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PubMed2002

Psychotic disorder following traumatic brain injury: a conceptual framework.

INTRODUCTION: Psychotic Disorder Following Traumatic Brain Injury (PDFTBI) is a relatively rare disorder that may provide clues to understanding schizophrenia and psychosis. The objective of this paper was to develop a conceptual framework describing how traumatic brain injury (TBI) can contribute to the development of a psychosis and potential neurobiological mechanisms that cause a psychosis in this population. METHODS: The literature on PDFTBI and previous conceptualisations of the disorder were reviewed. A model of psychosis was described as a context for a conceptualisation of PDFTBI. RESULTS: PDFTBI is associated with abnormalities to the temporal and frontal areas. The general presentation includes persecutory delusions and auditory hallucinations with an absence of negative symptoms. The mean onset is 4-5 years after TBI with the majority of cases occurring within 2 years. The progression and course of PDFTBI is variable. Neuroleptics appear to be the most efficacious medication. Previous conceptualisations of PDFTBI are varied and suggest that the relationship is not a simple one. CONCLUSION: We propose that psychosis results from damage to the frontal and temporal areas and dysregulation of the dopaminergic system. Everyone is vulnerable to a psychotic disorder and psychosis will result when a threshold of damage to these areas are attained. Traumatic brain injury can be the primary cause of psychosis or contribute to the development of a psychosis through secondary seizure disorder, increasing biological and psychological risk, and triggering psychosis in vulnerable patients. The relationship may also be coincidental. Traumatic brain injury triggers pathophysiological processes that generally result in a psychosis after a delay of 1-5 years. Directions for future research includes prospective studies examining the impact of TBI on developing psychosis, retrospective studies examining TBI as a risk factor in schizophrenia or other populations at risk for secondary psychosis, and studies examining prevention of psychotic illness.

Journal Article↗

PubMed2001

To do or not to do? Magnetic resonance imaging in mild traumatic brain injury.

Clinical quantification of mild traumatic brain injury (MTBI) patients should be based on Glasgow coma scale (GCS) score, duration of loss of consciousness (LOC) and post-traumatic amnesia (PTA). In addition, a short practicable neuropsychological test might be useful in detecting minor memory and attentional deficits. MRI appears to be the most sensitive imaging method for assessing MTBI so far, but information regarding a visualized lesion is not usually utilized in the classification of MTBI. Magnetic resonance imaging (MRI) should, therefore, play a major role in any MTBI classification scheme. An appropriate MRI protocol has to be chosen using at least T1 weighted, T2 weighted, proton density and gradient-echo (GRE) sequence images, all in at least two planes, in order to detect and classify all lesions precisely. Owing to the fact that acute lesions may be missed, it is advisable to perform MRI in the first 2 weeks following trauma. Further research is necessary to clarify the relationship between chronic symptoms after MTBI and MRI abnormalities. It may, thus, be possible to provide optimal strategies for emergency department management, to define a group of patients with a need for acute and rehabilitative intervention after MTBI, and to predict their outcome.

Adolescent↗

PubMed1993

Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance.

Intracranial hypertension following traumatic brain injury is associated with considerable morbidity and mortality. Hemorrhagic hypovolemia commonly coexists with head injury in this population of patients. Therapy directed at correcting hypovolemic shock includes vigorous volume expansion with crystalloid solutions. It is hypothesized that, following traumatic brain injury, cerebrovascular dysfunction results in rapid loss of brain compliance, resulting in increased sensitivity to cerebrovascular venous pressure. Increased central venous pressure (CVP) occurring with vigorous crystalloid resuscitation may therefore contribute to the loss of brain compliance and the development of intracranial hypertension. The authors tested this hypothesis in miniature swine subjected to traumatic brain injury, hemorrhage, and resuscitation. Elevated CVP following resuscitation from hemorrhage to a high CVP significantly worsened intracranial hypertension in animals with concurrent traumatic brain injury, as compared to animals subjected to traumatic brain injury alone (mean +/- standard error of the mean: 33.0 +/- 2.0 vs. 20.0 +/- 2.0 mm Hg, p < 0.05) or to animals subjected to the combination of traumatic brain injury, hemorrhage, and resuscitation to a low CVP (33.0 +/- 2.0 vs. 24.0 +/- 2.0 mm Hg, p < 0.05). These data support the hypothesis that reduction in brain compliance can occur secondary to elevation of CVP following resuscitation from hemorrhagic shock. This may worsen intracranial hypertension in patients with traumatic brain injury and hemorrhagic shock.

