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.     

Measurement and prediction of subjective fatigue following traumatic brain injury.

Numerous outcome studies have found fatigue to be a common problem following traumatic brain injury (TBI). This study examined the magnitude, causes and impact of fatigue following TBI using three subjective fatigue scales, and investigated its relationship with demographic and injury-related factors, and mood. Forty-nine controls and 49 TBI participants (36.2% with GCS score of 13-15, 29.8% with GCS score of 9-12, and 34% with GCS score of 3-8) were seen at a mean of approximately 8 months post injury. All participants completed three subjective fatigue measures, including the Fatigue Severity Scale (FSS), Visual Analogue Scale-Fatigue (VAS-F) and Causes of Fatigue Questionnaire (COF). TBI participants reported a significantly greater impact of fatigue on their lifestyle on the FSS relative to controls, and reported activities requiring physical and mental effort as more frequent causes of fatigue on the COF. There were, however, no significant group differences on subscales of the VAS-F. Greater time since injury and higher education levels were associated with higher fatigue levels, independent of the effects of mood. Injury severity and age were not found to be significant predictors of subjective fatigue severity in TBI participants.     

Two-point discrimination following traumatic brain injury.

This study investigated two point discrimination (TPD) perception in survivors of traumatic brain injury (TBI). Inpatient and outpatient survivors of severe TBI and age-matched healthy controls aged between 16 and 65 years were included in the study with a mean TPD of 3.61, 3.41 and 2.61 mm respectively. Significant group effects were seen in TPD between subjects with TBI and controls. TPD deficits did not appear to be influenced by GCS or PTA duration, nor did they show evidence of improvement over time. Similarly, CT scan data did not explain the observed TPD differences in TBI survivors. Admission functional independence measure (FIM), a global measure of functional independence, had a strong negative correlation with TPD. The lack of change in TPD over time mirrors other basic markers of neurological recovery but is at odds with TBI outcome literature reporting continuing improvements in function for at least 5 years post injury.     

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.     

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.     

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.     

Persisting insomnia following traumatic brain injury

Persisting insomnia secondary to traumatic brain injury, rarely reported and documented, is described in an adult male following head injury. The neuronal mechanisms underlying this sleep disorder as well as the neuropsychological concomitants and therapeutic approaches are discussed.     

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.     

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.     

Long-term neuropsychological outcomes following mild traumatic brain injury.

Mild traumatic brain injury (MTBI) is common, yet few studies have examined neuropsychological outcomes more than 1 year postinjury. Studies of nonreferred individuals with MTBI or studies with appropriate control groups are lacking, but necessary to draw conclusions regarding natural recovery from MTBI. We examined the long-term neuropsychological outcomes of a self-reported MTBI an average of 8 years postinjury in a nonreferred community-dwelling sample of male veterans. This was a cross-sectional cohort study derived from the Vietnam Experience Study. Three groups matched on premorbid cognitive ability were examined, those who (1) had not been injured in a MVA nor had a head injury (Normal Control; n = 3214), (2) had been injured in a motor vehicle accident (MVA) but did not have a head injury (MVA Control; n = 539), and (3) had a head injury with altered consciousness (MTBI; n = 254). A MANOVA found no group differences on a standard neuropsychological test battery of 15 measures. Across 15 measures, the average neuropsychological effect size of MTBI compared with either control group was -.03. Subtle aspects of attention and working memory also were examined by comparing groups on Paced Auditory Serial Addition Test (PASAT) continuation rate and California Verbal Learning Test (CVLT) proactive interference (PI). Compared with normal controls, the MTBI group evidenced attention problems in their lower rate of continuation to completion on the PASAT (odds ratio = 1.32, CI = 1.0-1.73) and in excessive PI (odds ratio = 1.66, CI = 1.11-2.47). Unique to the MTBI group, PASAT continuation problems were associated with left-sided visual imperceptions and excessive PI was associated with impaired tandem gait. These results show that MTBI can have adverse long-term neuropsychological outcomes on subtle aspects of complex attention and working memory.     

