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)

In 1983, a previously healthy 21-year old mother came to University Hospital in Dijon, France feeling weak and had a severe frontal headache with vomiting. Clinical and biochemical tests were normal. She smoked 20 cigarettes/day and used a high dosed combined oral contraceptive (OC) (ethinyl estradiol and cyproterone acetate). 15 days later, the headache returned and she could not understand spoken words and the bilateral section of the brain had slowed. Yet her mental status was normal as were cerebrospinal fluid and cerebral computerized tomography tests. The antiherpes virus drug, vidabarine, did not alleviate symptoms. At least 1 month later, a severe left pulmonary embolism caused acute right heart failure. She also had a prethrombotic left iliac vein, so physicians began heparin therapy, adding nifedipine and buflomedil to control the spasms in the right internal iliac artery and both external iliac arteries. Acute ischemia of the lower limbs eased within a week but sensory disorders remained for 2 months. Satisfactory collaterality transpired due to a blocked left external iliac artery and left iliac vein. The following signs and symptoms indicated her condition to be homocystinuria: blond hair with deep blue eyes, macrocytic anemia, factor VII deficit (51%), strong positive Brandt's reaction, cystine homocystine in the plasma, and presence of homocystine, cystathionine, and methionine in the urine. Physicians took her off the OC and discharged her on vitamin B6/day, folic acid/day, betaine citrate/day, and the anticoagulant Coumadin. A subsequent check of her 19-year old sister found she had it too. They assessed the patient's condition yearly. In 1988, her left leg developed edema and she limped when not using elastic stockings. Effects of iliac vein phlebitis were evident. She no longer suffered from headaches. Since plasma methionine was within the normal range and homocystine no longer was present in plasma and urine, the physicians halted the anticoagulant therapy. In conclusion, the OC precipitated this partial form of homocystinuria.
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PMID:Vascular manifestations in homocystinuria. 161 Jun 63

A review of the sensitivity of genetically hypertensive rats to cerebral ischemia was presented together with original data describing the systematic comparison of the effects of focal ischemia (permanent and temporary with reperfusion) performed in hypertensive and normotensive rats (i.e., blood pressures verified in conscious instrumented rats). Microsurgical techniques were used to isolate and occlude the middle cerebral artery (MCAO) of spontaneously hypertensive (SHR), Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats at the level of the inferior cerebral vein. Following permanent (24 h) MCAO, persistent and similar decreases in local microvascular perfusion (i.e., to 15.6 +/- 1.7% of pre-MCAO levels) were verified in the primary ischemic zone of the cortex for all strains using Laser-Doppler flowmetry. A contralateral hemiplegia that occurred following MCAO, evidenced by forelimb flexion and muscle weakness, was greater in SHR (neurological grade = 2.0 +/- 0.1) than SD (1.0 +/- 0.4) or WKY (0.7 +/- 0.4) rats (N = 7-9, p less than 0.05). SHR also exhibited sensory motor deficits following MCAO compared to sham-operation, with decreased normal placement response of the hindlimb (% normal = 20 vs. 83, N = 23-30, p decreased rota-rod (41 +/- 7 vs. 126 +/- 19 on rod, N = 10-15, p less than 0.05) and balance beam (25 +/- 5 vs. 116 +/- 29 s on beam, N = 5-7, p less than 0.05) performance. However, an index of general motor activity was not affected by permanent MCAO. Triphenyltetrazolium-stained forebrain tissue analyzed by planimetry revealed a significantly larger and more consistent cortical infarction in SHR (hemispheric infarction = 27.9 +/- 1.5%) compared to SD (15.4 +/- 4.1%) and WKY (4.0 +/- 2.4%) rats (N = 7-9, p less than 0.05), occupying predominantly the frontal and parietal areas. Also, a significant degree of ipsilateral hemispheric swelling (4.6 +/- 0.9%, N = 7-9, p less than 0.05) and increased brain water content (78.4 +/- 0.3% to 80.4 +/- 0.2%, N = 8-9, p less than 0.05) was identified in SHR that was not observed in SD or WKY rats. A novel model of temporary MCAO also was evaluated in the hypertensive and normotensive rat strains. Initially, the effect of increasing MCAO-time followed by 24 h reperfusion in SHR was studied. During temporary MCAO (20 to 300 min), persistent and stable decreases in local microvascular perfusion (i.e., to 15-20% of pre-MCAO levels) were verified in the primary ischemic zones of the cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetic hypertension and increased susceptibility to cerebral ischemia. 163 Jul 32

