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Anyone working in the field of drinking problems must cultivate an awareness of the range of psychiatric disorders that may result from or lie behind the drinking. Very serious issues will otherwise be overlooked. Similarly, a lack of appreciation about the impact of alcohol and other substances on mental state may also result in substance misuse being ignored. Psychiatric disorders occur more commonly in individuals with drinking problems (and other substance use disorders [SUDs]) than in the general population. Although the term “dually diagnosed” is sometimes used to describe such individuals, they often have multiple problems; for example, alcohol and drug misuse, one or more psychiatric disorders, and physical health, behavioural, forensic, and social problems.
The aetiology of comorbidity is most likely to be multifactorial and due to an interaction between biological, psychosocial, environmental, and personality factors. Many psychiatric symptoms experienced by problem-drinking individuals are directly related to intoxication and/or withdrawal and will disappear with extended abstinence. At the same time, heavy alcohol consumption and dependence can also put individuals at increased risk for developing a psychiatric disorder (e.g., major depression) that persists even if abstinence is attained. In the same fashion, individuals with psychiatric disorders may be vulnerable to developing an alcohol or drug use disorder that has a life of its own. Drinking problems and psychiatric disorders may also co-occur independently. Comorbidity complicates treatment and prognosis and poses significant challenges to mental health services as well as primary care services. Clinicians are best able to meet these challenges when they focus on assessing the needs and problems of the patient rather than focusing solely on the diagnostic category(ies) into which they have been classified.
Clinical samples have higher prevalence rates of comorbidity than community samples because the presence of the comorbid disorder increases the likelihood of help-seeking. Indeed, comorbid individuals may seek help for a psychiatric symptom or disorder rather than their alcohol problems. They may not acknowledge or even realize that their alcohol consumption is contributing to their difficulties.
Epidemiology
The U.S. National Comorbidity Survey (Table 6.1) indicated that individuals with a lifetime history of an alcohol use disorder (AUD) have a higher risk of a mental health disorder and vice versa (Kessler, Crum, & Warner, 1997; Kessler et al., 1994). The 10-year follow-up of this study revealed that mood disorders and many anxiety disorders (panic, specific and social phobia, post-traumatic stress disorder [PTSD], separation anxiety) were predictive of developing subsequent substance dependence, with a particularly strong association with bipolar disorder (Swendsen et al., 2010). Notably, these psychiatric disorders had negligible to moderate impact on the risk of starting drinking or of “alcohol abuse” (in the nomenclature of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders [DSM-IV]), but did increase the likelihood of a problem-drinking individual transitioning into alcohol dependence.
| Psychiatric Disorder | Individuals with Alcohol Dependence | |||
|---|---|---|---|---|
| Men | Women | |||
| (%) | OR | (%) | OR | |
| Anxiety | 35.8 | 2.2 | 60.7 | 3.1 |
| Mood | 28.1 | 3.2 | 53.5 | 4.4 |
| Drug dependence | 29.5 | 9.8 | 34.7 | 15.8 |
| Antisocial personality | 16.9 | 8.3 | 7.8 | 17.0 |
The evidence for lifetime comorbidity was stronger for alcohol dependence than for alcohol abuse, and comorbidity was more likely to occur in women than in men. The predominant comorbid disorders among men were other substance use disorders, conduct disorder, and antisocial personality disorder. Anxiety and affective disorders were the main contributors to comorbidity in women. The National Epidemiologic Survey on Alcohol Problems and Related Conditions (NESARC) in the United States found that, among individuals with AUDs (alcohol abuse and dependence) seeking treatment, 40.7 percent had at least one recurrent independent mood disorder and 33 percent had at least one current independent anxiety disorder (Grant et al., 2004). NESARC also revealed that transition from abuse to dependence occurs in 26.6 percent of individuals with alcohol abuse, mostly within about 3 years. Similar to the National Comorbidity Survey findings, NESARC data showed that a history of any mood, psychotic, or personality disorder showed an increased risk of transition to dependence on alcohol.
