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Alcohol misuse disorders

Acute intoxication The symptoms of alcohol intoxication will vary depending on the blood alcohol concentration (BAC), individual alcohol tolerance, and to some extent the setting in which the alcohol is taken. In general, as BAC rises from mild intoxication (BAC <100mg%) to moderate intoxication (BAC 100–200mg%) to severe intoxication (BAC >200mg%) a characteristic syndrome of acute intoxication is observed. Initial symptoms are elevated mood, disinhibition, and impaired judgement, followed by slurred speech, unsteady gait, nystagmus, ataxia, aggressiveness, lability of mood and impaired concentration, and eventually sopor and coma.

At-risk drinking There are reported benefits to health (lowered risk of coronary artery disease and strokes) associated with low levels of alcohol consumption as compared with those who are abstinent (the ‘J-shaped curve’), though this remains a contentious area. Above this low level, health risks increase with increasing alcohol consumption. It is therefore arbitrary at which point drinking is considered ‘at risk’. Patient and situational factors are important (e.g. any alcohol consumption while driving or in pregnancy carries increased risks; for patients with established alcohol-related organ damage any consumption is risky).

Harmful drinking (DSM-IV—alcohol abuse) Non-dependent drinking which continues despite established harm to the patient’s physical or mental health secondary to the alcohol consumption. ICD-10 diagnosis considers only physical and mental health harm, not harm related to social sanction.

Alcohol dependence Harmful use of alcohol + established dependence syndrome (b p. 542). Usually daily, stereotyped drinking pattern with increased tolerance, withdrawal features on abstinence, and ‘relief drinking’ (i.e. further drinking to alleviate the effects of withdrawals).

Pathological intoxication (‘mania à potu’) This is a medically and legally disputed syndrome which was not included in DSM-IV due to

lack of empirical evidence. It is described as an idiosyncratic reaction to a small amount of alcohol characterized by severe agitation, belligerence, and violent behaviour followed by collapse, profoundly deep sleep, and amnesia for the events which followed the alcohol consumption. It is a dubious diagnosis which is mainly sought after by defence lawyers, as most legal systems do not regard normal self-induced intoxication as a valid defence. There is of course a strong association between alcohol and violent crime. Careful re-examination of the history will usually demonstrate that significant quantities of alcohol have been consumed.

Alcohol-induced amnesia (‘blackouts’ or ‘palimpsest’) This term refers to transient amnesic episodes related to periods of intoxication. Characteristically the patient will report a ‘gap’ in their memory lasting several hours with global or partial amnesia for their actions during that time. The patient’s behaviour as reported by witnesses is usually characteristic of their normal behaviour when intoxicated. This amnesia seems to be a failure of recall rather than initial registration and represents a reversible form of brain damage. Its occurrence is not predictive of longer-term cognitive impairment. It occurs in the later stages of a drinking career, if at all, and tends to recur once established. Two forms are described:

  • ‘En bloc’—dense amnesia with well demarcated start and finish points.
  • Partial—episodes with indistinct start and end point with islands of preserved memory and variable degrees of recall.

There is some degree of state-dependent recall in blackouts and a return to intoxication may aid recall. Because of the potential confusion of the term ‘blackout’ with periods of loss of consciousness, the term ‘alcoholic palimpsest’ is to be preferred.

Alcoholic hallucinosis This is a substance-induced psychotic illness (defined in ICD-10), which is a rare complication of prolonged heavy alcohol abuse. The sufferer experiences hallucinations—usually auditory—in clear consciousness and while sober. The auditory hallucinations may begin as elemental hallucinations (e.g. bangs or murmurings) before, with continued alcohol use, being experienced as formed voices, most usually derogatory in nature. There may be secondary delusional elaboration. The nature of hallucinations tends to worsen during periods of alcohol detoxification, and at times, when intoxicated with alcohol.

  • Differential diagnosis Transitory hallucinatory or illusionary experiences while intoxicated, delirium tremens, psychotic illnesses.
  • Course In 795% of patients there is rapid resolution of these symptoms on ceasing alcohol consumption but the symptoms rapidly recur on restarting drinking. In 75% there are prolonged symptoms (<6mths after abstinence) and an emergence of more typical schizophrenic symptomatology.
  • Management Persisting symptoms may be treated with antipsychotic medication (bearing in mind the medical comorbidities seen in this population).

Alcohol-induced psychotic disorder with delusions Long recognized, but only recently included in DSM-IV. Development of persecutory or grandiose delusions after long history of heavy drinking. No other features of delirium tremens. Resolves on abstinence.

Alcohol-related cognitive impairment/alcohol-related brain damage (ARBD)

The classification of alcohol-related cognitive impairment is unclear, with both ICD-10 and DSM-IV viewing it as a number of discrete entities, as opposed to a continuum. ICD-10 describes amnesic disorder (F10.6), dementia (F10.73), and other persisting cognitive disorder (F10.74), DSMIV-TR using the terms alcohol-induced persisting amnestic disorder and alcohol-induced persisting dementia. It is worth noting that the DSMIV-TR categories ignore the possibility of slow recovery over 1–2yrs in this patient group.

