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Travmatik Beyin Hasarı Sonrası Ruhsal Belirtiler ve Bilişsel Bozulma
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OBJECTIVE
Traumatic brain injury (TBI)—the “silent epidemic”—contributes to worldwide death and disability more than any other traumatic insult. Yet, TBI incidence and distribution across regions and socioeconomic divides remain unknown. In an effort to promote advocacy, understanding, and targeted intervention, the authors sought to quantify the case burden of TBI across World Health Organization (WHO) regions and World Bank (WB) income groups.
METHODS
Open-source epidemiological data on road traffic injuries (RTIs) were used to model the incidence of TBI using literature-derived ratios. First, a systematic review on the proportion of RTIs resulting in TBI was conducted, and a meta-analysis of study-derived proportions was performed. Next, a separate systematic review identified primary source studies describing mechanisms of injury contributing to TBI, and an additional meta-analysis yielded a proportion of TBI that is secondary to the mechanism of RTI. Then, the incidence of RTI as published by the Global Burden of Disease Study 2015 was applied to these two ratios to generate the incidence and estimated case volume of TBI for each WHO region and WB income group.
RESULTS
Relevant articles and registries were identified via systematic review; study quality was higher in the high-income countries (HICs) than in the low- and middle-income countries (LMICs). Sixty-nine million (95% CI 64–74 million) individuals worldwide are estimated to sustain a TBI each year. The proportion of TBIs resulting from road traffic collisions was greatest in Africa and Southeast Asia (both 56%) and lowest in North America (25%). The incidence of RTI was similar in Southeast Asia (1.5% of the population per year) and Europe (1.2%). The overall incidence of TBI per 100,000 people was greatest in North America (1299 cases, 95% CI 650–1947) and Europe (1012 cases, 95% CI 911–1113) and least in Africa (801 cases, 95% CI 732–871) and the Eastern Mediterranean (897 cases, 95% CI 771–1023). The LMICs experience nearly 3 times more cases of TBI proportionally than HICs.
CONCLUSIONS
Sixty-nine million (95% CI 64–74 million) individuals are estimated to suffer TBI from all causes each year, with the Southeast Asian and Western Pacific regions experiencing the greatest overall burden of disease. Head injury following road traffic collision is more common in LMICs, and the proportion of TBIs secondary to road traffic collision is likewise greatest in these countries. Meanwhile, the estimated incidence of TBI is highest in regions with higher-quality data, specifically in North America and Europe.
Mild traumatic brain injury (mTBI) frequently challenges the integrity of sleep function by affecting multiple brain areas implicated in controlling the switch between wakefulness and sleep and those involved in circadian and homeostatic processes; the malfunction of each causes a variety of disorders. In this review, we discuss recent data on the dynamics between disorders of sleep and mental/psychiatric disorders in persons with mTBI. This analysis sets the stage for understanding how a variety of physiological, emotional and environmental influences affect sleep and mental activities after injury to the brain. Consideration of the intricate links between sleep and mental functions in future research can increase understanding on the underlying mechanisms of sleep-related and psychiatric comorbidity in mTBI.
In this paper we explore the evidence for post-traumatic stress disorder (PTSD) after traumatic brain injury (TBI). We examine its possible mediating mechanisms after brain injury, the evidence for its occurrence, risk, and protective factors, and the implications for intervention and service demands. In the first section we review the current literature relevant to cause, maintenance, and treatment of PTSD in general, before addressing issues associated with the assessment and management of PTSD after TBI. It is argued that PTSD may occur after a brain injury, and can be, relatively, a common disorder. However, explanatory mechanisms for its occurrence may be speculative. In this context, we argue, assessment and treatment need to be carefully considered, and comprehensive.
Traumatic brain injury (TBI) is known to lead to a range of adverse psychiatric sequelae but the question of whether TBI is a risk factor for psychosis and, in particular, schizophrenia remains unclear. Studies examining this issue have yielded conflicting results. We carried out a systematic review of the literature on TBI and psychosis in order to identify all population-based controlled studies which provide estimates of risk for schizophrenia following TBI. Odds ratios (ORs) were combined using random effects meta-analysis. Our literature search yielded 172 studies which were considered to be potentially relevant. From these, we identified 9 studies that could provide estimates of risk in the form of ORs. The pooled analysis revealed a significant association between TBI and schizophrenia (OR = 1.65; 95% CI = 1.17-2.32), with significant heterogeneity between the studies. Estimates from the family studies (OR = 2.8: 95% CI =1.76-4.47) were higher than those from the cohort/nested case-control studies (OR = 1.42: 95% CI = 1.02-1.97) by a factor of almost 2. There did not appear to be a dose-response relationship between severity of head injury and subsequent risk of schizophrenia. This meta-analysis supports an increased risk of schizophrenia following TBI, with a larger effect in those with a genetic predisposition to psychosis. Further epidemiological and neuroscientific studies to elucidate the mechanisms underlying this association are warranted.
Psychiatric disorders are common following traumatic brain injury (TBI). However, few studies have examined the course of disorder development and the influence of pre-injury psychiatric history. The present study aimed to examine the frequency of, and association between, psychiatric disorders occurring pre- and post-injury, and to examine the post-injury course of disorders.
