Comorbidity of mental disorders and substance use: A brief guide
for the primary care clinician
ACKNOWLEDGEMENT
INTRODUCTION
ABRIDGED PRINCIPLES
OF MANAGEMENT OF PEOPLE WITH DUAL DIAGNOSIS OR COMORBIDITY OF
MENTAL HEALTH PROBLEMS AND SUBSTANCE USE
THE COMMON DRUG GROUPS
Cannabis/Hallucinogens
Alcohol
Opioids
Stimulants
Benzodiazepines
Tobacco
DEPRESSION AND SUBSTANCE USE
Comorbidity
Major
clinical issues with cannabis, hallucinogens and depression
Major clinical
issues with alcohol and depression
Major
clinical issues with opiates and depression
Major clinical
issues with stimulants and depression
Major clinical
issues in benzodiazepine use and depression
ANXIETY DISORDERS
AND SUBSTANCE USE
Anxiety Subtypes
Comorbidity
Major
clinical issues with anxiety disorders and cannabis/hallucinogens
Major
clinical issues with anxiety disorders and
alcohol
Major
clinical issues anxiety disorders and opiate use
Major clinical
issues anxiety disorders and stimulant use
Major
clinical issues with anxiety disorders and benzodiazepines
PSYCHOSIS (SCHIZOPHRENIA
AND BIPOLAR DISORDER) AND SUBSTANCE USE
Comorbidity with psychosis
Major clinical
issues with psychosis and cannabis/hallucinogens.
Major clinical
issues with psychosis and alcohol
Major
clinical issues with schizophrenia and opiate use
Major
clinical issues with psychosis and stimulant use.
Major
clinical issues with the psychoses and. benzodiazepine use
PERSONALITY
DISORDERS AND SUBSTANCE USE
Comorbidity with personality
disorders
Major issues
with personality disorders and cannabis/hallucinogen use
Major
issues with the personality disorders and alcohol use
Major issues
with personality disorders and opiate use
Major issues
with people with personality disorders and stimulant use
Major issues
with personality disorder and benzodiazepine use
EATING DISORDERS AND SUBSTANCE USE
Anorexia and bulimia
Physical
and Medical Complications of Eating Disorders
Comorbidity of
eating disorders and substance use
Major
clinical issues with eating disorders and cannabis/hallucinogen
use
Major
clinical issues with eating disorders and alcohol abuse
Major
issues with eating disorders and opiate use
Major
issues with eating disorders and stimulants
Major
issues with eating disorders and benzodiazepines
SOMATOFORM DISORDERS AND SUBSTANCE
USE
Comorbidity
with the Somatoform disorders
Somatoform
disorders and cannabis/hallucinogens
Somatoform disorders
and alcohol use
Somatoform disorders and opioids
Somatoform disorders and stimulants
Somatoform
disorders and benzodiazepine use.
RERERENCES
APPENDIX 1 SEROTONIN
SYNDROME
Acknowledgments
Comorbidity of mental disorders and substance use: A brief guide
for the primary care clinician
by Chris Holmwood
Primary Mental Health Care Australian Resource Centre 2002
Copyright: Commonwealth of Australia 2002
This publication is also available in pdf format on the PARC
website at http://www.parc.net.au/Publications
Many thanks to Damian McCabe who was the project officer for
the 2001 Comorbidity Scoping Study. The need for this more
clinical resource arose as a result of this initial work.
PARC would like to acknowledge the assistance of the following
people in the development of this resource.
Dr Paul Williamson (Drug and Alcohol Services South Australia)
Dr Chris Wurm (National Centre for Education and Training on Addiction)
Associate Professor Chris Alderman. (Drug and Therapeutics Information
Service, Repatriation General Hospital)
Dr Michael Baigent (Department of Psychiatry Flinders University)
Ms Jody Braddon (Pharmacist, Drug and Therapeutics Information
Service, )
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Introduction
Comorbidity or the co-occurrence of mental disorders and substance
use disorders is common. The prevalence of comorbidity in the community
and the complex interactions that occur between the two sets of
disorders, should raise doubts about the manner in which we continue
to deal with each entity separately. As clinicians we need to consider
these problems as part of a whole complex of phenomena that are
closely linked to one another.
However there are significant problems with the management of people
with comorbidity. There is a dearth of evidence about best practice.
Specialist mental health or alcohol and other drugs services where
they are available, are usually separated physically administratively
and philosophically. Until recently training for general practitioners
has been inadequate for the problems that we face on a day to day
basis either in the mental health field or the alcohol and other
drugs field.
This resource has been developed as a result of work that PARC
undertook in 2001 with the development of a set of principles
for the management of people with comorbidity. These principles
are outlined at the start of this resource.
More detailed information about specific aspects of management
of the different types of co-existing mental disorders and substance
use problems then follows. Of course things are never that
simple. The information available is patchy and much of it is
not based on high levels of evidence. In addition many people
with co-morbidity have more than one mental disorder and may have
problematic use of several drugs. This resource is a simple guide
for clinicians to start to work from.
Chris Holmwood
Primary Mental Health Care
Australian Resource Centre
June 2002
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Abridged
principles of management of people with dual diagnosis or comorbidity
of mental health problems and substance use
Mental disorders and substance use occur together very frequently
and interact negatively on one another. Their management requires
a long-term perspective. Actual GP interventions may be brief or
extended over a period of time. A doctor-patient relationship based
on honesty, trust and respect will form the basis for effective
therapy. Active listening skills and a patient centered clinical
method should be used to establish rapport, to develop a common
understanding of the problems and an agreed management plan.
Detection
GPs should routinely enquire about substance use.
When a patient presents with either a substance use related problem
or a mental disorder then the GP should enquire about the other.
Comorbidity should be suspected when progress or response to
therapy is not straightforward.
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Assessment
A full assessment often takes several consultations.
This assessment should include determination of:
- the patterns of drug use;
- the day to day problems associated with the substance use;
- the reasons for the use;
- the effect that it might be having on the mental health problem;
- andthe nature of the mental disorder itself, diagnosis, previous
treatments and responses.
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General Management
Management should be based on the patient’s readiness for change.
This readiness for change might be different for the management
of the substance use than it is for the mental disorder.
Management should aim to increase the patient’s awareness of
the negative effect that the substance use and the mental disorder
are having on each other.
Management should involve family or carers where appropriate.
Specific management
Detoxification should be offered as a first step to enable engagement
in long-term approaches and decision making.
Specific management steps should include where appropriate:
- information provision;
- structured problem solving;
- motivational interviewing;
- brief behavioural or cognitive approaches.
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Pharmacological approaches
Clinicians should avoid using drugs of dependence unless as part
of a harm reduction plan (eg methadone or buprenorphine)
Benzodiazepines should not be used for more than a few days. Generally
longer acting benzodiazepines are preferable.
Clinicians should consider whether the current medication for
the mental disorder is adequate or causing side-effects as the
patient may be self medicating with non prescribed drugs to relieve
symptoms or side effects.
The clinician should consider potential interactions between
all substances used.
If there is drug-seeking behaviour then engagement of the patient
in a planned and limited prescribing program is required. (eg
HIC consent for all prescribing information to go to the one prescriber)
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Referral
Consider referral when:
- self harm risk or risk to others is present;
- acute exacerbation of mental disorder occurs;
- drug dependence with major associated problems (legal, health,
social) is present;
- complicated detox is anticipated.
It is important for GPs to develop links with local specialist mental
health or drug and alcohol services (where they exist)
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The Common Drug Groups
Cannabis/Hallucinogens
Cannabis (marijuana, hash, grass, dope), LSD (acid), Psilocybin
(Magic Mushrooms)
Datura (Angel’s trumpet), Anticholinergic drugs, e.g. benztropine,
benzhexol, orphenadrine.
In small quantities, users find cannabis both relaxing and stimulating.
The senses are enhanced and it improves the appetite. The drug
is often used in a group as it enhances sociability and at low
doses it causes a high that includes feelings of relaxation and
happiness.
In larger quantities (or with stronger strains), cannabis may
produce effects similar to LSD. LSD (Lysergic Acid Diethylamide
or acid) is a hallucinogenic or psychedelic drug. LSD and large
amounts of cannabis can trigger underlying mental problems and
produce delusions, paranoia and schizophrenia-like states. They
can also produce extreme anxiety states or panic attacks, not
only while the person is under the influence of the drug, but
for some time after. In this way these drugs may produce long
standing changes in the personality of the user.
Anticholinergic drugs, e.g. benztropine, benzhexol, orphenadrine
may be prescribed to alleviate extrapyramidal symptoms in patients
with psychosis. However these drugs may themselves lead to hallucinations,
and are therefore sometimes sold for recreational use. Several
psychotropic drugs have less marked anticholinergic effects, e.g.
tricyclic antidepressants, thioridazine and may interact with
prescribed or unsanctioned drugs to produce an anticholinergic
psychosis.
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Positive effects (cannabis): Relaxation, increased appetite,
feelings of happiness, sleepiness
Problematic effects (cannabis): Nausea, hallucinations,
anxiety, panic attacks, paranoia, psychological dependency, impaired
judgement, reduced motivation, acute and chronic lung problems.
Long term effects include reduced motivation and persistent cognitive
impairment.
