Addiction is not a fixed and rigid event. Like psychiatric
disorders, addiction is a dynamic process, with fluctuations in severity, rate of
progression, and symptom manifestation and with differences in the speed of onset.
Both disorders are greatly influenced by several factors, including genetic
susceptibility, environment, and pharmacologic influences. Certain people have a high
risk for these disorders (genetic risk); some situations can evoke or help to
sustain these disorders (environmental risk); and some drugs are more likely than
others to cause psychiatric or AOD use disorder problems (pharmacologic risk).
Pharmacologic effects can be therapeutic or detrimental. Medication often produces both
effects. Therapeutic pharmacologic effects include the indicated purposes and desired
outcomes of taking prescribed medications, such as a decrease in the frequency and
severity of episodes of depression produced by antidepressants.
Detrimental
pharmacologic effects include unwanted side effects, such as dry mouth or constipation
resulting from antidepressant use. Side effects perceived as noxious by patients
may decrease their compliance with taking the medications as directed.
Some detrimental pharmacologic effects relate to abuse and addiction potential.
For example, some medications may be stimulating, sedating, or euphorigenic
and may promote physical dependence and tolerance. These effects can promote
the use of medication for longer periods and at higher doses than prescribed.
Thus, prescribing medication involves striking a balance between therapeutic
and detrimental phar-macologic effects. For instance, therapeutic antianxiety
effects of the benzodiazepines are balanced against detrimental pharmacologic effects
of sedation and physical dependency. Similarly, the desired therapeutic effect
of abstinence from alcohol is balanced by the possibility of damage to the
liver from prescribed disulfiram (Antabuse).
Side effects of prescription
medications vary greatly and include detrimental pharmacologic effects that may promote
abuse or addiction. With regard to patients with dual disorders, special attention
should be given to detrimental effects, in terms of 1) medication compliance,
2) abuse and addiction potential, 3) AOD use disorder relapse, and 4) psychiatric
disorder relapse (Ries, 1993a).
Not all psychiatric medications are psychoactive. The term psychoactive describes the ability of certain medications, drugs, and other substances
to cause acute psychomotor effects and a relatively rapid change in mood or
thought. Changes in mood include stimulation, sedation, and euphoria. Thought
changes can include a disordering of thought such as delusions, hallucinations,
and illusions. Behavioral changes can include an acceleration or retardation
of motor activity. All drugs of abuse are by definition psychoactive.
In contrast, certain nonpsychoactive medications such as lithium (Eskalith)
can, over time, normalize the abnormal mood and behavior of patients with bipolar
disorder. Because these effects take several days or weeks to occur, and do not
involve acute mood alteration, it is not accurate to describe these drugs as psychoactive,
euphorigenic, or mood altering. Rather, they might be described as mood regulators.Similarly, some drugs, such as antipsychotic medications, cause normalization
of thinking processes but do not cause acute mood alteration or euphoria.
However, some antidepressant and antipsychotic medications have pharmacologic side
effects such as mild sedation or mild stimulation. Indeed, the side effects of
these medications can be used clinically. Physicians can use a mildly sedating
antidepressant medication for patients with depression and insomnia, or a mildly stimulating
antipsychotic medication for patients with psychosis and hypersomnia or lethargy
(Davis and Goldman, 1992). While the side effects of
these drugs include a mild effect on mood, they are not euphorigenic. Nevertheless,
case reports of misuse of nonpsychoactive medications have been noted, and use
should be monitored carefully in patients with dual disorders.
While psychoactive
drugs are generally considered to have high risk for abuse and addiction, mood-
regulating drugs are not. A few other medications exert a mild psychoactive effect
without having addiction potential. For example, the older antihistamines such
as doxylamine (Unisom) exert mild sedative effects, but not euphoric effects.
