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PubMed1993

Traumatic brain injury and chronic pain: differential types and rates by head injury severity.

Traumatic brain injury has been associated with many physical and neurobehavioral consequences, including pain problems. Documented most has been the presence of posttraumatic headaches that are associated with the postconcussion syndrome. This study therefore examined types and rates of chronic pain problems in patients seen in an outpatient brain injury rehabilitation program. A total of 104 patients were evaluated, 66 of whom were male and 38 female, and the average time postinjury was 26 months. Headaches were the most frequent chronic pain problem across both mild and the moderate/severe groups, although in the former, a significantly higher frequency was noted (89%) when compared against the latter group. The same relative rates were seen for chronic neck/shoulder, back, and other pain problems. The mild group also showed a higher frequency of concurrent pain problems, whereas in the moderate/severe group only one patient had more than one chronic pain problem. Results also showed that in the mild group neck/shoulder accompanied headaches 47% of the time, and back pain coexisted with headaches 44% of the time. These results underscore the high frequency of chronic pain problems in the mild head injury population and implicate the need for avoiding the mislabeling of symptoms such attentional deficits or psychological distress as attributable only to head injury sequelae in those with coexisting chronic pain. Early identification and intervention of pain syndromes in the mild head-injury population is also suggested.

Adolescent↗
PubMed2006

Enhanced catecholamine synthesis in the prefrontal cortex after traumatic brain injury: implications for prefrontal dysfunction.

Traumatic brain injury (TBI)--induced dysfunction of the prefrontal cortex causes many high-level cognitive deficits, including working memory (WM) dysfunction. WM lies at the core of many high-level functions, yet the cellular and molecular mechanisms underlying its dysfunction are poorly understood. Lesion and pharmacological studies in rodents have implicated the medial prefrontal cortex (mPFC), which includes the prelimbic/infralimbic (PL/IL) cortices, in WM tasks. These studies have shown that optimal levels of catecholamine neurotransmission are critical for normalcy of WM function, suggesting that alterations in their synthesis may play a role in WM dysfunction. Using the cortical impact injury model of traumatic brain injury which reproducibly causes working memory deficits in rodents, we have measured the protein levels and activity of tyrosine hydroxylase (TH), the rate-limiting enzyme for catecholamine biosynthesis, and tissue dopamine (DA) and norepinephrine (NE) levels in microdissected PL/IL tissues. Our results show that TBI increases TH protein levels, its activity and tissue DA and NE content in the PL/IL. These findings suggest that altered catecholamine signaling within the PL/IL may contribute to impaired PFC function, and may have implications in the design and implementation of strategies to alleviate prefrontal dysfunction in brain injury patients.

Animals↗
PubMed2002

Pre-injury status and adaptation following traumatic brain injury.

There are an estimated two million traumatic brain injuries (TBI) each year in the US. Behavioural and psychosocial sequelae are the most disabling consequences of TBI, but relatively little empirical data exist that identify factors underlying the variability in patient outcomes. There is an increasing appreciation that pre-injury coping liabilities are likely to contribute to persistent disability and that outcome reflects the combined effects of pre-morbid, injury-related, and post-injury factors. Despite this, most outcome studies focus on the effects of injury-related and post-injury variables. The present study evaluated outcome in 45 adults who suffered a moderate or severe TBI at least 2 years earlier. It was hypothesized that severity of pre-morbid psychiatric and substance abuse problems and less social support following brain injury would be associated with poorer post-injury adaptation as measured by employment status, independent living status, and neurobehavioural symptomatology. The authors found that pre-injury psychiatric and substance abuse histories predicted employment status and that pre-injury substance abuse predicted independent living status. Social support following TBI predicted significant other's assessment of the patients' neurobehavioural status. None of the independent variables were found to predict patient assessment of his or her own neurobehavioural functioning. These findings support the premise that pre-morbid coping liabilities are related to the degree of post-injury disability.

Activities of Daily Living↗
PubMed1988

Peripheral nerve injuries in the adult with traumatic brain injury.

Fifty adult patients who sustained a traumatic brain injury (TBI) were screened for the presence of a peripheral nerve injury (PNI). All suspected patients had diagnostic electromyography performed in order to confirm the clinical findings. The incidence of PNI with TBI was 34%. A variety of nerve injuries were seen, the most frequent of which were ulnar nerve entrapment at the elbow (10%) and brachial plexus injuries (10%). No patient initiated a complaint that led to the diagnosis. In addition, all the neuropathies were missed prior to admission. The neuropathies commonly were found in the neurologically impaired extremity and associated with spasticity. The results of this study suggest that patients sustaining a TBI have a significant and higher incidence of PNI as a complication than previously reported.

