Alcoholic Neuropathy Research Articles

S100b protein as a biological marker of nerve tissue damage in laboratory animals in preclinical studies

Background. For preclinical studies of drugs a relevant task is the selection of specific biochemical markers reflecting damage to the central nervous system, both in toxicological and pharmacological experiments. One of such markers may be protein S100b, the level of which will make it possible to assess the damage of the central nervous system of various genesis. Objective. The aim of the study was to assess changes in the level of S100b protein in the blood and in brain homogenates in brain tissue injuries of various genesis. Design and methods. The study was conducted on males of outbred rats and mice. A total of 62 animals were used: 47 rats and 15 mice. To determine the concentration of S100b protein, ELISA kits Rat S100b/S100 beta Elisa kit (Sandwich Elisa) were used) for rats and Mouse S100b/S100 beta Elisa kit (Sandwich Elisa) for mice. Statistical analysis was performed using licensed GraphPad Prism 9 software. Results: Changes of protein S100B was explored on models of alcohol neuropathy, bilateral and focal cerebral ischemia, traumatic brain injury. Forming of all pa[1]thologies led to increasing of protein S100B both in blood plasma and in brain tissues in case of traumatic brain injury. For alcohol neuropathy, focal and cerebral ischemia and traumatic brain injury changings of this marker level reached statistic meaning. Conclusion. Increased concentration of S100b is a sign of neuronal damage as a result of ischemic, traumatic and toxic factors, as well as in hypoclycemic conditions. Thus, protein S100b can be used in preclinical studies as a marker of brain damage, responding to damage of various genesis in studies of pharmacodynamics and pharmacological safety of drugs.

Late diagnosis of chronic inflammatory demyelinating polyneuropathy on the background of misdiagnosed alcoholic polyneuropathy: a clinical case

Chronic inflammatory demyelinating polyneuropathy is a rare immune-mediated polyneuropathy pathology of the peripheral nervous system. The presence of etiological factors in the patient, such as type 1 and 2 diabetes mellitus, alcohol intoxication in the anamnesis or other causes of polyneuropathy, which are often found in practice, can disguise chronic inflammatory demyelinating polyneuropathy and lead to delayed diagnosis of potentially curable polyneuropathy, which further increases the likelihood of disability of the patient and a significant decrease in the quality of his life. The clinical case under consideration is a demonstration of such diagnostic difficulties, which led to a delayed diagnosis of chronic inflammatory demyelinating polyneuropathy against the background of alcohol abuse in the debut of neurological disorders.

Structure, functions and metabolic features of the peripheral nervous system

Among diseases of the peripheral nervous system, polyneuropathies rank second in frequency of occurrence after vertebrogenic lesions, and among all polyneuropathies, diabetic and alcoholic polyneuropathies account for more than 50 % in prevalence. Knowledge of the structure, function, and metabolic features of the peripheral nervous system is relevant and will allow using pathogenetic approaches in the management of polyneuropathy patients, improving their standard of living and quality of life.

Modern view on the use of alpha lipoic acid in neurological practice

Modern view on the use of alpha lipoic acid in neurological practice

Effectiveness of gabapentin in treatment of pain in patients with alcoholic polyneuropathy

Alcoholic polyneuropathy is a pressing problem in modern society. This neurological disease is characterized by impaired functions of many peripheral nerves due to the toxic effects of alcohol and its metabolites on nerve fibers. A study was conducted to assess the effectiveness of the use of Gabapentin-SZ (North Star Co., Russia) in alcohol polyneuropathy, involving 47 adult patients (31 men and 16 women). The study found significant efficacy of Gabapentin-SZ in treating pain in patients with alcohol polyneuropathy. Significant improvement was noted after 14 days of therapy.

Exploring causal correlations between plasma proteins and peripheral neuropathy: a Mendelian randomization.

