Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three cases of bilateral deafness with cytologically-demonstrated meningeal carcinomatosis are reported. The first patient, a 64-year old man, presented with bilateral deafness, gait disturbances, and bilateral facial paresis. The second patient, a 78-year-old man, had bilateral deafness, unsteady gait and fluctuations in consciousness. The last patient, a 69-year-old man, complained of bilateral deafness and severe headache, and presented with right facial paresis and left laterodeviation while walking. All three patients had abnormal cochleo-vestibular findings and brainstem auditory evoked responses (BAER) that suggested peripheral lesions with absent or very delayed I waves. The brain CT scans with an without contrast enhancement were entirely normal, and the diagnosis was established by lumbar puncture. From our own cases and a review of the literature, deafness in meningeal carcinomatosis may start unilaterally but becomes bilateral in less than a week. Vestibular disturbances may not be apparent, but they can be demonstrated in almost all cases. Facial paresis or plegia is also a very frequent finding. The destruction of the eighth and seventh cranial nerves is probably due to direct infiltration by neoplastic cells as well as to ischemia through compression of the nerve supplying vessels. The 3 cases presented here emphasize once again the important fact that meningeal carcinomatosis remains a cytological diagnosis, several lumbar punctures being sometimes necessary, and that cerebrospinal fluid studies cannot yet be supplanted by other diagnostic techniques like contrast-enhanced CT or MRI with gadolinium.
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PMID:[Bilateral deafness, an initial manifestation of meningeal carcinomatosis]. 160 23

A 69-year-old man developed acute-onset confusion and hypertension with systolic pressures in the 160s 1 day after carotid endarterectomy for right facial droop from left hemispheric lacunar infarcts. CT perfusion (figure, A-D) demonstrated findings consistent with cerebral hyperperfusion syndrome (CHS) following revascularization. CHS is caused by loss of autoregulation, hypertension, and ischemia-reperfusion injury resulting in increased regional blood flow and vascular congestion.(1) CHS following revascularization may present as ipsilateral headache, focal seizure, or neurologic deficit. Nonperfusion imaging may show intraparenchymal hemorrhage or edema. Labetalol and clonidine are used for aggressive blood pressure control until cerebral autoregulation is restored.(2.)
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PMID:Teaching NeuroImages: perfusion imaging of cerebral hyperperfusion syndrome following revascularization. 2387 1

Background The syndrome of transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL) is a self-limited benign disorder of unclear pathogenesis, with diverse clinical manifestations. Cases We report two unusual presentations of this entity. The first case developed a catastrophic picture, characterized by acute elevation of intracranial pressure, necessitating emergency life support. The second case presented with hyperacute-onset mixed aphasia and facial droop, masquerading as acute ischemia of the middle cerebral artery territory. Both patients made full recoveries. Conclusion The possibility of HaNDL should be considered in individuals presenting with unusual patterns of headaches and transient neurological symptoms. Our report will expand the spectrum of this disorder, which will help physicians not only to recognize the unusual manifestations of this rare disorder, but also consider potential therapeutic interventions.
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PMID:Syndrome of transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis presenting as acute neurological emergencies. 2703 41

We present a case of a 58-year-old man with delayed diagnosed moyamoya disease who underwent encephaloduroarteriosynangiosis (EDAS) procedure. This patient with a history of three strokes presented to our facility with new left facial droop. Neurological examination revealed left facial droop and hemiparesis. Brain magnetic resonance imaging (MRI) described right frontal lobe acute ischemia. Head computed tomography (CT) angiography revealed bilateral supraclinoid internal carotid artery (ICA) occlusions. Cerebral angiography demonstrated diffuse intracranial vascular irregularity with stenosis, more above the bilateral supraclinoid ICAs and the right middle cerebral artery (MCA) suggestive of moyamoya disease. Due to the lack of MCA patency, he underwent EDAS. Superficial temporal artery (STA) was dissected inferiorly and the posterior branch was bipolared, then STA was movable. A bur hole made at the superior and inferior portion along the STA. Dura was opened, and STA was brought on top of the pia. His facial droop gradually improved after that. Nine months later, no new strokes reported. Moyamoya disease is a rare neurovascular disorder characterized by narrowing and occlusion of the ICA branches. Its symptoms include recurrent ischemic/hemorrhagic strokes. Incidence in Hispanics has not been studied. The gap between the first manifestations and disease progression is one to eight years. Its diagnosis is often delayed. Our patient had recurrent strokes for five years. Despite therapy with antiplatelets, new ischemic stroke brought him to our institution. Rate of recurrent strokes despite antiplatelets was reported 10.3% per year. Brain CTs and MRIs had failed to detect strokes' etiology. Catheter-directed angiography is the gold standard test for diagnosis of moyamoya disease. Antiplatelet alone is ineffective and surgery is the effective method to prevent further strokes, although there are no studies in adults regarding the efficacy of indirect revascularization. In direct revascularization, usually STA anastomoses to MCA. Indirect method works through the development of leptomeningeal collaterals. Postoperative complications are infarction and hyperperfusion syndrome. Seong-eun et al. proposed that modified EDAS is simpler with less complications in comparison with direct revascularization. Some other studies showed higher chance of stroke in indirect method versus direct technique. In conclusion, it is important to consider moyamoya disease as a differential diagnosis in patients with recurrent strokes.
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PMID:A Case of Delayed Diagnosis of Moyamoya Disease After Recurrent Strokes. 3201 May 32

A 30-year-old female with a history of seizure disorder and hypoplastic left heart syndrome treated with a Norwood procedure in 1986 followed by a modified non-fenestrated Fontan (Left SVC to IVC to pulmonary arteries) with a known baffle leak presented to the emergency department. On day of presentation, the patient became unresponsive, with perioral cyanosis, rightward gaze and a left facial droop near the end of a platelet transfusion. An emergent non-contrast head CT revealed intracranial air in the right MCA distribution. She was taken to the hyperbaric chamber and was treated with a U.S. Navy Table 6 in a multiplace chamber with no extensions. Ten minutes into the treatment patient became more alert and spontaneously asked questions. The following day she was treated with a U.S. Navy Table 5. Patient had repeat CT of the head, which showed resolution of intracerebral gas and small areas of ischemia in right frontal lobe and right caudate. On hospital day five neurologic exam was normal, with 5/5 strength and no residual deficits. Treating the patient was a concern because patient has a single ventricle, in which the pulmonary artery is connected directly to the vena cava. There is very little data regarding the effects of hyperbaric oxygen (HBO2)therapy on single-ventricle physiology. Only two case reports of three pediatric patients treated with HBO2 for CAGE in a similar setting are known. In these cases the patients had improvements in their symptoms following HBO2. These cases and ours indicate HBO2 is feasible and indicated for CAGE in patients with cyanotic congenital heart disease.
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PMID:Cerebral arterial gas embolism in a patient with hypoplastic left heart syndrome treated with emergent hyperbaric oxygen: case report. 3293 69