Accidents, Traffic↗
PubMed1990

The effect of acetylcholine depletion on behavior following traumatic brain injury.

Rats were injected with either saline; A-4 (40 mg/kg, i.p.), a bis tertiary amine derivative of hemicholinium-3; or A-5 (50 micrograms/kg, i.p.), a bis quaternary amine derivative of hemicholinium-3, 1 h prior to moderate fluid percussion brain injury. A variety of reflexes and responses were measured up to 60 min following injury, and body weight and several neurological measures were taken daily up to 10 days following injury. Pretreatment with either A-4 or A-5 significantly attenuated components of transient behavioral suppression, as well as more enduring deficits in body weight and beam walk and beam balance performance. A-4 administered prior to fluid percussion was found to reduce striatal, but not pontine, acetylcholine content. A-5 did not significantly reduce acetylcholine content in either area. Both A-4 and A-5 pretreatment prevented a significant increase in acetylcholine content in the cerebrospinal fluid following fluid percussion injury; however, only A-5 significantly reduced plasma acetylcholine content. These results confirm cholinergic involvement in the production of both transient and longer-lasting behavioral deficits following traumatic brain injury. Furthermore, traumatic brain injury may allow plasma constituents to gain access to the central nervous system.

Acetylcholine↗
PubMed2000

Dose-response curve and optimal dosing regimen of cyclosporin A after traumatic brain injury in rats.

Acute neuropathology following experimental traumatic brain injury results in the rapid necrosis of cortical tissue at the site of injury. This primary injury is exacerbated in the ensuing hours and days via the progression of secondary injury mechanism(s) leading to significant neurological dysfunction. Recent evidence from our laboratory demonstrates that the immunosuppressant cyclosporin A significantly ameliorates cortical damage following traumatic brain injury. The present study extends the previous findings utilizing a unilateral controlled cortical impact model of traumatic brain injury in order to establish a dose-response curve and optimal dosing regimen of cyclosporin A. Following injury to adult rats, cyclosporin A was administrated at various dosages and the therapy was initiated at different times post-injury. In addition to examining the effect of cyclosporin A on the acute disruption of the blood-brain barrier following controlled cortical impact, we also assessed the efficacy of cyclosporin A to reduce tissue damage utilizing the fluid percussion model of traumatic brain injury. The findings demonstrate that the neuroprotection afforded by cyclosporin A is dose-dependent and that a therapeutic window exists up to 24h post-injury. Furthermore, the optimal cyclosporin dosage and regimen markedly reduces disruption of the blood-brain barrier acutely following a cortical contusion injury, and similarly affords significant neuroprotection following fluid percussion injury. These findings clearly suggest that the mechanisms responsible for tissue necrosis following traumatic brain injury are amenable to pharmacological intervention.

Animals↗
PubMed2005

The effect of therapeutic hypothermia on the expression of inflammatory response genes following moderate traumatic brain injury in the rat.

Traumatic brain injury (TBI) initiates a cascade of cellular and molecular responses including both pro- and anti-inflammatory. Although post-traumatic hypothermia has been shown to improve outcome in various models of brain injury, the underlying mechanisms responsible for these effects have not been clarified. In this study, inflammation cDNA arrays and semi-quantitative RT-PCR were used to detect genes that are differentially regulated after TBI. In addition, the effect of post-traumatic hypothermia on the expression of selective genes was also studied. Rats (n = 6-8 per group) underwent moderate fluid-percussion (F-P) brain injury with and without hypothermic treatment (33 degrees C/3 h). RNA from 3-h or 24-h survival was analyzed for the expression of IL1-beta, IL2, IL6, TGF-beta2, growth-regulated oncogene (GRO), migration inhibitory factor (MIF), and MCP (a transcription factor). The interleukins IL-1beta, IL-2, and IL-6 and TGF-beta and GRO were strongly upregulated early and transiently from 2- to 30-fold over sham at 3 h, with normalization by 24 h. In contrast, the expressions of MIF and MCP were both reduced by TBI compared to sham. Post-traumatic hypothermia had no significant effect on the acute expression of the majority of genes investigated. However, the expression of TGF-beta2 at 24 h was significantly reduced by temperature manipulation. The mechanism by which post-traumatic hypothermia is protective may not involve a general genetic response of the inflammatory genes. However, specific genes, including TGF-beta2, may be altered and effect cell death mechanisms after TBI. Hypothermia differentially regulates certain genes and may target more delayed responses underlying the secondary damage following TBI.

