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PubMed1992

Posttraumatic epilepsy in civilians: clinical and electroencephalographic studies.

Posttraumatic epilepsy (PTE) is a known consequence of head trauma. The factors involved in posttraumatic seizures generation and the relationship between acute seizures and posttraumatic epilepsy are not without controversy. This also applies to the evolution of the electroencephalographic characteristics. The study here reported was performed analysing data from patients with posttraumatic epilepsy (N = 205) and data from patients followed-up since trauma and considered as a high risk population for the development of PTE (patients with acute seizures and/or patients with focal lesions--contusion, haematomas or penetrating head injury) (N = 152). Seizure type was associated with age and trauma severity (children, elderly and worst trauma cases present with a higher proportion of partial seizures). Neurological deficit and lesion location were associated with the seizure occurrence. The increased incidence of seizures was found when the most diffused brain dysfunction was combined with neurological deficits. The analysis of sequential EEGs performed at first, at 6th and 12 months post trauma revealed a non-stationary pattern throughout these time periods with EEG focal abnormalities remaining frequent for more than two years after the trauma. Children and old people have a higher proportion of EEG abnormalities with more frequent abnormal generalized activity in children and more frequent abnormal focal EEG activity in the elderly.

Adult↗
PubMed1992

Risk factors for late posttraumatic epilepsy.

The usually accepted risk factors for late post-traumatic seizures (LPTS) are those identified years ago by Jennet: early post-traumatic seizure (EPTS), depressed fracture, intracranial haematoma. Prolonged unconsciousness (PTA greater than 24 hrs) is another factor usually added. More recently, personal experience of the Authors and the data of the literature, compel us to question the validity of known risk factors based on clinical data. Authors believe that the identification of patients at risk for LPTS depends mainly on the precise definition of trauma severity and on CT or surgically documented lesions of brain substance. Three groups of patients, characterized by the presence of one or more of the accepted risk factors of LPTS, have been studied. In our experience, while in adults the presence of documented cortico-subcortical lesions represents the main risk factor of LPTS, in children the appearance of EPTS per se increases the risk of LPTS, irrespective of the presence of documented brain lesions. Alteration of consciousness without a focal lesion, even if prolonged and severe, is not a risk factor for LPTS.

Adolescent↗
PubMed1992

Comparative study of magnetic resonance and CT scan imaging in cases of severe head injury.

The distribution, frequency, and appearance of head injuries were evaluated with MRI and CT in a prospective study of 155 patients with acute (n = 124) and chronic (n = 31) head injuries. MRI was significantly more sensitive than CT in the detection of intraaxial injury at any stage. In severe cases, central structure lesions were detected in approximately 80% of patients. Severity on admission was compatible with MR findings. However it was difficult to decide on neurobehavioural prognosis from initial MRI findings only.

Adolescent↗
PubMed1992

Early post-traumatic cerebral blood flow mapping: correlation with structural damage after focal injury.

Focal post traumatic mass lesions such as contusions and intracerebral haematomas are common, and often difficult for neurosurgeons to manage, because little is known of their pathophysiology. We have mapped cerebral blood flow, and studied small vessel ultrastructure at different time points within the first three weeks of head injury, in patients with these lesions. A zone of ischaemic brain is always present around these lesions, and persists for weeks or months. This accords with astrocyte swelling and microvascular compression seen on electron microscopy. Focal zones of hyperaemia were also present in 42% of patients, within the first two weeks of injury, and this appeared only within apparently normal tissue as judged by late MRI or CT.

Astrocytes↗
PubMed1993

Monitoring of regional cerebral blood flow (CBF) in acute head injury by thermal diffusion.

During the last few years continuous measurements of CBF by means of a thermal diffusion blood flow probe have been proposed as a possible means for monitoring the patient's CBF in a clinical setting. Also, it has been suggested that continuous CBF data from head injured patients can be correlated with other continuously recorded clinical parameters, such as ICP and blood pressure, in order to clarify pathophysiological mechanisms such as "plateau-waves". We measured regional cortical blood flow continuously with a thermal diffusion flow probe in 13 comatose head injured patients after undergoing craniotomy for evacuation of a traumatic intracranial mass lesion in order to assess the reliability and usefulness of the method. In seven patients stable Xenon-CT CBF studies were performed with the flow probe in place, in order to compare the two methods. The continuous blood flow values did not correlate with regional or global stable Xenon-CT values. These results indicate that continuous monitoring of CBF with the thermal diffusion method as currently used cannot be used in the clinical management of the patient. Further research will have to be directed to the question as to whether changes in CBF are reliably measured with this method. If this is true, the thermal diffusion flow probe with its high temporal resolution may still be useful in investigating pathophysiological mechanisms such as interaction between CBF, ICP, mean arterial blood pressure (MABP), and end-expiratory CO2 (etCO2).

