Traumatic brain injury: A hidden consequence for battered women.

The inability of substantial numbers of battered women to terminate or extricate themselves from violent relationships is of grave concern to clinical practitioners. Despite professional intervention, many victims of domestic violence return to the batterer and to repetitive battering, demonstrating that, for these women, traditional psychosocial interventions are ineffective. In a sample of 53 battered women, 92% reported having received blows to the head in the course of their battering; 40% reported loss of consciousness. Correlations between frequency of being hit in the head and severity of cognitive symptoms were significant, strongly suggesting that battered women should be routinely screened for traumatic brain injury and postconcussive syndrome. Development of treatment strategies to address the potentially damaging sequelae of head trauma in this population is essential. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Traumatic brain injury and memory: The role of hippocampal atrophy.

In traumatically brain-injured (TBI) patients (n?=?83), memory performance was examined on the Warrington Recognition Memory Test, Rey-Osterrieth Complex Figure, and the Logical Memory and Visual Reproduction subtests of the Wechsler Memory Scale-Revised in relationship to time postinjury and structural changes based on MRI volumetry, including hippocampus volume. Significant trauma-induced changes were observed, including hippocampal atrophy. Structure-function relationships generally became significant only after 90 days postinjury. Memory tended to relate more to the degree of hippocampal atrophy, particularly left hippocampus, than to nonspecific indicators such as the temporal horns or the ventricle-to-brain ratio. A stronger relationship with left versus right hippocampus was evident for measures of verbal and supposedly nonverbal memory. These results are discussed with regard to the role the hippocampus may play in a neural system of memory. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Traumatic brain injury in children and adolescents: psychiatric disorders at two years

OBJECTIVE: To extend findings regarding predictive factors of psychiatric outcome from the first to the second year after traumatic brain injury (TBI) in children and adolescents. METHOD: Subjects were children aged 6 to 14 years at the time they were hospitalized after TBI. The study used a prospective follow-up design. Assessments of preinjury psychiatric, behavioral, adaptive functioning, family functioning and family psychiatric history status were conducted. Severity of injury was assessed by standard clinical scales and neuroimaging was analyzed. The outcome measure was the presence of a psychiatric disorder, not present before the injury ("novel"), during the second year after TBI. RESULTS: Fifty subjects enrolled, and the analyses focused on 42 subjects followed at 24 months. Severity of injury, preinjury family function, and preinjury lifetime psychiatric history predicted the development of a "novel" psychiatric disorder present in the second year. CONCLUSION: These data suggest that there are children, identifiable through clinical assessment, at increased risk for "novel" psychiatric disorders in the second year after TBI.     

Traumatic brain injury: Psychological and medical factors related to rehabilitation outcome.

Examined the relationship of medical and psychological factors of adaptive physical functioning (APF) at discharge and length of rehabilitation stay following traumatic brain injury. 32 Ss (aged 16–55 yrs) with severe traumatic brain injury underwent interdisciplinary rehabilitation evaluations, including the MMPI, WAIS, and the Wechsler Memory Scale, at admission to and discharge from an inpatient rehabilitation program. Results suggest that the actual status of APF at discharge was related to initial assessments of medical, not psychological, factors. However, psychological factors were related to relative improvement in APF when change occurred. Even Ss who were minimally aware of their physical abilities and limitations at admission improved in their APF during treatment. Length of rehabilitation stay was determined by both physical and psychological functioning. (13 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Traumatic brain injury alters synaptic homeostasis: implications for impaired mitochondrial and transport function