As the proportion of older people grows in the population, it becomes increasingly important to understand problem drinking and comorbidity among the elderly. Findings in younger adults may not generalize to older adults. For example, in NESARC participants aged 60 or older, substance use disorders did not predict incident mood or anxiety disorders, unlike for whole sample (Hasin & Kilcoyne, 2012). Researchers have less information on substance misuse and psychiatric disorders in late life than would be optimal. The National Comorbidity Survey, for instance, did not enroll older adults. Alcohol appears to be the main substance misused in mid to late life, with increasing use of prescribed opioids and benzodiazepines often co-occurring (Crome et al., 2011; Wu & Blazer, 2014).
There are gender differences in comorbidity patterns. Alcohol dependent women are at higher risk than alcohol dependent men for most externalizing disorders. On average, alcohol dependence remits earlier in women despite lower treatment utilization than men (Khan et al., 2013).
Psychiatric comorbidity also affects whether individuals attempt to quit drinking and whether they succeed. In the NESARC study, about 10 percent of those with alcohol abuse and 18 percent with alcohol dependence tried to quit in a 3-year period (Chiappetta, García-Rodríguez, Jin, Secades-Villa, & Blanco, 2014). Of these individuals, about a third were successful. Quit attempts were more likely in those who were single, younger than 40 years, of low income, and who had a co-occurring psychiatric disorder and greater number of dependence symptoms. A greater severity of dependence, a greater number of psychiatric disorders, and a substance use disorder (including tobacco use disorder) decreased the likelihood of a quit attempt being successful.
Epidemiological studies conducted outside the United States generated results similar to NESARC and the National Comorbidity Survey. The British Psychiatric Morbidity Survey (Farrell et al., 2001) showed that individuals with nicotine, alcohol, and drug dependence had an increased risk of psychiatric morbidity compared with the nondependent population (Table 6.2). Most users of drug and alcohol services also experience mental health problems. In Australia, 18 percent of those with an AUD had an affective disorder, 15 percent had an anxiety disorder, and 17 percent had another drug use disorder (DUD). Looked at from the other direction, 16 percent of those with depression, 24 percent with PTSD, and 37 percent of those with a cannabis use disorder had an AUD (Burns, Teeson, & Lysnkey, 2001).
| Nondependent population (%) | Nicotine-dependent population (%) | Alcohol-dependent population (%) | Drug-dependent population (%) | |
|---|---|---|---|---|
| No disorder | 87.5 | 77.0 | 69.4 | 52.9 |
| Mixed anxiety disorder | 6.2 | 10.2 | 9.9 | 16.3 |
| Generalized anxiety disorder | 2.4 | 4.1 | 5.3 | 7.3 |
| Depression | 1.2 | 3.7 | 7.3 | 9.1 |
| Phobia | 0.8 | 1.5 | 1.0 | 5.4 |
| Panic disorder | 0.5 | 1.5 | 2.7 | 2.5 |
There are two broad categories of co-occurring psychiatric problems: (1) alcohol-induced disorders such as hallucinations, delirium, and delusions; and (2) common comorbid diagnoses such as depression, anxiety disorders, and the like. These will be discussed in turn. This section of the book should be considered a supplement to some of the material presented in Chapter 5 (e.g., regarding Wernicke–Korsakoff syndrome).
Alcohol-induced disorders
Transient hallucinatory experience
Transient hallucinatory experience deserves note for two reasons. First, it may herald the onset of delirium tremens (DTs) or alcoholic hallucinosis, and it can often give early warning of the likelihood of these much more serious illnesses. It may therefore be viewed as continuous with those states, rather than an altogether discrete clinical entity. Second, it is important to be aware that transient hallucinations may occur without the illness progressing to either of the major presentations. The diagnostician who is unfamiliar with these transient phenomena may be tempted to record incorrectly that the patient has “suffered from DTs” when this was not the case. Whether other drug use could have contributed should also be carefully assessed.
