Medical News Today publishes that medical procedures and therapies, medications, and adjunctive and alternative therapies are commonly used to treat alcoholic polyneuropathy. To diagnose alcoholic neuropathy, medical professionals will generally perform a few tests or exams to determine the severity of the disorder and what can be done to treat and manage the symptoms. Many different stimuli, including growth factors, cytokines, viral infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. There are many studies suggesting the role of MEK/ERK signaling in inflammatory pain in male [60–63] and female rats [64]. It is important to stop drinking if you suffer from alcoholic polyneuropathy in order to stop the disease from getting worse and to correct the nutritional imbalance that is damaging the nerves and interfering with the nervous system. A medical detox program followed by a comprehensive alcohol rehab program can manage alcoholism and help a person to get sober and stay that way.
Medical Care
It was proposed that ALN pathogenesis, besides thiamine deficiency itself, could be due to its inappropriate use in the organism or transketolase deficiency [150]. Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153]. ALN is characterized by spontaneous burning pain, hyperalgesia, and allodynia. Besides, the key mechanism of chronic pain includes the alcohol neuropathy stages long-term potentiation of glutamatergic transmission. The percentage of alcohol-dependent patients affected by ALN is estimated to be 66% [50, 51]. The pathophysiology of ALN involves underlying mechanisms that include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters [52,53,54].
- You may then be referred to a doctor trained in nervous system disorders, also called a neurologist.
- These can be achieved by alcohol abstinence, a nutritionally balanced diet supplemented by all B vitamins, and rehabilitation.
- However, the pathophysiology of alcohol-induced PN is different than other forms of PN.
- Verywell acknowledges that a private nurse or caretaker may not be feasible for everyone and that readers do not have uniform access to safe, affordable, high-quality health care.
How does this condition affect my body?
- However, alternative therapies do not have side effect and tackle nutritional deficiencies and oxidative stress.
- Making the correct diagnosis can be difficult due to the varied clinical presentation and the many possible causes.
- Alcoholic neuropathy is caused by nutritional deficiency, as well as toxins that build up in the body.
- When alcohol is responsible for damage to the peripheral nerves, a person has alcoholic neuropathy.
A nutritious diet; vitamin supplements, especially vitamins B1 and B12; and reduction of or abstinence from alcohol use is the only way to improve the patient’s PN by allowing nerves to slowly regenerate. Antiepileptic drugs, such as the gamma aminobutyric acid (GABA) analogue (gabapentin), have proven helpful in some cases of neuropathic pain. These drugs have central and peripheral anticholinergic effects, as well as sedative effects, and they block the active re-uptake of norepinephrine and serotonin. Recently, extended release gabapentin relieved symptoms of painful polyneuropathy [120]. Valproate demonstrated varying effects in different studies of neuropathic pain, with three studies from one group reporting high efficacy [125–127] and others failing to find an effect [128, 129]. Tricyclic antidepressants (TCAs) are often the first line drugs to alleviate neuropathic pain symptoms.
What Are the Causes of This Type of Nerve Damage?
Additionally, chronic heavy alcohol consumption is toxic to the metabotropic glutamate receptor 5, which activates neuronal protein kinase C and causes neuropathic pain. In one clinical study, aimed at studying distinct clinicopathologic features of alcoholic neuropathy, 64 patients were assessed. In 47 of these patients sural nerve biopsy was performed, with discrimination in terms of their thiamine status [3]. The ethanol consumption of these patients was more than 100 g day–1 for more than 10 years. The subgroup without thiamine deficiency consisted of 36 patients, while the subgroup with thiamine deficiency consisted of 28 patients.
How is peripheral neuropathy diagnosed?
A mechanism of cisplatin chemotherapy-induced peripheral neuropathy was elucidated in an in vitro mouse model. Apoptosis of neurones was induced by cisplatin, but pre-incubation with N-acetylcysteine completely blocked apoptosis [112]. Nine studies reported EMG findings in alcohol-related peripheral neuropathy patients. Reduced recruitment pattern of motor units was a frequently reported outcome [16, 28, 67, 70].
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