Participants were 102 adults (75.5% male) with predominantly moderate-severe TBI. Participants were initially assessed for pre-injury and current disorders, and reassessed at 3, 6 and 12 months post-injury using the Structured Clinical Interview for DSM-IV Disorders (SCID).
Over half of the participants had a pre-injury psychiatric disorder; predominantly substance use, mood, and anxiety disorders. In the first year post-injury, 60.8% of participants had a psychiatric disorder, commonly anxiety and mood disorders. Post-injury disorders were associated with the presence of a pre-injury history (p<0.01), with 74.5% of participants with a pre-injury psychiatric history experiencing a post-injury disorder, which commonly presented at initial assessment or in the first 6 months. However, 45.8% of participants without a pre-injury history developed a novel post-injury disorder, which was less likely to emerge at the initial assessment and generally developed later in the year.
Despite evidence that most post-injury psychiatric disorders represent the continuation of pre-existing disorders, a significant number of participants developed novel psychiatric disorders. This study demonstrates that the timing of onset may differ according to pre-injury history. There seem to be different trajectories for anxiety and depressive disorders. This research has important implications for identifying the time individuals are most at risk of psychiatric disorders post-injury.
When the landmark patient Phineas Gage died in 1861, no autopsy was performed, but his skull was later recovered. The brain
lesion that caused the profound personality changes for which his case became famous has been presumed to have involved the
left frontal region, but questions have been raised about the involvement of other regions and about the exact placement of
the lesion within the vast frontal territory. Measurements from Gage's skull and modern neuroimaging techniques were used
to reconstitute the accident and determine the probable location of the lesion. The damage involved both left and right prefrontal
cortices in a pattern that, as confirmed by Gage's modern counterparts, causes a defect in rational decision making and the
processing of emotion.
Severe disturbances of sleep architecture and circadian rhythms are common in traumatic brain injured patients; however, complete absence of the rapid eye movement sleep stage is very rare. We describe a brain injured patient with cognitive disturbances who developed severe alterations of sleep architecture, accompanied by paranoid and jealousy delusions. Following several trials with conventional antipsychotics his psychotic state stabilized but he continued to complain of insomnia and daytime fatigue. When treated with risperidone 2 mg/day, both his sleep and the delusional thoughts improved markedly and his daytime alertness increased. Severe deterioration of his support system brought about discontinuation of treatment with re-emergence of all symptoms.
The goal of this study was to measure the very long-term mental and psychosocial outcomes of severe traumatic brain injury (TBI). Seventy-six persons with severe TBI were evaluated extensively by means of standardized scales, neuropsychological tests and evaluations by family members, at an average of 14.1 (SD = 5.5) years post-injury. Six mental and functional domains were examined: psychiatric symptomatology, cognitive abilities, vocational status, family integration, social functioning, and independence in daily routines. The findings indicate a long-term differential effect of severe TBI, with seriously affected psychiatric symptomatology, family and social domains, as compared to moderately influenced cognitive, vocational and independent functioning. Relatively high rates of depression, psychomotor slowness, loneliness and family members' sense of burden were found. In addition to their epidemiological importance, the results indicate that persons with TBI and their families may need professional assistance to maintain a reasonable psychosocial quality of life, even more than a decade post-injury.
To determine the association of report of any history of head injury with loss of consciousness or confusion and a lifetime diagnosis of psychiatric disorder in a general population.
A probability sample of adults from the New Haven portion of the NIMH Epidemiologic Catchment Area programme were administered standardized and validated structured interviews. The main outcome measures were lifetime prevalence of psychiatric disorders and suicide attempt in individuals with and without a history of traumatic brain injury.
Among 5034 individuals interviewed, 361 admitted to a history of severe brain trauma with loss of consciousness or confusion (weighted rate of 8.5/100). When controlling for sociodemographic factors, quality of life indicators and alcohol use, risk was increased for major depression, dysthymia, panic disorder, OCD, phobic disorder and drug abuse/dependence. In addition, lifetime risk of suicide attempt was greater in those who had suffered head injury.
Individuals with a history of traumatic brain injury have significantly higher occurrence for psychiatric disorders and suicide attempts in comparison with those without head injury and have a poorer quality of life. Future studies should examine the nature of this relationship, focusing on the severity of the brain injury and the temporal contiguity of the brain injury and psychiatric disorder.
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.
Study functional changes between one and five years after traumatic brain injury (TBI).
Prospective cohort.
TBI Model Systems National Database subjects using cohort with complete one and five year data (n = 301).
Disability Rating Scale (DRS) Level of Functioning and Employability Items.
On Level of Functioning, 53 (18%) individuals improved, 228 (76%) stayed the same, and 20 (7%) worsened by more than one point from Year 1 to Year 5. On Employability, 50 (17%) individuals improved, 237 (79%) stayed the same, and 14 (5%) worsened by greater than one point. Level of Functioning improvement was predicted by FIM-Motor, FIM-Cognitive, Rey Auditory Verbal Learning Test, Symbol Digit Modalities Test (written and oral), and Wechsler Adult Intelligence Scale-Revised Block Design, and worsening predicted by Symbol Digit Modalities Test (written and oral). Improvement in Employability was predicted by race, while Glasgow Coma Scale Eye Opening was predictive of worsening.
