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 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medulloblastoma and acute lymphocytic leukemia patients treated by intrathecal methotrexate and radiation were investigated by means of computerized axial tomography. More than 50% of them turned out to have acquired encephalopathy. Only gross morphologic brain defects, as visualized by computerized tomography, caused manifest clinical signs of brain dysfunction, such as epilepsy, mental retardation, paresis, and apallic syndrome. Mild morphologic changes were found even in asymptomatic children. The preferred site of defects in brain substance was the paraventricular white matter.
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PMID:Findings in computerized axial tomography after intrathecal methotrexate and radiation. 28 21

The author, after pointing out the rare occurence and peculiarities of pattern-sensitive forms of epilepsy, reports the case of a seven-year-old boy with infantile cerebral paresis characterized by symptomatic attacks, who was observed to show absence-like conditions when looking at small-checkered patterns of nylon fabric. Grasping and looking at such fabrics assumed the form of an addiction, with a sense of pleasure being believed to be derived therefrom. Although anticonvulsive therapy resulted in attacks of epilepsy being no longer detectable clinically and by electroencephalography, seizures were still triggered by looking at patterns. Also discussed in this article is the problem of transition from real to psychogenic attacks.
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PMID:[Epilepsy by looking at patterns]. 40 19

A case of corpus callosum lipoma with presumptive diagnosis is presented. Review of the literature disclosed 84 cases with such diagnoses. Lipoma of the corpus callosum is a rare intracranial lesion, perhaps congenital and often asymptomatic, but can present with seizure disorder, headache, mental changes, paresis or paralysis. Twenty-one patients had been operated upon. Surgical treatment seems to be of no value in this disease.
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PMID:Lipoma of the corpus callosum. 45 41

We report a 55-year-old right-handed man with frontal lobe epilepsy manifesting recurrent speech arrest. He was known to have hypertension, hypertriglyceridemia, and gout. In the three days prior to admission, he had episodes of sudden inability to talk. These episodes lasted 10 to 30 seconds and recurred ten to twenty times a day. On admission, speech comprehension and other mental functions were normal, as were findings on neurologic examination. During the period of speech arrest, he understood spoken commands, and there was no abnormal motor activity or paresis. The episodes of speech arrest were thought to be short aphasic periods due to transient ischemic attacks in the left carotid territory. Computed tomography and magnetic resonance imaging demonstrated a small calcified lesion in the upper medial portion of the left frontal lobe. Left internal carotid angiography demonstrated no abnormal findings. After neuroradiological examination finished, he suddenly raised his right hand and followed it with his gaze and a right head turn. The EEG seizure pattern in which 20-25 Hz activity began in the left fronto-central region and spread rapidly to the right fronto-central region, which after about 8 seconds was replaced by 12-14 Hz flattening rhythmic polyspikes was detected 9 times within 60 minutes. It is most unusual for supplementary motor area seizure to present pure paroxysmal speech arrest without accompanying paroxysmal motor activity. As in our case, epileptic arrest of speech may be confused with a transient ischemic attack of the dominant hemisphere.
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PMID:[A case of frontal lobe epilepsy presenting with recurrent speech arrest]. 129 18

An 18-year-old mentally normal epileptic boy had frequent left brachiofacial or unilateral motor seizures which started at age 4 years and ceased 10 years later. Seizures were exclusively sleep-related. No relapse followed antiepileptic drug (AED) discontinuation. Left arm slight paresis and left hand astereognosia occurred at age 10 years. Awake EEGs showed persistent right rolandic discharges increased by sleep. Somatosensory evoked potentials (SEPs) were giant with left median nerve stimulation. Computed tomography (CT) and magnetic resonance imaging (MRI) disclosed right opercular macrogyria. We suggest that the structural brain lesion was causally related to his "idiopathic" partial epilepsy. Similar case reports and pathologic studies will elucidate the morphologic substrate of the underlying functional disorder in idiopathic partial epilepsies.
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PMID:Unilateral opercular macrogyria and benign childhood epilepsy with centrotemporal (rolandic) spikes: report of a case. 159 27