Animals↗
PubMed2006

Emergency department assessment of mild traumatic brain injury and prediction of post-concussion symptoms at one month post injury.

Mild traumatic brain injury (mTBI) is a common injury and a significant proportion of those affected report chronic symptoms. This study investigated prediction of post-concussion symptoms using an Emergency Department (ED) assessment that examined neuropsychological and balance deficits and pain severity of 29 concussed individuals. Thirty participants with minor orthopedic injuries and 30 ED visitors were recruited as control subjects. Concussed and orthopedically injured participants were followed up by telephone at one month to assess symptom severity. In the ED, concussed subjects performed worse on some neuropsychological tests and had impaired balance compared to controls. They also reported significantly more post-concussive symptoms at follow-up. Neurocognitive impairment, pain and balance deficits were all significantly correlated with severity of post-concussion symptoms. The findings suggest that a combination of variables assessable in the ED may be useful in predicting which individuals will suffer persistent post-concussion problems.

Adult↗
PubMed2006

Severe human traumatic brain injury, but not cyclosporin a treatment, depresses activated T lymphocytes early after injury.

Severe traumatic brain injury (TBI) leads to an immunocompromised state responsible for an increased morbidity and mortality. Our understanding of the mechanisms responsible for this brain damage is incomplete. Damage maybe mediated by a complex cascade of neuroinflammation, and cytokine activation. In addition, translocation and accumulation of T cells in the brain parenchyma could take place and be related to detrimental effects. Our aims in this prospective randomized pilot study, were to detect the early effect of severe TBI upon cell-mediated immunity, to verify if early immunologic impairment correlates with neurologic outcome, and finally, to test the effect of early administration of iv infusion of cyclosporin A upon cell-mediated immunologic function. Forty-nine patients with severe TBI were studied. Thirty-six of these patients received a 24-h intravenous infusion of Cyclosporin A, or two 24-h infusions of the drug. 10 patients were in the placebo group. Three patients, not enrolled in the cyclosporin trial, were studied only for the relationship between cellular immunity, neurological outcome, and infection rate. T cell counts and microbiological cultures were performed in all patients. Sixty-five percent of patients demonstrated reduced T lymphocyte counts on admission. Furthermore, reduction of T cell numbers was related with significantly worse neurologic outcome and an increase in pulmonary infection. There was no significant difference between the placebo and CsA treated patients for the studied immunological parameters, or for incidence of infection. We also observed sequestration/diapedesis of T cells into the brain parenchyma, around contusions, after human TBI and we speculate that this could be responsible for further brain damage.

Adult↗
PubMed2005

Routine and quantitative EEG in mild traumatic brain injury.

This article reviews the pathophysiology of mild traumatic brain injury, and the findings from EEG and quantitative EEG (QEEG) testing after such an injury. Research on the clinical presentation and pathophysiology of mild traumatic brain injury is reviewed with an emphasis on details that may pertain to EEG or QEEG and their interpretation. Research reports on EEG and QEEG in mild traumatic brain injury are reviewed in this setting, and conclusions are drawn about general diagnostic results that can be determined using these tests. QEEG strengths and weaknesses are reviewed in the context of factors used to determine the clinical usefulness of proposed diagnostic tests. Clinical signs, symptoms, and the pathophysiologic axonal injury and cytotoxicity tend to clear over weeks or months after a mild head injury. Loss of consciousness might be similar to a non-convulsive seizure and accompanied subsequently by postictal-like symptoms. EEG shows slowing of the posterior dominant rhythm and increased diffuse theta slowing, which may revert to normal within hours or may clear more slowly over many weeks. There are no clear EEG or QEEG features unique to mild traumatic brain injury. Late after head injury, the correspondence is poor between electrophysiologic findings and clinical symptoms. Complicating factors are reviewed for the proposed commercial uses of QEEG as a diagnostic test for brain injury after concussion or mild traumatic brain injury. The pathophysiology, clinical symptoms and electrophysiological features tend to clear over time after mild traumatic brain injury. There are no proven pathognomonic signatures useful for identifying head injury as the cause of signs and symptoms, especially late after the injury.