Although the majority did not demonstrate meaningful change on the DRS items from year 1 to 5, some individuals made dramatic gains and a minority declined. There are demographic and functional indicators present at one-year post-injury that may be predictive of subsequent change.
This study delineated patterns of alcohol use 1 year after traumatic brain injury (TBI) in a large, population-based, epidemiological, nonclinical sample, and identified predictors of heavy alcohol use in these individuals. Participants were 1,606 adults identified by review of a South Carolina statewide hospital discharge data set, on the basis of satisfying the Centers for Disease Control case definition of TBI, and were interviewed by telephone 1 year after TBI-related discharge. Alcohol use in the month prior to interview was classified according to categories from the Quantity-Frequency-Variability Index; heavy drinking was defined as nearly daily use with > or = 5 drinks at least occasionally, or at least three occasions with > or = 5 drinks. A polychotomous logistic regression with 3 response levels (heavy, moderate, and abstinent/infrequent/light drinking) was used to identify predictors of heavy drinking. Heavy drinking in the month prior to interview was reported by 15.4% of participants, while 14.3% reported moderate drinking and 70.3% reported abstinence or light/infrequent drinking. Risk factors for heavy drinking included male gender, younger age, history of substance abuse prior to TBI, diagnosis of depression since TBI, fair/moderate mental health, and better physical functioning. There was no association between drinking patterns and TBI severity.
Depression is increasingly recognised as a common sequel to acquired brain injury and the use of antidepressant medication in this context has increased markedly over recent years. However, these drugs are not without side effects--some of them serious--and they should not be used without proper evaluation and monitoring. This set of concise guidance was developed jointly by the British Society of Rehabilitation Medicine, the British Geriatrics Society and the Royal College of Physicians, to guide clinicians working with people who have brain injury of any cause (i.e. stroke, trauma, anoxia, infection etc). The guidance covers (a) screening and assessment of depression in the context of brain injury, (b) issues to consider and discuss with the patient and their family before starting treatment, and (c) proper treatment planning and evaluation--including planned withdrawal at the end of treatment.
There is scattered but significant psychological and neuropsychological evidence to suggest that mild traumatic brain injury (mild TBI) plays a notable role in the emergence and expression of anxiety. Conversely, there is also empirical evidence to indicate that anxiety may exert a pronounced impact on the prognosis and course of recovery of an individual who has sustained a mild TBI. Although the relationship between mild TBI and anxiety remains unclear, the present body of research attempts to elucidate a number of aspects regarding this topic. Overall, the mild TBI research is rife with inconsistencies concerning prevalence rates, the magnitude and implications of this issue and, in the case of PTSD, even whether certain diagnoses can exist at all. This review obviates the need for greater consistencies across studies, especially between varying disciplines, and calls for a shift from studies overly focused on categorical classification to those concerned with dimensional conceptualization.
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 traumatic brain injury patients and the occurrence of post-traumatic stress-related symptoms 1 year after the trauma.
Blood samples were taken in patients (n = 88) on admission and approximately 7 hours later for analysis. Occurrence of post-traumatic stress-related symptoms was assessed for 69 patients using items from the Impact of Event Scale questionnaire (IES) at follow-up at 15 +/- 4 months after the injury.
Serum levels of cortisol were more increased in the first sample (cortisol/1, 628.9 +/- 308.9 nmol L-1) than in the second blood sample (cortisol/2, 398.2 +/- 219.4 nmol L-1). The difference between these samples was statistically significant (p < 0.001). Altogether 12 patients (17%) showed post-traumatic stress related symptoms at the time of the follow-up. Stepwise forward logistic regression analysis of symptoms and serum concentrations of markers revealed that only S-100B in the second sample was statistically significantly (p < 0.05) associated to symptoms (three symptoms of the avoidance sub-set of IES).
A major increase in serum concentrations of cortisol indicates that high stress levels were reached by the patients, in particular shortly ( approximately 3 hours) after the trauma. The association between the occurrence of post-traumatic stress related symptoms and serum levels of S-100B (generally considered as a biochemical marker of brain injury) seem to reflect the complexity of interactions between brain tissue injury and the ensemble of stress reactions.
There is currently a lack of evidence-based guidelines to guide the pharmacological treatment of neurobehavioral problems that commonly occur after traumatic brain injury (TBI). It was our objective to review the current literature on the pharmacological treatment of neurobehavioral problems after traumatic brain injury in three key areas: aggression, cognitive disorders, and affective disorders/anxiety/ psychosis. Three panels of leading researchers in the field of brain injury were formed to review the current literature on pharmacological treatment for TBI sequelae in the topic areas of affective/anxiety/ psychotic disorders, cognitive disorders, and aggression. A comprehensive Medline literature search was performed by each group to establish the groups of pertinent articles. Additional articles were obtained from bibliography searches of the primary articles. Group members then independently reviewed the articles and established a consensus rating. Despite reviewing a significant number of studies on drug treatment of neurobehavioral sequelae after TBI, the quality of evidence did not support any treatment standards and few guidelines due to a number of recurrent methodological problems. Guidelines were established for the use of methylphenidate in the treatment of deficits in attention and speed of information processing, as well as for the use of beta-blockers for the treatment of aggression following TBI. Options were recommended in the treatment of depression, bipolar disorder/mania, psychosis, aggression, general cognitive functions, and deficits in attention, speed of processing, and memory after TBI. The evidence-based guidelines and options established by this working group may help to guide the pharmacological treatment of the person experiencing neurobehavioral sequelae following TBI. There is a clear need for well-designed randomized controlled trials in the treatment of these common problems after TBI in order to establish definitive treatment standards for this patient population.
