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Diagnosing Co-Morbid Substance Use Disorders (SUDs)

Info: 5468 words (22 pages) Dissertation
Published: 12th Dec 2019

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What do the following have in common: alcoholism, obesity, smoking, drug abuse and compulsive gambling? Until recently, there were thought of as relatively independent and separate problem areas. Psychologists, psychiatrists, social workers, and other mental health professionals have previously specialised in the treatment of one of these behaviours, but few had attempted to extend their therapy and research efforts to cover more than one or two of these disorders. As well as their expertise, specialists in these areas have not worked in concert with one another, or communicated with each other about treatment and research issues. However, several changes have been induced in recent times with the concept of addictive behaviours, and this has led to possible commonalities among these seemingly diverse problems. There is also the increased awareness that workers in each of these areas have much to learn from one another, and that there may be significant and instructive similarities in aetiology, process and treatment.

The interesting similarity among the above mentioned problems has collectively come to be known as additive behaviours. According to Miller (1980) addictive behaviours involve some form of indulgence for short-term pleasure of satisfaction at the expense of longer-term adverse effects. The various substance abuse disorders all involve significant health risks as various chronic diseases. There are enormous social costs of addictive behaviours, both in personal expenditures as non-essentials and costs to the public as health care, crime control etc. The following essay aims to critically review DSM-IV guidelines for diagnosing co morbid substance use disorders (SUDs), the factors that undermine definitive diagnosis of co morbid disorders, and the potential diagnostic changes that could address these issues. In particular this essay shall examine alcoholism which is one form of substance abuse. Attempts shall also be made to investigate the types of research that would act as a support for the criteria and guidelines for diagnosing SUDs and psychosis.

Substance use disorder is caused due to psychoactive drug use and may be referred to as a condition arising from the abuse of alcohol and psychoactive drugs. Alcohol and other substances can have varied physiological and psychological effects. Although the effects of alcohol and drug consumption may appear as desirable, prolonged and heavy usage may result in physical harm, dependency and withdrawal problems and long term psychological damage or social harm. For the diagnosis of patients with co morbid psychotic symptoms and substance use disorders (SUDs) the Diagnostic and Statistical Manual of Mental Disorders 4th ed. (DSM-IV), makes clear distinctions between independent psychotic disorders (bipolar disorder, schizophrenia) and substance-induced syndromes (delirium, dementia etc.). Most substance-induced psychotic symptoms are considered to be short lived and that it subsides with sustained abstinence along with other symptoms of substance intoxication and withdrawal. One of the most frequent situations in psychiatric diagnosis are challenges posed by patients who experience the onset of psychotic symptoms during episodes of current or recent psychoactive substance use (Rosenthal & Miner, 1997). All major categories of non-organic psychotic disorders in DSM-IV have an exclusion criterion for symptoms that are not caused due to the direct physiological effects of a substance.

For patients with SUDs, psychotic disorders can be diagnosed as either independent or having one of the many substance-induced mental disorders. Psychosis forms a feature of this categorisation. When changes occur relating to the pharmacological effects of different categories of substances, the symptoms include – acute intoxication, intoxication delirium, withdrawal, substance-induced psychotic disorder with hallucinations etc (caused due to the use of substances such as, alcohol, stimulants etc.). The only exception is for alcohol-induced pathological dementia. All other substance-induced psychotic mental disorders are considered as time limited (Rounsaville, 2007). Alcohol dependence syndrome according to DSM-IV (APA,1994), is characterised by the presence of three or more of the following symptoms – a strong compulsion to drink; difficulty in controlling either the onset or termination of drinking or the levels of alcohol use; a physiological withdrawal state on the stopping of alcohol consumption or the use of alcohol to avoid withdrawal symptoms; increasing tolerance to alcohol (i.e. the need to consume larger quantities of alcohol to achieve a similar effect as produced originally from smaller amounts); digressive neglect of other interests; and persisting use of alcohol despite awareness of the harmful effects from consumption.

