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)

The effects of management of single forearm arterial injuries without other associated major muscular, vascular, or neurological trauma were studied. Ninety-six patients with acute injuries to either radial or ulnar arteries without obvious associated major injuries were evaluated. No patient had an ischemic hand secondary to arterial injury. The selection of operative treatment by arterial repair or ligation was by surgeon choice (50 injuries were ligated, and 46 were repaired). Six months to six years postoperative follow-up was done. The overall patency rate for all repaired vessels was 52% (24 cases). The collateral arteries appeared to be a factor causing the low patency rate. The remaining intact artery demonstrated a consistent increase in flow velocity. No subject had hand claudication; there were 51 cases (53%) of hand weakness, 27 incidents (28%) of parasthesia, and 14 incidents (15%) of cold sensitivity independent of patency of the damaged forearm vessel. In the absence of acute hand ischemia, ligation of a lacerated radial or ulnar artery is safe and cost effective.
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PMID:Management of isolated radial or ulnar arteries at the forearm. 774 46

In patients with dermatomyositis (DM) the earliest lesion is microvasculopathy mediated by deposition of C5b-C9 membranolytic attack complex (MAC) on intramuscular capillaries. This leads sequentially to muscle ischemia, necrosis of muscle fibers, and muscle weakness. High-dose intravenous immunoglobulin (IVIG), which can modulate complement-dependent tissue damage in animal models, has been shown to be effective in the treatment of patients with DM. We used an in vitro C3 uptake assay to examine 55 coded sera from 13 patients with DM and 5 patients with other non-complement-mediated neuromuscular diseases, before and after treatment with IVIG or placebo. Patients with active DM had a significantly higher baseline C3 uptake compared with the others (geometric mean 12,190 vs 3,090 cpm). Post-IVIG but not post-placebo sera inhibited the C3 uptake, without depleting the complement components, by 70.6-93.4%. The maximum inhibition of C3 uptake occurred within hours after IVIG infusion, started to rebound 2 d later, and reached pretreatment levels after 30 d. The serum levels of SC5b-9 complex production were high at baseline but normalized after IVIG therapy. Repeat biopsies from muscles of improved patients showed disappearance of C3b NEO and MAC deposits from the endomysial capillaries and restoration of the capillary network. We conclude that IVIG exerts its beneficial clinical effect by intercepting the assembly and deposition of MAC on the endomysial capillaries through the formation of complexes between the infused immunoglobulins and C3b, thereby preventing the incorporation of activated C3 molecules into C5 convertase. These findings provide the first serological and in situ evidence that IVIG modulates complement attack in a human disease.
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PMID:High-dose intravenous immunoglobulin exerts its beneficial effect in patients with dermatomyositis by blocking endomysial deposition of activated complement fragments. 796 20

Two cases of acute myopathy following the administration of high doses of glucocorticoids in patients requiring mechanical ventilation and who were also administered neuromuscular blockers are presented. The patients were two women of 57 and 73 years of age. The doses of methylprednisolone administered were of 810 and 1,180 mg during the first 7 and 17 days, respectively. With regard to the total doses of neuromuscular blockers the first patient received 76 mg of pancuronium over 4 days while the second received 1,180 mg of atracurium over 17 days. This myopathy is characterized by a clinical and histological picture which differs from that associated to the chronic use of glucocorticoids being attributed to a toxic action of these drugs somewhat favored by immobilization due to the use of neuromuscular blockers. Given the lack of references in the literature on this entity in Spain a review was undertaken with the need for correct early diagnosis allowing differentiation from other causes of weakness such as ischemia of the cerebral trunk, polyradiculoneuritis and polyneuritis of critical patients being of note. Muscular biopsy is therefore very useful since very suggestive signs of this myopathy may be found. The disease is reversible with no effective treatment. An early rehabilitation program is the only method of shortening the convalescence period.
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PMID:[Acute myopathy related to the administration of glucocorticoids and neuromuscular blockers]. 750 Jun 91

Esotropia from chronic sixth nerve palsy or paresis usually requires surgery. Chemodenervation of the antagonist medial rectus muscle, while popular for the treatment of acute sixth nerve palsies and pareses, has not been used extensively for chronic cases. In this study, 22 patients with sixth nerve palsies or partially recovered palsies of greater than 5 months duration were treated with chemodenervation. The etiologies of the sixth nerve palsies were trauma (n = 7), tumor (n = 4), infection/inflammation (n = 3), nerve compression from aneurysm or increased intracranial pressure (n = 4), congenital (n = 1), ischemia (n = 2), and idiopathic (n = 1). The mean preinjection deviation was 41 prism diopters. A total of 38 injections were administered (mean, 1.7 per patient). Each patient received an injection of 2.5 to 7.5 units (mean, 4.1) of botulinum neurotoxin A to the ipsilateral medial rectus muscle. Treatment success was assessed 6 months after the last injection. A course of chemodenervation significantly improved the alignment of 9 of the 22 patients (41%). The mean postinjection deviation was 8 delta. Seven patients (32%) had single binocular vision in primary position restored. These patients had a mean horizontal binocular field of 70 degrees (range, 40 degrees to 100 degrees). Thirteen patients (59%) had only modest improvement and required surgery. The data suggest that injection of botulinum neurotoxin A is a useful treatment for some patients with chronic sixth nerve weakness. A course of chemodenervation therapy compares less favorably with transposition surgery with concomitant neurotoxin injection for the treatment of these difficult problems.
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PMID:The efficacy of botulinum neurotoxin A for the treatment of complete and partially recovered chronic sixth nerve palsy. 771 9