This article outlines the epidemiology of psychiatric disorders in individuals with traumatic brain injury (TBI), with a focus on DSM axis I disorders diagnosed on the basis of structured clinical interview. The epidemiology of psychiatric disorders in the general population is described as a basis for understanding the disorders that occur before and after TBI. For each disorder category, including mood disorders, anxiety disorders, acute stress disorder, posttraumatic stress disorder (PTSD), substance use disorders, psychotic disorders, eating disorders, somatoform disorders, and adjustment disorders, the evidence from retrospective, cross-sectional and prospective studies is reviewed, showing the frequency, time course, and predictors of the disorders. Studies show elevated rates of depressive and anxiety disorders after TBI, most commonly major depressive disorder and PTSD, usually emerging in the first year postinjury but with delayed onset in severe injury cases. Although individuals with a preinjury history are more likely to develop these disorders, the nature of the disorders may change after injury, and novel psychiatric disorders are also common. Even though the frequency of anxiety disorders diminishes over the years postinjury, depressive disorders are more persistent during postinjury years. Substance use-while high before injury-declines after injury. The frequency of psychotic, eating, somatoform, and adjustment disorders do not exceed population rates.
Objective:
To investigate whether parental TBI increases the overall risk for psychiatric disorders and the risk for specific psychiatric diagnoses in the children affected by parental TBI.
Methods:
The 1987 Finnish Birth Cohort (n = 59 476) were followed up through national registers from birth to the end of 2008. The diagnoses of cohort members and their parents were obtained from the Care Register of Health Care, provided by the National Institute of Health and Welfare.
Results:
During the 21-year follow-up, the likelihood for psychiatric diagnoses being assessed in psychiatric care was significantly increased in males with any mental disorder (odds ratio (OR) = 1.43), substance-use-related disorders (OR = 1.71) and behavioural and emotional disorders (OR = 1.75), and in females with disorders of psychological development (OR = 1.85).
Conclusions:
Children affected by parental TBI are at increased risk for psychiatric disorders: males for externalizing disorders and females for developmental disorders. Observed gender interactions in the association between parental TBI and the psychiatric disorders of children warrant further study.
Background:
Psychiatric disorders commonly emerge during the first year following traumatic brain injury (TBI). However, it is not clear whether these disorders soon remit or persist for long periods post-injury. This study aimed to examine, prospectively: (1) the frequency, (2) patterns of co-morbidity, (3) trajectory, and (4) risk factors for psychiatric disorders during the first 5 years following TBI.
Method:
Participants were 161 individuals (78.3% male) with moderate (31.2%) or severe (68.8%) TBI. Psychiatric disorders were diagnosed using the Structured Clinical Interview for DSM-IV, administered soon after injury and 3, 6 and 12 months, and 2, 3, 4 and 5 years post-injury. Disorder frequencies and generalized estimating equations were used to identify temporal relationships and risk factors.
Results:
In the first 5 years post-injury, 75.2% received a psychiatric diagnosis, commonly emerging within the first year (77.7%). Anxiety, mood and substance-use disorders were the most common diagnostic classes, often presenting co-morbidly. Many (56.5%) experienced a novel diagnostic class not present prior to injury. Disorder frequency ranged between 61.8 and 35.6% over time, decreasing by 27% [odds ratio (OR) 0.73, 95% confidence interval (CI) 0.65-0.83] with each year post-injury. Anxiety disorders declined significantly over time (OR 0.73, 95% CI 0.63-0.84), whilst mood and substance-use disorder rates remained stable. The strongest predictors of post-injury disorder were pre-injury disorder (OR 2.44, 95% CI 1.41-4.25) and accident-related limb injury (OR 1.78, 95% CI 1.03-3.07).
Conclusions:
Findings suggest the first year post-injury is a critical period for the emergence of psychiatric disorders. Disorder frequency declines thereafter, with anxiety disorders showing greater resolution than mood and substance-use disorders.
It is not possible to provide a comprehensive forensic neuropsychiatric or psychiatric assessment of a person following traumatic brain injury without also including within the examination, at a minimum, structural brain imaging. Functional brain imaging may be useful in special circumstances but it is never the modality of first choice following traumatic brain injury (TBI). TBI follows a classic neurochemical cascade, which often results in structural and anatomical changes to brain tissue. These changes can be detected with neuroimaging using computed tomography, magnetic resonance imaging, single photon emission computed tomography, positron emission tomography, and magnetic resonance spectroscopy. The use of neuroimaging in forensic psychiatric cases of traumatic brain injury requires knowledge of the medical-legal distinctions between their uses in the clinic versus introduction of neuroimaging to a judge or jury. The American College of Radiology guidelines for uses of neuroimaging in subacute and chronic traumatic brain injury assessments by a psychiatrist are emphasized.