Peripheral neuropathy (PN) is a common neurological disorder, and circulating plasma proteins with causal genetic evidence are a major source of therapeutic targets. This study identifies several potential plasma proteins that are causally related to PN risk, providing new insights into protein-mediated pathogenesis of PN and potential targets for novel therapies. To identify potential therapeutic targets for PN, we employed two-sample Mendelian randomization (MR) to identify plasma proteins associated with six common PN. First, we screened for proteins related to PN using genome-wide association studies (GWAS), obtaining genetic data on plasma proteomes from 35,559 Icelanders. Summary data for six common PN, including Carpal Tunnel Syndrome (CTS), Trigeminal Neuralgia (TN), Alcoholic Neuropathy (AIP), Drug-induced Neuropathy (DIP), Diabetic Neuropathy (DP), and Guillain-Barré syndrome (GBS), were obtained from the FinnGen database. Two-sample MR and colocalization analyses were then conducted to further identify protein-PN pairs with presumed causal relationships. Enrichment analysis of positive proteins revealed potential biological processes and pathways. Based on drug-gene interaction analysis, we ultimately identified causal proteins associated with PN that could serve as potential drug targets for treating PN. Through MR analysis, we identified eight proteins (UBC12, SEM4C, IL23R, Prothrombin, CBS, Microglobulin, MATN4, COLEC12) with causal relationships to PN. We found that UBC12 is a protective factor for DP and CTS, while the remaining proteins are risk factors. Further colocalization analysis showed a posterior probability of hypothesis 4 (PPH4) less than 0.75, indicating no positive colocalization results were found. From the pathway enrichment analysis, we discovered that the proteins were mainly concentrated in pathways related to defense response to bacterium, receptor signaling pathway via STAT, cell killing, negative regulation of cytokine production, and leukocyte mediated immunity. Finally, in Drug-Gene Interaction database (DGIdb), we identified three protein-coding genes (IL23R, F2, CBS) as potential drug targets for PN. Mendelian randomization studies confirm the causal relationship between genetically predicted PN-related risk and genetically predicted plasma protein abundance. Plasma proteins, as biomarkers associated with PN, can provide potential drug targets for etiological intervention research in PN.

DEVELOPMENT OF PATHOLOGICAL CHANGES IN THE ORAL CAVITY ORGANS OF ANIMALS UNDER CONDITIONS OF POLYNEUROPATHIES OF DIFFERENT GENESIS

The aim of our research is to study the effect of polyneuropathy of different genesis on the development of pathological changes in the large salivary glands and periodontal tissues of animals. Methods. The study was conducted on 62 laboratory rats of both sexes. Toxic polyneuropathy was induced by paclitaxel injection, experimental type 1 diabetes mellitus was modeled by streptozocin injection, and alcoholic polyneuropathy was induced by chronic administration of increasing concentrations of ethanol. The development of polyneuropathy was confirmed by a change in the the pain sensitivity threshold (PST) using the Randall-Selitto tensoalgometric method. In the homogenate of oral cavity organs, total proteolytic and total antitryptic activity, catalase activity, content of TBARS, average mass molecules, oxidatively modified proteins, fucose and glycosaminoglycans (GAG), and amylase activity were determined. The level of total, protein-bound and non-protein sulfhydryl groups, activity of superoxide dismutase, glutathione peroxidase, glutathione transferase, glutathione reductase; content of reduced and oxidized glutathione, diene conjugates and Schiff bases were determined in blood serum. Results. We established the increasing of PST in animals that were simulated neuropathies of different genesis. All three types of polyneuropathies are accompanied by the development of carbonyl-oxidative stress in the soft tissues of the periodontium and large salivary glands of rats, which is evidenced by a probable increase in the content of oxidatively modified proteins and the content of TBARS, as well as average mass molecules compared to these indicators in intact animals . Under the conditions of modeling all three polyneuropathies, the protein-synthetic activity in the large salivary glands is suppressed, as evidenced by a decrease in the activity of α-amylase. Under conditions of experimental diabetic and toxic neuropathy in the salivary glands of animals, changes in the proteinase-inhibitor balance of the compensatory type are observed. We found that polyneuropathies of different genesis cause increased catabolism of biopolymers of the extracellular matrix of the periodontal connective tissue of rats, which confirms the increase in the content of GAG and fucose compared to these indicators in control animals. Conclusions. Under conditions of diabetic, toxic and alcoholic neuropathy, the amylolytic activity of the large salivary glands of animals is suppressed, the balance of the pro- and antioxidant system changes. When modeling peripheral polyneuropathy in animals by administration of paclitaxel, streptozocin, and ethanol, the development of periodontal syndrome is observed, the leading pathogenetic mechanisms of which are increased catabolism of connective tissue glycoconjugates and the development of oxidative stress and proteinase-inhibitor imbalance.