Adolescent↗
PubMed1994

Growth kinetics of a primary brain tissue necrosis from a focal lesion.

Secondary brain damage, such as brain edema or impairment of the cerebral microcirculation may evolve from tissue necrosis of the brain induced by trauma or ischemia. This laboratory has provided novel information on the secondary increase of a primary brain tissue necrosis resulting from a focal lesion. We have presently investigated more closely the growth kinetics of this process during 24 h after trauma. Rats were subjected to a standardized focal freezing injury of the brain. Area and volume of the resulting necrosis were quantitatively assessed by morphometry after different periods of survival (i.e., 5 min, 3, 6, 12, 18 and 24 h after trauma). The maximal area of necrosis increased by 45% (p < 0.001) during the posttraumatic observation period. Growth of necrosis after trauma was not limited to the early period, but continued between 12 and 24 h, amounting then to 29% (p < 0.05). The volume of necrosis calculated on the basis of histological serial sections was also observed to increase by 45%. The current findings confirm that a primary brain tissue lesion induced by a standard cryogenic injury, studied as model of a contusion focus in severe head injury, is subjected to secondary growth within a period of 24 h after trauma, longer periods of survival were not investigated yet. Quantification of lesion growth makes possible not only to study underlying mechanisms, but also of whether this process can be therapeutically inhibited.

Animals↗
PubMed1994

Focal brain injury: histological evidence of delayed inflammatory response in a new rodent model of focal cortical injury.

Cortical contusions are one of the most common characteristics in head injury and are regarded by many as the hallmark of significant injury. No experimental study has clarified the roles of mechanical forces, haemorrhage and ischaemia in the process of progressive acute brain damage and later neurobehavioural dysfunction. We have devised a new, simple reproducible rodent model of focal cortical injury which employs a 'pure' mechanical/physical force applied through the intact dura. Using this model we have investigated the time course and pattern of changes in neurons, glia and microvasculature. With the exception of haemorrhage, this model closely reproduces the light- and electron microscopy features of human contusion. In the absence of perivascular haemorrhage we have demonstrated delayed perivascular protein leakage and polymorphonuclear-leukocyte infiltration of the damaged cortex. We postulate that a component of the delayed blood brain barrier breakdown demonstrated in human focal head injury (which may contribute to swelling and brain damage) is due to an acute inflammatory response, the magnitude of which is dependent on the amount of tissue injury.

Acute-Phase Reaction↗
PubMed1994

Blood-brain barrier, cerebral blood flow, and cerebral plasma volume immediately after head injury in the rat.

The purpose of the present study was to determine blood-brain barrier (BBB) permeability, regional cerebral blood flow (rCBF) and regional cerebral plasma volume (rCPV) in the period immediately after head injury, and thereby to evaluate the effects of vascular factors in the pathophysiology of traumatic brain injury. Male Sprague-Dawley rats (350-450 g) anesthetized with 1.0-1.5% halothane were subjected to an impact acceleration closed head injury at the moderate level. BBB permeability (n = 5), rCBF (n = 8) and rCPV (n = 9) were measured by quantitative autoradiographic techniques using 14C-alpha-aminoisobutyric acid (AIB), 14C-iodoantipyrine and 14C-sucrose, respectively. Intravenous administration of each radiotracer was simultaneous with the traumatic impact. At 10 min after injury, BBB permeability, the transfer constant for AIB, was less than 0.1 ml/kg/min for all regions except for those with a relatively leaky BBB. At 30 s after injury, a significant and heterogeneous increase in rCBF was observed at 9 subcortical regions (p < 0.05). RCPV increased significantly in the frontal cortex, parietal cortex, thalamus, and hypothalamus (p < 0.05). In our closed head injury model without severe hypertension, BBB disruption did not occur immediately after trauma. Vascular responses in the period immediately after trauma may result from the derangement of cerebral autoregulation.

Animals↗
PubMed1994

Long term exposure to heat reduces edema formation after closed head injury in the rat.

