Alcohol-related peripheral neuropathy: a systematic review and meta-analysis.

The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case-control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7- 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy. The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor. There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine.

Peripheral systems: neuropathy.

Long-term, excessive consumption of alcoholic beverages produces a peripheral neuropathy with symptoms of decreased superficial sensation, hyperalgesia, and weakness. Alcoholic neuropathy is characterized by axonal degeneration with reduced density of both small and large fibers and axonal sprouting. Electrophysiologic studies reveal a marked reduction in the amplitude of sensory potentials and moderate slowing of nerve conduction, mainly in the lower extremities. Dietary deficiency of vitamins, which are often associated with chronic alcoholism, can contribute to the pathogenesis. Recent studies using animal models have identified several mechanisms by which ethanol impacts peripheral nerve function. Ethanol can exert direct neurotoxic effects on peripheral nerves via its metabolite acetaldehyde and by enhancing oxidative stress. Ethanol activation of protein kinase Cε signaling in primary afferent nociceptors plays an important role in lowering nociceptive threshold. Further, ethanol causes cytoskeletal dysfunction and inhibits both anterograde and retrograde axonal transport. Alcoholic neuropathy is potentially reversible and treatments include abstinence from alcoholic beverages and consumption of a nutritionally balanced diet supplemented with B vitamins. However, response to these treatment strategies can be variable, which underscores the need for novel therapeutic strategies. In this review, we provide an overview of the clinical findings and insights on molecular mechanisms from animal models.

[Peripheral neuropathies, from diagnosis to treatment, review of the literature and lessons from the local experience]. / Les neuropathies périphériques, du diagnostic au traitement, revue de la littérature et enseignements de l'expérience locale.

Peripheral neuropathy implies damages to neurons belonging to the peripheral nervous system which includes cranial nerves, spinal nerves' roots, spinal ganglia, nerve trunks and their divisions, and, the autonomic nervous system. Peripheral neuropathies are frequent in the general population (prevalence: 2,4%). We present a review of the recent literature and highlight diagnostic approaches for certain types of neuropathies particularly the most frequent ones or those requiring peculiar attention in first-line medicine. We also present epidemiologic data and data related to sural nerve biopsies from our centre. The determination of the location and the topography of the affected sites, integrated into the global context of the patient, is essential to provide an etiologic diagnosis. The median nerve compression within the carpal tunnel and polyneuropathies are the most frequent forms of peripheral neuropathies. More than one hundred causes of polyneuropathies are described and they are divided into acquired, genetically determined and idiopathic. We highlight a largely adopted diagnostic strategy concerning polyneuropathies and describe the Guillain-Barre syndrome, the alcohol-related polyneuropathy and the controversies about the benefit of the B vitamin therapy and its dangers. At the Hôpital Erasme, since 2008, more than 1372 patients with peripheral neuropathy were identified. Results of sural nerve biopsies performed in seventeen of them do not largely differ from those of other centres of expertise. We conclude that the diagnosis of peripheral neuropathy usually requires the expertise of a neurologist, but, first line caregivers must be able to recognize and refer patient when needed.

Illicit alcohol consumption and neuropathy--a preliminary study in Sri Lanka.

AIMS: To compare the effects on peripheral and autonomic nerve functions of Sri Lankan illicitly distilled alcohol consumption versus legal spirit consumption. METHODS: Peripheral nerve conduction and autonomic nerve functions were assessed in 40 healthy control subjects and two groups of chronic heavy drinkers: 41 illicit spirit drinkers and 17 legal spirit drinkers. RESULTS: Lower-limb motor and sensory nerve conduction parameters were affected in both groups of alcoholics. When compared with controls, in illicit spirit drinkers the mean heart rate indexes of all parasympathetic tests were lower while in legal spirit drinkers the heart rate response to standing was affected. There were no differences in the results of the above tests when the two groups of heavy drinkers were compared. CONCLUSIONS: Though chronic alcoholism results in peripheral and autonomic nerve damage, the damage caused by consumption of illicitly distilled spirit is not worse than the damage caused by consumption of legal spirits.

Multiple symmetric lipomatosis: Korean experience.

