View source for Alcoholic polyneuropathy

{{Infobox medical condition (new)
| name            = Alcoholic polyneuropathy
| synonyms        = Alcohol leg
| image           = Nerve.nida.jpg
| caption         = An illustration of a neuron's structure. In alcoholic polyneuropathy [[myelin]] loss and [[axon]]al degeneration occurs.
| pronounce       =
| field           = [[Neurology]]
| symptoms        =
| complications   =
| onset           =
| duration        =
| types           =
| causes          =
| risks           =
| diagnosis       =
| differential    =
| prevention      =
| treatment       =
| medication      =
| prognosis       =
| frequency       =
| deaths          =
}}
'''Alcoholic polyneuropathy''' is a [[neurological disorder]] in which peripheral [[nerve]]s throughout the body [[polyneuropathy|malfunction simultaneously]]. It is defined by [[axon]]al degeneration in [[neuron]]s of both the [[sensory system|sensory]] and [[motor system]]s and initially occurs at the [[Anatomical terms of location#Proximal and distal|distal]] ends of the longest axons in the [[Human body|body]]. This [[nerve injury|nerve damage]] causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by [[Alcoholism|chronic alcoholism]]; however, [[Avitaminosis|vitamin deficiencies]] are also known to contribute to its development. This [[disease]] typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.

==Signs and symptoms==

An early warning sign ([[prodrome]]) of the possibility of developing alcoholic polyneuropathy, especially in a chronic alcoholic, would be weight loss because this usually signifies a nutritional deficiency that can lead to the development of the disease.<ref name="brown"/>

Alcoholic polyneuropathy usually has a gradual onset over months or even years, although axonal degeneration often begins before an individual experiences any [[symptom]]s.<ref name="mawdsley"/>

The disease typically involves sensory issues and motor loss, as well as painful physical perceptions, though all [[Sensory system#Modality|sensory modalities]] may be involved.<ref name="laker"/>
Symptoms that affect the sensory and motor systems seem to develop symmetrically. For example, if the right foot is affected, the left foot is affected simultaneously or soon becomes affected.<ref name="brown"/>
In most cases, the legs are affected first, followed by the arms. The hands usually become involved when the symptoms reach above the ankle.<ref name="laker"/> This is called a stocking-and-glove pattern of sensory disturbances.<ref name="lisak"/>

===Sensory===
Common manifestations of sensory issues include numbness or painful sensations in the arms and legs, abnormal sensations like "pins and needles," and [[heat intolerance]].<ref name="medline"/> [[Pain]] experienced by individuals depends on the severity of the polyneuropathy. It may be dull and constant in some individuals while being sharp and lancinating in others.<ref name="lisak"/> In many subjects, tenderness is seen upon the palpitation of muscles in the feet and legs.<ref name="brown"/> Certain people may also feel [[cramp]]ing sensations in the muscles affected and others say there is a burning sensation in their feet and calves.<ref name="lisak"/>

===Motor===
Sensory symptoms are gradually followed by motor symptoms.<ref name="laker"/> Motor symptoms may include muscle cramps and weakness, [[erectile dysfunction]] in men, problems urinating, [[constipation]], and [[diarrhea]].<ref name="laker"/> Individuals also may experience muscle wasting and decreased or absent [[deep tendon reflex]]es.<ref name="brown"/> Some people may experience frequent falls and gait unsteadiness due to [[ataxia]]. This ataxia may be caused by [[cerebellar]] degeneration, sensory ataxia, or distal muscle weakness.<ref name="lisak"/> Over time, alcoholic polyneuropathy may also cause difficulty swallowing ([[dysphagia]]), speech impairment ([[disarthria]]), [[muscle spasms]], and [[muscle atrophy]].<ref name="medline"/>

In addition to alcoholic polyneuropathy, the individual may also show other related disorders such as [[Wernicke–Korsakoff syndrome]] and cerebellar degeneration that result from alcoholism-related nutritional disorders.<ref name="brown"/>

===Severity===
Polyneuropathy spans a large range of severity. Some cases are seemingly [[asymptomatic]] and may only be recognized on careful examination. The most severe cases may cause profound [[physical disability]].<ref name="brown"/>

