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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical ergotism as seen today results almost exclusively from the excessive intake of ergotamine tartrate in the treatment of migraine headache. Although both gangrenous and convulsive symptoms are seen in naturally occurring ergotism resulting from the ingestion of fungus infected rye, only gangrenous ergotism has been reported following the excessive ingestion of ergotamine tartrate. The symptoms of both iatrogenic and naturally occurring ergotism appear to result from regional ischemia caused by ergot induced vasospasm. This report discribes experiences in the diagnosis and management of two patients with unusual manifestations of iatrogenic ergotism. One patient presented with ischemia of all extremities and bilateral foot drop probably due to ischemic damage to the common peroneal nerves, a finding not previously described in ergot intoxication. The foot drop totally resolved in several months following the discontinuation of ergot. A second patient presented with unilateral leg ischemia and transient monocular blindness, both of which resolved after discontinuation of ergot. Both patients displayed typical angiographic findings of ergotism. There is no convincing evidence that any treatment other than discontinuation of ergotamine is of benefit in the treatment of iatrogenic ergotism.
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PMID:Ergot intoxication: historical review and description of unusual clinical manifestations. 437 16

Visual functions were examined in 18 survivors of perinatal hypoxia/ischemia with mild to severe neurological sequelae, aged between 3 months and 17 years, and in two patients, aged 8 and 13 years, who had suffered postnatal hypoxic events. All but two patients showed clear visual deficits ranging from mild defects in visual acuity, visual field size, and/or optokinetic nystagmus to blindness. In 5 patients, the visual field was restricted to tunnel vision, a finding which appeared to be specifically related to the hypoxic/ischemic nature of the brain damage. The severity of the visual defects after perinatal hypoxia was related to the occurrence of neonatal seizures, later neurological outcome, and gestational age at birth. This is discussed in relation to previous studies of the effects of perinatal hypoxia/ischemia.
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PMID:Visual defects in children after cerebral hypoxia. 652 37

An 11 year old boy was admitted to the Department of Pediatrics Medical School of Vienna with 2nd and 3rd degree burns covering 30% of his body. He presented with complications--high fever, vomiting, diarrhea and dehydration--which had led to acute renal failure. After 6 hemodialyses renal function recovered after two weeks and the patient entered a polyuric phase. In connection with a transient dehydration the patient showed a sudden bilateral cortical blindness. The computerized tomogram (CT) showed vague evidence of an occipital cortical ischemia. We assume that several factors have played a role in this sudden occurrence. As a result of hypovolemia and coincident anemia and electrolyte inbalance, cerebral edema and cortical tissue hypoxia with emphasis in the occipital cortical region developed in the brain possibly already damaged by burn injury. A complete reversal of the clinical state was achieved. The patient was discharged with normal vision and normalized renal function.
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PMID:[Acute cortical blindness: a reversible complication of acute kidney failure in a child with burns]. 683 79

Blindness following blepharoplasty is a well-documented complication. Removal of orbital fat is common to most cases in which such blindness occurs. We present a patient who was referred to us following blepharoplasty involving orbital fat removal in all four lids with subsequent onset of bilateral visual loss. Visual acuity in the right eye has remained no light perception and in the left eye improved from 20/400 to 20/20 following bilateral orbital decompression. An electroretinogram was within normal limits in both eyes. A normal response from the visual evoked response in the left eye and an abnormal response from the visual evoked response in the right eye indicate ganglion cell damage or visual pathway disruption in the right eye, probably secondary to optic nerve ischemia. We conclude that the small nutrient vessels to the optic nerve are more easily compromised than the central retinal artery and are responsible for the visual loss in many of these cases. We believe this to be the first documented case of bilateral visual loss following blepharoplasty and the first electrophysiological study demonstrating the pathophysiology of blindness following blepharoplasty. We advocate rapid orbital decompression to treat this catastrophic complication.
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PMID:Bilateral visual loss after blepharoplasty. 698 7

Only four cases of chaismal syndromes caused by arteriovenous malformations (AVMs) have been reported. We have examined two patients with chiasmal dysfunction caused by an AVM. In one patient, the AVM was suspected only after angiography. However, the presence of an angioma of the lip might have been a clue to the diagnosis. In the other patient, seizures and pulsating proptosis led to the correct diagnosis before angiography was performed. This patient also had episodes of transient bilateral blindness, presumably caused by postictal states or by periodic shunting with ischemia (chiasmal steal).
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PMID:Chiasmal syndrome caused by arteriovenous malformations. 706 62

