Alcohol-Related Neurological Disorders

Alcohol-related cognitive decline may result in a dementia-like illness and occur with injury. It may be unrecognized due to its multi-factorial nature, often contributed or confounded by head and brain trauma, frontal lobe impairment, cerebellar atrophy, hepatic encephalopathy, Wernicke’s and other nutritional deficiencies and seizures. 

Frontal lobe injury is a major site of neurologic injury from alcohol. The frontal lobe has a major role of moderating affective drive and impairment can result in disinhibition and impulsiveness, key targets for cognitive-focused psychological interventions to prevent relapse. 

Apart from acute alcohol intoxication-related injuries (through gamma-aminobutyric acid (GABA) and glutamate effects), the well-known neurological sequelae of continued problematic alcohol use are alcohol withdrawal and memory loss. Additionally,  in the presence of thiamine deficiency, alcohol use causes diffuse cortical injury and atrophy diagnosed as Wernicke’s encephalopathy and Korsakoff’s psychosis (Chapter 9). Alcohol-related brain injury is likely underestimated as it often occurs with variable contributions and is confounded by head and brain trauma, age-related brain disease such as involutional change and hypertension related small vessel ischaemic disease, hepatic encephalopathy, nutritional deficiencies and seizures.  

Alcohol can effect multiple regions of the brain, particularly the cerebellum and frontal lobe, with injury to the later posing a significant barrier to impulse control and cognitive focused psychological interventions to prevent relapse. Neurologic disability may affect mobility and interaction which in turn fosters social isolation that may exacerbate alcohol intake and alcohol-related harms. Even in younger people, alcohol-related neurological injury can impact the ability for self-care and sadly necessitate prolonged nursing home placement, at significant cost to the community. 

Alcohol-Related Seizures 

Epileptiform seizures are very common in people with AUD. Chronic alcohol misuse increases seizure threshold through adaption in the glutamate, N-methyl-D-aspartate (NMDA) and GABA receptors, leading to alcohol withdrawal-related seizures. Alcohol intake is also associated with seizure risk that increases with dose, independent of withdrawal. This seizure risk is frequently confounded by structural brain injury, which lowers the seizure threshold independent of alcohol intake or timing.  

Epileptiform seizures occur more frequently in patients who consume a large volume of alcohol. Patients with epilepsy should be counselled about the increased risk for seizures related to heavy alcohol consumption. 

Chronic alcohol misuse alters seizure thresholds through adaption in the glutamate, N-methyl-D-aspartate (NMDA) and GABA receptors, leading to alcohol withdrawal-related seizures. For individuals withdrawing from alcohol, both primary and secondary prevention of seizures is necessary and is particularly important in patients with a history of seizures or head injury. The risk for new-onset seizure appears to return to baseline after 12 months abstinence. Despite an early interest in their use and effect, multiple studies have shown no or little benefit for seizure prevention from phenytoin administration, and non-benzodiazepine anticonvulsants (NBAC), such as carbamazepine, oxcarbazepine and valproic acid, gabapentin, pregabalin, levetiracetam, topiramate and zonisamide.  

Alcohol-Related Neuropathy 

AUD can be complicated by a disabling painful peripheral neuropathy (PN), classically occurring in a “glove and stocking” distribution with small-fibre-predominant axonal degeneration of peripheral nerve fibres, sensory nerve fibre involvement and secondary demyelination. Nerve damage leads to unusual sensation in the limbs, reduced mobility, and loss of some bodily functions. Duration of alcohol use and total lifetime dose are associated with more severe PN as well as family history. Thiamine deficiency commonly occurs with chronic alcohol use, and this can also cause a PN indistinguishable from alcohol-related PN, so much so that there is conjecture whether they are in fact the same disease. Irrespective, high dose thiamine in addition to other vitamins is a cornerstone of treatment of the nutritionally deplete individuals with a history of alcohol abuse. 

Early recognition of symptoms of neuropathy and seeking treatment can reduce the risk of permanent disability. Assessment involves alcohol use history, neurologic examination, electromyography, and nerve conduction testing. Alcohol-related neuropathy is often associated with nutritional and vitamin deficiency that is comorbid in severe AUD. The treatment of alcohol-related neuropathy involves alcohol abstinence, analgesia, podiatry review, physical therapy, vitamin supplementation, and encouraging a nutritionally balanced diet.  

Chapter Recommendation Grade of recommendation
22.5 Alcohol abstinence, analgesia, high dose thiamine and a balanced diet supplemented with thiamine and other B vitamins, are recommended in persons with alcohol-related neuropathy who present with AUD or neurologic symptoms. B
22.6 Patients with AUD should be screened for risk of seizures and be provided with prevention treatment (in case of withdrawal symptoms) B