Gender And Peripheral Neuropathy In Chronic Alcoholism: A Clinical‐Electroneurographic Study

Abstract

In some alcohol‐related pathologies of chronic alcoholism women are more vulnerable than men. A consecutive sample of 62 chronic alcoholics was studied, 18 females and 44 males, aged between 28 and 69 years to assess the incidence and distribution of peripheral neuropathy with regard to gender. All patients underwent clinical and neurological observations, laboratory tests, and electroneurography. Total lifetime dose of ethanol (TLDE) and other risk factors for neuropathy (disease duration, age, nutritional status) were calculated and correlated to sural nerve sensory‐evoked potential (SEP) amplitude. In 42 patients (67.7%), we observed the presence of clinical and/or infraclinical neuropathy, mostly axonal, in 29 males (65.9%) and 13 females (72.2%). In women, compared to men, TLDE and disease duration were significantly inversely correlated to sural nerve SEP amplitude, i.e in women, SEP amplitude is significantly reduced in relation to TLDE and disease duration increase. These data indicate a higher sensitivity of females towards the toxic effects of ethanol, other than malnutrition, on peripheral nerve fibres.

Pattern of Peripheral Neuropathy Among Patients With Alcohol Dependence Syndrome

“…This was similar to the findings of Ammendola et al [11] reporting an occurrence of 67.7%. However, in another study, they noticed that the frequency of alcoholic neuropathy was only 30.3%.…”

“…She developed moderate neuropathy despite comparatively fewer years of alcohol abuse and low LTDE as compared to males. This also correlates with the findings of Ammendola et al [11] where females demonstrated lower tolerance to toxic levels of alcohol.…”

Neurotoxic Consequences of Chronic Alcohol Withdrawal: Expression Profiling Reveals Importance of Gender Over Withdrawal Severity

“…For example, alcoholic women develop cirrhosis (Loft et al, 1987), alcoholinduced cardiomyopathy (Fernandez-Sola and NicolasArfelis, 2002) and peripheral neuropathy (Ammendola et al, 2000) after fewer years of heavy drinking than do alcoholic men. Although sex differences have been only infrequently addressed with respect to EtOH-induced brain damage, accumulating data indicate that brain damage may also be enhanced in females, with males showing relative neuroprotection (Hommer et al, 2001).…”

Central somatosensory conduction slowing in adults with isolated elevated plasma level of homocysteine

“…[18] Elevated plasma level of homocysteine may result from deficiency of vitamin B12 and/or folate, and genetic predispositions such as C677T polymorphism of MTHFR. [19,20] Additionally, it may also result from various pathophysiologic conditions including aging, [21,22] obesity, [23,24] diabetes mellitus, [25][26][27] renal function impairment, [27] medications and/or toxic substances such as levodopa, [7,28] anti-gastric acid agents, [29,30] anti-epileptics, [31,32] tobacco, [33] and alcohol. [34][35][36] Because of its excitatory property which may promote the vulnerability of neuronal cells to excitotoxic-and oxidative-stress-induced injury, Hcy, especially eHcy, can be neurotoxic.…”