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Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Alcohol withdrawal syndrome occurs in a predictable manner in chronic alcoholics and is related to the degree of preceeding alcohol intake.247,604 The withdrawal symptoms are connected with irregular tremors, severe tremulousness, disordered perception, and frank visual and auditory hallucinations. In a small percentage of patients, generalized seizures occur and alcoholic polyneuropathy develops.316 Delirium tremens constitutes a major withdrawal syndrome. Patients display confusion and extreme agitation, restlessness, and excess motor activity. In fatal cases, hyperthermia or circulatory collapse may lead to death.584.
The Epidemiology and Public Health Burden of Addictive Disorders
Published in James MacKillop, George A. Kenna, Lorenzo Leggio, Lara A. Ray, Integrating Psychological and Pharmacological Treatments for Addictive Disorders, 2017
Kevin D. Shield, Sameer Imtiaz, Charlotte Probst, Jürgen Rehm
Over 230 three-digit ICD-10 code diseases (communicable as well as non-communicable) and injuries are causally linked to alcohol consumption [32, 33] (see Table 1.1 for an overview). Furthermore, for more than 30 of these conditions, alcohol consumption is a necessary cause (and the burdens caused by these diseases and injuries are wholly attributable to alcohol consumption), such as alcoholic cirrhosis of the liver, poisoning by alcohol, alcoholic polyneuropathy, and AUDs.
Neuropathic Pain †
Published in Gary W. Jay, Chronic Pain, 2007
Some other diagnoses related to SFN include: Chronic alcohol-dependent subjects, possibly via the direct toxic effect of alcohol on peripheral nerve fibers; painful alcoholic polyneuropathy effects the small myelinated and unmyelinated fibers more than large fibers, particularly early in the disease process. Hyperglycemia and impaired vitamin B (12) utilization may also be involved (100).Symptomatic HIV neuropathy, as a measure of small sensory fibers (decreased intraepidermal fiber density, abnormal cold, and heat pain thresholds) appears to be associated with transition to symptomatic HIV-associated distal sensory neuropathy up to 6 to 12 months later (101).Celiac disease, a T-cell mediated autoimmune disorder resulting from a lack of tolerance to gluten, is also associated with SFN as seen on skin biopsies. Idiopathic ataxia may also be seen (102,103).Sjogren syndrome patients with neuropathy exhibited either a decreased intraepidermal nerve fiber density or abnormal nerve morphology (104).Systemic lupus erythematosus, an inflammatory, autoimmune disease, is also found to be associated with a pure small-diameter nerve fiber neuropathy (105).Vasculitic neuropathy has infrequently been associated with skin denervation in spite of many manifestations of SFN, including reduced sensitivity to QST and neuropathic pain; epidermal nerve fiber densities were decreased, in addition to the more typical vasculitic effect on large diameter nerves (106,107).A case report of four patients with SFN responsive to steroid usage indicates that the patients had acute onset neuropathic pain, normal EMGs, and provocative/diagnostic QST and skin biopsies. The authors raised the question of this being a new entity (108).
Alcohol and melatonin
Published in Chronobiology International, 2021
In addition to these internal diseases, alcohol abuse leads to injury of the nervous system. This includes neurological and mental disorders, such as alcoholic polyneuropathy and typical alcoholic lesions of the central nervous system like seizures, typical variants of alcohol delirium, Wernicke’s encephalopathy, Korsakoff psychosis, or alcohol dementia (Tsuang et al., 2011). This was convincingly shown in the report of the Institute of Alcohol Studies (2007). It is additionally the cause of atypical alcohol delirium, alcoholic paranoia, acute and chronic alcohol hallucinosis, and alcohol delusions (Mukherjee 2013). Elucidation of the basic mechanisms of the course of these diseases has helped to identify and determine the main direct alcohol markers (Brien et al. 2011; Cabarcos et al. 2015; Philibert and Erwin 2015).
Alcohol addiction - the safety of available approved treatment options
Published in Expert Opinion on Drug Safety, 2018
Mariangela Antonelli, Anna Ferrulli, Luisa Sestito, Gabriele A. Vassallo, Claudia Tarli, Carolina Mosoni, Maria M. Rando, Antonio Mirijello, Antonio Gasbarrini, Giovanni Addolorato
Neurological adverse events account for 28% of all disulfiram side effects, making the nervous system the most affected apparatus by disulfiram toxicity [82]. Disulfiram neurotoxicity is mostly attributable to the accumulation of acetaldehyde and other toxic metabolites, such as carbon disulfide. This mechanism is mainly involved in the development of polyneuropathy which causes ataxia, paresthesias, and optic neuritis [83]. It seems to be dose-dependent and independent from gender and age [84]. In addition, other disulfiram neurotoxic side effects are attributable to the inhibition of dopamine-β-hydroxylase, an enzyme that catalyzes the conversion of dopamine to noradrenaline, affecting the level of brain biogenic amines [85]. Headache, delirium, convulsions, myoclonus, dysarthria, frontal release signs, anxiety, impaired memory, decreased concentration, depression, and psychosis could be related to this pathophysiological mechanism [86]. Moreover, the use of disulfiram in alcohol dependent patients may worsen preexisting conditions, such as alcoholic polyneuropathy and Wernicke encephalopathy [87].
Impaired thiol-disulphide homeostasis in patients with axonal polyneuropathy
Published in Neurological Research, 2018
Gonul Vural, Hesna Bektas, Sadiye Gumusyayla, Orhan Deniz, Murat Alışık, Ozcan Erel
All patients diagnosed with axonal polyneuropathy were evaluated by a neurology specialist, and the possible aetiological cause of polyneuropathy was determined in light of the anamnesis and performed examinations. The patients were classified in two groups according to the fact that they had diabetes or not. If the HbA1c levels of the patients, who have already been diagnosed with diabetes and who have been receiving oral antidiabetics or insulin treatment, were higher than normal and there were not any other comorbid diseases, it was considered that the primary reason for polyneuropathy was diabetes and these patients were included in the group of patients with diabetic axonal polyneuropathy. The others, who were diagnosed with axonal polyneuropathy but who were non-diabetic, were included in the group of patients with non-diabetic axonal polyneuropathy. This group consisted of the following: (i) the patients, who were followed up due to the diagnosis of chronic renal failure (CRF), who had sub-clinical neuropathy screening for haemodialysis indication and who were diagnosed with possible uremic polyneuropathy, (ii) the patients, who have frequently and continuously consumed too much alcohol for years, and who were referred since they demonstrated the clinical findings of polyneuropathy and who were consequently diagnosed with alcoholic polyneuropathy, (iii) the patients, who were examined due to the neuropathic complaints that started when they received chemotherapy for cancer and who were considered to have polyneuropathy associated with a chemotherapeutic agent. Fasting blood glucose and HbA1c were measured in order to exclude the possibility of non-diagnosed diabetes in these patients, who were included in the group of patients with non-diabetic axonal polyneuropathy, and the patients with newly diagnosed diabetes were not included. The patients, who were diagnosed with axonal polyneuropathy as a result of electrodiagnostic examination but who had multiple diseases that could cause polyneuropathy, or the patients for whom a priori etiological cause could not be presented, were similarly excluded from the study. The healthy individuals, who did not have diabetes or other chronic disease and who did not have any symptoms and signs that are associated with polyneuropathy, were included in the study as a control group.