Bipolar Disord. 2008 Feb;10(1):111-3. Homicidal ideation with intent during a manic episode triggered by antidepressant medication in a man with brain injury. Dealberto MJ, Marino J, Bourgon L. Department of Psychiatry, Ottawa Hospital, Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, Ontario, Canada. firstname.lastname@example.org BACKGROUND: Mood disorders are more frequent after brain injury and both depressive and manic episodes are associated in these patients with an increased risk of aggression. Antidepressant medications are associated with a risk of manic induction. CASE REPORT: We describe a case of homicidal ideation with intent during the onset of a manic episode in a patient with prior brain injury on antidepressant medication at low dosage. The manic episode could have been secondary to brain injury and/or triggered by antidepressant medications. This case raises the possibility of the sensitizing role of brain injury for antidepressant-induced mania. CONCLUSIONS: Further studies are needed to assess the role of brain injury as a risk factor for antidepressant-induced mania. Physicians should be cautious when prescribing antidepressants to patients with prior brain injury and inform them and their relatives of the possibility of a switch into mania. CNS Spectr. 2007 Oct;12(10):764-9. Quetiapine for mania due to traumatic brain injury. Oster TJ, Anderson CA, Filley CM, Wortzel HS, Arciniegas DB. Brain Injury Rehabilitation Unit, HealthONE Spalding Rehabilitation Hospital, Aurora, CO, USA. Secondary mania develops in as many as 9% of persons with traumatic brain injuries. The treatment of posttraumatic mania is not well defined, and agents traditionally used for the treatment of idiopathic manic episodes may not be well suited for use among individuals with traumatic brain injuries. Atypical antipsychotics are indicated for the treatment of idiopathic bipolar disorder, and have been used for other purposes among individuals with posttraumatic neuropsychiatric disturbances. This article offers the first description of the treatment of posttraumatic mania using the atypical antipsychotic quetiapine. Beneficial effects of this agent on posttraumatic mania, cognitive impairments, and functional disability in the subacute post-injury period are described. Possible mechanisms of action are discussed and the need for additional investigation of quetiapine for posttraumatic mania is highlighted. Psychosomatics. 2007 Sep-Oct;48(5):433-5. Manic behavior resulting from left frontal closed head injury in an adult with fetal alcohol syndrome. Camden JR, Spiegel DR. Eastern Virginia Medical School Department of Psychiatry and Behavioral Sciences, 825 Fairfax Ave., Norfolk, VA 23507, USA. Closed head trauma has been associated with various neuropsychiatric sequelae, including mood disturbances such as depression and mania. Although mood disturbances can occur with injury to either hemisphere, mania has been primarily associated with right-side frontal lobe injury. We present a case of manic behavior after a closed head injury to the left hemisphere in an adult with preexisting fetal alcohol syndrome. J Neuropsychiatry Clin Neurosci. 2007 Spring;19(2):106-27. Neuropsychiatric complications of traumatic brain injury: a critical review of the literature (a report by the ANPA Committee on Research). Kim E, Lauterbach EC, Reeve A, Arciniegas DB, Coburn KL, Mendez MF, Rummans TA, Coffey EC; ANPA Committee on Research. Bristol-Myers Squibb Company, Neuroscience Medical Strategy, 777 Scudders Mill Road, Plainsboro, NJ 08536, USA. email@example.com Psychiatric disorders frequently complicate recovery and rehabilitation from traumatic brain injury (TBI). This study reviews the literature from 1978 to 2006 on psychosis, depression, posttraumatic stress disorder, mania, and aggression following nonpenetrating TBI. The studies were reviewed using the American Academy of Neurology's criteria for classification of articles on diagnostic methods. No studies were found to be Class I or II. Of the 66 studies reviewed, the majority were Class IV. There are significant gaps in the literature on post-TBI psychiatric conditions with respect to nosology, epidemiology, and risk factors. Larger multicenter prospective studies using standardized diagnostic instruments are needed to further clarify the nosology, risk factors, and clinical course of these disorders. Specific directions for research are provided. Prog Neuropsychopharmacol Biol Psychiatry. 2007 Mar 30;31(2):551-6. Epub 2006 Nov 14. Late onset bipolar disorder associated with white matter hyperintensities: a pathophysiological hypothesis. Zanetti MV, Cordeiro Q, Busatto GF. Laboratory of Psychiatric Neuroimaging (LIM 21), Institute and Department of Psychiatry, University of São Paulo, Brazil. firstname.lastname@example.org Vascular depression is, nowadays, a well-established concept in the literature. However, the possible emergence of late onset bipolar disorder in subjects with no antecedents of mood disorder or after a chronic or recurrent course of unipolar depression constitutes a poorly studied issue, despite its importance in clinical practice. Here, we present the case of a 72-year-old female patient who began to present recurrent major depressive symptoms, resistant to pharmacological treatment, from the age of 58. Three years later, she started to present phases of mania with rapid cycling features. A brain MRI scan showed prominent white matter hyperintensities (WMH). WMH are frequently found in the elderly population, but with greater burden in individuals with hypertension and cerebrovascular disease. WMH impair cortical function and damage the cerebral tissue. WMH have been associated with adult-onset bipolar disorder and late onset depression, and are linked to a worse prognosis of both conditions. The present case report highlights the possibility that vascular-related WMH may provoke late onset bipolar disorder by damaging frontolimbic circuits implicated in the pathophysiology of mania. J Neurotrauma. 