Some drugs promote reinforcement, or the increased likelihood of repeated use. Reinforcement can occur by either
the removal of negative symptoms or conditions or the amplification of positive
symptoms or states. For example, self-medication that delays or prevents an unpleasant
event (such as withdrawal) from occurring becomes reinforcing. Thus, using a
benzodiazepine to avoid alcohol withdrawal can increase the likelihood of continued use.
Positive reinforcement involves strengthening the possibility
that a certain behavior will be repeated through reward and satisfaction, as
with drug-induced euphoria or drug-induced feelings of well-being. A classic
example is the pleasure derived from moderate to high doses of opiates or stimulants.
Drugs that are immediately reinforcing are more likely to lead to psychiatric
or AOD use problems.
Long-term or chronic use of certain medications can cause tolerance to the subjective
and therapeutic effects and prompt dosage increases to recreate the desired
effects. In addition, many drugs cause a well-defined withdrawal phenomenon after
the cessation of chronic use. Patients' attempts to avoid withdrawal syndromes
often lead them to additional drug use.
Thus, drugs that promote tolerance and withdrawal generally have higher risks
for abuse and addiction.
As can be seen, there are pharmacologic as well as hereditary and environmental
factors that influence the development of AOD use problems. All of these factors
should be considered prior to prescribing medication, especially when the patient
is at high risk for developing an AOD use disorder. High-risk patients include
people with both psychiatric and AOD use disorders, as well as patients with a
psychiatric disorder and a family history of AOD use disorders.
One aspect of
this issue relates to the pharmacologic profile of certain medications that
are used in the treatment of specific psychiatric disorders. For instance,
many medications used to treat symptoms of depression and psychosis are not
psychoactive or euphorigenic. However, many of the medications used to treat symptoms
of anxiety, such as the benzodiazepines, are psychoactive, reinforcing, have
potential for tolerance and withdrawal, and have an abuse potential, especially among
people who are at high risk for AOD use disorders. Other antianxiety medications,
such as buspirone (BuSpar), are not psychoactive or reinforcing and have low
abuse potential, even among people at high risk.
Thus, decisions about
whether and when to prescribe medication to a high-risk patient should include
a risk-benefit analysis that considers the risk of medication abuse, the
risk of undertreating a psychiatric problem, the type and severity of the psychiatric
problem, the relationship between the psychiatric disorder and the AOD use disorder
for the individual patient, and the therapeutic benefits of resolving the psychiatric
and AOD problems.
For example, the early and aggressive medication of
high-risk patients who have severe presentations of psychotic depression, mania,
and schizophrenia is
often necessary to prevent further psychiatric deterioration and possible death.
For these patients, rapid and aggressive medication can shorten the length
of the psychiatric episodes. In contrast, prescribing benzodiazepines to
high-risk patients with similarly severe anxiety involves a substantial risk of promoting
or exacerbating an AOD use disorder. For these high-risk patients, the use
of psychoactive medication should not be the first line of treatment.
Rather, for some high-risk patients, treatment efforts should involve a stepwise
treatment model that begins with conservative approaches and progressively becomes
more aggressive if the treatment goals are not met (Landry
et al., 1991a). For example, the stepwise treatment model for treating
high-risk patients with anxiety disorders may involve three progressive levels of
treatment: 1) nonpharmacologic approaches when possible; 2) nonpsychoactive medication
when nonpharmacologic approaches are insufficient; and 3) psychoactive medications
when other treatment approaches provide limited or no relief (Landry et al., 1991).
Reinforcement potential (decreases negative
symptoms and increases positive symptoms)
Tolerance and withdrawal potential
(a higher does is needed to gain the effect or to avoid ill effects).
A Stepwise Management Approach For Mild and Moderate Mental Disorders *
Step One:
Try nonpharmacologic approaches
Step Two:
Add nonpsychoactive
medications if Step One is unsuccessful
Step Three:
Add psychoactive
medications if Steps One and Two are unsuccessful.
* For
severe conditions, such as psychotic depression, mania, and schizophrenic disorders,
rapid and aggressive use of medications is needed to prevent danger to self or
others and further psychiatric deterioration.
