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PubMed1988

The epidemiology of mild, uncomplicated brain injury.

Mild brain injury accounts for a substantial proportion of all persons admitted to a hospital for brain trauma, yet the amount of information on the epidemiology of this problem is quite sparse. Data on mild brain injuries for San Diego County residents injured in 1981 were analyzed for incidence, external cause, prehospital factors, diagnoses, alcohol use, and in-hospital treatment costs. More than 80% of all San Diego County residents hospitalized for an acute brain injury had a mild uncomplicated brain injury: a rate of 130.8 per 100,000 per year. Three quarters of these had an ER Glasgow Coma Scale of 15. Rates are twice as high for males compared to females, with peak occurrence for males at ages 15-19 years. More than 40% of mild brain injuries are caused by motor-vehicle-related events. The most common diagnosis was concussion (80%) or other intracranial injury (14%). Median length of hospital stay was 2-3 days and depended on brain injury diagnosis or Glasgow Coma Scale. Although less than 30% of those aged 15 years and older were blood tested for alcohol, two thirds of those tested had a level of 100 mg% or higher. In-hospital treatment costs for concussion or other mild intracranial injury for San Diego County residents exceeded six million dollars in 1981.

Adolescent↗
PubMed2002

Local and systemic increase in lipid peroxidation after moderate experimental traumatic brain injury.

Traumatic brain injury is a common event associated with neurological dysfunction. Oxidative damage, may contribute to some of these pathologic changes. We used a specific and sensitive marker of lipid peroxidation, the isoprostane 8,12-iso-iPF(2alpha) -VI, to investigate whether local and also systemic lipid peroxidation were induced following lateral fluid percussion (FP) brain injury in the rat. Animals were anesthetized and subjected to lateral FP brain injury of moderate severity, or to sham injury as controls. Urine was collected before anesthesia (baseline), 6 and 24 h after injury. Blood was collected at baseline, 1, 6 and 24 h after injury. Animals were killed 24 h after surgery and their brains removed for biochemical analysis. No significant difference was observed at baseline (preinjury) for urine and plasma 8,12-iso-iPF(2alpha) -VI levels between injured and sham-operated animals. By contrast, plasma and urinary levels increased significantly already at 1 and further increased 24 h following brain injury, when compared to sham-operated animals. Finally, compared with sham, injured animals had a significant increase in brain 8,12-iso-iPF(2alpha) -VI levels. These results demonstrate that moderate brain injury induces widespread brain lipid peroxidation, which is accompanied by a similar increase in urine and plasma. Peripheral measurement of 8,12-iso-iPF(2alpha) -VI levels after brain injury may be a reliable marker of brain oxidative damage.

Animals↗
PubMed2002

Interleukin-1beta messenger ribonucleic acid and protein levels after fluid-percussion brain injury in rats: importance of injury severity and brain temperature.

OBJECTIVE: Posttraumatic temperature manipulations have been reported to significantly influence the inflammatory response to traumatic brain injury (TBI). The purpose of this study was to determine the temporal and regional profiles of messenger ribonucleic acid (mRNA) expression and protein levels for the proinflammatory cytokine interleukin-1beta (IL-1beta), after moderate or severe TBI. The effects of posttraumatic hypothermia (33 degrees C) or hyperthermia (39.5 degrees C) on these consequences of TBI were then determined. METHODS: Male Sprague-Dawley rats underwent fluid-percussion brain injury. In the first phase of the study, rats were killed 15 minutes or 1, 3, or 24 hours after moderate TBI (1.8-2.2 atmospheres), for reverse transcription-polymerase chain reaction analysis. Other groups of rats were killed 1, 3, 24, or 72 hours after moderate or severe TBI (2.4-2.7 atmospheres), for protein analysis. In the second phase, rats underwent moderate fluid-percussion brain injury, followed immediately by 3 hours of posttraumatic normothermia (37 degrees C), hyperthermia (39.5 degrees C), or hypothermia (33 degrees C), and were then killed, for analyses of protein levels and mRNA expression. Brain samples, including cerebral cortex, hippocampus, thalamus, and cerebellum, were dissected and stored at -80 degrees C until analyzed. RESULTS: The findings indicated that mRNA levels were increased (P < 0.05) as early as 1 hour after TBI and remained elevated up to 3 hours after moderate TBI. Although both moderate and severe TBI induced increased levels of IL-1beta (P < 0.05), increased protein levels were also noted in remote brain structures after severe TBI. Posttraumatic hypothermia attenuated IL-1beta protein levels, compared with normothermia (P < 0.05), although the levels remained elevated in comparison with sham values. In contrast, hyperthermia had no significant effect on IL-1beta levels, compared with normothermic values. Posttraumatic temperature manipulations had no significant effect on IL-1beta mRNA levels. CONCLUSION: Injury severity determines the degree of IL-1beta protein level elevation after TBI. The effects of posttraumatic hypothermia on IL-1beta protein levels (an important mediator of neurodegeneration after TBI) may partly explain the established effects of posttraumatic temperature manipulations on inflammatory processes after TBI.