Overdose risk: Small
Withdrawal: Unlikely, although symptoms may include anorexia,
disturbed sleep, irritability and moodiness.
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Alcohol
Alcohol (ethanol) is one of the most commonly used and abused drugs.
It is a depressant drug that slows down body reactions and general
brain function. In Australia the 12 month prevalence of harmful
use of alcohol is 3.0% while the prevalence of dependence is 3.5%.
Men are twice as likely to suffer dependence compared with women.
It is the secondary effects of alcohol that make it dangerous
with motor vehicle accidents, alcohol-related violence (including
domestic violence) and liver disease all major causes of morbidity
and mortality.
Alcohol is readily available and its consumption, even in excess,
has become part of our culture. The depressive effects of alcohol
makes it a significant risk factor in the development of mental
health problems, particularly depression.
Short term effects: Relaxation, reduced social inhibition,
slurring of speech, reduced motor-coordination, reduced vision,
reduced consciousness.
Long term effects: Liver disease, gastrointestinal disease,
anemia, malnutrition (thiamine deficiency), central nervous system
disturbances, depression.
Overdose risk: Moderate, becomes particularly dangerous
when used in conjunction with other substances (prescription benzodiazepines
for example).
Withdrawal: If dependence is established then withdrawal
effects include nausea and vomiting, agitation, tremour, sweating,
hallucinations, and seizures. It is potentially life threatening.
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Opioids
Heroin, codeine, morphine, pethedine, diconal, palfium, methadone.
Opioids are analgesic drugs derived from the opium poppy that
have a wide range of effects on the mind and body. Opioids are
generally taken to produce a sense of well-being and to reduce
effects of stress and pain.
Opioids are highly addictive and habit forming. Regular use quickly
creates tolerance leading the user seeking increasingly larger
doses of the drug to achieve the same effect.
Accompanying tolerance is a powerful psychological craving for
the drug and physical addiction that may produce strong withdrawal
effects. It is these effects of opioids that create significant
physical and mental health problems for the individual as they
engage in behaviour that becomes increasingly focussed on obtaining
and consuming the drug. Chemical contaminants may include talc,
glucose, quinine and strychnine with associated harmful consequences.
Short term negative effects: Depressed respiration, clouded
mental functioning, nausea, vomiting, sweating, itchy skin and
constipation. There is also a high risk of overdose that may lead
to fatal respiratory depression.
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Long term effects: Poor health, lung complications, scarred
or collapsed veins, abscesses, bacterial infections, blood borne
viruses (eg. hepatitis, HIV).
Associated problems: Generally problems are associated
with overdose and with injecting use. Hepatitis B and C, HIV,
severe thrombophlebitis and intravascular sepsis, endocarditis,
accidental arterial injection and peripheral ischaemia occur regularly
in the injecting drug using community.
Overdose risk: Opioids may be lethal in overdose.
Overdose results in respiratory and cardiovascular depression,
loss of consciousness and death. Tolerance develops rapidly to
opioids. Illicit drug availability varies considerably and hence
purity of street available drugs vary, increasing the risk of
accidental overdose.
Withdrawal: In the dependent person withdrawal is uncomfortable.
Features include sleeplessness, restlessness and agitation, abdominal
and general muscular pains, diarrhoea and nausea, shivers and
pilo-erection.
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Stimulants
Cocaine, amphetamine, methamphetamine, ecstasy (MDMA), methylphenidate,
ephedrine, pseudoephedrine (Sudafed).
Stimulants are recreational drugs that are purported to enhance
sociability, confidence and alertness while reducing inhibition.
The sensation of euphoria and well being that is associated with
the use of stimulants becomes highly sought after but is usually
only short lasting. The physiological effects of stimulants are
well documented and include increased heart rate and energy level
while reducing the influence of tiredness. The psychological effects
of stimulants, particularly prolonged use, are not so well documented.
There is some evidence that stimulants may have significantly
negative effects on consciousness and mental state. Indeed it
has been suggested that it may be difficult to distinguish primary
psychotic and primary mood disorders from chronic stimulant use
induced symptoms.
Short term effects: Periods of euphoria, increased
sexual activity, paranoia, empathy, enhanced sociability, fear
dissolution, hallucinations, appetite suppression, increased energy
level, stamina and racing thoughts followed by periods of depression
and low energy.
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Associated problems: Anxiety, depression, paranoia, tremor,
mydriasis, tachycardia, diaphoresis, hypertension, hypothermia,
risk of suicide, dehydration, acute renal failure, seizures, arrhythmias,
hyponatremia, nausea, muscle cramping, jaw clenching, jitteriness.
Injecting drug use associated with risks as stated above for opioids.
Overdose risk: Low to medium for oral use, however there
is a high risk of overdose associated with injecting use.
Withdrawal: symptoms include depression, dysphoria, fatigue,
exhaustion and somnolence, and loss of appetite lasting up to
two weeks. Following prolonged use insomnia, intense dreaming
and irritability may ensue and last several weeks to months.
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Benzodiazepines
Flunitrazepam (rohypnol), lorazepam, diazepam, temazepam, clonazepam,
oxazepam.
Benzodiazepines are sedative drugs that may be prescribed to
reduce anxiety, to encourage sleep or to act as a muscle relaxant.
The non-prescribed use of these psychotherapeutic medications
is frequent. The most likely to be abused are those that are short
acting or rapidly absorbed, producing a more rapid feeling of
intoxication. These prescribed medications have become the target
of doctor shoppers and they are sold or exchanged on the street.
Benzodiazepines are often used in combination either with other
benzodiazepines or with other illicit drugs eg. Flunitrazepam
may be taken by heroin users to prolong the effect of a heroin
injection and to reduce the effects of withdrawal. In non-poly
drug users psychological addiction may occur when benzodiazepines
are taken in an attempt to medicate (self-medicate) symptoms that
are associated with an undiagnosed mental health problem.
Short term effects: Euphoria, hallucinations, disinhibition,
skeletal muscle relaxation, sedation, light and sound sensitivity,
memory impairment.
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Associated problems: Drowsiness, forgetfulness, confusion,
depression, digestive problems, tachycardia, apnea, ataxia, hypotension,
seizures, nausea. When injected intravenously vein damage is common.
When injected arterially accidentally they can result in peripheral
ischaemia an gangrene.
Risk of overdose: Variable depending upon the strength
of particular tablets. However, taken in large amounts and/or
in-conjunction with other substances (usually alcohol) benzodiazepines
there is a high risk of overdose, particularly in people with
a high suicide risk.
Withdrawal: There is an established withdrawal effect
associated with use of benzodiazepines. Likelihood of withdrawal
is higher for stronger, shorter acting types that are used for
a long period of time. Withdrawal effects include anxiety, depression,
problems sleeping, irritability, palpitations and sensory disturbances.
Seizures can occur with sudden withdrawal from more than 50mg/day
of diazepam.
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Tobacco
While tobacco use is fairly common in the general adult population,
it is particularly widespread in patients with psychosis (87%
in one study) and probably accounts for a significant component
of the increased morbidity and premature death seen in patients
with chronic psychosis.
The use of Bupoprion (Zyban) is relatively contraindicated in
bipolar disorder as its antidepressant effects may lead
to hypomania.
Tobacco may induce the metabolism of some of the anti-psychotics
and hence lessen their side-effects. Nicotine may lessen
some side-effects of neuroleptic directly.
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Depression and Substance
Use
Depression is a debilitating disorder that disrupts relationships
and daily lives. It is common, affecting approximately 10 percent
of the general population. It is twice as common in women as in
men, although both sexes suffer its effects.
Depression may be characterised by the presence of a majority
of the following symptoms:
- Depressed mood most of the day, nearly every day, as indicated
by either subjective report (e.g. the person feels sad or empty
or appears tearful). In children and adolescents, this may be
characterised as an irritable mood.
- Markedly diminished interest or pleasure in all, or almost
all, activities most of the day, nearly every day.
- Significant weight loss when not dieting or weight gain (a
change of more than 5% of body weight in a month), or decrease
or increase in appetite nearly every day.
- Insomnia or hypersomnia nearly every day.
- Psychomotor agitation or retardation nearly every day.
- Fatigue or loss of energy nearly every day.
- Feelings of worthlessness or excessive or inappropriate guilt
nearly every day.
- Diminished ability to think or concentrate, or indecisiveness,
nearly every day.
- Recurrent thoughts of death (not just fear of dying), recurrent
suicidal ideation without a specific plan, or a suicide attempt
or a specific plan for committing suicide
To be described as suffering a major depressive episode a person
must either have a depressed mood or a loss of interest or pleasure
in daily activities consistently for at least a 2 week period. This
mood must represent a change from the person's normal mood. Social,
occupational, educational or other important functioning must also
be negatively impaired by the change in mood.
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Comorbidity
People develop co-existing depression and substance use problems
for a variety of reasons. The question about which came first is
vexed but should not delay treatment of either disorder. Preferably
the substance use should be ceased but this is not always possible.
People self medicate with a variety of drugs to alleviate the symptoms
of the depression. The effect that the drugs have depends on the
drug itself, the particular individual’s response to the drug, the
duration of the drug use and the particulars of the mental disorder,
in this case depression.
