Cases reported "Epilepsy"

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1/7. Aplasia of the retinal vessels combined with optic nerve hypoplasia, neonatal epileptic seizures, and lactic acidosis due to mitochondrial complex I deficiency.

    A newborn male with mitochondrial complex I deficiency suffered from neonatal epileptic seizures, which later developed into infantile spasms. The infant was blind due to aplasia of the retinal vessels and hypoplasia of the optic nerve. There was congenital lactic acidosis, which persisted in later life. The boy was microcephalic and retarded. Muscular hypotonia later shifted to spasticity. succinic acid was increased in urine. We assume that the aplasia of the retinal vessels is due to damage of the retinal ganglion cells caused by the mitochondrial disease in the first 3 to 4 months of pregnancy.
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keywords = ganglion
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2/7. Podiatric implications of psychogenic seizures.

    Psychogenic seizures can mimic epileptic conditions and are often difficult to diagnose. The present study reviews one such unusual occurrence in a patient having a complex psychiatric history who required surgery for the removal of a ganglionic cyst in her foot. The differential diagnosis and treatment of psychogenic seizures is discussed.
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3/7. Neuropathology of secondary generalized epilepsy--(Lennox-Gastaut syndrome)--a case report.

    Neuropathological considerations were performed on a case, who went into Lennox syndrome after an acute encephalopathy at the infantile period, and moreover who fell into an akinetic-mute state derived from brain damage by herniation caused by a head injury and subsequent status epilepticus. Neuropahtological background in the present case of Lennox syndrome is thought to be based on the widespread unilateral cerebral lesions and the basal ganglional, especially thalamic, degenerations derived secondarily from the diffuse cerebral damage. The patient revealed akinetic mutism with the disappearance of the epileptic seizures and the desynchronization of the EEG's, when the brain lesions formed at the adult period spread over the opposite hemispheric limbic system and the brain stem tectum.
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keywords = ganglion
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4/7. Lhermitte-Duclos disease (diffuse hypertrophy of the cerebellum). Report of two cases.

    Two cases of Lhermitte-Duclos disease or diffuse hypertrophy of the cerebellum are presented. This brings the total number of such cases reported in the literature to 42. Pathologically the disease is characterized by a circumscribed cerebellar lesion consisting of thickening of the cortex with closely packed dysplastic ganglion cells in the granular layer and with large myelinated axons in the molecular layer. purkinje cells are missing and the central white matter is greatly reduced. The first patient, a man 39 years of age, had in association to the cerebellar lesion, a megalencephalic brain (2320 g). He had suffered from epilepsy since he was 24-years-old and died with metastasizing colon carcinoma. An electron microscopic study of the cerebellar lesion disclosed perikarya containing large amounts of rough endoplasmic reticulum, cell processes filled with coated and dense core vesicles. In addition, there were numerous enlarged myelinated axons in the molecular layer. The second patient, a woman 74 years of age, had a small area of diffuse hypertrophy of the left cerebellar hemisphere measuring one centimeter in diameter. Specific symptoms were very scant in the first case and absent in the second one indicating a very slow evolution - if any - of the disease process. The etiology and pathogenesis remain unknown. However, the organoid structure of the lesion, the frequent association of megalencephaly and other congenital abnormalities, and the occurrence of familiar cases would favor the disease being basically a developmental disorder.
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keywords = ganglion
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5/7. pyridoxine dependent epilepsy with iatrogenic sensory neuronopathy.

    An 18-year-old man was treated from birth with chronic high dose pyridoxine (vitamin B6) up to 2000 mg per day for pyridoxine-dependent seizures. Within two years of onset of treatment, he developed a sensory neuropathy which did not progress over the following 16 years. Electrophysiological studies were consistent with a pure sensory neuronopathy expressed as centripetal degeneration of processes of the dorsal root ganglion cells.
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keywords = ganglion
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6/7. A rare case of achalasia coexistent with sigmoid megacolon and associated with epilepsy.

    A case of achalasia coexistent with sigmoid megacolon in a 38-year-old man with known epilepsy is described. The patient was referred to the Ryukyu University Hospital with a 4-year history of dysphagia and heartburn and a 1-year history of abnormal bowel movement. On admission, upper gastrointestinal (GI) series demonstrated a dilated, tortuous thoracic esophagus with a flask-type configuration. barium enema studies showed a dilated sigmoid colon from the rectosigmoid junction to the descending colon. Myotomy (modified Jekler-Lhotka's procedure) for achalasia and simple sigmoidectomy for sigmoid megacolon were carried out. The biopsied wall of the narrowed esophageal segment at operation showed decreased numbers of ganglion cells in Auerbach's plexus and atrophy of the muscle fibers. The resected dilated sigmoid colon revealed degeneration and markedly decreased numbers of ganglion cells in Auerbach's and Meissner's plexuses. The patient's postoperative course was uneventful and he has been doing well since surgery. The present case is very interesting and to our knowledge, such a case is rare in the literature. We believe that the abnormalities of the ganglion cells may be due to the same etiologic factor as the sigmoid megacolon. The association of the two pathologic processes is discussed, together with a brief review of the literature.
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keywords = ganglion
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7/7. heat stroke-like episode in a child caused by zonisamide.

    A 2-year-old mentally retarded boy with frontal lobe epilepsy presented with an episode that resembled heat stroke during the administration of zonisamide. He developed hyperpyrexia with oligohidrosis and central neurological symptoms, including, chorea-like involuntary movements, resting tremor, and cogwheel rigidity. A sweat test using pilocarpine iontophoresis revealed a marked reduction in the sweat response, which suggested a postganglionic sweating dysfunction. A skin biopsy examined by light and electron microscopy showed no morphological abnormality in the sweat glands. The oligohidrosis caused by zonisamide was reversible in that the patient regained the ability to sweat within 2 weeks of the cessation of drug administration. Children receiving zonisamide should be monitored for oligohidrosis and the development of neurological symptoms associated with an elevation of body temperature.
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keywords = ganglion
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