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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Neurotoxicity is a recognized complication of cyclosporin A (CsA) therapy in patients undergoing organ transplantation. It is most commonly manifested by fever, seizures, and altered mental status. Cortical blindness and speech and motor disturbances can also occur. Changes seen in cerebral white matter on imaging studies are nonenhancing areas of hypoattenuation on CT and T2 prolongation on MR. We report three cases of CsA-induced neurotoxicity in which reversible changes were observed in the cerebral white matter. In the first patient, CsA neurotoxicity occurred 1 week following orthotopic liver transplantation. In the second patient, CsA neurotoxicity coincided with an episode of severe systemic hypertension 4 weeks after cardiac transplantation. The third patient experienced seizures 1 month after heart/lung transplantation for cystic fibrosis. A current theory postulates a relationship between diminished serum cholesterol and CsA neurotoxicity. This theory, however, does not satisfactorily address all cases of CsA neurotoxicity. In particular, serum cholesterol measurements were normal in cases 2 and 3 and probably were normal in case 1, despite diminished cholesterol levels preoperatively. Although the matter of CsA-induced neurotoxicity remains unresolved, we suggest that endothelin, a newly described neuropeptide that causes intense vasoconstriction and that has been implicated in cerebral vasospasm, may potentiate CsA-induced damage to endothelium and promote CsA neurotoxicity.
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PMID:MR imaging of reversible cyclosporin A-induced neurotoxicity. 188 38

Cortical blindness is rarely an ictal manifestation. We report the case of a man who developed transient cortical blindness followed by permanent visual deficits during repeated partial seizures. Intermittent visual impairment began at age 14 years. After he had the first generalized seizure at age 28 years, neurologic, ophthalmologic, angiographic, and brain computed tomographic (CT) examinations were normal. Several EEGs showed almost continuous biposterior spike-waves. Over the next several years, frequent partial seizures were associated with transient visual loss and left body twitching or paresthesias. When he was 32, transient blindness occurred during several days of repeated occipital seizures. Permanent left homonymous hemianopia, right homonymous central scotoma, dyschromatopsia, and altered stereopsis followed these seizures. Brain CT demonstrated a new right occipital lesion. Partial seizures arising posteriorly may cause transient cortical blindness and result in permanent visual deficits.
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PMID:Ictal cortical blindness with permanent visual loss. 249 21

We present ten patients with classical or common migraine of increasing severity accompanied by seizures of multiple patterns and increasing severity leading to episodes of epilepsia partialis continua. Long lasting deficits associated with hypodense lesions on CT and abnormal signals on MRI, then developed. Cortical blindness, cortical deafness and dementia were common. Five of the patients died in 1-10 years. Some of these patients had markers of mitochondrial disease (ragged red fibers and serum lactate elevation) and others with the same clinical picture did not. This group of patients indicates that mitochondrial encephalopathy may exist without evidence of myopathy, that the clinical syndrome is characteristic and that it should suggest the diagnosis even in the absence of muscular abnormalities.
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PMID:Malignant migraine: the syndrome of prolonged classical migraine, epilepsia partialis continua, and repeated strokes; a clinically characteristic disorder probably due to mitochondrial encephalopathy. 311 51

Cortical blindness following grand mal seizures occurred in five adult patients. The causes of seizures included idiopathic epilepsy, vascular accident, brain cyst, acute encephalitis and chronic encephalitis. Blindness was permanent in one patients, but the others recovered within several days. Since most of the patients were either unaware of or denied their blindness, it is possible that this event often goes unrecognised. Cerebral hypoxia is considered the most likely mechanism.
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PMID:Postictal blindness in adults. 641 6

Cortical blindness without retinal changes is a rare complication in preeclampsia. We report two patients, both of whom developed cortical blindness one and two days post partum. In one of these patients, the blindness occurred following eclamptic seizure. In both patients the total blindness recovered fully after two and three days respectively following treatment for hypertension and cerebral edema. Spasm of small vessels in the occipital cortex is assumed to be the cause of this complication.
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PMID:[Postpartum amaurosis in patients with pre-eclampsia]. 668 42