Anti-Hu antibody seropositive neuropathy with large and small fiber involvement mimicking alcoholic neuropathy: a case report

BackgroundAnti-Hu antibody neuropathy is considered a rare acquired peripheral neuropathy, but common among paraneoplastic syndromes. Typically, is described as subacute sensory neuronopathy and electrophysiological findings are usually suggestive of a sensory axonal neuropathy.Case presentationWe report the case of a 67-year-old man referred to our clinic with a 4-month history of progressive pain and paresthesias of distal lower limbs. He had a 30-year history of alcohol abuse and smoking. Alcoholic neuropathy was considered the most likely diagnosis, considering his history and evaluation. The patient’s neurological examination revealed symmetric bilateral superficial and deep sensory loss in the lower extremities, reduced Achilles tendon reflexes and wide based gait. Electrophysiological testing was suggestive of axonal sensory-motor polyneuropathy and small fiber involvement. Even though alcohol consumption was discontinued, symptoms gradually worsened. Further testing was performed and the patient was found seropositive for anti-Hu antibody. Small-cell lung cancer was detected later, but patient passed away before treatment for cancer was administrated.ConclusionsThe aim of our paper is to report a case of a rare paraneoplastic syndrome that can cause progressive sensory-motor neuropathy with large and small fiber involvement, which should be rapidly differentially diagnosed from other neuropathies, so that the underlying cause can be identified and, potentially, treated.

Peripheral neuropathy occurring during pregnancy (literature review)

Peripheral neuropathy is a general scientific term used to describe disorders of the peripheral nerves of any etiology. Along with postinfectious, diabetic, paraneoplastic, and alcoholic neuropathy, neuropathy of pregnancy represents one of the forms of this pathology. In this study, the authors conducted an analysis of domestic and foreign literature from open sources over the past 20 years. The study of available data revealed that the most common peripheral neuropathies observed during pregnancy are carpal tunnel syndrome, Bells palsy, and neuropathies affecting the lower extremities. Despite the paucity of information on peripheral neuropathy in pregnant women, its relevance is very high as it can significantly impair the quality of life during pregnancy and does not always disappear immediately after delivery, sometimes persisting for a certain period of time. The literature search was conducted in Scopus, Web of Science, PubMed, ScienceDirect, CyberLeninka, and RSCI databases using the following keywords: pregnancy; neuropathy; carpal tunnel syndrome; Bells palsy; review.

Female Binge Drinkers may be at Higher Risk of Acute Alcoholic Neuropathy (P13-4.007)

<h3>Objective:</h3> This study is a case series of female patients who presented with significant disability attributed to acute alcoholic neuropathy. It describes their clinical presentation, laboratory, electrodiagnostic findings, and pathology of muscle and nerve biopsies. <h3>Background:</h3> Recent studies have shown that binge drinking may lead to more harm to health than chronic average alcohol consumption. Prior research on alcoholic neuropathy has predominantly focused on chronic, slowly progressive alcoholic neuropathies. Females are at increased risk for alcoholic polyneuropathy. Sexually dimorphic rats respond differently in models of alcohol induced neuropathy. <h3>Design/Methods:</h3> This is a retrospective analysis of patients who presented with acute, axonal polyneuropathy in the context of binge drinking. Three patients were identified with a sensorimotor polyneuropathy that developed acutely (up to 4 weeks). Symptoms were neuropathic pain, paresthesias, muscle weakness, areflexia, disability and weight loss. Nutrient deficiency was not identified as an etiology. Extensive studies were performed ruling out other etiologies including inflammation and other toxins. Trials of immunomodulators were variable in objective improvement. <h3>Results:</h3> Extensive studies including serology, electrodiagnostic studies, nerve and muscle biopsy failed to identify an alternative etiology for acute polyneuropathy. Trials of treatment response were variable in objective improvement. Following extensive diagnostic studies, risk factors in these three patients include self-professed or family-ascertained history about binge drinking, nausea and vomiting prior to acute polyneuropathy. All patients were female and this was similar to other published case series of acute alcoholic/nutritional neuropathies. <h3>Conclusions:</h3> We hypothesize that female patients have a predilection to developing acute/subacute axonal neuropathy after binge drinking. This could be related to a direct nerve toxicity or sexually dimorphic features given that nutrient deficiencies were not identified. <b>Disclosure:</b> Dr. Cornejo has nothing to disclose. Dr. Nguyen has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for Argenx. Dr. Nguyen has received personal compensation in the range of $5,000-$9,999 for serving on a Speakers Bureau for ArgenX. Dr. Nguyen has received publishing royalties from a publication relating to health care.

