Abnormal electroencephalography in first unprovoked seizure in Rajavithi Hospital.

BACKGROUND: Electroencephalography (EEG) has an important role in epilepsy diagnosis, classification of epilepsy syndrome, lesion localization, and prediction of seizure recurrence, but no study of EEG in the first unprovoked seizure had been carried out in Rajavithi Hospital prior to the current one. OBJECTIVE: The present research aimed to find the prevalence of abnormal EEG in the first unprovoked seizure and the prevalence of abnormal EEG in partial seizure and generalized seizure. MATERIAL AND METHOD: This was a retrospective study of 28 adult patients who presented with first unprovoked seizure. EEG was performed in all patients and baseline characteristics were recorded. RESULTS: Of the 28 patients with first unprovoked seizure, abnormal EEG was found in 16 patients (57.41%). 95% CI of the prevalence of abnormal EEG was 37.60-76.68%. EEG abnormalities were found in 7 patients (46.7%) who had partial seizure, and 8 patients (53.3%) who had generalized seizure. Eight patients (28.6%) had epileptiform discharges. The patients who were taking medication for underlying diseases and patients with abnormal neurological examinations were associated with a statistically significant higher risk of EEG abnormality (OR 6.43, 95% CI 1.05-39.33, p = 0.044, and OR 13.2, 95% CI 1.24-140.68, p = 0.027, respectively). CONCLUSION: Abnormal EEG was detected in more than half of the patients with first unprovoked seizure, which is comparable to previous studies. EEG should be considered for all patients with first unprovoked seizure.

An outbreak of botulism in Thailand: clinical manifestations and management of severe respiratory failure.

BACKGROUND: Northern Thailand's biggest botulism outbreak to date occurred on 14 March 2006 and affected 209 people. Of these, 42 developed respiratory failure, and 25 of those who developed respiratory failure were referred to 9 high facility hospitals for treatment of severe respiratory failure and autonomic nervous system involvement. Among these patients, we aimed to assess the relationship between the rate of ventilator dependence and the occurrence of treatment by day 4 versus day 6 after exposure to bamboo shoots (the source of the botulism outbreak), as well as the relationship between ventilator dependence and negative inspiratory pressure. METHODS: We reviewed the circumstances and timing of symptoms following exposure. Mobile teams treated patients with botulinum antitoxin on day 4 or day 6 after exposure in Nan Hospital (Nan, Thailand). Eighteen patients (in 7 high facility hospitals) with severe respiratory failure received a low- and high-rate repetitive nerve stimulation test, and negative inspiratory pressure was measured. RESULTS: Within 1-65 h after exposure, 18 of the patients with severe respiratory failure had become ill. The typical clinical sequence was abdominal pain, nausea and/or vomiting, diarrhea, dysphagia and/or dysarthria, ptosis, diplopia, generalized weakness, urinary retention, and respiratory failure. Most patients exhibited fluctuating pulse and blood pressure. Repetitive nerve stimulation test showed no response in the most severe stage. In the moderately severe stage, there was a low-amplitude compound muscle action potential with a low-rate incremented/high-rate decremented response. In the early recovery phase, there was a low-amplitude compound muscle action potential with low- and high-rate incremented response. In the ventilator-weaning stage, there was a normal-amplitude compound muscle action potential. Negative inspiratory pressure variation among 14 patients undergoing weaning from mechanical ventilation was observed. Kaplan-Meier survival analysis identified a shorter period of ventilator dependency among patients receiving botulinum antitoxin on day 4 (P=.02). CONCLUSIONS: Patients receiving botulinum antitoxin on day 4 had decreased ventilator dependency. In addition, for patients with foodborne botulism, an effective referral system and team of specialists are needed.

Neuroleptics and migraine.

Many dopamine antagonists are proven acute migraine treatments. Genetic studies also imply that polymorphisms in dopamine genes (DRD2 receptors) in persons with migraine may create dopamine hypersensitivity. However, treatment is limited by the adverse event profiles of conventional neuroleptics including extrapyramidal symptoms, anticholinergic and antihistaminergic effects, hyperprolactinemia, and prolonged cardiac QT interval. Atypical neuroleptics cause less extrapyramial symptoms and some atypical neuroleptics, including olanzapine and quetiapine, may be beneficial as both acute and preventive migraine treatment. The combination of prochlorperazine, indomethacin, and caffeine is effective in the treatment of the acute migraine attack. The mechanism of action by which neuroleptics relieve headache is probably related to dopamine D2 receptor antagonist. Other actions via serotonin (5HT) receptor antagonists may also be important, particularly for migraine prevention. Additional studies to clarify the mechanism of action of neuroleptics in migraine could lead to new drugs and better management of migraine.