Post-traumatic epilepsy: its complications and impact on occupational rehabilitation--an epidemiological study from India. (1/68)

The objective of this study was to assess the prevalence of seizure disorder, neuropsychiatric disorders and reproductive outcome of employees with post-traumatic epilepsy (PTE) and their effect on occupational rehabilitation. A case-comparison group study design was used to compare 30 subjects with PTE with (1) 129 non-PTE and (2) 55 non-PTE matched control employees. The 55 non-PTE matched controls were selected from the 129 non-PTE employees on the basis of age, age at onset of seizure, age at marriage and length of employment. The PTE group had a lower fertility rate than the controls and more neuropsychiatric disorders and seizure disability. PTE employees were more occupationally rehabilitated than non-PTE employees (p = 0.033). Of the 30 PTE subjects, thirteen who were rehabilitated by placement had more seizure disability (p = 0.007) and a higher fertility rate (p = 0.018). High prevalence of seizure disability and increased fertility rate among the placed PTE employees suggested that there might be some association between severity of seizures and increased production of live offspring and work placement. Work suitability or placement should not be judged on clinical assessment only but psychosocial seizure assessment, disability evaluation and other psychometric tests which are of equal importance.  (+info)

Acute psychotic symptoms induced by topiramate. (2/68)

The incidence of psychosis during clinical trials of topiramate was 0.8%, not significantly different from the rate for placebo or reported rates of psychosis in patients with refractory epilepsy. We observed psychotic symptoms in five patients soon after initiation of topiramate therapy. We performed a retrospective chart review of the first 80 patients who began on topiramate after approval for clinical use, between January and April 1997. Symptoms suggestive of psychosis, including hallucinations and delusions, were sought for analysis. Cognitive effects such as psychomotor slowing, confusion, and somnolence were not included. Five patients developed definite psychotic symptoms 2 to 46 days after beginning topiramate. Dosages at symptom onset were 50-400 mg/day. Symptoms included paranoid delusions in four patients and auditory hallucinations in three. Symptoms of psychosis and other psychiatric symptoms resolved quickly with discontinuation of topiramate in three patients, dose reduction from 300 to 200 mg/day in one and with inpatient treatment and neuroleptics in another. One patient had a history of auditory hallucinations, one of aggressive and suicidal thoughts, but three had no significant psychiatric history. Physicians should be aware of the possibility of psychotic symptoms, even in patients without a previous psychiatric history, when prescribing topiramate. Symptoms resolve quickly with discontinuation.  (+info)

Increased pyramidal excitability and NMDA conductance can explain posttraumatic epileptogenesis without disinhibition: a model. (3/68)

Partially isolated cortical islands prepared in vivo become epileptogenic within weeks of the injury. In this model of chronic epileptogenesis, recordings from cortical slices cut through the injured area and maintained in vitro often show evoked, long- and variable-latency multiphasic epileptiform field potentials that also can occur spontaneously. These events are initiated in layer V and are synchronous with polyphasic long-duration excitatory and inhibitory potentials (currents) in neurons that may last several hundred milliseconds. Stimuli that are significantly above threshold for triggering these epileptiform events evoke only a single large excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). We investigated the physiological basis of these events using simulations of a layer V network consisting of 500 compartmental model neurons, including 400 principal (excitatory) and 100 inhibitory cells. Epileptiform events occurred in response to a stimulus when sufficient N-methyl-D-aspartate (NMDA) conductance was activated by feedback excitatory activity among pyramidal cells. In control simulations, this activity was prevented by the rapid development of IPSPs. One manipulation that could give rise to epileptogenesis was an increase in the threshold of inhibitory interneurons. However, previous experimental data from layer V pyramidal neurons of these chronic epileptogenic lesions indicate: upregulation, rather than downregulation, of inhibition; alterations in the intrinsic properties of pyramidal cells that would tend to make them more excitable; and sprouting of their intracortical axons and increased numbers of presumed synaptic contacts, which would increase recurrent EPSPs from one cell onto another. Consistent with this, we found that increasing the excitability of pyramidal cells and the strength of NMDA conductances, in the face of either unaltered or increased inhibition, resulted in generation of epileptiform activity that had characteristics similar to those of the experimental data. Thus epileptogenesis such as occurs after chronic cortical injury can result from alterations of intrinsic membrane properties of pyramidal neurons together with enhanced NMDA synaptic conductances.  (+info)

The risks of epilepsy after traumatic brain injury. (4/68)