==Causes==
The general cause of this disease appears to be prolonged and heavy consumption of [[alcohol (drug)|alcohol]] accompanied by a nutritional deficiency. However, there is ongoing debate over the active mechanisms,<ref name="Chopra">{{cite journal |last1=Chopra |first1=Kanwaljit |last2=Tiwari |first2=Vinod |title=Alcoholic neuropathy: possible mechanisms and future treatment possibilities |journal=British Journal of Clinical Pharmacology |date=March 2012 |volume=73 |issue=3 |pages=348–362 |doi=10.1111/j.1365-2125.2011.04111.x |pmid=21988193 |pmc=3370340 }}</ref><ref name=NBK499856>{{cite book |last1=Sadowski |first1=Adam |last2=Houck |first2=Richard C. |title=StatPearls |date=2021 |publisher=StatPearls Publishing |id={{NCBIBook2|NBK499856}} |chapter=Alcoholic Neuropathy }}</ref> including whether the main cause is the direct [[toxicity|toxic]] effect of alcohol itself or whether the disease is a result of alcoholism-related [[malnutrition]].<ref name="brown"/> A 2019 metastudy found that the relationship between ethanol toxicity and neuropathy remained unproven.<ref>{{cite journal |last1=Julian |first1=Thomas |last2=Glascow |first2=Nicholas |last3=Syeed |first3=Rubiya |last4=Zis |first4=Panagiotis |title=Alcohol-related peripheral neuropathy: a systematic review and meta-analysis |journal=Journal of Neurology |date=1 December 2019 |volume=266 |issue=12 |pages=2907–2919 |doi=10.1007/s00415-018-9123-1 |pmid=30467601 |pmc=6851213 }}</ref>

===Effects due to nutritional deficiency===
Frequently alcoholics have disrupted social links in their lives and have an irregular lifestyle. This may cause an alcoholic to change their eating habits including more missed meals and a poor dietary balance.<ref name ="preedy"/> Alcoholism may also result in loss of [[appetite]], alcoholic [[gastritis]], and vomiting, which decrease food intake. Alcohol abuse damages the lining of the [[gastrointestinal system]] and reduces absorption of nutrients that are taken in.<ref name="Vittadini">{{cite journal |last1=Vittadini |first1=G. |last2=Buonocore |first2=M |last3=Colli |first3=G |last4=Terzi |first4=M |last5=Fonte |first5=R |last6=Biscaldi |first6=G |title=Alcoholic polyneuropathy: a clinical and epidemiological study |journal=Alcohol and Alcoholism |date=1 September 2001 |volume=36 |issue=5 |pages=393–400 |doi=10.1093/alcalc/36.5.393 |pmid=11524304 |doi-access=free }}</ref> The combination of all of them may result in a nutritional deficiency that is linked to the development of alcoholic polyneuropathy.<ref name ="preedy">{{cite book |last1=Santolaria |first1=Francisco |last2=González-Reimers |first2=Emilio |chapter=Alcohol and Nutrition: an Integrated Perspective |pages=3–17 |chapter-url=https://books.google.com/books?id=bTdyW8fBQZoC&pg=PA3 |editor1-last=Watson |editor1-first=Ronald Ross |editor2-last=Preedy |editor2-first=Victor R. |title=Nutrition and Alcohol: Linking Nutrient Interactions and Dietary Intake |date=17 December 2003 |publisher=CRC Press |isbn=978-0-203-50763-6 }}</ref>

There is evidence that providing individuals with adequate vitamins improves symptoms despite continued alcohol intake, indicating that vitamin deficiency may be a major factor in the development and progression of alcoholic polyneuropathy.<ref name="mawdsley">{{cite journal |last1=Mawdsley |first1=C. |last2=Mayer |first2=R. F. |title=Nerve conduction in alcoholic polyneuropathy |journal=Brain |date=1965 |volume=88 |issue=2 |pages=335–356 |doi=10.1093/brain/88.2.335 |pmid=4284013 }}</ref> In experimental models of alcoholic polyneuropathy utilizing [[brown rat|rats]] and monkeys no convincing evidence was found that proper nutritional intake along with alcohol results in polyneuropathy.<ref name="brown"/>

[[File:Thiamine pyrophosphate V2.svg|thumb|[[Thiamine pyrophosphate]] structure. As a result of nutritional deficiency in those with alcoholic polyneuropathy, low thiamine levels are usually present and have been proposed as a cause of the nerve destruction.]]

