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PubMed1993

Mechanisms of brain injury.

Head injuries vary widely in their etiology, pathophysiology, clinical presentation, and optimal treatment strategies. Broadly speaking, there are two categories of brain injury: focal injuries and diffuse injuries. Focal brain injuries, which are usually caused by direct blows to the head, comprise contusions, brain lacerations, and hemorrhage leading to the formation of hematoma in the extradural, subarachnoid, subdural, or intracerebral compartments within the head. Diffuse brain injuries, which are usually caused by a sudden movement of the head, comprise classical brief cerebral concussion and more prolonged posttraumatic coma, also known as diffuse axonal injury. Primary traumatic effects involve neural or vascular elements of the brain, which can be affected by delayed effects such as deafferentation or secondary events such as ischemia, swelling, cerebral edema, and increased intracranial pressure. Axonal damage at the node of Ranvier results in a traumatic defect in the axonal membrane that causes the excessive accumulation of calcium ions within the intracellular compartment of the axon. Brain ischemia can result in a similar effect, further increasing the accumulation of calcium ions, which can lead to axonal degeneration. Injury-specific treatments are now being designed to alter the various pathophysiological mechanisms of brain injury.

Axons↗
PubMed2003

The effects of combined fluid percussion traumatic brain injury and unilateral entorhinal deafferentation on the juvenile rat brain.

The current study was designed to address the effects of traumatic brain injury (TBI) on plasticity and reorganization in the juvenile brain. Given that two of the major pathological sequelae of TBI involve a generalized neuroexcitation insult and diffuse axonal injury, we have employed models of these pathologies, delivered either independently or in combination, to examine their effects on injury-induced synaptic reorganization of the dentate gyrus in the developing rat. Postnatal day 28 rats received either sham, central fluid percussion traumatic brain injury (TBI), unilateral entorhinal cortical lesion (UEC), or TBI+UEC (TUEC) injury. Cognitive performance was assessed in the Morris water maze (MWM) between 11 and 15 days post-injury and the brains were processed for synaptophysin immunohistochemistry and routine electron microscopy. The MWM results revealed that TBI or UEC lesions delivered independently do not produce significant morbidity in P28 rats. However, when these injuries are combined, they reveal significant deficits in the MWM, accompanied by measurable changes in the distribution of presynaptic synaptophysin immunoreactivity over the deafferented dentate molecular layer. These observations are further supported by qualitative ultrastructural alterations in synaptic architecture in the same subregions of the dentate neuropil. The present findings show that the resilience of the immature brain following TBI is reduced when neuroexcitatory insult is combined with deafferentation. Moreover, when deafferented tissue is assessed morphologically, evidence exists for aberrant plasticity and abnormal synaptic reorganization in the juvenile brain.

Animals↗
PubMed1999

Peripheral nerve injection injury with antiemetic agents.

Antiemetics are widely used drugs, frequently administered to alleviate postoperative and postchemotherapeutic nausea and vomiting. While antiemetics do not induce peripheral neurotoxicity when administered systemically, it is not known whether peripheral nerve injury can occur as a result of inadvertent intraneural injection during intramuscular administration. The purpose of this study was to characterize the neurotoxic effect of three commonly used antiemetic agents (promethazine, dimenhydrinate, and prochlorperazine) as compared to saline in the rat sciatic nerve model. Intrafascicular and extrafascicular injection as well as direct application of the antiemetic drugs were performed. Nerves were harvested at 2 weeks postoperatively for histology and morphometry, with an additional sacrifice point at 8 weeks for the intrafascicular injection group. Injection injuries caused by antiemetic drugs differed depending on the agent injected and the location of injection. Extrafascicular injection and direct application caused no damage. Intrafascicular injection caused diffuse axonal injury in the promethazine and dimenhydrinate groups, while prochlorperazine caused only focal injury. Regeneration was prominent at 8 weeks in all intrafascicular injection groups in this rat model. Prochlorperazine thus appears to be less neurotoxic when injected intraneurally and should preferentially be used for intramuscular injections.

Animals↗
PubMed2006

In vivo characterization of traumatic brain injury neuropathology with structural and functional neuroimaging.

Quantitative neuroimaging is increasingly used to study the effects of traumatic brain injury (TBI) on brain structure and function. This paper reviews quantitative structural and functional neuroimaging studies of patients with TBI, with an emphasis on the effects of diffuse axonal injury (DAI), the primary neuropathology in TBI. Quantitative structural neuroimaging has evolved from simple planometric measurements through targeted region-of-interest analyses to whole-brain analysis of quantified tissue compartments. Recent studies converge to indicate widespread volume loss of both gray and white matter in patients with moderate-to-severe TBI. These changes can be documented even when patients with focal lesions are excluded. Broadly speaking, performance on standard neuropsychological tests of speeded information processing are related to these changes, but demonstration of specific brain-behavior relationships requires more refined experimental behavioral measures. The functional consequences of these structural changes can be imaged with activation functional neuroimaging. Although this line of research is at an early stage, results indicate that TBI causes a more widely dispersed activation in frontal and posterior cortices. Further progress in analysis of the consequences of TBI on neural structure and function will require control of variability in neuropathology and behavior.

