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)

A nuclear oculomotor nerve syndrome is rarely caused by mesencephalic lesions. We describe 5 patients, 4 with unilateral syndrome (3 due to ischemia and 1 to mesencephalic hemorrhage) and 1 with bilateral nuclear ischemia of the third cranial nerve. These patients represent 0.2% of those admitted with cerebral vascular pathology over the last 12 years. Symptoms are consistent with descriptions of the anatomic organization of this nucleus, with peripheral paralysis of the contralateral superior rectus and possible bilateral involvement of the eyelid elevator and the pupillary constrictor muscles. A noteworthy symptom seen in these cases is supranuclear paralysis of the upward gaze on the side of the lesion, with ocular elevation achieved in response to oculocephalic stimuli in 2 cases and with Bell's synkinesis in 4. We analyze the nature of 22 published cases of unilateral nuclear damage and of 14 published cases of bilateral nuclear damage. Unilateral damage may or may not lead to ipsilateral pupillary involvement, uni- or bilateral eyelid ptosis, contralateral ocular hypotropia, and possible horizontal paresis of the contralateral gaze. Associated deficits are hemiparesis or crossed hemiataxia. Unresponsive pupils and bilateral ptosis associated with tetraparesis, bilateral ataxia and altered states of consciousness were seen with bilateral nuclear lesions. Infarction is the main cause (in 32 out of 41) and recovery of full ocular movement is uncommon.
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PMID:[Nuclear oculomotor nerve syndrome due to mesencephalic infarction or hemorrhage. Five cases and a review of literature]. 808 84

A 52 year old heavy smoker complained of paresthesiae and pain at the ventral side of the right thigh and the antero-medial side of the right lower leg as well as weakness of the right quadriceps femoris during exercise. Clinical examination revealed a paresis of the right quadriceps, hypesthesia and hypalgesia in the area of the femoral nerve and a reduced right patellar reflex after 10 min walking. An occlusion of the right common iliac artery was diagnosed by angiography. Following transluminal angioplasty and implantation of an intravascular stent, the patient was free of symptoms. On the basis of the clinical observations following recanalisation of the common iliac artery, the symptoms can best be explained by a reduced perfusion of the iliolumbar artery supplying the upper part of the femoral nerve, causing ischemia of the femoral nerve during exercise. In conclusion, stenosis/occlusion of the common iliac artery should be considered as a differential diagnosis of quadriceps weakness and paresthesia in the area of the femoral nerve associated with exercise.
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PMID:[Neurogenic intermittent claudication of the femoral nerve caused by occlusion of the common iliac artery]. 823 83

Four patients presented with hemiballism-hemichorea as a clinical manifestation of white matter ischemia. These patients illustrate "positive" motor phenomena rather than limb weakness as a consequence of cerebral ischemia. In each patient, the involuntary movements disappeared following worsening of paresis. Subcortical white matter infarction in three patients and hemodynamic hypo-perfusion in the cerebral hemisphere contralateral to dyskinetic movements were possible causes. Neuroradiologically, none had pathological changes in the vicinity of the subthalamic nucleus. We presume from these observations that ischemia of the subcortical white matter, without involvement of the basal ganglia or the subthalamic nucleus, may cause hemiballism-hemichorea.
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PMID:Hemiballism-hemichorea induced by subcortical ischemia. 831 49

Acute arterial occlusions of the extremities present with the classical five P's: pain, pallor, pulselessness, paresthesia, paresis. Loss of sensitivity and motility are symptoms of the most severe grade of ischemia. The occlusions are due to embolism in about 70% of subjects and to local thrombosis in 30%. These patients have to be treated immediately with heparin. In the mildest forms, deobliteration is desirable, but in the more severe cases rapid restoration of flow not only saves limbs but also life. Deobliteration may be performed surgically or by means of catheters (local thrombolysis or thrombus aspiration) if available. Deep vein thrombosis, the other kind of emergency situation, requires immediate anticoagulation as soon as pulmonary embolism is suspected. It should be initiated by heparin and followed by oral anticoagulation. In patients presenting without pulmonary embolism but a swollen leg, ruptured Baker cysts or muscle hematomas should be ruled out before anticoagulation is started. Systemic thrombolysis or surgical thrombectomy is reserved for young patients with acute isolated thromboses. Thrombectomy must also be kept in reserve for the most severe form of deep venous thromboses, the phlegmasia cerulea dolens. In thrombophlebitis, no anticoagulation is indicated except in bedridden patients. The others must remain mobile and may be treated by systemic and local antiinflammatory drugs, incision of thrombosed varices, and bandages.
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PMID:[Emergencies in angiology]. 849 73

Eighty-nine male veterans presenting to a vascular surgery clinic with symptomatic lower extremity atherosclerosis were prospectively screened by duplex scan for asymptomatic carotid artery stenosis (CAS). Their chief complaint was: claudication (90%), rest pain (6%), and ischemic ulcer or gangrene (4%). The mean ankle-brachial index (ABI) was 0.77. Twenty-five CAS > 50% were detected in 18 (20%) patients. Twelve CAS > 75% were detected in 11 (12%) patients. There was no difference between patients with and without CAS > 50% with regards to mean ABI, history of angina, diabetes, hypertension, prior coronary artery bypass, or history of smoking. Carotid bruit was associated with ipsilateral CAS > 50% [p < 0.0001, sensitivity (52%), specificity (88%), positive predictive value (41%), negative predictive value (92%)]. As a result of the screening, eight elective carotid endarterectomies have been performed to date in six (7%) patients with one transient twelfth cranial nerve paresis as the only postoperative complication. We conclude that: (1) male patients presenting with symptomatic lower extremity atherosclerosis have a 20% prevalence of asymptomatic CAS > 50%, (2) there is no correlation between the degree of lower extremity ischemia and CAS > 50%, (3) carotid bruit is significantly associated with CAS > 50%, but has a low sensitivity, and (4) routine CAS screening should be considered for all male patients with symptomatic lower extremity atherosclerosis regardless of whether a bruit is present.
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PMID:Asymptomatic carotid artery stenosis screening in patients with lower extremity atherosclerosis: a prospective study. 923 93