2006 Oct;23(10):1468-501. Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. Neurobehavioral Guidelines Working Group, Warden DL, Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, Drake A, Gentry T, Jagoda A, Katz DI, Kraus J, Labbate LA, Ryan LM, Sparling MB, Walters B, Whyte J, Zapata A, Zitnay G. Defense and Veterans Brain Injury Center, Department of Neurology and Neurosurgery, Walter Reed Army Medical Center, USA. 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. J Pharmacol Sci. 2005 Dec;99(4):307-21. Epub 2005 Dec 7. Lithium: potential therapeutics against acute brain injuries and chronic neurodegenerative diseases. Wada A, Yokoo H, Yanagita T, Kobayashi H. Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan. email@example.com In addition to the well-documented mood-stabilizing effects of lithium in manic-depressive illness patients, recent in vitro and in vivo studies in rodents and humans have increasingly implicated that lithium can be used in the treatment of acute brain injuries (e.g., ischemia) and chronic neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, tauopathies, and Huntington's disease). Consistent with this novel view, substantial evidences suggest that depressive illness is not a mere neurochemical disease, but is linked to gray matter atrophy due to the reduced number/size of neurons and glia in brain. Importantly, neurogenesis, that is, birth/maturation of functional new neurons, continues to occur throughout the lifetime in human adult brains (e.g., hippocampus); the neurogenesis is impaired by multiple not-fully defined factors (e.g., aging, chronic stress-induced increase of glucocorticoids, and excitotoxicity), accounting for brain atrophy in patients with depressive illness and neurodegenerative diseases. Chronic treatment of lithium, in agreement with the delayed-onset of mood-stabilizing effects of lithium, up-regulates cell survival molecules (e.g., Bcl-2, cyclic AMP-responsive element binding protein, brain-derived neurotrophic factor, Grp78, Hsp70, and beta-catenin), while down-regulating pro-apoptotic activities (e.g., excitotoxicity, p53, Bax, caspase, cytochrome c release, beta-amyloid peptide production, and tau hyperphosphorylation), thus preventing or even reversing neuronal cell death and neurogenesis retardation. Clin Sports Med. 2005 Jul;24(3):663-79, x. Psychiatric and neuropsychological issues in sport medicine. Broshek DK, Freeman JR. Division of Neuropsychology, Department of Psychiatric Medicine, University of Virginia School of Medicine, Box 800203, Charlottesville, VA 22908, USA. firstname.lastname@example.org This article reviews what is known about training room psychiatric/psychological issues and how to recognize them, and provides an initial framework for how to manage them. There is some focus on psychiatric issues involved in collegiate sports medicine environments, because the majority of research on this topic has been done with this population, but it is believed that this information generalizes to other athletic settings. Greater awareness of these problems, empirical research, and education about mental health issues in the sports medicine community is clearly needed. J Nerv Ment Dis. 2004 Jun;192(6):430-4. Suicidal behavior and mild traumatic brain injury in major depression. Oquendo MA, Friedman JH, Grunebaum MF, Burke A, Silver JM, Mann JJ. Department of Neuroscience, New York State Psychiatric Institute, Columbia University, New York, NY 10032, USA. Traumatic brain injury (TBI) is associated with psychiatric illness, suicidal ideation, suicide attempts, and completed suicide. We investigated the relationship between mild TBI and other risk factors for suicidal behavior in major depressive episode. We hypothesized that mild TBI would be associated with suicidal behavior at least partly because of shared risk factors that contribute to the diathesis for suicidal acts. Depressed patients (N = 325) presenting for treatment were evaluated for psychopathology, traumatic history, and suicidal behavior. Data were analyzed using Student t -test, chi-square statistic, or Fisher exact test. A backward stepwise logistic regression model (N = 255) examined the relationship between attempter status and variables that differed in the TBI and non-TBI patients. Forty-four percent of all subjects reported mild TBI. Subjects with TBI were more likely to be male, have a history of substance abuse, have cluster B personality disorder, and be more aggressive and hostile compared with subjects without TBI. They were also more likely to be suicide attempters, although their suicidal behavior was not different from that of suicide attempters without TBI. Attempt status was mostly predicted by aggression and hostility, but not the presence of TBI. Of note, for males, a history of TBI increased the likelihood of being a suicide attempter, whereas the risk was elevated for females regardless of TBI history. Our data suggest that suicidal behavior and TBI share antecedent risk factors: hostility and aggression. Future studies may yield confirmation using a prospective design. Int Rev Psychiatry. 