Animals↗
PubMed2005

Dose-dependent neuronal injury after traumatic brain injury.

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

Analysis of Variance↗
PubMed1996

Dextrorphan reduces infarct volume, vascular injury, and brain edema after ischemic brain injury.

Focal cerebral ischemia confined to the cerebral cortex in the right middle cerebral artery (MCA) territory was induced by temporary ligation of the MCA and both common carotid arteries (CCAs). Reperfusion was initiated by releasing all three arterial occlusions after 90 min of ischemia. Infarct volume was morphometrically measured after triphenyltetrazolium chloride staining 24 h postischemia. Blood-brain barrier breakdown was assessed 4 h postischemia by measuring vascular permeability to fluorescein isothiocyanate-conjugated dextran (FITC-D), a macromolecule tracer. Ischemic brain edema was measured based on percent water content, 24 h postischemia. Dextrorphan (DX) 20-10 mg/kg given ip 15 min before ischemia reduced infarct volume in a dose-dependent manner with an apparent U-shaped dose-response curve; best protection was observed at 30 mg/kg. Posttreatment at 30 min, but not 60 min, was still effective. DX (30 mg/kg, given 15 min before ischemia) also reduced the postischemic increase in vascular permeability and brain edema in the right MCA cortex. Results from this study support the idea that NMDA receptor activation contributes to blood-brain barrier breakdown and brain edema after ischemic insults

Analysis of Variance↗
PubMed1997

Measurement and treatment of agitation following traumatic brain injury: II. A survey of the Brain Injury Special Interest Group of the American Academy of Physical Medicine and Rehabilitation.

OBJECTIVE: Determine national patterns of measuring and treating agitation after traumatic brain injury (TBI) by physiatrists with expressed interest in treating TBI survivors. DESIGN: A 70% random sample of members of the Brain Injury Special Interest Group of the American Academy of Physical Medicine and Rehabilitation was surveyed by telephone. MAIN OUTCOME MEASURE: The survey instrument was designed to determine the most common pharmacologic interventions for agitation and, where possible, match each drug with the target behavioral and cognitive characteristics for which it is prescribed. Data were also collected on the manner in which participants measured agitation and judged treatment efficacy. RESULTS: One hundred twenty-nine of 157 responded, yielding an 82% response rate. The majority of respondents were not measuring agitation in a standard fashion. The five most frequently prescribed drugs by the expert stratum were carbamazepine, tricyclic antidepressants (TCAs), trazodone, amantadine, and beta-blockers. In comparison, the nonexperts most often reported prescribing carbamazepine, beta-blockers, haloperidol, TCAs, and benzodiazepines. Desyrel (p = .06) and amantadine (p = .001) were significantly more likely to be chosen by experts than by nonexperts. Experts chose haloperidol significantly less often than nonexperts (p = .01). Prescription of sedating drugs such as haloperidol or benzodiazepines was not found to be associated with the acuity of injury of TBI patients in the respondent's practice, practice setting, or years of practice since completing residency. Choice of haloperidol to treat agitation was not significantly associated with the degree to which explosive anger, verbal aggression, or physical aggression were considered important to the respondent's definition of agitation. CONCLUSIONS: The majority of physiatrists surveyed did not formally measure agitation. Treatment strategies differ significantly between general physiatrists and those who specialize in the treatment of patients with TBI. The breadth of pharmacologic agents and strategies identified in this survey probably reflects the lack of research specific to the pathophysiology of the disorder of posttraumatic agitation.

