NEUROPSYCHIATRIC

MANIFESTATION OF ALCOHOL

BY
DR. BABA MUSA MUHAMMAD
DEPARTMENT OF MENTAL HEALTH
FRDERAL NEUROPSYCHIATRIC HOSPITAL MAIDUGURI
01/04/2024

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OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• FORMS
• METABOLISM
• MANIFESTATION
• SIGNS AND SYMPTOMS
• MANAGEMENT
• HISTORY
• INVESTIGATIONS
• TREAMENT
• CONCLUSION
REFERENCES
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INTRODUCTION
• Alcohol is the most commonly used psychoactive substance in most
part of the world, heavy alcohol consumption is associated with many
health and social problem.In 2010, alcohol accounted for 4.9million
death and 5.5% of gobal burden of disease (Lim et al, 2013)
• Nigeria ranks second for per capita alcohol consumption and heavy
episodic drinking in Africa (WHO,2014)
• This does not include the fact that a quarter of the alcohol consumed
in the country is unrecorded. (Obot, 2007).

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EPIDEMIOLOGY
• It is estimated that over 2billion people use alcohol, 1.3 billion smoke
tobacco and 185 million are drug users globally (Anderson et al, 2006)
• A cross sectional study on alcohol use disorder done in kuru village of
Jos community shows alcohol use disorder to be common among the
elderly population (Okonoda et al,2020)
• Alcohol and other substances are more commonly among young
adult, however the expected rise in the population of adult may lead
to an increase among elderly people who abuse alcohol and other
substances. (Wang et al, 2013)

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FORMS OF ALCOHOL

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FORMS CONT……

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METABOLISM
• The chemical name for alcohol is ethanol. The body processes and eliminates
ethanol in separate steps.
• Chemical called enzymes help to break apart the ethnol molecule into other
compounds (or metabolites), which can be processed more easily by the
body. Some of these intermediate metabolites can have harmful effects on
the body.
• Most the ethanol in the body is broken down in the liver by an enzyme called
alcohol dehydrogenase (ADH), which transforms ethanol into a toxic
compound called acetaldehyde, a known carcinogen. However , acetyldehyde
is generally short lived; it is quickly broken down to a less toxic compound
called acetate by another enzyme called aldehyde dehydrogenase (ALDH).
• Actate then is broken down to carbondioxide and water, mainly in tissues
other than the liver.
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METABOLISM CONT..
• Other enzymes; the cytochrome P450 2E1 (CYP2E1) and catalase also
break down alcohol to acetaldehyde. However, CYP2E1 only is active
after a person has consumed large amount of alcohol, and catalase
metabolizes only a fraction of alcohol in the body. (Edenberg et al,
2007)
• Small amounts of alcohol also are removed by interacting with fatty
acids to form compounds called fatty acid ethyl esters (FAEEs). These
compounds have been shown to contribute to damage to the liver
and pancreas (Vonlaufen et al, 2006)

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METABOLISM CONT…

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MANIFESTATIONS
NEUROPSYCHIATRIC MANIFESTATIONS CAN BE CLASSIFIED AS;
1. Direct effects – alcohol intoxication, aggression, blackouts.
2. Disorders due to withdrawal – tremors, seizures, hallucinoses,
delirium tremens.
3. Associated nutritional deficiencies – Wernicke’s encephalopathy,
karsakoff’s syndrome, peripheral neuropathy, cerebellar
degeneration.
4. Alcohol induced conditions – dementia, mood disorder, anxiety
disorder, psychotic disorder

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CLASSIFICATION OF ALCOHOLISM

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BLOOD ALCOHOL
CONCENTRATRION (BAC)

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ALCOHOLIC INTOXICATION
• There is a generalised central nervous system depression with alcohol
use. With increasing intoxication, there is increased reaction time,
slowed thinking, distractibility and poor motor control. Later,
dysarthria, ataxia and incoordination can occur.
• The duration of intoxication depends on the amount and the rapidity
of ingestion of alcohol. Usually the signs of intoxication are obvious
with blood levels of 150-200 mg%. With blood alcohol levels of 300-
450 mg%, increasing drowsiness followed by coma and respiratory
depression develop. Death occurs with blood alcohol levels between
400 to 800 mg% (Ahuja, 2011)

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AGGRESSION
• Presents as an outburst of uncontrollable rage and excitement leading
to destructive actions against other persons and property, behavior is
described out of character for the individual concerned, duration is
short, and there is subsequently amnesia for entire episode.
• Severe form include pathological intoxication (manie a potu) ; Applies
only to alcohol. Sudden onset of aggression and often violent
behavior that is not typical of the individual when sober, very soon
after drinking drinking amounts of alcohol that would not produce
intoxication in most people.

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ALCOHOLIC BLACKOUT’S
• Characterised by memory impairment (anterograde amnesia) for the
period when a person was drinking heavily but remained awake.
• Is the result of the ability of high doses of any brain depressant (e.g.,
alcohol or benzodiazepines) to interfere with the acquisition and
solidification of memory.
• 40% of drinkers have at some time had a blackout.