Alcohol-related psychosis is a secondary psychosis with hallucinations occurring as the predominating feature in many alcohol-related conditions. These include but are not limited to acute intoxication; withdrawal, after a major decrease in alcohol consumption, and alcohol idiosyncratic intoxication. According to Larson (2008), alcohol is a neurotoxin that affects the brain in a complex manner through prolonged exposure and repeated withdrawal. This results in significant morbidity and mortality. Larson further argues that, alcohol-related psychosis is often an indication of chronic alcoholism. As such, it is associated with medical, neurological, and psychosocial complications. The discontinuation of alcohol rapidly clears alcohol-related psychosis but may continue on later alcohol related exposure. Although distinguishing alcohol-related psychosis from schizophrenia through clinical presentation often is difficult, the general consensus is that alcohol-related psychosis suspends with abstinence, unlike schizophrenia. Larson (2008) has also noted that, alcohol-related psychosis lacks the in-depth research needed to understand its pathophysiology, demographics, characteristics, and treatment when compared to alcoholism.

According to Rassool (2006) psychoactive drugs are substances which have an effect on the central nervous, as they alter mood, cognitive processes and behaviour. Rassool (2006), states that, the uses of psychoactive drugs are considered illegitimate depending on the social customs and laws of different cultures and societies. In most societies, no adjustments are made in the interest of the use and misuse of tranquilisers, heroine, volatile substances, and stimulants such as amphetamines and cocaine. Legal drugs such as alcohol, caffeine and nicotine are used as a social lubricant and as self-medication, as a means to relieve tensions and anxieties of everyday life. They are also used as a mechanism to ease social intercourse. He further agues that, although there is an increased risk of morbidity and morality, alcohol is actively encouraged and socially reinforced in some societies. There have also been observations that consumption levels are on the rise in most countries and hence, statistics have been obtained for the UK to demonstrate this fact below.

According to the NHS Information Centre (2009), an estimated 863,000 alcohol related admission in hospital in 2007/08. This is an increase of 69% since 2002/03 when the alcohol related admission was at 510,200. The statistics bulletin further states that, in England in 2007, the number of individuals who were on prescription items for the treatment of alcohol dependency were 134,429. These were prescriptions that were dispensed in primary care settings or NHS hospitals and those dispensed in the community. This shows a marked difference since 2003 when there were 102,741 prescription items (an increase by 31%). Further findings from the bulletin indicate that, there were 6,541 deaths in England in 2007, and these were directly related to alcohol (an increase by 19% since 2001). Of these alcohol related deaths, majority of the individuals died from alcoholic liver disease (estimate of 4,249). Alcohol misuse related harm is estimated to cost the NHS in England approx. £2.7 billion in 2006/07.

As an attempt to ensure a moderately even account of the statistics on alcohol misuse in UK, the Audit Scotland report has been reviewed and provides further evidence of Scotland’s growing problem with drug and alcohol misuse. The Audit Scotland (2009) report presents that Scotland has a higher level of drug and alcohol misuse compared to the rest of the UK. According to the report, the levels of alcohol dependency are three times higher than that of England. The report states that estimating the size of Scotland’s alcohol problem is not accurate due to lack of national data and under-reporting of consumption. Based from findings from the Office of National Statistics (2002), an estimated 4.9% of the population in Scotland aged 16 and over are dependant of alcohol. The higher prevalence of alcohol dependency is Scotland has been argued to be found due to high rates of alcohol dependency in Scottish women. There were 42,430 discharges from acute general hospitals with an alcohol-related diagnosis in 2007/08. When compared to statistics from the past five years, there has been an increase by 5% in discharge rates (Alcohol Statistics Scotland, 2008).

In Scotland, 11% of all accident and emergency attendances are considered to be as a result of alcohol. The busiest time of alcohol-related attendances are recorded as Friday night of Saturday morning ranging between midnight and four in the morning (NHS Quality Improvement Scotland, 2006). Scotland has the highest alcohol-related death rate in the UK with 1,399 alcohol-related deaths in 2007. This is a 75% increase over ten years and over 100% increase over fifteen years (General Register Office for Scotland, 2009). A report from Strathclyde Police in 2007 showed that between April 2006 and March 2007, two-thirds of those in custody at three Glasgow police stations were for violent offending under the influence of alcohol.

The reasons for highlighting the statistics on alcohol misuse in UK as well detailed statistics from Scotland is not just to emphasise the ever growing alcohol and drug consumption in the country, but also to understand the common co-occurring psychiatric disorders related with the misuse of these substances. The recent recognition of this co morbidity can be attributed to a number of reasons. Abou-Saleh & Janac (2004), state that, the development of drug abuse services was separate from that of the development of general psychiatric services, with little interference between them. Furthermore, the move from hospitals to community care of individuals with severe mental disorders has exposed these individuals to the risk of developing alcohol and drug problems, thereby merely heightening their psychopathology and disability. There is also the high risk of self-harm not just to individuals who are within general psychiatric services, but also those with severe personality disorders within addiction services.

