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PubMed1986

[Amnesia and responsibility following brain concussion. A study of 70 patients].

Hit- and run traffic accidents frequently occur because an intention to hide drunkenness. Later, the accused claims that he or she had amnesia due to concussion at the time of accident and what followed. In most cases, the question arises as to whether it is the truth or just a story to protect the defendant from punishment. To study this question, 70 patients (39 male, 31 female) were interrogated. They were asked about the duration of their amnesia and their ability to recall their own actions, or what they had been told. In 80% of the persons examined there was only a short period of amnesia (less than 30 min). Of 12 cases with a longer period of amnesia, 7 were also intoxicated from alcohol (one case had a concentration of 3.1%). In only one person suffering from concussion could it definitely be proved that the actions taking place long after the accident, were usually not comparable with evidence given in court.

Accidents, Traffic↗
PubMedDate not supplied

[Additional studies in the assessment of brain concussion].

Following minor head traumas nervous system injuries develop at cellular level. In these cases only multidirectional analysis using various techniques can contribute to easier detection of focal lesions. The importance of neurophysiological methods, including electroencephalography (EEG), polysomnography, neuroimaging methods, such as cerebral tomography (CT), magnetic resonance (MRI), single photon emission computerised tomography (SPECT) and positron emission tomography (PET) in cases of minor head trauma. A brief review of the diagnostic methods applicable in the assessment of brain commotion shows that the dynamic development of new diagnostic techniques such as SPECT and MRI made possible a better insight into the processes taking place after minor trauma to the head. Together with traditional methods it can contribute to more objective demonstration of the symptoms, dynamics of the pathological process and more exact expertise of late sequelae of the trauma.

Brain Concussion↗
PubMed1990

[Deontological aspects of the diagnosis and treatment of patients with a history of brain concussion].

Follow-up and therapeutic data obtained for 200 patients at the age of 15-75 who had a craniocerebral injury lead the author to the conclusion on the specificity of the deontological approach in acute and subsequent periods of the trauma. Due attention should be paid to the patients' premorbid status, pre-existent chronic somatic and neurological diseases, age, individual characteristics of the injury and personality traits.

Adolescent↗
PubMed1998

[Computed tomography as an alternative to observation in brain concussion].

In Sweden, patients with minor head injury (i.e., history of loss of consciousness or posttraumatic amnesia) are routinely admitted for neurological observation. The article reports the results of a small study of current clinical practices at St Göran's Hospital in Stockholm, and briefly reviews published reports of different management strategies. The findings suggest that computed tomography scanning might constitute better management than routine hospitalisation, both medically and economically. However, further investigation from a Swedish perspective is needed before any evidence-based recommendations can be made.

Adolescent↗
PubMedDate not supplied

[Sonographic follow-up of pronounced brain concussion in a 3-week-old infant following trauma caused by shaking].

Cerebral sonography was performed in a 3 week old whiplash shaken baby who had no external marks of injury and no skull fracture. On the day of admission, increased echogenicity in the white matter could be correlated with hypodense contusional lesions in the cranial computerized tomography. Sonographic follow-up showed multiple cystic defects in the white matter and later on marked dilatation of the adjacent lateral ventricle. In all infants with open anterior fontanel presenting with unexplained clouding of consciousness and/or external marks of child abuse, cerebral sonography should be a basic diagnostic method.

Brain↗
PubMed1976

Sinistrad mirror writing and reading after brain concussion in a bi-systemic (oriento-occidental) polyglot.

The problem of mirror writing and reading is discussed in the light of a clinical case, where this disturbance appeared after an apparently minor head injury. Mirror writing and reading in this polyglot individual affected only the sinistrad (Hebrew) writing and reading system, leaving the dextrad (Latin) system unimpaired. This disturbance appeared together with dyscalculia, left-right disorientation and slight temporal confusion, suggestive of parieto-occipital lobe pathology. The clinical picture also showed apparently "conversional" traits, such as are sometimes seen in incomplete parietal lobe syndromes. The relevant literature is reviewed and patho-physiological mechanisms of mirror reversal are discussed.

