Hot Water Epilepsy: Presentation of Three Cases

Hot water epilepsy (HWE) is a reflex epilepsy that develops after pouring hot water on the head; seizures are induced through tactile and temperature-related stimuli. The number of cases reported worldwide is low, with most cases in Turkey and India. The exact pathophysiology of HWE is unknown but patients are thought to have abnormal thermoregulation systems with seizures that emerge due to the stimulation of a particular region in the brain cortex via contact of hot water on the skin of the head. We investigated the pathogenesis of this disorder through a literature review and by presenting the clinical and laboratory findings of three patients with HWE. Fortunately, HWE can largely be prevented; however, if non-reflexive seizures co-occur with HWE, proper medical treatment can be added to ensure seizure-free follow-up

Hot Water Epilepsy: Presentation of Three Cases

Hot water epilepsy (HWE) is a reflex epilepsy that develops after pouring hot water on the head; seizures are induced through tactile and temperature-related stimuli. The number of cases reported worldwide is low, with most cases in Turkey and India. The exact pathophysiology of HWE is unknown but patients are thought to have abnormal thermoregulation systems with seizures that emerge due to the stimulation of a particular region in the brain cortex via contact of hot water on the skin of the head. We investigated the pathogenesis of this disorder through a literature review and by presenting the clinical and laboratory findings of three patients with HWE. Fortunately, HWE can largely be prevented; however, if non-reflexive seizures co-occur with HWE, proper medical treatment can be added to ensure seizure-free follow-up

Early cyclosporin A treatment retards axonal degeneration in an experimental peripheral nerve injection injury model

Injury to peripheral nerves during injections of therapeutic agents such as penicillin G potassium is common in developing countries. It has been shown that cyclosporin A, a powerful immunosuppressive agent, can retard Wallerian degeneration after peripheral nerve crush injury. However, few studies are reported on the effects of cyclosporin A on peripheral nerve drug injection injury. This study aimed to assess the time-dependent efficacy of cyclosporine-A as an immunosuppressant therapy in an experimental rat nerve injection injury model established by penicillin G potassium injection. The rats were randomly divided into three groups based on the length of time after nerve injury induced by penicillin G potassium administration (30 minutes, 8 or 24 hours). The compound muscle action potentials were recorded pre-injury, early post-injury (within 1 hour) and 4 weeks after injury and compared statistically. Tissue samples were taken from each animal for histological analysis. Compared to the control group, a significant improvement of the compound muscle action potential amplitude value was observed only when cyclosporine-A was administered within 30 minutes of the injection injury (P < 0.05); at 8 or 24 hours after cyclosporine-A administration, compound muscle action potential amplitude was not changed compared with the control group. Thus, early immunosuppressant drug therapy may be a good alternative neuroprotective therapy option in experimental nerve injection injury induced by penicillin G potassium injection