Depending upon the psychiatric
disorders and personal variables, numerous nonpharmacologic approaches can help patients
manage all or some aspects of their psychiatric disorders (Weiss and Billings,
1988). Examples include psychotherapy, cognitive therapy, behavioral therapy,
relaxation skills, meditation, biofeedback, acupuncture, hypnotherapy, self-help groups,
support groups, exercise, and education.
Some medications are not psychoactive and do not cause acute psychomotor effects
or euphoria. Some medications do not cause psychoactive or psychomotor effects
at therapeutic doses but may exert limited psychoactive effects at high doses
(often not
euphoria, but sometimes dysphoria).
For practical purposes, all of these medications
can be described as nonpsychoactive, since the psychoactive effect is not prominent.
Medications used in psychiatry that are not euphorigenic or significantly
psychoactive include but are not limited to the azapirones (for example, buspirone),
the amino acids, beta-blockers, antidepressants, monoamine oxidase inhibitors,
antipsychotics, lithium, antihistamines, anticonvulsants, and anticholinergic medications.
Some medications can cause significant and acute alterations in psychomotor,
emotional, and mental activity at therapeutic doses. At higher doses, and for some
patients, some of these medications can also cause euphoric reactions. Medications
that are potentially psychoactive include opioids, stimulants, benzodiazepines,
barbiturates, and other sedative-hypnotics.
One of the emphases of stepwise treatment is to encourage nondrug treatment
strategies for each emerging symptom before medications are prescribed. Nondrug treatment
strategies alone are inappropriate for acute and severe symptoms of schizophrenia
and mood disorders, but nondrug strategies do have their place in the treatment
of virtually any psychiatric problem, and may provide partial or total relief
of some symptoms related to severe psychiatric disorders. For example, relaxation
therapy can minimize or eliminate somatic symptoms of anxiety that may accompany
an agitated depression.
A second emphasis of stepwise treatment is to
encourage the use of medications that have a low abuse potential. This conservative
approach must be balanced against other therapeutic and safety considerations in
acute and severe conditions, such as
psychosis or mania. On the other hand, a conservative approach is not the same as
undermedication of psychiatric problems. Undermedication often leads to psychiatric deterioration
and may promote AOD relapse. There should be a balance between effective treatment
and safety.
A third emphasis of stepwise treatment is to encourage the
idea that different treatment approaches should be viewed as complementary,
not competitive. For example, if psychotherapy or group therapy does not provide
complete relief from a situational depression (such as prolonged grief), then antidepressants
should be considered as an adjunct to the psychotherapy, but not as a substitute
for psychotherapy.
In practice, treatment providers often use a combination
of drug and nondrug strategies. This practice includes medication to treat
the acute manifestations of the disorder while the individual learns long-term
management strategies. For example, an individual may be prescribed nonpsychoactive
buspirone to reduce anxiety symptoms while learning stress reduction techniques and
attending group therapy.
These guidelines are broad, general, and more applicable
to chronic than to acute psychiatric problems. Also, these guidelines have
limited application to very severe psychiatric problems.
Several antihistamines are approved for sale as over-the-counter hypnotics, including
diphenhydramine (Nytol, Benadryl), doxylamine (Unisom), and pyrilamine (Quiet World).
The efficacy of these drugs is not uniform, and tolerance to the anxiolytic
and hypnotic effects is rapid, limiting their utility for episodic use. Antihistamines
are frequently prescribed for mild anxiety and insomnia, particularly for patients
in general hospitals, patients with physical illness (Salzman, 1989), and
elderly patients.
