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)

A 29-yr-old writer presented with seizures and left hemiparesis 8 days post-partum. Studies revealed right parietal hemorrhagic infarction secondary to superior sagittal sinus thrombosis. An anticoagulant was given for clot extension associated with increasing cerebral edema and coma. Inpatient rehabilitation was undertaken for residual left hemiparesis, most severe in the leg. Left arm strength rapidly returned to normal. Significant improvement in left leg strength occurred but was delayed for many months. Intracerebral thrombosis is an uncommon but significant cause of stroke in young adults. It frequently occurs in the puerperium and may be associated with unilateral or bilateral neurologic deficits. Treatment with anticoagulants is controversial because of the risk of hemorrhagic cerebral infarction, but may be beneficial in some cases. Recovery may be delayed for several months pending recanalization of the sinus or the development of collateral circulation. The overall prognosis for neurologic and functional recovery in survivors of intracerebral thrombosis is good.
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PMID:Intracerebral thrombosis. Case report and brief clinical review. 155 32

11 cases of cerebral venous thrombosis in adults are reported. Main clinical signs are: intracranial hypertension (headache, nausea, papilledema in 7 cases, loss of consciousness in 6 cases, neurological deficit in 6 cases, seizure in 4 cases. 1 patient is dead, who did not receive heparin treatment. Delay before diagnosis is between 2 and 20 days, and is shortened when arteriography or MRI are available and prescribed. At least one (or several) CT examination was performed in 10 patients. Direct signs of thrombosis are uneasily detected without contrast injection, seen here in 4 cases. Empty delta sign is observed in 7 patients, lately in 4 cases, and once only afterwards. Cerebral infarction is visualized in 7 cases over 10. Its features frequently seem evocative for cerebral venous thrombosis: triangularin 4 cases or nodular shape in 3 cases with hemorragic infarct in 7 cases, with bilateral topography in 6 cases, in frontal or central areas in 7 cases. 6 patients had a MRI examination. All cerebral infarctions appeared haemorragical, even at early stages. During subacute period, venous thrombosis is constantly and easily detected by the mean of methemoglobin high signal intensity on T1 weighted images. The prediagnosis delay is short, without necessity of arteriography. MRI should take the place of CT and arteriography in investigation of a clinically suspected cerebral venous thrombosis.
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PMID:[Thrombosis of the cerebral veins. X-ray computed tomography and MRI imaging. 11 cases]. 160 50

Three cases of patients with unusual neuronal tumors in the cerebral hemisphere are reported. All were associated with long-standing epileptic seizures. Computed tomography disclosed low-density lesions without contrast enhancement, which were interpreted as either arachnoid cysts or a cerebral infarction at initial diagnosis. Magnetic resonance imaging scans, however, revealed the lesions to be solid tumors. At surgery, the tumors were found to be relatively well demarcated, soft, and gelatinous. Histologically, all tumors were composed of small uniform stellate cells, which proliferated in a loose myxoid fibrillary matrix and resembled either oligodendroglial or astrocytic tumors. Ultrastructurally, however, all tumors showed neuronal differentiation, including numerous clear and occasional dense-core vesicles, microtubules, and a number of synapses. A review of the literature uncovered no other such cases, and therefore it was decided to classify these tumors as a distinct group of benign neuronal tumors, designated as "cerebral" neurocytoma compared with "intraventricular" neurocytoma. Related nosologic problems of neuronal tumors of the central nervous system and their possible histogenesis are also discussed.
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PMID:Cerebral neurocytoma. A new subset of benign neuronal tumors of the cerebrum. 161 3

Severe watery diarrhea and eosinophilic colitis induced by carbamazepine (CBZ) has not been described previously. We report the first known case of CBZ-induced watery diarrhea and eosinophilic colitis in a 57-year-old man receiving CBZ for secondarily generalized tonic-clonic seizures that developed after a cerebral infarction.
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PMID:Carbamazepine-induced eosinophilic colitis. 173 44

Cerebral arterial infarction is a very rare condition during the neonatal period. In recent times, cerebral infarctions with an atypical bland course are reported in healthy, unsuspected newborns. For the first time, we saw focal seizures and a transient syndrome of inappropriate ADH secretion in a full-term, male newborn with an infarction of the middle cerebral artery as the first sign of this disorder. On the basis of these rare clinical manifestations, the literature about neonatal cerebral infarction is reviewed. The diagnostic possibilities and prognostic expectations are discussed. It is the aim of this case report to call attention to this rare disease in order to avoid a delay in diagnosis and therapy, even if the initial manifestations are atypical.
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PMID:[Neonatal focal seizures and transitory inappropriate ADH secretion syndrome due to an infarction in the region of the middle cerebral artery]. 177 Sep 60

