Duration Of Coma Research Articles

Mannitol as adjunct therapy for childhood cerebral malaria in Uganda: A randomized clinical trial

BackgroundSeveral reports have suggested that raised intracranial pressure (ICP) is a major contributor to death among children with cerebral malaria. Mannitol, an osmotic diuretic, effectively lowers ICP and is used to treat post-traumatic raised ICP. It is not clear whether intravenous mannitol given to children with cerebral malaria improves clinical outcome. The objective of this study was to determine the effect of mannitol as adjunct therapy on the clinical outcome of children with cerebral malaria.MethodsThis randomized double-blind placebo controlled clinical trial was carried out at the Emergency Paediatric ward of Mulago Hospital, Uganda's national referral and teaching hospital. One hundred and fifty six children aged 6 to 60 months with cerebral malaria were randomized to either one dose of mannitol 1 g/kg or placebo, in addition to intravenous quinine. Main outcome measures included coma recovery time; time to sit unsupported, begin oral intake; duration of hospitalization; death and adverse effects.ResultsTime to regain consciousness (p = 0.11), sit unsupported (p = 0.81), time to start oral intake (p = 0.13) and total coma duration (p = 0.07) were similar in both groups. There was no significant difference in the mortality between the placebo (13/80 or 16.3%) and mannitol (10/76 or 13.2%) groups: RR = 1.2 (CI 0.5–2.7). No adverse effects were observed after administration of mannitol.ConclusionMannitol had no significant impact on clinical outcome of cerebral malaria. It is difficult to recommend intravenous mannitol as adjunct therapy for childhood cerebral malaria.Clinical registration numberClinicalTrials.gov ID: NCT00113854

Pediatric Head Injury

Pediatric Head Injury

Brain injury severity and autonomic dysregulation accurately predict heterotopic ossification in patients with traumatic brain injury

Objective : To assess brain injury severity, autonomic dysregulation and systemic infection as risk factors for the occurrence of heterotopic ossification in patients with severe traumatic brain injury. Design : Historic cohort study. Setting : Radboud University Medical Centre. Subjects : All consecutively admitted patients with severe traumatic brain injury (admission Glasgow Coma Scale score 8 or less) during the years 2002—2003. Main measures : The development of clinically relevant heterotopic ossification, defined as painful swelling of joints with redness and decreased range of motion, confirmed radiographically. Results : Seventy-six (64%) of the 119 patients survived and were eligible for further follow-up. Nine patients (12%) developed 20 symptomatic heterotopic ossifications, in one or more joints. Patients with heterotopic ossification had sustained more severe brain injuries, compared to the group without heterotopic ossification. The mean coma duration in the heterotopic ossification group was 28.11 days (SD 20.20) versus 7.54 days (SD 7.47) in the patients without heterotopic ossification (P < 0.001). The occurrence of autonomic dysregulation (relative risk (RR) 59.55, 95% confidence interval (CI) 8.39—422.36), diffuse axonal injury (RR 20.68, 95% CI 4.92—86.91), spasticity (RR 16.96, 95% CI 3.96—72.57) and systemic infection (RR 13.12, 95% CI 3.01—57.17) were all associated with an increased risk of developing symptomatic heterotopic ossification. However, only autonomic dysregulation had a high positive (88.9%, 95% CI 51.7—99.7) and negative (98.5%, 95% CI 91.9—99.9) predictive value with regard to heterotopic ossification. Conclusions : The occurrence of autonomic dysregulation may predict the chance of developing heterotopic ossification in patients with severe head injury.

Longitudinal Changes in Global Brain Volume between 79 and 409 Days after Traumatic Brain Injury: Relationship with Duration of Coma

Neuropathological and experimental animal studies indicate that traumatic brain injury (TBI) results in long-term, neurodegenerative changes. Structural image evaluation using normalization of atrophy (SIENA) offers an automated analysis of the subtle changes in percent brain volume change (%BVC) associated with TBI. In the present study, SIENA was used to evaluate %BVC in individuals who had sustained a mild to severe TBI. We obtained three-dimensional (3D) T1-weighted anatomical magnetic resonance imaging (MRI) scans approximately 79 days and again 409 days post-injury. TBI patients (n = 37) displayed significantly greater decline in %BVC (-1.43%) relative to a normal comparison group (+0.1%, n = 30). Greater %BVC was associated with longer duration of post-injury coma. These results confirm previous findings from cross-sectional studies and argue that the brain undergoes continued structural change for several months post-injury.

