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Concussive convulsions. Incidence in sport and treatment recommendations.

Concussive convulsions (CC) are nonepileptic phenomena which are an immediate sequelae of concussive brain injury. Although uncommon, occurring with an approximate incidence of 1 case per 70 concussions, these episodes are often confused with post-traumatic epilepsy which may occur with more severe structural brain injury. The pathophysiological mechanism of CC remains speculative, but may involve a transient traumatic functional decerebration with loss of cortical inhibition and release of brainstem activity. The phenomenology of the CC is somewhat akin to convulsive syncope, with an initial tonic phase occurring within 2 seconds of impact, followed by a clonic or myoclonic phase which may last several minutes. Lateralising features are common during the convulsions. There is no evidence of structural or permanent brain injury on clinical assessment, neuropsychological testing or neuroimaging studies. Long term outcome is universally good with no evidence of long term epilepsy and athletes are usually able to return to sport within 2 weeks. The correct management of these episodes centres on the appropriate management of the associated concussive injury and the exclusion of other cerebral injury by medical assessment. The CC requires no specific management beyond immediate onfield first aid measures such as protection of the airway. Antiepileptic therapy is not indicated and prolonged absence from sport is unwarranted. These episodes, although dramatic, are relatively straightforward to manage and all team physicians and those involved in athlete care need to be aware of this condition.

Adult↗

Sideline management of sport-related concussions.

Concussions remain one of the most troublesome injuries sports physicians face. Studies suggest recovery takes hours to weeks, but at what point is the concussed brain no longer at increased risk for reinjury is unknown. Physicians must be alert to the symptoms of concussion and be familiar with the available tools to assess neurocognitive dysfunction. Prospectively validated signs and symptoms include amnesia, loss of consciousness, headache, dizziness, blurred vision, attention deficit, memory, postural instability, and nausea. A player with any signs or symptoms of a concussion should not be allowed to return to the current game or practice and should be monitored closely for deterioration of symptoms. Return-to-play should be individually based and proceed in a step-wise manner. The ongoing risk-benefit analysis of return-to-play must currently be based on experience, corollary data from traumatic brain injuries in animals and humans, and limited prospective data with sports-related concussions.

Athletic Injuries↗

Phantom and amputation illusions in paraplegic patients.

In paraplegic patients, amputation illusions and anosognosia with phantom position illusions are distinct phenomena which do not concur in any one patient. A permanent amputation illusion regularly follows a complete spinal injury with concomitant brain concussion, whereas all patients who are conscious during their spinal trauma remain aware of their paralyzed limbs in definite phantom positions which are clearly related to the position of the body at the moment of injury.

Adolescent↗

Second impact syndrome.

Diffuse cerebral swelling with delayed catastrophic deterioration, a known complication of brain trauma, has been postulated to occur after repeated concussive brain injury in sports--the "second impact syndrome" (SIS). Certain current concussion management guidelines are contingent upon this assumption. We established criteria for definite, probable, and possible SIS and analyzed all published cases. A total of 17 cases were identified in which the reports described the cases as being consistent with SIS. Of these, only five probable cases of SIS were found based on our diagnostic criteria. We also studied the accuracy of recalled episodes of minor concussion in football players by their teammates because the diagnosis of SIS is usually based on such accounts. We found overreporting of recalled episodes of concussion in teammates when compared with self reports and videotape analysis. Based on case reports, the claim that SIS is a risk factor for diffuse cerebral swelling is not established. Prevention strategies for sports-related cerebral swelling are difficult to implement in the absence of established risk factors.

Athletic Injuries↗

[Disruption of the functional interrelationships between specific and nonspecific brain systems in mild craniocerebral injuries].

An examination of the topographic distribution of evoked visual potential over the scalp after a brain concussion revealed a pronounced disturbance of the regular changes of the amplitude-temporal characteristics of nonspecific components in most patients. A diminution or an increase of the amplitude of the N2 component in the specific projection zone and an increase of the amplitude of the N3 component in the non-specific zone were noted, and so was an increase of the latent period of the P3N3 and P4N4 components in all deflections. The changes revealed point to a disturbance of the functional relations between the specific and nonspecific systems of the brain as a result of craniocerebral injury.