Acquired supranuclear ocular motor paresis is a rare disorder characterized by impaired saccadic and smooth pursuit eye movements in one or more directions of gaze. Vestibularly induced eye movements, however, are preserved. Six adult patients developed an acquired supranuclear ocular motor paresis following cardiopulmonary bypass surgery. Neuroimaging studies were normal in two patients and were consistent with small vessel ischemia in four patients. The mean cardiopulmonary bypass time was 132.3 min, and mean circulatory arrest time was 38.7 min; these were not outside established norms for this type of surgery. Patients undergoing cardiopulmonary bypass procedures with deep hypothermia are at risk for acquired supranuclear ocular motor paresis, but the development of this syndrome may not be predictable by duration of circulatory arrest or cardiopulmonary bypass times.
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PMID:Acquired supranuclear ocular motor paresis following cardiovascular surgery. 930 32

A flock of 15-wk-old tom turkeys experienced an acute onset of paresis and ataxia in 75% of the birds after handling. Cartilaginous emboli were found in the spinal cord vasculature from one of five turkeys at this initial presentation. Most of the flock recovered within 6 days, but 3% remained paretic. Myelomalacia was present in three turkeys that failed to recover. Two of these turkeys had cartilaginous and osseous emboli within the medullary spaces of the vertebral bodies, internal vertebral venous sinuses, and spinal cord. The third turkey had vascular and spinal cord necrosis consistent with thrombosis and resultant ischemia. These changes suggest that turkeys may be susceptible to a syndrome analogous to fibrocartilaginous embolism of the spinal cord in mammals. The articular cartilage of the vertebral body endplate may be the source of the emboli. The turkeys with emboli had articular cartilage defects consisting of matrix eosinophilia, chondrocyte loss, multicellular cluster formation, cartilage detachment, and cartilage clefts. Cartilaginous emboli in the spinal cord should be considered as a potential cause for acute paresis and ataxia, especially in flocks with preexisting abnormalities of the vertebral articular cartilage surfaces.
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PMID:Intravascular cartilaginous emboli in the spinal cord of turkeys. 964 39

A 67 year-old normotensive woman had a syncope followed by shock and remained anuric after hemodynamic stabilization. Paraplegia and paresis of the right upper limb, as well as signs of ischemia of the distal lower limbs were noted. The possibility of acute aortic dissection was raised and confirmed by computed tomography. The paraplegia was attributed to an ischemic infarction of the spinal cord. The patient died on the fourth hospital day due to a pericardial temponade. This rare and not well recognized complication of aortic dissection is briefly reviewed.
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PMID:[Acute paraplegia. A rare complication of aortic dissection]. 968 28

Little is known about how ischemia affects hemodynamic responses to neural activation in the brain. We compare the effects of a motor activation task and a cerebral vasodilating agent, acetazolamide (ACZ), on regional cerebral blood flow (rCBF) in primary sensorimotor cortex (PSM) in six patients with major cerebral artery steno-occlusive lesions without paresis of the upper extremities. Quantitative rCBF was measured in all patients using H2(15)O autoradiographic method and positron emission tomography. The CBF was determined at rest, during a bimanual motor activation task, and 10 minutes after ACZ administration. With bimanual motor activation, rCBF increased significantly in both PSM compared with at rest (P < 0.01 on lesion side, and P < 0.02 on contralateral side). However, rCBF did not increase after ACZ injection in the PSM on the lesion side, whereas rCBF increased significantly in the contralateral PSM after ACZ injection compared with the level at rest. This result suggests that despite a decreased hemodynamic reserve, there is a nearly normal flow response to neural activation, indicating that the mechanism of vasodilation responsible for perfusion change is different for acetazolamide and neural activation. The relations among neural activation, hemodynamic status, and cerebral metabolism in the ischemic stroke patients are discussed.
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PMID:Neural activation of the brain with hemodynamic insufficiency. 974 99

The most common initial symptom of aortic dissection is chest pain. Other initial symptoms include pain in the neck, throat, abdomen and lower back, syncope, paresis, and dyspnoea. Headache as the initial symptom of aortic dissection has not been described previously. A 61-year-old woman with a history of migraine and arterial hypertension developed continuous bifrontal headache. Two hours later, right-sided thoracic pain and a diastolic murmur were suggestive of aortic dissection that was confirmed by echocardiography and subsequent surgery. The dissection commenced in the ascending aorta and involved all cervical arteries until the base of the skull. Headache as the initial manifestation of aortic dissection was assumed due to either vessel distension or pericarotid plexus ischemia. Aortic dissection has to be considered as a rare differential diagnosis of frontal headache, especially in patients who develop aortic regurgitation or chest pain for the first time.
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PMID:Headache as the initial manifestation of acute aortic dissection type A. 982 52


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