Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four members of a family with an autosomal dominant form of cerebellar degeneration all had slow eye-movements, i.e. slow pursuit with absence of both nystagmus and rapid saccadic movements. Three showed progressive mental deterioration. One patient had nevus of Ota (oculodermal melanocytosis) and a history of grand mal epilepsy. In these four patients the symptoms first occurred between the ages of 10 and 31 years--the onset apparently appearing earlier with successive generations. Current studies implicate a brain-stem lesion of the paramedian pontine reticular formation in the pathogenesis of the oculomotor abnormality. The possibility of a neurocutaneous syndrome, specifically a 'melanophakomatosis', in the patient with seizures and nevus of Ota is discussed; however, absence of these findings in other affected relatives makes a fortuitous association more probable. The literature on nevus of Ota associated with neurological disease is considered.
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PMID:Familial cerebellar degeneration with slow eye-movements, mental deterioration and incidental nevus of ota (oculo-dermal melanocytosis). 93 51

The study concerns an epileptic patient whose absence attacks were contingent on the viewing of striped patterns. A series of experiments demonstrated first that seizures were not due to the intermittent stimulation of retinal cells produced as physiological nystagmus vibrated the image of the pattern, and secondly that seizures were triggered at the cortical level, probably by the firing of complex cells. Spectacles which occluded pattern vision in one eye were highly effective in reducing seizure incidence.
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PMID:Stripes, complex cells and seizures. An attempt to determine the locus and nature of the trigger mechanism in pattern-sensitive epilepsy. 118 83

Phencyclidine is now one of the most frequently used main ingredients of "street drug" preparations. Its effects are highly dose dependent and three varieties of acute intoxication have been seen clinically associated with different dosages and routes of administration. Most persons using phencyclidine smoke it sprinkled on parsley in low doses. The presence of horizontal and vertical nystagmus associated with hypertension in a patient who is agitated or comatose are diagnostic of a phencyclidine intoxicated state. Sensory isolation and intravenous administration of diazepam in the event of seizure activity have proved effective in the treatment of acute intoxicated states. Phencyclidine has pronounced behavioral toxicity and several deaths due to this agent have now been documented. It is unknown whether seizure activity or respiratory depression is the primary cause of death in pharmacological overdoses.
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PMID:Phencyclidine--states of acute intoxication and fatalities. 121 Mar 29

In nine cases of phencyclidine hydrochloride poisoning, early signs of overdose included drowsiness, nystagmus, miotic pupils, blood pressure elevation, increased deep tendon reflexes, ataxia, anxiety, and agitation. In more severe cases, seizures, spasticity, and opisthotonos were seen in addition to deep coma and respiratory depression. Treatment included removal by emetics or lavage, hydration, and a quiet, reassuring environment. Spasticity, agitation, and ocular manifestions responded to diazepam. Psychiatric intervention was instituted after the patients were stable and no longer agitated.
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PMID:Phencyclidine. Nine cases of poisoning. 124 71

Serum hyperviscosity syndrome was diagnosed in 2 cats with multiple myeloma. Clinical signs included pale mucous membranes, dehydration, retinal hemorrhages, dilated and tortuous retinal vessels, seizures, head-tilt, nystagmus, systolic murmur, and gallop rhythm. Laboratory abnormalities included hyperglobulinemia, azotemia, hyperphosphatemia, nonregenerative anemia, and thrombocytopenia. Both cats had IgG monoclonal gammopathy, Bence Jones proteinuria, increased numbers of bone marrow plasma cells, and high values for relative serum viscosity. Renal disease was suspected in both cats. Cardiac hypertrophy was documented in 1 cat and was suspected in the other cat. Chemotherapy, using melphalan, prednisone, and vincristine, caused short-term remission in both cats, and plasmapheresis was used to lower serum protein concentration in 1 cat. Serum hyperviscosity syndrome rarely develops in cats, but should be suspected when monoclonal gammopathy exists with signs of neurologic, cardiac, or retinal disease.
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PMID:Serum hyperviscosity syndrome associated with multiple myeloma in two cats. 153 97

Chronic intoxication of phenytoin (PHT) is a well known cause of cerebellar atrophy or irreversible cerebellar ataxia. Little attention, on the other hand, is paid for acute PHT intoxication because its clinical signs are believed to be reversible. We here report a patient with acute PHT intoxication, which resulted in irreversible cerebellar ataxia with radiologically definite cerebellar atrophy. A 39-year-old man admitted to our hospital because of cerebellar ataxia and confusional state. He had been treated with PHT for convulsive seizures after receiving craniotomy for left parietal brain abscess 9 years before. The concentration of his serum PHT had been 4 to 7 micrograms/ml because he had frequently omitted taking drug, and the dose of PHT had been increased to 600 mg/day one year before. He had admitted to another hospital 2 months before for left Bell's palsy and had been obliged to take drug regularly. Cerebellar signs and confusion had gradually developed for 7 weeks. On admission to our hospital, he was awake but in severe confusional state with slurred speech and nystagmus. His serum PHT was 86 micrograms/ml, which returned to therapeutic range 2 weeks after the discontinuation of PHT. His consciousness normalized and nystagmus disappeared. However, slurred speech continued and neurological examination revealed postural tremor and severe limb ataxia. During the subsequent 10 months, his cerebellar signs showed minimal improvement. Computed tomographies of his brain on 3rd and 5th month after the onset of his cerebellar dysfunction showed the definite cerebellar atrophy which had not been noted on the CTs 7 months before and 7 weeks after the onset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebellar atrophy and persistent cerebellar ataxia after acute intoxication of phenytoin]. 156 34