Brain Concussion↗

A fluid percussion model of experimental brain injury in the rat.

Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head injury.

Animals↗

[Parasagittal white matter shearing injury (so-called gliding contusion): possible radiological evidence of spastic hemiplegia in diffuse axonal injury].

Severe head injury or diffuse axonal injury is frequently associated with spastic hemiplegia/paraplegia. However, the causative lesion has not been well elucidated. Especially, the relationship between the gliding contusion and spastic hemiplegia has not been inferred yet. We have analyzed 6 brain concussion cases and 19 cases of diffuse axonal injury. None of the concussion cases experienced hemiplegia in their courses. Among the 19 cases, 10 were left with persistent and disabling hemiplegia/quadriplegia, whereas 5 showed persistent but mild hemiplegia. Among the 10 cases, one was incapacitated by a brainstem hemorrhage. The remaining 9 cases exhibited, in the parasagittal white matter, small hemorrhagic spots in the acute phase CT, low-density areas in the chronic phase CT, and/or T2 high and T1 low signal lesions in the MRI. In 8 cases, the lesion was in accord with the hemiplegic side, but in one case the low density area was on the ipsilateral side. Two of the 3 cases showing quadriplegia exhibited bilateral parasagittal lesions. None of the 5 mild hemiplegia cases and 10 nonhemiplegia cases showed such abnormality. Superficial brain contusions were found in 17 cases altogether, but they were not at all correlated with the occurrence of hemiplegia. Thus, it was concluded that parasagittal white matter shearing injury or so called gliding contusion could be the manifestation of injury to the corticospinal tract in the corona radiata.

Adolescent↗

Diagnostic confusion in mild traumatic brain injury (MTBI). Lessons from clinical practice and EFNS--inquiry. European Federation of Neurological Societies.

A 1997 inquiry of 130 neurosurgeons throughout Germany, dealing with diagnosis and therapy of patients with mild traumatic brain injury showed a mainly inhomogeneous picture. The European Federation of Neurological Societies inquiry form 'Management of Patients with Mild Head Injury' was sent on behalf of the German Society of Neurological Surgeons to every leading neurosurgeon in Germany, of whom only 74 (57%) answered. The diagnosis 'mild brain injury' is used by 63%, 'commotio cerebri' by 49%, and 'brain concussion' by 4% of the institutions. GCS is used for classification by 60%, PTA 48%, retrograde amnesia by 50%, and LOC by 63% of institutions. Guidelines are used in 78%. Diagnostic x-ray of the skull is used in 77%, cervical spine in 62%, CT in 66%, MRT in 7%; and routine EEG in 35%. Fourteen per cent of the patients are not admitted; home observation is used in 45% of institutions, full bedrest in 19%, working pause in 48%, pain medication in 27%, control in 51%. Seperate guidelines for children in 54% of those departments.

Adult↗

Injuries among disabled children: a study from Greece.

OBJECTIVE: To compare the differential implications of sociodemographic and situational factors on the risk of injury among disabled and non-disabled children. DESIGN: Data from the Emergency Department Injury Surveillance System (EDISS) were used to compare, in a quasi case-control approach, injured children with or without disability with respect to sociodemographic, event and injury variables, and to estimate adjusted odds ratios for the injury in a disabled rather than a non-disabled child. SETTING: Two teaching hospitals in Athens and two district hospitals in the countryside that participate in the EDISS. PATIENTS: In the five year period 1996-2000, 110 066 children were recorded with injuries; 251 among them were identified as having a motor/psychomotor or sensory disability before the injury event. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Mechanism of injury, type of injury, risk-predisposing socioeconomic and environmental variables, odds ratio for injury occurrence. RESULTS: Falls and brain concussion are proportionally more common among disabled children, whereas upper limb and overexertion injuries are less common among them. Urban environment, migrant status, and cold months are also associated with increased odds for injuries to occur among disabled rather than non-disabled children. The odds ratio for the occurrence of an injury among disabled children increases with increasing age. CONCLUSIONS: The results of the study provide the information for the targeting of trials of preventive measure in disabled children at increased risk of severe injuries.