Animals↗

PubMed2005

Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury.

The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment.

Analysis of Variance↗

PubMed1999

Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury.

In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. Here we investigate whether this CsA-linked protection was related to the concomitant blunting of intra-axonal, Ca2+-induced cytoskeletal changes in traumatic axonal injury, assessed with antibodies targeting spectrin proteolysis and neurofilament compaction. CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons.

Animals↗

PubMed2007

Correlates to traumatic brain injury in nonhuman primates.

BACKGROUND: Traumatic brain injury (TBI) is a major health problem, both in terms of the economic cost to society and the survivor's quality of life. The development of devices to protect against TBI requires criteria that relate observed injury to measurements of head kinematics. The objective of this study is to find the best statistical correlates to impact-induced TBI in nonhuman primates using a qualified, self-consistent set of historical kinematic and TBI data from impact tests on nonhuman primates. METHODS: A database was constructed and qualified from historical head impact tests on nonhuman primates. Multivariate logistic regression analysis with backwards stepwise elimination was performed. Variables considered are the peak rotational acceleration (Omegamax), the peak linear acceleration (Amax), and the number of impacts (N). RESULTS: Bivariate combinations of angular acceleration and the number of impacts are the best correlates to all modes of TBI considered, i.e., concussion, subarachnoid hemorrhage, brain contusion, and subdural hematoma. For a nonhuman primate with 100-g brain mass, the criteria that the probability of TBI is less than 10% by injury mode are:Concussion: OmegamaxN(0.84) < 70 krad/s/s SAH: OmegamaxN(0.70) < 160 krad/s/s Contusion: Omegamax N(0.35) < 160 krad/s/s SDH: Omegamax N(0.60) < 280 krad/s/s CONCLUSIONS: Based on this dataset, the best statistically based risk factor for all modes of TBI in nonhuman primates is the bivariate combination of rotational acceleration and number of impacts.

Acceleration↗

PubMed1999

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.

Adult↗

PubMed1999

Postconcussive symptoms and posttraumatic stress disorder after mild traumatic brain injury.

Postconcussive symptoms after mild traumatic brain injury (MTBI) may be exacerbated by anxiety associated with posttraumatic stress. The aim of this study was to investigate the relationship between postconcussive symptoms and posttraumatic stress disorder (PTSD) in an MTBI population. Survivors of motor vehicle accidents who either sustained an MTBI (N = 46) or no TBI (N = 59) were assessed 6 months posttrauma for PTSD and postconcussive symptoms. Postconcussive symptoms were more evident in MTBI patients with PTSD than those without PTSD, and in MTBI patients than non-TBI patients. Further, postconcussive symptoms were significantly correlated with PTSD symptoms. These findings indicate that postconcussive symptoms may be mediated by an interaction of neurological and psychological factors after MTBI.

Accidents, Traffic↗

PubMed2006

Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury.

