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Alcoholism

Category: Illness or disabilities

Type

Involuntary

Introduction and description

The following provides a good description of alcoholism and its effects on the brain.

Molecular and behavioral aspects of the actions of alcohol on the adult and developing brain
- Alfonso-Loeches S, Guerri C;
Cell Pathology Laboratory, Prince Felipe Research Centre, Valencia, Spain.

The brain is one of the major target organs of alcohol actions. Alcohol abuse can lead to alterations in brain structure and functions and, in some cases, to neurodegeneration.

Cognitive deficits and alcohol dependence are highly damaging consequences of alcohol abuse. Clinical and experimental studies have demonstrated that the developing brain is particularly vulnerable to alcohol, and that drinking during gestation can lead to a range of physical, learning and behavioral defects (fetal alcohol spectrum disorders), with the most dramatic presentation corresponding to fetal alcohol syndrome.

Recent findings also indicate that adolescence is a stage of brain maturation and that heavy drinking at this stage can have a negative impact on brain structure and functions causing important short- and long-term cognitive and behavioral consequences.

The effects of alcohol on the brain are not uniform; some brain areas or cell populations are more vulnerable than others. The prefrontal cortex, the hippocampus, the cerebellum, the white matter and glial cells are particularly susceptible to the effects of ethanol. The molecular actions of alcohol on the brain are complex and involve numerous mechanisms and signaling pathways.

Some of the mechanisms involved are common for the adult brain and for the developing brain, while others depend on the developmental stage.

During brain ontogeny, alcohol causes irreversible alterations to the brain structure. It also impairs several molecular, neurochemical and cellular events taking place during normal brain development, including alterations in both gene expression regulation and the molecules involved in cell-cell interactions, interference with the mitogenic and growth factor response, enhancement of free radical formation and derangements of glial cell functions. However, in both adult and adolescent brains, alcohol damages specific brain areas through mechanisms involving excitotoxicity, free radical formation and neuroinflammatory damage resulting from activation of the innate immune system mediated by TLR4 receptors.

Alcohol also acts on specific membrane proteins, such as neurotransmitter receptors (e.g. NMDA, GABA-A), ion channels (e.g. L-type Ca(2+) channels, GIRKs), and signaling pathways (e.g. PKA and PKC signaling). These effects might underlie the wide variety of behavioral effects induced by ethanol drinking.

The neuroadaptive changes affecting neurotransmission systems which are more sensitive to the acute effects of alcohol occur after long-term alcohol consumption. Alcohol-induced maladaptations in the dopaminergic mesolimbic system, abnormal plastic changes in the reward-related brain areas and genetic and epigenetic factors may all contribute to alcohol reinforcement and alcohol addiction.

This manuscript reviews the mechanisms by which ethanol impacts the adult and the developing brain, and causes both neural impairments and cognitive and behavioral dysfunctions. The identification and the understanding of the cellular and molecular mechanisms involved in ethanol toxicity might contribute to the development of treatments and/or therapeutic agents that could reduce or eliminate the deleterious effects of alcohol on the brain.

PMID: 21657944

How it works

Alcoholism produces hallucinations both auditory and visual, but it does it via two mechanisms of action – one is brain damage, the other is by excitation of the neurons in a manner similar to epilepsy.

Brain damage

Excessive consumption of alcohol causes brain damage in the longer term, particularly affecting the prefrontal cortex, the hippocampus, the cerebellum, the white matter and glial cells.  Damage to the hippocampus, for example,  produced by chronic alcohol abuse prevents new memories being laid down even though it does not interfere with the retrieval of older memories.  And this plus other brain damage produces hallucinations.

As we saw in the section on brain damage, damage to any number of organs can have its effect.

Brain excitation

But there are other causes of hallucinations and one key cause appears to be alcohol withdrawal. 

  • Alcoholic hallucinosis  - or alcohol-related psychosis develops about 12 to 24 hours after drinking stops and involves auditory and visual hallucinations, most commonly accusatory or threatening voices. Alcoholic hallucinosis results from a very short term cessation in drinking.  This condition develops and resolves rapidly, involves a limited set of hallucinations and has no other physical symptoms.  The risk of developing alcoholic hallucinosis is increased by long-term heavy alcohol abuse.  Alcoholic hallucinosis occurs in approximately 20% of hospitalised alcoholics and does not carry a significant mortality.
  • Acute alcoholic hallucinosis –  is the half way stage between alcoholic hallucinosis and delirium tremens
  • Delirium tremens - In contrast, delirium tremens is a condition brought on by withdrawal from alcohol on a more permanent basis.  DT is characterized by the presence of “altered sensorium”; that is, a complete hallucination without any recognition of the real world – a vision.

The main symptoms of Delirium Tremens are confusion, diarrhea, insomnia, tremor, disorientation and agitation and other signs of severe autonomic instability (fever, tachycardia, hypertension). These symptoms may appear suddenly but can develop 2–3 days after cessation of drinking heavily with its highest peak/ intensity on the fourth or fifth day. Also, these symptoms are characteristically worse at night. Other common symptoms include intense perceptual disturbance such as visions of insects, snakes, or rats. These may be hallucinations, or illusions related to the environment, e.g., patterns on the wallpaper or in the peripheral vision that the patient falsely perceives as a resemblance to the morphology of an insect.

Delirium tremens hallucinations are primarily visual, in the peripheral field of vision, but are also associated with tactile hallucinations such as sensations of something crawling on the subject — a phenomenon known as formication. Delirium Tremens usually includes extremely intense feelings of "impending doom" or that "something terrible is about to happen" to the patient suffering from DT. Severe anxiety and feelings of imminent death are at the foundation of DT.

DT occurs in 5-10% of alcoholics and carries up to 5% mortality with treatment and up to 35% mortality without treatment.

If we thus summarise up to now, excessive alcohol consumption causes brain damage, but withdrawal from alcohol consumption causes most of the hallucinatory activity.

According to the research of Dr Adams, the damage is more like the uncontrolled firing of neurons experienced by an epileptic than the sort of effect produced by tumours, dementia or other serious brain damage – see Epilepsy.

THE GORDON WILSON LECTURE - NUTRITIONAL DISEASES OF THE NERVIOUS SYSTEM IN THE ALCOHOLIC PATIENT
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 RAYMOND D. ADAMS, M.D.; BOSTON

One must postulate, therefore, that in the habituated patient the neurological symptoms are the results of excessive and disorganized activity of those parts of the central nervous system normally acted upon by alcohol, after a diminution of the levels of blood alcohol, viz., after sleep  or during enforced abstinence. Presumably the elevation of the levels of blood alcohol by oral ingestion or injection of alcohol would suppress them but this has not been studied systematically.

We can perhaps postulate that when an alcoholic withdraws from alcohol, it causes such a chemical inbalance that it produces nerve impulses of extremely high frequency perhaps at frequencies far higher than is normal to trigger the function the impulse is targetting.

Damage to the neuron itself can cause malfunction.  So the brain damage may have not reached the stage where whole sections of the brain have been wiped out, but severe damage may have been suffered causing it to misfire.

Related observations