Brain Concussion↗
PubMed1991

Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study.

Utilizing a lateral fluid percussion injury as a model of cerebral concussion, rats were studied histochemically measuring the degree of cytochrome oxidase activity present within different structures at different times following injury. After concussion, the cerebral cortex ipsilateral to the site of injury exhibited a diffuse decrease in its level of chromotome oxidase (CO) activity beginning at as soon as one day and lasting for up to 10 days after the insult. The ipsilateral dorsal hippocampus also exhibited an injury-induced decrease in CO activity, however, it was not as severe as in the cortex. These results indicate that oxidative metabolism is depressed primarily within the cerebral cortex and hippocampus for several days following a cerebral concussion. We propose that this period of metabolic depression may delineate a period of time during which the injured brain is unable to function normally and thus would be vulnerable to a second insult.

Animals↗
PubMed2002

Genes preferentially induced by depolarization after concussive brain injury: effects of age and injury severity.

Fluid percussion (FP) brain injury leads to immediate indiscriminate depolarization and massive potassium efflux from neurons. Using Northern blotting, we examined the post-FP expression of primary response/immediate early genes previously described as induced by depolarization in brain. RNA from ipsilateral and contralateral hippocampus was harvested from immature and adult rats 1 h following mild, moderate, or severe lateral fluid percussion injury and compared against age-matched sham animals. C-fos gene expression was used as a positive control and showed marked induction in both pups (6-25-fold with increasing severity) and adults (9.7-17.1-fold). Kinase-induced-by-depolarization-1 (KID-1) and salt-inducible kinase (SIK) gene expression was increased in adult (KID-1 1.5-1.6-fold; SIK 1.3-3.9-fold) but not developing rats. NGFI-b RNA was elevated after injury in both ages (pups 1.8-6.1-fold; adults 3.5-5-fold), in a pattern similar to that seen for c-fos. Secretogranin I (sec I) demonstrated no significant changes. Synaptotagmin IV (syt IV) was induced only following severe injury in the immature rats (1.4-fold). Our results reveal specific severity- and age-dependent patterns of hippocampal immediate early gene expression for these depolarization-induced genes following traumatic brain injury. Differential expression of these genes may be an important determinant of the distinct molecular responses of the brain to varying severities of trauma experienced at different ages.

Age Factors↗
PubMed2001

Clinical features of diffuse axonal injury.

OBJECTIVE: To analyze the mechanism of diffuse axonal injury (DAI) and study the relationship between DAI and brain concussion, brain contusion, and primary brain stem injury. METHODS: The clinical data and iconographic characteristics of 56 patients with DAI were analyzed retrospectively. RESULTS: Traffic accidents were the main cause of DAI. Among t he 56 cases, 34 were injured for at least twice, and 71.43% of the patients were complicated with contusion. CONCLUSIONS: It is considered that DAI is a common pattern of primary brain injury, which is often underestimated. And DAI includes cerebral concussion and primary brain injury, and is often complicated by cerebral cortex contusion. Therefore, it is very simple and practical to divide primary brain injuries into local and diffuse injuries.

Adolescent↗
PubMedDate not supplied

[Ultrastructural analysis of changes in the synapses in the rabbit brain after experimental concussion of the brain].

The authors discuss the results of electron-microscopic study of the synaptic contacts in the brain of rabbits during 4 months after experimental brain concussion. A complex of ultrastructural changes of the cerebral synaptic apparatus with a characteristic dynamics of development in time and space is described, and its peculiarities and features distinguishing it from other types of pathology as well as its role in the pathogenesis of craniocerebral injury are discussed.

Animals↗
PubMed1985

Leukotriene production in gerbil brain after ischemic insult, subarachnoid hemorrhage, and concussive injury.