Subacute sclerosing panencephalitis (SSPE) is a subacute encephalopathy of childhood and young adolescence. Infrequently, SSPE can occur in adults and pregnant women. It is caused by an aberrant measles virus, known as the SSPE virus. SSPE virus differs from wild-type measles viruses in the form of several mutations affecting the viral genome. The matrix gene is most commonly affected by these mutations. The characteristic clinical manifestations of SSPE include behavioral changes, cognitive decline, myoclonic jerks, seizures, abnormalities in vision, bilateral pyramidal signs and coma. Ocular changes may occur in up to 50% of patients. The most characteristic ophthalmological lesion is necrotizing retinitis. Cortical blindness can be the early feature of SSPE. The diagnosis of SSPE is often difficult in the early stages. In a typical case diagnosis is based on clinical, electroencephalographic, and cerebrospinal fluid findings. At present, there is no effective treatment to completely cure SSPE. Oral isoprinosine and intrathecal or intraventricular alpha-interferon may prolong survival to some extent. Immunization against measles is currently the most effective strategy against SSPE.
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PMID:Subacute sclerosing panencephalitis. 1884 16

A 10-year-old male presented with vision loss and behavioral changes. He had midpoint pupils with no reaction to light and normal funduscopic examination. Cranial magnetic resonance imaging revealed bilateral cortical lesions at parieto-occipital lobes. Elevated measles antibody titers in the cerebrospinal fluid confirmed the diagnosis of subacute sclerosing panencephalitis. Despite oral inosiplex and supportive care, patient developed generalized seizures with frequent myoclonic jerks and rapidly progressed into coma. Cortical blindness in subacute sclerosing panencephalitis can be an early indicator for fulminant course.
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PMID:Rapidly progressive subacute sclerosing panencephalitis presenting with acute loss of vision. 2236 74

Post-traumatic seizures can be a cause of multiple clinical and behavioral abnormalities. We present an unusual case of post-traumatic epilepsy resulting in blindness. The patient was a 35-year-old female with a past history of toxemia of pregnancy who was assaulted, sustaining a traumatic brain injury (TBI). Glasgow Coma Score upon presentation to the emergency department was 10. Initial CAT scan was negative. Subsequent MRI revealed occipital edema. On examination, she was found to be blind in both eyes. Consistent with cortical blindness, extra-ocular movements, pupillary reflexes and fundoscopic examination were normal. Unusual scanning eye movements were noted. Electroencephalography (EEG) revealed epileptiform discharges in both occipital regions consistent with occipital status epilepticus. Seizures were eventually controlled with Phenytoin and Phenobarbital, with subsequent conversion to Carbamazepine. Central vision returned, but peripheral sight was never regained. Follow up EEG revealed no evidence of epileptiform activity. Post-traumatic occipital status epilepticus is rare. Cortical blindness in TBI patients with minimal occipital pathology on imaging is generally transient. This case points out the need for the treating rehabilitation professional to be vigilant in assessing for post-traumatic seizures in patients with persisting visual deficits.
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PMID:Occipital status epilepticus: an unusual case of post-traumatic blindness. 2452 92

Cortical blindness (CB) due to contrast-induced encephalopathy is a rare complication in endovascular procedure. Although exact mechanism is not known, disruption of blood-brain barrier (BBB) by contrast agent is supposed to be caused. We report two cases of contrast-induced encephalopathies after coil embolization of unruptured aneurysm. A 68-year-old woman with unruptured basilar artery aneurysm was treated with endovascular stent-assisted coil embolization. The procedure was successfully accomplished within 172 min using about 160 ml of contrast medium (iopamidol). However, she manifested with CB 3 h after the procedure and seizure on the next day. Immediate computed tomography revealed the cortical enhancement in both occipital lobes. Diffusion-weighted imaging-magnetic resonance imaging and fluid-attenuated inversion recovery sequence 1 day after the procedure revealed edema in both occipital lobes with no findings of ischemia or hyperperfusion. Electroencephalography showed sharp and slow waves in both occipital lobes. She required endotracheal intubation on day 2 to maintain airways and breathing. Her sensorium improved 4 days after the procedure with administration of steroid and anticonvulsant. She was extubated on day 4 after the procedure. She was discharged with persisting CB as a sequel.
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PMID:Rare Cases of Contrast-Induced Encephalopathies. 3314 56


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