Accidental Falls↗

Retrospective study of concussive convulsions in elite Australian rules and rugby league footballers: phenomenology, aetiology, and outcome.

OBJECTIVES: To study the ictal phenomenology, aetiology, and outcome of convulsions occurring within seconds of impact in violent collision sport. DESIGN: Retrospective identification of convulsions associated with concussive brain injury from case records from medical officers of football clubs over a 15 year period. SUBJECTS: Elite Australian rules and rugby league footballers. MAIN OUTCOME MEASURES: Neuroimaging studies, electroencephalography, neuropsychological test data, and statistics on performance in matches to determine presence of structural or functional brain injury. Clinical follow up and electroencephalography for evidence of epilepsy. RESULTS: Twenty two cases of concussive convulsions were identified with four events documented on television videotape. Convulsions began within 2 seconds of impact and comprised an initial period of tonic stiffening followed by myoclonic jerks of all limbs lasting up to 150 seconds. Some asymmetry in the convulsive manifestations was common, and recovery of consciousness was rapid. No structural or permanent brain injury was present on clinical assessment, neuropsychological testing, or neuroimaging studies. All players returned to elite competition within two weeks of the incident. Epilepsy did not develop in any player over a mean (range) follow up of 3.5 (1-13) years. CONCLUSIONS: These concussive or impact convulsions are probably a non-epileptic phenomenon, somewhat akin to convulsive syncope. The mechanism may be a transient traumatic functional decerebration. In concussive convulsions the outcome is universally good, antiepileptic treatment is not indicated, and prolonged absence from sport is unwarranted.

Adult↗

[Subjective syndrome after head injury].

UNLABELLED: DEFINITION AND CLASSIFICATION PROBLEMS: Post-traumatic or post-commotion syndrome is one of the most controversial entities in studying consequences of craniocerebral trauma. Part of this problem arises from impossibility of adequate translation of the term brain concussion. Post-concussion syndrome is a broader concept than post-commotion and includes, if not a whole, than part of the post-contusion syndrome. There are also some other terms in the literature: post-traumatic syndrome, post head injury syndrome, post head injury syndrome or symptoms and the old term post-traumatic encephalopathy. Terminological imprecisions have not been solved yet, but the notion itself is determined by relative standard symptoms often associated with closed craniocerebral trauma, but without precise connection with the severity of the trauma. In the classification of mental disorders and behavior disorders, this syndrome is coded as FO7.2. ETIOLOGY: In regard to the etiology of this syndrome some authors speak in favor of psychogenic and some of organic etiology, while Levin considers symptoms of post-commotion syndrome to start as organic and persist as psychic. Wechsler classified subjective disorders after head injuries into 4 categories: simulation, traumatic hysteria, traumatic encephalopathy and traumatic neurosis. The author does not deal with the origin of symptoms, whereas the classification itself suggests priority of psychic to organic factors (11). Those who speak in favor of organic etiology, think that axon damage and neuron damage are organic substrate in mild brain injuries, while fibrous degenerations of the cerebral hemisphere and brain stem are the organic base in severe traumas. On the other hand, many scientists primarily point to psychic moments, especially to importance of aggravation and simulation as well as compensation or rental neurosis in persistent post-traumatic syndrome. Most scientists agree that personality characteristics influence the development of post-traumatic syndrome and can predispose aggravation and simulation, whereas these symptoms more often occur in neurotic persons. The latest investigations reveal that classification in regard to etiologic factors--organic and psychogenic--is an anachronism. Long and Novac state that 80% of persons with cerebral trauma spontaneously speak about symptoms of the post-traumatic syndrome, while by targeted evaluation the percentage rises to 90%, so that they think that universality of symptoms points to their common origin. CONCLUSION: If the post-traumatic syndrome is though of as a line with organic dementia at one end and traumatic neuroses at the other, then this syndrome can be placed at different positions. Some authors put it close to the neurotic syndrome or regard it to be the neurotic syndrome itself, while others, mostly due to homogenity of the clinical picture, believe that this syndrome has an organic cause.