This study utilized a unilateral controlled cortical impact model of traumatic brain injury to assess disruptions of synaptic homeostasis following trauma. Adult rats were subjected to a moderate (2 mm) cortical deformation and synaptosomes were prepared from the entire ipsilateral (injured) hemisphere or dissected into different regions (hippocampus, injured cortical area including penumbra, residual hemisphere) at various times postinjury (10 and 30 min, and 1, 6, and 24 h). Synaptosomes from the corresponding regions of the contralateral hemisphere were used as controls to assess alterations in synaptic ATP levels, lipid peroxidation, and glutamate and glucose transport. The results demonstrate significant time-dependent alterations in synaptic homeostasis, which included an immediate reduction in ATP levels, coupled with a significant increase in lipid peroxidation within 30 min postinjury. Lipid peroxidation demonstrated a biphasic response with elevations observed 24 h postinjury, a time at which decreases in glutamate and glucose transport occurred. These results suggest that disruption of synaptic homeostasis is an extremely early event following trauma that should be considered when designing pharmacological interventions.     

Traumatic injury of ciliary ganglion

The authors report a case in which slight cranial trauma was followed by manifestations of damage to the right ciliary ganglion. After 3 weeks the signs of damage began to regress and disappeared completely. Laboratory investigations failed to demonstrate any abnormalities. Apart from this trauma there were no other detectable causes, and especially there were no history data suggesting past infection, botulism or syphilis. The mechanism of ciliary ganglion injury is not known (contusion, haematoma, oedema etc.).     

Traumatic brain injury in the developing rat: effects of maturation on Morris water maze acquisition

Previous work has demonstrated that postnatal and adult rats show different physiological responses to lateral fluid percussion (FP) brain injury. Compared to adult animals, the younger rats showed longer apnea and shorter unconsciousness, and sustained hypotension at all injury severities, with higher mortality following severe traumatic brain injury (TBI). To determine if these younger rats exhibit differential cognitive impairments, the Morris water maze (MWM) was used to compare the degree of spatial learning deficits between moderately injured postnatal day 17 (P17), P28, and adult rats, as well as their age-matched controls. Comparisons between shams of different ages showed a maturational time course for MWM acquisition, where adult rats learned the task 34-58% faster than younger age groups. Injured adults showed escape latency deficits throughout the entire training period, took 39% fewer direct paths to the platform during training, took 24% longer to reach criterion performance, and showed poor probe trial performance than adult shams. Injured P28s exhibited escape latency deficits during the first week, with 23% more trials to criterion and 24% fewer direct paths compared to P28 shams. In contrast, injured P17 rats showed no significant difference from age-matched controls in terms of escape latency, number of direct paths taken, or time to criterion performance. This work suggests that, upon surviving the insult, P17 injured rats show remarkable sparing compared to P28 and adult injured animals.     

外伤性迟发性脑血肿的CT诊断

目的:总结23例颅内迟发血肿的CT表现,以期进一步提高对该病的重视.方法:23例头部外伤患者均行多次CT扫描.结果:23例外伤患者首次CT均未发现明显血肿,隔时症状加重,恶心呕吐,病情恶化,CT复查发现有脑血肿存在,10例中线结构偏移,出现脑疝.结论:外伤病人首次CT扫描没有发现脑血肿,对症治疗后病情不见好转,症状加重者应立即CT扫描,以便及时明确诊断,采取正确的治疗方法.     

Traumatic brain injury, polytrauma, and pain: Challenges and treatment strategies for the polytrauma rehabilitation.

Problem: Chronic pain conditions are common sequelae of traumatic brain injury (TBI). Unfortunately, the incidence of TBI among personnel deployed for Operations Enduring Freedom and Iraqi Freedom (OEF/OIF) is significant, and there is growing evidence that ongoing pain, particularly headaches, will be a primary concern for these individuals. Objective: This article synthesizes empirical data from civilian and veteran populations and clinical experience with OEF/OIF personnel with polytrauma to provide recommendations for the assessment and treatment of chronic pain among those with TBI. Conclusions: The available data signal the need for the incorporation of early and aggressive pain management strategies into existing treatment models. Challenges to providing effective pain management for OEF/OIF veterans are numerous and include comorbid cognitive, medical, and emotional impairments that complicate readjustment to civilian life. It is likely that the problem of polytrauma pain and associated comorbid conditions such as posttraumatic stress disorder and postconcussive syndrome will require the development of integrated approaches to clinical care which bridge traditional subspecialty divisions. A proposed model of treatment is presented. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Traumatic injury induces interleukin-6 production by human astrocytes

