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)

A rare case of criminal, chronic thallium poisoning is described. In spite of the general prohibition of the cosmetics, drugs and rodent exterminators containing thallium thallium intoxications are still observed occasionally. In the reported case typical symptoms as initial pain, dryness of the skin, constipation and insomnia were missing. The clinical picture was dominated by a polyneuropathy more pronounced in the lower extremities, a lesion of the optic nerve and the psychic symptoms of organic damage. A particular feature was the early loss of sensitivity of the anterior rami of the intercostal nerves.
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PMID:[Chronic thallium poisoning (author's transl)]. 46 65

Simple bedside measurements of blood pressure and systolic pressure response to the Valsalva maneuver will confirm a clinical impression of orthostatic hypotension. Careful questioning of the patient usually elicits other symptoms of autonomic nervous system dysfunction, such as impotence, urinary and fecal incontinence, constipation or diarrhea, blurred vision, or sweating changes. Drugs are the most common cause of autonomic dysfunction, and their benefits should be weighed against the severity of the dysfunction. In addition, diabetes mellitus, uremia, amyloidosis, acute intermittent porphyria, myeloma, tabes dorsalis, and alcohol-nutritional problems may produce symptoms of autonomic dysfunction. Thus, patients who present with autonomic features but no history of dysfunction-producing drugs should undergo complete laboratory evaluation. A regimen of tyramine or L-dopa or a diet rich in cheese, processed meats, and wine (a monoamine), coupled with a monoamine oxidase inhibitor have beneficial effects in patients with orthostatic hypotension due to preganglionic autonomic dysfunction. Patients who do not respond to catecholamine precursors have stable, isolated orthostatic hypotension or a polyneuropathy such as that caused by diabetes.
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PMID:Evaluating dysfunction of the autonomic nervous system. 63 67

In a man aged 28 years abdominal pains with constipation appeared, and were followed after 2 weeks by generalized maximal epileptic seizures, gradually progressing signs of proximal polyneuropathy, numerous brownish patches on the face and trunk, and hepatomegaly. In the urine raised levels were found of delta aminolaevulinic acid, prophobilinogen, coproporphyrins and uroporphyrins. Examination of stools demonstrated an increase of protoporphyrins and coproporphyrins, with prevalence of the former, characteristic of porphyria variegata. A gradual regression of changes was observed after treatment with high doses of propranolol and intravenous glucose infusions.
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PMID:[Porphyria variegata--a case report]. 356 76

A patient experienced an acute dysautonomia manifested by an inability to eat without vomiting, severe constipation, dry mouth, and orthostatic hypotension. One month later, a severe polyneuropathy supervened. The patient subsequently experienced an atonic bladder. Biopsy specimens obtained from the bowel wall disclosed an inflammatory infiltrate within the autonomic nerves consisting of lymphocytes and plasma cells. To our knowledge, this is the first time that inflammatory infiltrates have been demonstrated within the autonomic nerves in a patient with an acute dysautonomia, suggesting a relationship between this illness and the inflammatory polyneuropathies. The patient subsequently had a severe polyneuropathy, lending support to this conclusion.
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PMID:Acute dysautonomia and polyneuropathy. 608 19

We found degeneration of aminergic nerves in nine patients with type I familial amyloid polyneuropathy by histochemical study of rectal mucosa obtained by biopsy. There was prominent degeneration of aminergic nerves in four patients with uncontrollable alternating constipation and diarrhea, but aminergic nerves were relatively preserved in two patients with intermittent constipation or diarrhea. Sympathetic denervation of the gastrointestinal tract was probably important in causing bowel symptoms.
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PMID:Histochemical study of rectal aminergic nerves in type I familial amyloid polyneuropathy. 668 1

We found degeneration of enteric nerve plexuses in two patients with type I familial amyloid polyneuropathy. Amyloid deposition was more severe in the wall of the stomach than in the rectum. Hypomotility of the upper gastrointestinal tract, resulting from both amyloid deposition in the stomach and upper bowel and degeneration of the intrinsic autonomic nerves, may be responsible for anorexia, nausea, and vomiting. Diarrhea and constipation may be caused by degeneration of the enteric nerve plexuses. Gastric biopsy is valuable and safe in the diagnosis to type I familial amyloid polyneuropathy.
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PMID:Gastrointestinal amyloid deposition in familial amyloid polyneuropathy. 689 Jun 42