Long-term use of stimulants, such as amphetamines and MDMA have
been identified as producing depletion of neurotransmitters, thus
causing or aggravating depression. Alcohol dependence frequently
causes depressive symptoms. However psychosocial effects such
as stigma, poverty and isolation associated with drug use may
also be highly relevant.
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Major
clinical issues with cannabis, hallucinogens and depression
Effect of substance on mental disorder.
- Some people may use cannabis to self manage their depressive
symptoms.
- However the sedative effect of cannabis may exacerbate depression.
- Amotivational syndrome (associated with long term heavy usage)
may simulate the cognitive and psychomotor features of depression.
- Long-term heavy use also thought to cause a depression like
syndrome.
- Cannabis may mask appetite loss, thus concealing the extent
of vegetative changes in more severe depression.
- Drug interaction with therapeutic agents. Cannabis
will augment the sedative effect of benzodiazepines and tricyclic
antidepressants.
- Cannabis has been reported to cause mania with fluoxetine.
Confusion, depersonalisation, psychosis and hypomania have also
been reported with concurrent use of cannabis and SSRIs.
LSD may induce a serotonin syndrome with SSRIs.
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Management approaches
Because of the sedative effect of cannabis patients should be
advised to reduce or stop their use so that depressive symptoms
can be better evaluated.
While adverse effects have been reported as above with concurrent
use of SSRIs and cannabis, the risk is probably small. Patients
should be counselled accordingly. Patients should be counselled
re the signs of serotonin syndrome if SSRIs are to be used while
the patient is using cannabis.
Major
Clinical issues with alcohol and depression
Effect of substance on mental disorder.
Depression is a common feature of alcohol dependence. In many instances
the depression will resolve if the alcohol is ceased.
In addition the depressant effect of alcohol will exacerbate a clinical
depressive disorder. In fact chronic heavy use has been shown to
induce a depression-like condition that is difficult to distinguish
from major depressive disorder itself.
Similarly a depression like set of symptoms may emerge during or
after alcohol withdrawal.
Drug interactions
Alcohol induced sedation will exacerbate the effects of benzodiazepines,
tricyclic antidepressants, nefazodone and mirtazepine. Chronic
alcohol use has a variable effect on the metabolism of some antidepressants.
There is limited experience with drug interactions with acamprosate.
Does not interact with imipramine, diazepam or disulfiram. Naltrexone
will have a blocking effect on opiates used as analgesics.
Management approaches
If a patient is clinically depressed and drinks harmful quantities
of alcohol then they should be advised to stop drinking so that
the symptoms can be evaluated in a drug-free setting. In men this
commonly results in a resolution of the depressive symptoms.
Women more commonly drink in response to a primary depression.
Management therefore may involve the use of an anti-depressant
as well as cessation of the alcohol. If this is not possible then
use of antidepressants is indicated (SSRIs are safer than
tricyclics in overdose with/without combination with alcohol).
Response to antidepressants is less satisfactory in a heavy drinking
situation.
Cognitive therapy may not be possible or beneficial with persons
drinking heavily. Acamprosate or naltrexone may be used
to assist with abstinence supported by structured counselling.
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Major
clinical issues with depression and opiate use
Effect of opioids on mental disorder
Opioids’ depressive effects will exacerbate depressive disorders.
Again the euphoric effects may assist with some of the more negative
cognitive symptoms of depression.
Some depression resolves once patients are stabilised on methadone.
Drug interactions
Opioids will exacerbate the effects of the sedative antidepressants,
especially the tricyclics.
Fluoxetine, fluvoxamine, paroxetine and nefazodone potently inhibit
some of the cytochrome systems in the liver; these enzyme systems
metabolise several opioids including methadone.
Fluvoxamine has been associated with methadone toxicity, and
then when ceased, opioid withdrawal has developed. Citalopram
and sertraline are less likely to have this effect.
Carbamazepine (used as a mood stabiliser) will induce the metabolism
of methadone and reduce levels. Sodium valproate does not have
this effect.
Management approaches
Evaluation of depression is difficult while the patient is using
opioids heavily. Therefore initial cessation is recommended.
Non sedating antidepressants (SSRIs, venlafaxine) are preferable.
Watch for interactions if using methadone or buprenorphine.
Overdose risk is greater with combined tricyclic and opiate use.
CBT difficult while using opioids but it provides additional benefit
in combination with a methadone program.
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Major
clinical issues with depression and stimulant use
Effect of substance on mental disorder.
Depression is a common feature of the cycle of dependence in stimulant
users. People with depression sometimes use stimulants to self-treat
the lack of energy associated with the depression. However tolerance
to this effect develops quite quickly. There is a risk that stimulants
might provide the severely psycho-motor retarded depressed person
with the ability to self harm.
Depression is exacerbated when the stimulant effect wears off.
Stimulant effect on sleep may worsen sleep wake cycle disturbances
associated with depression.
Depression is common in the months following cessation of stimulants.
Interactions between stimulants and antidepressants
Irreversible monoamine oxidase inhibitors (tranylcypromine or
phenelzine) should not be prescribed if stimulants are used.
Some stimulants inhibit the metabolism of tri- and tetra-cyclic
antidepressants. If the clinician is aware of stimulant use then
other anti-depressants are probable better choices.
Most anti-depressants, as well as cocaine both lower seizure
thresholds. Increased seizures have been reported.
Serotonin syndrome may occur with cocaine or MDMA/ecstasy and
SSRIs and patients should be warned about this.
MDMA metabolised through CYP 2D6. This is inhibited by fluoxetine,
paroxetine and norfluoxetine.
Patients should be told about the signs of serotonin syndrome
(see appendix 1).
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Management approaches
The predictable depressive symptoms that occur when drug levels
drop just exacerbate the depression. The person using stimulants
and who is depressed should be encouraged to reduce and stop the
stimulant use.
If the person is dependent then formal drug detoxification should
be considered. There is little consistent evidence that antidepressants
are beneficial in management of stimulant withdrawal per se but
if there is established coexisting major depression and stimulant
use then antidepressants should be used. Benzodiazepines or pericyazine
can also be helpful in the short-term management of withdrawal.
Citalopram and sertraline have least cytochrome mediated drug
interactions but all SSRIs are potential precipitators of serotonin
syndrome in people using cocaine and MDMA.
If use is only occasional and dependence is not present is not
present then treatment as for depression can be commenced.
If the depression persists despite adequate withdrawal from the
stimulants then treat as for primary depression.
CBT is best used when the patient is not intoxicated and stimulant
use is minimal.
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Major
clinical issues in depression and benzodiazepine use
Effect of substance on mental disorder
Benzodiazepines can relieve some of the symptoms of depression such
as insomnia and agitation. However their sedative and depressive
actions exacerbate the more negative symptoms of depression such
as lack of energy, negative cognitions and anhedonia.
Sleep quality is impaired by benzodiazepines with suppression
of REM sleep.
Adverse reactions to the benzodiazepine. For example paradoxical
reactions such as aggression.
Drug interactions
Benzodiazepines will exacerbate the sedative effect of the tricyclic
and other antidepressants.
Disulfiram will increase the plasma concentrations of diazepam.
The addition of nefazodone, fluoxetine and fluvoxamine will increase
the levels of alprazolam, midazolam and triazolam potentially
to toxic levels.
Management approaches
Benzodiazepines can be useful for short term management of acute
agitation, anxiety, panic and insomnia associated with depression
but tolerance develops within a few weeks. Therefore this use
should be restricted to a few days. Their long term use exacerbates
depressive symptoms so that cessation should be a long term goal.
In general short acting benzodiazepines should be replaced with
long half-life benzodiazepines and dosages reduced steadily over
a few weeks or months.
Anti-depressant medication (SSRIs or other non-sedating antidepressants)
can be commenced with the patient still taking benzodiazepines.
Citalopram and sertraline are the least likely SSRIs to have cytochrome
mediated drug interactions.
CBT will be more effective if there is minimal sedation and anxiolysis
due to the benzodiazepine use.
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Anxiety Disorders
and Substance Use
In contrast to fear, which is a response to a realistic immediate
danger, anxiety is a fearful response occurring in the absence of
a specific danger.
According to the National Survey of Mental Health and Wellbeing
anxiety disorders are the most common form of mental disorder
in the population with a one-year prevalence of 9.7%. Patients
experiencing anxiety may present with complaints of excessive
fear or worry, or repetitive, intrusive thoughts or actions including
worry about the future, health or relationships. These people
may find it hard to relax, concentrate and sleep with physical
symptoms such as heart palpitations, tension and muscle pain,
sweating, hyperventilation, dizziness, faintness, headaches, nausea,
indigestion, bowel disturbance and loss of sexual pleasure. In
anxiety disorders the symptoms associated with anxiety are accompanied
by changes in thoughts, emotions and behaviour that substantially
interfere with the person’s ability to love and work.
In general anxiety disorder the person experiences constant worry
about harm befalling themselves or loved ones, about financial
disaster, their health, work or personal relationships.
Diagnostic indicators include:
- Excessive anxiety and worry more days than not for at least
6 months, about a number of events or activities.
- Difficulty controlling this worry.