2003 Nov;15(4):317-27. Mood disorders following traumatic brain injury. Jorge R, Robinson RG. Department of Psychiatry, University of Iowa College of Medicine, Iowa City, IA 52242, USA. Ricardoemail@example.com Mood disorders are a frequent complication of traumatic brain injury that exerts a deleterious effect on the recovery process and psychosocial outcome of brain injured patients. Prior psychiatric history and impaired social support have been consistently reported as risk factors for developing mood disorders after traumatic brain injury (TBI). In addition, biological factors such as the involvement of the prefrontal cortex and probably other limbic and paralimbic structures may play a significant role in the complex pathophysiology of these disorders. Preliminary studies have suggested that selective serotonin reuptake inhibitors such as sertraline, mood stabilizers such as sodium valproate, as well as stimulants and ECT may be useful in treating these disorders. Mood disorders occurring after TBI are clearly an area of neuropsychiatry in which further research in etiology as well as treatment is needed. J Affect Disord. 2003 Sep;76(1-3):79-83. Head injury as a risk factor for bipolar affective disorder. Mortensen PB, Mors O, Frydenberg M, Ewald H. National Centre for Register-based Research, Aarhus University, Taasingegade 1 DK-8000 Aarhus C, Denmark. firstname.lastname@example.org BACKGROUND: 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. METHODS: 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. RESULTS: 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). LIMITATIONS: 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. CONCLUSIONS: 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. Brain Inj. 2003 Apr;17(4):355-8. Rapid cycling bipolar disorder after left temporal polar damage. Murai T, Fujimoto S. Department of Psychiatry, Faculty of Medicine, Kyoto University, Kyoto, Japan. email@example.com The case of a 48-year-old woman with rapid cycling bipolar disorder subsequent to a traumatic brain injury is reported. Both depressive and manic episodes had an average duration of approximately 1 month, alternating without stable euthymic periods. Neuroradiological examinations revealed a circumscribed lesion in the left temporal pole. After 1 year without treatment, psychiatric intervention and pharmacotherapy was initiated. Her mood swings were successfully treated with the co-administration of valproate and lithium. Case reports of rapid cycling bipolar disorder after traumatic brain injury are very rare and this case supports the idea that temporal polar dysfunction is a candidate for the neurobiological basis of rapid cycling bipolar disorder. J Neuropsychiatry Clin Neurosci. 2002 Spring;14(2):202-5. Divalproex in the management of neuropsychiatric complications of remote acquired brain injury. Kim E, Humaran TJ. Department of Psychiatry, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, 671 Hoes Lane, Piscataway, NJ 08855-1392, USA. firstname.lastname@example.org A retrospective chart review was conducted on 11 patients with a remote history of acquired brain injury (ABI) referred for psychiatric treatment who were treated with divalproex sodium alone or in combination with other psychotropic medications. The patients were highly heterogeneous. They had a variety of psychiatric symptoms and frequently received concomitant psychotropic medications. The mean daily dose of divalproex was 1,818+/-791 mg/day, serum valproic acid level 85.6+/-29.6 microg/ml. Mean Clinical Global Impression improvement score was 1.9+/-0.5. This is the largest postacute case series reported. It demonstrates that divalproex sodium is well tolerated and effective in reducing a broad range of neurobehavioral symptoms in psychiatric patients with a remote history of ABI. Hypomania induced by herbal and pharmaceutical psychotropic medicines following mild traumatic brain injury. Spinella M, Eaton LA. Division of Social and Behavioral Sciences, Richard Stockton College of New Jersey, Pomona 08240-0195, USA. email@example.com The use of herbal medicines has become a very common practice. While many are safe enough to be available over-the-counter, they may pose risks due to interactions with pharmaceutical medications and effects in specific clinical populations. The case of a female patient with a history of mild traumatic brain injury and resulting depression is presented. She experienced hypomania after adding St John's wort and Ginkgo biloba to her regimen of fluoxetine and buspirone, which remitted after discontinuation of the herbal medicines. Implications for interactions between various psychopharmacologic agents, including herbal medicines and selective serotonin reuptake inhibitors (SSRIs), as well as the need for appropriate patient and health care provider education are discussed. Am J Psychiatry 2001 Mar;158(3):440-6 Traumatic brain injury and schizophrenia in members of schizophrenia and bipolar disorder pedigrees. Malaspina D, Goetz RR, Friedman JH, Kaufmann CA, Faraone SV, Tsuang M, Cloninger CR, Nurnberger JI Jr, Blehar MC. New York State Psychiatric Institute, Columbia University, New York 10032, USA. firstname.lastname@example.org 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 with no mental illness. However, multivariate analysis of within-pedigree data showed that mental illness was related to traumatic brain injury only in the schizophrenia pedigrees. Independent of diagnoses, family members of those with schizophrenia were more likely to have had traumatic brain injury than were members of the bipolar disorder pedigrees. The members of the schizophrenia pedigrees also failed to show the gender difference for traumatic brain