Giant-cell arteritis is a polysymptomatic disease of the elderly. Systemic symptomatology includes headaches, arthralgias, myalgias, tender temporal arteries, jaw claudication, low-grade fever, anemia, anorexia, malaise, and weight loss. Visual loss from anterior ischemic optic neuropathy and diplopia resulting from ischemia of the ocular muscles represents the major ocular manifestations of giant cell arteritis. When the diagnosis is suspected, blood for a sedimentation rate should be drawn, and, if it confirms the clinical impression, high dose prednisone should be started immediately and a temporal artery biopsy performed at a later date. Only by asking the proper questions and suspecting the diagnosis will this preventable form of blindness receive the prompt attention it deserves.
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PMID:Giant-cell arteritis. Signs and symptoms. 715 21

30 patients with acute onset of memory disturbances and visual impairment (cortical blindness or hemianopsia) are reported. For all of them, there was evidence of posterior cerebral artery ischemia. This clinical syndrome is compared with Dide and Botcazo's case report. The amnesia never recovered in 17 patients and was transient in 13 patients: in 4 of them it occurred during vertebral angiography and in 4 during general anaesthesia with anoxia. The main clinical features of the syndrome and the related bibliography are reviewed.
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PMID:[Amnesic syndrome of posterior cerebral ischemia]. 721 26

Cortical blindness is defined as a loss of vision due to bilateral retrogeniculate lesions (geniculocalcarine blindness). Gerstmann's syndrome is a combination of disorientation for left and right, finger agnosia, and profound agraphia, alexia, and acalculia. It is due to a lesion in the left angular gyrus, situated at the confluence of the temporal, parietal, and occipital lobes. We report on a patient who suffered from severe underdiagnosed eclampsia and who developed bilateral extensive medial temporal, parietal, and calcarine ischemic infarctions during an eclamptic fit. In addition, ischemia destroyed the left angular gyrus. The combination of these lesions led to Gerstmann's syndrome with additional cortical agnosia and cortical diplopia. For the first few months following the ischemic insult, the patient had been cortically blind. Thereafter, the patient slowly regained a visual acuity of 0.1 in both eyes. She then experienced monocular and binocular diplopia. Her ocular motility was normal; there was no phoria or tropia. Monocular and binocular diplopia slowly became less severe over the following year. Now, 2 years after the incident, the patient has a visual acuity of 0.2 in both eyes and no double vision. However, the handicapping symptoms of Gerstmann's syndrome, which make leading a normal life impossible, have persisted--the patient still cannot cope alone, mainly due to the severe disorientation for left and right. The picture of cortical agnosia, cortical diplopia, and Gerstmann's syndrome is a very rare combination. Visual recovery and rehabilitation in cortical blindness are severely affected and made difficult by the symptoms of Gerstmann's syndrome. In our case the reason for such a dramatic clinical picture was eclampsia, whose prodomes had not been diagnosed in time.
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PMID:Eclamptogenic Gerstmann's syndrome in combination with cortical agnosia and cortical diplopia. 749 36

Midfacial injuries, surgery of the orbit or the paranasal sinuses as well as retrobulbar anesthesia can be the cause of a traumatic laceration of the ophthalmic artery and/or its branches prompting an extensive orbital hemorrhage with consecutive blindness. Since the neurosensory retina does not tolerate an ischemia of more than 1-3 hours, therapy has to be emergent: an extensive lateral horizontal canthotomy and vertical cantholysis, and if the hypertony of the globe persists, splitting of the periorbita in the temporal lower lid region are mandatory. The surgical details are presented.
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PMID:[Emergency therapy of traumatic orbital hematoma with acute visual impairment]. 760 75

We describe a series of six patients who experienced severe retrograde amnesia (five cases) or cortical blindness (one case) during selective vertebral angiography. All angiograms were obtained with the same nonionic contrast medium. Analysis of the contrast batch demonstrated no abnormalities, but investigation of the angiographic suite revealed a faulty contrast warming cabinet resulting in injection of contrast material above body temperature. The warming cabinet was withdrawn, and the complication has not recurred. We believe that these symptoms reflect ischemia caused by vertebral arterial spasm.
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PMID:Transient global amnesia and cortical blindness after vertebral angiography: further evidence for the role of arterial spasm. 761 Oct 84


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