Brain Concussion↗

Prolonged and extensive IgG immunoreactivity after severe fluid-percussion injury in rat brain.

The relationships between protein extravasation, morphological changes in neurons, and reactive changes in axons were evaluated in rats subjected to right lateral fluid-percussion injury to the brain (4.8-5.6 atm, 20 ms). Serial sections of the brain were immunostained with antibodies to rat immunoglobulin G (IgG) and 68-kDa neurofilament at 1 h to 2 weeks after injury or sham injury. Ischemic changes in neurons were noted in the injured cortex at 6-48 h after injury, and macroscopic hemorrhages were noted in the right corpus callosum and external capsule at 1 h to 1 week after injury. Extracellular IgG immunostaining was observed in the right cortex and right hippocampus at 1 h to 1 week after injury, and in the cortices and hippocampi bilaterally at 2 weeks after injury, but was most prominent in those regions at 24 h after injury. Intracellular IgG staining was noted in the neurons of cortices, hippocampi, brainstem, and cerebellum at 1 h to 2 weeks after injury. The number of IgG immunoreactive neurons was greatest at 1 week after injury. Thickened IgG immunoreactive axons and reactive axonal changes seen with neurofilament immunostaining were both in the similar region of the brainstem at 1 h to 1 week after injury. It appears that prolonged and widespread breakdown of the blood-brain barrier to plasma protein occurs after severe concussive brain injury and that this breakdown is not always accompanied by morphological changes. Intra-axonal IgG immunostaining provides additional clues to the pathogenesis of axonal damage following diffuse brain injury.

Animals↗

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↗

[Clinical manifestation and outcomes of concussion of the brain: comparison of the results in patients admitted to hospital and in those who have refused admission].

The clinical manifestations and outcomes of concussion of the brain (CB) were comparatively analyzed in two groups of victims with acute brain injury (BI): those who had admitted to hospital and in those who had refused admission. A total of 355 individuals aged 16-35 years without concomitant somatic and neurological diseases were examined. The follow-up lasted 1 year. Clinical and neurological studies, computed tomography, and MR-imaging were used. In the acute period, the regression of neurological symptomatology and the better status of health were noted in the victims of both groups almost at the same time (on days 4-6 after injury). The psychovegetative syndrome was the basis of neurological disorders in the victims from both groups in the posttraumatic period. The follow-up has provided evidence for nearly equal numbers of victims with CB in both groups 1 year after BI.

Adolescent↗

Effects of experimental fluid-percussion injury of the brain on cerebrovascular reactivity of hypoxia and to hypercapnia.

To test the hypothesis that concussive brain injury interferes with the normal vasodilator response of the cerebral circulation to hypoxemia, 30 cats were subjected to mild (PaO2 50 mm Hg) and severe (PaO2 30 mm Hg) hypoxemia while measurements were made of arterial and intracranial pressure, regional cerebral blood flow (CBF), and arterial blood gases. Ten cats served as controls, 10 were subjected to mild fluid-percussion injury of the brain (0.8 to 1.7 atmospheres (atm)), and 10 to severe injury (2.4 to 4.1 atm). The CBF response to hypercapnia (PaCO2 50 mm Hg) was also tested in most animals, and the response of CBF autoregulation to hemorrhagic hypotension was tested in four animals of each group. Trauma was found to severely attenuate the capacity of CBF to increase during hypoxemia. Responsiveness to hypoxemia appeared to be better preserved in traumatized animals than was autoregulation, but was less robust than the response to hypercapnia.

Animals↗