injury (more common in men than in women) that was expected and was present in the bipolar disorder pedigrees. Subjects with a schizophrenia diagnosis who were members of the bipolar disorder pedigrees (and thus had less genetic vulnerability to schizophrenia) were less likely to have had traumatic brain injury (4.5%) than were subjects with schizophrenia who were members of the schizophrenia pedigrees (and who had greater genetic vulnerability to schizophrenia) (19.6%). CONCLUSIONS: Members of the schizophrenia pedigrees, even those without a schizophrenia diagnosis, had greater exposure to traumatic brain injury compared to members of the bipolar disorder pedigrees. Within the schizophrenia pedigrees, traumatic brain injury was associated with a greater risk of schizophrenia, consistent with synergistic effects between genetic vulnerability for schizophrenia and traumatic brain injury. Posttraumatic-brain-injury schizophrenia in multiplex schizophrenia pedigrees does not appear to be a phenocopy of the genetic disorder. J Am Acad Child Adolesc Psychiatry 2000 Apr;39(4):525-8 Case study: bipolar disorder after head injury. Sayal K, Ford T, Pipe R. Bethlem Hospital, London, England. email@example.com A case of bipolar disorder subsequent to a mild head injury in a 15-year-old girl is reported. Review of the literature indicates that this is an extremely rare outcome. Lack of adequate follow-up studies makes it difficult to accurately predict type and severity of psychiatric outcome. Assessment and management involves ongoing consideration of both organic and psychosocial factors even after initial negative investigations. Psychiatry Res 1999 Dec 27;89(3):281-6 Traumatic brain injury in individuals convicted of sexual offenses with and without bipolar disorder. DelBello MP, Soutullo CA, Zimmerman ME, Sax KW, Williams JR, McElroy SL, Strakowski SM. Department of Psychiatry, University of Cincinnati College of Medicine, OH 45267-0559, USA. firstname.lastname@example.org The authors examined the occurrence of traumatic brain injury (TBI) in individuals convicted of sexual offenses with and without bipolar disorder and a comparison group of patients with bipolar disorder without a history of sexual offending behaviors. Individuals convicted of sexual offenses and diagnosed with bipolar disorder had greater rates of brain injury resulting from head trauma than individuals convicted of sexual offenses without bipolar disorder and comparison patients with bipolar disorder. TBI predated the first sexual offense and/or the onset of bipolar disorder in most subjects. J Head Trauma Rehabil 1998 Aug;13(4):24-39 Axis I psychopathology in individuals with traumatic brain injury. Hibbard MR, Uysal S, Kepler K, Bogdany J, Silver J. Department of Rehabilitation Medicine, The Mount Sinai Medical Center, New York, New York 10029, USA. OBJECTIVES: To assess the incidence, comorbidity, and patterns of resolution of DSM-IV mood, anxiety, and substance use disorders in individuals with traumatic brain injury (TBI). DESIGN: The Structured Clinical Interview for DSM-IV Diagnoses (SCID) was utilized. Diagnoses were determined for three onset points relative to TBI onset: pre-TBI, post-TBI, and current diagnosis. Contrasts of prevalence rates with community-based samples, as well as chi-square analysis and analysis of variance were used. Demographics considered in analyses included gender, marital status, severity of injury, and years since TBI onset. SETTING: Urban, suburban, and rural New York state. PARTICIPANTS: 100 adults with TBI who were between the ages of 18 and 65 years and who were, on average, 8 years post onset at time of interview. MAIN OUTCOME MEASURES: SCID Axis I mood diagnoses of major depression, dysthymia, and bipolar disorder; anxiety diagnoses of panic disorder, obsessive-compulsive disorder (OCD), posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), and phobia; and substance use disorders. RESULTS: Prior to TBI, a significant percentage of individuals presented with substance use disorders. After TBI, the most frequent Axis I diagnoses were major depression and select anxiety disorders (ie, PTSD, OCD, and panic disorder). Comorbidity was high, with 44% of individuals presenting with two or more Axis I diagnoses post TBI. Individuals without a pre-TBI Axis I disorder were more likely to develop post-TBI major depression and substance use disorders. Rates of resolution were similar for individuals regardless of previous psychiatric histories. Major depression and substance use disorders were more likely than were anxiety disorders to remit. CONCLUSION: TBI is a risk factor for subsequent psychiatric disabilities. The need for proactive psychiatric assessment and timely interventions in individuals post TBI is indicated. Med Pregl 1997 Sep-Oct;50(9-10):391-3 [A manic syndrome after cerebral trauma: case report] [Article in Serbo-Croatian (Roman)] Mitrovic D, Misic-Pavkov G, Ivanovic S, Dickov A. Institut za neurologiju, psihijatriju i mentalno zdravlje, Medicinski fakultet, Novi Sad. This case report describes a 17-year-old female patient in whom a clinical picture of manic syndrome developed four days after craniocerebral trauma. The diagnostic procedure comprised neuropsychological, neurophysiological and neuroanatomical examination. The diagnosis revealed discrete organicity on the level of psychic functions, whereas magnetic resonance imaging revealed changes of the right hemisphere. One case cannot reveal the etiology of affective disorders after cerebral injuries, but gathered results point to the possibility of causal connection between craniocerebral