Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physiological and pharmacological studies of more than 150 patients with movement disorders are reported. Particular attention is paid to the differentiation of various types of tremor on the basis of rate, rhythm, and pattern of EMG activity in antagonistic muscles. The typical 'tremor-at-rest' of Parkinson's disease--3-7 Hz activity which alternates between antagonistic muscles--is suppressed, at least briefly, during voluntary activity, at which time typical 8--12 Hz 'physiological tremor' may be seen. Essential tremor and its familial or senile variants also have a characteristic EMG pattern during voluntary activity--5-8 Hz bursts of activity which are synchronous in antagonistic muscles. This type of tremor may also be present in patients with Parkinson's disease and in certain kinships with a Charcot-Marie-Tooth polyneuropathy. Other tremors in association with polyneuropathy ('neuropathic tremor') have different physiological characteristics. Myoclonus is of essentially two types ('positive' with EMG bursts and 'negative' with brief pauses in ongoing activity, as with asterixis) and may, at times, mimic tremor. Certain specific tremors respond predictably to specific pharmacological therapy.
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PMID:Physiological and pharmacological aids in the differential diagnosis of tremor. 0 92

Electromicroscopial changes were observed in arterioles, nerves, and striated skeleton muscle cells in a case of clinically and histologically definite polyarteritis nodosa with polyneuropathy. Inflammatory infiltrates were found in and around arteriolar walls; motor nerves were partly demarkated and presynaptic motor endplates were degenerated. The myofibrills of skeleton muscle cells showed a disorganization that is regarded as the morphological substrate for the clinically observed muscular weakness in this case.
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PMID:[Electron microscopic findings in a polyneuropathy complicating panarteritis nodosa]. 0 99

In a 50-year-old woman, working as a dental assistant for more than ten years, chronic mercury poisoning developed insidiously, apparently from careless handling of mercury-amalgam. The main signs consisted of mental and neurological changes such as erethism, tremor and mercurial psellism. Peripheral arterial circulatory disorders occurred in the course of the disease, as well as abdominal colic and a polyneuropathy, which provided the first clues to panarteritis nodosa subsequently confirmed histologically.
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PMID:[An unusual case of panarteritis nodosa associated with chronic mercury poisoning (author's transl)]. 1 86

The authors describe a case of flaccid tetraplegia due to a polyneuropathy in a man aged 50 years, progressing rapidly to death from mesenteric infarction. As significant abnormalities, the hematologic examinations revealed a very high erythrocyte sedimentation rate, a marked leukocytosis and a positive Australia antigen in repeated controls. In spite of the clinical picture being that of a symmetrical polyneuropathy rather than that of mononeuritis multiplex, the diagnose of a collagenosis was suspected. Nevertheless steroid treatment was not given because the patient had a peptic ulcer. On histological investigation many focal infarctions were found in several internal organs but the brain was pratically normal. Instead the nerve trunks examined (the sciatic nerve and the lumbo-sacral plexus) showed gross changes in the vasa nervorum represented by abundant perivascular cuffing and marked evidence of axonal degeneration secondary to an ischaemic damage. In the kidneys there were definite signs of membranous glomerulitis. The pathological findings in this fatal case of diffuse peripheral involvement were not those of classical periarteritis nodosa, but showed the picture of so-called "allergic vasculitis". This type of blood vessels inflammation is now assumed to be part of an immune-complex disease, in which the Australia antigen could be one of the causative agents.
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PMID:[Polyneuropathy due to "allergic vasculitis" possibly related to australia antigen. (author's transl)]. 1 14

The clinical consequences (therapeutic and toxic) of drug acetylation polymorphism are reviewed for procainamide, hydralazine, phenelzine, isoniazid, and salicylazosulfapyridine. Genetic slow acetylators are more likely than rapid acetylators to experience the following adverse drug reactions: (1) earlier development of procainamide-induced antinuclear antibody; (2) earlier and more frequent development of procainamide-induced systemic lupus erythematosus (SLE); (3) hydralazine-induced SLE; (4) spontaneous SLE; (5) drowsiness and nausea from phenelzine; (6) cyanosis, hemolysis, and transient reticulocytosis from salicylazosulfapyridine; and (7) polyneuropathy after isoniazid therapy. The incidence of isoniazid hepatitis may, however, be more common in rapid than than in slow acetylators. Genetic slow acetylators are also more likely than rapid acetylators to experience greater therapeutic responses from similar doses of the following: phenelzine, hydralazine provided beta blockers are concurrently used, and isoniazid if once weekly therapy is used. Thus, knowledge of the acetylator phenotype of a patient can help determine the relative risk for some drug-related toxic and therapeutic responses.
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PMID:Clinical consequences of polymorphic acetylation of basic drugs. 1 87