The brain is being evaluated as a de novo source of cytokines. Because recent evidence indicates that interleukin-6 (IL-6) may influence blood-brain barrier function and vascular permeability, we have sought to determine whether mechanical injury can directly induce in situ cerebral IL-6 production. Adult human astrocyte cultures were subjected to mechanical injury by the in vitro method of fluid percussion barotrauma, developed in our laboratory. Serial supernatant samples were collected for 8 h and evaluated for IL-6 activity using a proliferation assay employing the dependent B cell hybridoma cell line, B9. At optimum injury, the IL-6 level became significantly (P < 0.0001, analysis of variance) elevated from baseline 2 h after trauma and continued to increase over the observation period. Our study shows that following mechanical injury human astrocytes produce IL-6, which may contribute to post-traumatic cerebrovascular dysfunction. Elucidating the precise role of intracerebral cytokines is essential to our understanding of the mechanism responsible for post-traumatic cerebrovascular dysfunction.     

Traumatic brain injury causes delayed motor and cognitive impairment in a mutant mouse strain known to exhibit delayed Wallerian degeneration

Delayed Wallerian degeneration after neuronal injury is a feature of the C57BL/Wld(s) mouse mutant. In the present study, we examined the effect of unilateral controlled cortical impact (CCI) on motor and cognitive performance in C57BL/6 and C57BL/Wld(s) mice. Performance on a beam-walking task was impaired in both injured groups over the first 3 weeks; however, between 28 and 35 days post injury, C57BL/6 mice continued to improve whereas C57BL/Wld(s) mice showed increased footfaults. In a spatial learning task, C57BL/Wld(s) animals performed consistently better than C57BL/6 mice when tested 7-10 days and 14-17 days following CCI. C57BL/Wld(s) mice also demonstrated improved working memory performance as compared with C57BL/6 mice when trained on days 21-22 after injury; this effect was lost on days 23 and 24, and was not evident in other animals tested in the same task at 28-31 days following injury. These results indicate a marked delay in motor and cognitive impairment following CCI in C57BL/Wld(s) mice compared with injured C57BL/6 controls. This is consistent with previous work showing delayed temporal evolution of neuronal degeneration in C57BL/Wld(s) mice and suggests CCI may be a suitable model for examining the functional consequences of traumatic brain injury (TBI) in genetically altered mice.     

Perinatal hypoxic-ischemic brain injury

A highly sensitive radioimmunoassay for the measurement of plasma prostaglandins A and B, expressed in equivalents of PGA1, is described. This method was used for the measurement of prostaglandins A and B (PGA/B) in 23 healthy volunteers and 25 hypertensive patients. The PGA/B concentration in peripheral venous plasma of 23 healthy normotensive subjects is 115 +/- 15 pg/ml. The repeated measurement of the same plasma samples kept frozen for 60 days at -20 degrees C shows mean 194% increase of PGA/B concentration. The major site of synthesis of PGA/B seems to be the kidney. However in two patients PGA/B concentration in arterial blood was greater than in venous blood suggesting the possibility of cardio-pulmonary synthesis. The major site of inactivation is the hepatic circulation, as PGA/B concentration in hepatal venous blood is by 30% lower than in vena caval blood. The arterial concentration is 3% lower than venous PGA/B demonstrating very low pulmonary inactivation. Therefore the prostaglandins of the A and B series may represent a "circulating hormone". The plasmatic PGA/B is significantly increased in reno-vascular and essential hypertension.     