Life after survival: long-term daily life functioning and quality of life of patients with hypoxic brain injury as a result of a cardiac arrest

Objectives : To determine the level of daily functioning and quality of life of patients with hypoxic brain injury after a cardiac arrest and to investigate the predictive value of the duration of coma and post-traumatic amnesia in long-term functioning. Design : A retrospective cohort study. Setting : A Dutch rehabilitation centre. Subjects : Thirty-two patients with hypoxic brain injury caused by a cardiac arrest 2—7 years ago, who were admitted to a brain injury rehabilitation programme. Main outcome measures : Cognitive Failures Questionnaire (CFQ), Frenchay Activities Index (FAI), Impact on Participation and Autonomy Questionnaire (IPAQ) and Quality of Life after Brain Injury questionnaire (QOLIBRI). Data on duration of coma and post-traumatic amnesia were retrieved from medical files. Results : A significant association was found between duration of coma, complaints of cognitive functioning (r = 0.57, P < 0.05) and quality of life after brain injury (r = —0.70, P < 0.01). Duration of post-traumatic amnesia was associated with both daily functioning (r = —0.70, P < 0.01) and quality of life (r = —0.70, P < 0.01). Furthermore complaints of cognitive functioning were associated with both the level of participation in society (r = 0.76, P < 0.01) and quality of life (r = 0.77, P < 0.01). Conclusions : Long-term outcome of patients with hypoxic brain injury after a cardiac arrest shows that this group is limited in cognitive and daily functioning, participation and quality of life. Based on the duration of coma and post-traumatic amnesia, an estimation of daily life functioning and quality of life 2—7 years after a cardiac arrest can be made.

Neurodevelopmental Outcome After Severe Traumatic Brain Injury in Very Young Children: Role for Subcortical Lesions

Traumatic brain injury is a major cause of mortality and morbidity in children younger than 15 years of age. To evaluate the role of subcortical lesions on neurodevelopmental outcomes, long-term outcomes of 50 children with severe traumatic brain injury before 4 years of age (accidental injury, n = 21, nonaccidental injury, n = 29) were reviewed retrospectively and compared with late magnetic resonance imaging (MRI) findings: no visible lesions, cortical lesions, or subcortical lesions. Subcortical lesions occurred in both accidental and nonaccidental traumatic brain injuries. Traumatic brain injury severity (initial Glasgow Coma Scale or coma duration) was significantly associated with subcortical lesions. Long-term motor or visual deficiencies occurred in one third of patients and cognitive deficiencies in 52.1%. Although deficiencies occurred without visible MRI lesions, global outcome scores, motor delay, visual impairment, head growth slowing, global intellectual quotients, and planning performances were significantly worse in patients with subcortical lesions. An alarming deterioration in intellectual quotient over time was noted. It was concluded that neurodevelopmental outcomes are worrisome after severe traumatic brain injury in young children, and subcortical lesions affect the prognosis.

Prognostic Factors of Organophosphate Poisoning Between the Death and Survival Groups

In this prospective case series study, we consider the different factors between death and survival groups of organophosphate poisoning. Patients in tertiary-care medical center who had been exposed to organophosphate were included in the study. Pralidoxime (PAM) was discontinued after atropine had controlled the clinical situation. We recorded the demographic data, amount of organophosphate consumption, duration of coma, duration of ventilator use, duration of hospitalization, findings of chest X-ray, white blood cell count, acetylcholinesterase concentration, plasma cholinesterase concentration, total atropine amount, duration of atropine use, total PAM amount, duration of PAM use, urine organophosphate peak concentration, duration of urine organophosphate and mortality rate. Urine was collected every 8 hours and was analyzed by gas chromatography equipped with a flame photometric detector and gas chromatography with mass spectrometer detector for organophosphate determination. The urine organophosphate peak concentration was recorded. Wilcoxon rank sum test was used to compare the factors between death and survival groups. Fisher's exact test was used to compare the different findings of chest X-ray between the death and survival groups. Evidently, the death group had a higher amount of organophosphate consumption, duration of coma, and higher white blood cell count than those in the survival group. Also, the death group had lower duration of hospitalization, and decreased concentrations of acetylcholinesterase and plasma cholinesterase. Total PAM amount use and duration of PAM use were lower. However, the duration of ventilator use, findings of chest X-ray, total atropine amount, duration of atropine, urine organophosphate peak concentration and duration of urine organophosphate were similar in both groups. The mortality rate of our 50 cases was 20%. As stated earlier, the cases of the death group had insufficient PAM therapy. The maximum duration of PAM use was shorter than the maximum duration of urine organophosphate, although the medians of duration of PAM use were more than the medians of duration of urine organophosphate in both the survival and death groups. Prolonged coma duration, lower level of acetylcholinesterase and lower level of plasma cholinesterase were related to the poor prognosis of the patients.