Cerebral edema is one of the major consequences of head trauma (HT); its evolution may cause secondary ischemia and neuronal damage. In a closed head injury model in rats, we have shown BBB disruption and edema formation during the post traumatic period. We have previously shown that chronic exposure to moderate heat improves clinical outcome of rats subjected to HT. Long term exposure to heat results in the achievement of a stable acclimated state, characterized by a lower metabolic rate and improved heat tolerance. In the present study, we investigated the effect of chronic exposure to heat on edema formation after HT. Rats were held at 24 degrees C (CON) or 34 degrees C (ACC) for one month. Injury was then induced under ether anesthesia by a weight drop device. Four or 48 hours later, they were sacrificed for evaluation of BBB integrity (Evans blue, EB, extravasation) or edema formation (specific gravity, SG, or percent water). We found that EB uptake by the contused hemisphere was 6 fold lower in the ACC rats as compared to CON (p < 0.001). Furthermore, edema measured at 48 h by both SG and percent water methods was significantly lower in the acclimated rats (p < 0.01). We suggest that heat acclimation offers protection to rats subjected to head injury, possibly by reduction of plasma proteins extravasation.

Acclimatization↗
PubMed1994

Metabolic changes following cortical contusion: relationships to edema and morphological changes.

Rats with contusion injury to the right cortex exhibited significant formation of edema 6 and 24 hours after injury which resolved by 8 days and was replaced by cavitation necrosis. The contusions produced hyperglycolysis and ischemia in the impacted cortical tissue and underlying hippocampus immediately through 30 minutes post-injury. Glucose utilization was depressed throughout the contused cortex and in ipsilateral subcortical regions, as was blood flow, at chronic (1 and 10 days) periods after injury.

Animals↗
PubMed1994

Gadolinium DTPA-enhanced magnetic resonance imaging of cerebral contusions.

The morphological characteristics of cerebral contusions in head trauma patients suggest that an increase in cerebrovascular permeability is responsible for the contusion edema which develops within 1-3 days posttrauma. In the present study, 10 patients with cerebral contusions (mean age, 38 years old; 8 males and 2 females) were examined by gadolinium (Gd)-DTPA enhanced magnetic resonance imaging (MRI) at 1-2 days after trauma. Gd-DTPA (0.3 mmol/kg) was infused intravenously over a period of 30 min. MRIs were taken before, and at 2 and 4 hours after initiation of the Gd-DTPA administration. It was found that contusion edema areas were frequently enhanced by Gd-DTPA at 2 hours. The enhancement diminished at 4 hours. These findings appear to be inconsistent with the results of previously reported similar studies in which enhancement was detected at 6-9 days posttrauma but not during the period earlier than 6 days. This discrepancy may be attributable to the presence of a high blood concentration of Gd-DTPA for a longer period of time and a delay in the time at which MRIs were taken in the present study. The present data indicate that an increased cerebrovascular permeability occurs at as early as 1-2 days posttrauma, and suggest that contusion edema which progresses during the initial 1-3 days may be at least partially vasogenic in nature.

Adolescent↗
PubMed1994

Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema.

Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.

Adolescent↗
PubMed1994

Administration of an omega-conopeptide one hour following traumatic brain injury reduces 45calcium accumulation.

The omega-conopeptide, SNX-111 (NEUREX Corporation) was administered to rats 1 hour following a lateral fluid percussion brain injury to determine if the drug could reduced the extent and duration of trauma-induced calcium accumulation. Administration at doses of 3 or 5 mg/kg (i.v.) markedly reduced the extent of calcium accumulation as determined using 45calcium autoradiography primarily within the cerebral cortex and hippocampus. The reduction of calcium accumulation was particularly event within the parietal cortex beginning as early as 6 hours and lasting out to 48 hours following injury. Although not as effective as in the cerebral cortex, SNX-111 did exhibit a reduction of calcium accumulation within the dorsal hippocampus especially at 24 and 48 hours after the insult. These preliminary results demonstrate that SNX-111 can reduce the injury-induced accumulation of calcium even when administered 1 hour after the insult and offers this compound as a potential therapeutic treatment for traumatic brain injury.

Animals↗
PubMed1994

Excitatory amino acid release from contused brain tissue into surrounding brain areas.

The EAA release from contused brain tissue and its effect on the extracellular EAA levels in brain areas surrounding the contusion were investigated with microdialysis technique in the rat. A significant increase in extracellular EAA levels was observed in the contused brain tissue. The EAA increase was significantly greater in the contused brain tissue than in the isolated but non-contused brain tissue. It was further demonstrated that EAAs were released from non-contused brain areas 1-2 mm distant from contused brain tissue. No such EAA release from surrounding brain areas was demonstrated when the cavity was filled with isolated but non-contused brain tissue. The increase in EAAs was attenuated by KYN administered through microdialysis, suggesting that the EAA release from the surrounding brain areas appears to be a consequence that is secondary to the EAA release from the contused brain tissue. Such a diffusion-reaction process is probably mediated by the neurotransmitter actions of EAAs. The results of the present study are of clinical importance, since surgical removal of contused brain tissue and administration of EAA antagonists may serve to protect the surrounding brain areas from EAA neurotoxicity.