Adult↗
PubMed1997

Definition of agitation following traumatic brain injury: I. A survey of the Brain Injury Special Interest Group of the American Academy of Physical Medicine and Rehabilitation.

OBJECTIVE: To determine national patterns of defining agitation after traumatic brain injury (TBI) by physiatrists with expressed interest in treating TBI survivors. DESIGN: A random sample of 70% of the members of the Brain Injury Special Interest Group (SIG) of the American Academy of Physical Medicine and Rehabilitation (AAPM&R) were surveyed by telephone. RESULTS: The 129 members who responded yielded an 82% response rate. Respondents rated 18 characteristics from established rating scales on a 5-point scale according to each characteristic's relation to its clinical definition of agitation. Physical aggression, explosive anger, increased psychomotor activity, impulsivity, verbal aggression, disorganized thinking, perceptual disturbances, and reduced ability to maintain or appropriately shift attention were rated by at least 50% of the sample as very important or essential to agitation. Delirium, as defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM), has been proposed as a standard definition of agitation. The degree to which all characteristics from the 3rd revised edition of the DSM (DSM-IIIR), considered together, were perceived to relate to agitation predicted 24% of the degree to which the term "delirium" was perceived to relate to agitation (Canonical correlation r = .48, p = .0002). Physicians' ratings of individual delirium characteristics from the DSM-IIIR were examined to determine if a sufficient number were similarly ranked to fulfill the diagnostic criteria for delirium. A significant number of physicians rated diagnostic criteria for delirium in one direction, yet did not rank the term "delirium" accordingly (McNemar's p = .04). CONCLUSIONS: There is considerable variation among physiatrists in their rating of characteristics that define agitation. Many define agitation during the acute recovery phase as posttraumatic amnesia plus an excess of behavior such as aggression, disinhibition, and/or emotional lability. Less support was given to defining agitation by the DSM-IIIR or DSM-IV diagnostic criteria for delirium. Delirium appears related to, but is not sufficient for, a diagnosis of agitation.

Adult↗
PubMed2006

Serum biomarkers after traumatic and hypoxemic brain injuries: insight into the biochemical response of the pediatric brain to inflicted brain injury.

Inflicted traumatic brain injury (iTBI) involves a combination of mechanical trauma and hypoxemia. Serum biomarker concentrations may provide objective information about their relative importance to the pathophysiology of iTBI. We compared the time course of neuron-specific enolase (NSE), S100B and myelin basic protein after pediatric hypoxic-ischemic brain injury, iTBI and noninflicted TBI (nTBI). The time to reach peak concentrations of all three biomarkers was shorter after nTBI. Initial and peak S100B, initial and peak myelin basic protein and peak NSE concentrations were no different between the three groups. Initial NSE concentration was highest after nTBI. These results suggest that the biochemical response of the brain to iTBI is distinct from the response to nTBI and shares temporal similarities with hypoxic-ischemic brain injury. This may have important implications for the treatment and prognosis of children with iTBI.

Age Factors↗
PubMed2002

Secondary injury in traumatic brain injury patients--a prospective study.

OBJECTIVE: Secondary insults of hypotension and hypoxia significantly impact on outcome in patients with traumatic brain injury (TBI). More than 4 hours' delay in evacuation of intracranial haematomas has been demonstrated to have an additional impact on outcome. The objective of this study was to document the incidence of these preventable secondary insults in patients admitted with moderate or severe brain injury. METHODOLOGY: All moderate and severe head injury patients admitted to Groote Schuur Hospital over a 3-month period were studied prospectively. Data were obtained from ambulance dockets, referral letters, patient charts and attending medical staff. Preventable secondary insults (hypotension, hypoxia) and time delay to assessment and surgery were documented. Outcome was assessed using the Glasgow outcome scale (GOS) at discharge or outpatient follow-up. RESULTS: Ninety-six patients were studied. Forty-nine patients experienced at least one recorded preventable event of hypoxia or hypotension. Seventeen had an intracranial haematoma requiring evacuation. The mean time interval between injury and surgery was 455 minutes. No haematoma was evacuated within 4 hours of injury. Patients referred via a primary or secondary care facility experienced a mean additional delay of 70 minutes. These results demonstrated a significant incidence of secondary injury and delay to assessment and surgery. We believe that education and a raised awareness of the impact of secondary insults may have a positive impact on TBI outcome in our referral area.