In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency. Alcohol, a [[carbohydrate]], increases the [[metabolic]] demand for [[thiamine]] (vitamin B1) because of its role in the [[carbohydrate metabolism|metabolism of glucose]]. Thiamine levels are usually low in alcoholics due to their decreased nutritional intake. In addition, alcohol interferes with intestinal absorption of thiamine, thereby further decreasing thiamine levels in the body.<ref name="mendell"/> Thiamine is important in three reactions in the [[carbohydrate metabolism|metabolism of glucose]]: the [[decarboxylation]] of [[pyruvic acid]], d-ketoglutaric acid, and [[transketolase]]. A lack of thiamine in the cells may therefore prevent neurons from maintaining necessary [[adenosine triphosphate]] (ATP) levels as a result of impaired [[glycolysis]]. Thiamine deficiency alone could explain the impaired nerve [[Electrical conductance|conduction]] in those with alcoholic polyneuropathy, but other factors likely play a part.<ref name="mawdsley"/>

The malnutrition many alcoholics experience deprives them of important [[cofactor (biochemistry)|cofactors]] for the oxidative metabolism of glucose. Neural tissues depend on this process for energy, and disruption of the cycle would impair cell growth and function. [[Schwann cell]]s produce myelin that wraps around the sensory and motor nerve axons to enhance [[action potential]] conduction in the periphery. An energy deficiency in Schwann cells would account for the disappearance of myelin on peripheral nerves, which may result in damage to axons or loss of nerve function altogether. In peripheral nerves, oxidative enzyme activity is most concentrated around the [[nodes of Ranvier]], making these locations most vulnerable to cofactor deprivation. Lacking essential cofactors reduces myelin impedance, increases current leakage, and slows signal transmission. Disruptions in conductance first affect the peripheral ends of the longest and largest peripheral nerve fibers because they suffer most from decreased action potential propagation. Thus, neural deterioration occurs in an accelerating cycle: myelin damage reduces conductance, and reduced conductance contributes to myelin degradation. The slowed conduction of action potentials in axons causes segmental demyelination extending proximally; this is also known as retrograde [[degeneration (medical)|degeneration]].<ref name="mawdsley"/>

Many of the studies conducted that observe alcoholic polyneuropathy in patients are often criticized for their criteria used to assess nutritional deficiency in the subjects because they may not have completely ruled out the possibility of a nutritional deficiency in the genesis of the polyneuropathy.<ref name="brown"/> Many researchers favor the nutritional origin of this disease, but the possibility of alcohol having a toxic effect on the peripheral nerves has not been completely ruled out.<ref name="brown"/>

===Effects due to alcohol ingestion===
The consumption of alcohol may lead to the buildup of certain toxins in the body. For example, in the process of breaking down alcohol, the body produces [[acetaldehyde]], which can accumulate to toxic levels in alcoholics. This suggests that there is a possibility [[ethanol]] (or its metabolites) may cause alcoholic polyneuropathy.<ref name="lisak"/> There is evidence that polyneuropathy is also prevalent in well-nourished alcoholics, supporting the idea that there is a direct toxic effect of alcohol.<ref name="Chopra"/>

The metabolic effects of liver damage associated with alcoholism may also contribute to the development of alcoholic polyneuropathy. Normal products of the liver, such as [[lipoic acid]], may be deficient in alcoholics. This deficiency would also disrupt glycolysis and can alter metabolism, transport, storage, and activation of essential nutrients.<ref name="mawdsley"/>

[[Acetaldehyde]] is toxic to peripheral nerves. There are increased levels of acetaldehyde produced during [[ethanol]] metabolism. If the acetaldehyde is not metabolized quickly the nerves may be affected by the accumulation of acetaldehyde to toxic levels.<ref name="lisak"/><ref name="koike"/>

==Pathophysiology==
The [[pathophysiology]] of alcoholic polyneuropathy is unclear.<ref name="koike"/>

==Diagnosis==
Alcoholic polyneuropathy is very similar to other [[neurodegeneration|axonal degenerative]] polyneuropathies and therefore can be difficult to diagnose. When alcoholics have sensorimotor polyneuropathy as well as a nutritional deficiency, a diagnosis of alcoholic polyneuropathy is often reached.<ref name="brown" /><ref name=shields>{{cite journal |last1=Shields |first1=Robert W. |title=Alcoholic polyneuropathy |journal=Muscle & Nerve |date=March 1985 |volume=8 |issue=3 |pages=183–187 |doi=10.1002/mus.880080302 |pmid=4058462 |s2cid=13623097 }}</ref>

