Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nervous control of gastrointestinal motility is extremely complex, is regulated by the enteric system, the "brain of the gut", and modulated by extrinsic nerves. This system with its multiplicity of transmitters and receptors does not always allow a clear interpretation of experimental data, especially with compounds lacking specificity. In this review the complex situation is described particularly in relation to receptor populations (cholinergic, adrenergic, dopamine, histamine, 5-hydroxytryptamine, opioid, gamma-aminobutyric acid (GABA), prostanoid and dihydropyridine receptors), therapeutic aspects of drugs and their usefulness in children. Newer principles with known drugs and promising new compounds with a more appropriate kinetic or fewer side-effects, deriving from distinct pharmacological groups, as candidates for the treatment of gastrointestinal disorders are considered e.g. anticholinergics (prifinium or actilonium bromide), adrenergic alpha 2-agonists (clonidine, lidamidine) for diarrhoea in diabetic neuropathy, adrenergic beta-blockers for shortening postoperative ileus (propranolol), dopamine receptor antagonists (metoclopramide, domperidone, alizapride) and another prokinetic substance (cisapride) which may be useful for a number of applications as gastro-oesophageal reflux, gastro-paresis, intestinal pseudo-obstruction, cystic fibrosis and constipation, morphine derivatives (e.g. loperamide) for intractable diarrhoea and calcium antagonists (e.g. nifedipine) for achalasia. Increasing experience in digestive tract pharmacology and reliable clinical studies will furthermore be the basis for a more specific and better tolerated therapy of gastrointestinal motility disorders in adults and children.
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PMID:Rational pharmacotherapy of gastrointestinal motility disorders. 266 4

Out of an unselected group of 160 patients with diabetic neuropathy 51 patients were followed up for an average of 5, 6 years by repeated neurological examinations and by means of a questionnaire. The control of the diabetes was requested from the house physicians. The patients were classified as presenting (1) a symmetrical, predominantly sensory neuropathy (2) a mixed syndrome with additional autonomic neuropathy and (3) multiple mononeuropathy. Individual symptoms and objective signs of neuropathy revealed a remarkable variety of changes. The outlook in multiple mononeuropathy and distal paresis was favorable while autonomic failures, in particular of male sexual function, progressed. There seemed to be some beneficial effect of improved glycemic control. However, despite satisfactory metabolic control some progression of diabetic neuropathy occured.
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PMID:The natural course of diabetic neuropathy. A follow-up. 692 85

In order to produce a model of ischemic neuropathy with neural microvascular alterations, sodium laurate was injected into a femoral artery and saline into the contralateral artery at the mid-thigh level in Sprague-Dawley rats aged 11 weeks. In view of the dose-related findings, 0.3 mg sodium laurate dissolved in 0.1 ml saline was used for the main experiment. The laurate-injected leg showed paresis during the experimental period. On day 1-7, various stages of Wallerian degeneration and acute microvascular changes were found. At 1 month, regenerating myelinated nerve fibers (MNFs) were found at the central or total fascicular area mainly in the distal tibial nerve. Morphometric analyses suggested that MNFs other than regenerating fibers are atrophic ones. The proliferative changes of nutrient microvascular walls were striking. The percent of closed epineurial microvessels was significantly larger on the laurate-injected sides and inversely associated with the diameter of MNFs. At 7 months, the attenuation of MNFs was more prominent and microvascular alterations were persistently observed. These pathological findings resemble those of chronic ischemic neuropathy including diabetic neuropathy, suggesting that this neuropathy model might provide some valuable and useful clues for clarifying the pathogenesis of chronic ischemic neuropathy.
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PMID:An animal model of chronic ischemic neuropathy with proliferative changes of nerve microvessel wall. 828 80

The most common form of diabetic neuropathy is the distal symmetrical sensorimotor variety. It is all the more likely to develop, the longer diabetes mellitus has been clinically manifest. Clinical signs of this neuropathy include the loss of the Achilles tendon reflex, sensory disorders beginning distally, distal muscle paresis and such signs of autonomic nerve involvement as erectile disorders, disordered bladder emptying, diaphoretic disorders or orthostatic hypotension. The diagnostic work-up should also include a number of laboratory investigations to exclude other causes of neuropathy. The basis of treatment is the earliest detection of diabetes mellitus and the establishment of normoglycemia. The individual manifestations are treated symptomatically. For the treatment of pain, it may become necessary to apply opioids if antidepressants and anticonvulsants fail to prove effective.
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PMID:[Diabetic Neuropathy. Diagnosis and Treatment in the Physician's Office]. 1537 4

Twenty-three diabetic patients -- 16 men and seven women (mean age: 50.7 +/- 17.4 years; mean duration of diabetes: 13.6 +/- 6.9 years) -- with diabetic mononeuropathy of the cranial nerves participated in the study. Four of them were with mononeuropathia multiplex and total ophthalmoplegia, affecting the oculomotor, trochlear and abducent nerves; 12 with paresis of the oculomotor nerve, one -- of the trochlear nerve and six -- of the abducent nerve. They were treated with alpha-lipoic acid (600 mg) for 10 days daily intravenously, thereafter one film tablet of 600 mg daily for 60 days. On the 10th day, we found significant improvement in the clinical signs of diabetic mononeuropathy - double vision, motility and position of the eyeball, ptosis of the upper eyelid and mydriasis. The mean period of oral treatment was 69.1 +/- 23.8 days, following the 10-day intravenous application of alpha-lipoic acid, and full recovery of the diabetic mononeuropathy was achieved with this therapeutic approach. Peripheral neuropathy was present in 17 patients (74%). On the 10th day, we established a decrease in total symptom score by an average of 2.7 +/- 1.4 points and by the end of the treatment period it was improved by 5.9 +/- 1.9 points (p = 0.04). On the 10th day, we found a decrease of 33% in foot pain and by the end of the second month, it fell by 65.5% (p < 0.0001). Vibration perception threshold was reduced in these patients at entry -- mean: 2.42 +/- 1.8 at the great toe, 2.89 +/- 1.8 at the first metatarsal and 3.65 +/- 1.7 at the medial malleolus. By the end of the second month, it reached mean 4.7 +/- 1.8 (p < 0.002) at the great toe, 4.92 +/- 2.1 (p = 0.004) at the first metatarsal and 5.3 +/- 1.4 (p < 0.01) at the medial malleolus. Cardiovascular autonomic neuropathy was present in two of the patients and there was improvement after treatment in the Ewing's tests -- Valsalva manoeuvre, deep-breathing test and lying-to-standing test. The results of our study demonstrate that alpha-lipoic acid appears to be an effective drug in the treatment for not only peripheral and autonomic diabetic neuropathy, but also diabetic mononeuropathy of the cranial nerves leading to full recovery of the patients.
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PMID:Treatment for diabetic mononeuropathy with alpha-lipoic acid. 1592 91

Oculomotor nerve palsy can be due to varied causes that include diabetic neuropathy, myasthenia gravis, brainstem infarction, demyelinating conditions, and cerebral aneurysms. Among the aneurysmal causes of oculomotor nerve palsy, aneurysm of the posterior communicating artery has been observed to be the most common. Pupillary dysfunction is considered to be an important feature of aneurysmal oculomotor nerve paresis. A case of a 7-year-old boy with partial oculomotor nerve palsy with pupillary sparing is being reported here, the etiology of which is tortuous and ectatic distal internal carotid artery. This is a rare cause of oculomotor nerve paresis and to the best of our knowledge has not yet been reported in children. Ischemia rather than compression seems to be the most plausible cause in this case.
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PMID:Partial oculomotor nerve palsy in a 7-year-old child. 2760 31