The effect of oxiracetam (CGP 21690E, CAS 62613-82-5) on cerebrovascular impairment was investigated in rats. 1. After injection of tranylcypromine (a MAO inhibitor), spontaneously hypertensive rats (SHR) which had been previously infused with norepinephrine (NE) for 14 days displayed stroke-related behaviour including kangaroo-like posture, seizures and death. Administration of oxiracetam at doses of 400 and 800 mg/kg/d p.o. for 14 days before tranylcypromine injection inhibited the stroke-related behaviour. 2. Bilateral common carotid and vertebral artery occlusion induced electroencephalogram (EEG) flattening, the EEG recovering gradually after re-perfusion of cerebral blood flow. Oxiracetam administered after the re-perfusion at a dose of 100 mg/kg, i.v. accelerated the recovery. This facilitatory effect was not seen when either piracetam (50 and 100 mg/kg i.v.) or idebenone (50 and 100 mg/kg i.v.) were administered. 3. Occlusion of middle cerebral artery produced cerebral infarction and disturbed the circadian rhythm of spontaneous motor activity with an relative increase of activity in the light period. Treatment with oxiracetam (400 mg/kg/d p.o.) for 14 days after the occlusion showed a tendency to an improvement in the disturbed circadian rhythm but did not influence the size of brain infarction. From these results, oxiracetam is thought to have a protective effect in cerebrovascular impairment.
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PMID:Effect of oxiracetam on cerebrovascular impairment in rats. 177 53

A 34 year old woman developed cerebral infarction, following a tonic-clonic seizure. A vertebral artery dissection was demonstrated and may have been caused by arterial trauma during the seizure. This cause of morbidity following convulsive seizures may have been overlooked in the past and needs to be recognised in view of the potential benefits of anticoagulation.
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PMID:Extracranial vertebral artery dissection following tonic clonic seizure. 190 46

We studied the pattern and outcome of strokes in 200 Saudi patients. Cerebral infarction constituted 87% of strokes, subarachnoid hemorrhage 4.5%, cerebral hemorrhage 6.5%, and venous infarction 2%. The vessel most commonly involved was part or all of the middle cerebral artery, constituting 52% (90) of the 174 arterial infarcts. Lacunar infarcts were seen in 21% (37) of the patients with arterial infarcts. Among all 200 patients, 8% died and 8% had secondary generalized seizures. Hypertension occurred in 41% of the 174 patients with arterial infarcts and 62% of the 13 with cerebral hemorrhages. The highest incidence of hypertension as a risk factor was among those with lacunar infarcts (81%), ganglionic cerebral hemorrhages (80%), and infarcts of deep branches of the middle cerebral artery (57%). Embolic infarcts due to rheumatic heart disease constituted 11% of all arterial infarcts. We conclude that our pattern of strokes is similar to that of the west rather than that of the Japanese, but with less frequent arteriovenous malformations and aneurysms.
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PMID:Cerebrovascular disease in Saudi Arabia. 192 60

A 54 year-old man, who had a hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease; O-W-R) accompanied by pulmonary arteriovenous fistulas (PAVFs) and congestive heart failure, developed seizure, right hemiparesis and dysphasia. A brain CT scan revealed a cystic lesion with perifocal edema in left frontoparietal lobe. A contrast enhanced CT scan showed a ring-like enhancement. Dynamic CT scans disclosed that the ring in the cortical side was enhanced more thickly than that in the ventricular side. Considering the severity of the cardio-pulmonary condition, and the deep location of the abscess, we performed an echo-guided aspiration and drainage of the abscess under local anesthesia. No bacteria were demonstrated in the culture of the contents of the abscess. After the surgery, the right hemiparesis and dysphasia were much improved and a CT scan showed the marked reduction of the abscess. However, around eight days after the surgery, the patient showed severe pleural effusion due to progressive heart failure and died on the 11th postoperative day. Autopsy disclosed a shrunken brain abscess, multiple cerebral infarction, multiple PAVFs and severe constrictive pericarditis which was regarded as the cause of death in the patient. In this report, we presented the therapeutic advantage of echo-guided surgery for the treatment of brain abscess in a high-risk patient. We also discussed the mechanism of the formation of brain abscess in patients of O-W-R disease by reviewing published cases.
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PMID:[A case of Osler-Weber-Rendu disease with brain abscess; the mechanism of the formation of brain abscess and its treatment in Osler-Weber-Rendu disease]. 194 83

Clinical and necropsy findings in 11 patients with sickle cell anemia (SS) indicate that intracranial hemorrhage (IH) is a delayed sequela of the same vasculopathy that causes cerebral infarction during childhood. Evidence of prior cerebral infarction during childhood included hemiparesis, seizures, an episode of coma, or mental retardation. Computerized tomography (CT) scans showed cerebral infarcts with lucent areas and dilated ventricles or cerebral atrophy. CT or magnetic resonance imaging (MRI) scans after the intracranial hemorrhage demonstrated intraventricular or intracerebral hemorrhages. Angiography or autopsy in seven patients showed widespread vascular occlusion and narrowing of arterial vessels. Moyamoya with internal carotid artery occlusion was identified in two cases. At the time of the IH, three patients were being treated with prophylactic transfusion regimens. We hypothesize that the central nervous system vasculopathy progresses over time and that arterial narrowing in both large and small vessels secondary to endothelial hyperplasia is followed by neovascularization and hemorrhage. Recognition of this pattern of delayed intracranial hemorrhage following cerebral infarction should encourage more intensive evaluation aimed at developing rational interventional therapy prior to a terminal intracranial hemorrhage.
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PMID:Delayed intracranial hemorrhage following cerebral infarction in sickle cell anemia. 213 21


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