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Results for “EPILEPSY, TRAUMATIC”

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PubMed1977

Laughing and running fits as manifestation of early traumatic epilepsy.

Early traumatic epilepsy, whose frequency is rather high, especially in children, is usually characterized by focal motor seizures (57%) or by generalized seizures (43%). The association of both running and laughing fits in the same patient on the contrary is quite exceptional, as only three cases have been reported in literature. There are no observations about temporal lobe epilepsy, nor, particularly, about running or laughing fits in early traumatic epilepsy. We report here the interesting case of a boy whose early traumatic epilepsy manifested itself as temporal lobe epilepsy characterized by running and laughter.

Child↗

PubMed1998

[Post-traumatic epilepsy].

Post-traumatic epilepsy is a well-known complication of head injury (TCE). There is extensive bibliography on the subject which contains contradictory data and unanswered questions. In this paper, we review and update the literature emphasizing particularly current definitions, incidence, risk factors and evaluation of prophylactic treatment in relation to the physio-pathology. We give data of a retrospective study of the cases observed during the past 15 years in our unit, analyzing the factors which may help to predict the evolution of these crises. There is a relationship between the incidence of post-traumatic epilepsy and the severity of injury. One of the main risk factors is the presence of focal lesions, particularly haemorrhagic lesions. Prophyllactic treatment with anti-epileptic drugs is only effective during the first week in the group at risk of developing early crises. It has not been shown to be of use in preventing post-traumatic epilepsy. Other treatments, such as antioxidants, calcium antagonist and glutamate inhibitors are still only at an experimental stage.

Adult↗

PubMed2003

Indriven sphenoid wing as a cause of post-traumatic epilepsy.

Post-traumatic epilepsy is more frequent after severe head injuries, however the severity of the trauma is not always correlated with the injured brain tissue. We report a patient whose seizures developed 4 years after a face trauma. Upward displacement of the sphenoid wing caused a contusion at the orbital surface of the frontal lobe. Computed tomography, magnetic resonance imaging and electroencephalographic findings are presented. The patient responded well to commonly used antiepileptic drugs.

Adult↗

PubMed2006

Prevention and treatment of post-traumatic epilepsy.

Post-traumatic epilepsy is reported after 2-5% of closed head injuries but up to 50% or more following penetrating head injury. Despite several studies, no drug strategy has been able, to date, to quench the biochemical events leading to epileptogenesis. One possibility is that treatment with available antiepileptic drugs has been implemented too late, and thus, ultra-early treatment might still be able to stop the neurochemical epileptogenic cascade dead in its tracks. However, currently drug therapy should be instituted only after the first late unprovoked seizure.

Aged↗

PubMedDate not supplied

Post traumatic epilepsy: a review of scientific evidence.

Post traumatic epilepsy is the development of recurrent seizures following head trauma and has a high clinical relevance. Several risk factors including some genetic factors increase the susceptibility of post traumatic epilepsy. The precise mechanisms of epileptogenesis in post-traumatic epilepsy are still poorly understood. Many structural, physiologic and biochemical changes in the brain may account for epileptogenesis. The reactive oxygen species (ROS), especially *OH and excitotoxicity are primarily involved. Antioxidants, like tocopherol, antiepileptic drug zonisamide, condensed tannins, melatonin, adenosine, trans-resveratrol, and some other agents have been proposed to prevent epileptogenic focus formation. The review also discusses various aspects of post traumatic epilepsy, mechanisms of epileptogenesis, and clinical implications.

Animals↗

PubMed2001

[The forensic determination of post-traumatic epilepsy in 21 patients].

UNLABELLED: To evaluate the forensic determination of post cerebral traumatic epilepsy. METHODS: In 21 patients, traumatic history and previous history were analysied combined with the demonstrations of electroencephalogram(EEG), X-ray, CT and MRI. RESULTS: Post-traumatic epilepsy, manily in late stage, usually occurred following serious cerebral trauma. The type of traumatic epilepsy was determined by the traumatic location and extent. Abnormal epileptic wave in scalp EEG and 24 h dynamic EEG and medical image examinations were helpful for qualitative analysis. CONCLUSION: The forensic determination of post traumatic epilepsy must be on the basis of traumatic and previous history combined with EEG, CT and MRI analysis.

Adult↗

PubMed2005

Post-traumatic epilepsy: an overview.

Post-traumatic epilepsy (PTE) is a recurrent seizure disorder secondary to brain injury following head trauma. PTE is not a homogeneous condition and can appear several years after the head injury. The mechanism by which trauma to the brain tissue leads to recurrent seizures is unknown. Cortical lesions seem important in the genesis of the epileptic activity, and early seizures are likely to have a different pathogenesis than late seizures. Anti-epileptic drugs available for treatment are phenytoin, sodium valproate, and carbamazepine. Newer anti-epileptics are helpful, particularly in patients with associated post-traumatic stress disorders; however, no randomized controlled studies are available to prove that one of these drugs is better than the other. Current evidence is that the treatment of early post-traumatic seizures does not influence the incidence of post-traumatic epilepsy. Routine preventive anticonvulsants are not indicated for patients with head injuries, and treatment in the acute phase does not reduce death or disability rates.