Adolescent↗
PubMed1999

Does growth hormone augment brain edema caused by brain injury? A study with a freeze brain injury model in the rat.

OBJECTIVE: Because of the known sodium and water retention associated with growth hormone (GH) therapy, it is crucial to evaluate the safety of GH after brain injury. To clarify this issue, we investigated whether GH affects brain edema in a rat brain freeze-injury model. METHODS: Male Wistar rats (n = 29) were divided into four groups according to the substance injected (GH vs. normal saline) and whether the brain was injured or not. The subcutaneous injections of GH (0.8 IU/kg) or saline were given 24 hours apart. In the injury groups, after the second injection, an aluminum rod (4-mm diameter) cooled to -50 degrees C was placed on the exposed dura mater in the right parietal region for 4 minutes, under anesthesia. At 4 hours after the insult, brain and skeletal muscle were excised and their water content was measured by drying. RESULTS: Freeze injury of the brain caused an increase in water and sodium content in skeletal muscle. GH injection augmented this edema in skeletal muscle. Freeze injury of the brain also caused an increase in water and sodium content in the injured hemisphere of the brain. GH injection did not exacerbate this edema in injured brain tissue. Neither freeze injury nor GH injection caused brain edema in the noninjured hemisphere or in the cerebellum. CONCLUSION: GH administration did not augment brain edema caused by brain injury in our model.

Animals↗
PubMed2006

Response of the contralateral hippocampus to lateral fluid percussion brain injury.

Traumatic brain injury is a leading cause of death and disability in the United States. Pathological examinations of humans and animal models after brain injury demonstrate hippocampal neuronal damage, which may contribute to cognitive impairments. Data from our laboratories have shown that, at 1 week after brain injury, mice possess significantly fewer neurons in all ipsilateral hippocampal subregions and a cognitive impairment. Since cognitive function is distributed across both cerebral hemispheres, the present paper explores the morphological and physiological response of the contralateral hippocampus to lateral brain injury. We analyzed the contralateral hippocampus using design-based stereology, Fluoro-Jade (FJ) histochemistry, and extracellular field recordings in mice at 7 and 30 days after lateral fluid percussion injury (FPI). At 7 days, all contralateral hippocampal subregions possess significantly fewer healthy neurons compared to sham-injured animals and demonstrate FJ-positive neuronal damage, but not at 30 days. Both the ipsilateral and contralateral dentate gyri demonstrate significantly increased excitability at 7 days post-injury, but only ipsilateral dentate gyrus hyperexcitability persists at 30 days compared to sham. In the contralateral hippocampus, the transient decrease in the number of healthy neurons, concomitant with FJ damage, and electrophysiological alterations establish a stunned period of cellular and circuit dysfunction. The return of healthy neuron number, absence of FJ damage, and sham level of excitability in the contralateral hippocampus suggest recovery of structure and function by 30 days after injury. The cognitive recovery observed after human traumatic brain injury may stem from a differential injury exposure and time course of recovery between homologous regions of the two hemispheres.

Animals↗
PubMed2006

Hypopituitarism after acute brain injury.

Acute brain injury has many causes, but the most common is trauma. There are 1.5-2.0 million traumatic brain injuries (TBI) in the United States yearly, with an associated cost exceeding 10 billion dollars. TBI is the most common cause of death and disability in young adults less than 35 years of age. The consequences of TBI can be severe, including disability in motor function, speech, cognition, and psychosocial and emotional skills. Recently, clinical studies have documented the occurrence of pituitary dysfunction after TBI and another cause of acute brain injury, subarachnoid hemorrhage (SAH). These studies have consistently demonstrated a 30-40% occurrence of pituitary dysfunction involving at least one anterior pituitary hormone following a moderate to severe TBI or SAH. Growth hormone (GH) deficiency is the most common pituitary hormone disorder, occurring in approximately 20% of patients when multiple tests of GH deficiency are used. Within 7-21 days of acute brain injury, adrenal insufficiency is the primary concern. Pituitary function can fluctuate over the first year after TBI, but it is well established by 1 year. Studies are ongoing to assess the effects of hormone replacement on motor function and cognition in TBI patients. Any subject with a moderate to severe acute brain injury should be screened for pituitary dysfunction.

Brain Injuries↗
PubMedDate not supplied

Who's teaching whom? A study of family education in brain injury.

