This phenomenon may be responsible for the induction of the neuropathic pain like behaviour following chronic ethanol consumption. Not only mGluRs but ionotropic glutamate (NMDA) receptors are also involved in alcoholic-induced neuropathic pain. The value of these approaches is that they could potentially detect neuropathologic effects of chronic alcohol abuse and/or thiamine deficiency and thereby aid in diagnosis and treatment management. For example, these approaches have been used to quantify volume reductions in gray and white matter, and detect microstructural disruption of white matter tracts [78, 87]. Moreover, these tools could be used to evaluate reversibility of structural lesions [49] and assess activity in the specific brain regions. For instance, fMRI has been used to demonstrate that alcohol relapse tendencies could be predicted by increased activity in the mesocorticolimbic system [19].
- In addition, a support group can help you cope with the life changes you’re experiencing as a result of your condition.
- Nonetheless, the pathogenesis of alcoholic myopathy is likely to be multifactorial because the histopathologic changes are only partly reversed by cessation of drinking [42], and disease is more prevalent in alcoholics who have cirrhosis [121].
- Doctors tailor specific treatments and alcohol abstinence programs to the individual.
Because ALN is a length-dependent axonopathy, it manifests mainly in a “stocking-glove” form, affecting the lower extremities at the beginning [28, 113]. The main symptoms of ALN include dysesthesia, paresthesia, numbness, and pain in the lower extremities which progressively reach higher parts of the body [114,115,116,117]. The pain is described as burning, cramp-like, or itching; also, a common symptom is a subjective feeling of cold in both feet [118,119,120,121,122,123]. The symptoms deteriorate through touch and pressure which intensify pain while standing or walking [124].
Peripheral neuropathy
Patients may have difficulty buttoning a shirt or blouse and with handwriting and holding objects. Patients may also have a deficiency in vitamin B12 (cobalamin), affecting the axon and causing muscle weakness, sensory disturbances, and anemia. Vitamin B9 (folic acid) levels tend to be decreased, reducing the density of small and large nerve fibers. Important in carbohydrate metabolism and neuron function, vitamin B3 (niacin) may also be decreased.
They have central effects on pain transmission and block the active re-uptake of norepinephrine and serotonin. TCAs have been shown to relieve various neuropathic pain conditions in many trials [115]. In agreement with this, one recent study has confirmed the efficacy of TCAs in central pain [116]. The serotonin/norepinephrine https://ecosoberhouse.com/article/alcohol-neuropathy-symptoms-and-treatment/ re-uptake inhibitors (SNRIs), duloxetine and venlafaxine, have a well-documented efficacy in painful polyneuropathy [117, 118]. SSRIs have been studied in a few trials which have demonstrated a weak analgesic effect but the clinical relevance of these compounds is questionable [119].
Cerebellar degeneration
Use of this website and any information contained herein is governed by the Healthgrades User Agreement. Nerve damage typically affects the axons, which are the projections that send electrical signals from one nerve to another, as well as the myelin, which is the fatty coating that protects the nerves. By Sarah Jividen, RN
Sarah Jividen, RN, BSN, https://ecosoberhouse.com/ is a freelance healthcare journalist and content marketing writer at Health Writing Solutions, LLC. She has over a decade of direct patient care experience working as a registered nurse specializing in neurotrauma, stroke, and the emergency room. It is important to share any history of alcohol use with your doctor to get an accurate diagnosis.