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Other Common Peripheral Neuropathies
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
Alcoholic neuropathy is common in western countries. These patients present with painful symmetrical and distal sensorimotor neuropathy with complete absence of reflexes. History of heavy alcohol drinking is the only way to relate the clinical presentation with pathological findings. The main histological feature is axonal degeneration with regeneration. There is no specific morphological sign associated with alcoholic neuropathy. In very rare cases, segmental demyelination coexists. The diagnosis of alcoholic neuropathy is very difficult through nerve biopsy. It may be expected when the alcoholic patient presents only with neuropathy, free from other abnormal systemic conditions.
Systemic Illnesses (Diabetes Mellitus, Sarcoidosis, Alcoholism, and Porphyrias)
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Alcohol can affect the central nervous system in several ways. Polyneuropathy is the most common manifestation, affecting 5%–15% of alcoholics.30 Ethanol can interfere with the absorption of both fat and water soluble vitamins, e.g., thiamine (B1), nicotinic acid (B3), pyridoxine (B6), folate (B9), and vitamin A.29 Polyneuropathy can be a result of nutritional deficiency (mainly thiamine deficiency) and/or direct toxic effect of ethanol and acetaldehyde.31 Studies that propose direct toxicity of alcohol on the peripheral nervous system show cytochrome P450E1, an isozyme of cytochrome P450, to induce oxidative stress causing neurotoxicity32 or a direct neurotoxic effect of ethanol or its metabolites.33 Alcoholic neuropathy is uniformly shown to be slow progression of distal and symmetric sensory and motor disease. In some cases, damage can lead to loss of ganglionic neurons and sympathetic and parasympathetic nerve fibers.40
Gastrointestinal Motility Disorders Induced by Ethanol
Published in Victor R. Preedy, Ronald R. Watson, Alcohol and the Gastrointestinal Tract, 2017
Ali Keshavarzian, Jeremy Z. Fields
Winship et al.23 were the first to report esophageal dysrnotility in chronic alcoholics. The abnormalities included nonperistaltic, low amplitude, distal esophageal contractions with normal LES pressure. This dysrnotility, however, was observed only in alcoholics with peripheral neuropathy. The observed abnormality could therefore be secondary to peripheral neuropathy rather than to alcoholism. Indeed, Fischer et al.34 reported similar findings in a group of patients with neuropathy, only some of whom had alcoholic neuropathy. It is important to note that Winship et al.23 studied alcoholics 3 to 6 weeks after cessation of drinking. None of these patients had esophageal symptoms in spite of abnormal esophageal motility. Hodes and Korsten24 reported a patient with dysphagia and persistent corkscrew esophagus who happened to be an actively drinking alcoholic. The manometric recording of the esophagus of this patient demonstrated high amplitude peristaltic contractions compatible with nutcracker esophagus.
Quality of life and pain perception in alcohol dependence: A comparative examination of patients, their relatives, and healthy controls
Published in Journal of Substance Use, 2019
Irem Ekmekci Ertek, Mustafa Ender Taner, Rabia Nazik Yüksel, Vahap Ozan Kotan, Erol Göka
No relationship between pain and addiction level (e.g. duration of addiction, the number of treatments) was found in our study. The analgesic effect of alcohol and pain sensitivity in alcohol withdrawal is well known (Gatch & Lal, 1999). Another pain-related situation due to alcohol is alcoholic neuropathy. There are studies indicating that all of these are the results of the neurotoxic effect of alcohol (De Witte, Pinto, Ansseau, & Verbanck, 2003). Instead of these situations, we aimed to investigate the general effect of alcohol dependence on pain and the genetic relationship through first-degree relatives. However, both addiction level and genetic factors did not seem to be related to pain perception. Jochum et al. in 2010 gave painful stimuli to patients in alcohol withdrawal, sober alcoholics, and controls. In the application of electrical stimulation, they found no difference in pain threshold or pain tolerance between the three groups, but with thermal stimulation, patients with alcohol withdrawal were found to be more sensitive to pain (Jochum, Boettger, Burkhardt, Juckel, & Bär, 2010). In the study of Ralevski et al. (2010), who tested pain with electrical stimuli in those with and without alcoholism in the family history, there was no difference in pain threshold and tolerance between the groups at the beginning, but there was a difference in the analgesic response to ethanol infusion. In our study, there was no specific response to pain in the relative group. Accordingly, it could be more meaningful to use thermal stimulation rather than electrical stimulation in assessing pain threshold or tolerance. Or the main distinguishing feature in pain applications may be the response to ethanol administration. There is a need for more extensive work in this regard with various painful stimulation methods and abstinence periods.
SFN-SIQ, SFNSL and skin biopsy of 55 cases with small fibre involvement
Published in International Journal of Neuroscience, 2018
Bo Sun, Yifan Li, Lizhi Liu, Zhaohui Chen, Li Ling, Fei Yang, Jiexiao Liu, Hong Liu, Xusheng Huang
A detailed medical history was obtained, including history of smoking and/or alcohol consumption, renal disorders, nutritional diseases, hyper/hypothyroidism, haematological disorders, malignancy, connective tissue diseases, hepatitis C and/or other hepatic disorders, paraneoplastic syndrome, history of past medication, history of neurotoxic agents and family history of neuropathy. Alcoholic neuropathy was diagnosed according to the Alcohol Use Disorders Identification Test manual [12].
Decreases in retinal nerve fiber layer thickness correlates with cumulative alcohol intake
Published in Journal of Addictive Diseases, 2020
Mehmet Hamdi Orum, Aysun Kalenderoglu
Chronic alcoholic neuropathy involves sensory more than motor nerve fibers, and the histological studies demonstrated axonal degeneration as the primary pathophysiological mechanism.25 Furthermore, the studies showed that small myelinated and unmyelinated fiber densities were more severely reduced than large myelinated fiber densities in the early stages of chronic alcoholic neuropathy.26 Evidence from postmortem human central nervous system tissue from individuals with an AUD indicated a loss in brain weight primarily due to the loss of white matter.2,3In vivo imaging in human individuals with an AUD further revealed perturbation in the microstructure of white matter in brain.27 The literature demonstrated that the nerve fiber layers have the equivalent of WM; the nuclear and the GCL have the equivalent of GM.28 The RNFL involves only non-myelinated axons of ganglion cells.29 In our study, significant differences were detected between the patient and control groups in terms of OCT values. However, when age effect and age plus APRI effects were excluded, only RNFL values were correlated with alcohol unit/year in the patient group. This finding about RNFL is valuable because in many other psychiatric disorders,5,6 GCL and IPL are affected before RNFL. Previous studies have found that RNFL damage can be detected by ophthalmologic examination only after 50% of the ganglion cells were damaged. Therefore, RNFL damage may also be observed in latter stages of the disorders.5 While this information is valid for other psychiatric disorders progressing with neurodegeneration, the situation seems different in alcohol exposure. The effects of alcohol on RNFL, the non-myelinated white matter tissue,29 suggest that it is more affected than other OCT parameters. This makes RNFL a possible biomarker candidate for chronic alcohol use-induced neuronal degeneration. In addition, when age effect is controlled, a possible significant correlation between alcohol unit/year and GCL and IPL may be indicative of further neuronal damage than RNFL. Regression analysis findings also support this interpretation.