In general, the early antihistamines exert very mild anxiolytic and hypnotic
effects, but lack euphoric properties and do not promote physical dependence (Meltzer,
1990). While lacking significant abuse potential themselves, antihistamines may
cause problems for some patients by reinforcing the idea of self-medication of
insomnia and anxiety. Taken in high doses, antihistamines may cause acute delirium,
alter mood (often causing dysphoria), or cause morning-after depression. Under
close medical supervision, the conservative use of antihistamines can be valuable
in treating brief episodes of insomnia during an otherwise drug-free recovery
process. Patients in recovery should be discouraged from purchasing and using over-the-counter
antihistamines.
The antidepressants include several
types of medication, such as tricyclics, monoamine oxidase inhibitors (MAOIs),
and other, newer, antidepressants such as trazodone (Desyrel), bupropion (Wellbutrin),
sertraline (Zoloft), and fluoxetine (Prozac). Antidepressants are effective for the
treatment of depression, and several are valuable for the treatment of anxiety disorders,
including generalized anxiety disorder, phobias, and panic disorder.
The antidepressants are not euphorigenic, and do not
cause acute mood alterations. Rather, they are mood regulators and diminish
the severity and frequency of depressive episodes; they also have anti-panic
capabilities unrelated to sedation.
While the general effects of most of the older
tricyclic antidepressants are similar, they differ considerably with regard to side
effects. For example, some antidepressants such as doxepin (Sinequan) exert a mild
sedating effect, while others such as protriptyline (Vivactil) exert a mild stimulating
effect. These side effects can be clinically useful. For example, clinicians
might give antidepressants with slight sedating effects to depressed patients
with insomnia or give those with mild stimulating effects to depressed patients
who experience low energy and hypersomnia (Davis and Goldman,
1992).
Other side effects of tricyclic antidepressants are common. Anticholinergic
effects such as dry mouth, blurred vision, constipation, urinary hesitancy, and
toxic-confusional states are common anticholinergic effects. Adrenergic activation symptoms
may include tremor, excitement, palpitation, orthostatic hypotension, and weight
gain. These noxious side effects are frequently the cause of requests to switch
from one medication type to another. Also, side effects often prompt discontinuation
of medication, which may provoke reemergence of the psychopathology. Tricyclics
unfortunately are quite toxic when combined with AODs. Therefore use of tricyclic antidepressants
in early recovery should be carefully monitored.
More expensive, but
much less toxic when used with AODs, are the newer serotonin reuptake inhibitors
including fluoxetine, paroxitine (Paxil), and sertraline. These agents also have
anticompulsive effects, and their side effects tend to be slight to moderate stimulation
rather than sedation. They are much safer to use in early recovery.
Overall,
the use of antidepressants is consistent with a psychoactive-drug-free philosophy,
does not compromise recovery from addiction, and enhances recovery from depressive
and panic disorders. However, patient information must include clear explanations
of the reasons for prescribing, the expected results, and the risks of adverse
effects, including overdose. The risk-benefit analysis must include the risk of
lethal overdose with tricyclic antidepressants, especially for depressed patients
(Reid, 1989).
The beta-blockers such as propranolol (Inderal) are well-recognized medications
for the treatment of hypertension, cardiac arrhythmias, and angina pectoris.
They also have clinical efficacy as an adjunct in the treatment of anxiety
(Lader, 1988). The b-blockers may reduce or eliminate the adrenergic discharge
associated with panic attacks, thus blocking the somatic components of some anxiety
states, especially when somatic symptoms predominate (Trevor and Way, 1989). b-blockers
diminish the tremor and restlessness related to lithium or antipsychotics in some
patients.
The Beta-blockers
are not psychoactive, euphorigenic, or mood altering. Since tolerance to the
anti-panic effects of b-blockers develops rapidly, they cannot be used for extended
periods of time for this purpose. Rather, they are often used prophylactically
for anticipated panic-producing situations, or for episodes of anxiety that
may last a few days. The b-blockers are also used to decrease acute and subacute
anxiety symptoms during detoxification from sedative-hypnotics such as the benzodiazepines.
Overall, the use of b-blockers is consistent with a psychoactive-drug-free
philosophy, does not compromise recovery from addiction, and can be an important adjunct
to anxiety management.