Brain Injuries↗
PubMed1995

The neuropsychiatric aspects of boxing.

OBJECTIVE: To review the neuropsychiatry of boxing. METHOD: This update considers the clinical, neuropsychological, diagnostic, neurobiological, and management aspects of boxing-related brain injury. RESULTS: Professional boxers with multiple bouts and repeated head blows are prone to chronic traumatic encephalopathy (CTE). Repeated head blows produce rotational acceleration of the brain, diffuse axonal injury, and other neuropathological features. CTE includes motor changes such as tremor, dysarthria, and parkinsonism; cognitive changes such as mental slowing and memory deficits; and psychiatric changes such as explosive behavior, morbid jealousy, pathological intoxication, and paranoia. Screening with neuropsychological tests and neuroimaging may help predict those boxers at risk for CTE. CONCLUSIONS: Boxing results in a spectrum of CTE ranging from mild, nonprogressive motor changes to dementia pugilistica. Recent emphasis on safety in the ring, rehabilitation techniques, and other interventions do not eliminate the risk for CTE. For this reason, there is an active movement to ban boxing.

Athletic Injuries↗
PubMed1986

Gliding contusions in nonmissile head injury in humans.

"Gliding" contusions, ie, hemorrhagic lesions in the parasagittal white matter, were analyzed in 434 fatal nonmissile head injuries in humans. It is concluded that gliding contusions are a type of diffuse brain damage occurring at the moment of injury. Gliding contusions are significantly associated with road-traffic accidents, with the absence of a skull fracture or a "lucid interval," and with the presence of diffuse axonal injury and deep hemispheric traumatic hematomas.

Accidents, Traffic↗
PubMed1990

Wartime neurosurgical experience in Lebanon, 1982-85. II: Closed craniocerebral injuries.

This report presents 64 patients who sustained military-related closed craniocerebral injuries during the Lebanon conflict of 1982-85, all of whom underwent CT scanning at the initial assessment. Of these, 59% required surgery for removal of hematomas, depressed fractures and for monitoring intracranial pressure, in addition to intensive care management of elevated intracranial pressure and associated insults. CT scan revealed brain concussion only in 23%, depressed fracture in 9%, brain contusion alone in 17%, extracerebral hematomas in 17%, intracerebral hematomas in 11%, and diffuse axonal injury in 22%. Overall mortality was 19%, and the outcome was good in 69%. Various factors affecting survival are discussed, and our findings are compared with those in the literature concerning closed head injuries among civilians. Attention is drawn to the high proportion of diffuse brain injury due to blasts caused by side mines. Despite continued efforts to hasten evacuation from the field and improve the management of warfare-related head trauma, the outcome is still far from satisfactory.

Blast Injuries↗
PubMed2003

Preinjury administration of the calpain inhibitor MDL-28170 attenuates traumatically induced axonal injury.

Traumatic brain injury (TBI) evokes diffuse (traumatic) axonal injury (TAI), which contributes to morbidity and mortality. Damaged axons display progressive alterations gradually evolving to axonal disconnection. In severe TAI, the tensile forces of injury lead to a focal influx of Ca2+, initiating a series of proteolytic processes wherein the cysteine proteases, calpain and caspase modify the axonal cytoskeleton, causing irreversible damage over time postinjury. Although several studies have demonstrated that the systemic administration of calpain inhibitors reduces the extent of ischemic and traumatic contusional injury a direct beneficial effect on TAI has not been established to date. The current study was initiated to address this issue in an impact acceleration rat-TBI model in order to provide further evidence on the contribution of calpain-mediated proteolytic processes in the pathogenesis of TAI, while further supporting the utility of calpain-inhibitors. A single tail vein bolus injection of 30 mg/kg MDL-28170 was administered to Wistar rats 30 min preinjury. After injury the rats were allowed to survive 120 min when they were perfused with aldehydes. Brains were processed for immunohistochemical localization of damaged axonal profiles displaying either amyloid precursor protein (APP)- or RMO-14-immunoreactivity (IR), both considered markers of specific features of TAI. Digital data acquisition and statistical analysis demonstrated that preinjury administration of MDL-28170 significantly reduced the mean number of damaged RMO-14- as well as APP-IR axonal profiles in the brainstem fiber tracts analyzed. These results further underscore the role of calpain-mediated proteolytic processes in the pathogenesis of DAI and support the potential use of cell permeable calpain-inhibitors as a rational therapeutic approach in TBI.