- Restlessness or feeling keyed up or on edge
- Being easily fatigued
- Difficulty concentrating or mind going blank
- Irritability
- Muscle tension
- Sleep disturbance (difficulty falling or staying asleep,
or restless unsatisfying sleep)
- Clinically significant distress or impairment in social,
occupational, or other important areas of functioning but not
due to the physiological effects of a substance, a general medical
condition, or another mental disorder.
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Anxiety Subtypes
There are also a number of anxiety subtypes including:
· Panic disorder, where a person suffers recurrent
panic attacks that cause significant distress or disability. Panic
attacks involve an abrupt onset of intense fear.
· Obsessive-Compulsive disorder, where a person experiences
constant unwanted thoughts and conducts elaborate rituals in an
attempt to control or banish these.
· Social Phobia, where a person experiences fear
that others will judge everything they do in a negative way, particularly
when in the presence of unfamiliar people or under specific scrutiny.
· Posttraumatic Stress Disorder, where a person experiences
flashbacks, intrusive thoughts or nightmares for years following
major traumas like assault, war, torture, rape, vehicle accidents,
and fires.
Anxiety usually begins in early adulthood and is often, bit
not always, triggered by a series of significant life events. It
frequently occurs in-conjunction with other mental disorders, for
example between 30 and 40 percent of people with panic disorder
and obsessive-compulsive disorder also suffer depression. Anxiety
disorders may are also often complicated by self-medication with
alcohol and other substances. Similarly substance use may be complicated
by the development of anxiety symptoms. At times, it can be hard
to distinguish primary symptoms of anxiety from withdrawal symptoms
in a person with dependence on alcohol or benzodiazepines.
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Comorbidity
Anxiety is commonly seen in association with substance use, however
the relationship between the two is complex. Anxiety is common in
withdrawal from alcohol, benzodiazepines, and opioids and is also
common during intoxication with stimulants, marijuana and hallucinogens.
The failure to recognise and treat anxiety can lead to worsening of
substance use and associated problems vice versa.
Major
clinical issues with anxiety disorders and cannabis/hallucinogens
Effect of substance on mental disorder.
Cannabis and the other hallucinogens can induce anxiety in susceptible
people. This occurs during intoxication and when high doses have been
used, for some time afterwards when drug levels have dropped.
Some people use cannabis to help them cope with the symptoms of an
anxiety disorder that is not being properly managed.
Drug interaction with therapeutic agents.
Cannabis will augment the sedative effect of benzodiazepines and
tricyclic antidepressants. It has also been reported
to cause mania with fluoxetine. Confusion, depersonalisation, psychosis
and hypomania have also been reported with concurrent use of cannabis
and SSRIs.
LSD may induce a serotonin syndrome with SSRIs.
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Management approaches
Because of the anxiety provoking effect of cannabis in some patients,
they should be advised to reduce or stop their use so that their
anxiety symptoms can be better evaluated. In many cases this will
result in an overall reduction in anxiety symptoms.
If the anxiety symptoms started after commencement of the cannabis
or other hallucinogen then the anxiety is probably a secondary phenomenon
and cessation is indicated.
If the patient has been using cannabis or other hallucinogens to
self medicate, then appropriate anxiety specific CBT or drug based
treatment is obviously indicated.
While adverse effects have been reported as above with concurrent
use of SSRIs and cannabis, the risk is probably small. Patients
should be counselled accordingly.
Patients should be counselled re the signs of serotonin syndrome
if SSRIs are to be used while the patient is using cannabis.
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Major
clinical issues with alcohol and anxiety disorders
Effect of substance on mental disorder
Alcohol has long been used to self medicate for symptoms of anxiety
disorders. The effect is sustained although tolerance occurs. When
alcohol levels drop then there is a reappearance of the anxiety symptoms
given the appropriate environment.
Drug interactions
Alcohol will enhance the sedation that occurs with tricyclic antidepressants,
some of which are still used for severe anxiety disorders.
·Nefazodone has caused liver toxicity so its use with people
with established liver disease is best avoided.
Management approaches
Regardless of aetiology and “what developed first” the combination
of an anxiety disorder and alcohol use disorder is problematic as
both exacerbate each other. Early assessment and management of the
anxiety disorder using a behavioural approach is indicated.
Assessment of the alcohol use is indicated at the same time together
with detox if required.
Drug management of the anxiety disorder with SSRIs nefazodone or
venlafaxine may be indicated if behavioural therapy is not possible
or successful.
Specific anti-craving therapies such as naltrexone or acamprosate
are worth considering in this group of people.
Major
clinical issues anxiety disorders and opiate use
Effect of substance on mental disorder
Opioids can have a positive effect on some symptoms of anxiety through
their soporific and sedative effects and euphoria. However withdrawal
effects can exacerbate and be exacerbated by anxiety disorders.
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Drug interactions
Benzodiazepines are often used in the management of anxiety despite
problems with tolerance and dependence.
Benzodiazepines and opioids used together increase the risk of
fatal opiate overdose.
Similarly the use of methadone and benzodiazepines increases the
risk of sedation. Fluoxetine, fluvoxamine, paroxetine and
nefazodone potently inhibit some of the cytochrome systems in the
liver; these enzyme systems metabolise several opioids including
methodone and buprenorphine. Citalopram and sertraline have less
risk of this effect.
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Management approaches
The rapidly fluctuating blood levels of heroin exacerbate anxiety
disorders due to withdrawal effects when levels are low. Therefore
patients should be encouraged to reduce their use and if possible
cease.
Methadone or buprenorphine maintenance improves health status and
should be encouraged/offered.
If medication is indicated for treatment of the anxiety disorder,
then non sedating medication (SSRIs, venlafaxine) favoured.
If long term benzodiazepine use is indicated then this should involve
the use of contracts, registration with the relevant local government
health authority and the prescribing doctor should be identified
as the sole prescriber through the Health Insurance Commission.
(Australia)
Daily dispensing of benzodiazepines with methadone or buprenorphine
should be considered.
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Major
clinical issues anxiety disorders and stimulant use
Effect of substance on mental disorder
Stimulants generally make the symptoms of anxiety disorders worse.
Chronic amphetamine, and cocaine use can precipitate anxiety states
and panic attacks. High dose use can precipitate obsessive cognitions
and compulsive behaviour.
Drug interactions
Irreversible monoamine oxidase inhibitors (tranylcypramine or phenylzine)
should not be prescribed if stimulants are used.
Some stimulants inhibit the metabolism of tri- and tetra-cyclic
antidepressants. If the clinician is aware of stimulant use then
other anti-depressants are probably better choices.
Serotonin syndrome may occur with cocaine, amphetamines or MDMA/ecstasy
and SSRIs.
Paroxetine, fluoxetine and norfluoxetine and nefazodone potently
inhibit CYP 2D6 which metabolises cocaine and MDMA. This may result
in elevated levels of these latter substances.
Management approaches
Reduction or cessation of stimulants is a first step in management
as this will help to clarify the situation regarding the relative
effects of the stimulant vs the disorder in generating anxiety symptoms.
Benzodiazepines may be helpful in the management of acute withdrawal
and emergent acute symptoms but dosages should be slowly reduced.
· When benzodiazepine use is minimised or stopped behavioural
therapy can be effective.
Cognitive therapy can be commenced prior to this provided the person
is not acutely intoxicated with stimulants or with benzodiazepines.
If stimulants have been used to self assist with social phobia
then low dose benzodiazepines can be used to assist engagement with
group therapy.
SSRIs (accepting theoretical risks with stimulants causing serotonin
syndrome) can be very effective for a variety of anxiety disorders
if CBT is not successful or appropriate.
Citalopram and sertraline have least cytochrome mediated drug interactions
but all SSRIs are potential precipitators of serotonin syndrome
in people using cocaine and MDMA.
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Major
issues with benzodiazepines and anxiety disorders
Effect of substance on mental disorder
Benzodiazepines are very effective for treating the acute symptoms
of anxiety. However tolerance and dependence develop within a short
period of time. If short acting benzodiazepines are used (eg alprazolam,
oxazepam, temazepam) rapidly fluctuating blood drug levels may exacerbate
the symptoms of the anxiety disorder.
Drug interactions
Benzodiazepines will exacerbate the sedative effect of the tricyclic
and other antidepressants
Disulfiram will increase the plasma concentrations of diazepam.
The addition of nefazodone, fluoxetine and fluvoxamine will increase
the levels of diazepam, alprazolam, midazolam and triazolam potentially
to toxic levels.
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Management approaches
Benzodiazepines should be reduced or stopped. This can be done gradually
over a few weeks or months with safety. There should be a management
plan that is agreed to prospectively by the patient.
The patient can sign an authority form to allow all prescribing
information to be sent by the HIC to the chief prescribing doctor.
The assistance of the clinical pharmacist or family member can
be invaluable in ensuring restricted daily dispensing.
Once benzodiazepine dosage is minimised the patient can engage
in CBT. Behavioural therapy involving desensitisation will only
be effective if the patient feels anxious during exposure. Therefore
benzodiazepine dosage should be minimised. In general short acting
benzodiazepines should be replaced with long half-life benzodiazepines
and dosages reduced steadily over a few weeks or months.
Specific anti-anxiety medication such as SSRIs can be commenced
with the patient still taking benzodiazepines.