While all of the benzodiazepines have anxiolytic characteristics, they differ
in their effectiveness in treating generalized anxiety disorder, mixed anxiety
and depression, panic attacks, phobic-avoidance
behaviors, and insomnia. In general, the benzodiazepines promote sedation, central
nervous system depression, and muscle relaxation, and thus are effective for anxiety
reduction and, at higher doses, for short-term management of insomnia.
The benzodiazepines
are psychoactive, mood altering, and reinforcing. Chronic use and subsequent
cessation can cause withdrawal symptoms. Studies have shown that the benzodiazepines
are not uniformly euphorigenic. Also, patients with a family and personal history
of AOD abuse and addiction are more likely to experience euphoria with the
benzodiazepines (Ciraulo et al., 1988,1989).
Benzodiazepines are the most commonly
used agents to moderate alcohol withdrawal and prevent dangerous withdrawal
conditions such as delirium tremens and seizures. They are also widely used during
detoxification from sedative-hypnotics. The benzodiazepines are frequently prescribed
for use alone and in combination with antipsychotics during the treatment of
acute psychotic symptoms caused by mania, schizophrenia, and drugs of abuse such
as cocaine. Such treatment should be limited to the acute episode for most
patients with dual disorders, so that one problem (psychosis) is not replaced by
another problem (physical dependence or addiction). The benzodiazepines are not
usually recommended for long-term use in patients with dual disorders unless all
nonpsychoactive approaches have failed. That is, if all other less potentially adverse
medications have proven inadequate and the benzodiazepines are indicated, then careful
dispensing, regulation of dose, and scrupulous monitoring are required.
Overall,
the use of benzodiazepines after the medical management of withdrawal is not
consistent with a psychoactive-drug-free philosophy and may compromise recovery from
addiction (Zweben and Smith, 1989). However, they can be used in the management
of acute and severe withdrawal, panic, and psychosis with special guidelines
in nonroutine situations.
Buspirone is the most well known of a new group of drugs (the azapirones) that selectively
diminish multiple symptoms of anxiety without the acute mood alteration, sedation,
or associated somatic side effects seen in the sedative-hypnotic anxiolytics.
Buspirone is useful for generalized anxiety disorder, chronic anxiety
symptoms, anxiety with depressive features, and anxiety among elderly patients.
Buspirone is
generally equivalent to the benzodiazepines with regard to anxiety management
(Petracca et al., 1990; Strand et al., 1990). However,
it takes several weeks for the maximal therapeutic effect of buspirone to
occur.
Buspirone is not psychoactive,
mood altering, or euphorigenic (Balster, 1990). In particular,
buspirone does not cause the mood alteration, central nervous system depression,
sedation, and muscle relaxation associated with the benzodiazepines. However, many
people with experience taking benzodiazepines may associate these mood alterations
with relief of anxiety. As a result, patients who have experience with the
benzodiazepines may misinterpret the absence of these side effects as evidence that the
medication is ineffective. Educating patients about the distinction between anxiety
reduction and sedation and about treatment expectations can avoid these misinterpretations.
Overall, the use of buspirone is consistent with a psychoactive-drug-free philosophy,
does not compromise recovery from addiction, and enhances recovery from anxiety
disorders.
Used in the form of a patch (Catapres Transdermal
Therapeutic System patches) or tablets (Catapres), clonidine is well recognized as
a treatment for symptoms of hypertension, including hypertensive symptoms
that occur during withdrawal from depressant drugs, especially the opioids.
In addition, clonidine appears to have anxiolytic and anti-panic properties
comparable to the antidepressant imipramine. Patients may become less anxious but
remain symptomatic. Some patients who have anxiety-depression or panic-anxiety
experience significant antianxiety effects from clonidine. The anti-panic effect
is the result of clonidine's ability to decrease locus ceruleus firing and
thus decrease adrenergic discharge. Thus, clonidine may be useful for short-term
use in the treatment of refractory anxiety with panic (Domisse
and Hayes, 1987; Uhde et al., 1989).