On principle one has to distinguish between inflammatory (infectious) and non-inflammatory intestinal diseases. These may affect merely certain parts of the gastrointestinal tract or influence the entire digestive system. Leading symptoms of all these diseases are disturbances of intestinal motility and of secretion, both causing diarrhoea or, rarely, constipation. The clinical picture can be acute or chronic. Acute manifestations, especially with high temperatures, include various florid psychopathological phenomena of an exogenous type of reaction. Chronic diseases of the gastrointestinal system do not show the above-mentioned picture. Very rarely encephalopathy causes organic psychosyndromes. Neurological findings point to lesions of the peripheral nerves (polyneuropathy), funicular defects within the spinal cord (funicular myelitis) and, very rarely, to encephalopathy. Syndromes of polyneuritis can be seen in acute, as well as in chronic enteropathies. Spinal lesions are only found in cases with chronic gastro-intestinal disease. With the exception of funicular myelosis in genuine pernicious anaemia (here parenteral substitution with vitamin B 12 is the therapy of choice) -- all gastroenterogenous neurological signs are only minimally accounted for by disturbances of B 1 and B 12 absorption. These substances should be used only in combination with other agents combating the basic disease.
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PMID:[Neuro-psychiatric aspects of gastrointestinal disease (author's transl)]. 725 12

We report three cases of histologically verified systemic amyloidosis with polyneuropathy. Common to them were early onset progressive peripheral sensorimotor disturbance starting in the legs and prominent autonomic dysfunctions such as postural hypotension, anhidrosis, and loss of pupillary light reflexes. Other characteristic features included vomiting, alternating diarrhea and constipation, opacities of the vitreous bodies, and congestive heart failure. All these clinical manifestations resemble type I familial amyloid polyneuropathy described by Andrade in 1952 from Portugal. Sural nerve biopsy stained with Congo red showed typical green birefringence under polarized light microscope. Histologically verified familial cases of this form of amyloid polyneuropathy have not been reported from Taiwan before.
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PMID:Type I familial amyloid polyneuropathy--report of a family in Taiwan. 822 Dec 94

A Portuguese female, aged 47 years, who had emigrated to Spain, was admitted to the hospital in 1991 for pontine haematoma. The patient, four siblings and her father were affected by a peripheral neuropathy, indicating autosomal dominant inheritance. The patient presented in the 2nd decade with sensory and motor neuropathy beginning in the lower extremities. Alternating constipation and diarrhoea, and urinary incontinence became uncontrollable. She had to be colostomised, and, eventually, confined to a wheelchair from the age of 43. Neurological examination showed bilateral facial involvement, and severe signs of sensory and motor peripheral neuropathy, and later right hemiplegia. There were abnormalities of atrial rhythm and left bundle branch block. Computerised axial tomography and magnetic resonance images demonstrated left-sided pontine haemorrhage. Nerve conduction studies revealed severe diminution of motor conduction velocity and absence or reduction of amplitude of sensory and motor action potentials. Inanition and a respiratory infection led to her death. Clinical diagnosis was type I familial amyloid polyneuropathy (FAP). Postmortem examination demonstrated amyloid deposits in peripheral nerves, including spinal roots and cranial nerves, leptomeninges, thyroid, breasts, heart, adrenal glands, kidneys, intestines, pancreas, and meningeal and some pontine vascular structures. Advanced pontine haematoma was verified. Cerebral haemorrhage usually occurs with cerebrovascular amyloidosis, but exceptionally with FAP. A minority of patients presenting with CNS haemorrhage showed arteriovenous malformation or embolism [Da Silva Horta and Dias Coelho (1960) Arch 'de Vecchi' Anal Patol Med Clin 31 = 163-172].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Type I familial amyloid polyneuropathy and pontine haemorrhage. 831 Aug 8

Diabetic neuropathy is the most frequent complication of diabetes and the leading cause of polyneuropathy in the Western world. A distal symmetric predominantly sensory polyneuropathy is the most common of the diverse neuropathies that occur secondary to diabetes. Pain is often the most bothersome and difficult to treat symptom of diabetic neuropathy. Autonomic neuropathy is a frequent feature of diabetic neuropathy and the source of many significant problems including postural hypotension, gastroparesis, diarrhea, constipation, neurogenic bladder, and male impotence. Physicians need to be familiar with the multiple, less common forms of diabetic neuropathy, as these often mimic other medical or neurologic conditions. The cause of diabetic neuropathy is not determined, but abundant evidence suggests that both metabolic and ischemic nerve injury are likely factors. These should not be considered mutually exclusive causes of diabetic neuropathy as both factors likely operate to different degrees to produce the clinical spectrum of neuropathies that are seen in diabetes. Although no effective treatment exists to cure diabetic neuropathy, improvement is possible with glycemic control and symptomatic therapy.
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PMID:Neuropathies associated with diabetes. 841 16


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