Psychosocial Impact of Brain Injury: A Review
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paper_title: A systematic review of brain injury epidemiology in Europe

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BACKGROUND ::: The world's literature on traumatic brain injury (TBI) grows annually including new reports on epidemiologic findings from many regions. With the wide variety of reports emphasizing various factors it is useful to compile these findings, hence the objective of this report. Thus, we describe epidemiological factors from European studies largely published in the last 20 years. ::: ::: ::: METHOD ::: The Medline was searched for TBI related articles from about 1980 to 2003 including terms such as "epidemiology", "head injury", "brain injury" and others. From the research reports identified, we checked references for additional relevant reports and from those reports we abstracted data on TBI incidence, severity, external cause, gender, mortality, prevalence, cost and related factors. ::: ::: ::: RESULTS ::: Twenty three European reports met inclusion criteria and included findings from national studies from Denmark, Sweden, Finland, Portugal, Germany, and from regions within Norway, Sweden, Italy, Switzerland, Spain, Denmark, Ireland, the U.K. and France. An aggregate hospitalized plus fatal TBI incidence rate of about 235 per 100,000 was derived. Prevalence rate data were not reported from any European country. An average mortality rate of about 15 per 100,000 and case fatality rate of about 11 per 100 were derived. The TBI severity ratio of hospitalized patients was about 22:1.5:1 for mild vs. moderate vs. severe cases, respectively. The percentages of TBI from external causes varied considerably and several reports reported an association of alcohol use with TBI. Outcome or disability findings were mixed and inconsistent. ::: ::: ::: INTERPRETATION ::: It was difficult to reach a consensus on all epidemiological findings across the 23 published European studies because of critical differences in methods employed across the reports. We highly recommend the development of research guidelines to standardize definitional, case finding, and data reporting parameters to help establish a more precise description and hence utility of the epidemiology of TBI in Europe.
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paper_title: Depression following traumatic brain injury.

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OBJECTIVE ::: Review the existing literature on the incidence, neurobiological and psychosocial correlates, and methods of assessment and treatment of depression following traumatic brain injury (TBI). ::: ::: ::: DATA SOURCES ::: Computerized database searches of the English-language literature from Index Medicus, Psychological Abstracts, Excerpta Medica, and Cumulative Index of Nursing and Allied Health Literature. ::: ::: ::: STUDY SELECTION ::: Given the relatively small number of publications specifically related to TBI and depression, all studies appearing in the peer-reviewed literature were included in the review. In addition, studies examining depression and other neurologic diseases (eg, stroke) were also reviewed as to the potential applicability of the theoretical model or methodology used. ::: ::: ::: CONCLUSIONS ::: Depression occurs with sufficient frequency to be considered a significant consequence after TBI. Depression can impede the achievement of optimal functional outcome, whether in the acute or chronic stages of recovery. It appears that a combination of neuroanatomic, neurochemical, and psychosocial factors is responsible for the onset and maintenance of depression. Its treatment is typically psychopharmacologic, with best results obtained from nontricyclic antidepressants. These results have not been confirmed in double-blind clinical trials, however. Future research should use comprehensive, integrative models of depression that include demographic, biologic, and psychosocial factors; enhanced functional neuroimaging techniques; controlled studies of psychopharmacologic and other interventions; and prospective designs with long-term follow-up.
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paper_title: The Beck Depression Inventory: Is It a Suitable Measure of Depression for Individuals with Traumatic Brain Injury?

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OBJECTIVE: This study examined the relationship between Beck Depression Inventory (BDI) scores and current diagnosis of depression, based on The Structured Clinical Interview for DSM-IV Diagnosis (SCID). DESIGN: Correlation. SETTING: Community-based sample. PARTICIPANTS: 100 individuals with traumatic brain injury (TBI) participated in this study, 25 of whom were diagnosed as depressed and 75 as not depressed at the time of interview. MAIN OUTCOME MEASURES: BDI scores, number of symptoms reported on a symptom checklist and DSM-IV diagnosis of depression. RESULTS: BDI symptoms correlated significantly with the SCID diagnosis of depression (r = .30) but were more strongly related (r = .67) to the number of non-depression-related problems reported, using the TIRR Symptom Checklist, a list of symptoms frequently found post TBI. The BDI had low sensitivity for discriminating depressed from nondepressed individuals (sensitivity = 36% when specificity was set at 80%). These results suggest that for individuals with TBI, high BDI scores may reflect hyperreactivity to post-TBI symptoms to a greater extent than clinical depression. CONCLUSIONS: Further study is needed to (1) understand the physiological, functional, and psychosocial factors that are associated with depression in individuals with TBI; (2) provide the basis for developing better measures of depression; and (3) understand how depression is experienced after TBI. Language: en
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paper_title: Obsessive-compulsive disorder secondary to bilateral frontal damage due to a closed head injury.

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OBJECTIVE ::: To describe a patient who exhibited obsessive-compulsive disorder and frontal lobe dysfunction signs after a closed head trauma. ::: ::: ::: BACKGROUND ::: Recent evidence indicates that frontal-subcortical circuits are involved in the pathogenesis of primary obsessive-compulsive disorder. There are a number of case reports of secondary obsessive-compulsive disorder after lesions involving certain parts of these circuits. ::: ::: ::: METHOD ::: Clinical examinations, cognitive and behavioral assessments, and-lesion analysis based on magnetic resonance imaging were conducted. ::: ::: ::: RESULTS ::: The patient displayed marked obsessive-compulsive behavior along with hyperorality and apathy. Magnetic resonance imaging showed symmetrical frontal-polar abnormal signal intensity. Topographic lesion analysis revealed involvement of Brodmann areas 11, 10, 24, 25, and 32. ::: ::: ::: CONCLUSIONS ::: The patient presented in this report had both frontal lobe dysfunction signs and obsessive-compulsive disorder secondary to bilateral frontal damage due to a closed head injury. The etiological significance of head injury and frontal lobe involvement in obsessive-compulsive disorder is discussed in the context of the clinical and neuroimaging findings and of previous series of brain injured patients.
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paper_title: Obsessive-compulsive disorder after traumatic brain injury