A leukotriene-like immunoreactivity was measured by radioimmunoassay in the gerbil forebrain following ischemia and reperfusion, subarachnoid hemorrhage (SAH), or nonlethal concussive brain injury. In each paradigm an increase in immunoreactivity levels was found. Peak levels were reached 15 to 30 minutes after each insult, and slowly returned to baseline over the next 24 hours. The study supports the suggestion that cerebral vessels and circulating blood are capable of producing leukotrienes, and that a major source of production is a nonvascular component within gray matter, possibly the cortical neuron. Leukotrienes may play a role in the pathophysiology of cerebral edema formation, cerebral vasospasm, seizure activity, and other central nervous system abnormalities. These studies are the first to demonstrate leukotriene production in gerbil brain following SAH or concussive brain injury.

Animals↗
PubMed1997

A concussive-like brain injury model in mice (I): impairment in learning and memory.

The modeling of human concussive brain injury (CBI) in the laboratory has been challenging. In the present study, we developed an experimental CBI model in mice using a novel weight-drop device. Various injury levels were examined by adjusting the height of the falling weight (diameter 10 mm, length 20 cm, weight 21 g). At a height of 50 cm, the impact resulted in a mortality rate of 46.7% with a skull fracture rate of 28.6%. At a height of 25 cm, however, the impact produced a concussive-like brain injury (CLBI) to the mice without skull fracture. A series of pathophysiological and neurobehavioral responses was evaluated at this injury level. The CLBI mice lost muscle tone and righting reflex response immediately following the trauma and recovered from the latter within a short duration of 1.6 +/- 0.32 min (mean +/- SE). Brain edema formation started at 12 h, reached a maximum at 24 h and recovered 48 h. Typically edema was found in the neocortex, hippocampus, and cerebellum, but not in the brain stem. Deficits in the feeding behaviors lasted for 2 days, accompanied by lower body weight persisting for 5 days. The body weight growth rate for 24 h returned to the control levels by the third day postinjury. Learning and memory were evaluated at the end of 1-3 weeks after the trauma using a water-finding task. At 1 week, exploratory behaviors were slightly inhibited while learning and memory were profoundly impaired. Interestingly, the learning and memory deficits lasted for 2 weeks while recovering to the control levels by 3 weeks. No motor disability was found in the CLBI mice during the 3-week evaluations. These results indicate that the weight-drop impact produced graded injury to the brain, and at the injury level of 25 cm it produced a CLBI in the mice in which the characteristics of transient loss of neurobehavioral responses, short duration of brain edema, and long-lasting learning and memory deficits are similar to those of human CBI.

Animals↗
PubMedDate not supplied

[Multimodal evoked potentials in the early period after cranio-cerebral trauma].

In 83 patients aged 17-68 years somatosensory evoked potentials by median nerve stimulation, and visual and auditory evoked potentials were studied 5-28 days after craniocerebral trauma. Brain concussion was diagnoses in 43 cases on the basis of neurological examination, CT and duration of unconsciousness. In the remaining 40 cases brain contusion was diagnosed. In SSEP the latency was calculated of waves N9, N13, P16, N20, P22, N35 and P40: in the visual evoked potentials the latency of the P100 component, and in auditory evoked potential the latency of waves I, III and V, and interpeak latency I-III, III-V and I-V SSEP changes were found in 39% of cases of brain concussion and 52.9% of brain contusion cases. The abnormalities in both groups involved mainly the component of latency and deviation P100 of visual evoked potential P40 and N35. Prolongation of the latency of P100 of the visual evoked potential was recorded in 20% of patients with brain concussion and 16.7% with brain contusion. Auditory evoked potentials were abnormal in 10.3% of brain concussion and 26.5% of brain contusion cases. In 64 cases all three types of evoked potentials were studied and pathological changes in at least one of these types were found in 56.4% of brain concussion and 72% of brain contusion cases. The results show that as least in a part of cases diagnosed as brain concussion according to generally accepted criteria, central nervous system injury is present.