Most spinal dural arteriovenous malformations are located in the thoracic and lumbar regions. The symptoms include pain, weakness, sensory disturbances, and sphincter dysfunction, which are usually gradual in onset. They are attributed to venous hypertension with a resultant ischemia of the cord, and hemorrhage from them is rare. The authors report an unusual case of a patient with a dural arteriovenous malformation in the cervical spine who was admitted with a sudden onset of severe headache and dysesthesia due to subarachnoid hemorrhage.
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PMID:Dural arteriovenous malformation in the cervical spine presenting with subarachnoid hemorrhage: case report. 164 Oct 89

We describe conduction block as an unusual electrophysiologic manifestation in a patient with necrotizing angiopathy. The patient developed subacute symptoms over a 1-month period consisting of progressive pain, tingling, and weakness of the lower extremities. Physical examination revealed a pattern consistent with a polyneuropathy. Electrodiagnostic studies provided evidence of a conduction block in the left ulnar nerve. Pathologic studies confirmed the process to be a necrotizing angiopathy. This report establishes the role of conduction block in human nerve ischemia.
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PMID:Necrotizing angiopathy presenting with multifocal conduction blocks. 162 80

Although atrophy of the lower cervical and upper thoracic cord in juvenile muscular atrophy of distal upper extremity has been reported, the atrophic patterns of the cord, especially in the transverse section, have not been studied extensively. The aim of this study is to clarify the atrophic patterns of the cord by CT myelography (CTM) and to discuss the pathogenesis of cord atrophy. Sixteen patients with juvenile muscular atrophy of distal upper extremity were examined by CTM. Atrophy of the lower cervical and upper thoracic cord, consistent with the segmental weakness, was seen in all patients. Flattening of the ventral convexity was a characteristic atrophic pattern of the cord. Bilateral cord atrophy was commonly observed; eight of 12 patients with unilateral clinical form and all four patients with bilateral form showed bilateral cord atrophy with dominance on the clinical side. There was no correlation between the degree of cord atrophy and duration of symptoms. Flattening of the ventral convexity, associated with purely motor disturbances, reflects selective atrophy of the anterior horns in the cord, which is attributable to chronic ischemia. Cord atrophy proved to precede clinical manifestations. The characteristic atrophy of the cord provides useful information to confirm the diagnosis without long-term observation.
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PMID:Computed tomographic myelography characteristics of spinal cord atrophy in juvenile muscular atrophy of the upper extremity. 175 50

Lateral medullary syndrome is known to cause hemiparesis ipsilateral to the medullary lesion. However, it's clinical significance has not been fully evaluated. In this study, we made clinical and angiographic studies in patients with syndrome to elucidate the pathogenesis of ipsilateral hemiparesis. Thirty-four patients with cerebral infarction presenting with this syndrome were studied. Their mean age was 51 years and all the patients were examined within 6 months of their first attack. Diagnosis of ipsilateral hemiparesis was made if subjective feeling of weakness in the upper and lower extremities was associated with increased deep tendon reflexes. Ipsilateral hemiparesis was observed in 38% of all the patients. Cerebral angiography was performed in 26 patients and divided into two groups; group A with ipsilateral hemiparesis (n = 9) and group B without ipsilateral hemiparesis (n = 7). In 56% of patients in group A, angiography showed non-visualization of ipsilateral vertebral artery (VA) and posterior inferior cerebellar artery (PICA). Non-visualization of these two arteries never occurred in the patients of group B. On the other hand, non-visualization of VA alone was observed in 35% of the patients in group B, but it was none in the patients of group A. However, there were no differences in concerning the frequency of non-visualization of PICA alone or non-occlusion at all between both groups. Therefore, the focal ischemia in the region below the pyramidal decussation due to the occlusion of both VA and PICA, regardless of thrombotic or embolic episode, was considered to be responsible for ipsilateral hemiparesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pathogenesis of ipsilateral hemiparesis in patients with lateral medullary syndrome]. 191 24

We report a case of adult polymyositis with peculiar muscular pathology of innumerable muscle fiber necrosis and regeneration accentuated in the perifascicular area. A 51-year-old woman developed generalized weakness of the extremities, trunk and bulbar muscles subacutely for two months. Anterior tibial muscle biopsy showed numerous tube-like necrotic/regenerative muscle fibers predominantly in the perifascicular area. The diameters of the muscle fibers were smaller in the periphery of the fascicles. Small arteries at the center of the fascicles occasionally showed marked perivascular cuffing, although complement component C9 was negative in the vessel wall. The gradient of the diameters of necrosis/regeneration fibers was thought to have been caused by ischemia of the muscles, which persisted at the perifascicular area leading to recurrent necrosis and regeneration and gradually invaded towards the center of the fascicles. We designated this muscular pathology as perifascicular necrosis and regeneration, and regarded it was an acute severe form of the perifascicular ischemic lesions of myositis.
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PMID:[Perifascicular necrosis and regeneration in a case of adult polymyositis]. 191 31