Cognitive Impairment After Cerebral Malaria in Children: A Prospective Study

This study was conducted to assess prospectively the frequency of cognitive deficits in children with cerebral malaria. Cognitive testing in the areas of working memory, attention, and learning was performed for Ugandan children 5 to 12 years of age with cerebral malaria (n = 44), children with uncomplicated malaria (n = 54), and healthy community children (n = 89) at admission and 3 and 6 months later. Six months after discharge, 21.4% of children with cerebral malaria had cognitive deficits, compared with 5.8% of community children. Deficits were seen in the areas of working memory (11.9% vs 2.3%) and attention (16.7% vs 2.3%). Children with cerebral malaria had a 3.7-fold increased risk of a cognitive deficit, compared with community children, after adjustment for age, gender, nutritional status, school level, and home environment. Among children with cerebral malaria, those with a cognitive deficit had more seizures before admission (mean: 4.1 vs 2.2) and a longer duration of coma (43.6 vs 30.5 hours), compared with those without a deficit. Children with uncomplicated malaria did not have an increased frequency of cognitive deficits. Cerebral malaria may be a major cause of cognitive impairment in children in sub-Saharan Africa. Cognitive deficits in children with cerebral malaria are more likely for those who have multiple seizures before effective treatment for cerebral malaria.

Prediction of recovery from a post-traumatic coma state by diffusion-weighted imaging (DWI) in patients with diffuse axonal injury

To determine whether diffusion-weighted magnetic resonance (MR) imaging findings combined with initial clinical factors indicate the depth of shearing lesions in the brain structure and therefore relate to coma duration in diffuse axonal injury (DAI). A total of 74 adult patients (48 male and 26 female) with DAI were examined with conventional MR imaging and diffusion-weighted MR imaging between 2 hours and 20 days after injury. Apparent diffusion coefficient (ADC) maps were obtained and the mean ADC values of each region of interest (ROI) were measured using MRI console software. The involvement of the brainstem, deep gray matter, and corpus callosum was determined for each sequence separately as well as for the combination of all sequences. The correlations between MR imaging findings indicating the presence of apparent brain injury combined with initial clinical factors were determined. Clinical characteristics, such as initial score on the Glasgow coma scale (GCS), age and number of all lesions, and ADC scores were predictive of the duration of coma. It was possible to predict post-traumatic coma duration in DAI from cerebral MR imaging findings combined with clinical prognostic factors in the acute to subacute stage after head injury. Age, ADC scores, GCS score and number of lesions were highly significant in predicting coma duration. The technique presented here might provide a tool for in vivo detection of DAI to allow the prediction of the coma duration during the early stages in patients with traumatic brain injury.

Apolipoprotein E4 polymorphism as a genetic predisposition to delirium in critically ill patients*

To test for an association between apolipoprotein E (APOE) genotypes and duration of intensive care unit delirium. Prospective, observational cohort study. A 541-bed, community-based teaching hospital. Fifty-three mechanically ventilated intensive care unit patients. None. All patients were managed with standardized sedation and ventilator weaning protocols as part of an ongoing clinical trial and were evaluated prospectively for delirium with the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). DNA was extracted from whole blood samples obtained on enrollment, and APOE genotype was determined using polymerase chain reaction followed by restriction enzyme digestion by investigators blinded to the clinical information. Delirium occurred in 47 (89%) patients at some point during the intensive care unit stay. Of the 53 patients, 12 (23%) had an APOE4 allele (APOE4+) and 41 (77%) had only APOE2 or APOE3 alleles (APOE4-). APOE4+ patients were younger (53.2 +/- 21.9 vs. 65.4 +/- 13.4, p = .08) and less often admitted for pneumonia (0% vs. 29.3%, p = .05) compared with APOE4- patients, yet they had a duration of delirium that was twice as long: median (interquartile range), 4 (3, 4.5) vs. 2 (1, 4) days (p = .05). No other clinical outcomes were significantly different between the APOE4+ and APOE4- patients. Using multivariable regression analysis to adjust for age, admission diagnosis of sepsis or acute respiratory distress syndrome or pneumonia, severity of illness, and duration of coma, the presence of APOE4 allele was the strongest predictor of delirium duration (odds ratio, 7.32; 95% confidence interval, 1.82-29.51, p = .005). APOE4 allele represents the first demonstrated genetic predisposition to longer duration of delirium in humans.