OBJECTIVES: Posttraumatic hypotension is believed to increase morbidity and mortality in traumatically brain-injured patients. Using a clinically relevant model of combined traumatic brain injury with superimposed hemorrhagic hypotension in rats, the present study evaluated whether a reduction in mean arterial blood pressure aggravates regional brain edema formation, regional cell death, and neurologic motor/cognitive deficits associated with traumatic brain injury. DESIGN: Experimental prospective, randomized study in rodents. SETTING: Experimental laboratory at a university hospital. SUBJECTS: One hundred nineteen male Sprague-Dawley rats weighing 350-385 g. INTERVENTIONS: Experimental traumatic brain injury of mild to moderate severity was induced using the lateral fluid percussion brain injury model in anesthetized rats (n = 89). Following traumatic brain injury, in surviving animals one group of animals was subjected to pressure-controlled hemorrhagic hypotension, maintaining the mean arterial blood pressure at 50-60 mm Hg for 30 mins (n = 47). The animals were subsequently either resuscitated with lactated Ringer's solution (three times shed blood volume, n = 18) or left uncompensated (n = 29). Other groups of animals included those with isolated traumatic brain injury (n = 34), those with isolated hemorrhagic hypotension (n = 8), and sham-injured control animals receiving anesthesia and surgery alone (n = 22). MEASUREMENTS AND MAIN RESULTS: The withdrawal of 6-7 mL of arterial blood significantly reduced mean arterial blood pressure by 50% without decreasing arterial oxygen saturation or Pao2. Brain injury induced significant cerebral edema (p < .001) in vulnerable brain regions and cortical tissue loss (p < .01) compared with sham-injured animals. Neither regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assessed at 7 days postinjury was significantly aggravated by superimposed hemorrhagic hypotension. Brain injury-induced neurologic deficits persisted up to 20 wks after injury and were also not aggravated by the hemorrhagic hypotension. Cognitive dysfunction persisted for up to 16 wks postinjury. The superimposition of hemorrhagic hypotension significantly delayed the time course of cognitive recovery. CONCLUSIONS: A single, acute hypotensive event lasting 30 mins did not aggravate the short- and long-term structural and motor deficits but delayed the speed of recovery of cognitive function associated with experimental traumatic brain injury.

Animals↗

PubMed1995

Psychiatric disorders and functional disability in outpatients with traumatic brain injuries.

OBJECTIVE: This study examined psychiatric sequelae of traumatic brain injuries in outpatients and their relation to functional disability. METHOD: Fifty consecutive outpatients with traumatic brain injuries who came to a brain injury rehabilitation clinic for initial evaluation were examined for DSM-III-R diagnoses with the use of the National Institute of Mental Health Diagnostic Interview Schedule. The patients completed the Medical Outcomes Study Health Survey to assess functional disability and a questionnaire to assess postconcussion symptoms and self-perceptions of the severity of their brain injuries and cognitive functioning. RESULTS: Thirteen (26%) of the patients had current major depression, and an additional 14 (28%) reported a first-onset major depressive episode after the injury that had resolved. Twelve (24%) had current generalized anxiety disorder, and four (8%) reported current substance abuse. The group with depression and/or anxiety was significantly more impaired than the nondepressed/nonanxious patients according to the Medical Outcomes Study Health Survey measures of emotional role functioning, mental health, and general health perceptions. The depressed/anxious group also rated their injuries as significantly more severe and their cognitive functioning as significantly worse, despite the lack of significant differences in objective measures of severity of injury and Mini-Mental State examination scores. The depressed patients reported significantly more postconcussion symptoms that were increasing in severity over time. CONCLUSIONS: Depression and anxiety are common in outpatients with traumatic brain injuries. Patients with depression or anxiety are more functionally disabled and perceive their injury and cognitive impairment as more severe. Depressed patients report more increasingly severe postconcussion symptoms.

Adult↗

PubMed2003

The development of acute lung injury is associated with worse neurologic outcome in patients with severe traumatic brain injury.