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Traumatic brain injury ( TBI) neuropsychiatric sequelae are a significant cause of morbidity in TBI victims. Among the recognized sequelae are anxiety, obsessions, compulsions and obsessive-compulsive disorder (OCD). This review addresses the emergence of OCD and OCD symptoms after TBI with an emphasis on neural circuits that underlie OCD symptom expression that may be affected by the injury. Current studies suggest that post-TBI emergent psychopathology, including OCD, is influenced by underlying sub-clinical diathesis, brain injury lesions sites, environmental stressors and the rehabilitation process. Pre-morbid status can be obtained by structured psychiatric interviews, and TBI brain lesions can be defined with advanced neuroimaging techniques. This information along with the management of family and environmental stressors and the enhanced clinical identification of symptoms of anxiety and OCD can be used in the rehabilitation process to improve prognosis after TBI.
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paper_title: Memory of the traumatic event as a risk factor for the development of PTSD: lessons from the study of traumatic brain injury.

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Traumatic memories, and the mechanisms by which they operate, continue to occupy a central role in the scientific investigation of risk factors for the development of posttraumatic stress disorder (PTSD). However, empirically based studies are constrained by practical and ethical considerations and are limited to naturalistic models. Consequently, the paradigms most appropriate for the exploration of the relationship between traumatic memories and PTSD have been identified in conditions involving traumatic events where memories may be compromised. Indeed, traumatic brain injury, a condition that is commonly associated with memory impairment, has often been utilized as a naturally occurring model for the study of traumatic memory and its contribution to the development of PTSD. This article presents a critical review of these research efforts and discusses their theoretical and clinical implications.
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paper_title: Interaction of posttraumatic stress disorder and chronic pain following traumatic brain injury.

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OBJECTIVE ::: To investigate the association between posttraumatic stress disorder (PTSD) and chronic pain in patients who had sustained a severe traumatic brain injury (TBI). ::: ::: ::: DESIGN ::: Correlational relationships between pain variables and PTSD measures were examined in a cohort study. ::: ::: ::: SETTING ::: An adult tertiary care center brain injury clinic. ::: ::: ::: PATIENTS ::: Ninety-six persons with severe TBI. ::: ::: ::: OUTCOME MEASURES ::: The Posttraumatic Stress Disorder Interview (PTSD-I), a modified McGill Pain Questionnaire, the Beck Depression Inventory (BDI), the General Health Questionnaire (GHQ), the Community Integration Questionnaire (CIQ), the Satisfaction with Life Scale (SWL), and the Coping Style Questionnaire (CSQ). ::: ::: ::: RESULTS ::: More persons with chronic pain reported PTSD than did those without pain. The relationship between pain severity and depression, functional adjustment, and satisfaction with life was mediated by severity of PTSD. Pain severity was significantly associated with an avoidant coping style. ::: ::: ::: CONCLUSIONS ::: Effective rehabilitation of persons with chronic pain following severe TBI should recognize the role of posttraumatic stress in the maintenance of dysfunctional reactions. Specific interventions that address adaptive coping mechanisms to reduce PTSD may enhance rehabilitation for persons with TBI who suffer chronic pain.
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paper_title: One-year follow-up of patients with mild traumatic brain injury: Occurrence of post-traumatic stress-related symptoms at follow-up and serum levels of cortisol, S-100B and neuron-specific enolase in acute phase

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OBJECTIVE: To investigate serum levels of cortisol (a biochemical marker of stress), S-100B and neuron-specific enolase (two biochemical markers of brain tissue injury), in acute phase in mild trau ...
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paper_title: Mild traumatic brain injury does not produce post-traumatic stress disorder.

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It has been widely assumed that patients who sustain mild traumatic brain injury (MTBI) or post-concussive syndrome develop post-traumatic stress disorder (PTSD) in response to their cognitive difficulties, diminished coping skills, or other losses. This study examined 70 patients who had previously been diagnosed as having either PTSD or MTBI. Each patient was asked to provide a highly detailed chronological history of the events which preceded, followed, and occurred during the traumatic event, to indicate whether they were rendered unconscious or had amnesia for the event, and to describe the various symptoms they developed. All (100.0%) of the PTSD patients were able to provide a highly detailed and emotionally charged recollection of the events which occurred within 15 minutes of the traumatic event in comparison to none (0.0%) of the MTBI patients. None of the MTBI patients reported symptoms such as intrusive recollections of the traumatic event, nightmares, hypervigilance, phobic or startle reactions, or became upset when they were asked to describe the traumatic event or were exposed to stimuli associated with it. These data suggest that PTSD and MTBI are two mutually exclusive disorders, and that it is highly unlikely that MTBI patients develop PTSD symptoms. Furthermore, these findings suggest that clinicians should exercise considerable caution in ruling out PTSD prior to making the diagnosis of MTBI.
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paper_title: Psychiatric consequences of road traffic accidents.