trauma and manic syndrome. Singapore Med J 1996 Aug;37(4):448-50 Mania following left hemisphere injury. Lim LC. Department of Psychological Medicine National University Hospital, Singapore. A case of mania following closed head injury to the left hemisphere is reported. The patient presented with a self-limiting manic episode that recovered without treatment. It is postulated that the head injury is the causative factor in this case. This was supported by laboratory results as well as psychological investigations. It is believed that non-dominant right hemisphere injury is related to the development of mania. However, a search of the literature revealed five other cases of mania following left hemispheric injury. Although the mechanisms implicated in the pathogenesis of secondary mania have not been established, this case adds to the growing evidence that head injury may be directly causative in affective psychoses. Therefore, it is premature to conclude that mania is a pathology of the non-dominant right hemisphere. Brain Inj 1996 May;10(5):319-27 Psychiatric disorders after traumatic brain injury. van Reekum R, Bolago I, Finlayson MA, Garner S, Links PS. Department of Psychiatry, University of Toronto, Canada 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. Br J Psychiatry 1996 May;168(5):647-50 Bipolar affective disorder minus left prefrontal cortex equals schizophrenia. Pang A, Lewis SW. Chinese University of Hong Kong, Hong Kong. BACKGROUND. An investigation of the relationship between bipolar affective disorder and schizophrenia, following a severe head injury and removal of the left prefrontal cortex. METHOD. A single case report. RESULTS. An individual with past history of bipolar affective disorder suffered traumatic damages to the left prefrontal cortex with a second lesion in the left temporal lobe. The patient developed typical schizophrenia nine months later. The relevance of his brain lesions in determining the schizophrenic symptoms is discussed. CONCLUSION. We propose that the specific pattern of brain injury in this patient was sufficient to change the phenotype from bipolar affective disorder to schizophrenia. Ann Med Psychol (Paris) 1995 May;153(3):161-8 [Secondary mania caused by cerebral organic pathology] [Article in French] Verdoux H, Bourgeois M. Centre Carreire, Universite de Bordeaux II. The so-called "secondary mania" are manic syndromes complicating various kinds of somatic illness. Cases of secondary mania following brain injury (i.e., tumors, cerebrovascular lesions, head traumas, infectious diseases, etc.) offer the opportunity to better elucidate the pathophysiology of "primary" mania. Published case reports of secondary mania are reviewed. J Geriatr Psychiatry Neurol 1994 Jan-Mar;7(1):55-7 Valproate in the treatment of posttraumatic bipolar disorder in a psychogeriatric patient. Yassa R, Cvejic J. Psychogeriatric Unit, Douglas Hospital, Verdun, Quebec, Canada. The authors present an 83-year-old man who had developed posttraumatic bipolar disorder 22 years earlier. His condition was characterized by recurrent manic and depressive attacks. Valproate was found effective in controlling his symptoms. Am J Psychiatry 1993 Jun;150(6):916-21 Secondary mania following traumatic brain injury. Jorge RE, Robinson RG, Starkstein SE, Arndt SV, Forrester AW, Geisler FH. Department of Psychiatry, College of Medicine, University of Iowa. OBJECTIVE: In this study patients were examined during the first year after traumatic brain injury to determine the presence of secondary mania. METHOD: A consecutive series of 66 patients with closed-head injury were evaluated in the hospital and at 3-, 6-, and 12-month follow-ups. The patients were examined with a semistructured psychiatric interview and scales for measurement of impairment in activities of daily living, intellectual function, and social functioning. Patients fulfilling the DSM-III-R criteria for mania were compared to patients with major depression and to patients without affective disturbances in regard to their background characteristics, impairment variables, and lesion locations. RESULTS: Six patients (9%) met the criteria for mania at some point during follow-up. The presence of temporal basal polar lesions was significantly associated with secondary mania even when the effect of other lesion locations was taken into account. Secondary mania was not found to be associated with the severity of brain injury, degree of physical or cognitive impairment, level of social functioning, or previous family or personal history of psychiatric disorder. The duration of mania, however, appeared to be brief, lasting approximately 2 months. CONCLUSIONS: The 9% frequency of secondary mania in these patients with traumatic brain injury is significantly greater than that seen in other brain-injured populations (e.g., patients with stroke). The major correlate was the presence of a temporal basal polar lesion. Brain Inj 1993 Mar-Apr;7(2):147-52 Ultra-rapid cycling bipolar affective disorder following a closed-head injury. Zwil AS, McAllister TW, Cohen I, Halpern LR. Department of Psychiatry and Human Behavior, Jefferson Medical College and Thomas Jefferson University Hospital, Philadelphia, PA. A young adult with no prior history of affective disease suffered the onset of a rapid cycling bipolar illness, marginally responsive to psychotropic medications, following a mild closed-head injury, and persisting after the cognitive effects of the injury had resolved. A concurrence of findings on the neurological examination, neurobehavioural examination, SPECT scan, EEG and neuropsychological test