OBJECTIVE: The purpose of this study was to determine the incidence of acute lung injury (ALI) in trauma patients with severe traumatic brain injury (TBI), to evaluate the impact of ALI on mortality and neurologic outcome after severe traumatic brain injury (TBI), and to identify whether the development of ALI correlates with the severity of TBI. METHODS: Clinical data were collected prospectively over a 4-year period in a Level I trauma center. Patients included in the study met the following criteria: mechanical ventilation > 24 hours, head Abbreviated Injury Scale score >or= 3, no other body region Abbreviated Injury Scale score >or= 3, and age between 18 and 54 years. ALI was defined using international consensus criteria. Glasgow Outcome Scale scores were assessed at 3 and 12 months. Bivariate comparisons were made between ALI and non-ALI groups. Multivariate analysis with stepwise logistical regression was used to assess independent factors on mortality. The patient's admission head computed tomographic (CT) scan was graded using the Marshall system, and the presence and size of specific intracranial abnormality was noted. Glasgow Coma Scale (GCS) score, Marshall CT scan score, and intracranial abnormality were correlated with the development of ALI. RESULTS: One hundred thirty-seven patients with isolated head trauma were enrolled in the study over a 4-year period. Thirty-one percent of patients with severe TBI developed ALI. Head trauma patients with ALI had a significantly higher ISS, a greater number of days on the ventilator, and a worse neurologic outcome for those who survived their hospitalization. Mortality was 38% in the ALI group and 15% in the non-ALI group (p = 0.004). Only 3 of 16 (19%) of the deaths within the ALI group were directly related to ALI. By multivariate analysis, only the presence of ALI, older age, and lower initial GCS score were associated with higher mortality. There was no association between ISS, the presence of arterial hypotension (arterial systolic pressure < 90 mm Hg) at admission to the hospital, or the amount of blood transfused and mortality. No correlation was found between the severity of head injury (GCS score, Marshall score, or intracranial abnormality) and development of ALI. CONCLUSION: The development of ALI is a critical independent factor affecting mortality in patients suffering traumatic brain injury and is associated with a worse long-term neurologic outcome in survivors. The risk of developing ALI is not associated with specific anatomic lesions diagnosed by cranial CT scanning.

Abbreviated Injury Scale↗

PubMed2004

Common patterns of bcl-2 family gene expression in two traumatic brain injury models.

Cell death/survival following traumatic brain injury (TBI) may be a result of alterations in the intracellular ratio of death and survival factors. Bcl-2 family genes mediate both cell survival and the initiation of cell death. Using lysate RNase protection assays, mRNA expression of the anti-cell death genes Bcl-2 and Bcl-xL, and the pro-cell death gene Bax, was evaluated following experimental brain injuries in adult male Sprague-Dawley rats. Both the lateral fluid-percussion (LFP) and the lateral controlled cortical impact (LCI) models of TBI showed similar patterns of gene expression. Anti-cell death bcl-2 and bcl-xL mRNAs were attenuated early and tended to remain depressed for at least 3 days after injury in the cortex and hippocampus ipsilateral to injury. Pro-cell death bax mRNA was elevated in these areas, usually following the decrease in anti-cell death genes. These common patterns of gene expression suggest an important role for Bcl-2 genes in cell death and survival in the injured brain. Understanding the regulation of these genes may facilitate the development of new therapeutic strategies for a condition that currently has no proven pharmacologic treatments.

Animals↗

PubMed2005

Hypopituitarism induced by traumatic brain injury in the transition phase.

Traumatic brain injury (TBI) has been associated with hypopituitarism in general and GH deficiency (GHD) in particular; the consequences of this on growth and development are likely to be critical in children and adolescents in the so-called "transition phase". In order to verify the consequences of TBI on pituitary function in the transition phase, we studied a population of adolescents and young adults 3 and 12 months after brain injury [no. = 23, 9 females, 14 males; age: 16-25 yr; body mass index (BMI): 21.9 +/- 0.6 kg/m2]. At 3 months, hypopituitarism was present in 34.6%. Total, multiple and isolated deficits were present in 8.6, 4.3 and 21.7%, respectively. Diabetes insipidus (DI) was present in 8.6% patients and mild hyperprolactinemia in 4.3%. At 12 months, hypopituitarism was present in 30.3%. Total, multiple and isolated deficits were present in 8.6, 4.3 and 17.4%, respectively. DI was present in 4.3% of patients and mild hyperprolactinemia in 4.3%. Total hypopituitarism was always confirmed at retesting. Multiple and isolated hypopituitarism were confirmed in 0/1 and 2/5, respectively. Two/23 patients showed isolated hypopituitarism at 12 months only; 1 patient with isolated at 3 months showed multiple hypopituitarism at retesting. GHD and secondary hypogonadism were the most common acquired pituitary deficits. These results show the high risk of TBI-induced hypopituitarism also in the transition age. Thus it is recommended that pediatric endocrinologists follow-up pituitary function of children and adolescents after brain injuries.