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OBJECTIVE ::: To determine the psychiatric consequences of being a road traffic accident victim. ::: ::: ::: DESIGN ::: Follow up study of road accident victims for up to one year. ::: ::: ::: SETTING ::: Emergency department of the John Radcliffe Hospital, Oxford. ::: ::: ::: SUBJECTS ::: 188 consecutive road accident victims aged 18-70 with multiple injuries (motorcycle or car) or whiplash neck injury, who had not been unconscious for more than 15 minutes, and who lived in the catchment area. ::: ::: ::: MAIN OUTCOME MEASURES ::: Present state examination "caseness"; post-traumatic stress disorder and travel anxiety; effects on driving and on being a passenger. ::: ::: ::: RESULTS ::: Acute, moderately severe emotional distress was common. Almost one fifth of subjects, however, suffered from an acute stress syndrome characterised by mood disturbance and horrific memories of the accident. Anxiety and depression usually improved over the 12 months, though one tenth of patients had mood disorders at one year. In addition, specific post-traumatic symptoms were common. Post-traumatic stress disorder occurred during follow up in one tenth of patients, and phobic travel anxiety as a driver or passenger was more common and frequently disabling. Emotional disorder was associated with having pre-accident psychological or social problems and, in patients with multiple injuries, continuing medical complications. Post-traumatic syndromes were not associated with a neurotic predisposition but were strongly associated with horrific memories of the accident. They did not occur in subjects who had been briefly unconscious and were amnesic for the accident. Mental state at three months was highly predictive of mental state at one year. ::: ::: ::: CONCLUSIONS ::: Psychiatric symptoms and disorder are frequent after major and less severe road accident injury. Post-traumatic symptoms are common and disabling. Early information and advice might reduce psychological distress and travel anxiety and contribute to road safety and assessing "nervous shock."
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paper_title: Neurological, Cognitive and Attributional Predictors of Posttraumatic Stress Symptoms After Traumatic Brain Injury

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We investigated the relationship between the reporting of symptoms of posttraumatic stress disorder (PTSD) in a community sample of 66 survivors of severe traumatic brain injury (TBI) and measures of injury severity, memory, insight, and index-event attributions. Correlational analyses revealed that reporting of PTSD symptoms was related to level of insight and not associated with the severity of survivors' injury, educational background, premorbid or current IQ, or memory impairment. The severity of PTSD symptoms was also associated with external attributions to others of causality for the event.
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paper_title: Posttraumatic Stress Disorder in patients with traumatic brain injury

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BackgroundSevere traumatic stressors such as war, rape, or life-threatening accidents can result in a debilitating psychopathological development conceptualised as Posttraumatic Stress Disorder (PTSD). Pathological memory formation during an alarm response may set the precondition for PTSD to occur. If true, a lack of memory formation by extended unconsciousness in the course of the traumatic experience should preclude PTSD.Methods46 patients from a neurological rehabilitation clinic were examined by means of questionnaires and structured clinical interviews. All patients had suffered a TBI due to an accident, but varied with respect to falling unconscious during the traumatic event.Results27% of the sub-sample who were not unconscious for an extended period but only 3% (1 of 31 patients) who were unconscious for more than 12 hours as a result of the accident were diagnosed as having current PTSD (P < .02). Furthermore, intrusive memories proved to be far more frequent in patients who had not been unconscious. This was also the case for other re-experiencing symptoms and for psychological distress and physiological reactivity to reminders of the traumatic event.ConclusionTBI and PTSD are not mutually exclusive. However, victims of accidents are unlikely to develop a PTSD if the impact to the head had resulted in an extended period of unconsciousness.
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paper_title: Posttraumatic Stress Disorder Symptoms During the First Six Months After Traumatic Brain Injury

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Controversy exists regarding the rate and risk factors for posttraumatic stress disorder (PTSD) following traumatic brain injury (TBI). The authors determined the rate and phenomenology of PTSD symptoms in the 6 months after TBI by conducting a prospective cohort study of 124 subjects who completed the PTSD Checklist–Civilian Version. The cumulative incidence of meeting PTSD symptom criteria at 6 months was 11% and full criteria 5.6%. Prevalence peaked at 1 month (10%). Eighty-six percent had another psychiatric disorder and 29% a history of PTSD. Symptoms were associated with not completing high school, assault, recalling being terrified or helpless, and positive toxicology. PTSD after TBI is rare and the relation to risk factors and comorbidities must be examined.
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paper_title: Psychosis following head injury: a critical review

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Schizophrenia is the most common form of psychotic mental disorder, with a point prevalence generally estimated to lie between 0.6–1.0%. Genetically informative studies have indicated a multifactorial aetiology, with an important heritable (genetic) component, but with environmental exposures also undoubtedly relevant. The “neurodevelopmental hypothesis” has informed a body of research that fairly consistently identifies birth complications as a risk factor for the later onset of schizophrenia.1,2 ::: ::: Injury to the head or brain after birth and beyond has been posited as a risk factor for psychosis for many decades but has enjoyed little systematic research (see Lishman,3 van Reekum et al ,4 and Fujii and Ahmed5 for reviews). The purpose of this article is to review this information systematically. Computerised databases including Medline and PsychInfo were searched using head/brain injury and psychosis or schizophrenia as search terms, covering the period from 1966 to end 2003. Citations from published reviews were also retrieved and yielded important articles and monographs, some published more than two decades ago, not included in these databases. ::: ::: Four types of study design have been used to assess the relation between head injury and schizophrenia: the case report; the long term follow up of series of head injured persons; the cross sectional survey; and the case–control study. ::: ::: Case reports document individual unusual clinical events or episodes. The report from O’Callahan and colleagues6 is a good recent case in point. The striking circumstance here was the onset of schizophrenia in a previously well 16 year old, with no other risk factors, two years after a significant head injury involving a blow to the left frontotemporal region. His parents commented that “he was never the same since the accident”. However, it is possible that the onset of schizophrenia was incidental to the head injury, and …
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paper_title: Schizophrenia-like psychosis following traumatic brain injury: a chart-based descriptive and case-control study.