Increasing evidence indicates that posttraumatic stress disorder (PTSD) may develop following traumatic brain injury (TBI), despite most patients having no conscious memory of their accident. This prospective study examined the frequency, timing of onset, symptom profile, and trajectory of PTSD and its psychiatric comorbidities during the first four years following moderate to severe TBI. Participants were 85 individuals (78.8% male) with moderate or severe TBI recruited following admission to acute rehabilitation between 2005 and 2010. Using the Structured Clinical Interview for DSM-IV Disorders (SCID-I), participants were evaluated for pre- and postinjury PTSD soon after injury and reassessed at 6 and 12 months, 2, 3, and 4 years postinjury. Over the first four years postinjury 17.6% developed injury-related PTSD, none of whom had PTSD prior to injury. PTSD onset peaked between 6- and 12-months postinjury. The majority of PTSD cases (66.7%) had a delayed-onset, which for a third was preceded by subsyndromal symptoms in the first six months postinjury. PTSD frequency increased over the first year postinjury, remained stable during the second year and gradually declined thereafter. The majority with PTSD experienced a chronic symptom course and all developed one or more comorbid psychiatric disorder, with mood, other anxiety and substance-use disorders being the most common. Despite event-related amnesia, posttraumatic stress symptoms, including vivid re-experiencing phenomena, may develop following moderate to severe TBI. Onset is typically delayed and symptoms may persist for several years postinjury.
Severe traumatic brain injury (TBI) is one of the most complex and diverse pathologic medical conditions. Each year, approximately 100,000 patients require neurosurgical evacuation of an intracranial hematoma in the United States. It is essential, early in the clinical course, to distinguish those patients with severe TBI who require operative intervention from those who can be managed with only conservative measures. The surgical technique employed is determined primarily by the specific underlying pathology in conjunction with the patient's other comorbidities.
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Psychiatric disorders are common following traumatic brain injury (TBI) and can include depression, anxiety, and psychosis, as well as other maladaptive behaviors and personality changes. The epidemiologic data of psychiatric disorders post-TBI vary widely, although the incidence and prevalence rates typically are higher than in the general population. While the experience of psychiatric symptoms may be temporary and resolve in the acute period, many patients with TBI can experience psychopathology that is persistent or develop in the post-acute period. Long-term psychiatric disorder, along with cognitive and physical sequelae and greater risk for substance use disorders, can pose a number of life-long challenges for patients and their caregivers, as they can interfere with participation in rehabilitation as well as limit functional independence in the community. The current review of the literature will consider the common psychiatric problems afflicting individuals with TBI in the post-acute period including personality changes, psychosis, executive dysfunction, depression, anxiety, and substance misuse. While treatment considerations (pharmacological and non-pharmacological) will be referred to an extensive description of such protocols is beyond the scope of the current review. The impact of persistent psychiatric symptoms on perceived caregiver burden and distress will also be discussed.
The development of anxiety disorders following a traumatic brain injury is a strong predictor of social, personal, and work dysfunction; nevertheless, the emergence of anxiety has been largely unexplored and poorly understood in the context of TBI. This paper provides an overview of the limited published research to date on anxiety disorders that are known to develop following TBI, including post-traumatic stress disorder, generalized anxiety disorder, obsessive-compulsive disorder, panic disorder, specific phobia, and social anxiety disorder. This review also examines diagnostic criteria, the epidemiology of each disorder, and the factors that influence the expression of these conditions, including injury-related and psychosocial variables. Putative neural correlates will be reviewed where known. A discussion of current treatment options and avenues for further research are explored.
Traumatic brain injury (TBI) is a major health and socioeconomic problem that affects all societies. In recent years, patterns of injury have been changing, with more injuries, particularly contusions, occurring in older patients. Blast injuries have been identified as a novel entity with specific characteristics. Traditional approaches to the classification of clinical severity are the subject of debate owing to the widespread policy of early sedation and ventilation in more severely injured patients, and are being supplemented with structural and functional neuroimaging. Basic science research has greatly advanced our knowledge of the mechanisms involved in secondary damage, creating opportunities for medical intervention and targeted therapies; however, translating this research into patient benefit remains a challenge. Clinical management has become much more structured and evidence based since the publication of guidelines covering many aspects of care. In this Review, we summarise new developments and current knowledge and controversies, focusing on moderate and severe TBI in adults. Suggestions are provided for the way forward, with an emphasis on epidemiological monitoring, trauma organisation, and approaches to management.
To retrospectively establish the nature and frequency of Axis I psychiatric disorders pre- and post-TBI.
One hundred participants who were 0.5 to 5.5 years post mild to severe TBI and 87 informants, each evaluated at a single time point.
The Structured Clinical Interview for DSM-IV Disorders (SCID-I).