Adolescent↗

PubMed2006

Psychiatric disturbances after traumatic brain injury: neurobehavioral and personality changes.

Traumatic brain injuries (TBI) are frequently accompanied by psychiatric disturbances, which can include striking to relatively minor alterations in personality, behavior, and emotional regulation. The persistence of these neurobehavioral syndromes often leads to deleterious effects on recovery and rehabilitation outcomes. A recent surge of studies has emerged in the past several years to quantify the extent of psychiatric disorders in TBI and to describe differential clinical presentations. Various pre- and post-injury factors also have been hypothesized to contribute to the development and maintenance of psychiatric symptoms in survivors of brain injuries. The identification of high-risk individuals with distinct neuropathophysiological and psychosocial features permits the development of multidisciplinary and tailored approaches to the assessment, prevention, and management of the negative effects of personality and behavioral changes in TBI. This article summarizes the most recent research in these areas and highlights the gaps that need to be filled in subsequent future.

Adaptation, Psychological↗

PubMed2002

Cognitive Impairment Following Traumatic Brain Injury.

Cognitive impairments due to traumatic brain injury (TBI) are substantial sources of morbidity for affected individuals, their family members, and society. Disturbances of attention, memory, and executive functioning are the most common neurocognitive consequences of TBI at all levels of severity. Disturbances of attention and memory are particularly problematic, as disruption of these relatively basic cognitive functions may cause or exacerbate additional disturbances in executive function, communication, and other relatively more complex cognitive functions. Because of the high rate of other physical, neurologic, and psychiatric syndromes following TBI, a thorough neuropsychiatric assessment of the patient is a prerequisite to the prescription of any treatment for impaired cognition. Psychostimulants and other dopaminergically active agents (eg, methylphenidate, dextroamphetamine, amantadine, levodopa/carbidopa, bromocriptine) may modestly improve arousal and speed of information processing, reduce distractibility, and improve some aspects of executive function. Cautious dosing (start-low and go-slow), frequent standardized assessment of effects and side effects, and monitoring for drug-drug interactions are recommended. Cognitive rehabilitation is useful for the treatment of memory impairments following TBI. Cognitive rehabilitation may also be useful for the treatment of impaired attention, interpersonal communication skills, and executive function following TBI. This form of treatment is most useful for patients with mild to moderate cognitive impairments, and may be particularly useful for those who are still relatively functionally independent and motivated to engage in and rehearse these strategies. Psychotherapy (eg, supportive, individual, cognitive-behavioral, group, and family) is an important component of treatment. For patients with medication- and rehabilitation-refractory cognitive impairments, psychotherapy may be needed to assist both patients and families with adjustment to permanent disability.

Journal Article↗

PubMed2006

Deficits in predictive smooth pursuit after mild traumatic brain injury.

Given that even mild traumatic brain injury (TBI) may produce extensive diffuse axonal injury (DAI), we hypothesized that mild TBI patients would show deficits in predictive smooth pursuit eye movements (SPEM), associated with impaired cognitive functions, as these processes are dependent on common white matter connectivity between multiple cerebral and cerebellar regions. The ability to predict target trajectories during SPEM was investigated in 21 mild TBI patients using a periodic sinusoidal paradigm. Compared to 26 control subjects, TBI patients demonstrated decreased target prediction. TBI patients also showed increased eye position error and variability of eye position, which correlated with decreased target prediction. In all subjects, average target prediction, eye position error and eye position variability correlated with scores related to attention and executive function on the California Verbal Learning Test (CVLT-II). However, there were no differences between TBI and control groups in average eye gain or intra-individual eye gain variability, or in performance on the Wechsler Abbreviated Scale of Intelligence (WASI), suggesting that the observed deficits did not result from general oculomotor impairment or reduced IQ. The correlation between SPEM performance and CVLT-II scores suggests that predictive SPEM may be a sensitive assay of cognitive functioning, including attention and executive function. This is the first report to our knowledge that TBI patients show impaired predictive SPEM and eye position variability, and that these impairments correlate with cognitive deficits.