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BACKGROUND: Head injury has been reported to increase the likelihood of the development of schizophrenia-like psychosis (SLP), but its features and risk factors have been insufficiently investigated. METHOD: Between 1987 and 1997, we examined 45 referred patients with SLP following brain trauma. These subjects were matched with 45 head-injured subjects without SLP on age (current and at injury) and gender, and their case records reviewed systematically. The groups were compared and logistic regression analyses performed. RESULTS: The psychoses had a mean age of onset of 26.3 years, a mean latency of 54.7 months after head injury, usually a gradual onset and a subacute or chronic course. Prodromal symptoms were common and depression often present at onset. Paranoid delusions and auditory hallucinations were the predominant features, with formal thought disorder, catatonic features and negative symptoms being uncommon. The SLP group had more widespread brain damage on neuroimaging, especially in the left temporal and right parietal regions, and were more impaired cognitively. Fewer (non-significantly) SLP subjects had epilepsy which was more likely to be well-controlled in this group. On regression analysis, a positive family history of psychosis and duration of loss of consciousness were the best predictors of SLP. CONCLUSIONS: Head injury-related psychosis is usually paranoid-hallucinatory and subacute or chronic in its presentation. A genetic predisposition to schizophrenia and severity of injury with significant brain damage and cognitive impairment may be vulnerability factors. Language: en
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paper_title: Magnetic resonance imaging of schizophrenia-like psychoses associated with cerebral trauma: clinicopathological correlates

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Three patients with schizophrenia-like psychosis and two with schizoaffective-like psychosis who experienced cerebral trauma before the onset of their illness underwent clinical and magnetic resonance imaging evaluation. Each patient with a schizophrenia-like psychosis, but neither of those with a schizoaffective-like psychosis, showed abnormalities confinedto or including the left temporal lobe. These observations complement recent findings in schizophrenia
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paper_title: Psychiatric Illness Following Traumatic Brain Injury in an Adult HealthMaintenance Organization Population

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Background Psychiatric illness after traumatic brain injury (TBI) has been shown to be prevalent in hospitalized and tertiary care patient populations. Objective To determine the risk of psychiatric illness after TBI in an adult health maintenance organization population. Design Prospective cohort study. Setting Large staff-model health maintenance organization. Participants Nine hundred thirty-nine health plan members diagnosed as having TBI in 1993 and enrolled in the prior year, during which no TBI was ascertained. Three health plan members per TBI-exposed subject were randomly selected as unexposed comparisons, matched for age, sex, and reference date. Main Outcome Measure Psychiatric illness in the 3 years after the TBI reference date, determined using computerized records of psychiatric diagnoses according to the International Classification of Diseases, Ninth Revision, Clinical ::: Modification , prescriptions, and service utilization. Results Prevalence of any psychiatric illness in the first year was 49% following moderate to severe TBI, 34% following mild TBI, and 18% in the comparison group. Among subjects without psychiatric illness in the prior year, the adjusted relative risk for any psychiatric illness in the 6 months following moderate to severe TBI was 4.0 (95% confidence interval [CI], 2.4-6.8) and following mild TBI was 2.8 (95% CI, 2.1-3.7; P P = .005). Prior psychiatric illness significantly modified the relationship between TBI and subsequent psychiatric illness ( P = .04) and was a significant predictor ( P Conclusions Both moderate to severe and mild TBI are associated with an increased risk of subsequent psychiatric illness. Whereas moderate to severe TBI is associated with a higher initial risk, mild TBI may be associated with persistent psychiatric illness.
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paper_title: Psychotic disorder and traumatic brain injury

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Traumatic brain injury (TBI) can result in serious and disabling neuropsychiatric disorders, such as cognitive deficits and personality change, as well as severe and chronic psychosis. This review focuses on the relationship between TBI and schizophrenia-like psychosis (SLP) including its epidemiology, diagnostic criteria, clinical presentation, psychopathology, risk factors, and pathophysiology. The relationships between post-traumatic epilepsy and SLP, and brain trauma and schizophrenia, are also discussed. The risk of SLP does increase after TBI. The clinical presentation has considerable overlap with primary schizophrenic disorder, with a prominence of persecutory and other delusions and auditory hallucinations, as well as a lack of negative symptoms. The onset is often gradual, with a subacute or chronic course. More severe and diffuse brain injury, especially of the temporal and frontal lobes, is the most prominent risk factor. Genetic load may also play a role, but presence of epilepsy could be a protective factor. Further large and systematic longitudinal studies are needed.
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paper_title: Traumatic Brain Injury and Schizophrenia in Members of Schizophrenia and Bipolar Disorder Pedigrees

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OBJECTIVE: Schizophrenia following a traumatic brain injury could be a phenocopy of genetic schizophrenia or the consequence of a gene-environment interaction. Alternatively, traumatic brain injury and schizophrenia could be spuriously associated if those who are predisposed to develop schizophrenia have greater amounts of trauma for other reasons. The authors investigated the relationship between traumatic brain injury and psychiatric diagnoses in a large group of subjects from families with at least two biologically related first-degree relatives with schizophrenia, schizoaffective disorder, or bipolar disorder. METHOD: The Diagnostic Interview for Genetic Studies was used to determine history of traumatic brain injury and diagnosis for 1,275 members of multiplex bipolar disorder pedigrees and 565 members of multiplex schizophrenia pedigrees. RESULTS: Rates of traumatic brain injury were significantly higher for those with a diagnosis of schizophrenia, bipolar disorder, and depression than for those wit...
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paper_title: Alcohol abuse and traumatic brain injury: quantitative magnetic resonance imaging and neuropsychological outcome.

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Prior or concurrent alcohol use at the time of traumatic brain injury (TBI) was examined in terms of post-injury atrophic changes measured by quantitative analysis of magnetic resonance imaging (MRI) and neuropsychological outcome. Two groups of TBI subjects were examined: those with a clinically significant blood alcohol level (BAL) present at the time of injury (TBI + BAL) and those without a significant BAL (TBI-only). To explore the potential impact of both acute and chronic alcohol use, subjects in both groups were further clustered into one of four subgroups (NONE, MILD, MODERATE or HEAVY) based upon available information regarding their pre-injury alcohol use. One-way analysis of covariance (ANCOVA) and multiple analysis of covariance (MANCOVA) were used with subject grouping as the main factor. Age, injury severity as measured by Glasgow Coma Scale (GCS) score, years of education, total intracranial volume (TICV), and the number of days post-injury were included as covariates where appropriate. Increased general atrophy was observed in patients with (a) a positive BAL and/or (b) a history of moderate to heavy pre-injury alcohol use. In addition, performance on neuropsychological outcome variables (WAIS-R and WMS-R Index scores) was generally worse in the subgroups of patients with positive BAL and a history of preinjury alcohol use, as compared to the other TBI groups though not statistically significant. Implications of alcohol use, at the time of brain injury, are discussed.
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paper_title: Substance abuse as a mediating factor in outcome from traumatic brain injury