Preinjury, 52% received a psychiatric diagnosis, most commonly substance use disorder (41%), followed by major depressive disorder (17%) and anxiety (13%). Postinjury, 65% received a diagnosis, of which major depression became the most common (45%), followed by anxiety (38%) and substance use disorder (21%). Frequency of depression, generalized anxiety disorder, posttraumatic stress disorder, panic disorder, and phobias rose from preinjury to postinjury. More than two-thirds of postinjury depression and anxiety cases were novel and showed poor resolution rates. Few novel cases of substance use disorder were noted. Psychotic disorders, somatoform disorders, and eating disorders occurred at frequencies similar to those in the general population.
A high frequency of postinjury psychiatric disorders was evident up to 5.5 years postinjury, with many novel cases of depression and anxiety. Individuals with TBI should be screened for psychiatric disorders at various time points post-injury without reliance on history of psychiatric problems to predict who is at risk, so that appropriate intervention can be offered.
Traumatic brain injury (TBI) is a significant public health concern. According to the Centers for Disease Control and Prevention, about 1.4 million people in the United States sustain a TBI annually.
This review places particular emphasis on the current knowledge of effective treatment of TBI symptoms, and proposes directions for future research.
Neuropsychiatric problems are more prevalent and longer-lasting in TBI patients than in the general population. About 40% of TBI victims suffer from two or more psychiatric disorders, and a similar percentage experience at least one unmet need for cognitive, emotional, or job assistance 1 year after injury. The entire spectrum of TBI severity, from mild to severe, is associated with an increase in psychiatric conditions.
Despite the high incidence of severe consequences of TBI, there are scarce empirical data to guide psychiatric treatment. Some approaches that have been helpful include cognitive and behavioral therapy and pharmacologic treatment. The authors list specific research recommendations that could further identify useful therapeutic interventions.
We collected data on all residents of San Diego County, California who were hospitalized for or died from a brain injury in 1981. The objectives were to assess the frequency of blood alcohol concentration (BAC) testing and the associations of BAC prevalence with the external cause of the brain injury and case outcome. We found that high BAC levels were most frequent among brain-injured subjects between the ages of 25 and 44 and among those subjects involved in motor vehicle crashes and assaults. Contrary to expectations, injury severity and hospital mortality were inversely related to BAC level, controlling for other predictors. We believe that these inverse associations might be due to differential rates of BAC testing by severity. Among brain-injured survivors with more severe injuries, however, we found that BAC level was positively associated with the prevalence of physician-diagnosed neurological impairment at discharge and with the length of hospitalization.
The authors present psychiatric and neurologic data on 20 patients who developed mania after closed head trauma. An association was seen between severity of head trauma (based on length of posttraumatic amnesia), posttraumatic seizure disorder, and type of bipolar disorder. The manic episodes were characterized by irritable mood rather than euphoria and by assaultiveness. Psychosis occurred in only 15% of the sample, and 70% had no depressive episodes. Bipolar disorders were absent among 85 first-degree relatives. The authors suggest that posttraumatic seizures may be a predisposing factor in posttraumatic mania.
Two cases of mania secondary to head injury are reported. Only four well-documented reports of head trauma as a cause of secondary mania were found in an English and foreign literature search, although such a search is made difficult by the paucity of cases meeting modern diagnostic criteria for mania. Previous reviews of the causes of secondary mania have not included head injury, but the two case reports confirm that head injury may be an additional cause. A diagnosis of mania secondary to head trauma should be considered in manic patients with atypical age of onset, absence of previous psychiatric illness, negative family history for bipolar illness, and close temporal proximity of head trauma to subsequent mania.
Substantial psychological and neurobehavioural evidence is available to support the hypothesis that traumatic brain injury (TBI) is a risk factor for subsequent psychiatric disorders. However, studies utilizing established psychiatric diagnostic schemes to study these outcomes after TBI are scarce, and no studies have included an assessment of personality disorders in addition to the major psychiatric disorders. This study utilizes structured psychiatric interviews to measure the prevalence of DSM-III(R) disorders in a sample of 18 subjects derived from a TBI rehabilitation programme. Results revealed high rates for major depression, bipolar affective disorder, generalized anxiety disorder, borderline and avoidant personality disorders. Co-morbidity was also high. A preliminary study of postulated predictive factors revealed possible roles for sex and for initial severity of injury. The study supports the association between TBI and psychiatric disorder, and suggests the need for monitoring, for prevention, and for treatment of psychiatric disorders after TBI.
To assess the ability of acute stress disorder to predict posttraumatic stress disorder (PTSD), the relationship between acute stress disorder and PTSD over the 2 years following mild traumatic brain injury was determined.
Survivors of motor vehicle accidents who sustained mild traumatic brain injuries were assessed for acute stress disorder within 1 month of the trauma (N=79) and for PTSD at 6 months (N=63) and 2 years (N=50) posttrauma.
Acute stress disorder was diagnosed in 14% of the patients. Among the patients who participated in all three assessments, 80% of the subjects who met the criteria for acute stress disorder were diagnosed with PTSD at 2 years. Of the total initial group, 73% of those diagnosed with acute stress disorder had PTSD at 2 years.
This study provides further support for the utility of the acute stress disorder diagnosis as a predictor of PTSD but indicates that the predictive power of the diagnostic criteria can be increased by placing greater emphasis on reexperiencing, avoidance, and arousal symptoms.