To confirm the diagnosis, a physician must rule out other causes of similar clinical syndromes. Other neuropathies can be [[Differential diagnosis|differentiated]] on the basis of typical clinical or laboratory features.<ref name="shields"/> Differential diagnoses to alcoholic polyneuropathy include [[amyotrophic lateral sclerosis]], [[beriberi]], [[Charcot-Marie-Tooth disease]], [[plexopathy|diabetic lumbosacral plexopathy]], Guillain Barre Syndrome, [[diabetic neuropathy]], [[mononeuritis multiplex]] and [[post-polio syndrome]].<ref name=laker>{{EMedicine|article|315159|Alcoholic Neuropathy}}</ref>

To clarify the diagnosis, medical workup most commonly involves laboratory tests, though, in some cases, [[medical imaging|imaging]], [[nerve conduction study|nerve conduction studies]], [[electromyography]], and vibrometer testing may also be used.<ref name="laker"/>

A number of tests may be used to rule out other causes of peripheral neuropathy.  One of the first presenting symptoms of [[diabetes mellitus]] may be peripheral neuropathy, and [[hemoglobin A1C]] can be used to estimate average [[blood sugar|blood glucose levels]].  Elevated blood [[creatinine]] levels may indicate [[chronic kidney disease]] and may also be a cause of peripheral neuropathy.  A heavy metal toxicity screen should also be used to exclude [[lead toxicity]] as a cause of neuropathy.<ref name="laker"/>

Alcoholism is normally associated with nutritional deficiencies, which may contribute to the development of alcoholic polyneuropathy. [[Thiamine]], [[Vitamin B12|vitamin B-12]], and [[folic acid]] are vitamins that play an essential role in the [[peripheral nervous system|peripheral]] and [[central nervous system]] and should be among the first analyzed in laboratory tests.<ref name="laker"/> It has been difficult to assess thiamine status in individuals due to difficulties in developing a method to directly [[assay]] thiamine in the blood and urine.<ref name="brown"/> A [[liver function test]] may also be ordered, as alcoholic consumption may cause an increase in liver enzyme levels.<ref name="laker"/>

==Management==
Although there is no known cure for alcoholic polyneuropathy, there are a number of treatments that can control symptoms and promote independence.  [[Physical therapy]] is beneficial for strength training of weakened muscles, as well as for gait and balance training.<ref name="laker"/>

===Nutrition===
[[File:Tpn 3bag.jpg|thumb|right|upright|An [[intravenous therapy|intravenous]] home [[parenteral nutrition]] formula may be a part of the treatment plan for those with alcoholic polyneuropathy who also have a nutritional deficiency.]]
To best manage symptoms, refraining from consuming alcohol is essential. Abstinence from alcohol encourages proper diet and helps prevent progression or recurrence of the neuropathy.<ref name="shields"/> Once an individual stops consuming alcohol it is important to make sure they understand that substantial recovery usually isn't seen for a few months. Some subjective improvement may appear right away, but this is usually due to the overall benefits of alcohol detoxification.<ref name="mendell">{{cite book |author1=Cornblath, David R. |author2=Jerry R. Mendell |author3=Kissel, John T. |title=Diagnosis and management of peripheral nerve disorders |publisher=Oxford University Press |location=Oxford [Oxfordshire] |year=2001 |pages=332–334 |isbn=978-0-19-513301-1 }}</ref>  If alcohol consumption continues, vitamin supplementation alone is not enough to improve the symptoms of most individuals.<ref name="lisak"/>

Nutritional therapy with [[parenteral]] multivitamins is beneficial to implement until the person can maintain adequate nutritional intake.<ref name="brown"/> Treatments also include [[vitamin]] supplementation (especially [[thiamine]]). In more severe cases of nutritional deficiency 320&nbsp;mg/day of [[benfotiamine]] for 4 weeks followed by 120&nbsp;mg/day for 4 more weeks may be prescribed in an effort to return thiamine levels to normal.<ref name="lisak"/>