A number of etiological models for co morbidity have been introduced in research. These include – common factor models, secondary substance misuse models, and secondary psychiatric illness models (Mueser, Bellack & Blanchard, 1998). According to Mueser et al (1998), the common factors models include common genetic factors and antisocial personality disorder. However, Abou-Saleh & Janac (2004) argue that studies have not supported the existence of a common genetic factor in the causation of substance misuse and psychiatric disorders. At the same time, the presence of antisocial personality disorder was shown to be a common factor in substance misuse. They further go on to argue that, patients with sever mental illness and antisocial personality disorder are morel likely to have substance misuse than those with no antisocial personality disorder. Adversity in childhood can seem omnipresent in patients with alcohol misuse who are co morbid with psychiatric conditions. A study conducted by Langeland, Dralijer & Van der Brink (2004), found that childhood detrimental influences such as early loss of a parent, witnessing domestic violence and parental alcoholism, exemplified as variations in types of co morbid psychiatric disorders in men with alcohol dependence. A further study by Mueser et al (2000), in a cohort study involving 325 patients with co morbid psychiatric disorder and substance misuse distinguished the predictors of co morbidity as – male, young age, lacking education, involved in criminal activity, conduct disorder, and antisocial personality disorder.

Secondary substance misuse models include those of self-medication, alleviation of depression, and super sensitivity. Abou-Saleh & Janac (2004), further state that the self-medication model depict psychiatric patients as using specific substances to alleviate specific symptoms. However, this argument has not been supported and psychiatric patients who use alcohol or drugs have worse outcomes. As depression can be associated with a general proneness to addiction and not the use of a specific substance, the alleviation of depression model is more acceptable. According to the super sensitivity model, patients with severe mental illnesses react in a highly sensitive manner to low doses of alcohol and drugs, in particular amphetamines leading to a hasty relapse in the individual’s illness. The secondary psychiatric illness model alcohol and drug use disorders are viewed as causing the co morbid mental disorder (Abou-Saleh & Janac, 2004). An interesting note about the above stated models is that, causality is one-directional. In clinical practice, substance abuse may form both a cause and a consequence of another mental disorder. A mental disorder at the same time may be both a cause and a consequence of substance abuse, thereby creating a vicious circle. In individual cases, multiple pathways of association between substance abuse and other mental disorders may act simultaneously in both directions.

A review of certain factors (bio physiological and genetic, socio cultural and psychodynamic) as well as a detailed review of other models (social learning and behavioural) which all put together helps formulate what is known and thought about why human beings come to abuse themselves by abusing alcohol. When split apart, each model explains a part of every abuser’s problem, together they provide a comprehensive etiological perspective. According to Miller (1980), one of the most obstinate theories of the bio physiological model of alcoholism is that alcoholics and non-alcoholics differ in the rate at which they metabolise alcohol. Identifying such a difference would suggest that the etiological factor resides in the rate-limiting mechanisms involved in the metabolism of ethanol. However, no metabolic studies of alcoholism indicate the existence of such a rate difference (given that the alcohol consumption is kept constant) (Mello & Mendelson, 1978). Charles Lieber, claims that alcoholics have two metabolic routes by which they break down alcohol while non-alcoholics have one (Korsten & Lieber, 1979). According to this theory, alcoholics metabolise alcohol differently from non-alcoholics and thus gain the capacity to consume larger amounts of alcohol for longer periods of time than non-alcoholics. Even if such proof were available, there still lie the important roles of environmental, behavioural and socio-cultural factors in alcoholism.

Numerous studies have been carried out, suggesting that alcoholism runs in families (Goodwin, 1979). Evidence that genetic factors play an important role in the development of alcoholism has been derived from twin studies, family studies, adoption studies, observations of ethnic differences, and studies of biological risk factors (Goodwin 1979, 1985). Studies of monozygotic (identical) and dizygotic (fraternal) twins generally suggest that there is some degree of heritability in the frequency and quantity of alcohol consumed (Schuckit 1987). Monozygotic twin pairs also tend to show a significantly higher level of concordance compared with dizygotic twin pairs (Schuckit 1987; Agarwal and Goedde 1990). Family studies indicate that approximately 40% of alcoholics have an alcoholic parent (Institute of Medicine 1987), and that the alcoholism rate is significantly higher in relatives of alcoholics than in relatives of non alcoholics (Cotton, 1979; Guze et al, 1986). Alcoholics with a family history of alcoholism tend to begin drinking earlier in life. They also tend to have more alcohol-related problems than those alcoholics without a family history of alcoholism (Cloninger et al. 1981). These data, taken together, suggest that there may well be a genetic component to alcoholism, though its extent and influence of inheritance is not a simple one, as both genetic and environmental factors may be involved (McNeece & DiNitto, 2005). The pharmacology and physiology of physical dependence and tolerance to the drugs of abuse continue to be explored, but this model alone cannot adequately define alcoholism.