Animals↗
PubMed2004

Applied psychophysiology, clinical biofeedback, and rehabilitation neuropsychology: a case study--mild traumatic brain injury and post-traumatic stress disorder.

This article presents a case study of a 39-year-old European American married woman with a history of child and adolescent incest,marital rape, and physical abuse from her husband for more than 10 years. She was referred to a pain clinic for treatment of headaches and Tourette's syndrome. The client was evaluated with the Ackerman-Banks Neuropsychological Rehabilitation Battery to identify neuropsychological strengths and weaknesses. The Vulnerability to Stress Audit was used to identify life events that were positively and negatively influencing her life. The client was treated for mild traumatic brain injury, post-traumatic stress disorder,cognitive difficulties, impulsivity, confabulation, low frustration tolerance, and inability to evaluate and make decisions about socially appropriate behaviors. Treatment involved traditional psychotherapy, hypnosis, cognitive rehabilitation, biofeedback training, electromyography, finger temperature, and blood pressure.

Adult↗
PubMed1998

Family burden and adaptation during the initial year after traumatic brain injury in children.

OBJECTIVE: Traumatic brain injury (TBI) often leads to long-term behavioral and cognitive deficits in children. However, little is known about the burden and psychosocial morbidity of pediatric TBI for families. The purpose of this study was to test the hypothesis that moderate and severe TBI in children has more adverse consequences than orthopedic trauma. DESIGN: The sample was comprised of children between the ages of 6 and 12 recruited from hospital trauma and inpatient units including 53 with severe TBI, 56 with moderate TBI, and 80 with orthopedic injuries not involving central nervous system insult. Measures of injury-related burden, parental distress, and family functioning were administered to the child's primary caregiver at baseline assessment conducted soon after injury and at 6- and 12-month follow-ups. Multivariate repeated measures analysis of covariance was used to examine group differences in these outcomes over time. RESULTS: Caregivers in the severe TBI group reported significantly higher levels of family burden, injury-related stress, and parental psychological symptoms than caregivers in the orthopedic injury group (ORTHO). The groups did not differ with respect to marital distress. Caregivers in the severe TBI group were significantly more likely than caregivers in the ORTHO group to exceed the clinical cutoff on the Brief Symptom Inventory and to report clinically significant levels of family dysfunction at follow-up. CONCLUSIONS: The findings suggest that severe TBI is a source of considerable caregiver morbidity, even when compared with other traumatic injuries. Caregivers in the severe TBI group had persistent stress associated with the child's injury, as well as the reactions of other family members, and a relative risk of clinically significant psychological symptoms nearly twice that of the ORTHO comparison group. These findings underscore the need for interventions that facilitate family adaptation after pediatric TBI.

Adaptation, Psychological↗
PubMed2000

Posttraumatic stress disorder after severe traumatic brain injury.

OBJECTIVE: This study indexed the profile of posttraumatic stress disorder (PTSD) after severe traumatic injury to the brain. METHOD: Patients who sustained a severe traumatic brain injury (N=96) were assessed for PTSD 6 months after the injury with the PTSD Interview, a structured clinical interview based on DSM-III-R criteria. RESULTS: PTSD was diagnosed in 26 (27.1%) of the patients. While only 19.2% (N=5) of the patients with PTSD reported intrusive memories of the trauma, 96.2% (N=25) reported emotional reactivity. Intrusive memories, nightmares, and emotional reactivity had very strong positive predictive values for the presence of PTSD. CONCLUSIONS: These findings indicate that PTSD can develop after severe traumatic brain injury. The predominance of emotional reactivity and the relative absence of traumatic memories in patients with PTSD who suffered impaired consciousness during trauma suggest that traumatic experiences can mediate PTSD at an implicit level.

Adolescent↗
PubMed2004

Lateral automobile impacts and the risk of traumatic brain injury.