Perceptions of care access: the experience of rural and urban women following brain injury

To examine care access among women with brain injuries, a qualitative, phenomenological study was conducted. Twenty-one women with acquired brain injuries were recruited for the inquiry, representing rural and urban regions of Colorado. The phenomenological approach allowed the investigators to examine the shared experiences of women with brain injuries as they sought rehabilitative supports and services, and attempted to re-enter their lives and communities. Each woman was interviewed one or two times, the interviews were transcribed and then coded and analysed by both authors separately. Thematic analysis of the data revealed two major emergent themes: issues surrounding diagnosis and barriers to accessing care. A total of 10 women interviewed experienced difficulty obtaining a diagnosis of brain injury and experienced serious personal and professional consequences as a result. All the women experienced barriers to accessing care, including problems with service providers and service systems, financial challenges, travelling for services, lack of information or services in their area, lack of care coordination and funneling. Some of the barriers cannot be changed secondary to cost, efficiency and logistics. Other barriers, could be changed through education, training and policy making.     

Traumatic spinal cord injury in Arkansas, 1980 to 1989

To develop and implement target prevention strategies, we studied the causes of spinal cord injuries in Arkansas and the groups most affected by SCI. Any Arkansas resident with a spinal cord injury who satisfied the state registry criteria was defined as a subject. Transportation-related incidents caused 319 (49.5%) of the SCIs. Males 15 to 24 years of age experienced the highest incidence of SCI because of transportation and sport-related injuries. The rate of SCI from falls was 2.8 times higher for people 65 years of age and older than for people 64 years of age and younger. Minority males 15 to 44 years of age were at the greatest risk of violence-related SCIs. More intervention is needed in the areas of transportation and sport-related causes involving males 15 to 24 years of age, fall-related causes involving the elderly, and violence-related causes involving minority males 15 to 44 years of age.     

Traumatic head injury: A challenge to rehabilitation psychologists.

Traumatic head injury is a tragedy for all whom it affects. Many families of injured individuals report that the most painful aspects of the injury are the lack of accurate information available to them at all points following the injury and the fact that, because a head injury's effects are so different from those of other illnesses and injuries, no one seems to understand. It is hoped that this Special Issue of Rehabilitation Psychology will not only help more people to understand, but will also impel some readers to participate in the search for answers. In pulling these papers together, I struggled with the question of whether to include papers from the wide spectrum of rehabilitation efforts in which psychologists are involved (including neuropsychological assessment, cognitive retraining, vocational rehabilitation, etc.), or to focus on one major area. Given the increasing number of books that provide the broader perspective, I have chosen the latter route, including papers dealing with the psychosocial issue that is a prerequisite for success in other areas—how patients and their families come to terms with the injury and its consequences. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cytokines and perinatal brain injury

A rapidly expanding body of data provides support for the hypothesis that pro-inflammatory cytokines including interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) are expressed acutely in injured brain and contribute to progressive neuronal damage. Little is known about the pathogenetic role of these cytokines in perinatal brain injury. Recent experimental studies have incorporated two closely related in vivo perinatal rodent brain injury models to evaluate the role(s) of pro-inflammatory cytokines in the progression of neuronal injury: a perinatal stroke model, elicited by unilateral carotid artery ligation and subsequent timed exposure to 8% oxygen in 7-day-old rats, and a model of excitotoxic injury, elicited by stereotactic intra-cerebral injection of the selective excitatory amino acid agonist NMDA. Each of these lesioning methods results in reproducible, quantifiable focal forebrain injury at this developmental stage. Acute brain injury, evoked by cerebral hypoxia-ischemia or excitotoxin lesioning, results in transient marked increases in expression of IL-1 beta, and TNF-alpha mRNA in brain regions susceptible to irreversible injury, and there is evidence that pharmacological antagonism of IL-1 receptors can attenuate injury in both models. Recent studies also suggest that complementary strategies, based on pharmacological antagonism of platelet activating factor and on neutrophil depletion can also limit the extent of irreversible injury. In summary, current data suggest that pro-inflammatory cytokines contribute to the progression of perinatal brain injury, and that these mediators are important targets for neuroprotective interventions in the acute post-injury period.