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)

Biopsies of the two heads of the sternocleidomastoid muscle were studied in 9 children with idiopathic torticollis, from 8 months to 17 years of age, who were undergoing surgical release of the sternal and clavicular attachments on the side of the contracture. Extensive fibrosis involved mainly the sternal head. Nonspecific myopathic changes, also mainly in the sternal head, included cytoarchitectural alterations of muscle fibers, necrosis, and focal inflammation. Histochemical type grouping and grouped atrophy were extensive in some cases and present in all except one, but the clavicular head was predominantly involved. Denervation and reinnervation are common chronic features in idiopathic torticollis, probably secondary to entrapment neuropathy: the accessory nerve reaches the clavicular head by passing through the sternal head. Separate arterial supplies predispose to ischemia in the sternal head, resulting in focal myopathy and fibrosis.
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PMID:Idiopathic torticollis: sternocleidomastoid myopathy and accessory neuropathy. 729 Jan 5

Thirty-eight patients with myokymic discharges localized to limb muscles on needle electromyography had various neurologic lesions, both acute and chronic. Of the 38 patients, 27 had had previous radiation therapy and the clinical diagnosis of radiation-induced plexopathy, myelopathy, or both. For the remaining 11 patients, the diagnoses included multiple sclerosis, inflammatory polyradiculoneuropathy, ischemic neuropathy, inflammatory myopathy, and chronic disorders of the spinal cord and peripheral nerves. The clinical presentations and results of local ischemia, peripheral nerve block, and percutaneous stimulation suggest that most limb myokymic discharges arise focally at the site of a chronic peripheral nerve lesion.
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PMID:Limb myokymia. 731 89

Three-hour oral glucose tolerance tests (GTTs) were performed for 58 men with secondary impotence (SI), 63 with normal sexual function (NL), and 69 with premature ejaculation (PRE). All were apparently nondiabetic. Diagnoses of diabetes and impaired glucose tolerance were based on serum glucose levels during GTT as recently defined by the National Diabetes Data Group. Covariance analysis corrected for weight and age differences. Mean glucose levels in patients with SI were significantly higher at one and two hours after glucose ingestion than in the other groups. Seven patients with SI (12.1%) were found to have diabetes. The three groups did not differ notably in frequency of impaired glucose tolerance. Inorganic serum phosphate levels were lower for the SI group. The high frequency of diabetes in subjects with SI who have no diabetic symptoms (12.1%) suggests that localized neuropathy or penile ischemia may produce impotence in otherwise asymptomatic patients.
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PMID:Previously unrecognized diabetes mellitus in sexually impotent men. 743 71

Angina pectoris and asymptomatic myocardial ischemia are part of the spectrum of coronary heart disease. Not the presence or absence of angina determines the future of the patient, but repeated ischemia and the progression of the coronaropathy. This progression is neither linear with time, nor is the moment of plaque rupture foreseeable. Silent myocardial infarctions increase with age and are very frequent in diabetics. In patients without neuropathy but with asymptomatic myocardial ischemia the central pain threshold is higher than in patients with angina pectoris. The best noninvasive test for the detection, localization and estimation of extension of myocardial ischemia, be it pain-free or symptomatic, is 201-thallium scintigraphy, combined with the exercise ECG. The fight against all amendable cardiovascular risk factors and pharmacotherapy are the first steps, if asymptomatic myocardial ischemia is suspected. Augmented dyspnea on effort and rhythm disturbances are indicators of advanced multivessel heart disease. Under these circumstances coronary angiography is indicated, and further treatment should follow the generally accepted rules such as for patients with angina pectoris.
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PMID:[Asymptomatic ischemia--an important part of the spectrum of coronary disease]. 748 31

We describe 2 patients in whom juvenile dermatomyositis (DM) was associated with well defined clinical polyneuropathies, and review the clinical and serological data. Light and electron microscopy were used to study muscle and nerve tissues from one patient. Neuropathy in our patients was associated with ulcerative skin lesions and elevated serum levels of factor VIII related antigen. Light microscopic studies of muscle revealed perifascicular atrophy and microinfarcts consistent with juvenile DM. Light microscopy of the affected sural nerve showed axonal degeneration. Electron microscopy of the same nerve demonstrated capillary endothelial inclusions characteristic of those observed as manifestations of early endothelial injury in juvenile DM muscle tissue. Polyneuropathy in patients with juvenile DM is a rare complication and is likely due to ischemia secondary to endothelial damage.
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PMID:Polyneuropathy in juvenile dermatomyositis. 897 68