The majority (50–60%) of heavy drinkers display some degree of cognitive impairment on cognitive testing while sober. There is impairment in short-term memory, long-term memory recall, new skill acquisition, executive function, relative preservation of language ability and mildly impaired visuospatial function. IQ (measured by the WAIS) is generally preserved (in comparison with pre-morbid IQ, measured using the NART). CT/MRI examination of the brains of heavy drinkers reveals cortical and subcortical atrophy. White matter loss is prominent, which correlates with neuropathology findings. Degree of structural abnormality poorly correlated with degree of functional impairment. In all patients with alcohol-related brain damage (including those with ‘alcohol dementia’ and Korsakoff

syndrome), a significant amount of medical comorbidity is seen, including small vessel disease, repetitive head injuries, and comorbid alcohol liver disease. The neurotoxic effects of alcohol on the brain are exacerbated significantly by thiamine deficiency, and there is evidence to suggest earlier onset in women. Abstinence from alcohol use has been shown to correlate with functional improvement and MRI improvement at 1yr.

The term alcohol dementia is used at times, describing a generalized dementia syndrome, in which there is intellectual decline and more pronounced neuropsychological deficits. The changes correlate with total lifetime drinking and length of drinking history.

Wernicke–Korsakoff syndrome

This is a monosymptomatic delusional disorder (see b p. 220) seen most commonly secondary to current or previous alcohol abuse. The form is a primary delusion in which the content is that the patient’s spouse or partner has been or is being unfaithful. Delusional evidence may be provided to back up this belief and the patient may go to great lengths to obtain ‘evidence’ (e.g. following her, planting tape recorders, examining discarded clothing). There is a significant association with violence and even homicide towards the supposedly unfaithful partner.

Management

  • Abstinence from alcohol with addition of antipsychotic medication.
  • It may be necessary for the couple to separate and advice to this effect may have to be given to the at-risk partner.

Psychiatric comorbidity

Anxiety and depressive disorders Symptoms such as generalized anxiety, panic attacks, and low mood are very frequently reported in alcohol abusers. Many patients with alcohol problems also merit diagnoses of depressive illness (750%) or anxiety disorder (775%). The phenomenology of these disorders is similar to that found when the disorders occur in isolation. The difficulty is deciding the sequence of events, as in some cases the alcohol problem is secondary to the patient ‘self-medicating’ with alcohol in order to relieve primary anxiety or depressive symptoms. Nonetheless, chronic alcohol use will act as a direct depressant, its secondary effects will produce depressogenic life events (e.g. loss of job) and alcohol-related effects such waking at 04.00hr due to withdrawal, or weight loss related to nausea may masquerade as, or mask, biological depressive features.

Patients may emphasize the primacy of the mood or anxiety features and seek their resolution before tackling the alcohol problem. Generally a primary mood or anxiety disorder diagnosis should not be made in the presence of continuing alcohol misuse and psychological or pharmacological treatment for mood disorder is unlikely to be effective. The correct course is to initiate detox if indicated and to reassess mood/anxiety symptoms after 4wks of abstinence, treating residual symptoms at this point. Only a minority will require formal treatment. An undiagnosed depressive illness preceding the alcohol problem is more common in women. Alcohol problems can also arise as a result of self-medication of agoraphobia and social phobia.

Suicide Classically quoted as lifetime risk of 10–15% in dependent drinkers. Now estimated at 74% lifetime risk of suicide in those with alcohol problems. Psychiatric comorbidity is important, as is social isolation, physical ill health, and repeated failed attempts at abstinence.

Schizophrenia High rates of alcohol and substance use found in schizophrenic patients (750%). Increased risk of violence, EPSEs, TD, noncompliance, relapses, and rehospitalizations. Alcohol is an easily available temporary treatment for some of the distressing symptoms of psychotic illness.

Drug misuse Comorbid alcohol and drug misuse can be to enhance effects (e.g. euphoriant effect of alcohol and cocaine combined) or to minimize unpleasant side-effects (e.g. alcohol to relax after taking stimulants), or as a substitute when the primary drug is unavailable. Comorbid drug misuse is associated with poorer outcome. Some comorbidity can have an iatrogenic component where there is mixed abuse or substitution of BDZs for alcohol. This can result from inappropriate prescribing of anxiolytics, misdiagnosis of alcohol problems as anxiety disorders, and repeated unsupervised withdrawals with hoarding of tablets. Aim to limit new prescriptions, review diagnosis in patients with treatment-resistance anxiety disorders, and avoid short-acting BDZs (e.g. lorazepam).

Wernicke–Korsakoff syndrome

Wernicke encephalopathy and Korsakoff psychosis represent the acute and chronic phases of a single disease process—Wernicke–Korsakoff syndrome—which is caused by neuronal degeneration secondary to thiamine deficiency, most commonly seen in heavy drinkers.

Neurological Effects

  • Wernicke–Korsakoff syndrome (b p. 572).
  • Peripheral neuropathy.
  • Central pontine myelinolysis (pseudobulbar palsy + quadriplegia).
  • Marchiafava–Bignami disease (corpus callosum degeneration).
  • Cerebellar degeneration.
  • Optic atrophy.
  • Alcoholic myopathy.
  • Erectile problems.
  • Hypogonadism in men.
  • Foetal alcohol syndrome
  • Gout.
  • Osteoporosis.
  • Impaired absorption and diminished intake of specific vitamins and food overall.
  • Contribution to accidents, particularly RTA.
  • Exacerbating factor in violent crime and assaults.
  • Diminished compliance with treatment for other medical and psychiatric disorders.

Last Updated: 10 Dec 2024