Decision-making after traumatic brain injury in children: a preliminary study

Decision-making under conditions of uncertainty was studied in 11 children with moderate to severe post-acute traumatic brain injury (TBI) using a modification of the Iowa Gambling Task (Bechara et al., 1994). We hypothesized that decision-making would be compromised in children with TBI. The results revealed that when divided into subgroups by lesion location, children with lesions in the amygdala (AM) were impaired on modified gambling task performance, but children with ventromedial (VM) lesions did not appear to be impaired on the task. These results are in contrast to studies of decision-making in adults with focal lesions of vascular etiology.     

Epidemiology of traumatic brain injury: a population based study in western Sweden

Background – This study on traumatic brain injury (TBI) is based on prospective and retrospective population based data from a head injury register in Borås. Methods – Data was collected from the hospital emergency unit, the discharge register, the regional neurosurgical clinic and the coroner's records during 1 year. This district is mixed urban and rural with a population of 138 000. Results – The 753 cases identified represent an incidence of 546 per 100 000 which includes deaths (0.7%), hospital admissions (67%) and attendance at the emergency department in patients not admitted (32%). Males (644 per 100 000), had 1.46 higher overall rate than females (442 per 100 000). The external causes were dominated by fall from same level (31%) and fall from different level (27%) followed by traffic accidents (16%) and persons hit by objects (15%). Conclusions – The incidence of TBI found in this study is high but well in accordance with earlier published Swedish studies.     

Neurogenic fever after traumatic brain injury: an epidemiological study

OBJECTIVES: To determine the incidence of neurogenic fever (NF) in a population of patients in the acute phase following severe traumatic brain injury (TBI); to identify factors associated with the development of NF following severe TBI in adults. METHODS: Charts of patients admitted from 1996 to 1999 with severe TBI at a large, urban mid-Atlantic teaching hospital were retrospectively evaluated based on diagnostic criteria for each episode of hyperthermia to determine the diagnosis of NF. Data were collected regarding mechanism and area of injury, severity of injury, and demographic factors to determine potential predictors of NF. RESULTS: Diffuse axonal injury (DAI) (OR 9.06, 95% CI 0.99 to 82.7) and frontal lobe injury of any type (OR 6.68, 95% CI 1.1 to 39.3) are independently predictive of an increased risk of development of NF following severe TBI. The presence of a skull fracture and lower initial Glasgow Coma Score (GCS) were individual predictors of development of NF, but did not contribute to the final model. CONCLUSIONS: These findings examine known and novel risk factors for this phenomenon in comparison to previously published literature on NF. A set of predictor variables was identified to help clinicians target patients at high risk for development of NF following severe TBI. It is hoped that earlier diagnosis and appropriate intervention for fever in the TBI patient will lead to improved outcomes.     

Hand movement span after mild traumatic brain injury: a longitudinal study.

This study examined whether memory span was impaired during the acute and post-acute phases following mild traumatic brain injury (mTBI). Twenty-two adults with mTBI were compared with 22 controls on computerized tasks of immediate memory for verbal, spatial, and hand movement sequences under no interference (baseline) and articulatory suppression conditions. Groups were assessed within a month and followed up 3-12 months post-injury. In the acute phase, there were no group differences across tasks under either condition. At follow-up, all spatial and verbal span scores and associated practice effects were equivalent across groups. Yet for the hand movement task, baseline movement span was worse for the mTBI group suggesting that they failed to benefit from practice to the same extent as controls. Furthermore, the fact that this group difference in span scores disappeared when articulatory suppression was imposed indicates that successful hand movement task performance involves verbal recoding.     

Transcranial magnetic stimulation for depression after a traumatic brain injury: a case study

Depression after a traumatic brain injury (TBI) is very common, yet there is a lack of evidence-based treatment options for people who experience depression after a TBI. Traditionally, a history of TBI has been considered an exclusion criterion for transcranial magnetic stimulation trials because of the increased risk of seizure after a TBI. We present what we believe to be the first case of a patient with depression after a TBI treated with transcranial magnetic stimulation.     

Dementia after traumatic brain injury

Early retrospective studies suggested that individuals with a history of a traumatic brain injury (TBI) had a higher risk for dementia than those without a history of TBI. Two meta-analyses demonstrated that the risk for dementia is higher among men, but not women, with a history of TBI. More recent prospective studies, however, are providing discrepant findings, probably due to important methodological differences. TBI is usually associated with significant neuropsychological deficits, primarily in the domains of attention, executive functioning and memory. These deficits may not improve with time. TBI may also lower the threshold for the clinical expression of dementia among predisposed individuals, and the onset of Alzheimer's disease (AD)-like neuropathological and biochemical changes immediately after severe TBI may play an important role in this mechanism.     