battery suggested the presence of a diffuse cerebral injury with a predominance of left frontotemporal findings. This case demonstrates that a severe and disabling mood disorder may follow a mild head injury, and that its course may be independent of cognitive impairment and recovery. Brain Topogr 1993 Winter;6(2):143-62 Standardized varimax descriptors of event related potentials: basic considerations. John ER, Easton P, Prichep LS, Friedman J. New York University Medical Center, Dept. of Psychiatry, NY. This paper describes a set of proposed standardized quantitative descriptors of event-related potentials, based upon principal component varimax analysis (PCVA). No claim is made that these mathematical descriptors correspond to discrete neurophysiological processes which generate the ERP. However, adoption and prospective evaluation of such a set of precise, standardized descriptors of the quantitative ERP may eventually result in advances like those which resulted from adoption of equally arbitrary standardized descriptors for QEEG. PCVA was performed on data from normal subjects and from groups of patients with a wide variety of psychiatric disorders ("Abnormals"). This yielded two sets of factor waveshapes, Normal and Abnormal, which were closely similar. Reconstruction of the normal and abnormal ERP data with either set of factors yielded almost identical allocation of variance. These results gave acceptable reassurance that factors derived from normal population could reasonably be used to describe ERP waveshapes from patients. The ERPs at each electrode of the 10/20 System in a "training group" of normal subjects were then reconstructed. The resulting distributions of factor scores were transformed to achieve Gaussianity. Mean values and standard deviations were obtained for the normative distribution of each factor score, the root mean square deviation, the residual and the absolute ERP power at each electrode. Individual ERPs could then be reconstructed with the normal factors, and the resulting factor scores rescaled to "probability of abnormal morphology" by Z-transformation. Statistical probability maps could be generated by using a color scale in standard deviation units. These methods were used to evaluate visual and auditory ERPs from an independent normal "test group" and the patients in the Abnormal sample. High specificity and sensitivity were obtained for many factor Z- scores. Multiple discriminant functions were constructed which separated normal from abnormal patients with high, replicable accuracy. Further development and testing of these descriptors may make them clinically useful. Psychiatr Clin North Am 1992 Jun;15(2):395-413 Neuropsychiatric sequelae of head injuries. McAllister TW. Section of Neuropsychiatry, Dartmouth Medical School, Hanover, New Hampshire. Based on the above review several general points can be highlighted: Head injuries are extremely common, affecting probably close to 2,000,000 people in this country each year. The most common are nonmissile, closed-head injuries, the majority of which occur in association with motor vehicle accidents. Virtually all studies of head injury suggest a peak incidence in the 15 to 24 years of age group. Coarse measures of outcome suggest that the very young and the elderly have poorer outcomes. Because of improved acute care, however, a large number of young, otherwise healthy patients are surviving head injuries with a variety of profound neuropsychiatric sequelae. Because of the mechanics of brain injury in acceleration-deceleration injuries, certain brain injury profiles are common including orbitofrontal, anterior and inferior temporal contusions, and diffuse axonal injury. The latter particularly affects the corpus callosum, superior cerebellar peduncle, basal ganglia, and periventricular white matter. The neuropsychiatric sequelae follow from the above injury profiles. Cognitive impairment is often diffuse with more prominent deficits in rate of information processing, attention, memory, cognitive flexibility, and problem solving. Prominent impulsivity, affective instability, and disinhibition are seen frequently, secondary to injury to frontal, temporal, and limbic areas. In association with the typical cognitive deficits, these sequelae characterize the frequently noted "personality changes" in TBI patients. In addition, these changes can exacerbate premorbid problems with impulse control. Marked difficulties with substance use, sexual expression, and aggression often result. The constellation of symptoms, which make up the postconcussive syndrome, are seen across the whole spectrum of brain injury severity. Even in so-called mild or minor head injury, these symptoms are likely to have an underlying neuropathologic, neurochemical, or neurophysiologic cause. Higher than expected rates of certain psychopathologic disorders occur in the TBI population, including psychotic syndromes and depressive syndromes. Manic syndromes also are associated with TBI; however, the incidence has not been established. Assessment and treatment of the neuropsychiatric sequelae is a complex and challenging process. The mixture of diffuse and focal injuries, the combination of cognitive, language, somatic, and behavioral difficulties do not fit easily into current diagnostic categories. Biol Psychiatry 1991 Jan 15;29(2):149-58 Manic-depressive and pure manic states after brain lesions. Starkstein SE, Fedoroff P, Berthier ML, Robinson RG. Department of Psychiatry and Behavioral Science, Johns Hopkins University School of Medicine, Baltimore, MD 21205. Although mania is a rare complication of brain