The essence of this condition is that the patient fleetingly and suddenly experiences any one of a variety of perceptual disturbances, often very much to their surprise and consternation, and with the episode then immediately over. These occurrences may be experienced during periods of continued, heavy, and chaotic dependent drinking or during withdrawal. There is no delirium or evidence of severe physiological disturbance as seen in DTs. Here are some examples of how patients described such experiences:
I would be walking down the road and, ZOOM, a car would come up behind me and I’d jump on the pavement. Frightened out of my life. But it was all imagination.
What used to happen was that I would turn around thinking someone had called my name.
The degree of insight is often characteristic; the patient immediately disconfirms the reality of the hallucination. A relatively stereotyped and limited kind of hallucinatory experience is also typical; for one patient, it is nearly always the car coming up from behind, for another a pigeon flying into the room. It is important to realize that some patients can experience such discomforting happenings for many months without progressing to a major disturbance. The meaning and significance of “continuity” will immediately become clear as we go on to discuss DTs and alcoholic hallucinosis.
Delirium tremens
DTs is a short-lived toxic confusional state that usually occurs as a result of reduced alcohol intake in alcohol dependent individuals with a long history of use (World Health Organization, 1992). It can produce a range of clinical pictures, but it is best viewed as a unitary syndrome with a continuum of severities and a variation in symptom clustering. The disturbance is often fluctuating, with the patient’s condition worsening in the evening or when the room is unlit and shadowy. The classical triad of symptoms includes clouding of consciousness and confusion, vivid hallucinations affecting any sensory modality, and marked tremor. Delusions, agitation, sleeplessness, and autonomic arousal are frequently also present.
Symptoms of delirium usually occur from about 24–150 hours after the last drink although typically peaking between 72 and 96 hours. Prodromal symptoms are usually evident but may be overlooked. The onset is often at night with restlessness, insomnia and fear:
A 65-year-old widower was admitted to a general hospital via ambulance following a period of heavy drinking. On admission, he was written up for one dose of chlordiazepoxide (25 mg orally). A reducing dose was not commenced, even though the nursing and medical staff were aware that he had an alcohol problem. During the first 2 days of admission he was “pleasantly confused.” On the third day, he went into the nursing office where he saw a nurse “organizing patients into groups.” He suddenly realized that this meant everyone had to be evacuated because of a bomb scare. He left the ward in his pyjamas and bare feet and walked out of the hospital into a busy street, shouting that the hospital was in danger. He was duly found, returned, and reassured by nursing staff. Ten days later, he had a hazy recall of the event: “I knew it wasn’t true, and yet I experienced a mounting and inexplicable fear and felt that I had to escape. Since then nothing extraordinary has happened.”
Delirium
In delirium, the patient is more or less out of contact with reality and potentially disoriented as to person, place, and time. For instance, the patient may believe that they are cruising on a liner, mistake the nurse for a steward, and order a drink, but 5 minutes later, the patient knows that they are in a hospital and can correctly identify the people around them.
Hallucinations
Hallucinations are characteristically vivid, chaotic, and bizarre and occur in any sensory modality – the patient may see visions, hear things, smell gases, or feel animals crawling over them. The classical visual hallucinations are vivid and horrifying and typically include snakes, insects, rats, and other small animals that may appear to attack the patient as they lie in bed. They may also take a “microscopic” form (small furry men dancing on the floor), but any type of visual hallucination can occur. Patients often become completely preoccupied by and interact with the hallucinated objects. Thus, they brush away the spiders or argue with the little men.
Hallucinatory voices or bursts of music may be heard, or the threatening screams of animals. Hallucinations are often based on a ready tendency to illusional misrepresentation: the wrinkles in the bedclothes become snakes, patterns in the wallpaper become faces.
Tremor
As the illness develops, the patient becomes anxious and more fearful and develops tremor. At worst, the patient may shake so severely that the bed rattles, but, as with other symptoms, there can be a continuum of severity, and the tremor may not be very noticeable unless the patient is asked to stretch out their hands.