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TREMORS

• Commonest, associated with general weakness, nausea and irritability

• Mild forms – occur after a single night’s abstinence and after a period
of drinking for ony several days.
• Severe forms – 12-24hrs after stopping, only after continuous weeks
of drinking.
• Subsides over several hours or days but after severe attacks may take
1-2wks

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ALCOHOLIC SEIZURE (‘RUM FITS’)
• Generalised tonic clonic seizures occur in about 10% of alcohol
dependence patients, usually 12-48 hours after a heavy bout of
drinking. Often these patients have been drinking alcohol in large
amounts on a regular basis for many years.
• Multiple seizures (2-6 at one time) are more common than single
seizures. Sometimes, status epilepticus may be precipitated. In about
30% of the cases, delirium tremens follows.

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DELIRIUM TREMENS
• Delirium tremens (DT) is the most severe alcohol withdrawal
syndrome. It occurs usually within 2-4 days of complete or significant
abstinence from heavy alcohol drinking in about 5% of patients, as
compared to acute tremulousness which occurs in about 34% of
patients.
• Characterised by vivid hallucinations, delusions, profound confusion,
tremor, agitation, and sleeplessness.
• The course is short, with recovery occurring within 3-7 days. This is an
acute organic brain syndrome

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ALCOHOLIC HALLUCINOSIS
• Alcoholic hallucinosis is characterised by the presence of
hallucinations (usually auditory) during partial or complete
abstinence, following regular alcohol intake. It occurs in about 2% of
patients.
• These hallucinations persist after the withdrawal syndrome is over,
and classically occur in clear consciousness. Usually recovery occurs
within one month and the duration is very rarely more than six
months.

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WERNIKE’S ENCEPHALOPATHY
This is an acute reaction to a severe defi ciency of thiamine, the
commonest cause being chronic alcohol use. Characteristically, the
onset occurs after a period of persistent vomiting. The important
clinical signs are:
• Ocular signs: Coarse nystagmus and ophthalmoplegia, with bilateral
external rectus paralysis occurring early. In addition, pupillary
irregularities, retinal haemorrhages and papilloedema can occur,
causing an impairment of vision.
• Higher mental function disturbance: Disorientation, confusion, recent
memory disturbances, poor attention span and distractibility are quite
common. Other early symptoms are apathy and ataxia.

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KARSAKOFF’S PSYCHOSIS
• Described by Korsakoff in 1887, named as psychosis polyneuritica
• As Korsakoff’s psychosis often follows Wernicke’s encephalopathy;
these are together referred to as Wernicke-Korsakoff syndrome.
• Clinically, Korsakoff’s psychosis presents as an organic amnestic
syndrome, characterised by gross memory disturbances, with
confabulation. Insight is often impaired.
• The underlying cause is believed to be usually severe untreated
thiamine deficiency secondary to chronic alcohol use.

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MARCHIAFAVA-BIGNAMI DISEASE
• This is a rare disorder, formerly thought to be restricted to Italian
males and vine consumption which is characterised by disorientation,
epilepsy, ataxia, dysarthria, hallucinations, spastic limb paralysis, and
deterioration of personality and intellectual functioning.
• The cause is probably an alcohol-related nutritional deficiency.

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PERIPHERAL NEUROPATHY
• Caused by thiamine deficiency with pyridoxine and pantothenic acid
deficiency, neurotoxic effect of alcohol, toxins in beverages
• Usually present with sensory disturbances – numbness, burning
sensation in feet

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ALCOHOLIC DEMENTIA
• Alcoholic dementia or alcoholic related dementia is a severe form of
alcohol related brain damage caused by many years heavy drinking, it
can lead to dementia like symptoms, including memory loss, erratic
mood and poor judgment.

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MANAGEMENT
• HISTORY
Detailed history from the patient/family members, regarding the
symptoms, and past history.
Age of onset of drinking
Age at which the patient develop psychiatric disorder
Period of abstinence
Rule out organic causes and independent psychiatric disorders

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INVESTIGATIONS
• Biological investigations include;
Liver function test (LFT)
Renal Function test (RFT)
Electrolytes
Blood sugar
Urine drug analysis/blood alcohol concentrations
ECG, ECHO, CXR
Lumber puncture and CSF analysis
CT/MRI/EEG/SPECT/PET
Breath analyser
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INVESTIGATION CONTI…
• Psychological investigations
MAST ( Michigan Alcoholism Screening Test)
CAGE questionnaire
Alcohol use disorders identification test (AUDIT)

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ALCOHOLISM SCREENING TOOL

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SOCIAL INVESTIGATIONS
• Assessment of social support system.
• Assessment of current and past social, interpersonal and occupational
functioning.