This study was undertaken to determine whether patients with silent ischemia (SI) (a positive thallium stress test without chest pain) have nonchest-pain symptoms that might serve as "anginal equivalents." Two hundred ninety-four individuals on completing a stress test were requested to score ten symptoms on a questionnaire (0 absent; 3 severe). Forty-three with a positive test had pains (chest, back, arm, and/or jaw) (no SI), whereas 93 with a positive test did not (SI). Patients with SI and patients without SI did not differ as to age, gender, or clinical features (including presence of diabetes or a history of myocardial infarction), but patients with SI were less likely to report a history of effort-related chest pains. Patients with SI exercised longer and had a higher peak heart rate. Patients were comparable with respect to myocardial ischemia (ST segment depression, double product, thallium lung uptake, and positive thallium scintigrams) and severity of coronary disease. Patients with SI complained less of weakness (p < 0.02) and tended to have lower overall symptom scores (4.2 +/- 0.3 vs 5.4 +/- 0.6), but breathlessness was comparable for both groups. On multivariate analysis, no nonanginal symptom was associated with SI. Only absence of a history of chest pain with activity and longer exercise time were related to SI. Patients with SI have similar clinical features as those with angina but tend to be less symptomatic with myocardial ischemia even for symptoms other than chest pain.
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PMID:Symptoms of patients with silent ischemia as detected by thallium stress testing. 816 17

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

Patients with acute vascular disorders of the CNS demonstrate an abundance of both rhythm and morphologic changes in their ECG. Of these a few will demonstrate myocardial dysfunction and or damage. The value of the ECG in evaluating and predicting which patients will have myocardial dysfunction or damage is questionable. One would assume the echocardiogram would be of more help than the ECG in identifying patients with myocardial damage; however, little data are available. The reason for the poor correlation between ECG findings and clinical correlates has not been explained to date, but it is possible to postulate a theory. There are two mechanisms that might mediate ECG changes in these patients, ie, autonomic neural stimulation from the hypothalamus or elevated circulating catecholamines. Hypothalamic stimulation may cause ECG changes without associated myocardial damage whereas elevated catecholamines may result in myocardial damage. This might explain why so many patients have ECG changes and very few have demonstrable myocardial damage in general, or ischemic damage in particular. That cardiac antiischemic therapy does not change mortality may relate to the fact that treatment has been directed towards patients with ECG changes, which in turn do not correlate with myocardial damage. Better patient selection for such therapy might rest upon demonstration of wall motion abnormalities on echocardiogram. The weakness of this strategy is that many patients with stroke have preexisting coronary disease and wall motion abnormalities and thus echo findings may only document remote infarction rather than acute ischemia.
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PMID:Electrocardiographic changes associated with acute cerebrovascular disease: a clinical review. 823 77

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

A 74-year-old man developed proximal muscular weakness and wasting of the left upper extremity without sensory disturbance or myelopathic symptoms. The muscle atrophy had not progressed for a few years. Radiological examination of the spine showed cervical disc herniation. These findings and electrophysiological studies excluded motor neuron diseases, permitting the diagnosis of dissociated motor loss syndrome. Interestingly, delayed computerized tomographic myelography disclosed cavities in the anterior horns of the spinal cord, which coincided with the clinical symptoms. Previous radiological and pathological examinations showed formation of such cavities within the spinal cord resulting from chronic compression, which was followed by ischemic change. In this context, the present case supports ischemia as a cause of dissociated motor loss syndrome.
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PMID:Dissociated motor loss syndrome with cavities in the anterior horns. 856 84

A 70-year-old man with prostatic cancer extending to the urinary bladder underwent transurethral resection of the bladder neck under spinal anesthesia and developed weakness of the proximal lower limbs a few hours after the procedure. The weakness persisted for several months. Because there were no local surgical complications (hematoma, infectious epiduritis, abscess) or bone metastases responsible for nerve root or spinal cord compression, a causal relation between the neurologic deficit and the spinal anesthesia was considered likely. Neurologic deficits are uncommon after spinal anesthesia and can be produced by complications of the surgical procedure (direct nerve injury, hematoma, abscess), arachnoiditis, neurotoxicity of disinfectants or of preservatives added to solutions of anesthetic drugs, or spinal cord ischemia. Precipitating factors for spinal cord ischemia include faulty patient position during the procedure, intraoperative arterial hypotension and injection of vasoconstricting agents.
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PMID:Proximal paraparesis following spinal anesthesia. 881 56


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