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Abstract A review of recent research addressed two questions: how common are problems of substance abuse in traumatic brain injury (TBI), and to what extent does alcohol and other drug use mediate outcome? Studies showed alcohol intoxication present in one third to one half of hospitalizations; data for other drug intoxication were not available. Nearly two thirds of rehabilitation patients may have a history of substance abuse that preceded their injuries. Intoxication was related to acute complications, longer hospital stays, and poorer discharge status; however, these relationships may have been caused by colinearity with history. History of substance abuse showed the same morbidity, and was further associated with higher mortality rates, poorer neuropsychological outcome, and greater likelihood of repeat injuries and late deterioration. The effect of history may be caused by subgroups with more severe substance abuse problems. Implications for rehabilitation are discussed, including the potential negative impact of untreated substance abuse on the ability to document efficacy of rehabilitation efforts.
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paper_title: Alcohol abuse and traumatic brain injury: effect on event-related potentials

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Abstract Objective: To examine the individual and combined impact that traumatic brain injury (TBI) and heavy social use of alcohol have on electrophysiologic correlates of working memory and evaluation of task-relevant information. Design: Case-control study Setting: University hospital brain injury rehabilitation unit. Participants: Forty male volunteers divided into four groups on the basis of their history of TBI and alcohol intake. Subjects with TBI had experienced a severe closed head injury at least 1 year before testing. Main Outcome Measure: Event-related potentials (ERPs) and neuropsychometric tests. Results: Groups showed no significant differences in average age or neuropsychological tests. TBI groups did not differ in time postinjury or on severity measures. Alcohol use measures were significantly greater in the two alcohol groups. N200 latency and P300 amplitude were impaired in heavy social drinkers and in nondrinking subjects with TBI relative to controls, but were significantly impaired in subjects with TBI who were also heavy social drinkers. Conclusion: The results indicate that although alcohol use and TBI independently produce mild alterations in some aspects of late ERP components, the ERP changes are significantly greater when alcohol use and TBI are combined. This study provides evidence that heavy social drinking after TBI has a measurable impact on electrophysiologic correlates of cognition.
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paper_title: Co-morbid traumatic brain injury and substance use disorder: Childhood predictors and adult correlates

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PRIMARY OBJECTIVE: To examine demographic factors, childhood experiences and behaviour problems and adult psychopathology associated with a history of adult traumatic brain injury (TBI) with unconsciousness in patients with substance use disorders (SUD). DESIGN AND METHODS: Voluntary patients (n = 550) undergoing treatment for SUD were compared for clinical and demographic variables based on report of TBI. RESULTS: Among the 218 (40%) patients reporting TBI, 61% were men. Childhood conduct problems and loss of a parent were strongly associated with adult TBI. Patients with TBI had more severe SUD and higher rates of depressive and anxiety symptoms, somatic concerns, physical trauma, attempted suicide and Antisocial Personality Disorder. CONCLUSIONS: Men have a higher rate of TBI than women, but women with SUD have an increased relative risk of TBI compared to women in the general population. Childhood conduct problems and loss of a parent in childhood may predict adult risk-taking behaviour that leads to TBI in patients with SUD. TBI is associated with higher rates of psychopathology in patients with SUD.
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paper_title: Traumatic brain injury, psychiatric disorders and suicide: A population-based study of suicide victims during the years 1988–2004 in Northern Finland

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Background: Depression and substance abuse are common among patients with traumatic brain injury (TBI). However, previous studies have not examined the temporal association between psychiatric disorders, TBI and suicide.Objective: To study the prevalence of TBI injury among suicide victims; to determine the association of suicide, psychiatric disorders and TBI severity; and to examine the effect of pre- and post-traumatic psychiatric disorders on their remaining life-time.Methods: This study examined all suicides (n = 1877) committed during a 16-year period in the province of Oulu, Finland. The information of suicide victims was extracted from the official death certificates and the National Hospital Discharge Registers.Results: TBI was found in 5.5% (n = 103) of the victims. Compared to the victims without TBI, those with TBI had significantly more hospital-treated psychiatric and alcohol disorders. If TBI subjects had comorbid psychiatric disorders, the time period between TBI and suicide was under 3 ye...
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paper_title: Disorders of diminished motivation.

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Disorders of diminished motivation occur frequently in individuals with traumatic brain injury. Motivation is an ever-present, essential determinant of behavior and adaptation. The major syndromes of diminished motivation are apathy, abulia, and akinetic mutism. Depending on their etiology, disorders of diminished motivation may be a primary clinical disturbance, a symptom of another disorder, or a coexisting second disorder. This article presents a biopsychosocial approach to the assessment and management of motivational impairments in patients with traumatic brain injury. The recognition and differential diagnosis of disorders of diminished motivation, as well as the mechanism and clinical pathogenesis, are discussed.
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paper_title: Pathological laughter and crying: a link to the cerebellum.