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TREATMENT
BIOLOGICAL TREATMENT
• Intoxication- acute episode/severely intoxicated; patients should be
observed closely
• Alcoholic coma- managed in hospital, rule out head injury,
hypoglycaemia and other complication of alcohol, maintain airway,
breathing and circulation
• Aggression- sedation with antipsychotic/benzodiazepines
• Withdrawal- watch for withdrawal symptoms use long acting
sedatives
• Complications- admission, sedatives titrated according to symptoms
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BIOLOGICAL TREATMENT CONTI…
• Delirium – adequate fluid replacement, and sedation.
• Wernicke’s encephalopathy which is an acute medical emergency –
IV/IM infusion of large doses of thiamine (200-300mg) slowly over
10mins twice daily for a period of minimum 5days and oral thiamine
for several months
• Karsakoff’s syndrome – high dose of thiamine replacement by
parenteral route followed by oral for many months
• Peripheral neuropathy – vitamin supplementation
• Alcohol induced psychotic disorder – no treatment required,
spontaneously remits on abstinence
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DETERRENT AGENTS
• The deterrent agents are also known as alcohol sensitising drugs.
• Disulfiram (tetraethyl thiuram disulfi de) was discovered in 1930s, when
it was observed that workers in the rubber industry developed
unpleasant reactions to alcohol intake, due to accidental absorption of
antioxidant disulfiram
• When alcohol is ingested by a person who is on disulfiram, alcohol-
derived acetaldehyde cannot be oxidised to acetate and this leads to an
accumulation of acetaldehyde in blood. This causes the important
disulfiram-ethanol reaction (DER) characterised by flushing, tachycardia,
hypotension, tachypnoea, palpitations, headache, sweating, nausea,
vomiting, giddiness and a sense of impending doom associated with
severe anxiety
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MODE OF ACTION OF DISULFIRAM

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OTHER DETERRENT AGENTS
• Citrated calcium carbimide (CCC): The mechanism of action is similar
to disulfiram but onset of action occurs within 1 hour and is
reversible. The usual dosage is 100 mg/d in two divided doses.
• Metronidazole.
• Animal charcoal, a fungus (Coprinus atramen - tarius), sulfonylureas
and certain cephalosporins also cause a disulfiram like action.

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ANTI-CRAVING AGENTS
• Acamprosate (the Ca++ salt of N-acetyl-homo taurinate) interacts
with NMDA receptor-mediated glutamatergic neurotransmission in
the various brain regions and reduces Ca++ fluxes through voltage-
operated channels.
• Naltrexone (oral opioid receptor antagonist) probably interferes with
alcohol-induced reinforcement by blocking opioid receptors.
• Fluoxetine (and other SSRIs) have been occasionally used as anti-
craving agents in their usual antidepressant doses.

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PSYCHOLOGICAL TREATMENT
• Behavioural therapy: covert sensitisation, relaxation techniques,
assertiveness training, selfcontrol skills, and positive reinforcement
have been used alone or in combination with aversion therapy.
Currently, in most settings, it is considered unethical to use aversion
therapy for the treatment of alcohol dependence.
• Psychotherapy: Both group and individual psychotherapy have been
used. The patient should be educated about the risks of continuing
alcohol use, asked to resume personal responsibility for change and
be given a choice of options for change. Motivational enhancement
therapy with or without cognitive behaviour therapy and lifestyle
modification is often used
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• Group therapy: Of particular importance is the voluntary self-help
group known as AA ( Alcoholics Anonymous), with branches all over
the world and a membership in hundreds of thousands. Although the
approach is partly religious in nature, many patients derive benefits
from the group meetings which are non-professional in nature.

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CONCLUSION
• The role of the psychiatrist is not only to manage the treatment of
withdrawal symptoms of alcoholic disorders and prevention of relapse
but also to treat the associated complications, especially
neuropsychiatric as they cause severe impairment and socio-
occupational dysfunction.
• Goal should be aimed at a better symptom free life for the patient
which not only improves the work performance but also may act to
prevent relapse.

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REFERENCES
• Anderson, P. (2006) global use of Alcohol, Drugs and Tobacco. Drug and Alcohol Review,
25, 489-502 http//doi.org10.1080/09595230600944444
• Wang, Y.P. and Andrade, L.H. (2013) Epidemiology of Alcohol and Drug use in the elderly
current opinion in Psychiatry, 26, 343-348. http//doi.org/10.1097/YCO. Obo13328360
• Edenberg, H.J. the genetic of Alcohol Metabolism: Role of Alcohol dehydrogenase variant.
Alcohol Research and Health 30(1):5-13, 2007. PMID: 17718394
• Vonlaufen, A., Wilson, J.S; Pirola, R.C.; and Apte, M.V. Role of Alcohol Metabolism in
Chronic pancreatitis. Alcohol Research and Health 30 (1): 48-54 2007, PMID:177184401
• Okonoda, K.M., James B.O., Piwuma C.G., Envuladu E.A., Alochol use disorders and
associated factors among elderly community sample in Nigeria. A cross sectional survey.
Open Journal of Psychiatry. Vol. 10 No. 3, July 2020.
• World Health Organisation. The ICD10 Classification of Mental and Behavioural disorders,
Clinical descriptions and diagnostic guidelines. World Health Organisation, Geneva, 1992.
• Niraj Ahuja, A short Textbook of Psychiatry, Seventh Edition, Jaypee, 2011.

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