Anticonvulsants↗

PubMed1991

[Surgical treatment of traumatic epilepsy].

Fifteen patients with traumatic epilepsy were treated surgically. Cortico-electroencephalography was used during the operation. Meningo-encephalo cicatrix was found in 8 patients, scar formation in brain parenchyma in 4, meningoencephalocele in 2, and porencephalia in 1. Seven of the 15 patients were examined by CT, showing more accurate localization of pathological changes. Seizure subsided in 8 patients. Anti-epileptic drugs were still used in 4 patients, but the frequency and severity of epileptic attack were obviously decreased. There was no operative mortality. The indications, techniques of the operation and the postoperative management were discussed.

Adolescent↗

PubMed1995

Causes, prevention, and treatment of post-traumatic epilepsy.

Post-traumatic seizures often occur after severe head injury. Acutely, these seizures complicate management of the head-injured patient by increasing intracranial pressure and causing postictal decreases in level of consciousness. In the long term, epilepsy can have a negative effect on the patient's functioning and integration into society. The more severe the head injury, the more likely that post-traumatic seizures will occur. The risk of late seizures exceeds 30% for patients with penetrating head injury, intracerebral hematoma, subdural hematoma, depressed skull fracture, or seizure within the first week after injury. Late post-traumatic seizures are treated the same as any epileptic seizures of the same type. Phenytoin and carbamazepine are effective in preventing seizures in the first week after head injury, but are not effective in preventing late seizures. Both additional antiepileptic drugs and neuroprotective agents that may lessen the damage that leads to seizures are being investigated to determine if they are effective in preventing the occurrence of post-traumatic epilepsy.

Anticonvulsants↗

PubMed2002

alpha-Tocopheryl-L-ascorbate-2-O-phosphate diester, a hydroxyl radical scavenger, prevents the occurrence of epileptic foci in a rat model of post-traumatic epilepsy.

Intracortical injection of iron ions has been used to model post-traumatic epilepsy. The results obtained using these models suggest that oxidation of neural membranes by active oxygen free radicals may be involved in the etiology of post-traumatic epilepsy. This is a study of the effects of alpha-tocopheryl-L-ascorbate-2-O-phosphate diester potassium salt (EPC-K1), known as a hydroxyl radical scavenger, on the peroxidation of neural membranes by FeCl(3) in vitro and on the occurrence of epileptic discharges in the FeCl(3) injected post-traumatic epilepsy model rats. EPC-K1 dose-dependently inhibited the production of thiobarbituric acid reactive substances (TBARS) and protein carbonyl (P-Carb), both indices of biogenic macromolecular peroxidation. In vivo studies, sporadic spike discharges and/or epileptiform activities were observed in electrocorticograms (ECoG) of male Sprague-Dawley rat 15-90 min after 500 nmol of FeCl(3) was injected into the motor cortex. On the other hand, when 200 mg/kg of EPC-K1 was injected intraperitoneally 60 min prior to the injection of FeCl(3), the occurrence of epileptic discharges was prevented or delayed. When EPC-K1 (2.5-5 nmol) was injected along with the ferric ions, the occurrence of epileptiform activities was also prevented or delayed. EPC-K1 prevented the induction of early convulsion, the major risk factor of post-traumatic epilepsy. Rats in the Fe+EPC group were injected with 500 nmol of FeCl(3) into the left motor cortex and were given an EPC-K1-diet (CE-2 chow contained 0.2% of EPC-K1, and daily EPC-K1 intake was about 80 mg/kg/day). In the Fe+EPC group rats, the percent induction of epileptic discharges in ECoGs was significantly lower than that in the Fe+CE group rats, which were fed CE-2 after FeCl(3) injection. In the homotropic contra lateral cortex, TBARS and P-Carb content did not show any changes. However, the relative TBARS content in the focal area significantly increased in the Fe+CE and Fe+EPC group rats 3 h after the injection. It became normal 3 days after in the Fe+EPC group. The relative P-Carb content in the focal area significantly increased in the Fe+CE and Fe+EPC group rats 3 h after the injection. However, it became normal after 3 days. In the present study, EPC-K1, which consists of vitamins E and C connected by a phosphate, protected the oxidation of neural membranes and prevented the occurrence of ferric ion-induced epileptic discharges by its radical scavenger activity. These data suggest that EPC-K1 may be clinically useful in not only preventing the focus formation of post-traumatic epilepsy, but also in treating and attenuating the progression of free radical-induced degenerative disorders.

Journal Article↗

PubMed1992

[Epidemiologic study of post-traumatic epilepsy on the Island of Majorca].

The epidemiological study of post-traumatic epilepsy after 10 years of follow-up on the island of Mallorca is reported. The double prospective and retrospective method was used for patient selection. Prospectively, 23,082 isolated head injuries were studied in the Hospital of Son Dureta in Palma de Mallorca between the years 1980 to 1988. Retrospectively, 663 epileptics proceeding from different data bases of different centers were studied. Two hundred and twelve post-traumatic epilepsies of certain etiology were identified. Results are discussed with regard to age, sex and latency time found. Special emphasis is made in that benign cerebral concussion is not causing seizures. A prevalence of 4% of post traumatic epilepsy is found in the population of risk head injuries, and post-traumatic epilepsy represents 7% of the total of the casuist of epileptic patients.