Amyloid beta-Protein Precursor↗
PubMed1988

Brain damage in fatal non-missile head injury without high intracranial pressure.

As part of a comprehensive study of brain damage in 635 fatal non-missile head injuries, the type and prevalence of brain damage occurring in the absence of high intracranial pressure were analysed. Of 71 such cases, 53 sustained their injury as a result of a road traffic accident; only 25 experienced a lucid interval. Thirty eight had a fractured skull, a mean total contusion index of 12.9 and diffuse axonal injury in 29: severe to moderate ischaemic damage was present in the cerebral cortex in 25, brain swelling in 13, and acute bacterial meningitis in nine. The prevalence and range of brain damage that may occur in the absence of high intracranial pressure are important to forensic pathologists in the medicolegal interpretation of cases of fatal head injury.

Adolescent↗
PubMed1995

[Lesions of the corpus callosum and syndromes of interhemispheric disconnection of traumatic origin].

We review the different kinds of injury to the corpus callosum in closed head trauma, as well as their different mechanisms. Most frequent lesions are either diffuse and at the microscopic level, secondary to disruption of axons at the time of the trauma, or focal and at macroscopic level, also due to torsion or shearing strains on the corpus callosum. They are associated with diffuse axonal injury of hemispheric and brainstem white matter. Focal macroscopic lesions, sometimes extensive, are encountered in 16-40% of autopsies after fatal head injury. Likewise, MRI allows nowadays to show them in 22-49% of nonfatal head injuries. Such lesions can produce an interhemispheric disconnection syndrome. However, clinical observation of an interhemispheric disconnection after head trauma has been only rarely reported in the literature, as it is showed by a brief overview of those cases, which suggests that this pathology is probably often overlooked. Focal damage to the corpus callosum seems to be a marker of severe injury, with often long-lasting coma and sometimes transitory vegetative state or mutism. Extension of posterior callosal lesions towards adjacent midline structures, such as the fornix, could contribute to the important memory impairment which is particularly frequently associated with posttraumatic interhemispheric disconnection syndromes.

Adolescent↗
PubMed2000

Recent advances in neurotrauma.

The frequency of and outcome from acute traumatic brain injury (TBI) in humans are detailed together with a classification of the principal focal and diffuse pathologies, and their mechanisms in extract laboratory models are outlined. Particular emphasis is given to diffuse axonal injury, which is a major determinant of outcome. Cellular and molecular cascades triggered by injury are described with reference to the induction of axolemmal and cytoskeletal abnormalities, necrotic and apoptotic cell death, the role of Ca2+, cytokines and free radicals, and damage to DNA. It is concluded that TBI in humans is heterogeneous, reflecting various pathologies in differing proportions in patients whose genetic background (APOE gene polymorphisms) contributes to the outcome at 6 months. Although considerable progress has been made in the understanding of TBI, much remains to be determined. However, a deeper understanding of the pathophysiological events may lead to the possibility of improving outcome from rational targeted therapy.

Animals↗
PubMed2001

Position paper on fatal abusive head injuries in infants and young children.

This article represents the work of the National Association of Medical Examiners Ad Hoc Committee on shaken baby syndrome. Abusive head injuries include injuries caused by shaking as well as impact to the head, either by directly striking the head or by causing the head to strike another object or surface. Because of anatomic and developmental differences in the brain and skull of the young child, the mechanisms and types of injuries that affect the head differ from those that affect the older child or adult. The mechanism of injury produced by inflicted head injuries in these children is most often rotational movement of the brain within the cranial cavity. Rotational movement of the brain damages the nervous system by creating shearing forces, which cause diffuse axonal injury with disruption of axons and tearing of bridging veins, which causes subdural and subarachnoid hemorrhages, and is very commonly associated with retinal schisis and hemorrhages. Recognition of this mechanism of injury may be helpful in severe acute rotational brain injuries because it facilitates understanding of such clinical features as the decrease in the level of consciousness and respiratory distress seen in these injured children. The pathologic findings of subdural hemorrhage, subarachnoid hemorrhage, and retinal hemorrhages are offered as "markers" to assist in the recognition of the presence of shearing brain injury in young children.

Battered Child Syndrome↗
PubMed2006

[Biochemical and immunohistochemical markers of brain injury].