===Pain===
Painful [[dysesthesias]] caused by alcoholic polyneuropathy can be treated by using [[gabapentin]] or [[amitriptyline]] in combination with over-the-counter pain medications, such as [[aspirin]], [[ibuprofen]], or [[acetaminophen]]. [[Tricyclic antidepressants]] such as [[amitriptyline]], or [[carbamazepine]] may help stabbing pains and have central and peripheral [[anticholinergic]] and [[sedative|sedative effects]]. These agents have central effects on pain transmission and block the active reuptake of norepinephrine and serotonin.<ref name="laker"/><ref name="medline"/>

[[Anticonvulsant|Anticonvulsant drugs]] like [[gabapentin]] or [[pregabalin]] block the active reuptake of [[norepinephrine]] and [[serotonin]] and have properties that relieve neuropathic pain.  However, these medications take a few weeks to become effective and are rarely used in the treatment of [[pain|acute pain]].<ref name="laker"/>

[[analgesics|Topical analgesics]] like [[capsaicin]] may also relieve minor aches and pains of muscles and joints.<ref name="laker"/>

==Prognosis==
Alcoholic polyneuropathy is not life-threatening but may significantly affect one's quality of life. Effects of the disease range from mild discomfort to severe disability.<ref name="medline">{{MedlinePlusEncyclopedia|000714|Alcoholic neuropathy}}</ref>

It is difficult to assess the [[prognosis]] of a patient because alcohol dependence results in difficulty maintaining abstinence from drinking alcohol. It has been shown that a good prognosis may be given for mild neuropathy if the person has abstained from drinking for 3–5 years.<ref name="koike">{{cite journal |last1=Koike |first1=Haruki |last2=Sobue |first2=Gen |title=Alcoholic neuropathy |journal=Current Opinion in Neurology |date=October 2006 |volume=19 |issue=5 |pages=481–486 |doi=10.1097/01.wco.0000245371.89941.eb |pmid=16969158 |s2cid=20621462 }}</ref>

===Early stage===
During the early stages of the disease the damage appears reversible when people take adequate amounts of vitamins, such as thiamine.<ref name="mawdsley"/> If the polyneuropathy is mild, the individual normally experiences a significant improvement and symptoms may be eliminated within weeks to months after proper nutrition is established.<ref name="brown"/> When those people diagnosed with alcohol polyneuropathy experience a recovery, it is presumed to result from regeneration and collateral sprouting of the damaged axons.<ref name="lisak"/>

===Progressed disease===
As the disease progresses, the damage may become permanent. In severe cases of thiamine deficiency, a few of the positive symptoms (including neuropathic pain) may persist indefinitely.<ref name="koike"/> Even after the restoration of a balanced nutritional intake, those patients with severe or chronic polyneuropathy may experience lifelong residual symptoms.<ref name="brown"/>

==Epidemiology==
[[File:Alcohol by Country.png|thumb|right|Total recorded alcohol consumption per capita of individuals 15 years or older, in liters of pure alcohol. Alcoholism is the main cause of alcoholic polyneuropathy.]]

In 2020 the NIH quoted an estimate that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy.<ref name=NBK499856/> The rate of incidence of alcoholic polyneuropathy involving sensory and motor polyneuropathy has been stated as from 10% to 50% of alcoholics depending on the subject selection and diagnostic criteria. If electrodiagnostic criteria are used, alcoholic polyneuropathy may be found in up to 90% of individuals being assessed.<ref name="lisak">{{cite book |author1=Roongroj Bhidayasiri |author2=Lisak, Robert P. |author3=Daniel Truong |author4=Carroll, William K. |title=International Neurology |publisher=Wiley-Blackwell |year=2009 |pages= 413–414 |isbn=978-1-4051-5738-4 }}</ref>

The distribution and severity of the disease depends on regional dietary habits, individual drinking habits, as well as an individual's [[genetics]].<ref name="koike"/> Large studies have been conducted and show that alcoholic polyneuropathy severity and incidence correlates best with the total lifetime consumption of alcohol. Factors such as nutritional intake, age, or other medical conditions are correlate in lesser degrees.<ref name="mendell"/> For unknown reasons, alcoholic polyneuropathy has a high incidence in women.<ref name="lisak"/>