Citalopram and sertraline are the least likely SSRIs to have cytochrome
mediated drug interactions.
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Psychosis
(Schizophrenia and bipolar disorder) and Substance Use
The person experiencing psychosis in the context of concurrent illicit
drug use presents a problem that is challenging for the diagnostic
and management skills of the clinician.
The psychoses are characterized by a loss of connectedness with
reality. A person may develop false ideas or beliefs about reality
(delusions). These may be based on false perceptions of reality
(hallucinations). There are also characteristic flaws in the ways
that people think. These are termed thought disorder. Examples are
tangential thinking, loose associations between words and thoughts,
and incoherence.
Psychoses can occur in response to physical conditions. Eg acute
delirium with septicemia. Alternatively psychoses can be functional.
There are two broad classes of functional psychotic disorders, schizophrenia
and bipolar disorder. Generally schizophrenia is a chronic condition
with exacerbations, but always with some background symptoms, while
bipolar disorder is generally an intermittent condition with full
recovery in between episodes. There is considerable overlap between
the two conditions and “fluidity of diagnosis”. Schizophrenia itself
has so called “negative symptoms” such as social withdrawal and
lack of energy and motivation that are similar to those found in
depression.
While the clinician may realise that the psychosis could be drug-induced
and is cautious in the prescription of neuroleptics or sedatives
to control the symptoms, they may be under pressure to respond to
the manifestation of bizarre or potentially destructive thinking
or behaviour. On the other hand alterations to the way the person
behaves and thinks may be subtle in their early stages when early
intervention may be most appropriate.
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Comorbidity with psychosis
It is important to differentiate between three different phenomena
with regard to psychosis and substance use:
- Firstly people can suffer from an acute psychotic episode in
response to substance use, in particular cannabis and the stimulants.
- Secondly these substances can precipitate a psychotic disorder
in predisposed individuals.
- Thirdly use of substances can exacerbate the symptoms in people
with a chronic psychotic disorder. Use of these drugs will often
exacerbate their condition and make rehabilitation much more difficult.
People with psychosis tend to use a broad range of substances for
a variety of reasons. However, because of cost, cannabis and alcohol
are the most used drugs in this group of people.
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Major
clinical issues in the management of psychosis and cannabis/hallucinogens.
Effect of substance on mental disorder
As mentioned above cannabis and other hallucinogens certainly can
precipitate acute psychotic episodes both in people with established
psychotic disorders and in those who do not. Psychotic episodes tend
to occur more frequently at high doses and in the person who is using
them for the first time. Many people using these drugs realize early
on that the drug makes them “a bit paranoid” and make the decision
not to use them again.
In some people regular cannabis use may augment metabolism of anti-psychotic
agents and lessen side-effects, thus re-inforcing the use of the
cannabis. A similar interaction is thought to underlie the high
rates of cigarette usage amongst people with psychotic disorders.
Generally outcomes for people with schizophrenia using cannabis
are not as good as for those who do not use cannabis.
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Drug interactions Most of the active ingredients of
cannabis are metabolised through the hepatic cytochrome system.
There is sparse evidence regarding drug interactions between cannabis
and most drugs including the anti-psychotic agents both “typical”
and “atypical”.
The sedative effect of cannabis will augment similar side-effects
of the antipsychotics.
Cigarette smoking will induce the metabolism of the typical anti-psychotics
and reduce plasma levels. It is unclear whether chronic cannabis
consumption does the same.
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Management approaches
As mentioned above it is important to distinguish between people
with an acute psychotic episode caused by the drug use, a first
episode of a psychotic disorder or an acute episode in someone with
an established chronic psychotic disorder.
In an acute psychotic episode caused by a drug, cessation
of the drug will often result in resolution of the episode. Sometimes
the use of an anti-psychotic medication or benzodiazepines is indicated
for the first few days.
In general people with psychotic disorders should be counselled
against using cannabis. In theory people with a psychotic disorder
should avoid cannabis. In practice there are some who use small
amounts infrequently and in whom there is no ill effect. For most
people with schizophrenia cannabis makes them worse. This needs
to be explored with the patient.
Education about the possible effects of cannabis on schizophrenia
should be provided in the context of motivational interviewing and
a “stages of change” model.
Anti-psychotic medications are generally required for the ealry
management of drug induced psychosis.
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Major clinical
issues with alcohol and psychosis
Effect of substance on mental disorder
Long term effects on the course of schizophrenia unclear. However
alcohol has the potential for making an already disordered lifestyle
even more disordered.
Relapse rates are higher for those people with schizophrenia and harmful
alcohol use.
Alcohol tends to make the negative symptoms of schizophrenia worse.
It probably has little effect on the positive symptoms.
Drug interactions
Alcohol will exacerbate the sedative effects of many of the anti-psychotics
and cause additional psychomotor incoordination.
Alcohol exacerbates the orthostatic hypotension problems associated
with many of the anti-psychotics.
Naltrexone: unknown interactions with anti-psychotics
Disulfiram: no major interactions with anti-psychotics
Acamprosate: no known drug reactions with the antipsychotics
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Management approaches
As mentioned above alcohol is used because of its relative accessibility
but is often not the preferred drug.
If there is obvious harmful consumption and dependence then abstinence
would be the strategy of choice. Patients need to be counselled
accordingly.
Detoxification needs to be supervised and psychiatric assistance/advice
available should there be a flare up of psychotic symptoms.
In combination with specific psychotherapy some consideration should
be given to the use of adjuvant drug therapies such as disulfiram,
naltrexone and/or acamprosate.
Major
clinical issues with schizophrenia and opiate use
Effect of substance on mental disorder
As mentioned above the effects of opioids tend to be sedative and
do not assist with self-management of the negative symptoms of schizophrenia.
However the euphoric response from the opioids may alleviate the
depression and isolation that is often associated with psychotic
illness.
Opioid use is associated with poorer outcomes for the psychotic
disorder.
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Drug interactions
Opioids (including methadone and buprenorphine) have an additional
sedative effect to that of the anti-psychotics. Care with driving
and machinery.
No significant pharmacokinetic interactions between methadone or
buprenorphine and anti-psychotics.
No interactions between naltrexone and antipsychotics.
Management approaches
Concurrent opiate dependence and psychotic disorder often means
high levels of dysfunction and harm minimisation approaches should
be pursued.
Psychotherapy may be interfered with by active psychotic symptoms.
Methadone or buprenorphine maintenance should be encouraged as these
will result in better adherence with anti-psychotic management.
Close liaison with dispensing pharmacist will assist with gaining
a good picture of adherence to treatment, levels of self care and
general stability.
Major
clinical issues with psychosis and stimulant use.
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Effect of substance on mental disorder
Stimulants certainly can precipitate acute psychotic episodes both
in people with established psychotic disorders and in those who
do not.
Psychotic episodes tend to occur more frequently at high doses
and in the person who is using them for the first time.
Psychotic symptoms are very common in those with stimulant dependence.
Many people using these drugs realize early on that the drug makes
them “a bit paranoid” and make the decision not to use them again.
Generally outcomes for people with schizophrenia using stimulants
are not as good as for those who do not use cannabis.
Occasional use of low dose stimulants is unlikely to induce an
acute psychotic episode in most people.
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Drug interactions
Stimulants generally do not interfere with anti-psychotics.
Management approaches
As mentioned above it is important to distinguish between people
with an acute psychotic episode caused by the drug use, a first
episode of a psychotic disorder or an acute episode in someone with
an established chronic psychotic disorder.
In an acute psychotic episode caused by a drug, cessation of the
drug will often result in resolution of the episode. Sometimes the
use of an anti-psychotic medication or benzodiazepines is indicated
for the first few days.
Any use of stimulants in someone with a chronic psychotic disorder
will probably exacerbate their symptoms. Patients should be counselled
accordingly.
An acute psychotic episode induced by stimulants is initially difficult
to distinguish from that associated with schizophrenia.
Drug induced psychotic reactions tend to settle more quickly (a
few days) than those due to functional psychoses.
Follow up of psychotic episode is important to ensure that the
patient has not developed an underlying functional psychotic disorder.
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Major
clinical issues with benzodiazepine use and the psychoses.
Effect of substance on mental disorder
Benzodiazepines can be used for the management of the acute agitation
and anxiety associated with an acute psychotic state.
They are used by patients to self manage positive psychotic symptoms.
May exacerbate negative symptoms such as depression and psychomotor
retardation as well as slowing of cognitions.
Drug Interactions
Benzodiazepines will increase the sedative effects of the antipsychotics.
This is sometimes used to assist with management of acute episodes.
Benzodiazepines may induce delirium, severe sedation and respiratory
collapse when used with clozapine.
Management approaches
Benzodiazepines can be very useful for the acute management of psychotic
episodes in conjunction with major tranquilizers. Eg lorazepam,
clonazepam and diazepam.
In general patients function better off benzodiazepines as they
may exacerbate some of the negative symptoms of schizophrenia.
If the patient is using these for management of positive symptoms
consider changing anti-psychotic medication to better address these.
When withdrawing benzodiazepines do this slowly. May result in
flare up of positive symptoms. Converting to an equivalent dose
of a long-acting benzodiazepine like diazepam will often make this
easier.