Alcoholic Neuropathy and Its Impact among the Tea Garden Workers in the Golaghat District of Assam

Alcoholic Neuropathy and Its Impact among the Tea Garden Workers in the Golaghat District of Assam

Effect of Allium Sativum on the Alcohol Induced Neuropathic Pain in Wistar Rats

Neuropathic pain is a severe pain condition associated with pathological changes which have deleterious effects like dysfunction of the brain. Alcohol abuse is known to be the most common reason at present for developing neuropathic pain. Alcohol-induced neuropathic pain can be assessed by ache studies such as hyperalgesia and allodynia which characterizes the response severity of induced pain. In the current research, we used the Allium Sativum (Garlic) bulb extract to study the effect on alcohol-administered rodents. The behavioral and biochemical studies have been done. It has been reported in the study, that Allium sativum has certain protective mechanisms such as analgesic and anti-inflammatory effects, free radical scavenger, and antioxidant effects which contribute to alcohol-induced neuropathic pain. Based on the results of the current investigation, it can be concluded that Allium sativum bulb extract, administered at doses of 200 and 300 mg/kg in 0.9 per cent saline, is helpful in reducing the symptoms of alcoholic neuropathy. Allium sativum may offer a protective effect in the revocation of alcoholic-induced neuropathic pain.

Sex-specific differences in alcohol-induced pain sensitization

Pain sensitization is a phenomenon that occurs to protect tissues from damage and recent studies have shown how a variety of non-noxious stimuli included in our everyday lives can lead to pain sensitization. Consumption of large amounts of alcohol over a long period of time invokes alcohol use disorder (AUD), a complex pathological state that has many manifestations, including alcohol peripheral neuropathy (neuropathic pain). We asked if ‘non-pathological’ alcohol consumption can cause pain sensitization in the absence of other pathology? Studies have pointed to glia and other immune cells and their role in pain sensitization that results in cell and sex-specific responses. Using a low-dose and short-term ethanol exposure model, we investigated whether this exposure would sensitize mice to a subthreshold dose of an inflammatory mediator that normally does not induce pain. We observed female mice exhibited specific mechanical and higher thermal sensitivity than males. We also observed an increase in CD68+ macrophages in the ipsilateral dorsal root ganglia (DRG) and Iba1+ microglia in the ipsilateral spinal dorsal horn of animals that were exposed to ethanol and injected with subthreshold inflammatory prostaglandin E2. Our findings suggest that short-term ethanol exposure stimulates peripheral and central, immune and glial activation, respectively to induce pain sensitization. This work begins to reveal a possible mechanism behind the development of alcoholic peripheral neuropathy.

Increased incidence of alcohol use disorder and alcohol-related psychiatric disorders in patients with obstructive sleep apnea: A nationwide population-based cohort study

BackgroundObstructive sleep apnea (OSA) and alcohol-related diseases (ARDs), including alcohol use disorder, alcohol-related psychiatric disorders, alcoholic liver disease, alcoholic polyneuropathy alcoholic cardiomyopathy, and alcoholic gastritis, are both highly prevalent conditions. Alcohol consumption is associated with a higher risk of sleep apnea. However, whether OSA increases the risk of ARD has not, as yet, been studied comprehensively. Our study aimed to determine whether OSA increases the subsequent risk of ARD. MethodsThis study utilized the data from Taiwan's National Health Insurance Database between 2000 and 2015. We identified 7722 individuals newly diagnosed with OSA and randomly selected sex-, age-, and index date-matched (1:3) 22,166 controls without OSA, with a total of 29,888 subjects. We used the Fine and Gray's survival analysis to estimate the effects of OSA on ARD. ResultsThe OSA cohort had an adjusted hazard ratio of subsequent ARDs as 1.486 (95% Confidence Interval: 1.301–1.698), when comparing the cohort without OSA. The Kaplan-Meier analysis showed that the cumulative incidence of ARDs was significantly higher in the OSA cohort than in the controls in the first year of follow-up, till the end of the follow-up. A post-hoc analysis showed that OSA was associated with alcohol use disorder, alcohol-related psychiatric disorders, and alcoholic liver disease, but not alcoholic polyneuropathy, alcoholic cardiomyopathy, and alcoholic gastritis. The use of psychoactive medication, including the sedative-hypnotics, antidepressants or antipsychotics were associated with a lower risk of ARDs. ConclusionsOur study demonstrates that the OSA patients are at a higher risk of developing ARDs.