Traumatic brain injury (TBI) may cause psychiatric illness. This article reviews the evidence on the basis of an established set of causation criteria. The evidence is convincing for a strong association between TBI and mood and anxiety disorders. Substance abuse and schizophrenia are not strongly associated with TBI, and there is little research into the rates of personality disorders after TBI. Evidence for a biologic gradient is lacking, but such a gradient may not be relevant to TBI. Evidence for the correct temporal sequence is present. Preliminary evidence suggests a biologic rationale for TBI causing psychiatric illness. Further and methodologically improved research is supported and required.
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.
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.
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.
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.
The authors analyzed data from 69 published case studies of Psychotic Disorder Due to Traumatic Brain Injury (PDTBI) in order to describe its common characteristics and assist in its diagnosis and differentiation from schizophrenia. The majority of these PDTBI patients were males with onset of symptoms occurring within the first 2 years after moderate to severe head injury. A majority showed abnormalities on MRI/CT and EEG with localization in the frontal and temporal areas. The general presentation included delusions and hallucinations without co-occurring negative symptoms. The findings demonstrate that patients with PDTBI have a profile that distinguishes itself from schizophrenia.
To characterize outcomes after traumatic brain injury (TBI) resulting from vehicular crashes, violence, falls, or other causes.
Prospective, multicenter, longitudinal.
Seventeen Traumatic Brain Injury Model Systems.
A total of 1,170 individuals with moderate to severe TBI with data from initial medical and rehabilitation stays and 1-year follow-up.
Not applicable.
At rehabilitation discharge, FIM instrument, Disability Rating Scale (DRS), and Rancho Los Amigo Levels of Cognitive Functioning Scale. At 1 year postinjury, FIM, DRS, Community Integration Questionnaire (CIQ), employment, residence, marital status, and seizure occurrence.
The 4 etiology groups could be distinguished based on premorbid characteristics. Severity of injury indices indicated that individuals in vehicular crashes showed a trend toward incurring more severe injuries than the other 3 groups. At rehabilitation discharge, there were no functional differences between groups. At 1 year postinjury, the groups could be differentiated: individuals in violence-related TBI had higher unemployment rates and lower CIQ scores; persons in vehicular crashes reported the best functional and psychosocial outcomes; and individuals in the falls and other groups had outcomes lying between the vehicular and violence groups.
This study elucidated important differences between persons with violence-related TBI and those with non-violence-related TBI. Further research is needed to find effective interventions to address these differences.
To identify the frequency and manifestations of depression after traumatic brain injury (TBI) and the factors that contribute to developing this mood disorder.
A prospective, nationwide, multicenter study; 17 centers supplied data from medical records and patient responses on a standardized criterion instrument.
Traumatic Brain Injury Model Systems programs.
A demographically diverse sample of 666 outpatients with TBI was evaluated 10 to 126 months after injury.
Not applicable.
Depressive symptoms were characterized with the Neurobehavioral Functioning Inventory by using the Diagnostic and Statistical Manual of Mental Disorders (4th ed; DSM-IV) diagnostic framework. Analysis of variance and Pearson correlations were used to identify factors that were significantly related to depression.
Fatigue (29%), distractibility (28%), anger or irritability (28%), and rumination (25%) were the most commonly cited depressive symptoms in the sample. Twenty-seven percent of patients with TBI met the prerequisite number (>/=5) of criterion A symptoms for a DSM-IV diagnosis of major depressive disorder. Feeling hopeless, feeling worthless, and difficulty enjoying activities were the 3 symptoms that most differentiated depressed from nondepressed patients. Patients who were unemployed at the time of injury and who were impoverished were significantly more likely to report DSM-IV criterion A symptoms than patients who were employed, were students, or were retired due to age. Time after injury, injury severity, and postinjury marital status were not significantly related to depression.
Patients with TBI are at great risk for developing depressive symptoms. Findings provide empirical support for the inclusion of depression evaluation and treatment protocols in brain injury programs. Unemployment and poverty may be substantial risk factors for the development of depressive symptoms. Future research should develop biopsychosocial predictive models to identify high-risk patients and examine the efficacy of treatment interventions.
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.
Case reports have associated head injury with psychoses including affective disorders, but little is known regarding head injury as a risk factor for the onset of bipolar affective disorder.
The Danish Psychiatric Case Register and the Danish National Patients Register were linked together with the Danish Population Register, thus identifying 10,242 patients with bipolar affective disorder, and 102,420 matched controls. History regarding head injury was recorded from the National Patients Register data. Data were analysed using conditional logistic regression.
Bipolar affective disorder was associated with an increased risk of a history of head injury (IRR=1.55; 95% CI 1.36-1.77). The increased risk was confined to head injury occurring less than 5 years before the first psychiatric admission. The finding could not be ascribed to increased accident proneness (as evaluated through the occurrence of other fractures not involving the skull).
In studies based on clinical diagnoses only and limited to patients who were hospitalised for psychiatric disorder, exposure was limited to injuries leading to admission to hospital.
Head injury may be a contributing factor to the onset of bipolar affective illness. However, this factor is probably only relevant to a relatively small minority of cases.
Major depression is a frequent psychiatric complication among patients with traumatic brain injury (TBI). To our knowledge, however, the clinical correlates of major depression have not been extensively studied.