As mentioned earlier, cultural patterns have a profound impact on drinking and rates of alcoholism. Miller (1980), states that although cultural influences can predispose a person to alcoholism, social variables play a major role in translating that predisposition to actual addiction. He further states that cultural influences can operate to maintain alcoholic drinking. For e.g. peer pressure, has a powerful influence on the development of deviant drinking among adolescents (Jessor & Jessor, 1975). Social historians have argued that the pervasiveness of social setting-related influences on persons to drink heavily (Zinberg & Fraser, 1979).

Psychoanalysts explain alcoholism in several ways. Alcoholism is seen by some psychoanalysts as fundamentally suicidal, trying to destroy “bad, depriving mothers” with whom the person has identified with. Others claim that alcoholics are defining themselves against underlying depression by drinking to oblivion (Williams, 1976). Critics of the psychoanalytic approach to alcoholism, argue that there is no empirical data to support these hypotheses. They also argue that psychoanalysis does not help alcoholics who seek treatment (Schuckit & Haglund, 1977). Dynamic theories of drug addiction, describe the addict as a person whose habit represents a return to the oral stage of psychosexual development. As such, dependency needs being paramount, the addict is frustrated with their inability to derive satisfaction of these needs. Inability to meet their oral dependency needs in more appropriate ways, leads the addicts to use drugs or alcohol to obtain gratification. Although the complex psychoanalytic theory has been simplified to a great extent, it has relatively little impact on the prevailing views of aetiology and treatment.

The cognitive behavioural approach views any type of psychopathology as a maladaptive learning process. As such, the central goal of cognitive behavioural approaches is to design techniques through which maladaptive responses can be disentangled and replaced with adaptive responses. The first behavioural explanation for alcoholism was that of tension-reduction. Tension-reduction is based on the hypothesis that, alcohol appears to reduce anxiety. Hence, alcohol is presumed to reinforce drinking by alcoholics. Empirical support for the theory came from earlier studies of experimentally-induced conflict in animals (Conger, 1951, 1956; Masserman & Yum, 1946). However, tension reduction has not received universal support (Cappell & Herman, 1972; Brown & Crowell, 1974).

The behavioural effects of alcohol involve a complex interaction of factors. The expectations an individual holds about alcohol effects their behaviour (Pliner & Cappell, 1974). Expectancies themselves are complex because it is based on belief systems, prior drinking experiences, the immediate social and physical setting of drinking, dosage levels etc. Such complexity suggests that the potential reinforcing capabilities of alcohol remain uncertain. The social learning model views alcohol and drug abuse as socially acquired, learned behaviour patters that are maintained by numerous anticipatory causes (classical conditioning) and consequent reinforces (operant conditioning). The causes and reinforces may be of a psychological, sociological or physiological nature (Miller & Eisler, 1975).

The relationship between SUDs and psychiatric disorders pose commonplace diagnostic challenges for both clinicians in treatment settings and researchers in community settings. This is because both SUDs and psychiatric disorders are intermeshed with resemblance of intoxication and withdrawal effects to the symptoms of psychiatric disorders in most patients who come for treatment. Research findings suggests that there are high rates of SUDs amongst individuals with schizophrenia (Regier et al 1990), and even higher rates were reported among samples with first episode psychosis (FEP) (Sevy et al, 2001; Kavanagh et al, 2004; & Wade et al, 2004). Addressing co morbidity is clinically relevant because SUD in schizophrenic patients is associated with poorer clinical outcomes (Swofford et al, 1996) and contributes significantly to their morbidity and morality (Rosen et la, 2008). The reasons for high co morbidity between SUD and schizophrenia although poorly understood, are considered to be an involvement of brain pathways and is likely to be a shared feature in co morbidity that is common to all drugs of abuse (Volkow et al, 2007). The co morbidity of SUD and schizophrenia could also be a direct consequence of the underlying neuropathology of schizophrenia. This may contribute to enhanced addiction vulnerability in individuals by disrupting the neural substrates that mediate positive reinforcement (Chambers, Krystal & Self, 2001).