Proteins released to circulation from affected tissues during primary or secondary trauma brain injury might be used as serum markers of glial or ganglial cells damage (neuron specific enolasis and S100 B protein). Other markers of trauma can be proved as relatively specific of diffuse axonal injury by immunohistochemical detectoin (amyloid prekurzor protein, neuron specific enolasis, glial fibrilar acidic protein and superficial antigen receptor CD 68). Some markers are associated with blood brain barrier damage (matrix metaloproteinases (MMP-2, MMP-9) and synthase of nitric oxide (iNOS)). We aimed in our short communication on biomechanics of developed of trauma, primary or secondary kinds of trauma brain injury and use of trauma brain injury markers for clinical diagnostics and management of patients.

Biomarkers↗
PubMed2003

Awakenings from persistent vegetative state: report of three cases with parkinsonism and brain stem lesions on MRI.

Three patients with a persistent vegetative state after severe head injury are reported. They recovered from a prolonged disturbance of consciousness after the administration of levodopa. These patients all had parkinsonian features. On magnetic resonance imaging, the distribution of lesions implied a diffuse axonal injury involving the substantia nigra or ventral tegmental area. The existence of patients whose dopaminergic systems may have been selectively damaged by a severe head injury should be recognised because such individuals may respond to levodopa treatment.

Adolescent↗
PubMed1992

Magnetic resonance identified ventricular dilation in traumatic brain injury: comparison of pre- and postin jury scan and postin jury results.

A case study is presented in which a patient received magnetic resonance (MR) imaging of the brain 3 months prior to a severe traumatic brain injury (TBI). The post-TBI MR findings are compared and contrasted with the pre-TBI MR images. The posttraumatic changes demonstrate a significant dilation of the ventricular system which reflects diffuse axonal injury and loss of brain substance. Correspondingly, the neuropsychological studies in this individual reflect global deficits which match the nonspecific, traumatically induced degenerative changes found in the postinjury MR scan. This case study is unique in that specific preinjury MR findings are available for direct comparison and quantitative analysis of TBI-associated changes in brain structure with neuropsychological outcome.

Clinical Conference↗
PubMed1993

Opportunities for neuroprotective drugs in clinical management of head injury.

Over the past 15 years, neuropathological studies, patient monitoring, and data emerging from the laboratory have significantly advanced the understanding of both primary and secondary brain damage. The challenge now rests with the clinician treating head injury, who must translate these recent developments into real benefits for the patient. Neurological deterioration after head injury may be due to the effects of secondary mechanisms in up to one-third of cases. These secondary events may follow early insults such as transient global ischemia, hematomas, or diffuse axonal injury. They may be mediated by complex cascades of biochemical processes. Many of these secondary posttraumatic events have been targeted as potential sites for pharmacological intervention. In models of focal brain ischemia, a new generation of compounds that inhibit activity of glutamate has been shown to ameliorate the severity of the ischemic insult. Other potential neuroprotective agents that are currently being clinically investigated include free radical scavengers and calcium antagonists. Preliminary findings show indications of improved neurological outcome with early administration of a number of these drugs. Because head-injured patients tend to be admitted to the hospital within hours of injury, which allows for pretreatment or early therapy, several ongoing trials are assessing safety, tolerance, and efficacy of many new therapeutic agents combined with standard management. It is hoped that the outcome of this novel approach to head injury management will be positive and will help to reduce the high morbidity and mortality associated with head injuries.

Animals↗
PubMed1993

Persistent facial myoclonus: a negative prognostic sign in patients with severe brain injury.

The determination of long-term prognosis is one of the most difficult tasks in the management of persons with brain injury (BI). Initial Glasgow Score, duration of coma, brain stem reflexes, and pupillary responses are all clinical findings that have been related to outcome in BI. We describe another easily observable clinical finding, persistent facial myoclonus (PFM), which may provide additional information on prognosis after severe BI. We retrospectively reviewed 295 consecutive admissions to an inpatient brain injury rehabilitation program. Data extracted included mechanism of injury, patient demographics, admission and discharge Rancho Level (RL), and presence of PFM plus first date of description. Of the total admissions, 68 (23%) were RL < or = 2 on admission and of those 68, nine (13%) demonstrated PFM. Twenty-seven of 59 patients without PFM advanced to RL > 3 but none of those with PFM progressed to RL > 2 (Fisher's exact probability = .007). Mean time from injury to PFM description was 10.5 months (SD = 11.8, range, 2.5 to 25.0 months) and mean time from description to discharge was 7.1 months (SD = 6.6, range, 2.0 to 22.5 months). Four of the nine PFM patients had evidence of brain stem injury on computed tomography or magnetic resonance imaging scans, a much higher percentage than in the larger population. We postulate that patients with PFM after TBI represent a subgroup of patients with severe diffuse axonal injury with brain stem lesions.

Adult↗