Alcoholic Myopathy: Causes, Symptoms & Treatment

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Brain MRI performed 6 weeks previously (for an episode of transient confusion in the context of urosepsis) revealed no abnormalities. No signal changes were evident on contrast-enhanced brain MRI; EEG revealed mild slowing, and CSF analyses were normal. Follow-up brain MRI performed 10 days after presentation (and 10 days of IV thiamine repletion) supported imaging resolution of the syndrome. His cognition gradually improved, and was unremarkable 1 month after thiamine repletion; however, fixed neuro-ophthalmic deficits, including right abducens paresis, remained at that time. The diagnosis of Wernicke syndrome is often suspected based on clinical grounds, and laboratory testing may not be additionally useful.

alcohol paralysis symptoms

Chronic Complications

Most patients with alcohol neuropathy initially present with symmetrical polyneuropathies in the lower distal extremities, however; heavier abuse can progress to distal upper extremity symptoms. The most common findings are sensory related and are varied to include pain, numbness, and paresthesias. Pain seems to be consistent through the literature to be one of the most common complaints and can be the first clinical indication of the disease.

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Are There Tests to Diagnose the Cause of Paralysis?

alcohol paralysis symptoms

Contrary to a previous study (Duka et al., 2004) in which only patients with severe alcohol withdrawal complications were included, we did not observe any association between multiple detoxifications and the severity of the current AWS. We also found that AUD patients with moderate-AWS reported higher alcohol alcohol neuropathy stages consumption during the month preceding withdrawal than those with mild-AWS. A 51-year-old man with a history of chronic alcoholism and colon adenocarcinoma with local intraabdominal metastases presented to the emergency department following several days of blurred vision followed by confusion and somnolence.

Alcoholic Neuropathy Symptoms

In addition to thiamine deficiency, recent studies indicate a direct neurotoxic effect of ethanol or its metabolites. Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5]. Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol [6, 13]. The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed.

  • But if you have developed neuropathy as a result of alcohol use, it’s important to stop drinking as soon as possible.
  • When identified, alcoholic neuropathy is indistinguishable from other distal sensorimotor axonal processes.
  • Several treatment options and interventions can help a person recover from alcohol dependence.
  • Additional hormones including insulin, testosterone, aldosterone, and catecholamines are also known to upregulate Na+-K+ ATPase pump activity [7, 8].
  • The prevalence of denervation findings on EMG ranged from muscle to muscle, with the highest being in the muscles of the lower limbs suggesting a length-dependent pattern [35, 45, 52, 59].
  • Generally, he was relatively well nourished, but he had been on a recent binge and had not eaten for 2 days during the past week.
  • When significantly limiting or cutting off alcohol consumption, receiving ongoing support is essential.
  • While peripheral neuropathy generally cannot be cured, there are several medical treatments that can be used to manage the pain of alcoholic neuropathy, aiding in your recovery.
  • Even if the person survives, an alcohol overdose like this can lead to long-lasting brain damage.

Review of additional medical history revealed that he had had three prolonged hospitalizations over the past 6 months for ileus and failure to thrive. In retrospect, a nationwide shortage of parenteral multivitamins limited his micronutrient intake to the rare days when he either briefly tolerated a liquid diet or received total parenteral nutrition, and he did not receive IV thiamine. Examination demonstrated disorientation to time and place, shortened attention span including impaired registration of unrelated words intended for subsequent recall, and amnesia without confabulation. Additionally, he had horizontal and vertical gaze–evoked nystagmus and weakness of right eye abduction and weakness of left eye elevation, as well as a distal symmetric sensory loss and diminished patellar and Achilles reflexes. MRI revealed T2 and FLAIR hyperintensities in the periaqueductal gray (Figure 7-2A and B), midbrain tectum (Figure 7-2C), and mammillary bodies (Figure 7-2D).

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Paralysis can include “paresis,” which is a partial weakness of part of the body. It can be hard to decide if you think someone is drunk enough to need medical help. You may worry about what will happen to you or a friend or family member, especially if underage. If you think that someone has alcohol poisoning, seek medical care right away. Alcohol poisoning also can occur when adults or children accidentally or intentionally drink household products that contain alcohol. Sometimes, these symptoms will build gradually and could be noticeable to family and friends long before the person with ARBD realises that something is wrong.

In an acute compressive lesion, electrodiagnostic studies are helpful for both diagnosis and prognosis. Demonstration of a conduction block across the site of compression after 5 to 10 days is a favorable prognostic sign and implies a degree of neurapraxia and short-term improvement over days to weeks. If significant axonal injury occurs (axonotmesis), Wallerian degeneration follows, and the nerve must regenerate by collateral sprouting or axonal regrowth from the distal stump over many months. Older patients with coexisting peripheral neuropathy have a less favorable outcome in this setting. Rare cases have been reported of alcoholics with severe acute or subacute neuropathy that mimics Guillain-Barré syndrome.37 Biopsy and electrodiagnostic data show an axonal pattern (not demyelinating) with normal CSF protein. A causal but unproven association with ethanol exists, and most cases have no report of thiamine levels.

  • Alcohol is a known teratogen (an agent capable of causing physical abnormalities in developing fetuses) that affects both the infant’s body and brain.
  • More recent findings show that loss-of-function mutations in KCNJ18, encoding Kir2.6, a skeletal muscle-specific Kir channel, result in decreased total potassium efflux and contribute to this phenomenon [7, 9].
  • If you feel that you sometimes drink too much alcohol, or your drinking is causing problems, or if your family is concerned about your drinking, talk with your health care provider.
  • If health care providers are open with patients and create a trusting environment, the patients are often happy to tell us what is going on with them.
  • There was not however, complete resolution of symmetric neuropathy with persistent mild loss of vibration sense or pinprick sensation in the feet or loss of ankle tendon reflexes.

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Gait disturbance due to sensory ataxia may be difficult to distinguish from, or be concomitant with, alcoholic cerebellar degeneration. Paresthesia is usually mild to moderate in severity but can become quite unpleasant or even frankly painful. Although patients may initially present with hand dysesthesia, more commonly hand symptoms follow anesthesia in the legs, which may be otherwise unrecognized or overlooked until more bothersome symptoms evolve. Neuropathic “Charcot” joints, a traumatic arthropathy typically of the ankle, may develop in advanced cases with severe loss of nociception as the patient forcefully strikes the ground to perceive placement of footing leading to joint destruction. Autonomic signs are difficult to demonstrate at the bedside unless frank orthostatic hypotension is present. Protein kinase C (PKC) is a family of protein kinases consisting of approximately 10 isozymes.

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