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

The scenario is all too familiar. A patient has a surgical procedure. Anesthesia is uneventful and the procedure goes well. Nothing untoward is observed in the recovery room. Later that evening the patient complains of numbness, weakness, or pain, and a neurological deficit is found. A neurologist is called, examines the patient, and it is concluded that a nerve lesion has occurred, because of stretch, ischemia, compression, or laceration. A subsequent electromyogram and nerve conduction study confirm the clinical impression, but offer little in the way of explanation. Over the subsequent months, the patient makes a slow recovery but there has been a prolonged period of pain and disability. Liability issues loom. This scenario could reflect a number of different nerve lesions. This review illustrates the different modes of pathogenesis that may occur and the variable nature of the neurological deficits. We grouped these lesions according to the clinical setting in which they occur.
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PMID:Perioperative nerve lesions. 255 97

Thirteen patients with peripheral neuropathy caused by necrotizing vasculitis were clinico-pathologically analyzed. These patients consisted of nine classical periarteritis nodosa (PN), four allergic granulomatous angitis (Churg-Strauss syndrome, AGA). All of them were proven to have a necrotizing vasculitis by sural nerve biopsy. The characteristics of peripheral neuropathy of these patients were summarized as follows. 1) Mononeuritis multiplex was a principal features in all patients preferentially localized in common peroneal, sural, radial median and ulnar nerves, with all modality of sensory impairment. 2) Radiation or diffuse deep-pain was a major initial symptom. Since this pain occurs frequently in the manner of sudden onset, the patient can tell the day of onset. 3) Local edema on the skin of involved region was initially observed. 4) Muscular atrophy and weakness was distributed more widely than sensory impairment. 5) Morphometric and teased-fiber study of biopsied sural nerves revealed axonal degeneration as a major pathological process. As compared to myelinated fibers, unmyelinated fibers were likely to be well preserved in morphology and population, which suggests that unmyelinated fibers are relatively resistant to ischemia. 6) Motor and sensory conduction study showed greatly decreased sensory and motor action potentials frequently resulting in absent of recordings. Conduction velocity is almost within normal range or just below the normal. Routine EMG recordings showed active denervation potentials in the involved muscles. 7) Protein in CSF was rarely elevated which suggested involvement of the spinal roots is infrequent. 8) Hypereosinophilia, thrombocythemia, fever, increased erythrocyte sedimentation rate, positive CRP and RA, and polyclonal hypergammaglobulinemia (IgG, IgA) were observed in most cases.
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PMID:[Clinical features of the peripheral nerve involvement in necrotizing angitis--characteristics in polyarteritis nodosa and allergic granulomatous angitis]. 256 7

This case report documents an acute rupture of the lateral head of the gastrocnemius muscle at the myotendinous junction and a lateral dislocation of the tibialis anterior tendon with a clinical presentation consistent with a compartment syndrome, despite the intraoperative finding of a rupture of the posterior and lateral compartments. Extensive hematoma formation led to marked edema, paresthesias, muscle weakness, and severe pain in the involved leg. Surgical repair of the torn muscle and dislocated tendon and evacuation of the dissecting hematoma resulted in a well-functioning extremity. The authors emphasize the importance of prompt diagnosis of soft tissue injuries, which may place a patient at risk for a compartment syndrome. A compartment syndrome may lead to severe ischemia and irreversible tissue necrosis if intracompartmental hemorrhage of a torn muscle persists, and may require a surgical decompression. The clinical presentation, as well as adjunctive techniques in the diagnosis of a patient with a partial rupture of the gastrocnemius muscle, and a compartment syndrome, were presented.
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PMID:Rupture of the lateral head of the gastrocnemius muscle at the musculotendinous junction mimicking a compartment syndrome. 258 26

Type I dissecting aortic aneurysm is not only the most common type of all but an extremely lethal event. It is important to create the experimental model of type I dissection for clarifying behavior of this disease and successful treatment. The purpose of this study is: (1) production of experimental model of type I aortic dissection; (2) examination of progression manner of dissection; (3) and investigation of influence of dissection upon aortic valve and coronary artery. The experimental model of type I aortic dissection was produced in adult mongrel dogs. Bilateral thoracotomy was made and intimal tear was created in the ascending aorta by modified Blanton's procedure. Hypertension and creation of large pocket of the aortic media were necessary to produce type I aortic dissection. Extension of dissection had a tendency toward the inner layer of the aortic wall at distal site. However, at proximal site the dissection progressed in the same layer of the aortic wall. In this series, retrograde extension of dissection remained blind above annulus of aortic valve, and no incidence of aortic regurgitation or coronary ischemia was occurred. But on histologic examination, degeneration of the aortic wall by the dissection was observed. Such weakness of aortic wall showed potentiality to developed into subsequent aortic regurgitation or coronary ischemia.
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PMID:[Experimental study on the dissecting aortic aneurysm]. 260 44