The potential for hypothermia to prevent or ameliorate ischemic injury to the central nervous system is well known. To determine if a more prolonged period of metabolic suppression with blood substitution is possible, a method was developed to lower body temperature to near the freezing point. Eight adult mongrel dogs underwent closed-chest extracorporeal circulation with both external and internal body cooling. As they were cooled, progressive hemodilution was employed until complete exsanguination and blood substitution with an aqueous solution was accomplished. Continuous circulation and a core temperature at a mean of 1.7 degrees C were maintained from 2 1/2 to 3 hours. After rewarming to 20 degrees C, the animals were autotransfused and allowed to recover. Of the eight animals, two died due to technical factors related to cardiac defibrillation. Of the six surviving animals, five survived over a long period and one died on the 10th postoperative day with hepatorenal failure resulting from a presumed blood transfusion incompatability reaction. All six showed normal neurological function and kennel behavior, except one dog with mild weakness of a hindlimb. When the dogs were sacrificed 1 to 2 months postoperatively, all organs were histologically normal. Specifically, there was no gross or microscopic evidence of ischemic or hypoxic injury to any central nervous system structures. This pilot study demonstrates that it is possible to successfully achieve complete exsanguination, blood substitution, and ultraprofound body temperature, while continuous circulation of the blood substitute is maintained. With the capability of controlling and repeatedly performing washout of the extracellular environment and by reaching lower temperatures, it may be possible to attain greater cellular metabolic suppression. This perhaps will extend the allowable times for circulatory arrest procedures. In addition, "bloodless ischemia" may be beneficial in removing both blood substances and formed elements which may mediate organ ischemia. With replacement of blood at warm temperatures, coagulopathy is avoided. This preliminary evidence demonstrates potential in the combination of ultraprofound hypothermia and complete blood component substitution. However, further study is required to confirm the potential of achieving circulatory arrest of longer duration.
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PMID:Ultraprofound hypothermia with complete blood substitution in a canine model. 201 79

Renal transplantation is an accepted treatment for patients with end stage renal disease from insulin-dependent diabetes mellitus. Acute lumbosacral plexopathy developed following renal transplantation in 4 female patients with insulin-dependent diabetes mellitus between January 1, 1981 and June 30, 1988. In all 4 patients the internal iliac artery was used for revascularization of the renal allograft with ligation of the anterior and posterior divisions. Within 24 hours of surgery they complained of ipsilateral buttock pain, numbness in the leg and weakness below the knee. This complication has not been observed in nondiabetic patients at our institution, nor in diabetic patients when the internal iliac artery was not used. However, lumbosacral plexopathy occurred in 4 of 27 (14.8%) female patients with insulin-dependent diabetes mellitus when the internal iliac artery was used (p less than 0.001). Age, duration of insulin-dependent diabetes mellitus, hypertension, cigarette smoking history and kidney donor were not significant predictors of this complication. This unusual and newly recognized complication appears to result from ischemia of the lumbosacral plexus following ligation of the internal iliac artery in patients with severe small vessel disease.
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PMID:Acute lumbosacral plexopathy in diabetic women after renal transplantation. 229 36

In 39 patients with angiographically documented coronary artery disease and silent or symptomatic myocardial ischemia under exertion it was investigated if there is a difference in forearm skeletal muscle ischemia and ischemic pain threshold. The degree of myocardial ischemia was determined by plethysmographically measured reactive hyperemia. In 12 asymptomatic and eight symptomatic patients maximal reactive hyperemia was induced by ischemic work in the forearm skeletal muscle. After termination of ischemia there was a significantly higher reactive hyperemia at 20, 90, and 180 s in the asymptomatic patients. Furthermore, nine asymptomatic and 10 symptomatic patients underwent symptom-limited ischemic work until weakness or pain developed. Under these conditions reactive hyperemia as a parameter of oxygen deficiency was higher in the asymptomatic patients. The difference was not statistically significant. There was, however, a significantly higher incidence of ischemic pain in the symptomatic patients. It can be concluded that patients with asymptomatic myocardial ischemia tolerate a higher oxygen deficit in the working forearm and have a higher pain threshold than patients with symptomatic ischemia.
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PMID:[Comparison of the oxygen deficit and ischemia pain threshold in patients with silent and symptomatic myocardial exercise-induced ischemia]. 231 73


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