BACKGROUND: Multiple symmetric lipomatosis (MSL) is a rare disorder that is characterized by abnormal adipose tissue growth mainly at the neck, abdominal wall, back, shoulder girdle, and arms. A suggested mechanism for accumulation of adipose tissue is a defect in the lipolytic pathway of fat cell. OBJECTIVE: To evaluate the clinical, morphologic, and biochemical findings in Korean patients. METHOD: A total of 32 patients with MSL were evaluated retrospectively. Ten patients were seen at our hospital. The remaining 22 patients from literature were reviewed. Biochemical analyses and neurologic studies were performed. RESULTS: All cases were a sporadic form of MSL. The age of onset ranged from 26 to 70 years (mean of 49.4 years). The male-to-female ratio was 31:1. All but two patients were alcoholics with a daily intake of more than 80 g of alcohol for at least 10 years. In metabolic studies of 17 patients, a Fredrickson type IIb or IV hyperlipoproteinemia was found in three patients. High-density lipoprotein cholesterol values were higher in three patients. A glucose tolerance test was abnormal in five patients. A high prevalence of neurologic abnormalities was observed. Clinical signs of peripheral neuropathy were present in 11 of 13 patients. Central nervous system involvement was found clinically in 3 of 13 patients. CONCLUSION: The surgical removal of the fatty tissue and abstinence from alcohol are essential for relieving the patients from functional impairment. Not only metabolic studies of lipid abnormalities but also a complete neurologic examination were required in order to improve the quality of life in MSL patients.

Peripheral neuropathy in young-old and old-old patients.

Diabetes is said to account for most cases of neuropathy in the elderly. We reviewed records of 223 young-old (65-79 years) and 77 old-old (>or=80 years) patients referred for evaluation of neuropathic symptoms over a 9-year period. We prospectively validated our findings in 102 consecutive elderly (77 young-old) patients receiving intensive evaluation for neuropathy. Diabetes was the most common cause of neuropathy (41%), but was less common in the old-old (25% versus 46%, P < 0.001). Idiopathic neuropathies were more common in the old-old (39% versus 9%, P < 0.001). Alcoholic and nutritional neuropathies were uncommon in the old-old. Electrophysiological studies showed that most patients had an axonal type of neuropathy. Sural and peroneal response amplitudes were poorly correlated with age. We obtained similar results in our prospective study. The distribution of causes of neuropathies in young-old and old-old patients, in a hospital-based sample, is age-related. Future studies need to include the old-old to better understand the nature of neuropathy in the elderly.

[Alcohol polyneuropathy]. / Alkoholpolyneuropathie.

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.

Alcoholic polyneuropathy: a clinical and epidemiological study.

In the present study, we investigated the frequency of polyneuropathy in a sample of 296 alcoholics who were admitted to the 'S. Maugeri' Medical Centre for detoxification from October 1997 to November 1999. Results revealed a high frequency of polyneuropathy in the sample under study. The disorder was often clinically asymptomatic and demonstrable only on electroneurographic investigation. Significant correlations were found between polyneuropathy, the duration of alcoholism, the type of alcoholic beverage consumed (wine) and the presence of liver disease and macrocytosis.

Cuban neuromyelopathy epidemic

During the last semester of 1991 an unexpected increase in the number of cases of optic neuropathy was detected by the Cuban Epidemiological Surveillance System in the Pina del Rio province of Western Cuba. Reported cases occurred mainly in middle-aged men, usually tobacco farmers with a history of cigarette smoking and moderate alcohol consumption. Patients complained of weight loss, blurred vision, photophobia, and progressive decrease in visual acuity over a period of 1-4 weeks. Examination disclosed the presence of bilateral and usually symmetrical central or cecocentral visual field defects with the loss of red-green colour vision, pallor of temporal border of optic disc and loss of fibres in maculopapillary bundle. A diagnosis of tobacco-alcohol amblyopia or nutritional optic neuropathy was made at the time. By the end of July 1992, a total of 168 cases had been reported (monthly range, 14-36), all confirmed to this province. By December 1992, the number had increases to 472 cases, including reports from five of fourteen provinces of Cuba, mainly in Havana, Sancti Spiritus, Holguin and Santiago de Cuba (AU)