Self-esteem in children after traumatic brain injury: an exploratory study

Children with a traumatic brain injury (TBI) often have difficulties in adjusting to their injury and altered abilities, and may be at risk of low self-esteem and loss of confidence. However, few studies have examined self-esteem in this client group. The current study measured the self-esteem of a group of children who were, on average, two years post-TBI and compared this to their performance on other psychometric measures. Participants were 96 children with TBI and 31 peer controls, their parents and teachers. Self-esteem was measured using the Coopersmith Self-esteem Inventory (CSEI). CSEI scores were compared with performance on Wechsler Intelligence Scales (WISC-III), Hospital Anxiety and Depression Scale (HADS); Children's Memory Scale (CMS), Vineland Adaptive Behaviour Scales (VABS) and Parental Stress Index (PSI). Self-esteem was highly correlated with IQ; HADS anxiety and depression; and parental stress (p< 0.001). Children with TBI had significantly lower self-esteem than controls and population norms (p=0.015). Many children with TBI demonstrate low self-esteem and this is closely linked with anxiety and depression. This may hamper academic performance and could lead to further psychosocial problems. It is recommended that self-esteem is routinely assessed after brain injury and rehabilitation strategies implemented to promote a sense of self-worth.     

Dose-dependent neuronal injury after traumatic brain injury

The Fluoro-Jade (FJ) stain reliably identifies degenerating neurons after multiple mechanisms of brain injury. We modified the FJ staining protocol to quickly stain frozen hippocampal rat brain sections and to permit systematic counts of stained, injured neurons at 4 and 24 h after mild, moderate or severe fluid percussion traumatic brain injury (TBI). In adjacent sections, laser capture microdissection was used to collect uninjured (FJ negative) CA3 hippocampal neurons to assess the effect of injury severity on mRNA levels of selected genes. Rats were anesthetized, intubated, mechanically ventilated and randomized to sham, mild (1.2 atm), moderate (2.0 atm) or severe (2.3 atm) TBI. Four or 24 h post-TBI, ten frozen sections (10 microm thick, every 15th section) were collected from the hippocampus of each rat, stained with FJ and counterstained with cresyl violet. Fluoro-Jade-positive neurons were counted in hippocampal subfields CA1, CA3 and the dentate gyrus/dentate hilus. At both 4 and 24 h post-TBI, numbers of FJ-positive neurons in all hippocampal regions increased dose-dependently in mildly and moderately injured rats but were not significantly more numerous after severe injury. Although analysis of variance demonstrated no overall difference in expression of mRNA levels for heat shock protein 70, bcl-2, caspase 3, caspase 9 and interleukin-1beta in uninjured CA3 neurons at all injury levels, post hoc analysis suggested that TBI induces increases in neuroprotective gene expression that offset concomitant increases in deleterious gene expression.     

Long-term survival after traumatic brain injury: a population-based analysis

This population-based retrospective cohort study identified all Olmsted County, MN residents with any diagnosis indicative of potential traumatic brain injury (TBI) during the years 1985 to 2000. The complete community-based medical records of a random sample (n = 7,175) were reviewed to confirm and characterize the event, and to determine vital status through 2002. The review identified 1,448 confirmed incident cases; 164 (11%) were moderate to severe; 1,284 were mild. The estimated 30-day case fatality rate was 29% for moderate to severe cases and 0.2% for mild cases. Comparison of observed mortality over the full period of follow-up with that expected revealed a risk ratio (95% CI) of 5.29 (4.11-6.71) for moderate to severe cases and 1.33 (1.05-1.65) for mild cases. Proportional hazards modeling showed the adjusted hazard of all-cause mortality for moderate to severe cases relative to mild cases was 5.18 (3.65-7.3) within six months of the event and 1.04 (0.57-1.88) for the remaining follow-up period. This analysis indicates that persons who experience mild TBI exhibit a small but statistically significant reduction in long-term survival compared to the general population. The case fatality rate for persons with moderate to severe TBI is very high, but among six-month survivors, long-term survival is similar to that for persons with mild TBI.     

Neuroendocrine disorders after traumatic brain injury

Traumatic brain injury (TBI) is the most common cause of death and disability in young adults living in industrialised countries, in which 180-250 persons per 100 000 per year die or are hospitalised as a result. Neuroendocrine derangements after TBI have received increasing recognition in recent years because of their potential contribution to morbidity, and possibly mortality, after trauma. Marked changes of the hypothalamo-pituitary axis have been documented in the acute phase of TBI, with as many as 80% of patients showing evidence of gonadotropin deficiency, 18% of growth hormone deficiency, 16% of corticotrophin deficiency and 40% of patients demonstrating vasopressin abnormalities leading to diabetes insipidus or the syndrome of inappropriate anti-diuresis. Longitudinal prospective studies have shown that some of the early abnormalities are transient, whereas new endocrine dysfunctions become apparent in the post-acute phase. There remains a high frequency of hypothalamic-pituitary hormone deficiencies among long-term survivors of TBI, with approximately 25% patients showing one or more pituitary hormone deficiencies. This is a higher frequency than previously thought and suggests that most cases of post-traumatic hypopituitarism (PTHP) remain undiagnosed and untreated. PTHP has been associated with adverse outcome both in the acute and chronic phases after injury. These data underscore the need for the identification and appropriate timely management of hormone deficiencies, in order to optimise patient recovery from head trauma, improve quality of life and avoid the long-term adverse consequences of untreated hypopituitarism.     

