ABSTRACT
Photosensitive epilepsy is a type of reflex epilepsy. Five percent of epileptics are photosensitive, i.e. they show photoconvulsive response (PCR) during intermittent photic stimulation. Patients with photogenic or photosensitive epilepsy have seizures with flickering light. They also exhibit heliotaxis. Sodium valproate and ethosuximide are the common drugs used. Even though benzodiazepines are useful, the specific effect of lorazepam is not mentioned. We report 5 cases of photosensitive epilepsy with inadequate response to usual antiepileptic drugs who had complete or near complete remission with lorazepam.
Subject(s)
Adolescent , Anticonvulsants/therapeutic use , Child , Epilepsy, Reflex/drug therapy , Female , Humans , Lorazepam/therapeutic use , Male , Middle Aged , SunlightABSTRACT
It has always been a controversial subject whether or not to treat a patient with first episode of seizure. The actual decision whether or not to treat patients who present with initial seizure must be individualized. It depends on probability of having a recurrence and on the perceived risk/benefit ratio of treatment. In a large majority of patients, it is prudent to defer treatment with antiepileptic drugs until a second episode has occurred, unless it is a remote symptomatic seizure, associated with definite epileptiform abnormalities in EEG or a partial seizure. However, in an occasional patient, treatment may be indicated even after a first seizure; for example, in patients involved in certain occupations like driving or operating dangerous machinery.
Subject(s)
Anticonvulsants/administration & dosage , Electroencephalography , Epilepsy/drug therapy , Humans , Prognosis , Recurrence , Seizures/drug therapyABSTRACT
The essential pathophysiological feature of dystonia is co-contraction of antagonistic muscles. This may be due to derangement of the spinal cord or cortical mechanism. In the cord, there is disruption of the normal reciprocal inhibition of antagonists during agonist contraction. This decreased reciprocal inhibition is due to reduced presynaptic inhibition of muscle afferent input to the inhibitory interneuron. The reduced presynaptic inhibition may in turn be either due to defective suprasegmental control or to changes in the tonic afferent input to the interneuron from cutaneous and muscle afferents. Alternatively, genesis of dystonia may entirely be a cortical mechanism. Overactivity of the premotor cortices, which receive projections from basal ganglia via ventral thalamus, could result in dystonia by abnormal activation of cortical motor neurons. This may again be due to a dopaminergic dysfunction of basal ganglia.