The challenge has been to design measures to differentiate three conditions. Firstly, differentiating between expected intoxication and withdrawal symptoms; secondly, being able to distinguish between psychiatric disorders occurring during periods of active substance use. The third measure includes being able to differentiate between psychiatric disorders that are clearly independent from substance use. Prior to the publication of DSM-Iv, there existed no specific criteria for making these differentiations in substance abusers. This gave rise to a number of reliability and validity problems, including low levels of agreement between study groups, even when the same measures were used (Hasin, Samet, Nunes, Meydan, Matseoane & Waxman, 2006). Eventually, DSM-IV clarified the guidelines to a considerable extent for differentiating independent and substance-induced disorders. According to DSM-IV, if a psychiatric episode occurs when substance use is insufficient to produce persistent intoxication or withdrawal, it would be diagnosed as primary (independent). Subsequently, substance-induced psychiatric disorders are defined as those that occur during periods of heavy substance use (or remitting shortly thereafter) and that have symptoms that exceed the expected effects of intoxication or withdrawal listed in DSM-IV. Hasin et al (2006), also argue that no study has yet addressed the reliability of the DSM-IV system of differentiating between intoxication/withdrawal symptoms. Disorders whose symptoms exceed intoxication/withdrawal effects and psychiatric disorders that is temporally independent from periods of substance use.

In order to create a diagnostic instrument that was reliable and valid for assessment of psychiatric disorders in substance abusers, the Psychiatric Research Interview for Substance and Mental Disorders (PRISM) was developed (Hasin, Trautman, Miele, Samet, Smith & Endicott, 1996). The pre-DSM-IV PRISM included standardised guidelines and probes to differentiate between organic and non organic syndromes and was administered by experienced clinical interviewers. Hasin et al (1996) conducted a study involving 172 dual-diagnosis or substance abuse patients. The result showed good to excellent reliability for many diagnoses, including SUDs, primary affective disorders, eating disorders, some anxiety disorders, and psychotic symptoms.

The need to incorporate the new DSM-IV criteria (including the criteria for substance-induced disorders), to shorten and simplify the interview, and to add assessment of specific psychotic disorders led to the development of the PRISM-IV (Hasin et al, 2006). The PRISM-IV is a semi structured interview. The covers the diagnosis for current and lifetime time frames. These include abuse and dependence (by substance), major depressive disorder, mania, schizophrenia, mood disorder with psychotic features, delusional disorder, brief psychotic disorder, personality disorders etc. The most fascinating feature of the PRISM-IV is that, diagnostic modules can be selected to suit specific research needs. Apart from this, substance use disorders that are unimportant to the research question can be omitted as well.

Other than PRISM-IV and DSM-IV, there are various other assessment tools that can be used for the assessment of psychiatric disorders in substance abusers. One such tool is the International Classification of Diseases Diagnostic Criteria (ICD-10). ICD-10 provides specific criteria to differentiate between primary disorders and disorders resulting from psychoactive substance use, but only for psychotic disorders. ICD-10 excludes psychotic episodes attributed to psychoactive substance use from a primary classification similar to DSM-IV. Unlike DSM-IV, ICS-10 does not provide a separate psychoactive substance-related category for any other type of psychiatric disorder. In ICS-10, organic mental disorders exclude alcohol or other psychoactive substance-related disorders. Furthermore, organic mood disorders and organic delusional disorders cannot be used to diagnose episodes co-occurring with heavy psychoactive substance use (Torrens, Matrin-Santos & Samet, 2006).

Different interviews for psychiatric diagnosis based on DSM-IV or ICD-10 criteria are available for clinical and research studies. These include Structured Clinical Interviews for Axis I disorders (SCID-I) for DSM-IV (First et al, 1997). There exists the Schedule for Clinical Assessment in Neuropsychiatry (SCAN) (Janca et al, 1994) and the Composite International Diagnostic Interview (CIDI) (WHO, 1998). The SCID-IV is a semi-structured interview that allows diagnosis of primary or substance-induced disorders. However, it does not provide any specific guidelines other than those stated in the criteria. The differentiation of primary and substance induced disorders is made on a syndrome level in SCID-IV (Torrens, Matrin-Santos & Samet, 2006). A range of clinical phenomena can be assessed by SCAN. A core instrument of the SCAN is the Present State Examination (PSE-10). PSE ratings are coded on score sheets and based on these ratings, a computer program generates ICD-10 and DSM-IV diagnoses. The PSE is a semi-structured clinical examination. The interviewer uses clinical judgment to attribute specified definitions to clinical phenomena using the SCAN Glossary. The glossary consists of a list of definitions of clinical symptoms and experiences (Torrens, Matrin-Santos & Samet, 2006).