Brain Dysfunction

Chronic critical illness is a devastating syndrome of prolonged respiratory failure and other derangements. To our knowledge, no previous research has addressed brain dysfunction in the chronically critically ill, although this topic is important for medical decision making. We studied a prospective cohort of 203 consecutive, chronically critically ill adults transferred to our hospital's respiratory care unit (RCU) after tracheotomy for failure to wean. We measured prevalence and duration of coma and delirium during RCU treatment using the Confusion Assessment Method for the Intensive Care Unit with the Richmond Agitation-Sedation Scale. To assess survivors (at 3 and 6 months after RCU discharge), we used a validated telephone Confusion Assessment Method. Before hospitalization, most (153 [75.4%]) of the 203 patients in the study were at home, completely independent (115 [56.7%]), and cognitively intact (116 [82.0%]). In the RCU, 61 (30.0%) were comatose throughout the stay. Approximately half of patients (66 of 142) who were not in coma were delirious. Patients spent an average of 17.9 days (range, 1-153 days) in coma or delirium (average RCU stay, 25.6 days). Half of survivors (79 of 160) had one of these disturbances at RCU discharge. At 6 months, three fourths (151) of the study patients were dead or institutionalized; of 85 survivors, 58 (68.2%) were too profoundly impaired to respond to telephone cognitive assessment, and 53 (62.4%) were dependent in all activities of daily living. Severe, prolonged, and permanent brain dysfunction is a prominent feature of chronic critical illness. These data, together with previous reports of symptom distress and rates of mortality and institutionalization, describe burdens for chronically critically ill patients receiving continued life-prolonging treatment and for their families.

Influence of activated charcoal on the pharmacokinetics and the clinical features of carbamazepine poisoning

Carbamazepine (CBZ) poisoning has been associated with cases of severe toxicity and death. Multiple-dose activated charcoal was proposed to enhance the clearance of CBZ elimination, but there are no prospective controlled studies that demonstrated a change in clinical outcome after the use of multiple-dose activated charcoal. The aim of this study was to determine the CBZ elimination kinetics and the evolution of clinical features according to the dose of activated charcoal in acute poisoning patients. It is a prospective study for 6 months, from January to June 2004, including all pure acute CBZ-poisoned patients. Twelve patients were randomized to receive a multiple-dose activated charcoal (G1) or a simple dose of 1g/kg (G2). Their mean age was 27.6 ± 12.2 years; the Simplified Acute Physiology Score (SAPS II), 16.37 ± 8.46; and the Acute Physiology and Chronic Health Evaluation (APACHE II), 8 ± 3.96. They were 8 men and 4 women. The mean concentration of blood CBZ at hospital admission was of 29.42 ± 6.68 mg/L. Each group includes 6 patients. The peak value of blood CBZ was comparable in the 2 groups: 33 ± 3.46 mg/L (G1) vs 32.6 ± 5.63 (G2) ( P = .5); the requirement of mechanical ventilation was similar also (3 in each group). The duration of both coma and mechanical ventilation was significantly decreased in the first group compared with the second: 20.33 ± 3.05 vs 29.33 ± 4.11 hours for coma ( P = .02) and 24.1 ± 4.2 vs 36.4 ± 3.6 hours for mechanical ventilation ( P = .001). The length of stay was also significantly decreased in the first group: 30.3 ± 3.4 vs 39.7 ± 7.3 hours in the second group ( P = .000006). Concurrently, we have noted a significant constant reduction of the half-life of CBZ from serum in the first group: 12.56 ± 3.5 hours after multiple dose vs 27.88 ± 7.36 hours after a simple dose ( P = .0004). This decrease was correlated to the dose of charcoal. In summary, we can conclude that multiple-dose activated charcoal is more efficient than simple-dose; it permits a constant decrease of the half-life of blood CBZ without any rebound effect and could improve the prognosis by reducing the duration of coma and the length of stay.

