Psychosis following traumatic brain injury

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.     

Psychosis following traumatic brain injury

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.     

Hysteria following brain injury.

Of 167 patients referred to a unit treating severe behaviour disorders after brain injury, 54 showed clinical features closely resembling those of gross hysteria as described by Charcot. Close correlation was found with very diffuse insults (hypoxia and hypoglycaemia), but not with severity of injury or with family or personal history of hysterical or other psychiatric disorder. The findings may have implications for the understanding of the nature of hysteria.     

Irritability following traumatic brain injury

This study was undertaken to identify the clinical and pathoanatomical correlates of irritability in patients with closed head injuries. A consecutive series of 66 patients was assessed in hospital and at 3, 6, 9, and 12-month follow-ups. Patients fulfilling criteria for irritability were divided into 2 groups based on the immediate or delayed onset of their irritability and compared with patients without irritability for background characteristics, impairment variables, and lesion characteristics. There were 12 patients (18.2%) with acute onset irritability and 10 (15.1%) with delayed onset irritability. Acute onset irritability patients had a higher frequency of left cortical lesions. Delayed onset irritability patients showed a strong association with poor social functioning and greater impairment in activities of daily living. The findings suggest that post-brain injury irritability may have different causes and treatment in the acute and chronic stages.     

Mood disorders following traumatic brain injury

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.     

Irreversible brain injury following status epilepticus

Described here is a patient with medically intractable generalized epilepsy who developed status epilepticus (SE) affecting his right cerebral hemisphere for about 48 hours, which led to irreversible injury to that hemisphere. His partial SE did not respond to the first-line therapies, repeated doses of midazolam, or continuous intravenous infusion of propofol. Extensive investigations failed to find a cause of his SE except for a low serum valproic acid. A minor trauma that he suffered 1 week prior to his SE was of questionable significance. Neurological examination, neuropsychological testing, electroencephalography, and magnetic resonance imaging all demonstrated striking abnormalities limited to the affected cerebral hemisphere that did not resolve with repeated testing. This case illustrates permanent focal brain injury following prolonged partial SE in a patient with previously known generalized seizure disorder.     

Recurrent hypersomnia following traumatic brain injury

BackgroundRecurrent hypersomnia (RH) following a traumatic brain injury (TBI) is a rare form of RH. According to the International Classification of Sleep Disorders, 2nd edition (ICSD-2), RH must be considered in the differential diagnosis as secondary to an organic insult of the central nervous system and not as the clinical subtype of RH, Kleine–Levin syndrome (KLS). The aim of our study was to investigate if cases of RH following TBI should be considered in the differential diagnosis of RH as indicated by the International Classification of Sleep Disorders, 2nd edition or as genuine, or indicated by ICSD-2, RH must cases of KLS.MethodsTwelve cases of RH developed after TBI were collected and analyzed for circumstance at onset, severity of TBI, delay between TBI and occurrence of first episode of RH, symptoms of RH, duration and cycle length of episodes of hypersomnia, physical signs, and brain morphological imaging at the time of hypersomnia episodes.ResultsFactors such as the delay between TBI and the first episode of RH, the presence of other triggering factors and potential genetic factors, the degree of the severity of TBI, the presence or absence of any consistent brain imaging abnormality, provided the following results: (1) two of the cases could be considered as symptomatic of the underlying pathological brain process, (2) eight of the cases could be considered as simply triggered by TBI in patients at risk for KLS, and (3) two cases could be considered neither symptomatic nor triggered by TBI, due to the long delay between TBI and occurrence of symptoms.ConclusionCases of RH following TBI do not present under a single mechanism. Clinical assessment and laboratory tests are necessary to correctly classify them.     

Major depression following traumatic brain injury

BACKGROUND: 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. OBJECTIVE: To determine the clinical, neuropsychological, and structural neuroimaging correlates of major depression occurring after TBI. DESIGN: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.     

Mood disorders following traumatic brain injury

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.     

创伤性脑损伤后脑红蛋白的表达变化

目的 观察创伤性脑损伤后伤灶周围皮质脑红蛋白（Ngb）的表达变化.方法 采用自由落体硬膜外撞击方法建立脑外伤模型,应用免疫组织化学和Western Blot技术,定量观察创伤性脑损伤后Ngb的表达变化.结果 各实验组之间阳性信号面积没有统计学差异（P＞0.05）;但外伤后,光密度或累积光密度均明显增高（P＜0.05或P＜0.01）.结论 脑外伤后伤灶周围皮质神经元Ngb的表达增高,提示Ngb可能参与了脑外伤后伤灶周围神经元的保护过程.     