lesions, recent reports have emphasized the importance of lesion location and genetic predisposition in these patients. In the present study we compared patients who developed a bipolar affective disorder (i.e., mania and depression) after a brain lesion with patients who only developed mania. Although no significant between-group differences were found on demographic variables, the manic-depressed group showed significantly more impairments on the Mini Mental State Exam than the mania only group. All the bipolar patients had subcortical lesions (mainly right head of the caudate and right thalamus), while patients with unipolar mania had significantly higher frequency of cortical involvement (mainly right orbitofrontal and basotemporal cortices). It is suggested that subcortical and cortical right hemisphere lesions may produce different neurochemical and/or remote metabolic brain changes that may underlie the production of either a bipolar disease or a unipolar mania. Br J Psychiatry 1991 Jan;158:117-9 Bipolar affective disorder following head injury. Bamrah JS, Johnson J. Withington Hospital, Didsbury, Manchester. A patient developed distinct episodes of major depressive illness, schizophreniform psychoses and mania as well as focal epilepsy following head injury. Head injury may be directly causative in the development of affective psychoses, in this case secondary bipolar (mixed) disorder. Ann Neurol 1990 Jun;27(6):652-9 Mania after brain injury: neuroradiological and metabolic findings. Starkstein SE, Mayberg HS, Berthier ML, Fedoroff P, Price TR, Dannals RF, Wagner HN, Leiguarda R, Robinson RG. Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD. We present a consecutive series of 8 patients who developed a manic episode after a brain injury. Five patients had cortical lesions (4 with damage to the right basotemporal region, and 1 with bilateral damage to the orbitofrontal area). While the other 3 patients had subcortical lesions (white matter of the right frontal lobe, right anterior limb of the internal capsule, and right head of the caudate), a fluorodeoxyglucose positron emission tomography scan showed hypometabolism in the right lateral basotemporal region in all 3 patients. These findings suggest a major role for the basal region of the right temporal lobe in the modulation of mood. Br J Psychiatry 1990 Jun;156:884-6 Seasonal affective disorder following brain injury. Hunt N, Silverstone T. Homerton Hospital, London. Seasonal affective disorder has not previously been linked with neuroanatomical abnormalities despite its relationship to biological rhythms. A 45-year-old woman is described with an arteriovenous abnormality in the right frontotemporal region who developed recurrent winter depression and summer hypomania. Acta Psychiatr Scand 1988 Jun;77(6):637-9 Mania following head injury: case reports and neuropsychological findings. Nizamie SH, Nizamie A, Borde M, Sharma S. Central Institute of Psychiatry, Bihar, India. Mania secondary to head injury is reported to be rare. Two cases of florid manic psychoses following head injury are reported along with neurological and neuropsychological investigations. Findings on the Luria Nebraska Neuropsychological Battery (LNNB) suggested residual cognitive deficits, predominantly of right hemisphere. Temporal proximity, clinical neurological findings, EEG changes and deficits on LNNB suggest a causal link between head injury and mania. Acta Psychiatr Scand 1988 Mar;77(3):359-60 Mania following head injury. Yatham LN, Benbow JC, Jeffers AM. St. Ita's Hospital, Portrane, Dublin, Ireland. A case of mania following head injury in an individual with a genetic predisposition to schizophrenia is reported. It is argued that the head injury is probably causative in his case and suggested that head injury should be considered as one of the aetiological factors in secondary mania. Am J Psychiatry 1988 Feb;145(2):172-8 Comparison of mania and depression after brain injury: causal factors. Robinson RG, Boston JD, Starkstein SE, Price TR. Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21205. Patients who developed secondary mania after brain injury (N = 17) had a significantly greater frequency of injury to right hemisphere areas connected with the limbic system than poststroke patients with major depression (N = 31), who had injury primarily in the left frontal cortex and basal ganglia. For patients without mood disturbance after brain injury (N = 28), the location of the lesion was not significant. Secondary mania patients also had a significantly greater frequency of family history of affective disorder than did the other two groups. These results suggest that an interaction between injury to certain areas of the right hemisphere and genetic factors or other neuropathological conditions produces secondary mania. J Nerv Ment Dis 1988 Feb;176(2):87-100 Mechanisms of mania after brain injury. 