A 22-year-old male developed a tic of neck-flexion at the age of 14. The tic occurred 40 to 50 times per minute on its peak at age 16. Since then he noticed the atrophy and weakness of his both upper limbs. His right leg became weak at age 22. On admission, neurological examination revealed tic of lip and neck, severe muscle atrophy and weakness of bilateral upper limbs, mild muscle weakness and spasticity of right lower limb and hyperreflexia in four limbs. Needle EMG studies revealed fibrillation, positive sharp wave and giant MUP in the biceps, triceps and first interossei muscles. There were no abnormal findings suggesting cervical spondylosis or disc herniation on neck roentgenogram and neck MRI in neutral position. Neck MRI in the ventro-flexed position showed a flattening of the lower cervical cord and a band-like isointensity lesion in the posterior epidural space at C4-6. This isointensity lesion was considered to represent a congestion of the internal vertebral venous plexus. These findings suggest that frequent neck flexion by itself causes the injury of the lower cervical cord through (1) over-stretching of the cord, (2) compression of the cord by dural sac, (3) arterior ischemia, and/or (4) stagnant hypoxia due to venous congestion. Flexion myelopathy may represent one of the most important mechanisms of cervical cord injury accompanied with involuntary movement of neck.
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PMID:[Flexion myelopathy due to tic of neck]. 275 44

We report 2 cases of cadaveric renal transplantation in which the grafts were placed in the right iliac fossa. Postoperatively, both patients complained of ipsilateral thigh weakness. Electromyography and nerve conduction studies indicated femoral nerve neuropathy. Muscle weakness gradually resolved. Difficulty was encountered in placing both grafts, and each kidney and limb were subjected to prolonged ischemia. We suggest that the femoral neuropathy was ischemic in origin.
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PMID:Femoral neuropathy after renal transplantation. 299 77

Forty-seven consecutive patients presenting acutely with repetitive symptoms indicative of anterior circulation ischemia ("crescendo" transient ischemic attacks) were evaluated to identify clinical features that might reliably predict the presence of significant stenosis, ulceration, or both in the presumably symptomatic internal carotid artery. Angiographic or intraoperative correlation was obtained in all patients, and 26 (55%) were found to have anatomically significant disease. Of 20 patients with signs or symptoms suggestive of cortical ischemia, amaurosis fugax, or both, 17 (85%) had "positive" angiograms; of 18 with numbness/weakness only, 9 (50%) had positive angiograms; of 9 whose symptoms suggested lacunar ischemia, none had positive angiograms.
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PMID:'Crescendo' transient ischemic attacks: clinical and angiographic correlations. 334 Feb 80

In 1980, 120 cases with late-life migrainous accompaniments resembling transient ischemic attacks were presented. In the present paper, 85 further cases examined in the past five years are analyzed. The findings support the concept advanced previously. In general, the cases are divided into the same categories: visual--21 cases, visual and paresthesias--6, visual and speech disturbance--2, visual, paresthesias and speech disturbance--3, visual, paresthesias, speech disturbance, and weakness--20, visual and brainstem symptoms--3, and cases without visual symptoms--32. The ages ranged from 40 to 73 years. Headache occurred in association with the episodes in only 40% of cases. There was a history of recurrent headache in 65%. The condition can justifiably be regarded as benign. Migrainous accompaniments account for some of the cases of transient ischemia with normal angiograms. Knowledge of the condition helps in the planning of rational management.
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PMID:Late-life migraine accompaniments--further experience. 353 32

Three patients presented with hand wasting and weakness secondary to mid-cervical spinal cord compression. This was due to cervical spondylosis in two patients and a meningioma in one case. This phenomenon is probably similar to that seen with foramen magnum lesions and may be due to spinal cord ischemia distal to the compression, secondary to venous stasis.
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PMID:Hand wasting due to mid-cervical spinal cord compression. 366 74

A 25-year-old white man presented with acute multiple sclerosis manifested by right blindness, difficulty urinating, and paresthesias and weakness of both legs. Retinal examination revealed a distal occlusion of the descending branch of the superior temporal arteriole leading to an area of retinal ischemia of the right eye. The optic disc was edematous, and there were focal areas of periphlebitis. All retinal signs resolved in three weeks, and the only abnormality that persisted was a pale right optic disc. The finding of small arteriolar disease is unusual and may represent another possible pathogenetic mechanism in multiple sclerosis.
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PMID:Retinal arteriolar occlusion in multiple sclerosis. 371 37


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