Fear
The patient may experience extremes of horror in reaction, for instance, to the snakes writhing all over their bed. But fearful reactions are not universal: on other occasions, the hallucinations may be enjoyable or entertaining, as if the patient is happily watching a private cinema show.
Paranoid delusions
The illness often has a degree of paranoid flavouring: enemies are blowing poisonous gas into the room, assassins lurk at the window, and there is a nameless conspiracy afoot. The mood can in fact be paranoid, with every happening and stimulus being misrepresented as it comes along, but the patient’s mental state is too muddled for the delusional ideas to become systematized.
Occupational delusions or hallucinations
The barman, for instance, may believe that he is serving in his cocktail bar and pour out imaginary drinks. The bricklayer may be building an imaginary wall.
Restlessness and agitation
Partly as a consequence of the fearfulness of the hallucinatory experiences, the patient is often highly restless, clutching and pulling at the bedclothes, starting at any sound, or attempting to jump out of bed and run down the ward. This overactivity, when combined with a degree of weakness and unsteadiness, can put the patient seriously at risk of falls and other accidents.
Heightened suggestibility
The patient who is suffering from DTs can show a heightened susceptibility to suggestion, which occasionally becomes evident spontaneously but may only come out on testing. The older textbooks often mention such stories as the patient agreeing to deal from an imaginary pack of cards or “drinking” from a proffered empty glass.
Physical disturbances
Heavy sweating is typical. Appetite is usually lacking, the pulse is rapid, the blood pressure is likely to be raised, and the patient feverish. If the illness continues over many days, the picture gradually becomes that of dehydration, exhaustion, and collapse, with the possibility of a sudden and disastrously steep rise in temperature.
Aetiology and course
DTs is today generally viewed as essentially an alcohol withdrawal state, even though other factors, such as infection or trauma, sometimes play an ancillary role. The withdrawal state precipitating the attack may have been occasioned by admission to hospital, arrest and incarceration, or a self-determined effort to give up drinking. Often, though, there is no history of abrupt withdrawal, and the illness starts while the patient is still drinking, although there has probably been at least partial withdrawal. In some instances, the patient seems to have hovered on the brink of DTs for many preceding weeks, with much evidence of transient hallucinatory experience; in other instances, the illness has a more explosive onset. It is unusual for a patient to experience DTs without a history of at least several years of severe alcohol dependence and many years of excessive drinking, but an attack may occur even after 1 or 2 weeks if a previously abstinent patient rapidly reinstates dependence. Recurrent attacks are common once a patient has had one such episode.
The condition usually lasts for 3–5 days, with gradual resolution. On rare occasions, the illness drags on for some weeks, fluctuating between recovery and relapse. The possibility of severe physical complications has been mentioned, and, before the advent of antibiotics, intercurrent chest infection or pneumonia constituted serious risks. Reported mortality rates have varied from centre to centre and even with skilled care a degree of risk remains, with death occurring in 1–4 percent of hospitalized patients (Schuckit, 2014). Death is typically due to cardiovascular collapse, hypothermia, or intercurrent infection.
Possibilities of diagnostic confusion
DTs may seem so vivid and distinct as to make diagnostic mistakes unlikely. But there is always the possibility that an underlying condition, which is contributing to the picture, is being overlooked. Liver failure, pneumonia, and head injury should always be borne in mind. Confusion may also occur when the possibility of DTs is entirely overlooked, although in retrospect the diagnosis was plainly evident. This is often the case in the setting of a general hospital ward, where the patient is noted to be suffering from “confusion,” to be “rambling a bit,” or trying to get out of bed at night. In this situation, the condition may be put down to the nonspecific effects of infection, trauma, or an operation. The diagnosis is at times overlooked in the psychiatric hospital setting when it may be misdiagnosed as an “acute schizophrenic reaction”; for instance, when the acutely disturbed person with DTs has florid paranoid ideas, is found running up the street with a knife in their hand, and presents as an emergency admission from the police.