Bipolar disorder after traumatic brain injury

Objective. We report the case of a 47-year-old man with no psychiatric antecedents who developed manic and depressive symptoms after traumatic brain injury (TBI). Methods and results. Findings on neurobehavioral examination, neuropsychological test battery, electrophysiological and imaging exams suggested the presence of a diffuse cerebral injury with a predominance of left fronto-temporal findings. Conclusions. This case demonstrates that TBI may cause vulnerability to psychiatric disorders, with long latency periods, and that its course may be independent of cognitive impairment and recovery.     

Obsessive-compulsive disorder after traumatic brain injury

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

Dysautonomia after severe traumatic brain injury

Background: Dysautonomia after traumatic brain injury (TBI) is characterized by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating. This study addresses the incidence of dysautonomia after severe TBI, the clinical variables that are associated with dysautonomia, and the functional outcome of patients with dysautonomia. Methods: A historic cohort study in patients with severe TBI [Glasgow Coma Scale (GCS) ≤ 8 on admission]. Results: Seventy‐six of 119 patients survived and were eligible for follow‐up. The incidence of dysautonomia was 11.8%. Episodes of dysautonomia were prevalent during a mean period of 20.1 days (range 3–68) and were often initiated by discomfort. Patients with dysautonomia showed significant longer periods of coma (24.78 vs. 7.99 days) and mechanical ventilation (22.67 vs. 7.21 days). Dysautonomia was associated with diffuse axonal injury (DAI) [relative risk (RR) 20.83, CI 4.92–83.33] and the development of spasticity (RR 16.94, CI 3.96–71.42). Patients with dysautonomia experienced more secondary complications. They tended to have poorer outcome. Conclusions: Dysautonomia occurs in approximately 10% of patients surviving severe TBI and is associated with DAI and the development of spasticity at follow‐up. The initiation of dysautonomia by discomfort supports the Excitatory: Inhibitory Ratio model as pathophysiological mechanism.     

Obsessive-compulsive disorder after traumatic brain injury

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

Rehabilitation outcome after traumatic brain injury

Rehabilitation goals after traumatic brain injury are improving function, increasing the level of independence as high as possible, preventing complications and providing an acceptable environment to the patient. Several complications can be encountered during the rehabilitation period which lead to physical, cognitive and neurobehavioral impairments that cause major delay in functional improvement. This prospective study was designed in order to investigate the complications and their relations with functional recovery in patients that were included in the acute phase of a rehabilitation program. Thirty traumatic brain injured patients admitted to the Intensive Care Units of Uludag University School of Medicine were included in the study. Rehabilitation program consisted in appropriate positioning, range of motion exercises, postural drainage and respiratory exercises. Complications that were encountered during intensive care rehabilitation program were recorded. All patients were evaluated by Functional Independence Measure, Disability Rating Scale and Ranchos Los Amigos Levels of Cognitive Function Scale at admission and discharge. Improvement was observed in patients in terms of functional outcome and disability levels. Pneumonia, athelectasis, anemia and meningitis were the most frequent complications. Deterioration in functional outcome and disability levels was noted as the number of these complications increased. In conclusion, rehabilitation has an important role in the management of traumatic brain injured patients. Reduction of frequency of complications and improvement in functional outcome and disability levels can be achieved through rehabilitation programs. Long-term controlled studies with large number of patients are needed in order to obtain accurate data on factors associated with rehabilitation outcomes.     

Pituitary insufficiency after traumatic brain injury

After traumatic brain injury (TBI), patients present with psychological disorders that may be explained by post-traumatic pituitary insufficiency (PI). The goal of this study was to determine the relationship between hypopituitarism, neuropsychological changes and findings on CT scans after TBI. Hospital charts of 55 TBI patients were screened for age, Glasgow Coma Scale (GSC) score, hypoxia or hypotension. The first two CT scans were analyzed for hemorrhagic lesions. Basal levels of the following hormones were recorded: cortisol, prolactin, estradiol, testosterone, insulin-like growth factor 1 and free thyroxine. Hormonal stimulation tests were performed either if the basal hormone screening revealed an abnormality or if the patient answered “yes” to at least one question in the non-evaluated neuropsychological questionnaire. Overall, 14 out of 55 patients (25.4%) presented with PI; one of them with two hormonal deficits. Growth hormone deficit, hypothyroidism and hypocortisolism were found in one, one and two patients, respectively. Neuropsychological complaints were present in 67% of the patients and were associated with intracerebral hemorrhagic lesions and not PI. Neuropsychological complaints after TBI are more frequent than PI. Brain tissue damage is most important than PI in the development of psychological changes after TBI.