Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 11584682

[Alcohol polyneuropathy].

B Neundörfer
View original source ↗Export metadata ↓

Abstract

The Alcoholic Polyneuropathy occurs in about 10-30% of alcoholics. It is the second most frequent type of polyneuropathies after the diabetic form. The clinical pattern is a symmetric sensory or symmetric motor sensory manifestation type. In almost all cases there is a pressure pain of the calves. In the beginning the disturbance of the proprioceptive sensation is predominant. Disturbances of the autonomic nervous system deal with the sympathetic as well as the parasympathetic nervous system. Morphologically there is a primary axonal degeneration. A direct toxic influence of the alcohol itself is discussed as the prevailing pathomechanism.

Explore related subjects

Alcoholic NeuropathyAnimalsHumansEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B Neundörfer. 2001. [Alcohol polyneuropathy].. https://doi.org/10.1055/s-2001-16507

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Involvement of mGluR5 in the ethanol-induced neuropathic pain-like state in the rat.

Alcohol neuropathy has been thought to involve decreased nerve function following chronic ethanol consumption. However, there is no reliably successful therapy, largely due to a lack of understanding of the central underlying mechanisms. The aim of this study was to investigate the mechanisms that contribute to the neuropathic pain-like state induced by chronic ethanol treatment in rats. Rats were chronically treated with ethanol diet (1.25-5% of ethanol) for over 70 days. Mechanical hyperalgesia was observed during ethanol consumption and even after ethanol withdrawal. Under these conditions, an immunohistochemical study showed an increase in metabotropic glutamate receptor 5 (mGluR5) immunoreactivity in the superficial spinal dorsal horn of chronic ethanol-fed rats. Furthermore, immunoblot analysis revealed that the protein level of mGluR5 was clearly increased following chronic ethanol consumption. These findings support the idea that the increased levels of mGluR5 in the spinal cord may be, at least in part, involved in the induction of ethanol-dependent neuropathic pain-like state.

Alcoholic Neuropathy↗
PubMed2006

Treatment of alcoholic polyneuropathy with vitamin B complex: a randomised controlled trial.

AIMS: To evaluate the therapeutic efficacy and safety of BEFACT Forte 'new formulation' and BEFACT Forte 'old formulation' in the treatment of sensory symptoms of alcoholic polyneuropathy. METHODS: A multi-centre, randomised, double-blind, placebo-controlled study was conducted on 325 patients with sensory symptoms and signs of alcoholic polyneuropathy. Patients were randomised to the 'old formulation' (i.e. vitamins B1, B2, B6, and B12), 'new formulation' [i.e. identical to the 'old formulation' with additional folic acid (vitamin B9)], or placebo in a 1:1:1 ratio. One tablet of the study medication ('new formulation' or 'old formulation') or placebo was taken orally, three times a day, over a 12-week treatment period. RESULTS: Therapeutic efficacy was assessed in 253 patients by measuring vibration perception threshold (biothesiometry), intensity of pain, sensory function, co-ordination, and reflex responses. Patients treated with the 'new formulation' or 'old formulation' showed significant improvement in the primary efficacy endpoint (vibration perception threshold at the big toe) and secondary efficacy endpoints in comparison to placebo. The active treatment groups were comparable to placebo in terms of safety. CONCLUSIONS: A specific vitamin B complex (with and without folic acid) significantly improved symptoms of alcoholic polyneuropathy over a 12-week treatment period.

Alcoholic Neuropathy↗
PubMed2006

Multiple lipomas, alcoholism, and neuropathy: Madelung's disease or MERRF?

We report a 51-year-old alcoholic man with a 10-year history of cervical lipomas and progressive symmetrical sensory neuropathy, initially diagnosed with Madelung's disease, an idiopathic syndrome often attributed to chronic alcoholism. The eventual development of proximal weakness led to pathological and genetic testing which identified a A8344G mutation in the mitochondrial tRNA lysine gene, associated with MERRF (myoclonic epilepsy with ragged-red fibers). This case demonstrates how the varied terminology for this syndrome has resulted in a lack of consistent recognition and assessment for mitochondrial cytopathy.

Alcoholic Neuropathy↗