Finally, the CIDI is a fully structured interview design. The interviewers read the questions as written without interpretation (Robins et al, 1988). CIDI relies heavily on the subject’s opinion for primary substance-induced differentiation. The CIDI generates ICD-10 and DSM-IV diagnoses. Symptoms attributed to alcohol, drugs, or physical illnesses are eliminated for consideration when making psychiatric diagnoses in CIDI. The method of evaluation used in CIDI is very varied in comparison to SCID-IV, SCAN or PRISM-IV. Torrens et al (2006) argues that, currently, most DSM-IV psychiatric disorders can be assessed in substance-abusing subjects with acceptable to excellent reliability and validity by specifically using the PRISM assessment tool.

Having reviewed the statistics, aetiology and assessment of co morbidity in alcohol abuse, the next section is going to analyse the different treatment approaches. One of the biggest problems in the treatment of SUDs is preventing a relapse after abstinence or controlled substance use has been achieved. Whilst there is no general theory of relapse, Marlatt & Gordon’s approach to treatment is based principles of social learning theory, and draws heavily on the concepts of self-efficacy (Bandura, 1977). The approach emphasises on the methods to enhance confidence in individuals to enable them to perform activities leading to an effective outcome. According to self-efficacy theory, individuals who possess a high self-efficacy on their ability to perform a particular task are more likely to initiate and maintain that behaviour (Wilson, 1996). Wilson (1996) argues that the self-efficacy theory has been criticised on a number of conceptual grounds including difficulty in distinguishing between response-outcome expectancies and performance self-efficacy (Lee, 1989).

The Stages of change model by Prochaska & DiClemente (1983), suggest four stages in the process of change. These include: pre-contemplation (not thinking about cessation); contemplation; action (attempting to engage in cessation); and maintenance (stopped using drug, and attempting to remain abstinent). Wilson (1996) argues that, although this model cannot be considered to be a general theory of relapse, there are opportunities different types of interventions for different individuals. He further argues that theory helps make specific and testable predictions about the matching of individuals for treatments. Other than the theoretical explanations for prevention of replace in individuals with alcohol abuse, there also exists medical treatment and social treatment approaches. Detoxification is an abrupt stop of alcohol drinking coupled with the substitution of drugs that have similar effects to offset the withdrawal symptoms. Detoxification treats only the physical effects of prolonged use of alcohol, but does not actually treat alcoholism. There is a high chance of relapse without further treatment. Various forms of group therapy or psychotherapy can be used to deal with underlying psychological issues that are related to alcohol addiction, as well as providing relapse prevention skills.

Miller (1980) states that when problem drinkers are treated, approximately one-third become abstinent and an additional one-third show substantial improvement without abstinence. He has based his findings from short-term studies; however, data from long-term studies suggest that on average only 26% of those treated remain abstinent or improved after one year. A few other treatment strategies for alcohol addiction include aversion therapies, family therapies, controlled drinking therapies etc.

To conclude, while progress is apparent in the study of substance abuse; more research is needed on the commonalities and differences among the addictions. Numerous theories have been developed to help explain the causes of addiction, but it is important not to lose sight of essential differences among substances and their effects. Individuals with recurrent or severe and enduring mental illness and co morbidity with substance-misuse have complex needs. This requires the continuing care of specialist mental health services and substance-misuse services. It has been reported that around 30% of those seeking help for mental health problems have current substance misuse problems, and of individuals seeking help for substance misuse, more than half have had a mental disorder in the previous six months (Department of Health, 1998). According to Appleby (1999), individuals with substance-misuse and psychiatric disorders find it hard to engage with appropriate services. He further states that suicide is a high risk factor amongst this group.

The different assessment tools that have been devised by DSM-IV for the diagnosis of co morbidity in SUDs, whether in primary or specialist care should consider how to access appropriate specialist input. Recent studies have examined the relationship

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