Coma Might Not Preclude Emergency Operation in Acute Aortic Dissection

Syncope or new onset focal neurologic deficits are described in as many as one fifth of patients with acute aortic dissection referred for surgery. Coma or stroke caused by involvement of the arch vessels and secondary brain malperfusion is considered a major contraindication for emergency aortic repair. Initial experience with emergency operation in selected patients with acute type A aortic dissection complicated by coma is described. Five comatose (median Glasgow coma score, 5.5), hemodynamically stable (systolic blood pressure > or = 100 mm Hg) patients with preserved pupillary reactivity and coma duration of less than 12 hours underwent emergency surgical repair. The ascending aorta was always replaced using profound hypothermic circulatory arrest. There were no operative deaths. No hemorrhagic brain infarction developed postoperatively. Ischemic strokes were documented by radiology in 3 patients, and were always right-sided. Four patients returned to normal life with no neurologic sequelae, whereas 1 patient showed partially recovered left hemiparesis and mild cognitive impairment. Coma may not represent an absolute contraindication for resuscitative surgery in hemodynamically stable patients with acute type A aortic dissection. A larger experience is necessary to draw more definitive conclusions.

Analysis of Neurological Complications in Children Transplanted Due to Fulminant Liver Failure

Treatment of patients with fulminant liver failure is a challenge of contemporary medicine. Liver transplantation, in this group, is presently the only reasonable alternative, but in many patients the disastrous condition of the patient results in serious life-threatening complications, including neurological sequelae, which may influence the quality of life after transplantation, and in some cases even cause death. From 1990 to 2004, we performed 241 liver transplantations in children, including 20 transplanted due to fulminant liver failure (8.2%). Serious neurological complications followed liver transplantation in five cases (20%), three of which were fatal. The analysis revealed that the duration of pretransplant coma (grade III or IV) strongly correlated with the incidence of neurological complications ( P < .05). Also a suboptimal quality of the donor liver and poor early graft function may contribute to these posttransplant complications.

Response Inhibition After Traumatic Brain Injury (TBI) in Children: Impairment and Recovery

Children who experience traumatic brain injury (TBI) often show cognitive impairments postinjury, some of which recover over time. We examined the recovery of motor response inhibition immediately following TBI and over 2 years. We assessed the role of injury severity, age at injury, and lesion characteristics on initial impairment and recovery while considering the role of pre-injury psychiatric disorder. Participants were 136 children with TBI aged 5–16 years. Latency of motor response inhibition was measured with the stop-signal task within 1 month of the injury and again at 3, 6, 12, and 24 months. The performance of the TBI participants at each measurement occasion was standardized with 117 children of similar age, but without injury. Residualized latency scores were calculated. Growth curve analyses showed an initial impairment in response inhibition and improvement over the 2 years following injury. Younger TBI patients were initially more impaired although they exhibited greater recovery of response inhibition than did older TBI patients. Longer duration of coma, but not reactivity of pupils or Glasgow Coma Scale score, predicted initial deficit. Lesion characteristics or pre-injury attention deficit hyperactivity disorder did not predict initial impairment or recovery. Replication with longitudinal testing of a comparison group of children sustaining extracranial injury is necessary to confirm our findings.

Neuropsychological profile following suicide attempt by hanging: two adolescent case reports

Hippocampal damage and amnesia following hypoxia and ischemia are described in the few published adult cases of suicide attempt by hanging. However, a recent review (Caine & Watson, 2000) suggests a variable pattern of brain involvement and neuropsychological impairments following hypoxic-ischemic injury that may or may not involve amnesia. To help clarify the impact of hanging on the developing brain, we examined neuropsychological functioning in two adolescents who survived suicide attempt by hanging. Despite differences in Glasgow Coma Scale (GCS), coma duration, and structural imaging findings, both patients had similar IQ (VIQ > PIQ) and presented with various combinations of deficits in expressive/receptive language, visual-constructional and perceptual ability, processing speed, attention, working memory, and/or executive functioning shortly after injury. In spite of their similarities, only one of the patients presented with classic amnesia symptoms in his early recovery. This patient was evaluated 1 year postinjury, and persistent deficits in processing speed and memory encoding were noted. Several hanging-related variables, including longer estimated hanging duration, greater weight, and severe airway edema, were thought to place this patient at increased risk for cognitive deficits. Clinical MRI scans of this patient obtained 6 weeks postinjury revealed mild volume loss as well as abnormalities in bilateral superior cortex. However, CT and MRI scans obtained throughout early recovery did not reveal overt evidence of injury to specific memory-related structures. Comprehensive neuropsychological evaluation of all adolescent survivors of suicide attempt by hanging is recommended, as a variety of postacute cognitive deficits were observed in these patients despite relatively short (≤ 15 minutes) estimated hanging durations.

