alcoholic neuropathy/neuralgia

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Tocotrienol ameliorates behavioral and biochemical alterations in the rat model of alcoholic neuropathy.

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Chronic alcohol consumption produces a painful peripheral neuropathy for which there is no reliable successful therapy, which is mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy is characterized by spontaneous burning pain, hyperalgesia (an exaggerated pain in response

Natural products evaluated in neuropathic pain models - a systematic review.

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Chronic pain conditions, such as neuropathic pain, are a common problem that poses a major challenge to health-care providers due to its complex natural history, unclear aetiology and poor response towards therapy. Despite the large number of drugs available, the adherence is limited by the large

Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status.

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BACKGROUND Although polyneuropathy related to chronic alcoholism has been reported frequently, its clinical features and pathogenesis remain to be clarified. OBJECTIVE To determine the clinicopathologic features and pathogenesis of alcoholic polyneuropathy associated with pain in patients with

Amelioration of functional, biochemical and molecular deficits by epigallocatechin gallate in experimental model of alcoholic neuropathy.

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Long term alcohol consumption leads to decreased nociceptive threshold characterized by spontaneous burning pain, hyperalgesia and allodynia. The mechanism involved in this pain includes increased oxidative-nitrosative stress, release of pro-inflammatory cytokines and neuronal apoptosis. The present

Alcoholic neuropathy: possible mechanisms and future treatment possibilities.

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Chronic alcohol consumption produces painful peripheral neuropathy for which there is no reliable successful therapy, mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy involves coasting caused by damage to nerves that results from long term excessive drinking of alcohol

Muscle pain in models of chemotherapy-induced and alcohol-induced peripheral neuropathy.

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OBJECTIVE While inflammatory pain is well described in skeletal muscle, neuropathic muscle pain remains to be clarified. We used 3 well-established rodent models of peripheral neuropathy to evaluate for muscle pain. METHODS In rats exposed to either of 2 neurotoxic cancer chemotherapies, paclitaxel

Evaluation of ameliorative effect of quercetin in experimental model of alcoholic neuropathy in rats.

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OBJECTIVE The objective of the present investigation was to study the neuroprotective effect of the quercetin in alcohol induced neuropathy in rats. METHODS Male Wistar rats were administered alcohol (10 gm/kg, 35% v/v, p.o. b.i.d.) for 10 weeks. Alpha tocopherol (vitamin E) was used as a standard

Schwann cells expressing nociceptive channel TRPA1 orchestrate ethanol-evoked neuropathic pain in mice.

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Excessive alcohol consumption is associated with spontaneous burning pain, hyperalgesia and allodynia. Although acetaldehyde has been implicated in the painful alcoholic neuropathy, the mechanism by which the ethanol metabolite causes pain symptoms is unknown. Acute ethanol ingestion caused delayed

Neurotoxic catecholamine metabolite in nociceptors contributes to painful peripheral neuropathy.

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The neurotoxic effects of catecholamine metabolites have been implicated in neurodegenerative diseases. As some sensory neurons express tyrosine hydroxylase and monoamine oxidase (MAO), we investigated the potential contribution of catecholamine metabolites to neuropathic pain in a model of

[Peripheral nerve disorders as common diseases].

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Peripheral neuropathy occurs as a component of several common and rare diseases. It is heterogeneous in cause, diverse in pathology, and varied in severity. The term peripheral neuropathy includes symmetric polyneuropathy, single and multiple mononeuropathy, and radiculopathy. The major disorders

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