The following predict DTs during alcohol withdrawal: scores above 15 on the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA)-Ar scale (see Chapter 11), particularly in association with cardiovascular disturbance (systolic blood pressure >150 mm Hg, pulse rate >100 beats per minute), recent withdrawal seizures (seen in 20 percent of individuals with delirium), prior withdrawal delirium or seizures, older age, recent misuse of other depressant agents, and concomitant medical problems (Schuckit, 2014).
In addition, patients may describe having had DTs but on closer questioning describe only “real bad shakes and sweats.” It is therefore important to clarify their understanding of DTs.
The treatment of DTs is outlined in Chapter 11.
Alcohol-induced psychotic disorder
Alcohol-induced psychotic disorder, which includes alcoholic hallucinosis, is a comparatively rare disorder with auditory or visual hallucinations occurring either during or after a period of heavy alcohol consumption (Glass, 1989a, 1989b; Tsuang, Irwin, Smith, & Schuckit, 1994). The hallucinations are vivid, of acute onset, and typically occur in the setting of clear consciousness, which makes them different from DTs. They may be accompanied by misidentifications, delusions, ideas of reference, and an abnormal affect. Alcohol-induced psychotic disorder typically resolves over a period of weeks but can occasionally persist for months. DTs and other psychotic disorders (including those related to other psychoactive substances) must be ruled out before a diagnosis of alcohol-induced psychotic disorder can be made.
In alcohol-induced psychotic disorder, the auditory hallucinations may consist of unformed noises or snatches of music but usually take the form of voices. These voices may be talking to the patient directly, but more often they take the form of a running commentary about the patient. Sometimes there is only one voice, but often several engage in discussion, and the same voice may come back again on different occasions. The commentary may be favourable and friendly but is usually accusatory, threatening, or involves jealousy. Sometimes the voices command the patient to do things against their will, and this may result in acting-out behaviour or a suicide attempt. There is a lack of insight, and the voices are considered as real, but the patient will seldom elaborate any complex explanation as to the supposed mechanism by which the voices are reaching them. The voices may come and go or haunt the patient more or less incessantly.
Alcohol-induced psychotic disorder is almost certainly not a form of latent schizophrenia. Nevertheless, it may superficially resemble acute paranoid schizophrenia, and the differential diagnosis may be difficult. The delusions associated with alcohol-induced psychotic disorder are usually attempts to explain the hallucinations. There is no evidence of a complicated delusional system, thought disorder, incongruity of affect, or negative symptoms, and insight is regained as the voices diminish (Lishman, 1998).
Although these guidelines provide useful indications, in practice, it can still be difficult to make the distinction, and, in such circumstances, the sensible course of action is to admit the patient to the hospital, withdraw the patient from alcohol, and observe what happens. Remission may take place abruptly, but more often there is a slow fading of the symptoms. The voices become less persistent, do not make such an urgent demand on attention, and their reality begins to be doubted. Prognosis is generally good, but 10–20 percent may have a chronic schizophrenic-like course. The possibility that the illness will finally declare itself to be schizophrenia has, of course, also to be borne in mind. If symptoms have not ceased within a couple of months, the latter diagnosis becomes more likely, although it has been reported that alcohol-induced psychotic disorder may sometimes require up to 6 months for complete recovery. Some drug intoxications, including most notably amphetamine psychosis, can also result in a picture mimicking alcohol-induced psychotic disorder; with a presentation of this sort, it is always wise to carry out urine testing for drugs.
Alcoholic blackouts (alcohol-induced amnestic episodes)
The widely used but somewhat confusing lay term “alcoholic blackout” refers to transient memory loss that may be induced by intoxication (i.e., alcohol-related amnesia). There is no associated loss of consciousness. As described, the blackout may be related to a hyperglutamatergic state (see Chapter 2) and therefore may indicate the severity of impact that alcohol is having on brain function. Indeed, it may be thought of as the brain’s equivalent of liver function tests. Clinicians should not enquire simply whether the patient has had a blackout and leave it at that. It is preferable to ask “Have you ever forgotten things you did while drinking?” Although such occurrences are reported in some two-thirds or more of alcohol dependent individuals, alcoholic memory blackouts are also relatively common in social drinkers after drinking too much, too fast. Approximately one-third of young men in the general population are likely to have experienced memory blackouts (Goodwin, Crane, & Guze, 1969a). Thus, although blackouts are an important warning sign of problem drinking, they are not necessarily pathognomonic of alcohol dependence.