Cerebrospinal fluid levels of markers of brain parenchymal damage in Vietnamese adults with severe malaria

A retrospective study of cerebrospinal fluid (CSF) markers of brain parenchymal damage was conducted in Vietnamese adults with severe malaria. Three markers were analysed by immunoassays: the microtubule-associated protein tau, for degenerated axons; neuron-specific enolase (NSE), for neurons; and S100B for astrocytes. The mean concentration of tau proteins in the CSF was significantly raised in patients with severe malaria compared with controls (P=0.0003) as reported for other central nervous system diseases. By contrast, the mean concentration of NSE and S100B remained within the normal range. Tau levels were associated with duration of coma (P=0.004) and S100B was associated with convulsions (P=0.006). Concentrations of axonal and astrocyte degeneration markers also were associated with vital organ dysfunction. No association was found between the level of markers of brain parenchymal damage on admission and a fatal outcome. On admission to hospital, patients with severe malaria had biochemical evidence of brain parenchymal damage predominantly affecting axons.

Role of premorbid factors in predicting safe return to driving after severe TBI

Primary objective: The present study explored the possibility of predicting post-injury fitness to safe driving in patients with severe traumatic brain injury (TBI) (n = 66).Methods and procedure: Sixteen different measures, derived from four domains (demo/biographic, medico-functional, neuropsychological, and psychosocial) were used as predictor variables, whereas driving outcomes were assessed in terms of driving status (post-TBI drivers versus non-drivers) and driving safety (number of post-TBI car accidents and violations).Main outcomes and results: About 50% of the patients resumed driving after TBI. Compared to post-TBI non-drivers, post-injury drivers had shorter coma duration. With regard to driving safety, the final multiple regression model combined four predictors (years post-injury, accidents and violations before TBI, pre-TBI-risky-personality-index, and pre-TBI-risky-driving-style-index) and explained 72.5% of variance in the outcome measure.Conclusions: Since the best three predictors of post-injury driving safety addressed patients’ premorbid factors, the results suggest that in order to evaluate the actual possibility of safe driving after TBI, it would be advisable to consider carefully patients’ pre-TBI histories.

Proton MR Spectroscopy Detected Glutamate/Glutamine Is Increased in Children with Traumatic Brain Injury

Adults with traumatic brain injury (TBI) have been shown by invasive methods to have increased levels of the excitatory neurotransmitter glutamate. It is unclear whether glutamate release contributes to primary or secondary injury and whether its protracted elevation is predictive of a poor outcome. Preliminary studies at our institution in adults found that early increases in magnetic resonance spectroscopy (MRS)–detected glutamate/glutamine (Glx) were associated with poor outcomes. We therefore studied 38 children (mean age, 11 years; range, 1.6–17 years) who had TBI with quantitative short-echo time (STEAM, TE = 20 msec) proton MRS, a mean of 7 ± 4 (range, 1–17) days after injury in order to determine if their occipital or parietal Glx levels correlated with the severity of injury or outcome. Occipital Glx was significantly increased in children with TBI compared to controls (13.5 ± 2.4 vs. 10.7 ± 1.8; p = 0.002), but there was no difference between children with good compared to poor outcomes as determined by the Pediatric Cerebral Performance Category Scale score at 6–12 months after injury. We also did not find a correlation between the amount of Glx and the initial Glasgow Coma Scale score, duration of coma, nor with changes in spectral metabolites, including N-acetyl aspartate, choline, and myoinositol. In part, this may have occurred because, in this study, most patients with poor outcomes were studied later than patients with good outcomes, potentially beyond the time frame for peak elevation of Glx after injury. Additional early and late studies of patients with varying degrees of injury are required to assess the importance to the pathophysiology of TBI of this excitatory neurotransmitter.

P.6.050 Anxiety depression and quality of life inpatients with solid cancer during the palliative chemotherapy

Conventional “staging ” of traumatic brain injury (TBI) typically uses depth of coma assessed by the Glasgow Coma Scale (GCS) score near admission as a severity marker. Frequently, early GCS scores are contaminated by alcohol or drug ingestion and other, nonneurological organ system trauma. As well, this measure's usefulness is limited due to its restricted range in survivors. Here we explore the utility of using length of posttraumatic amnesia, coma duration, and age as indirect markers of severity. Cluster analytic techniques were used to examine the relationship of severity so defined to long-term outcome in 106 mild, moderate, and severe TBI patients. Results indicate complex relationships between cluster groups with the influence of age of patient being highlighted as an important moderator in determining severity of injury and later psychosocial outcome.