Pathological laughing and crying following traumatic brain injury

The authors examined the prevalence and clinical correlates of pathological laughing and crying (PLC) using the Pathological Laughter and Crying Scale (PLAC) in 92 consecutive patients with acute symptoms 3, 6, and 12 months after traumatic brain injury (TBI). The prevalence of PLC during the first year after TBI was 10.9%. Compared to patients without PLC, patients with PLC had significantly more depressive, anxious, and aggressive behaviors and had poorer social functioning. Additionally, PLC was associated with the presence of anxiety disorder, and focal frontal lobe lesions, especially in the lateral aspect of the left frontal lobe. Findings revealed that prefrontal regulation of limbic circuits may be involved in the pathophysiology of this disturbed emotional expression.     

Profound amnesia and confabulation following traumatic brain injury

Amnesia and confabulation may persist following acute aneurysmal hemorrhage of the anterior communicating artery, chronic alcoholic Korsakoff's syndrome, and late-stage dementia of the Alzheimer type. However, there is a paucity of information regarding the persistence of these symptoms following traumatic brain injury. We present the case of JL, a 43-year-old male with persistent and severe anterograde amnesia for verbal and visual information with co-occurring provoked confabulation which persists well into the chronic phase of recovery after a severe traumatic brain injury. Neuropsychological testing at 7 weeks post-injury demonstrated severe anterograde amnesia with co-occurring confabulation. Follow-up testing at 9.5 months post-injury showed persistent and severe anterograde amnesia and provoked confabulation despite superior non-verbal intelligence and above average attentional and perceptual abilities. Late computed tomography showed chronic hypodense regions in the temporal lobes, bilaterally (L > R), and in the region of the left ventrolateral frontal lobe. This case demonstrates that anterograde amnesia and provoked confabulation may persist long after the acute phase of recovery after traumatic brain injury, and also supports previous research which asserts that medial temporal lobe damage must be accompanied by ventral frontal lobe pathology to produce the amnestic-confabulatory syndrome.     

Predicting depression following mild traumatic brain injury

CONTEXT: Minimizing negative consequences of major depression following traumatic brain injury is an important public health objective. Identifying high-risk patients and referring them for treatment could reduce morbidity and loss of productivity. OBJECTIVE: To develop a model for early screening of patients at risk for major depressive episode at 3 months after traumatic brain injury. DESIGN: Prediction model using receiver operating characteristic curve. SETTING: Level I trauma center in a major metropolitan area. PARTICIPANTS: Prospective cohort of 129 adults with mild traumatic brain injury. MAIN OUTCOME MEASURES: Center for Epidemiologic Studies Depression Scale score and current major depressive episode module of the Structured Clinical Interview for the DSM-IV. RESULTS: A prediction model including higher 1-week Center for Epidemiologic Studies Depression Scale score, older age, and computed tomographic scans of intracranial lesions yielded 93% sensitivity and 62% specificity. CONCLUSION: This study supports the feasibility of identifying patients with mild traumatic brain injury who are at high risk for developing major depressive episode by 3 months' postinjury, which could facilitate selective referral for potential treatment and reduction of negative outcomes.     

Fasting is neuroprotective following traumatic brain injury

To determine the neuroprotective effect of fasting after traumatic brain injury (TBI) and to elucidate the potential underlying mechanisms, we used a controlled cortical impact (CCI) injury model to induce either a moderate or a severe injury to adult male Sprague Dawley rats. Tissue-sparing assessments were used to determine the level of neuroprotection of fasting, hypoglycemia (insulin 10 U), or ketone (1.66 mmoles/kg/day or 0.83 mmoles/kg/day; D-beta-hydroxtbutyrate) administration. Mitochondrial isolation and respiratory studies were utilized to determine the functionality of mitochondria at the site of injury. We also investigated biomarkers of oxidative stress, such as lipid/protein oxidation, reactive oxygen species (ROS) production, and intramitochondrial calcium load, as a secondary measure of mitochondrial homeostasis. We found that fasting animals for 24 hr, but not 48 hr, after a moderate (1.5 mm), but not severe (2.0 mm), CCI resulted in a significant increase in tissue sparing. This 24-hr fast also decreased biomarkers of oxidative stress and calcium loading and increased mitochondrial oxidative phosphorylation in mitochondria isolated from the site of injury. Insulin administration, designed to mimic the hypoglycemic effect seen during fasting did not result in significant tissue sparing after moderate CCI injury and in fact induced increased mortality at some injection time points. However, the administration of ketones resulted in increased tissue sparing after moderate injury. Fasting for 24 hr confers neuroprotection, maintains cognitive function, and improves mitochondrial function after moderate (1.5 mm) TBI. The underlying mechanism appears to involve ketosis rather than hypoglycemia.