Adolescent↗

PubMed2005

Analysis of long-term gene expression in neurons of the hippocampal subfields following traumatic brain injury in rats.

After experimental traumatic brain injury (TBI), widespread neuronal loss is progressive and continues in selectively vulnerable brain regions, such as the hippocampus, for months to years after the initial insult. To clarify the molecular mechanisms underlying secondary or delayed cell death in hippocampal neurons after TBI, we compared long-term changes in gene expression in the CA1, CA3 and dentate gyrus (DG) subfields of the rat hippocampus at 24 h and 3, 6, and 12 months after TBI with changes in gene expression in sham-operated rats. We used laser capture microdissection to collect several hundred hippocampal neurons from the CA1, CA3, and DG subfields and linearly amplified the nanogram samples of neuronal RNA with T7 RNA polymerase. Subsequent quantitative analysis of gene expression using ribonuclease protection assay revealed that mRNA expression of the anti-apoptotic gene, Bcl-2, and the chaperone heat shock protein 70 was significantly downregulated at 3, 6 (Bcl-2 only), and 12 months after TBI. Interestingly, the expression of the pro-apoptotic genes caspase-3 and caspase-9 was also significantly decreased at 3, 6 (caspase-9 only), and 12 months after TBI, suggesting that long-term neuronal loss after TBI is not mediated by increased expression of pro-apoptotic genes. The expression of two aging-related genes, p21 and integrin beta3 (ITbeta3), transiently increased 24 h after TBI, returned to baseline levels at 3 months and significantly decreased below sham levels at 12 months (ITbeta3 only). Expression of the gene for the antioxidant glutathione peroxidase-1 also significantly increased 6 months after TBI. These results suggest that decreased levels of neuroprotective genes may contribute to long-term neurodegeneration in animals and human patients after TBI. Conversely, long-term increases in antioxidant gene expression after TBI may be an endogenous neuroprotective response that compensates for the decrease in expression of other neuroprotective genes.

Animals↗

PubMed1997

Risk factors for acute care transfer among traumatic brain injury patients.

OBJECTIVE: Acute inpatient traumatic brain injury (TBI) rehabilitation has seen a jump in complexity of medical patient care over the past several years, often necessitating transfer back to an acute care facility. The purpose of this study was to determine the association between selected clinical variables and transfer from inpatient rehabilitation to an acute care facility. DESIGN: A retrospective review of cases from 1992 to 1994. SETTING: A TBI unit in a freestanding rehabilitation hospital. PATIENTS: Twenty-two patients were identified as having received acute care transfer. This group was compared with 78 patients, admitted in the same interval, who did not require acute care transfer. The variables evaluated included recent surgery, pneumonia, fracture, intracranial blood, tracheostomy use, percutaneous feeding tube use, deep venous thrombosis, focal neurological examination, following simple commands, serum sodium level of < 135 mmol/L, serum white blood cell count of > 11,000 cells/microL, and serum hemoglobin level of < 10.0 g/dl. ANALYSIS: Chi-square analysis was performed on the association between acute care transfer and the noted variables. RESULTS: History of pneumonia (p < .03) and history of recent surgery (p < .02) were both associated with acute care transfer, and serum hemoglobin of < 10.0 g/dL had a trend towards association (p < .10). CONCLUSION: Physiatrists caring for the TBI patient may warrant more acute observation of individuals with these parameters to prevent the problems necessitating acute care transfer.

Brain Injuries↗