Certain alcoholic beverages can also contain [[Congener (alcohol)|congeners]] that may also be bioactive; therefore, the consumption of varying alcohol beverages may result in different health consequences.<ref name="koike"/> An individual's nutritional intake also plays a role in the development of this disease. Depending on the specific dietary habits, they may have a deficiency of one or more of the following: [[thiamine]] (vitamin B1), [[Niacin (nutrient)|niacin]] (vitamin B3), [[pantothenic acid]] (vitamin B5),  [[pyridoxine]] (vitamin B6) and [[biotin]] (vitamin B7), [[vitamin B12]], [[folic acid]], and [[vitamin A]].<ref name="medline"/>

===Acetaldehyde===
[[File:Ethanol_to_acetaldehyde.svg|thumb|Conversion of [[ethanol]] to [[acetaldehyde]]. The toxic buildup of acetaldehyde may result in alcoholic polyneuropathy.]]
{{Main|Acetaldehyde}}

It is also thought there is perhaps a genetic predisposition for some alcoholics that results in increased frequency of alcoholic polyneuropathy in certain ethnic groups. During the body's processing of alcohol, ethanol is oxidized to acetaldehyde mainly by [[alcohol dehydrogenase]]; acetaldehyde is then oxidized to acetate mainly by [[aldehyde dehydrogenase|aldehyde dehydrogenase (ALDH)]]. [[ALDH2]] is an isozyme of ALDH and ALDH2 has a polymorphism (ALDH2*2, Glu487Lys) that makes ADLH2 inactive; this allele is more prevalent among Southeast and East Asians and results in a failure to quickly metabolize acetaldehyde. The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of alcoholic polyneuropathy.<ref name="lisak"/><ref name="koike"/>

==History==
[[File:Johncoakleylettsome.jpeg|thumb|upright|right|[[John C. Lettsome]] noted in 1787 [[hyperesthesia]] and [[paralysis]] in legs more than arms of patients, a characteristic of alcoholic polyneuropathy.]]
The first description of [[symptom]]s associated with alcoholic polyneuropathy were recorded by [[John C. Lettsome]] in 1787 when he noted [[hyperesthesia]] and [[paralysis]] in legs more than arms of patients.<ref name="mawdsley"/> Jackson has also been credited with describing polyneuropathy in chronic alcoholics in 1822. The clinical title of alcoholic polyneuropathy was widely recognized by the late nineteenth century. It was thought that the polyneuropathy was a direct result of the toxic effect alcohol had on peripheral nerves when used excessively. In 1928, George C. Shattuck argued that the polyneuropathy resulted from a vitamin B deficiency commonly found in alcoholics and he claimed that alcoholic polyneuropathy should be related to [[beriberi]]. This debate continues today over what exactly causes this disease, some argue it is just the alcohol toxicity, others claim the vitamin deficiencies are to blame and still others say it is some combination of the two.<ref name=brown>{{cite book |author1=Aminoff, Michael J. |author2=Brown, William A. |author3=Bolton, Charles Francis |title=Neuromuscular function and disease: basic, clinical and electrodiagnostic aspects |publisher=W. B. Saunders |location=Philadelphia |year=2002 |pages=1112–1115 |isbn=978-0-7216-8922-7 }}</ref>

==Research directions==
In 2001 research directions included the effect that an alcoholics' consumption and choice of alcoholic beverage might have on their development of alcoholic polyneuropathy. Some beverages may include more nutrients than others (such as thiamine), but the effects of this with regards to helping with a nutritional deficiency in alcoholics is yet unknown.<ref name="Vittadini"/>

Research also continued on reasons for the development of alcoholic polyneuropathy. Some argue it is a direct result of alcohol's toxic effect on the nerves, but others say factors such as a nutritional deficiency or chronic liver disease may play a role in the development as well. Multiple mechanisms may be present.<ref name="mendell"/>

==References==
{{Reflist}}

== External links ==
{{Medical resources
|  DiseasesDB      = 9850
|  ICD10           = {{ICD10|G|62|1|g|60}}
|  ICD9            = {{ICD9|357.5}}
|  ICDO            =
|  OMIM            =
|  MedlinePlus     = 000714
|  eMedicineSubj   = article
|  eMedicineTopic  = 315159
|  eMedicine_mult  =
|  MeshID          = D020269
}}

{{PNS diseases of the nervous system}}
{{Psychoactive substance use}}

[[Category:Health effects of alcohol]]
[[Category:Peripheral nervous system disorders]]