability.14 While post-TBI manic syndromes may resemble the classic manic syndrome of euphoria, elation, increased energy, and grandiosity, a more common presentation is a dysphoric mixed bipolar syndrome.15

Treatment of post-TBI aggression aims to reduce disruptive behaviors without negatively impacting other areas of functioning. Anticonvulsants appear to be effective and well-tolerated in treating these disorders, although cognitive impairment may occur at higher doses.16 Traditional antipsychotics have been associated with cognitive impairment in TBI patients, but second-generation antipsychotics appear to be better tolerated.17


The prevalence of major depression following TBI ranges from 15% to 61%.18,19 Estimates are limited by the wide variety of methodologies and diagnostic criteria. Some investigators noted that fatigue, frustration, poor concentration, boredom, and distractibility were common in depressed TBI patients, but feeling sad or blue was not as common.20 On the other hand, Jorge and associates21 found that feelings of depression and sadness did, in fact, discriminate between depressed and nondepressed patients and suggested that cognitive impairment and fatigue were not useful diagnostic symptoms in this population. Treatment of post-TBI depression with antidepressants appears to be effective, as is psychotherapy and, when necessary, electroconvulsive therapy. Effective treatment is considered crucial to maximizing cognitive and psychosocial functioning, which are often compromised by depressive symptoms.22


TBI is frequently complicated by neuropsychiatric symptoms that are multiply determined. The complex interaction between neurobiologic changes and the external social environment may lead to devastating psychosocial morbidity, even in the absence of profound neurologic or cognitive impairment. Increased vigilance for previously undiagnosed or incidental TBIs in general mental health populations may lead to more effective clinical management.

Dr Kim is associate director of medical strategy, neuroscience at Bristol-Myers Squibb and clinical associate professor of psychiatry, Robert Wood Johnson Medical School, Piscataway, NJ. He reports that he has no conflicts of interest regarding the subject matter of this article.


References1. Kraus JF, McArthur DL. Incidence and prevalence of, and costs associated with, traumatic brain injury. In: Rosenthal M, Griffith ER, Kreutzer JS, Pentland B, eds. Rehabilitation of the Adult and Child With Traumatic Brain Injury. 3rd ed. Philadelphia: FA Davis; 1999:3-18.
2. Sparadeo FR, Strauss D, Barth JT. The incidence, impact, and treatment of substance abuse in head trauma rehabilitation. J Head Trauma Rehabil. 1990;5:1-8.
3. American Congress of Rehabilitation Medicine. Definition of mild traumatic brain injury. J Head Trauma Rehabil. 1993;8:86-88.
4. Adams JH, Graham DI, Gennarelli TA. Contemporary neuropathological considerations regarding brain damage in head injury. In: Becker DP, Polvishock JT, eds. Central Nervous System Trauma Status Report 1985. Richmond, Va: William Byrd Press; 1986:65- 78.
5. Maxwell WL, Povlishock JT, Graham DL. A mechanistic analysis of nondisruptive axonal injury: a review [published correction appears in J Neurotrauma. 1997;14:755]. J Neurotrauma. 1997;14:419-440.
6. Nilsson P, Hillered L, Ponten U, Ungerstedt U. Changes in cortical extracellular levels of energyrelated metabolites and amino acids following concussive brain injury in rats. J Cereb Blood Flow Metab. 1990;10:631-637.
7. Narayan RK, Michel ME, Ansell B, et al. Clinical trials in head injury. J Neurotrauma. 2002;19:503- 557.
8. Bruce JM, Echemendia RJ. Delayed-onset deficits in verbal encoding strategies among patients with mild traumatic brain injury. Neuropsychology. 2003;17:622-629.
9. Morey CE, Cilo M, Berry J, Cusick C. The effect of Aricept in persons with persistent memory disorder following traumatic brain injury: a pilot study. Brain Inj. 2003;17:809-815.
10. Whyte J, Vaccaro M, Grieb-Neff P, Hart T. Psychostimulant use in the rehabilitation of individuals with traumatic brain injury. J Head Trauma Rehabil. 2002;17:284-299.
11. Carlsson GS, Svardsudd K, Welin L. Long-term effects of head injuries sustained during life in three male populations. J Neurosurg. 1987;67:197-205.
12. Greve KW, Sherwin E, Stanford MS, et al. Personality and neurocognitive correlates of impulsive aggression in long-term survivors of severe traumatic brain injury. Brain Inj. 2001;15:255-262.
13. Kolakowsky-Hayner SA, Kreutzer JS. Pre-injury crime, substance abuse, and neurobehavioural functioning after traumatic brain injury. Brain Inj. 2001;15:53-63.
14. Jorge RE, Robinson RG, Starkstein SE, et al. Secondary mania following traumatic brain injury. Am J Psychiatry. 1993;150:916-921.
15. Shukla S, Cook BL, Mukherjee S, et al. Mania following head trauma. Am J Psychiatry. 1987;144:93- 96.
16. Kim E. The use of newer anticonvulsants in neuropsychiatric disorders. Curr Psychiatry Rep. 2002;4:331-337.
17. Kim E, Bijlani MV. A pilot study of quetiapine treatment of aggression due to traumatic brain injury. J Neuropsychiatry Clin Neurosci. In press.
18. Hibbard MR, Uysal S, Kepler K, et al. Axis I psychopathology in individuals with traumatic brain injury. J Head Trauma Rehabil. 1998;13:24-39.
19. Rapoport MJ, McCullagh S, Streiner D, Feinstein A. The clinical significance of major depression following mild traumatic brain injury. Psychosomatics. 2003;44:31-37.
20. Kreutzer JS, Seel RT, Gourley E. The prevalence and symptom rates of depression after traumatic brain injury: a comprehensive examination. Brain Inj. 2001;15:563-576.
21. Jorge RE, Robinson RG, Arndt SV, et al. Depression following traumatic brain injury: a 1 year longitudinal study. J Affect Disord. 1993;27:233-243.
22. Alderfer BS, Arciniegas DB, Silver JM. Treatment of depression following traumatic brain injury. J Head Trauma Rehabil. 2005;20:544-562.

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