Clonidine is not psychoactive,
euphorigenic, or mood altering. Clonidine may have significant antianxiety effects when
administered to patients with anxiety-depression and panic-anxiety. However, tolerance
to the anti-panic effects of clonidine can develop within several weeks.
Thus, clonidine may be most useful for
short-term use in the treatment of refractory panic disorder.
Overall, the use
of clonidine is consistent with a psychoactive-drug-free philosophy, does
not compromise recovery from addiction, and may be an adjunct in the treatment
of anxiety symptoms.
The neuroleptic medications are most effective in suppressing the positive
symptoms of psychosis such as hallucinations, delusions, and incoherence. In addition,
they may help reduce disturbances of arousal, affect, psychomotor activity,
thought content, and social adjustment (Africa and Schwartz,
1992). These psychotic symptoms may accompany schizophrenia, brief reactive
psychosis, schizophreniform disorder, mania, depression, and organic mental disorders
induced by AODs and medical conditions (Ries, 1993a).
Although neuroleptic medications are equally effective in suppressing psychotic
symptoms, individuals may respond to one medication better than another. The chief
differences among the neuroleptics relate to dosage, onset of effects, and (especially)
side effects. Some side effects may be clinically useful, such as nighttime
sedation with chlorpromazine or avoidance of appetite stimulation with molindone
(Moban) (Africa and Schwartz, 1992).
In general, low-potency neuroleptics,
for example, chlorpromazine, thioridazine (Mellaril), and clozapine (Clozaril),
have significant sedative and hypotensive properties. Tolerance to these properties
may develop within a few weeks. Also, low-potency neuroleptics are inherently
anticholinergic, so that the use of additional anticholinergic drugs to prevent extrapyramidal
symptoms may be unnecessary. The high-potency neuroleptics such as fluphenazine
(Prolixin) and haloperidol (Haldol) cause more extrapyramidal side effects than the
low-potency medications.
The extrapyramidal system is a network of nerve pathways that links nerves
in the surface of the cerebrum (the deep mass of the brain), the basal ganglia
deep within the brain, and parts of the brain stem. The extrapyramidal system
influences and modifies electrical impulses that are sent from the brain to the skeletal
muscles.
When this system is damaged or disturbed, execution of voluntary
movements and muscle tone
can be disrupted, and involuntary movements, such as tremors, jerks, or writhing
movements, can appear. These disturbances are called extrapyramidal syndromes, which
can be caused by all of the neuroleptic medications except clozapine.
Extrapyramidal
symptoms are unwanted, noxious, and uncomfortable. Compliance with neuroleptic
medications is worsened because of the onset of these drug-induced symptoms. A class
of medications called anticholinergic agents can eliminate the muscle spasms
in the neck, oral, facial, cheek, and tongue regions. Several other types
of medications may also be helpful, including amantadine and beta-blockers.
Anticholinergic agents can also reduce the extrapyramidal movement disorder called akathisia,
which consists of purposeless movements, usually of the lower extremities, often
accompanied by the experience of severe, uncomfortable restlessness. These medications
include benztropine (Cogentin), biperiden (Akineton), diphenhydramine (Benadryl),
trihexyphenidyl (Antitrem), and procyclidine (Kemadrin). Patient response should be monitored
because some anticholinergic medications may be mildly psychoactive for some AOD
patients.
Neuroleptic drugs are not euphorigenic and do not cause acute mood or psychomotor alterations.
However, side effects are common. Most of the neuroleptics cause sedation
as a side effect, although adaptation to the sedative (but not the antipsychotic)
effects develops within days or weeks. The anticholinergic side effects of neuroleptic
medications can include dry mouth, constipation, and blurred vision. The neuroleptics
can also cause extrapyramidal symptoms. The adverse side effects of neuroleptic
medications are a frequent cause of medication compliance problems. These adverse
effects can also prompt patients to use AODs to self-medicate noxious symptoms.