Blackouts have been described as being of two types (Goodwin, Crane, & Guze, 1969a, 1969b). The en bloc variety is characterized by a dense and total amnesia with abrupt points of onset and recovery and with no subsequent recall of events for the amnesic period, either spontaneously or with prompting. This period may extend from 30 to 60 minutes up to as long as 2 or 3 days. In contrast, “fragmentary” blackouts or “greyouts” are patchy episodes of amnesia, with indistinct boundaries and islands of memory within these boundaries. They are often characterized by partial or complete subsequent recall and usually extend over a shorter period than the en bloc variety. In reality, alcoholic memory blackouts can occur with every degree of gradation, and although it is useful to recognize the two types, the experience of each patient has to be described separately.
Blackouts may begin to occur at a late stage in a career of excessive drinking or never at all. Once they start to be experienced with any frequency, they tend to recur, and a patient may often be able to identify the phase at which they “began to get bad blackouts.” The reason for such varied susceptibility to the disorder is unknown, but blackouts are associated with an early onset of drinking, high peak levels of alcohol, and a history of head injury. Concurrent use of sedatives and hypnotics may increase the likelihood of amnesia. Blackouts are not predictive of long-term cognitive impairment.
During an alcoholic blackout, the individual can engage in any type of activity. To the observer, the drinker will not obviously be in an abnormal state of mind (other than being intoxicated), although a spouse or someone else who knows them well may claim to recognize subtle changes – for instance, “they get that glazed look.” Patients sometimes report that during an alcohol blackout period they wandered away from home, later “waking up” in a strange place. Here is an example:
When I came round I was sitting in a barber’s chair having a shave. Hadn’t a clue where I’d got to this time, terribly embarrassed, didn’t like to ask. I had to go outside and look at the shop signs until I found the answer, and then to my amazement I discovered I was in this town 150 miles from home. To this day, I don’t know how I got there. That was the worst experience of this kind, but time after time I woke up in strange places or found myself sitting on a train going to the coast.
Blackouts and their significance to the patient
One patient may mention blackouts only on direct questioning and appear untroubled about such experiences, whereas another patient may deem blackouts a leading reason for seeking help. Blackouts for that type of patient are often a matter of dread with, for instance, recurrent anguished fear that they may have hurt or killed someone while driving home; they do not remember getting their car into the garage the previous night, and they go out in the morning fearfully to check the paint work.
Alcohol-related brain damage and cognitive impairment
The question often arises as to whether the patient with a drinking problem is suffering from “brain damage” or cognitive impairment. In some individuals, it is immediately apparent that they are having difficulty giving accurate information about themselves and their drinking history. It is then important to determine if any impairment is due to Wernicke’s encephalopathy, which is a medical emergency requiring immediate treatment, or is due instead to acute effects of alcohol consumption:
A 53-year-old man comes into a drop-in session at the local alcohol treatment centre on and off over a number of weeks. Although he sees his drinking as “a bit heavy,” he is not particularly interested in stopping. Nevertheless, his support worker helps him make some reductions in his drinking although it is obvious that his main motivation for attending is to get help with filling in application forms for better-quality housing. Over the weeks, his support worker concludes that the man has poor reading and writing skills and attributed him forgetting their previous conversations to his current drinking. However, on one occasion, the man attended confused, unsteady on his feet, and not smelling of alcohol. A medical assessment confirmed Wernicke’s encephalopathy, and a medical admission was arranged for treatment with intravenous thiamine.