Acquired brain injury affects every aspect of life-cognition, emotional response, physical ability, and behavior. Although the changes affect the person with the brain injury most directly, people who provide care also experience changes. Family members play a critical role in the long-term rehabilitation of a person with a brain injury. The demands involved can deplete the most resourceful of families. Therefore, they must have multiple resources available to them to ensure the best possible outcome for the brain-injured member. A formalized family education program is an important resource in helping family members understand the brain injury and their ability to cope with and assist in the rehabilitation process (Maitz & Sachs, 1995). This article reports a qualitative study that measured the perceptions of 15 families that received an educational program about the care of a person with a brain injury.

Adolescent↗
PubMedDate not supplied

The effect of hypothermia and hyperthermia on acute brain injury.

The brain is extraordinarily susceptible to changes in temperature. Hyperthermia has been shown to exacerbate the biochemical cascade of secondary brain injury. Inversely, hypothermia limits the damaging effects of secondary brain injury. There has been a great deal of investigation regarding the detrimental effects of hyperthermia and the neuroprotection of hypothermia in animal studies. Within the last decade, clinical trials have begun to establish how the brain reacts to both temperature extremes. In the future, studies of hypothermia will continue in the quest of the optimal timing and degree of hypothermia. Hyperthermia will be examined in depth for its detrimental effects on an injured brain. Interventions for the prevention and treatment of hyperthermia will be explored. Nurses will implement cooling strategies to induce hypothermia, applying interventions to prevent complications, and they will also diagnose hyperthermia, deciding when and if to intervene pharmacologically and therapeutically. These advanced nursing actions will be guided by knowledge and understanding of available evidence. This article presents the pathophysiology of secondary brain injury and how it is affected by both hypothermia and hyperthermia. A review of the research leading up to clinical trials is explored, as well as a discussion of the future of temperature modulation for the brain injury patient. This information will help healthcare providers understand the effect that both hypothermia and hyperthermia have on the acutely injured brain.

Acute Disease↗
PubMed2000

Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury.

Prior evidence indicates that synaptically-released zinc enters postsynaptic neurons in toxic excess during ischemia and seizures. In addition, prevention of this zinc translocation has been shown to be neuroprotective in both ischemia and seizures. Here we show evidence that the same translocation of zinc from presynaptic boutons into postsynaptic neurons occurs after mechanical injury to the brain. Specifically, using a rat model of traumatic brain injury, we show that trauma is associated with (i) loss of zinc from presynaptic boutons (ii) appearance of zinc in injured neurons, and (iii) neuroprotection by intraventricular administration of a zinc chelator just prior to brain impact. The possible use of zinc chelators for neuroprotection after head trauma is considered.

Aminoquinolines↗
PubMed2000

Influences of secondary injury following traumatic brain injury in developing versus adult rats.

Hypoxia and hypotension are both common findings following traumatic brain injury occurring with a frequency of up to 46% according to data of the Traumatic Coma Data Bank. In the present study the influence of secondary injury on intracranial pressure and the cardiovascular response is investigated in developing rats. Differences from adult rats are determined. Diffuse brain injury was produced in intubated and ventilated 17-20 days old Sprague-Dawley rats (N = 16) using a modification of the Marmarou-model. Hypoxia was induced by reducing O2-concentration to 8% lasting for 15/30 min. Mean arterial blood pressure recordings and intracranial pressure recordings were performed continuously. Animals were divided into two groups, sustaining hypoxia alone (N = 9) and trauma/hypoxia (N = 7). The results were compared to readings in adult animals subjected to hypoxia (N = 5) and trauma/hypoxia (N = 5) (450 gm/150 cm). Immediately following the onset of hypoxia in the developing rat, MABP decreased from 76.5 +/- 13 mm Hg to 35.8 +/- 7 mm Hg. In the adult rat the decrease was more marked (from 93.3 +/- 8 mm Hg to 33.5 +/- 5.7 mm Hg) (p < 0.05). Mortality rate in developing rats with trauma/hypoxia was 43% with no significant change of ICP (from 13 +/- 5.2 to 22.3 +/- 11). All adult animals recovered following trauma/hypoxia with no relevant ICP-increase within one hour post-trauma. Hypoxia induces hypotension in adult and developing rats. However, developing rats appear to be more vulnerable to hypoxia associated with trauma.

Age Factors↗