Alcoholic neuropathy associated with chronic alcohol intake

Tessitore, Maria Eduarda; Pereira-Rufino, Laís da Silva; Panfilio, Carlos Eduardo; Sinigaglia, Rita de Cássia; Júnior, Odair Aguiar; Maluf, Luciana Le-Sueur; Conte, Rafael; Ladd, Fernando Vagner Lobo; Céspedes, Isabel Cristina

doi:10.1016/j.ibneur.2022.08.004

Cited by 4 publications

(2 citation statements)

References 62 publications

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“…To our knowledge, our study is the first to determine mechanical allodynia using von Frey filaments with the mouse CIE‐2BC paradigm in both sexes. Previous studies have mainly determined hyperalgesia in rats (Avegno et al, 2018; Dina et al, 2006; Edwards et al, 2020; Fu et al, 2021; Navarro et al, 2008; Pradhan et al, 2019; Roltsch Hellard et al, 2017; Tessitore et al, 2022). We found no sex differences between dependent male and female mice in the abstinence‐induced pain hypersensitivity.…”

Section: Discussionmentioning

confidence: 99%

Chronic alcohol induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol‐evoked neuropathic pain

Borgonetti

Roberts

Bajo

et al. 2023

British J Pharmacology

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Background and Purpose. Unrelieved chronic pain is considered a key factor contributing to the maintenance of alcohol use disorder (AUD). The mechanisms responsible for chronic pain associated with chronic alcohol consumption are still unknown. Thus, our goal was to evaluate the development of chronic pain in a mouse model of alcohol dependence and investigate the role of neuroinflammation in this chronic condition. Experimental Approach. We used the chronic-intermittent ethanol two-bottle choice CIE-2BC paradigm that generates three groups: (1) alcohol-dependent mice that exhibit escalating alcohol intake,(2) nondependent mice, mimicking moderate drinking, that experience voluntary drinking, and (3) alcohol-naïve control male and female mice. We measured mechanical allodynia using von Frey filaments during withdrawal and after the last voluntary drinking. Finally, we used immunoblotting to evaluate the protein levels of ionized calcium-binding adapter molecule-1 (IBA-1), macrophage-colony stimulating factor (CSF-1), interleukin 6 (IL-6), p38 and extracellular signal-regulated kinase 1/2 (ERK44/42) in spinal cord tissue of dependent and non-dependent animals. Key Results. We found significant escalation of drinking in the dependent group in male and female compared with the non-dependent group. The dependent group developed strong mechanical allodynia during 72 h of withdrawal, which was completely reversed immediately after the voluntary drinking. Moreover, we observed an increased pain hypersensitivity (allodynia) compared with the naïve group in 40% and 50% of non-dependent male and female mice, respectively. Increased IBA-1 and CSF-1 expression was observed in spinal cord tissue of both hypersensitivity-abstinence related and neuropathy-alcohol mice, and increased IL-6 expression and ERK44/42 activation in mice with hypersensitivity-related to abstinence, but not in mice with alcohol-evoked neuropathic pain. Conclusions and Implications. We showed that the CIE-2BC model induces two distinct pain conditions specific to the type of ethanol exposure: abstinence-related

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Section: Discussionmentioning

confidence: 99%

Chronic alcohol induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol‐evoked neuropathic pain

Borgonetti

Roberts

Bajo

et al. 2023

British J Pharmacology

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“…Клиническая картина включает потерю чувствительности в стопах и снижение (или отсутствие) рефлексов. Прогрессирование болезни продолжается несколько месяцев и проявляется нарушением походки, симметричной жгучей болью и онемением в ногах, к которому присоединяется слабость в мышцах ног [32].…”

Section: Note Alc -Amyotrophic Lateral Sclerosis; Dspk -Degenerative ...unclassified

Neurological disorders imitating spinal stenosis in elderly patients. Series of clinical observations

Seliverstova,

Kordonskiy,

Druzhinina

et al. 2023

Nejrohirurgiâ (Mosk.)

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Spinal stenosis is a pathological narrowing of the central spinal canal, lateral pocket, or intervertebral foramen due to age‑related changes, including pathology of the discs, facet joints, ligament hypertrophy, osteophyte formation and destruction of the arches. Clinically, the disease can manifest itself with pain, as well as numbness, or weakness in the arms or legs. The complexity of differential diagnosis is due to the lack of correlation between the degree of stenosis according to neuroimaging data and the severity of clinical manifestations. Spinal stenosis among 21 % of people may have an asymptomatic course.Spinal stenosis has to be differentiated from atherosclerosis of the vessels of the lower extremities, rheumatoid arthritis, piriformis syndrome, sacroiliitis, spondylitis/spondylodiscitis, amyotrophic lateral sclerosis, Guillain–Barré syndrome and other polyneuropathies. Isolated weakness should be of a particular concern in the clinical picture. Muscle hypotrophy, brisk tendon reflexes, the presence of pyramidal signs, muscle fasciculations, as well as patients’ complaints of simultaneous weakness in both the upper and lower extremities accompany them.We present and discuss three clinical cases of patients with a presumptive diagnosis of spinal stenosis. Two of them were held surgical treatment, which did not produce the expected result. Subsequently, it was found that the cause of progressive muscle weakness in the limbs was amyotrophic lateral sclerosis in two patients and the third one had Guillain–Barré syndrome, a form of acute demyelinating polyneuropathy.

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Chronic intermittent ethanol produces nociception through endocannabinoid-independent mechanisms in mice

Miliano,

Dong,

Profitt

et al. 2024

Preprint

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Alcohol use disorder (AUD) affects millions of people and represents a significant health and economic burden. Pain represents a frequently under-studied aspect of hyperkatifeia during alcohol withdrawal, yet to date no drugs have received FDA approval for the treatment of this indication in AUD patients. This study aims to evaluate the potential of targeting bioactive lipid signaling pathways as a therapeutic approach for treating alcohol withdrawal-related pain. We utilized a chronic intermittent ethanol (CIE) vapor exposure model in C57BL/6J mice to establish alcohol dependence, and demonstrated that CIE mice developed robust tactile allodynia and thermal hyperalgesia during withdrawal that was independent of prior blood alcohol levels. Next, we evaluated four drugs for their efficacy in reversing tactile allodynia during abstinence from CIE using a cross-over treatment design that included FDA-approved naltrexone as well as commercially available inhibitors targeting inflammatory lipid signaling enzymes including fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL), and 15-Lipoxygenase (LOX). None of these compounds produced significant therapeutic benefit in reversing established CIE-induced tactile allodynia, despite attenuating pain-like behaviors at these doses in other chronic pain models. These findings underscore the need for novel therapeutic approaches to mitigate pain in AUD patients.

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Alcoholic neuropathy associated with chronic alcohol intake

Cited by 4 publications

References 62 publications

Chronic alcohol induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol‐evoked neuropathic pain

Chronic alcohol induced mechanical allodynia by promoting neuroinflammation: A mouse model of alcohol‐evoked neuropathic pain

Neurological disorders imitating spinal stenosis in elderly patients. Series of clinical observations

Chronic intermittent ethanol produces nociception through endocannabinoid-independent mechanisms in mice

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