Adolescent↗

PubMed2002

Post-traumatic epilepsy in children requiring inpatient rehabilitation following head injury.

OBJECTIVE: To study the prevalence of, and identify possible risk factors for, the development of post-traumatic epilepsy in a cohort of children with severe head injury treated in an inpatient rehabilitation unit. METHODS: The hospital and community medical case notes of all children admitted prospectively to the unit and the records of the clinical EEG department over a seven year period were reviewed to identify those children who had developed late epilepsy after head injuries. RESULTS: 102 children received inpatient rehabilitation between 1 June 1991 and 28 February 1998. Follow up of these patients ranged from 18 months to over eight years. Nine patients (9%) developed post-traumatic epilepsy between eight months and over five years after the head injury. Three of the nine patients had experienced early tonic-clonic seizures in the first week after the injury. Other risk factors examined included the age of the patient, the cause of the head injury, initial Glasgow coma scale score, neuroimaging findings, and duration of ventilatory support. Only the presence of early seizures (p = 0.002) and possibly the Glasgow coma scale score (p = 0.043) were found to be specific risk factors for late late epilepsy. CONCLUSIONS: Post-traumatic epilepsy appears to be uncommon, even in children with severe head injuries. Early seizures may indicate increased risk of developing late post-traumatic epilepsy in this study population.

Adolescent↗

PubMed1986

[Prevention of traumatic epilepsy in ambulatory care facilities].

The causes of 1382 readmissions of 156 patients with traumatic epilepsy were studied with regard to the seasonal and pathogenic factors. It was established that readmissions of patients with traumatic epilepsy directly correlated with the spring and autumn seasons and 8 pathogenic factors (no maintenance therapy, psychogenias, dysphorias, intoxication with antiepileptic drugs, alcoholization, infectious diseases and inadequate rehabilitative measures). The data obtained will help neuropathologists and psychiatrists to time repeated prophylaxis of traumatic epilepsy under outpatient conditions.

Adult↗

PubMedDate not supplied

[Clinical course of post-traumatic epilepsy in children].

The authors review critically the traditionally accepted views on post-traumatic epilepsy in children. The analysis is based on 385 children hospitalized for craniocerebral injuries and 42 of these children (10.91%) in whom post-traumatic epilepsy developed. In the pathogenesis of this epilepsy development of essential importance were early beginning and frequently recurring attacks. Serial EEG was useful and the clinical pattern was initially non-characteristic. In the prevention of post-traumatic epilepsy careful prevention of secondary changes and primary neurosurgical management are of particular importance in the acute phase, while the effect of anticonvulsive treatment as prophylaxis is still a problem at issue.

Adolescent↗

PubMed1990

[Nootropic agents in the complex treatment of patients with traumatic epilepsy].

A study was made of the therapeutic efficacy of nootropic agents in multimodality treatment of 62 patients with traumatic epilepsy. The treatment efficacy was appraised with regard to the time-course of changes in psychopathological symptomatology. The data obtained have been processed statistically according to criteria for the signs. When applied in multimodality treatment of patients with traumatic epilepsy the nootropic agents turned out most efficacious for the psycho-organic syndrome and for the status of deranged consciousness. The use of the nootropic agents as part of rehabilitation therapy allows improvement of the secondary prophylaxis of traumatic epilepsy.

Adult↗

PubMed1989

[Early diagnosis of traumatic epilepsy].

The risk factors and clinical course of prodromal period were studied in 184 patients with traumatic epilepsy. Statistically reliable as predictors of traumatic epilepsy were: brain concussion++, open lesions of the skull, repeated craniocerebral trauma, comatose after-trauma states lasting over more than 6 hours, episodes of consciousness confusion, myoclonic spells. The establishment of the risk factors in the prodromal stage of posttraumatic epilepsy provides means for the early diagnose, secondary prevention and social-hygienic measures designing.

Adult↗

PubMed1982

CT scan prediction of late post-traumatic epilepsy.

Out of 233 patients admitted for head trauma during 1977-1978, 93 had a CT scan examination within the first 48 hours. Forty-nine of these had at least one clinical risk factor for post-traumatic epilepsy. Ten of this group developed post-traumatic epilepsy. In all cases early CT scan showed focal brain damage, which was related more significantly to post-traumatic epilepsy than to risk factors.

Brain Edema↗

PubMed1989

[The results of computed tomography in patients with traumatic epilepsy].

Computerized tomography in 134 patients with traumatic epilepsy allowed to reveal different changes in the brain tissue, meninges and CSF spaces. Early stages were characterized by signs of meningeal adhesions. With increased duration of the disease these changes were supplemented by signs brain atrophy in the form of dilatation of the subarachnoidal spaces, internal hydrocephalus. CSF cysts were diagnosed in 5 patients, porencephaly in 2, ischemia foci in the brain in 9 patients.

Adolescent↗