Adolescent↗
PubMed1996

[Changes in the cerebral cortex in closed craniocerebral trauma of gunshot origin (experimental research)].

Cerebral cortex was studied morphologically in rabbits with concussion of brain induced by gunshot injury. The extent of severity was modelled by the bullet rate. No significant bleeding followed the injury allowing to observe the animals during the necessary terms (7-14 d.) Morphological study included light optical and electron microscopy. In neurons, glial cells and synapses a series of essential destructive changes in shown detectable predominantly on ultrastructural level that might be the base of psychoneurological complications of a distant period. Ballistic properties of a bullet were obviously fundamental to pathogenesis of brain concussion in these experiments as kinetic energy of the bullet was only sufficient for non significant damage of the skull soft tissue. But in contrast to the dull trauma, the blow was of a high speed and despite mild clinical characteristics caused essential diffuse structural disturbances in brain tissues.

Animals↗
PubMed2001

The Neurometabolic Cascade of Concussion.

OBJECTIVE: To review the underlying pathophysiologic processes of concussive brain injury and relate these neurometabolic changes to clinical sports-related issues such as injury to the developing brain, overuse injury, and repeated concussion. DATA SOURCES: Over 100 articles from both basic science and clinical medical literature selected for relevance to concussive brain injury, postinjury pathophysiology, and recovery of function. DATA SYNTHESIS: The primary elements of the pathophysiologic cascade following concussive brain injury include abrupt neuronal depolarization, release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow, and impaired axonal function. These alterations can be correlated with periods of postconcussion vulnerability and with neurobehavioral abnormalities. While the time course of these changes is well understood in experimental animal models, it is only beginning to be characterized following human concussion. CONCLUSIONS/RECOMMENDATIONS: Following concussion, cerebral pathophysiology can be adversely affected for days in animals and weeks in humans. Significant changes in cerebral glucose metabolism can exist even in head-injured patients with normal Glasgow Coma Scores, underscoring the need for in-depth clinical assessment in an effort to uncover neurocognitive correlates of altered cerebral physiology. Improved guidelines for clinical management of concussion may be formulated as the functional significance and duration of these postinjury neurometabolic derangements are better delineated.

Journal Article↗
PubMed1997

A concussive-like brain injury model in mice (II): selective neuronal loss in the cortex and hippocampus.

A novel concussive-like brain injury (CLBI) model characterized by transient neurobehavioral depression, short duration of brain edema, and long-lasting memory deficits has been reported in our companion paper. This was achieved by dropping a 21-g weight from a height of 25 cm onto the head of a mouse. In the present study, we examined the histopathological changes in this model. Male ddY mice were subjected to either the trauma or sham injury. Gross pathological examination of the brain 1 h posttrauma did not demonstrate subdural, subarachnoid, intraventricular, periventricular, and intraparenchymatous hemorrhage, focal lesions or contusions. Microscopic examination 24 h posttrauma with Nissl staining (cresyl violet), however, revealed a selective bilateral neuronal cell loss in the cerebral cortex and hippocampus but not in the regions of the thalamus, cerebellum, and brain stem. The characteristics of neuronal cell loss in the cortex suggested that this pathology was related in part, to the head impact dynamics, since the cell loss was noted in the central portion of the supraventricular cerebral cortex (p < 0.001), the site of the weight impact, gradually decreasing peripheral to this site, and disappearing in the areas remote from this locus. In contrast, neuronal cell loss seen in the hippocampus did not suggest that this pathology was directly associated with the impact site. Neuronal cell loss was concentrated in the pyramidal cell layer of CA2 (p < 0.01) and CA3 (p < 0.01), and a lesser degree was noted in the subfields of CA3c (p < 0.05) and the hilar region (p < 0.05) but not in the subfields of CA1 and the dentate gyrus layers. The present study characterized the histopathological change seen in the CLBI model, demonstrating the selective neuronal cell loss following weight-drop concussion in mice.

Animals↗