Because patients with psychotic symptoms often experience significant biopsychosocial
problems, the neuroleptics allow them to engage in problem-solving and recovery-oriented
interpersonal activities. Overall, the use of neuroleptics is consistent with a psychoactive-drug-free
philosophy, does not compromise recovery from addiction, and enhances recovery from
psychotic disorders.
Lithium
is the standard and first-line treatment for
manic episodes, even though 10-14 days may be required before full effect is
achieved. The initial symptoms managed by lithium include increased psychomotor
activity, pressured speech, and insomnia. Later, lithium diminishes the symptoms
of expansive mood, grandiosity, and intrusiveness. Lithium also treats signs
related to disorganization of the form of thought such as flight of ideas and loosening
of association.
Lithium
does not cause acute mood alteration, and is not psychoactive or mood altering.
Rather, lithium is a mood regulator, and diminishes symptoms of acute
mania. The common adverse effects of lithium include thirst, urinary frequency,
tremor, and gastrointestinal distress. Lithium allows patients who may have seriously
disabling symptoms to engage in problem-solving and recovery-oriented interpersonal
activities. Overall, the use of lithium is consistent with a psychoactive-drug-free
philosophy, does not compromise recovery from addiction, and enhances recovery from
bipolar disorders.
Anticonvulsants have a role in the management of bipolar disorders, mania, schizoaffective
disorder, and alcohol and benzodiazepine withdrawal. In addition, these medications
may be prescribed for "flashbacks" related to drug use or post-traumatic stress
disorder. These medications, such as carbamazepine (Tegretol) and valproic acid,
are not psychoactive. The typically minor side effects of sedation and nausea
may emerge as treatment is initiated. Rarely, carbamazepine causes a decrease
in white blood cell count. Both medications are monitored according to blood
levels. For the treatment of bipolar disorder, the anticonvulsants are most often
used when lithium has failed. However, they are occasionally used by highly
skilled physicians as first-line treatment. These medications are consistent with
a psychoactive-drug-free philosophy, and may enhance the abilities of those
who need them to participate in the recovery process.
There are certain risks associated
with AOD use and withdrawal among patients who are also being administered medications
to treat psychiatric disorders. Because of these risks, serious consideration
should be given to inpatient treatment for withdrawal.
Alcohol and barbiturates
can cause increased tolerance by increasing the amount of liver enzymes responsible
for their metabolism. These same liver enzymes are also responsible for metabolizing
many antidepressant, anticonvulsant, and antipsychotic medications. Thus, serum
levels of medications will be decreased, possibly to subtherapeutic levels. Without
assessing for possible AOD use, some physicians may mistakenly increase medication
doses.
Alcohol interferes with the thermoregulatory center of the brain, as do antipsychotic
drugs. Patients taking both medications may be unable to adjust their body temperature
in response to extremes in the external environment.
The interaction
of stimulants in a person taking monoamine oxidase inhibitor antidepressants
can lead to a life-threatening hypertensive crisis.
Alcohol and cocaine
enhance the respiratory depression effects of opioids and some neuroleptics such
as the phenothiazines. This effect can increase vulnerability to overdose
death.
Marijuana has anticholinergic effects. In combination with the anticholinergic medications
such as Cogentin, marijuana use can lead to an anticholinergic (atropine) psychosis.
Patients who are vulnerable to hallucinations, such as schizophrenic patients, are
at high risk for having hallucinations during the withdrawal from alcohol
and other sedative-hypnotics.
Antipsychotics and antidepressants
lower the seizure threshold and enhance seizure potential during withdrawal from
sedative-hypnotics and alcohol.
Alcohol intoxication and withdrawal disturbs the fluid
electrolyte balance in the body, which can lead to lithium toxicity.
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