Wolfram syndrome is an autosomal recessive disorder beginning in childhood that consists of four cardinal features: optic atrophy, diabetes mellitus, diabetes insipidus, and neurosensory hearing loss. Aside from these features, the clinical picture is highly variable and may include other neurologic abnormalities such as ataxia, nystagmus, mental retardation, and seizures. We present two unrelated patients with Wolfram syndrome, both of whom had the four cardinal features and several other neurologic abnormalities. MRIs showed widespread atrophic changes throughout the brain, some of which correlated with the major neurologic features of the syndrome.
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PMID:Wolfram syndrome: evidence of a diffuse neurodegenerative disease by magnetic resonance imaging. 160 50

The clinical spectrum of toxic effects and serum concentrations after ingestion of carbamazepine were studied in 82 pediatric patients. Serum carbamazepine level was related to the depth of coma (p less than 0.001), convulsions (p = 0.002), hypotension (p less than 0.001), and the requirement for mechanical ventilation (p less than 0.001). In 10 patients in deep coma with a Glasgow Coma Scale (GCS) of 3-4, the mean serum level was 213 mumol/L (range 143 to 343); seizures, ventilatory failure, or hypotension caused by myocardial failure and conduction defects were observed. In four of these, large doses of inotropic agents were required, one patient was treated with plasmapheresis, and two died--one of cardiac failure and one of aspiration pneumonitis. In 27 patients with moderate coma (GCS 5-8), the mean serum level of carbamazepine was 112 mumol/L (range 63 to 176); convulsions were observed in two patients in this group. In 45 patients whose conscious state was mildly depressed or normal (GCS 9-15), the mean serum level was 73 mumol/L (range 37 to 128); additional effects were drowsiness (80%), ataxia (53%), nystagmus (38%), vomiting (17%), and dystonia (7%). I conclude that patients with serum carbamazepine levels of approximately 100 mumol/L require close observation, whereas those with levels greater than 150 mumol/L may require intensive life support.
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PMID:Acute toxic reaction to carbamazepine: clinical effects and serum concentrations. 164 Mar 2

Children with autism demonstrate "atypical" gaze or social "looking" and frequently manifest such sterotypies as eye pressing, hand flicking, and light gazing. This study's purpose was to evaluate autistic children for visual dysfunction that may be related to the manifested visual signs and symptoms. Thirty-four autistic children, ages 2 to 11 years (median age = 7 years, 6 months) were evaluated for ocular alignment, refractive error, visual acuity, oculomotility skills, and stereopsis. None of the children manifested ocular disease, known seizure disorders, or dysmorphic features. Their developmental levels ranged from average intelligence to severely retarded. Binocular visual acuity was measured with the acuity card procedure. Monocular visual acuity was not obtained. Refractive errors ranged from -4.25 to +3.25 D; the median was plano with the near retinoscopy technique. Of the 34 children, 21% were strabismic at far and 18% were strabismic at near. Lang stereo testing was attempted on all children and completed on 17. Of the 17, all but 3 exhibited 550 sec arc. Only 14.7% of the children exhibited voluntary pursuit movements, and all the children demonstrated saccadic fixations. Thirty-one children had atypical optokinetic nystagmus (OKN) responses such as delayed onset, short duration, gaze avoidance, or stereotypic behavior. Repeated testing revealed consistent visual responses on OKN and visual acuity. Given these findings, research with this population should be pursued further.
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PMID:Assessment of visual function in autistic children. 164 Dec 24

Two cases of epileptic nystagmus (EN) are described. The first patient had no history of seizures and experienced attacks of EN associated with oscillopsia and followed by horizontal diplopia and esotropia. These episodes could be triggered by certain visual stimuli and ocular pressure. The second patient had a history of generalized tonic-clonic seizures. He displayed episodes of EN that changed direction in the course of the attacks simultaneously with a shift of the EEG discharge from one occipital region to the other. Cortical blindness followed postictally. On recovery from the postictal state, both patients were neurologically normal. With standard electrodes, the EEG seizures associated with EN involved the occipital, posterotemporal, and parietal areas of the scalp contralateral to the fast phase of the nystagmus. In the first patient, use of supplementary scalp electrodes further localized the seizures to an anterior occipital site intermediate between standard occipital and posterotemporal electrodes. Thirty-six previously reported cases of EN were associated with partial seizures. Horizontal EN most commonly results from seizure activity involving the occipital cortex, although participation of adjoining portions of the parietal and temporal cortexes is possible.
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PMID:Epileptic nystagmus. 174 65


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