We present a patient with a clinical picture of multiple mononeuropathy in which muscle and sural nerve biopsy revealed the existence of vasculitis compatible with panarteritis nodosa. Along with classical axonal lesion signs, we observed multifocal conduction blocks (CB) in all the nerves explored electrophysiologically. Topographic evolution was atypical in that distal BC disappeared earlier, whereas proximal BC appeared later and in all cases persisted longer. Ischemia may play a pathogenic role in BC along with other more well-known factors such as compression and immunological processes. BC detection would probably be less exceptional if, when ischemic neuropathy is suspected, patients were subjected to early and follow-up electrophysiological exploration that included proximal nerve segments.
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PMID:[Ischemic neuropathy with conduction blocks]. 757 30

Diabetic foot infections, a common source of morbidity and mortality, often have been related to vasculopathy and neuropathy in its etiopathogenesis, especially in the elderly person with diabetes. However, blood flow in the neuropathic diabetic foot has not been evaluated extensively, and there is evidence of abnormal blood flow patterns in the neuropathic diabetic foot unrelated to ischemia. The authors studied young persons with diabetes, with varying degrees of neuropathy, to assess the extent of vasculopathy in their lower limbs. Twelve young persons with insulin-dependent (Type I) diabetes (mean age, 36.1 +/- 1.975 years) and peripheral neuropathy, all of whom had previous surgery for diabetic foot infections, were identified. Confirmatory evidence of neuropathy was made using electromyographic studies and clinical tests that showed severe peripheral neuropathy. The results of vascular assessment of both lower limbs did not reveal any change in the pulse wave velocities from the popliteal to the digital vessels of the big toe as compared with correspondingly matched controls. There also was no significant stenosis in any of the vessels studied as far as the level of the dorsalis pedis and posterior tibial vessels. The normal triphasic pattern of arterial blood flow was lost. A monophasic pattern was present in all patients with prolonged diastolic flow at the level of the dorsalis pedis and posterior tibial arteries and distally. The pulsatility index was 3.14 +/- 0.81 as compared with 9.85 +/- 4.2. Mean toe pressures in the patient with diabetes was 64.17 +/- 20.87 mm Hg as compared with 98.23 +/- 10.12 mm Hg in controls. A linear correlation of decreasing toe pressures with increasing severity of neuropathy was seen (R = 0.7). The data suggest that changes exist in the blood flow patterns in young patients with diabetes and neuropathy, even in the absence of lower limb ischemia.
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PMID:Vascular assessment in the neuropathic diabetic foot. 758 48

Optic nerve dysfunction can be secondary to mass lesions, osseous compression states, inflammatory disorders, ischemia, increased cerebrospinal fluid pressure, and trauma. Representative clinical material from each of these areas is described, with an institutional review of 70 cases that were managed surgically. It is evident that compromise of optic nerve function can resolve with medical and surgical therapy. This clinical review is designed to highlight factors that favor this recovery. Although each condition has unique characteristics, an evaluation of clinical disorders that affect the nerve from globe to optic chiasm is presented as a comprehensive review of optic neuropathy. It is apparent from the literature that many questions need to be answered concerning the pathophysiology of optic nerve injury and the factors that influence recovery. A basic animal model for the analysis of these questions has been developed. An optic nerve injury produced in the cat leads to progressive loss of myelin but preservation of axons, the precise theoretic state that may be reversible with corticosteroid therapy or surgical management. Finally, the model may allow future study of the biochemical mediators of injury and the factors that promote recovery.
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PMID:Harris P. Mosher Award thesis. The recovery potential of the optic nerve. 760 88

Sensory and motor neuropathy result in foot deformities highly susceptible to unrecognized trauma resulting in ulceration. Early, aggressive surgical debridement, adjunctive antibiotics, dressings, rest of the injured area, correction of ischemia, and control of diabetes are essential to prevent amputation.
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PMID:Diabetic foot infections. Anatomy and surgery. 776 14

Optic neuropathy occurred in two patients suffering from Graves' disease with marked limitation of eye movement. Optic nerve changes were moderate. They consisted of parapapillary flame-shaped hemorrhages, swelling of the disc, and bundle defects in the visual field on the involved side. This clinical pattern suggested that the optic neuropathy was anterior and ischemic in nature. In one patient, symptoms of optic neuropathy were noted 3 days after starting stretching exercises with the ocular muscles, performed following a friend's advice in an attempt to prevent increase in restrictive myopathy. In patients with Graves' disease, it is conceivable that mild optic neuropathy occasionally occurs as a result of elevation in intraocular pressure, and stretching exercises of the ocular muscles might consequently favor such ischemic events. In the mechanisms of optic nerve involvement associated with Graves' disease, the role of ischemia should be considered in addition to the widely accepted role of optic nerve compression by enlarged extraocular muscles, at the level of the orbital apex.
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PMID:Anterior ischemic optic neuropathy in Graves' disease. 780 22


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