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Personality
Disorders and Substance Use
Personality traits are conspicuous features of personality and are
not necessarily pathological, although certain styles of personality
traits may cause interpersonal problems. The personality disorders
are not regarded as illnesses and so treatment and recovery are not
really relevant. However some dominant personality traits and personality
disorders result in problematic habitual behaviours that can be modified
or at least managed on a system level.
Of all the different types of personality disorders the emotionally
unstable personality disorder (including explosive personality disorder
and borderline personality disorder) and the dissocial personality
disorder come to the attention of health providers and authorities
the most. The explosive PD and the dissocial PD tend to end up in
the criminal justice system. They are the groups with the highest
rates of comorbid drug use.
Other personality disorders include paranoid, schizoid, schizotypal,
histrionic, narcissistic, avoidant, dependent, obsessive-compulsive,
passive-aggressive, and self-defeating. Rates of comorbid drug use
are near average in these groups.
Borderline personality disorder is characterized by a pervasive
pattern of instability in interpersonal relationships, self-image,
and affect, as well as marked impulsivity as follows:
- Frantic efforts to avoid real or imagined abandonment
- Intense and unstable interpersonal relationships alternating
between extremes of idealisation and devaluation.
- Identity disturbances with markedly and persistently unstable
self-image or sense of self.
- Impulsivity in at least two areas that are potentially self-damaging
(eg. spending, sex, substance abuse, reckless driving and binge
eating)
- Recurrent suicidal behaviour, gestures or threats, or self-mutilating
behaviour
- Affective instability due to a marked reactivity of mood (ie
intense episodic dysphoria, irritability, or anxiety, usually
lasting a few hours and only rarely more than a few days)
- Chronic feelings of emptiness.
- Inappropriate, intense anger or difficulty controlling anger
- Transient, stress-related paranoid ideation or severe dissociative
symptoms.
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Comorbidity with personality
disorders
People with unstable emotional traits frequently use drugs in a non-functional
and destructive manner. As stated above drug use is most common in
the person with dissocial PD or the emotionally unstable PD group.
Drugs tend to be sought out and used early in an attempt to manage
the interpersonal difficulties and stresses that develop because of
their personality related problems. It is generally thought
that the PD predates and leads to the drug use and dependence but
one must consider the complex interplay of the drug related lifestyle
and its effects on the person over many years. The relationship between
the personality disorders and drug use is complex.
Drug use is generally counter productive and people should be counselled
through their use and brought to realise the problems that the drug
use produces for them given their particular personalities.
Limit setting and contracting is extremely important in this client
group.
Early case management with other primary care providers (emergency
department staff, locum service, after hours staff and even emergency
services and mental health staff) is indicated.
Drug use should be contracted. If benzodiazepine dependence is
a problem then some type of maintenance contract with a single prescriber
and pharmacist is indicated. If opiate use is a problem then consideration
should be given to opiate substitution programs such as methadone
or buprenorphine.
Regular scheduled consultations with restricted access to emergency
services/ last minute appointments. There needs to be a balance
between dependency fostering and providing the support that is required.
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Major
issues with personality disorders and cannabis/hallucinogen use
Effect of drug on disorder
Cannabis may be used in the context of poly drug use in the person
with dissocial PD. It may be used alone in many other types of PD,
for its euphoric and sedative effects in an attempt to relieve distress.
Drug interactions
The drug-based management of personality related problems is controversial.
A variety of medications have been tried for some types of behaviors
rather than diagnoses per se. Aggression and impulsivity have been
treated with carbamazepine, lithium, sodium valproate, and the SSRIs.
Good quality data on efficacy is limited.
Drug interactions therefore are similar to those encountered in
people with co-morbidity with depression and substance use, depending
on the medications being used.
Cannabis has been reported to cause mania with fluoxetine. Confusion,
depersonalisation, psychosis and hypomania have also been reported
with concurrent use of cannabis and SSRIs.
LSD may induce a serotonin syndrome with SSRIs.
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Clinical Considerations
Advice regarding cannabis usage in these disorders depends on the
degree of dysfunction associated with their use as well as the standard
range of problems associated with using an illicit substance.
Overall approach depends on the persons insight and readiness for
change.
Major
issues with the personality disorders and alcohol use
Effect of substance on mental disorder
Alcohol tends to cause disinhibition and blur judgement and thinking
and so is associated with more acting out in people with dissocial
and emotionally unstable PDs. This leads to violence or self-harm
attempts. The occurrence of problematic behaviours when intoxicated
is often stark.
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Drug interactions
The drug-based management of personality related problems is controversial.
A variety of medications have been tried for some types of behaviors
rather than diagnoses per se. Aggression and impulsivity have been
treated with carbamazepine, lithium, sodium valproate, and the SSRIs.
Good quality data on efficacy is limited.
Drug interactions therefore are similar to those encountered in
people with co-morbidity with depression and substance use, depending
on the medications being used.
Management approaches
Because of the problems associated with alcohol use and impulse
control the patient should be guided towards insight regarding this.
Depending on the amount of insight and readiness for change the
patient should be assisted with reducing or stopping alcohol use.
The use here of acamprosate or naltrexone should be considered.
However disulfiram may be problematic as these patients may drink
impulsively despite being warned of the risks.
Assistance with problem solving skills and with simple behavioural
management of stress can be helpful.
Formal CBT is more difficult with these people due to limited capacity
for insight.
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Major
issues with opiate use in people with personality disorders.
Effect of substance on mental disorder
Some people with personality disorders use opioids in the context
of poly-substance abuse.
In others opioids are used alone to relieve some of the distress
associated with their behavioural and interpersonal problems.
The chaotic lifestyle associated with opiate abuse certainly exacerbates
problems for people with dissocial PD and emotionally unstable PD.
Drug interactions
The drug-based management of personality related problems is controversial.
A variety of medications have been tried for some types of behaviors
rather than diagnoses per se. Aggression and impulsivity have been
treated with carbamazepine, lithium, sodium valproate, and the SSRIs.
Good quality data on efficacy is limited.
Drug interactions therefore are similar to those encountered in
people with co-morbidity with depression and substance use, depending
on the medications being used.
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Management approaches
People should be counselled according to the degree of problems
associated with the drug use.
Standard motivational interviewing techniques are useful here.
If dependence is present then maintenance opiate substitution should
be considered in an effort to re-instate some order in their lives.
Once stabilised then specific therapeutic interventions for problematic
behaviours can be considered.
Major
issues with people with personality disorders and stimulant use
Effect of substance on mental disorder
Use of stimulants may exacerbate the impulsivity of people with emotionally
unstable PD or dissocial PD.
People with other types of PD may use stimulants to assist with
symptom control or for recreation.
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Drug interactions
The drug-based management of personality related problems is controversial.
A variety of medications have been tried for some types of behaviors
rather than diagnoses per se. Aggression and impulsivity have been
treated with carbamazepine, lithium, sodium valproate, and the SSRIs.
Good quality data on efficacy is limited.
Drug interactions therefore are similar to those encountered in
people with co-morbidity with depression and substance use, depending
on the medications being used.
Serotonin syndrome may occur with cocaine or MDMA/ecstasy and SSRIs
and patients should be warned about this.
MDMA metabolised through CYP 2D6. This is inhibited by fluoxetine,
paroxetine and norfluoxetine.
Patients should be told about the signs of serotonin syndrome.
Citalopram and sertraline have least cytochrome mediated drug interactions
but all SSRIs are potential precipitators of serotonin syndrome
in people using cocaine and MDMA.
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Management approaches
People should be led to some insight regarding the negative effect
of the stimulants on their impulsive behaviour.
Education on the adverse health effects of stimulants should be
discussed.
Simple problem solving skills and behavioural strategies for managing
sress can be useful. However if frequent stimulant use if a factor
then success can be limited.
CBT is best used when the patient is not intoxicated and stimulant
use is minimal.
Major
issues with personality disorder and benzodiazepine use
Effect of substance on mental disorder
Benzodiazepines have been associated with reduced impulse control,
disinhibition and increased levels of violence, particularly with
people with dissocial PD, explosive PD and emotionally unstable PD.
The pattern of use is very important. Some people use benzodiazepines
in an intermittent binge pattern resulting in intoxication and disinhibition.
Consequently their use should be discouraged.
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Drug interactions
The drug-based management of personality related problems is controversial.
A variety of medications have been tried for some types of behaviors
rather than diagnoses per se. Aggression and impulsivity have been
treated with carbamazepine, lithium, sodium valproate, and the SSRIs.
Good quality data on efficacy is limited.
Drug interactions therefore are similar to those encountered in
people with co-morbidity with depression and substance use, given
that the SSRIs and mood stabilisers have been used in this group
of patients to assist with problematic violent and other extreme
behaviours.
The addition of nefazodone, fluoxetine and fluvoxamine will increase
the levels of diazepam alprazolam, midazolam and triazolam potentially
to toxic levels.
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Management approaches
As mentioned above benzodiazepines are used frequently by people
with dissocial, emotionally unstable and explosive PDs.
They are thought to have a negative effect on many of the problematic
behaviors associated with these disorders.
Patients should be counseled to reduce and stop these drugs. They
are addictive and dependence is common.