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Patients with pathological laughter and crying (PLC) are subject to relatively uncontrollable episodes of laughter, crying or both. The episodes occur either without an apparent triggering stimulus or following a stimulus that would not have led the subject to laugh or cry prior to the onset of the condition. PLC is a disorder of emotional expression rather than a primary disturbance of feelings, and is thus distinct from mood disorders in which laughter and crying are associated with feelings of happiness or sadness. The traditional and currently accepted view is that PLC is due to the damage of pathways that arise in the motor areas of the cerebral cortex and descend to the brainstem to inhibit a putative centre for laughter and crying. In that view, the lesions \`disinhibit' or \`release' the laughter and crying centre. The neuroanatomical findings in a recently studied patient with PLC, along with new knowledge on the neurobiology of emotion and feeling, gave us an opportunity to revisit the traditional view and propose an alternative. Here we suggest that the critical PLC lesions occur in the cerebro-ponto-cerebellar pathways and that, as a consequence, the cerebellar structures that automatically adjust the execution of laughter or crying to the cognitive and situational context of a potential stimulus, operate on the basis of incomplete information about that context, resulting in inadequate and even chaotic behaviour.
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paper_title: Pathological laughter and crying in patients with closed traumatic brain injury

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We report on the clinical and radiological features in 16 adult patients who suffered a traumatic brain injury and subsequently developed pathological laughter and crying. Patients with pathological laughter and crying were identified from among 301 consecutive brain-injured admissions to a trauma centre and subsequently to a rehabilitation facility. Patients displaying pathological laughter and crying had a greater severity of injury than patients without the syndrome; they also had other associated neurological features compatible with pseudobulbar palsy. Pathological laughter alone, or combined with crying, was more frequent than crying alone. An attempt to correlate clinical features with focal lesions on neuroimaging studies yielded inconsistent results. The theoretical anatomical substrate for pathological laughter and crying in patients with traumatic brain injury is discussed.
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paper_title: Defining and diagnosing involuntary emotional expression disorder.

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Uncontrollable episodes of emotional expression occur in a variety of neurological conditions. This emotional disinhibition syndrome is characterized by episodes of crying or laughing that are unrelated to or out of proportion to the eliciting stimulus. This syndrome is common among patients with amyotrophic lateral sclerosis, multiple sclerosis, stroke, and traumatic brain injury and a variety of terms and definitions have been used to describe it. The confusing nomenclature has been a barrier to understanding, diagnosis, and treatment of this disorder. The authors propose a unifying term, involuntary emotional expression disorder (IEED), and provide diagnostic criteria for this disorder.
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paper_title: Akinetic mutism: disconnection of frontal-subcortical circuits.

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Akinetic mutism may result from anterior cingulate lesions or a disconnection of the limbic connections projecting from the cingulate through subcortical circuits. Based on nonhuman primate primate tracer studies, ventral pallidal lesions should disrupt the anterior cingulate frontal-subcortical circuit. A patient developed a rigid akinetic mute state caused by bilateral lesions of the globus pallidus interna with ventral extension. The anatomic basis of the patient's clinical findings support a similarity in frontal-subcortical anatomy between humans and nonhuman primates. Isolated pallidal lesions are rare. Future studies should document whether ventral extension below the anterior commissure is associated with a loss of motivation.
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paper_title: Pathophysiology of involuntary emotional expression disorder.

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Extensive clinical experience and research suggest that a cortico-limbic-subcortico-thalamic-ponto-cerebellar network plays a significant role in the expression of human emotions. This network includes specific cerebral, cerebellar, and brainstem areas and their multiple projections/pathways, with activity modulated through serotonergic, dopaminergic, glutamatergic, and possibly sigma receptor neurotransmitter systems. Disruptions of regulatory and inhibitory mechanisms in the structure and function of this network likely constitute a pathophysiological basis for the crying and laughing episodes characteristic of involuntary emotional expression disorder. Pharmacologic interventions targeting the neurochemical modulators of the emotional expression systems may afford opportunities for symptom control among persons affected by this disorder.
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paper_title: Neuropsychological and Neurobehavioral Correlates of Aggression Following Traumatic Brain Injury

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This study aimed to establish the neuropsychological and neurobehavioral profile of individuals who develop aggression following traumatic brain injury. In a prospective cohort study, 134 brain-injured individuals who exhibited aggression were compared to 153 individuals who had sustained comparable injuries but were not aggressive. In the aggressive group, specific deficits were identified in verbal memory and visuo-perceptual skills. Compared to normative data, this group had impaired executive-attention function. It is tentatively suggested that significant impairment in verbal memory and visuospatial abilities against a background of diminished executive-attention functioning is associated with the development of aggression after brain injury, especially when other risk factors such as low premorbid IQ, low socioeconomic status, and male gender are present.
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paper_title: Frontal lobe injuries, violence, and aggression: a report of the Vietnam Head Injury Study.

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Knowledge stored in the human prefrontal cortex may exert control over more primitive behavioral reactions to environmental provocation. Therefore, following frontal lobe lesions, patients are more likely to use physical intimidation or verbal threats in potential or actual confrontational situations. To test this hypothesis, we examined the relationship between frontal lobe lesions and the presence of aggressive and violent behavior. Fifty-seven normal controls and 279 veterans, matched for age, education, and time in Vietnam, who had suffered penetrating head injuries during their service in Vietnam, were studied. Family observations and self-reports were collected using scales and questionnaires that assessed a range of aggressive and violent attitudes and behavior. Two Aggression/Violence Scale scores, based on observer ratings, were constructed. The results indicated that patients with frontal ventromedial lesions consistently demonstrated Aggression/Violence Scale scores significantly higher than controls and patients with lesions in other brain areas. Higher Aggression/Violence Scale scores were generally associated with verbal confrontations rather than physical assaults, which were less frequently reported. The presence of aggressive and violent behaviors was not associated with the total size of the lesion nor whether the patient had seizures, but was associated with a disruption of family activities. These findings support the hypothesis that ventromedial frontal lobe lesions increase the risk of aggressive and violent behavior.
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paper_title: Modulation of Anger and Aggression.

paper_content:

Traumatic brain injury commonly results in anger and aggressive behavior. The hypothalamus, limbic system, and prefrontal cortex mediate aggression, and frequently are injured during trauma. Many neurotransmitters that modulate aggressive behavior, including norepinephrine, serotonin, dopamine, and acetylcholine are affected by brain injury. The pharmacological treatment of aggression is divided into medications used for acute behavioral control, and those used for the prophylaxis of episodes. Specific recommendations are made for the choice of specific medications.
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paper_title: The role of injury severity in neurobehavioral outcome 3 months after traumatic brain injury.