Forty-two patients have been surgically treated for medically uncontrollable epilepsy, using the Talairach and Bancaud methodology. The mean age of the patients was 19 years (range 6-54 years). The location of the epileptogenic zone was:frontal in 18 patients, temporal in 14, temporo-parieto-occipital junction in 4, parietal in 4 and occipital in 2. The overall surgical results are: 20 patients are seizure free and 6 patients had occasional seizures (62% success rate). There has been a significant decrease in the number of seizures in 12 patients. The seizures persist in 4 patients. Only two patients, both with a parietal focus, presented additional postoperative neurological deficit (mild paresis in the contralateral lover limb). This was preoperatively foreseen, and accepted by the patient, on guarantees of the removal of the epileptogenic zone and amelioration of seizures.
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PMID:Surgical treatment for epilepsy. Results after a minimum follow-up of five years. 179 58

Cerebrotendinous xanthomatosis (CTX) is a rare hereditary disease characterized by xanthomata of tendons, osteoporosis, cataracts, cerebellar ataxia, spastic paresis, and dementia. Though electroencephalographic (EEG) abnormalities are frequent in CTX, epileptic seizures have not been recognized as a major feature. A CTX patient is reported who presented with a generalized epileptic seizure and was evaluated with EEG and neuropsychological testing. Epilepsy should be considered a feature of CTX, and CTX considered as a possible, though rare, cause of symptomatic seizures.
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PMID:Epileptic seizure as a presenting symptom of cerebrotendinous xanthomatosis. 191 72

Cleidocranial dysostosis (CCD) is a rare congenital disorder characterized by the heredity, the disturbance of the ossification of the skull and clavicles, and dental anomaly. The entity of CCD was established by Marie and Sainton in 1898. In Japan about 150 cases have been reported since Haneda's first report in 1933. Recently we experienced a rare case of CCD associated with the temporal arachnoid cyst. The patient was a 61-year-old male who had suffered from mild spastic paresis of the left upper extremity since his childhood. One morning he suddenly noticed motor weakness of the left upper and lower extremities and was transferred to our hospital. On admission we observed the left hemiparesis (MMT 3/5), the left central type facial palsy, and the left long tract signs. Physical examination disclosed frontal bossing, depression of the forehead, sloped shoulders, cone-shaped thorax, and thoracic scoliosis. Plain skull radiograph showed persistent metopic suture and frontal fontanelle, many wormian bones around coronal and lambdoid sutures. Plain radiographs of the systemic bones also showed typical features of CCD such as dysplasia of the lateral third of the bilateral clavicles, deformities of the cervical vertebral bodies, thoracic scoliosis, and wide symphysis. CT scan disclosed the right putaminal hemorrhage, the right temporal arachnoid cyst, enlargement of the right middle fossa, thinning of the temporal bone adjacent to the arachnoid cyst. It also showed the atrophy of the right cerebral peduncle and midbrain. Surgical treatment was performed to remove the hematoma and release the cyst. Several neurological disorders associated with CCD have been reported such as epilepsy, mental retardation, spastic paresis etc.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cleidocranial dysostosis associated with arachnoid cyst]. 343 33

Development of epilepsy was studied prospectively in a group of 77 consecutive stroke patients. Included were stroke patients less than 75 years old admitted within the first 3 days after the stroke. Excluded were patients with subarachnoid hemorrhage, vertebrobasilar stroke, and patients with other severe diseases. Cerebral angiography, CT, and EEG were performed in all patients. The patients were followed clinically for 2 to 4 years. Seven patients (9%) developed epilepsy. Of 23 patients with lesions involving the cortex, 6 (26%) developed epilepsy. Of 54 patients in whom the cortex was not involved, only 1 (2%) developed epilepsy. Patients with persisting paresis and cortical involvement seem to be at particularly high risk of developing epilepsy, as 50% of such patients (6 of 12) developed the disease.
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PMID:Epilepsy after stroke. 360 Oct 84

We report a family whose members have familial spastic paraplegia (FSP) associated with epilepsy. A man and his sister initially had primary generalized epilepsy with tonic-clonic seizures, but they have had no seizures for years. However, they developed spastic paresis of the lower extremities and presently show features of FSP. Their mother seemed to have suffered from FSP. One son of the female patient has epilepsy. The clinical picture of this family suggests a close relationship between FSP and epilepsy.
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PMID:Familial spastic paraplegia with epilepsy. 400 10


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