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1/3. Childhood-onset epilepsy associated with polymicrogyria.

    To study the electroclinical characteristics of patients with childhood-onset epilepsy who showed polymicrogyria (PMG) on MRI, we classified 15 patients according to the location of PMG on MRI. The composition of the subjects was as follows: four patients with PMG in both hemispheres; three with localized PMG in one hemisphere associated with other lesions such as porencephaly; and eight with only localized PMG in one hemisphere. We investigated the electroclinical characteristics of the epileptic syndromes associated with these different types of PMG. Four patients suffered from infantile spasms during their clinical course. Five patients suffered from epilepsy with electrical status epilepticus during slow sleep (ESES) and ESES-related epilepsy. The other six patients had only localization-related epilepsy throughout their clinical course. patients with PMG in both hemispheres, and localized PMG in one hemisphere associated with other lesions tended to have early-onset intractable seizures, especially infantile spasms. On the other hand, patients with only localized PMG in one hemisphere had ESES and ESES-related epilepsy or localization-related epilepsy, and their seizure prognosis was relatively favorable. These findings are useful in predicting the outcome of patients with PMG. ( info)

2/3. Lamotrigine-induced seizure aggravation and negative myoclonus in idiopathic rolandic epilepsy.

    The authors describe a paradoxical reaction to lamotrigine (LTG) treatment in a patient with idiopathic rolandic epilepsy characterized by seizure deterioration, the appearance of new seizure type, and transient cognitive impairment. This phenomenon was present at a low dose after a slow titration and promptly reverted on LTG discontinuation. This rare event may have similarities with carbamazepine-induced seizure worsening caused by the Na channel inhibitory effect of the two antiepileptic drugs. ( info)

3/3. sleep exacerbation of persistent sexual arousal syndrome in a postmenopausal woman.

    AIM: To investigate possible causes and treatment of persistent sexual arousal syndrome, which was exacerbated by sleep onset, in a postmenopausal subject. methods: A clinical examination and interviews with the patient to obtain her case history and follow-up of the effects of drug treatments. Pretreatment laboratory investigations monitored vaginal blood flow by photoplethysmography and heated electrode. Routine blood chemistry and endocrine assessments were undertaken. magnetic resonance imaging (MRI) scans of brain, pelvis, and spinal cord and genito-sensory neural analysis of clitoral and vaginal areas were performed. A selective internal iliac artery arteriogram was utilized to check the normality of the pelvic blood supply. RESULTS: genitalia appeared normal and uncongested. No structural abnormalities were observed in the MRI scans. Hormonal levels and blood chemistry were commensurate with the subject's postmenopausal status. Basal vaginal blood flow (heat electrode) was within the range of normal premenopausal women and showed (photoplethysmography) normal vasomotion. On becoming drowsy and falling lightly asleep in the laboratory the vaginal pulse amplitude (VPA) increased by 95% of the basal value and the low-amplitude VPAs were replaced by high-amplitude VPAs--all evidence of increased vaginal blood flow and congestion and confirming the subject's complaint of persistent sexual arousal during sleep. A simple cognitive task of repeatedly subtracting 7 from 500 out aloud did not hasten the reversion to the basal level. There was no evidence of malfunction of the brain, spinal cord, or pelvic area by MRI but genito-sensory analysis of the clitoral and vaginal area showed evidence of reduced sensory function. CONCLUSIONS: Of the treatments tried only risperidone has been effective allowing the subject to sleep throughout the night without disturbance and according to the subject has significantly reduced the aggravation of the arousal during the day. ( info)


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