paper_content:

Objective/Background: To assess neurobehavioral outcome using the Neurobehavioral Rating Scale-Revised (NRS-R), an instrument with established specificity and validity in Traumatic Brain Injury (TBI) in a sample including the full spectrum of TBI severity 3 months after injury. Method: A cohort group of 102 subjects with mild TBI, 41 with moderate TBI, and 139 with severe TBI, from multiple academic trauma centers, were assessed using the NRS-R and the Glasgow Outcome Scale. Results: Principal components analysis of the NRS-R resulted in a 3-factor model: (1) Cognitive, (2) Emotional, and (3) Hyperarousal. At 3 months, subjects with severe TBI show greater difficulties in cognitive and hyperarousal, but not emotional domains, than those with mild to moderate TBI. More than one third of subjects in all injury severity groups showed evidence of anxiety, depression, irritability, mental fatigability, and memory dysfunction. Scores on the NRS-R were related to outcome on the Glasgow Outcome Scale. Conclusions: Three months after injury, subjects with severe TBI have more dysfunction in cognitive and behavioral (but not emotional) domains than those with mild-to-moderate TBI. The NRS-R is a useful tool for assessing the full spectrum of neurobehavioral dysfunction at all ranges of TBI severity.
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paper_title: Depression following traumatic brain injury.

paper_content:

OBJECTIVE ::: Review the existing literature on the incidence, neurobiological and psychosocial correlates, and methods of assessment and treatment of depression following traumatic brain injury (TBI). ::: ::: ::: DATA SOURCES ::: Computerized database searches of the English-language literature from Index Medicus, Psychological Abstracts, Excerpta Medica, and Cumulative Index of Nursing and Allied Health Literature. ::: ::: ::: STUDY SELECTION ::: Given the relatively small number of publications specifically related to TBI and depression, all studies appearing in the peer-reviewed literature were included in the review. In addition, studies examining depression and other neurologic diseases (eg, stroke) were also reviewed as to the potential applicability of the theoretical model or methodology used. ::: ::: ::: CONCLUSIONS ::: Depression occurs with sufficient frequency to be considered a significant consequence after TBI. Depression can impede the achievement of optimal functional outcome, whether in the acute or chronic stages of recovery. It appears that a combination of neuroanatomic, neurochemical, and psychosocial factors is responsible for the onset and maintenance of depression. Its treatment is typically psychopharmacologic, with best results obtained from nontricyclic antidepressants. These results have not been confirmed in double-blind clinical trials, however. Future research should use comprehensive, integrative models of depression that include demographic, biologic, and psychosocial factors; enhanced functional neuroimaging techniques; controlled studies of psychopharmacologic and other interventions; and prospective designs with long-term follow-up.
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paper_title: The Overt Aggression Scale for the Objective Rating of Verbal and Physical Aggression

paper_content:

The authors describe the design and reliability of a rating scale that measures aggressive behaviors in adults and children. On the Overt Aggression Scale (OAS), aggression is divided into four categories: verbal aggression, physical aggression against objects, physical aggression against self, and physical aggression against others. In addition, specific interventions related to each aggressive event can be recorded on the OAS. The clinical and research applications of this scale are discussed. Language: en
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paper_title: Impaired social response reversal. A case of 'acquired sociopathy'.

paper_content:

In this study, we report a patient (J.S.) who, following trauma to the right frontal region, including the orbitofrontal cortex, presented with `acquired sociopathy'. His behaviour was notably aberrant and marked by high levels of aggression and a callous disregard for others. A series of experimental investigations were conducted to address the cognitive dysfunction that might underpin his profoundly aberrant behaviour. His performance was contrasted with that of a second patient (C.L.A.), who also presented with a grave dysexecutive syndrome but no socially aberrant behaviour, and five inmates of Wormwood Scrubs prison with developmental psychopathy. While J.S. showed no reversal learning impairment, he presented with severe difficulty in emotional expression recognition, autonomic responding and social cognition. Unlike the comparison populations, J.S. showed impairment in: the recognition of, and autonomic responding to, angry and disgusted expressions; attributing the emotions of fear, anger and embarrassment to story protagonists; and the identification of violations of social behaviour. The findings are discussed with reference to models regarding the role of the orbitofrontal cortex in the control of aggression. It is suggested that J.S.'s impairment is due to a reduced ability to generate expectations of others' negative emotional reactions, in particular anger. In healthy individuals, these representations act to suppress behaviour that is inappropriate in specific social contexts. Moreover, it is proposed that the orbitofrontal cortex may be implicated specifically either in the generation of these expectations or the use of these expectations to suppress inappropriate behaviour.
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paper_title: Clinical correlates of aggressive behavior after traumatic brain injury.

paper_content:

The authors assessed aggressive behavior in 89 patients with traumatic brain injury (TBI) and 26 patients with multiple trauma but without TBI using a quantitative scale (the Overt Aggression Scale) and examined its clinical correlates. Aggressive behavior was found in 33.7% of TBI patients and 11.5% of patients without TBI during the first 6 months after injury. Aggressive behavior was significantly associated with the presence of major depression, frontal lobe lesions, poor premorbid social functioning, and a history of alcohol and substance abuse. Interventions aimed at treatment of depression and substance abuse and enhancing social support may help reduce the severity of this disruptive behavior.
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paper_title: Episodic dyscontrol syndrome

paper_content:

Episodic dyscontrol syndrome may affect both children and adults. Those who treat children with neurological disorders are likely to see patients referred for investigation of outbursts of aggressive behaviour, especially if episodes are possibly of an epileptic nature. This may occasionally be the case, but in some children it seems that their threshold to such behaviour is abnormally low, and this may also result from defects in the biochemistry or structure of the brain. There is nothing calculated about this behaviour, and it cannot be explained by justifiable anger, such as the result of frustration. Boys are affected more frequently than girls, and the syndrome is more often seen among urban than rural populations. Such outbursts can occur in isolation, but also after a series of minor episodes such as the crying of a younger sibling for nights on end. The outbursts may be very brief or last several hours.
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paper_title: ['Frontal lobe syndrome' caused by severe head trauma or cerebrovascular diseases].