If dependence is present then gradual reduction is indicated. Initial
change to longer acting benzodiazepines for this withdrawal is preferable.
If this is unsuccessful then maintenance can have a role as part
of a containment strategy. However it must be emphasised that there
is evidence that even maintenance dosing of benzodiazepines may
be deleterious. If this approach is adopted then the relevant authorities
should be notified in each state jurisdiction, the drug use contracted;
there should be one dedicated prescriber and dispensing pharmacy.
Extreme caution should be exercised with maintenance doses above
40mg diazepam daily.
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Eating Disorders
Eating disorders such as anorexia and bulimia nervosa are more common
in women, but men sometimes develop these disorders too.
Anorexia
Anorexia is characterized by a significant weight loss resulting
from excessive dieting.
Most women and an increasing number of men are motivated by the
strong desire to be thin and a fear of becoming obese. Anorexics
consider themselves to be fat, no matter what their actual weight
is. In their attempts to become thinner, the anorexic will avoid
food and taking in calories at all costs, which can result in death.
People with anorexia usually strive for perfection. They set very
high standards for themselves and feel they always have to prove
their competence. They usually always put the needs of others ahead
of their own needs. A person with anorexia may also feel the only
control they have in their lives is in the area of food and weight.
If they can't control what is happening around them, they can control
their weight. Each morning the number on the scale will determine
whether or not they have succeeded or failed in their goal for thinness.
They feel powerful and in control when they can make themselves
lose weight. Sometimes focusing on calories and losing weight is
their way of blocking out feelings and emotions. Anorexics usually
have low self-esteem and sometimes feel they don't deserve to eat.
Signs and Symptoms (unique to anorexia nervosa)
- Noticeable weight loss
- Excessive exercise
- Fatigue & muscle weakness
- Obsession with food, calories, recipes
- Unusual eating habits (ie. cutting food into tiny pieces, picking
at food)
- Noticeable discomfort around food
- Complaining of being "too fat", even when thin
- Guilt or shame about eating
- Depression, irritability, mood swings
- Evidence of vomiting, laxative abuse, diet pills or diuretics
to control weight Wearing baggy clothes to hide weight loss
(or gain)
- Frequently checking weight
- Fainting spells and dizziness
- Difficulty eating in public
- Feelings of self worth determined by what is or is not eaten
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Bulimia
Bulimia is characterised by a cycle of binge eating followed by
purging to try and rid the body of unwanted calories. A binge is
different for all individuals. For one person a binge may range
from 1000 to 10000 calories, for another, one cookie may be considered
a binge.
Purging methods usually involve vomiting and laxative abuse. Other
forms of purging can involve excessive exercise, fasting, use of
diuretics, diet pills and enemas.
Bulimia sufferers are usually people that do not feel secure about
their own self worth. They usually strive for the approval of others.
They tend to do whatever they can to please others, while hiding
their own feelings. Food becomes their only source of comfort. Bulimia
also serves as a function for blocking or letting out feelings.
Unlike anorexics, people with bulimia do realize they have a problem
and are more likely to seek help.
Signs and Symptoms of Bulimia
- Binge eating
- Secretive eating
- Bathroom visits after eating
- Vomiting
- Laxative, diet pill or diuretic abuse
- Weight fluctuations (usually with 10-15 lb range)
- Harsh exercise regimes
- Fasting
- Severe self-criticism
- Self-worth determined by weight
- Fear of not being able to stop eating voluntarily
- Self-deprecating thoughts following eating
- Avoidance of restaurants, planned meals or social events
- Substance abuse
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Physical
and Medical Complications of Eating Disorders
A range of physical/medical complications can occur due to eating
disorders, generally associated with the dangerous eating habits and
compensatory activities of these disorders.
- Fatigue and lack of energy
- Irregular menstruation
- Dizziness & Headaches
- Dehydration & electrolyte imbalances
- Constipation and diarrhoea
- Shortness of breath & Chest pains Irregular heartbeat
- Depression
- Hair loss
- Stomach pain and bloating rosion of teeth enamel
- Chronic sore throat
- Kidney and liver damage
- Osteoporosis
- Insomnia
- Low blood pressure
- Gastric dilation and rupture, peptic
- Ulcers and pancreatitis
- Anemia
- Cardiac arrest and death
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Comorbidity
of eating disorders and substance use
People with bulimia have high rates of comorbid alcohol dependence.
In fact rates are much higher than normal healthy controls and higher
than people with anorexia nervosa.
Bulimic women with alcohol dependency have higher rates of self-harm,
higher rates of borderline personality disorders, and poorer outcomes
than those without alcohol related problems.
Cocaine and stimulants may also be used to control appetite and
dependence can develop.
The disruptive symptoms of eating disorders often interfere with
therapy for substance use disorders.
Drug use may assist with weight control, may be part of a risk
taking or self harm pattern of behaviour or part of impulsiveness
and loss of control.
Major
clinical issues with comobrbidity of eating disorders and cannabis/hallucinogen
use
Effect of substance on mental disorder
Cannabis is not often abused by people with eating disorders.
In moderate dosages cannabis stimulates the appetite. This may
give the false impression of recovery from anorexia.
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Drug interactions
Drug therapy is generally not used for the eating disorders with
the exception of the anti-depressants for co-occurring depression.
Management approaches
Management of the cannabis use should be determined by the level
of problem associated with the use.
Chronic intoxication will interfere with behavioural and cognitive
therapies for the eating disorder.
Major
clinical issues with the comorbidity of alcohol abuse and eating
disorders
Effect of substance on mental disorder
Alcohol abuse is common with people with bulimia. (probably 20-25%
incidence)
High rates of self harm and poorer prognosis in people with both
eating disorder and alcohol dependence.
Drug interactions
As drugs are usually not used in the management of the eating disorders
the scope for drug interactions is less.
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Management approaches
The alcohol dependence and the eating disorder need to be addressed
in an integrated manner.
Assistance with stress management (structured problem solving,
behavioural therapy, cognitive therapy) may assist both impulsive
binge eating behaviour and impulsive drinking.
Major
issues with eating disorders and opiate use
Effect of substance on mental disorder
People with eating disorders do not usually abuse opioids.
Drug interactions
As drugs are usually not used in the management of the eating disorders
the scope for drug interactions is less.
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Management approaches
Management of the opiate use will be directed by the level of problems
associated with this use.
While such a combination is unusual, the general approach should
be based on stages of change models, harm minimisation and opportunistic
management of both conditions in an integrated manner.
Major
issues with eating disorders and stimulants
Effect of substance on mental disorder
People with eating disorders frequently use stimulants in an attempt
to moderate appetite and assist with exercise bingeing.
Drug interactions
As drugs are usually not used in the management of the eating disorders
the scope for drug interactions is less.
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Management approaches
When assessing people with eating disorders a detailed drug history
should be elicited. This should include specific inquiry about alcohol,
stimulants, as well as diuretics, laxatives and thyroxine.
The use of stimulants at any level should be discouraged due to
the risk of dependence and toxicity.
Assistance with stress management may assist with impulsive use
of stimulants and with bingeing behaviours.
Standard management of the eating disorders should be commenced
if the patient is willing and engaged. The use of stimulants should
be addressed as this standard management is commenced.
Major
clinical issues with eating disorders and benzodiazepines
Effect of substance on mental disorder
People with eating disorders do not often use benzodiazepines.
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Drug interactions
As drugs are usually not used in the management of the eating disorders
the scope for drug interactions is less.
Management approaches
Benzodiazepine use should be discouraged. If some dependence has
been established then graduated withdrawal through slow reduction
of dosage should be negotiated.
Standard management of the eating disorders should commence if
the patient is willing and engaged.
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Somatoform disorders
Somatic presentations of underlying mental disorder or distress are
extremely common. Many of these presentations are easy to sort out
for the clinician with the underlying stressor or disorder quickly
coming to the fore and the patient quite willing to attribute the
physical symptoms to the underlying problem.
However within this broad phenomenon of somatic symptoms is a group
of people for whom somatic presentations become a predominant and
persistent feature of their illness behaviour . There are a number
of diagnostic subtypes.
Non simulated disorders
Where there is no insight into and even denial of the psychological
nature of the problem three diagnoses are used:
Somatization disorder.
Occurs when a person has the following features:
At least two years of multiple and varied presentations without
physical diagnosis.
- Persistent refusal to accept reassurance
- Impairment of social functioning.
- Persistent Somatoform pain disorder
- “Chronic pain syndrome” tend to have persistent pain
that is out of proportion with the underlying organic problem
and which is refractory to most biomedical treatments. There
is symptom hypervigilance , idiosyncratic beliefs in various
pharmacological regimes and treatments and a tendency to move
from one medical practitioner to another in the search of a
cure.
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Hypochondriacal disorder.
Occurs where a person presents repeatedly with physical symptoms
and refuses to accept reassurances despite thorough [and often repeated]
examination and investigation.
Simulated disorders
Where there is awareness that the symptoms and perhaps signs are
being simulated but no awareness of gain then factitious disorder
is likely. Where there is consciousness of the simulation as well
as the gain being sought then malingering is the correct conclusion.