Rare presentation of Waldenström’s macroglobulinaemia requiring bilateral above-knee amputations: a case report

BackgroundWaldenström’s macroglobulinaemia is a rarely encountered B-lymphocytic malignancy. Waldenström’s macroglobulinaemia-associated paraproteinaemia is linked to an increase in serum viscosity, which results in a hypercoagulable state. Burning bilateral foot pain in a man with alcohol dependence and controlled atrial fibrillation presenting to the emergency department was attributed to peripheral neuropathy, given satisfactory angiographic evidence of bilateral foot arterial blood supply. Subsequently, his presentation as an emergency with acute bilateral critical lower limb ischemia that was managed by bilateral above-knee amputations, prompted a wider search for other etiologies. We present a hitherto unreported case of Waldenström’s macroglobulinaemia-related acute bilateral lower limb ischemia, which required bilateral above-knee amputations.Case presentationA 50-year-old Caucasian man, who was an alcohol dependent heavy smoker, presented with burning pain in his right foot that was deemed to be related to alcoholic neuropathy. A computerized tomographic angiogram demonstrated an occluded right distal anterior tibial artery but a patent posterior tibial artery supplying the foot arch, findings that were associated with noncritical ischemia. After multiple presentations within a week, he was admitted following sudden clinical deterioration with acute confusion, hyponatremia, and bilateral foot pain. Over the course of 24 hours, the patient deteriorated rapidly, with bilateral lower limb ischemia requiring bilateral above-knee amputations. Subsequent investigations revealed a diagnosis of Waldenström’s macroglobulinaemia.ConclusionsTo the best of our knowledge, this is the only reported case of Waldenström’s macroglobulinaemia-induced bilateral lower limb ischemia requiring major bilateral amputations.

S3013 Home Brew Gone Wrong: A Case Report on Potential Auto-Brewery Syndrome Sequelae

Introduction: Auto-Brewery Syndrome (ABS) is a condition not often seen in medical practice. It involves the conversion of carbohydrates to alcohol by the intestinal microbiome in a subset of patients. However, when these patients deny any consumption of alcohol, they are often brushed off or worked up for other etiologies, including stroke or hypoglycemia. There are also many possible medical sequelae that are not as widely reviewed due to the rarity of this disease. These include symptoms of chronic alcohol consumption such as increased alcohol cravings addiction, possible neuropathy, and liver disease such as fatty liver disease or cirrhosis. Case Description/Methods: In this case, we present a 26-year-old male with a history of auto-brewery syndrome presenting with bilateral lower extremity paralysis, sensation loss, and neuropathy. These symptoms were similar to an episode which was inconclusive. He consumed alcohol occasionally but was sober at that time. During that stay, he was diagnosed with auto-brewery syndrome. In ED, his blood alcohol was 493mg/dL, although he was sober for 1 year, and his liver function tests were significantly elevated with AST twice the level of ALT, consistent with findings of alcoholic liver injury. There was some return of neurological and hepatic function over the hospital stay with supportive care. He was placed on a consistent carbohydrate diet and his LFTs subsequently improved. Discussion: While there is data on potential causes and causative organisms for this condition, there is little in the literature on the potential sequelae associated with auto-brewery syndrome. Chronic alcoholism and its effects are widely seen and studied. From alcohol neuropathy to cirrhosis, the effects of consistent alcohol consumption are deleterious to one’s health. The question that needs to be asked is: are patients with chronic exposure to endogenous alcohol at risk for the same complications seen in chronic alcoholism? Cirrhosis, which is seen as a risk factor for ABS, may actually be a consequence of ABS. In this patient, his AST and ALT were mildly elevated, even during previous admission. Therefore, the patient may have been experiencing chronic liver injury from alcohol use while sober, placing him at increased risk for NASH and eventually cirrhosis at a much earlier onset than expected. It would be imperative in this case to ensure that the patient is on a limited intake of carbohydrates, or antifungals if necessary.