STUDY OBJECTIVES: We determine the relative risk and severity of traumatic brain injury among occupants of lateral impacts compared with occupants of nonlateral impacts. METHODS: This was a secondary analysis of the National Highway Traffic Safety Administration's National Automotive Sampling System, Crashworthiness Data Systems for 2000. Analysis was restricted to occupants of vehicles in which at least 1 person experienced an injury with Abbreviated Injury Scale score greater than 2. Traumatic brain injury was defined as an injury to the head or skull with an Abbreviated Injury Scale score greater than 2. Outcomes were analyzed using the chi2 test and multivariate logistic regression, with adjustment of variance to account for weighted probability sampling. RESULTS: Of the 1,115 occupants available for analysis, impact direction was lateral for 230 (18.42%) occupants and nonlateral for 885 (81.58%) occupants. One hundred eighty-seven (16.07%) occupants experienced a traumatic brain injury, 14.63% after lateral and 16.39% after nonlateral impact. The unadjusted relative risk of traumatic brain injury after lateral impact was 0.89 (95% confidence interval [CI] 0.51 to 1.56). After adjusting for several important crash-related variables, the relative risk of traumatic brain injury was 2.60 (95% CI 1.1 to 6.0). Traumatic brain injuries were more severe after lateral impact according to Abbreviated Injury Scale and Glasgow Coma Scale scores. The proportion of fatal or critical crash-related traumatic brain injuries attributable to lateral impact was 23.5%. CONCLUSION: Lateral impact is an important independent risk factor for the development of traumatic brain injury after a serious motor vehicle crash. Traumatic brain injuries incurred after lateral impact are more severe than those resulting from nonlateral impact. Vehicle modifications that increase head protection could reduce crash-related severe traumatic brain injuries by up to 61% and prevent up to 2,230 fatal or critical traumatic brain injuries each year in the United States.

Abbreviated Injury Scale↗
PubMed1998

Rehabilitation after traumatic brain injury in adults.

PURPOSE: Traumatic brain injury (TBI) stands as a major public health problem and one of the most important challenges for neurological rehabilitation. This review discusses advances that have occurred in the past 10 years in rehabilitation after severe TBI in adults. METHOD: First, theoretical concepts, goals of rehabilitation and organization of resources are reviewed. Then specific questions that arise in the rehabilitation of severe TBI patients are considered. RESULTS: Three phases are distinguished in post-traumatic evolution. Acute rehabilitation takes place during coma and arousal states. Specific aims are to prevent orthopaedic and visceral complications, and to provide sensory stimulations with the hope of accelerating arousal. Secondly subacute (generally inpatient) rehabilitation is designed to facilitate and accelerate recovery of impairments, and to compensate for disabilities. Motility, cognition, behaviour, personality and affect should be simultaneously addressed in an holistic approach. Physical as well as psychological independence and self-awareness are the major goals to emphasize. A third, post-acute rehabilitation phase includes outpatient therapy for achieving physical, domestic and social independence, reduction of handicaps and re-entry into the community. CONCLUSIONS: Problems with returning home, obtaining financial independence, driving, returning to work, participating in social relationships and leisure activities, and the importance of psychosocial adjustment and self-acceptance, are outlined. Questions about economic aspects and rehabilitation in the future are addressed.

Activities of Daily Living↗
PubMed2004

Suicidal behavior and mild traumatic brain injury in major depression.

Traumatic brain injury (TBI) is associated with psychiatric illness, suicidal ideation, suicide attempts, and completed suicide. We investigated the relationship between mild TBI and other risk factors for suicidal behavior in major depressive episode. We hypothesized that mild TBI would be associated with suicidal behavior at least partly because of shared risk factors that contribute to the diathesis for suicidal acts. Depressed patients (N = 325) presenting for treatment were evaluated for psychopathology, traumatic history, and suicidal behavior. Data were analyzed using Student t -test, chi-square statistic, or Fisher exact test. A backward stepwise logistic regression model (N = 255) examined the relationship between attempter status and variables that differed in the TBI and non-TBI patients. Forty-four percent of all subjects reported mild TBI. Subjects with TBI were more likely to be male, have a history of substance abuse, have cluster B personality disorder, and be more aggressive and hostile compared with subjects without TBI. They were also more likely to be suicide attempters, although their suicidal behavior was not different from that of suicide attempters without TBI. Attempt status was mostly predicted by aggression and hostility, but not the presence of TBI. Of note, for males, a history of TBI increased the likelihood of being a suicide attempter, whereas the risk was elevated for females regardless of TBI history. Our data suggest that suicidal behavior and TBI share antecedent risk factors: hostility and aggression. Future studies may yield confirmation using a prospective design.

Adult↗
PubMed1995

Long-term potentiation deficits and excitability changes following traumatic brain injury.

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation.

Action Potentials↗