To determine the clinical, neuropsychological, and structural neuroimaging correlates of major depression occurring after TBI.
Prospective, case-controlled, surveillance study conducted during the first year after the traumatic episode occurred. Settings University hospital level I trauma center and a specialized rehabilitation unit.
The study group consisted of 91 patients with TBI. In addition, 27 patients with multiple traumas but without evidence of central nervous system injury constituted the control group. The patients' conditions were evaluated at baseline and at 3, 6, and 12 months after the traumatic episode. Psychiatric diagnosis was made using a structured clinical interview and DSM-IV criteria. Neuropsychological testing and quantitative magnetic resonance imaging were performed at the 3-month follow-up visit.
Major depressive disorder was observed in 30 (33%) of 91 patients during the first year after sustaining a TBI. Major depressive disorder was significantly more frequent among patients with TBI than among the controls. Patients with TBI who had major depression were more likely to have a personal history of mood and anxiety disorders than patients who did not have major depression. Patients with major depression exhibited comorbid anxiety (76.7%) and aggressive behavior (56.7%). Patients with major depression had significantly greater impairment in executive functions than their nondepressed counterparts. Major depression was also associated with poorer social functioning at the 6-and 12-month follow-up, as well as significantly reduced left prefrontal gray matter volumes, particularly in the ventrolateral and dorsolateral regions.
Major depression is a frequent complication of TBI that hinders a patient's recovery. It is associated with executive dysfunction, negative affect, and prominent anxiety symptoms. The neuropathological changes produced by TBI may lead to deactivation of lateral and dorsal prefrontal cortices and increased activation of ventral limbic and paralimbic structures including the amygdala.
Psychosis is a relatively infrequent but potentially serious and debilitating consequence of traumatic brain injury (TBI), and one about which there is considerable scientific uncertainty and disagreement. There are several substantial clinical, epidemiological, and neurobiological differences between the post-traumatic psychoses and the primary psychotic disorders. The recognition of these differences may facilitate identification and treatment of patients whose psychosis is most appropriately regarded as post-traumatic. In the service of assisting psychiatrists and other mental health clinicians in the diagnosis and treatment of persons with post-traumatic psychoses, this article will review post-traumatic psychosis, including definitions relevant to describing the clinical syndrome, as well as epidemiologic, neurobiological, and neurogenetic factors attendant to it. An approach to evaluation and treatment will then be offered, emphasizing identification of the syndrome of post-traumatic psychosis, consideration of the differential diagnosis of this condition, and careful selection and administration of treatment interventions.
This study indexed the relationship between resting heart rates (HRs) after injury and subsequent posttraumatic stress disorder (PTSD) in patients who sustained severe traumatic brain injury (TBI).
Patients who sustained a severe TBI (N = 68) had their resting HR assessed 1 week and 1 month after injury, and they were assessed for PTSD 6 months after injury with the PTSD Interview, a structured clinical interview based on the criteria of the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revised.
PTSD was diagnosed in 23% of patients. PTSD participants had higher HRs at 1 week but not at 1 month after trauma than non-PTSD participants. This difference remained significant when the effect of posttraumatic amnesia was controlled, but it was not significant when the effect of Glasgow Coma Scale was controlled.
These findings accord with the proposal that fear conditioning can occur outside the level of awareness and contribute to PTSD development.
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 Reckurn et al,(4) and Fujii and Ahmed(5) 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, sonic 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.
Depression is a common consequence of traumatic brain injury (TBI), and is a source of substantial distress and disability for persons with TBI and their families. This article offers a practical approach to the evaluation and treatment of this condition. Diagnostic and etiologic considerations relevant to this issue are reviewed first. Next, somatic therapies for posttraumatic depression, including antidepressant medications and electroconvulsive therapy, are discussed. Use of these therapies is also considered in the context of the common medical and neurological comorbidities among persons with TBI. Finally, psychosocial interventions relevant to the care of persons with posttraumatic depression are presented.
Posttraumatic stress disorder (PSTD), classified as an anxiety disorder, has become increasingly important because of wars overseas, natural disasters, and domestic violence. After trauma exposes the victim to actual or threatened death or serious injury, 3 dimensions of PTSD unfold: (1) reexperiencing the event with distressing recollections, dreams, flashbacks, and/or psychologic and physical distress; (2) persistent avoidance of stimuli that might invite memories or experiences of the trauma; and (3) increased arousal. Traumatic events sufficient to produce PTSD in susceptible subjects may reach a lifetime prevalence of 50% to 90%. The actual lifetime prevalence of PTSD among US citizens is approximately 8%, with the clinical course driven by pathophysiologic changes in the amygdala and hippocampus. Comorbid depression and other anxiety disorders are common. General principles of treatment include the immediate management of PTSD symptoms and signs; management of any trauma-related comorbid conditions; nonpharmacologic interventions including cognitive behavioral treatment; and psychopharmacologic agents including antidepressants (selective serotonin reuptake inhibitors most commonly), antianxiety medications, mood stabilizing drugs, and antipsychotics. This review of PTSD will provide the reader with a clearer understanding of this condition, an increased capacity to recognize and treat this syndrome, and a greater appreciation for the role of the internist in PTSD.