A case of panarteritis nodosa with positive Australia antigen is presented. Panarteritis appeared following serum hepatitis and caused arthromyalgia, abdominal pain, prolonged fever of unknown origin, peripheral polyneuropathy, blood hypertension, and renal insufficiency. A muscular biopsy showed atrophy due to denervation and necrotizing arteritis in various stages causing serious damage to the arteries. Abdominal arteriography clearly demonstrated the existence of aneurismal dilations in the liver, pancreas, and kidneys. The angiographic findings in panarteritis nodose are discussed with special reference to the aneurysms localized in several organs. Their situation is described in detail; it is usually abdominal and more specifically intrarenal. The fact that they occur in a high percentage of cases is helpful when establishing the diagnosis. Lastly, the role of Australia antigen in the development of panarteritis nodose is discussed. It stimulates an immune response and the production of circulating immunocomplexes which are depostied on the vascular walls with complement fixation and damage to the blood vessels. The possibility that other viral agents may be present in the various types of necrotizing vasculitis in humans is commented on.
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PMID:[Panarteritis nodosa with positive Australia antigen (author's transl)]. 3 58

A series of 20 cases of polyarteritis nodosa (PAN) is presented. Clinical features of 2 cases are described in more detail to illustrate the most common neurological complications. PAN is an uncommon disease but one which usually presents with some form of neurological disturbance, often a mononeuritis multiplex or a symmetrical polyneuropathy. Diagnosis requires a high degree of clinical suspicion as serological tests are at best non-specific, and absolute biopsy proof often requires examination of multiple sites. Early diagnosis is important, as treatment with corticosteriods usually induces symptomatic relief and provides a better chance of long term survival. If an acute remission is obtained the patient not only should have a good quality of life but in a proportion of cases, where the remission is prolonged, steroid therapy may be ceased.
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PMID:Neurological features of polyarteritis nodosa. 4 Feb 17

A 33-year-old man with Refsum disease exhibited clinical features of night blindness, dysequilibrium, hearing loss, itchy dry skin, symmetrical polyneuropathy, distal muscle weakness, pes cavus, and hammer toe. His total serum protein was increased, nerve conduction velocities were slow, and serum phytanic acid levels were high. Dietary restriction of phytol resulted in a decrease in serum phytanic acid without any visual and autitory changes; however, coordination, skin lesions, and nerve conduction velocities definitely improved.
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PMID:Heredopathia atactica polyneuritiformis (phytanic acid storage disease). A new case with special reference to dietary treatment. 4 80

2 patients, who were treated with clioquinol after radical resection of carcinoma of the rectum and colostomy, developed symmetrical sensorimotor polyneuropathy, mild posterior tract ataxia, bilateral pyramidal tract lesions and optic neuropathy, a clinical picture compatible with subacute myelo-optic-neuropathy (S.M.O.N.). One patient had neurological symptoms after having received 750 g of clioquinol, 3 years after treatment started, and impairment of vision was noted after having received 1200 g. The other patient had neurological symptoms 6 weeks after clioquinol was first given, having received 65 g, the average daily dose being 1.5 g, and vision was impaired after 765 g had been administered. On examination 12 and 14 months after clioquinol had been discontinued, the first patient's vision was slightly improved, but he was otherwise unchanged, while the vision of the other patient was unchanged, but she had otherwise deteriorated slightly neurologically. Electrophysiological examinations confirmed the clinical observations. A multifactor etiology of the syndrome: neurotoxicity of clioquinol, paraneoplastic neuropathy and malabsorption, is discussed.
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PMID:[Subacute myelo-optic-neuropathy (S.M.O.N.) following treatment with clioquinol (author's transl)]. 5 Oct 51

A man, age 50, fell ill with polyneuropathy followed by parkinsonism and organic psychosis and died in a shock 6 weeks later. Serologic examination suggested bacillary dysentery, but the patient had no diarrhoea. The neuropathological examination did not reveal any organic substrat of parkinsonism. Peripheral nerves showed mucoid degeneration, segmental demyelination and lymphocytic infiltration of peri- and endoneurium. Many Renaut bodies were found which seemed to arise from mucoid masses organized by cells of the endoneurium. Polyneuropathy and parkinsonism are well known neurological complications of bacillary dysentery and favour this diagnosis in accord with the serological findings.
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PMID:[Bacillary dysentery with involvement of the central and peripheral nervous system (author's transl)]. 5 Oct 59


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