Finally there are the conversion disorders where the patient mimics
neurological or other phenomena but this mimicry reflects the patients
understanding of how the phenomena present. During the simulation
the neurological structures said to be non-functional can clearly
be made to function by the examining medical practitioner.
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Comorbidity
with the Somatoform disorders
With people with these groups of disorders there is obvious
scope for inappropriate drug use and comorbidity as the medical practitioner
attempts to deal with some of the symptomatology before the correct
diagnosis is recognised. The Somatoform disorders are best managed
behaviourally and with cognitive therapy. However to engage in these
some degree of insight is required. If this insight cannot be achieved
then a health system based containment strategy is required.
Probably the most common Somatoform disorder to end up with comorbidity
with substance use problems is persistent Somatoform pain disorder.
Because of delay with diagnosis people with this disorder may well
end up having opioids, benzodiazepines and other psychotropic drugs
prescribed and dependence may occur in its own right.
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Somatoform
disorders and cannabis/hallucinogens
Effect of the cannabis/hallucinogen use on the disorder
These may have an effect on somatic symptoms in terms of making them
more accentuated.
Some people with persistent Somatoform pain disorder use cannabis
to assist with pain relief or with nausea associated with opiate
use. Cannabis has no analgesic properties and its role in modulating
pain and other symptoms is still being investigated.
Drug interactions
Drug management is not recommended in most Somatoform disorders.
However many people with persistent Somatoform pain disorder are
on opioids so there is a potential for increased sedation and psychomotor
problems with cannabis
Clinical considerations
Approach depends on the nature of the drug use, what other drugs
the person is taking and what problems there are associated with
the drug use.
If use is frequent an intoxication regular then this may interfere
with cognitive behavioural therapy. Use at this level should be
discouraged.
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Somatoform disorders
and alcohol use
Effect of alcohol on the disorder
People with chronic Somatoform pain disorder may use alcohol to reduce
pain symptoms. However it is not an analgesic and may interfere with
the person’s ability to use cognitive strategies to manage their behaviour
and their symptoms.
Alcohol use and intermittent withdrawal may result in exacerbation
of a variety of physical symptoms particularly associated with anxiety.
Depending on the nature of the Somatoform disorder this may be
an issue.
Drug interactions
Drug management is not recommended in most Somatoform disorders.
However many people with persistent Somatoform pain disorder are
prescribed opioids or tricyclics so there is a potential for increased
sedation and psychomotor problems with alcohol at any level.
There is no major interaction between disulfiram or acamprosate
with the opioids if these are being used. Naltrexone will obviously
interfere with opioid management.
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Clinical considerations
If alcohol consumption is hazardous or harmful then the person should
be counselled accordingly.
Alcohol use that results in intoxication will interfere with CBT
and will interfere with any structured problem solving or motivational
therapy.
Look for links between the patient’s symptomatology and alcohol
use so that insight can be raised.
Somatoform disorders and
opioids
Effect of opioids on the disorder
People with chronic Somatoform pain disorder frequently use opioids.
These may be helpful in the management of organic aspects of the pain
but because of the chronic nature of the pain and hence the opiate
use, dependence is common.
In some instances the actual prescription of the opiate is
seen as a legitimization of the pain and an acknowledgement of its
physical source.
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Drug interactions
Several analgesics and pain modulators cause sedation and the addition
of an opiate will exacerbate this.
This is a concern with the use of benzodiazepines as well.
Clinical approaches
If opioids are to be used then the advice of a specialist pain clinic
is advisable. This type of clinic will provide a multi-disciplinary
approach to the management of the patient’s pain that is not possible
in general practice.
If opiate dependence is identified then this needs to be discussed
with the patient and their readiness for change identified.
Change to a long acting opiate is preferable.
Use of methadone as part in a formalised program is also possible,
as this will allow probable control of the pain and the drug seeking
lifestyle.
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Somatoform disorders and
stimulants
Effect of the stimulant on the disorder
Stimulants may cause a variety of sympathetic nervous system related
symptoms that may become clinical presentations. However these are
generally short lived and drug level related.
Stimulant use may contribute to the anxiety associated with some
of the Somatoform disorders and resultant impulsively may result
in presentation to the health practitioner at a lower threshold
than usual.
Drug interactions
Potential interactions between stimulants and SSRIs. These latter
may be being used for secondary depression but they should not be
used as pain moderators as there is little evidence to support their
use. (in contrast with tricyclic antidepressants)
No particular interactions between stimulants and opioids and tricyclics.
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Major clinical considerations
Depends on the nature of the stimulant use. The clinician needs
to explore the reasons for the drug use and the possible negative
effect on the person’s health and the Somatoform disorder. As discussed
above stimulant use may contribute to symptoms and frequent presentations.
If the use is harmful then the patient needs to be guided towards
that realisation and readiness for change determined.
Somatoform
disorders and benzodiazepine use.
Effect of benzodiazepines on the Somatoform disorder
· People with Somatoform disorders often use benzodiazepines
to alleviate anxiety symptoms or to moderate pain. Dependence is frequent.
· Especially with short acting benzodiazepines fluctuating
levels may result in exacerbation of the disorder, with lowered thresholds
for presenting to the health system and withdrawal symptoms or “breakthrough
anxiety”.
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Drug interactions
Care with other potentially sedating drugs the person may be using
(either prescribed or non prescribed)
Major clinical considerations
Benzodiazepine use is common and dependence frequent. In general
use should be discouraged due to dependence potential and psychomotor
effects.
Withdrawal or dose reduction should be negotiated.
Change to a longer acting benzodiazepine is preferable both if
they are being maintained or for dosage reduction.
If the person is ready for change and willing to engage in CBT
specifically for their Somatoform disorder then minimisation of
benzodiazepine dosage is required so that the CBT is not interfered
with.
If maintenance use of benzodiazepines is anticipated then this
should be subject to a contract with the patient. Authorities should
be advised. Advice from a psychiatrist should be sought.
Benzodiazepines are frequently prescribed to induce “muscle relaxation”.
In reality very large (near anaesthetic doses) doses are required
for this and benzodiazepines are not recommended for the relief
of acute back pain.
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References
American Psychiatric Association (1996) Diagnostic and Statistical
Manual of Mental Disorders (4th Edition) Primary Care Version
Australian Medicines Handbook. (2000) Adelaide South Australia
Baigent M, Holme G, Hafner RJ Self-reports of the interaction between
substance abuse and schizophrenia. Aust N Z J Psychiatry (Australia),
Mar 1995, 29(1) p69-74
Bazire S Psychotropic Drug Directory 2001/2 QUAY BOOKS Bath
Brown T, Skop B Mareth T Pathophysiology and Management of the
Serotonin Syndrome Annals of Pharmacotherapy 1996 vol 30 527-33
Drug and Therapeutics Information Service Depression (2001)
Adelaide South Australia
Evans K, Sullivan JM (1990) Dual Diagnosis: Counselling the mentally
ill substance .abuser. New York: Guilford Press.
Gold M and Slaby A (Eds.), Dual diagnosis in substance abuse. New
York: Dekker Press.
Goldberg D, Benjamin S, Creed F Psychiatry in General Practice
(1994) Routledge London
Lane R Baldwin D Selective Serotonin Reuptake Inhibitor-Induced
Serotonin Syndrome: Review Journal of Clinical Pharmacotherapy 1997,
17: 208-221
O’Connell D 1998 Dual Diagnosis Essentials for Assessment and Treatment
Ware, Herts, Wynne Howard Books.
Prochaska J, DiClemente C (1986) Toward a comprehensive model of
change. In WR Miller and N Heather (eds) Treating Addictive Behaviours:
Process of change. Plenum New York
Ries (1995) Assessment and Treatment of patients with co-existing
mental illness and alcohol and other drug abuse. DIANE Publishing
Company
Sadock BJ, Sadock VA Psychiatric Drug Treatment 3rd Edition (2001)
Lippincott Williams and Wilkin Philadelphia
Sporer K The Serotonin Syndrome Drug Safety 1996 13 (2): 94-104
Stern T, Herman J, Slavin P MGH Guide to Psychiatry in Primary Care
(1998) McGraw Hill New York
Troisi A, Pasini A, Saracco M et al (1998) Psychiatric symptoms
in male cannabis users not using other illicit drugs. Addiction
93 (4): 487-92
Watson S, Benson J, Joy J Marijuana and medicine: assessing the
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Archives of General Psychiatry (2000) 57: 547-552
Zeidonis D, Brady K Dual Diagnosis in Primary Care Medical Clinics
of North America (1997) 81 (4): 1017-1036
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Appendix 1 Serotonin
syndrome
Some medication combinations can cause the development of a condition
called serotonin syndrome, due to too much serotonin being released
into the nervous system and the rest of the body. The syndrome is
potentially fatal.
Common features are as follows:
· Severe restlessness
· Over-excitability and hyperactivity (hypomania)
· Sweating and shivering
· Diarrhoea
· Fever
· Lack of coordination
· Confusion and altered consciousness
· Tremour
· Jerking limb movements (termed myoclonus)
It is important to let your doctor know or attend an emergency
department should you develop these symptoms.
The syndrome can be treated with withdrawal of the medications
that caused it in the first place. Sedative medications such as
diazepam or lorazepam are sometimes needed. If more severe then
intensive care is required.
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