12 case reports and review of the literature. Starkstein SE, Boston JD, Robinson RG. Department of Psychiatry and Behavioral Science, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205. Twelve patients who developed mania after a brain lesion are reported. Ages ranged from 20 to 83 years. Five patients had brain tumors (three frontal meningiomas, one temporal meningioma, and one temporal astrocytoma), four patients had stroke lesions (one frontal, one temporal, and two thalamocapsular), two patients had a traumatic frontal closed head injury, and one patient had a pituitary adenoma resection. Although seven patients had lesions restricted to the right hemisphere, four had bilateral or midline damage and one had a left hemisphere lesion. Damage to structures functionally connected to the obitofrontal cortex, mainly in the right hemisphere, seems to be associated with secondary mania. The possible roles of monoaminergic, genetic, and perinatal factors in the pathogenesis of secondary mania are discussed. J Clin Psychiatry 1988 Feb;49(2):74-5 Bipolar illness following traumatic brain injury: treatment with lithium and carbamazepine. Stewart JT, Hemsath RH. Gainesville VA Medical Center, FL 32602. A case is described of a 22-year-old woman in whom bipolar disorder developed after a traumatic brain injury. Her symptoms initially responded well to lithium carbonate, but she eventually relapsed. Carbamazepine was added to her treatment regimen with good results. Arch Neurol 1987 Oct;44(10):1069-73 Mania after brain injury. A controlled study of causative factors. Starkstein SE, Pearlson GD, Boston J, Robinson RG. Eleven patients who developed manic syndromes after brain injury (secondary mania) were studied. Six patients had depressive episodes before mania and five had a definite or possible family history of affective disorder. Eight had lesions involving limbic areas, and nine had right hemisphere involvement. In addition to focal brain injury, mean values for bifrontal and third ventricle/brain ratios of manic patients were significantly increased when compared with non-manic patients who had lesions matched for cause, location, volume, and time since injury. Results indicate that the confluence of either anterior subcortical atrophy and a focal lesion of a limbic or limbic-connected region of the right hemisphere, or genetic loading and a limbic-connected right hemisphere lesion may account for the rare occurrence and specific factors necessary to produce secondary mania. Psychiatry Res 1987 Aug;21(4):303-6 Childhood head trauma and psychosis. Wilcox JA, Nasrallah HA. The medical histories of 200 schizophrenic patients were compared to those of 203 depressed patients, 122 manic patients, and 134 surgical controls. All subjects were hospital inpatients. Charts were specifically examined to record any head injury before age 10 that had required medical attention or caused loss of consciousness. Schizophrenics had a significantly greater history of head trauma than the manics, depressives, and surgical controls. There were no significant differences between manics and depressives or between affective disorders as a group and surgical controls. Childhood trauma may be a contributing factor to the development of psychosis in some individuals. Br J Psychiatry 1987 Jun;150:841-4 Mania following head injury. A report of two cases and a review of the literature. Clark AF, Davison K. Royal Victoria Infirmary, Newcastle-upon-Tyne. Secondary mania has been described in association with a variety of physical conditions. While there have been a number of reports of mania occurring in individuals with intracranial cerebral lesions, there have been few reporting its occurrence in association with non-penetrating cerebral trauma. Two further cases of mania following non-penetrating head injury and the efficacy of ECT in its management are reported, and a brief review of the literature relating to the subject is given. Br J Psychiatry 1987 May;150:690-2 Mania following head injury. Bracken P. Cork Regional Hospital, Wilton, Ireland. A case of mania subsequent to head injury is presented. The literature reporting cases of mania after head injury is reviewed. It is suggested that the concept of Secondary Mania be broadened to include cases occurring after head injury. It is also suggested that a true bipolar illness can be secondary. J Clin Psychiatry 1987 Jan;48(1):29-30 Manic syndrome following head injury: another form of secondary mania. Riess H, Schwartz CE, Klerman GL. 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. Am J Psychiatry 1987 Jan;144(1):93-6 Mania following head trauma. Shukla S, Cook BL, Mukherjee S, Godwin C, Miller MG. 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. J Dev Behav Pediatr 1985 Dec;6(6):352-4 Effective management with lithium of a persistent, post-traumatic hypomania in a 10-year-old child. Joshi P, Capozzoli JA, Coyle JT. A 10-year-old child who suffered closed head trauma resulting in a coma of 1 week's duration at the age of 4, developed a persistent, severe behavioral disorder characterized by hyperactivity, impulsivity, distractability, irritability, and grandiosity. Prior attempts at treatment with stimulants and behavioral modification were unsuccessful. Treatment with lithium carbonate resulted in a marked reduction in symptoms and attenuation in her emotional lability. No To Shinkei 1977 Jul;29(7):787-90 [An autopsy case of head injury with a manic-depressive states (author's transl)] [Article in Japanese] Deshimaru M, Miyakawa T, Suzuki T. M. M. a man aged 49. He suffered from a head injury at the aged of 41. At that time he lost consciousness for a few minutes and he was diagnosed as a consquassatio cerebri. The sequelaes of his head injury were a change of character and a disturbance of autonomic nerve function. The changes of character were decreased of activity, lie-down for all day, decrease of speech and depressive mode, and occasionally he was ill-humored, restless and irritative. Periodically he became euphoris, talkative and childisch. He had a disturbance of autonomic nerve function which became worse in parallel to the depressive states. We speculated that character changes, such as manic-depressive states and disturbances of autonomic nerve function were due to the bruising of the bilateral orbital surfaces of frontal lobes.