paper_content:

The term "frontal lobe syndrome" comprises a variety of different clinical syndromes produced by focal lesions involving the prefrontal cortex. However, similar syndromes can be observed after lesions involving subcortical structures connected with the prefrontal cortex in neuronal networks. With respect to the different clinical pictures and underlying brain lesions, prefrontal lobe dysfunction may be divided into a disorganized type, caused by lesion of the dorsolateral prefrontal lobe and its connections, a disinhibited type that can be observed following lesions of the orbitofrontal cortex, and an apathetic type following lesions affecting the functional balance between the cingulum and the supplementary motor area. As intracerebral lesions are rarely limited to the brain regions described, in the majority of patients various degrees of behavioural dysfunction can be observed. The case reports of four patients illustrating the three major prefrontal syndromes following severe head injury (n = 2) or cerebrovascular disease (n = 2) are presented and diagnostic implications as well as possible treatment strategies are discussed.
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paper_title: CSF testosterone and 5-HIAA correlate with different types of aggressive behaviors

paper_content:

We studied the potential roles of testosterone and serotonin in various forms of aggressive and violent behaviors by measuring each biochemical and behavior in free-ranging adolescent male nonhuman primates. Our results showed that (1) CSF free testosterone concentrations were positively correlated with overall aggressiveness, but not with measures of impulsivity. (2) CSF 5-HIAA concentrations were negatively correlated with impulsive behavior, and severe, unrestrained aggression, but not with overall rates of aggression. High rates of impulsive behavior were positively correlated with severe, unrestrained aggression, but not overall rates of aggression. (3) Dimensional analyses showed that while subjects with low CSF 5-HIAA exhibited high rates of aggression, high CSF testosterone further augmented rates and intensity of aggression in subjects with low CSF 5-HIAA. We conclude that high CSF free testosterone concentrations are associated with competitive aggression, while low CSF 5-HIAA concentrations are associated with severe aggression which results from impaired impulse control, and perseverance.
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paper_title: Sex Offending as a Psychosocial Sequela of Traumatic Brain Injury

paper_content:

Objective: To describe the nature and extent of sexual offending after traumatic brain injury (TBI). Design: Retrospective file review. Setting: A brain injury unit providing inpatient and outpatient rehabilitation services. Participants: A review of five years of admissions to the Brain Injury Rehabilitation Unit (N = 477) identified a sample of 29 males who committed 128 incidents of sex offending. Main Outcome Measures: A protocol to record data on demographic, injury, radiological, and psychosocial variables and offending behaviors. Results: Of the total population of 445 clients with TBI, 6.5% (n = 29) were identified as having committed some form of sexual offense. Alcohol was a factor in only three (2.3%) of the incidents, and only two clients had a preinjury history of sexual offending. The most common offenses were the “touching” offenses, followed by exhibitionism and overt sexual aggression. Staff members were the most common targets of the offenses, followed by members of the general public, other people with TBI, and family members. Conclusions: Sex offending is a significant clinical problem among a small minority of men after TBI. The absence of alcohol and preinjury histories of sexual offending suggest that the brain injury and contingent sequelae were a significant etiological factor underlying the offenses. A number of implications for the clinical management of clients with sexually aberrant behaviors is identified and discussed.
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Title: Psychosocial Impact of Brain Injury: A Review

Section 1: Introduction
Description 1: Provide an overview of traumatic brain injury (TBI) including its incidence, primary causes, affected demographics, and the general lack of awareness about its delayed symptoms and psychosocial impacts.

Section 2: Impact on Individual Depression
Description 2: Discuss the prevalence, symptoms, and neurological causes of depression post-TBI, including the co-occurrence of psychiatric disorders and the influence of lesion sites.

Section 3: Mania
Description 3: Examine the prevalence, symptoms, and neurological factors associated with mania following TBI, highlighting the common sites of brain lesions and related psychiatric comorbidities.

Section 4: Obsessive-Compulsive Disorder
Description 4: Outline the prevalence, symptoms, and brain regions involved in obsessive-compulsive disorder (OCD) post-TBI, along with insights into its rehabilitation challenges and psychiatric comorbidity.

Section 5: Posttraumatic Stress Disorder
Description 5: Address the prevalence, symptoms, and contributing factors to posttraumatic stress disorder (PTSD) following TBI, including the role of brain structures and the impact on patients’ quality of life.

Section 6: Psychotic Disorders
Description 6: Detail the incidence, symptoms, and neurological underpinnings of psychotic disorders post-TBI, discussing the association with genetic predispositions and the types of psychotic symptoms observed.

Section 7: Disorders Related to Alcohol
Description 7: Explore the link between alcohol use and TBI, covering the prevalence of alcohol dependence/abuse in TBI cases, the impact of alcohol on brain structures, and the exacerbation of psychiatric symptoms.

Section 8: Personality Changes Apathy
Description 8: Describe the prevalence and neurological basis of apathy post-TBI, emphasizing the role of specific brain regions and neurotransmitters in these motivational disturbances.

Section 9: Affective Lability
Description 9: Investigate the emotional instability and rapid mood changes observed post-TBI, detailing the neurological pathways and neurotransmitters involved.

Section 10: Aggression
Description 10: Analyze the incidence and characteristics of aggression following TBI, explaining the neurological mechanisms and environmental factors contributing to aggressive behavior.

Section 11: Other Personality Changes
Description 11: Summarize additional personality changes such as behavioral disinhibition and hypersexuality post-TBI, focusing on the role of frontal lobe impairment.

Section 12: Conclusion
Description 12: Conclude the review by summarizing the various psychosocial impacts of TBI, emphasizing the importance of recognizing psychiatric disorders and the need for well-planned follow-up studies for better outcomes.