The aim of this study is to present the incidence of traumatic brain injury (TBI) and identify those characteristics of brain injuries that are associated with the development of seizures. We identified 5984 episodes of TBI (loss of consciousness, post-traumatic amnesia, or skull fracture) in Olmsted County, Minnesota, from 1935 to 1984. Of these, 4541 were followed for seizure. Injuries were classified as mild (loss of consciousness or amnesia less than 30 minutes), moderate (loss of consciousness 30 minutes to 1 day or a skull fracture), or severe (loss of consciousness of more than 1 day, subdural hematoma, or brain contusion). The incidence of TBI in the period from 1975 to 84 peaked at 800 per 100 000 in males aged 15-24. The relative risk of seizures was 1.5 (95 percent confidence interval 1.0-2.2) after mild injuries, but with no increase after 5 years; 2.9 (95 percent confidence interval 1.9-4.1) after moderate injuries; and 17.2 (95 percent confidence interval 12.3-23.6) after severe injuries. Significant risk factors were brain contusion with subdural hematoma, skull fracture, loss of consciousness or amnesia of 1 day or more, and age over 65 years. We conclude that TBI is a major public health problem and contributes to the occurrence of seizures and epilepsy.  (+info)

Current perception thresholds of epileptic patients treated with valproate. (5/68)

We investigated the current perception threshold (CPT) of epileptic patients treated with valproate. The CPTs at frequencies of 5 Hz, 250 Hz and 2000 Hz in the control group of patients were 198.9 +/- 15.8, 62.0 +/- 18.9 and 35.3 +/- 15.8, respectively. The CPTs at 5 Hz, 250 Hz and 2000 Hz in the epileptic group of patients were 350.6 +/- 61.3, 338.6 +/- 64.3 and 193.2 +/- 21.1, respectively. The CPTs at 5 Hz, 250 Hz and 2000 Hz in the epileptic group were significantly higher than those of the control group. We measured the CPTs for 6 months after the administration of valproate in three patients with traumatic epilepsy. Their CPTs were higher than that of the epileptic group. The CPTs at 5 Hz, 250 Hz and 2000 Hz reached a maximum 4 weeks after the administration of valproate for two of these patients and in 6 weeks for the other patient. When the administration of valproate to a patient was stopped, CPTs decreased.  (+info)

The attitude of courts in England to compensation for post-traumatic epilepsy. (6/68)

The attitudes of courts in England to the assessment of damages for post-traumatic epilepsy have dramatically changed over the last 20-30 years. In assessing damages for post-traumatic epilepsy the courts are faced with a number of considerations: epilepsy can appear several years after the injury; epilepsy is not a homogeneous condition; the eventual prognosis is unknown; the epilepsy may not have been directly due to the trauma; and epilepsy affects life expectancy and employment. Damages were originally fixed at the point of compensation, and these rather crude calculations led to both over- and under-compensation. This situation was improved in 1985, when courts were permitted to award damages on the assumption that epilepsy would not occur or worsen, and further damages should these assumptions prove to be incorrect. The courts in England still depend, however, upon the evidence of expert witnesses chosen by the plaintiff and defendant. A tension thus exists between the duty of expert witnesses to the court and the understandable inclination of expert witnesses to support the party that has instructed them. The Woolf report has led to changes in the responsibilities of expert witnesses, and will hopefully remedy many of the inconsistencies and inequities that occur.  (+info)

The structural basis of moderate disability after traumatic brain damage. (7/68)

The objective was to discover the nature of brain damage in survivors of head injury who are left with moderate disability. Macroscopic and microscopic examination was carried out on the brains of 20 persons who had died long after a head injury that had been treated in a neurosurgical unit. All had become independent but had various disabilities (moderate disability on the Glasgow outcome scale) Most deaths had been sudden, which had led to their referral from forensic pathologists. Post-traumatic epilepsy was a feature in 75%. An intracranial haematoma had been evacuated in 75%, and in 11 of the 15 with epilepsy. Diffuse axonal injury was found in six patients, five of the mildest type (grade 1) and one of grade 2. No patient had diffuse thalamic damage but one had a small focal ischaemic lesion in the thalamus. No patient had severe ischaemic brain damage, but three had moderate lesions which were bilateral in only one. No patient had severe cortical contusions. In conclusion, the dominant lesion was focal damage from an evacuated intracranial haematoma. Severe diffuse damage was not found, with diffuse axonal injury only mild and thalamic damage in only one patient.  (+info)

Long-term outcome after severe head injury. (8/68)

From a consecutive series of 7000 patients with head injuries admitted to the regional accident service, Radcliffe Infirmary, Oxford between 10 and 24 years earlier, every patient was taken who had been amnesic or unconscious for one week or longer. Of these 479 patients, all but ten were traced, and either the cause of death was established or the survivors examined. Ten years after injury 4% were totally disabled, and 14% severely disabled to a degree precluding normal occupational or social life. Of the remainder, 49% had recovered, and the rest were dead. Additionally, a selected series of 64 patients whose unconsciousness had been prolonged for a month or more were studied. Forty of these had survived between three and 25 years after injury and were re-examined. On the basis of age at injury, the worst state of neurological responsiveness, and the duration of posttraumatic amnesia, the outcome of head injury can be predicted reliably in most cases. Patients and relatives need more reassurance and simple psychotherapeutic support, especially in the first few months after injury. Extrapolation from our figures suggests that each year in England and Wales 210 patients survive totally disabled and another 1500 are severely disabled.  (+info)