A familiar scenario, however, is that of alcohol-related brain damage (ARBD) and is discussed more fully in Chapter 5 in relation to the physical damages that can result from drinking. Much the same sort of picture is seen when the patient is developing a dementia for any other reason (presenile dementia, for instance, or senile or multi-infarct dementia). The patient with ARBD will typically give a history of many years of heavy drinking with ultimate development of brain damage. With dementia due to other causes, the sequence of events is the other way round: the patient develops dementia and, as a result of the ensuing disinhibition and personality deterioration, becomes involved in drinking.
The fact that brain damage can be a cause as well as a consequence of drinking needs to be written into any diagnostic checklist. In addition to brain damage due to degenerative processes such as those already mentioned, the significance of a history of brain injury deserve particular attention. Instances occur when personality change as a sequel to head injury is disproportionate to any fall-off in intellectual functioning, and this type of personality change may, for instance, result in drinking problems as a late sequel of a road accident. The following brief case extracts show some of the many possible organic relationships that should be on that checklist:
A 48-year-old career civil servant of previously unblemished record suffered a subarachnoid haemorrhage (a bleed into the space around the brain). The leaking blood vessel was operated on, and she felt she had “recovered completely.” But she had, in fact, sustained a degree of brain damage. Work habits, which had for a lifetime been almost overmeticulous, now deteriorated, and she was found to be drinking secretly in the office.
A divorced woman of 60 presented with alcohol dependence, seemingly of recent onset. Over the past few months, friends had also noticed that she seemed increasingly unhappy and irritable but put this down to her son and family moving away. They realized something was wrong when, on a night out, she acted out-of-character by being very flirtatious with the waiter and attempted to grab him. She was found to have a brain tumour.
Some of these case histories illustrate only rather rare associations, and the precise part that brain damage played in the aetiology of the drinking is in some instances difficult to establish. However, the general picture, which is being built up by listing these diverse cases, is valid and important. Some associations between brain damage and alcohol dependence are relatively common (personality deterioration following head injury, for example), whereas others, such as tumour, are rare; the general message has to be stressed that no diagnostic assessment is complete without thinking about the possible significance of brain involvement. Alcohol dependence can also supervene as a complication of learning disability of any origin.
Whatever the underlying brain syndrome associated with alcohol dependence, the clinical features can be grouped under a number of headings. There are, of course, first the primary symptoms of the brain damage itself. Features of the drinking problem will also stand in their own right, but it is the interaction of the underlying brain damage and the drinking that gives these cases their colouring. Personal and social deterioration may seem to be disproportionate to the drinking or suddenly to have accelerated. Drunken behaviour when there is underlying brain damage often appears to be particularly heedless of consequences or antisocial. There may be increasing episodes of violence, or the patient sets their lodgings on fire. There is also an increased sensitivity to alcohol; the patient gets drunk on less drink, and, with relatively little alcohol, becomes disinhibited or begins to fall about.
Given proper alertness to the possibility of such underlying problems, what, then, are the practical implications? If involvement of an underlying brain condition is in any way suspected, appropriate neurological and psychological investigations need to be carried out with a sober patient, which may require hospital admission. The sad fact is that most of the possibly relevant brain conditions are going to prove more diagnosable than treatable. Even so, an accurate diagnostic formulation is the necessary basis for working out what is best to be done. If, for instance, an individual with alcohol dependence is severely cognitively impaired, the only kind and safe policy may be to propose care in a supportive residential community. If there is milder impairment, the patient will be able to keep going outside an institution, but they may be more likely to drink alcohol, and further troubles are probably to be expected. The continuing treatment plan must be set up to meet these sorts of eventualities and be designed to support the family in what may well be a difficult situation. The emphasis may sometimes have to be placed on directive intervention, such as ensuring that money is properly handled or that local pub owners will not serve the person drinks. But, even here, there is no cause for absolute pessimism because sometimes a patient with significant cognitive impairment will be able to stop drinking, the progression of such damage will be arrested, and the patient’s behaviour will improve.
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