Animals↗
PubMed1994

High colloid oncotic therapy for contusional brain edema.

We investigated whether prolonged high colloid oncotic therapy for two weeks can suppress contusional brain edema. Eighteen patients with cerebral contusion were randomly divided into two groups of patients receiving high oncotic pressure (HOP; 26-30 mmHg) treatment and those receiving normal oncotic pressure (NOP; 22-26 mmHg) treatment. Oncotic pressure was maintained for two weeks with administration of a 25% albumin solution with additional use of furosemide. Edema volume was calculated by summation of all measured low-density areas in each CT slice multiplied by 1.0 cm of slice of thickness. We expressed contusional brain edema volume as a percent increase based on each patient's initial CT. The mean percent increase of contusional brain edema in the NOP group was significantly higher than that in the HOP group at 9-15 days (208.9% and 14.0%, respectively) and 16-25 days (188.8% and 10.0%, respectively). There were no complications such as heart failure or renal failure during treatment. All the patients in the HOP group recovered with minimal or no neurological deficit. On the other hand, 30% of patients in the NOP group remained in poor condition. With frequent measurement of oncotic pressure and adjustment of fluids and electrolytes, continuous oncotic therapy for two weeks effectively and safely reduced contusional brain edema.

Adolescent↗
PubMed1994

Effect of barrier opening on brain edema in human brain tumors.

Blood-brain barrier (BBB) opening was carried out in 10 patients with cerebral lesions, and the MRI findings were evaluated following the barrier opening. An intra-arterial injection of 10% glycerol (4 ml/kg, 1 approximately 2 ml/s) was given as a hyperosmotic solution. T2-weighted MRI was undertaken using a TOSHIBA 22A at 30 minutes after BBB opening. Barrier-opening MRI was performed 10 times in 10 patients, including 5 cases of glioblastoma multiforme, 2 cases of astrocytoma, 1 case of malignant lymphoma, 1 case of cerebral contusion and 1 case of neurinoma. The high-intensity area (HIA) was compared with that in MRI without barrier opening. Three types of changes of HIA in MRI were observed after BBB opening as follows. Type 1: Expansion of the HIA was noted in 4 of 5 cases of glioblastoma multiforme, the 1 case of malignant lymphoma and the 1 case of cerebral contusion. Type 2: Almost no change was observed in the 1 case of neuronoma. Type 3: A decrease in HIA was noted in the 2 cases of astrocytoma and in 1 case of glioblastoma multiforme. The MRI following BBB opening evidently showed 3 types of changes according to the degree of BBB disruption. Glioblastoma multiforme or contusion with a severely disrupted BBB revealed an increase in HIA following barrier opening. Benign posterior fossa neurinoma showed no change in HIA after barrier opening. Moderate malignant tumors exhibited a decrease in HIA on barrier-opening MRI. It was concluded that malignant tumors have a severely damaged BBB, which is readily disrupted by osmotic barrier opening.

Adult↗
PubMed1996

Traumatically induced axonal damage: evidence for enduring changes in axolemmal permeability with associated cytoskeletal change.

Recent studies have demonstrated that delayed or secondary axotomy is a consistent feature of traumatic brain injury in both animals and man. Moreover, these studies have shown that the pathogenesis of this secondary axotomy involves various forms of initiating pathology, with the suggestion that, in some cases, only the axonal cytoskeleton is perturbed, while, in other cases, both the axonal cytoskeleton and related axolemma manifest traumatically induced perturbations. In the current communication, we continue in our investigation of the significance of these traumatically induced alterations in axolemmal permeability and their relation to any related intra-axonal cytoskeletal change. This was accomplished in cats which received intrathecal infusions of peroxidase, an agent normally excluded by the intact axolemma. These animals were subjected to traumatic brain injury, and sites showing altered axolemmal permeability to the peroxidase were assessed at the light and electron microscopic level. Through this approach, we recognized that a traumatic episode of moderate severity evoked changes in axolemmal permeability which surprising endured for up to 5 hrs postinjury. At such focal sites of altered permeability, the related cytoskeleton showed a statistically significantly neurofilament compaction, with the strong suggestion of concomitant neurofilament sidearm loss, microtubular dispersion, and mitochondrial abnormality. Over time, these events led to further disorganization of the axonal cytoskeleton which translated into impaired axoplasmic transport and secondary axotomy. Most likely, these alterations in axolemmal permeability result in either the direct or indirect effects upon the axonal cytoskeleton that precipitate the damaging sequences resulting in delayed axotomy.

Animals↗