Working memory brain activation following severe traumatic brain injury

Functional magnetic resonance imaging (fMRI) has shown that brain activation during performance of working memory (WM) tasks under high memory loads is altered in adults with severe traumatic brain injury (TBI) relative to uninjured subjects (Perlstein et al., 2004; Scheibel et al., 2003). Our study attempted to equate TBI patients and orthopedically injured (OI) subjects on performance of an N-Back task that used faces as stimuli. To minimize confusion in TBI patients that was revealed in pilot work, we presented the memory conditions in two separate tasks, 0- versus 1-back and 0- versus 2-back. In the 0- versus 1-back task, OI subjects activated bilateral frontal areas more extensively than TBI patients, and TBI patients activated posterior regions more extensively than OI subjects. In the 0- versus 2-back task, there were no significant differences between the groups. Analysis of changes in activation over time on 1-back disclosed that OI subjects had decreases in bilateral anterior and posterior regions, while TBI patients showed activation increases in those and other areas over time. In the 2-back condition, both groups showed decreases over time in fusiform and parahippocampal gyri, although the OI group also showed increases over time in frontal, parietal, and temporal areas not seen in the TBI patients. The greatest group differences were found in the 1-back condition, which places low demand on WM. Although the extent of activation in the 2-back condition did not differ between the two groups, deactivation in the 2-back condition was seen in the OI patients only, and both groups' patterns of activation over time varied, suggesting a dissociation between the TBI and OI patients in recruitment of neural areas mediating WM.     

Linguistic outcomes following traumatic brain injury in children

Recent studies of outcome after traumatic brain injury (TBI) emphasize the adverse effect of diffuse brain injury on linguistic development. This article reviews studies of lexical development, discourse processes, and reading in children and adolescents with TBI. The child's developmental level at the time of injury is related to the pattern of deficits. Young children who sustain severe TBI are particularly vulnerable to linguistic deficits at both lexical and discourse levels. TBI in older children and adolescents preferentially disrupts higher-order discourse functions. The contribution of deficits in fundamental processes, such as working memory and processing speed, to linguistic outcomes requires further investigation.     

Muscarinic cholinergic receptor binding in rat brain following traumatic brain injury

Recent evidence suggests that excessive activation of muscarinic cholinergic receptors (mAChRs) contributes significantly to the pathophysiological consequences of traumatic brain injury (TBI). To examine possible alterations in mAChRs after TBI, the affinity (K_d) and maximum number of binding sites (B_max) of mAChRs in hippocampus, neocortex, brain stem and cerebellum were determined by [³H]QNB binding. Three groups of rats were examined: 1 h post-TBI (n = 21), 24 h post-TBI (n = 21) and sham-injured rats (n = 21). K_d values were significantly higher in hippocampus and brain stem at 1 but not 24 h post-TBI compared with sham-injured controls (P < 0.05). K_d values did not significantly differ in neocortex and cerebellum at 1 or 24 h post-TBI compared with sham-injured controls. B_max values did not significantly differ in any brain areas at 1 or 24 h post-TBI compared with sham-injured controls These results show that TBI significantly decreases the affinity of mAChRs in hippocampus and brain stem at an early stage post-TBI, which may contribute to desensitization of mAChRs after TBI. The findings of no change in B_max values are consistent with a transient elevation in ACh concentrations after TBI.     

谷氨酸氧化毒性在脑外伤后继发性脑损伤中作用的实验研究

目的 用大鼠脑外伤模型研究谷氨酸氧化毒性在脑外伤后继发性脑损伤中的作用.方法 用自由落体致伤的方法制作大鼠重型颅脑外伤模型,D609为治疗药物;SD大鼠按随机数字表法分为对照组、外伤组和治疗组,各组内均分为三组,分别检测实验性外伤后24h的脑皮质谷胱苷肽(GSH)含量、脑组织含水量、神经元凋亡情况.结果 治疗组伤侧皮质GSH含量显著高于外伤组(P<0.01),但显著低于对照组(P<0.01);治疗组脑水肿显著低于外伤组(P<0.01),但显著高于对照组(P<0.01);脑组织TUNEL染色显示,外伤组伤侧海马见大量凋亡细胞,治疗组伤侧海马凋亡细胞明显减少,显著低于外伤组(P<0.01),外伤组及治疗组对侧海马和对照组海马均未见凋亡细胞.结论 谷氨酸氧化毒性是引起大鼠颅脑外伤后继发性脑损伤的重要机制.     

Sleepiness and fatigue following traumatic brain injury

ObjectivesTo compare individuals with traumatic brain injury (TBI) to healthy controls (CTLs) on measures of sleepiness, fatigue, and sleep, and explore correlates of sleepiness and fatigue separately for each group.MethodsParticipants were 22 adults with moderate/severe TBI (time since injury ?1 year; mean = 53.0 ± 37.1 months) and 22 matched healthy CTLs. They underwent one night of polysomnographic (PSG) recording of their sleep followed the next day by the Maintenance of Wakefulness Test (MWT). They also completed a 14-day sleep diary, the Epworth Sleepiness Scale (ESS), the Functional Outcomes of Sleep Questionnaire (FOSQ), and the Multidimensional Fatigue Inventory (MFI).ResultsThere were no significant group differences on measures of objective (MWT) or subjective (ESS) sleepiness, both groups being quite alert. However, TBI participants reported greater consequences of sleepiness on their general productivity (FOSQ), spent more time in bed at night, and napped more frequently and for a longer time during the day. Subjective fatigue was significantly higher in TBI participants on the general, physical, and mental fatigue MFI subscales. There were no between-group differences on any sleep parameters derived either from PSG or sleep diary.ConclusionsFatigue appeared to be a more prominent symptom than sleepiness when assessed between 1 and 11 years after TBI. Participants with TBI used compensatory strategies such as increasing time spent in bed and daytime napping in this sample. Future research should document the time course of sleepiness and fatigue after TBI and investigate treatment options.