Alcoholic neuropathy associated with chronic alcohol intake

Alcoholic neuropathy (AN), a debilitating condition that mainly affects chronic alcohol drinkers, is thought to cause lesions in the peripheral nervous system leading to sensory, autonomic, and motor dysfunctions. Despite many studies, the pathogenesis of these lesions is still not completely understood. We investigated few aspects on the development of alcohol-induced peripheral neuropathy, by assessing sensory, motor and autonomic functions, as well as stereological analysis of axonal fibers and myelin sheath of the sciatic nerve. Twelve male Wistar rats were divided into Control group and Alcohol group that was submitted to Two Bottle-Choice Paradigm of intermittent and voluntary alcohol solution intake (20%; v/v) during eight weeks. At the end of treatment, three different sensorium-motor tests were applied - Tactile Sensitivity, Thermal Sensitivity, and Functional Observational Battery (FOB). Quantitative morphometric analysis of sciatic nerve structures was performed by stereological method. Alcohol concentration in the blood was measured to analyze possible correlation between availability of alcohol in the blood and the magnitude of the peripheral nerve lesion. Our data showed a peripheral effect of chronic alcohol intake associated with hyperalgesia and a process of demyelination with a strong correlation with alcohol consumption. This process was associated with increased tactile sensitivity, with behavioral reflexes such as locomotor hyperactivity, changes in gait and balance, and autonomic reflexes such as piloerection.

NEUROLOGICAL DISORDERS ASSOCIATED WITH CHRONIC ALCOHOLIC CONSUMPTION IN PATIENTS ADMITTED TO SVS HOSPITAL, MAHABUBNAGAR, TELANGANA STATE – A FIVE-YEAR STUDY WITH REVIEW OF LITERATURE.

Background: The neurological complications of alcoholism include both the peripheral and the central nervous system like the alcohol withdrawal syndrome which includes alcohol withdrawal seizures, delirium tremens, alcohol hallucinosis, alcoholic peripheral neuropathy, alcoholic myopathy, Wernicke encephalopathy, combination of Wernicke encephalopathy with Korsakoff's psychosis. AMaterials and methods: total of 134 consecutive patients without a prior diagnosis of neurologic disease presenting with seizures or other neurologic disorder, and a chronic use of various alcohol intake were studied and investigated. 74(53.33%) cases had withdrawal seizures, polyneuropathy inObservations: 18(13.43%) cases, Alcoholic compressive neuropathy and Korsakoff's psychosis noted in 12(8.96%) cases each, alcoholic myopathy in 10 and Wernicke's neuropathy was seen in 8(7.42%). The present study was compared with various earlier studies and tabulated.

Еxperimental justification of the efficacy of cocarnite for correction of disorders in rat periodont tissues under alcohol neuropathy

Еxperimental justification of the efficacy of cocarnite for correction of disorders in rat periodont tissues under alcohol neuropathy

A Young man with Delirium Tremens, Pellagra and Alcoholic neuropathy. Case report and review of pharmacological treatment

IntroductionWe present the case of a 36-year-old male with chronic alcoholism who suffered Delirium Tremens and other complications during hospital admission and who recovered thanks to treatment with benzodiazepines and antiepileptics using a cross tapering strategy.ObjectivesPresentation of a case and review of the available literature on the pharmacological treatment of alcohol withdrawal.MethodsA 36-year-old man was hospitalised for extensive dermatological lesions suggestive of Pellagra. He acknowledged a daily consumption of six litres of beer, was homeless and had a poor and unvaried diet. After 48 hours, the patient began to present hyperreflexia, disorientation and delusions of harm and was diagnosed with Delirium Tremens.ResultsThe case was managed jointly by Internal Medicine and Psychiatry. High doses of Chlorazepate (up to 400 mg daily), Tiapride (up to 600 mg daily) and Thiamine (300 mg daily) were prescribed. After 5 days of treatment, the patient started to improve but severe pain appeared in the lower limbs suggestive of alcoholic neuropathy. Gradually the treatment was replaced by Pregabalin (up to a dose of 1200 mg daily) which was effective in calming the late withdrawal and partially controlling the lower limb pain.ConclusionsBenzodiazepines remain the first-line agent for severe withdrawal, while some antiepileptic drugs have proven useful in mild-moderate withdrawal and relapse prevention. Switching to antiepileptic drugs during follow-up should be considered because of the lower risk of dependence and respiratory depression, as well as the positive effects on the “kindling” phenomenon.DisclosureNo significant relationships.