German Journal of Psychiatry
ISSN 1433-1055
¹Department of Psychiatry, Columbia University/ New York State Psychiatric Institute, New York
Corresponding
author: Carlos Blanco, M.D. Ph.D., Department of Psychiatry,
Columbia
University/New York State Psychiatric Institute, Box 69, 1051 Riverside Drive,
New York NY
10032, USA
Objective: Pathological
gambling is an increasing public health problem. Many mental health
professionals have limited information regarding the etiology, phenomenology and
treatment of this patient population. Method: Computerized literature search
using PsycLIT and MEDLINE for the years 1984 to 1999. Results and conclusion:
There are several competing conceptualizations of pathological gambling: as an
impulse control disorder, a mood disorder, an obsessive-compulsive spectrum
disorder, or a non-pharmacological addiction. An alternative model of
pathological gambling is as a heterogeneous disorder with different subtypes
sharing certain characteristics. Both biological and psychological factors play
a role in the etiology of pathological gambling. Treatment options include
several medications, psychotherapies and attendance to Gamblers Anonymous,
although none of them are established treatments. There is the need for further
research in order to improve the understanding of this disorder and improve the
quality of the treatments available (German J Psychiatry, 2000;3:37-52).
Pathological
gambling is a frequently underdiagnosed and disabling disorder the prevalence of which appears to be
increasing along with the increment of gambling opportunities (Volberg, 1994).
Many decades have passed since excessive gambling was recognized as a form of
psychopathology. But the attention paid to this disorder grew considerably when
pathological gambling started to be considered a public health issue, as well as
when the American Psychiatric Association (APA) included pathological gambling
in the third edition of its Diagnostic and Statistical Manual of Mental
Disorders (DSM-III) in 1980. Over the last decade, there has been a growing
interest to refine the diagnostic criteria of pathological gambling, assess its
prevalence, identify the possible causes of this disorder, and find effective
treatments for it.
Pathological
gambling is a chronic and progressive condition that disrupts the life of the
individual and those close to him. Not only is pathological gambling associated
with financial problems due to the large amounts of money spent on the activity
or the loss of a job, but this disorder increases the likelihood of other
emotional and psychiatric problems, and general health problems in the
individual or his family (Lorenz and Yaffee, 1986, 1988). Suicide is a possible
consequence of pathological gambling. Exceeded only by mood disorders,
schizophrenia and some neurological conditions, the suicide rate due to
pathological gambling has been found to be very high.
At present,
there are several competing conceptualizations for pathological gambling.
(1) The World
Health Organization (WHO), as well as the APA, classify pathological gambling as
an impulse control disorder, because the individual becomes increasingly
incapable of resisting his impulses to gamble. All the impulse control disorders
share the following characteristics: difficulties to resist an impulse, desire
or temptation to perform some behavior that is detrimental for the individual or
others; a progressive emotional discomfort or tension before performing the act;
pleasurable or gratifying feelings while performing the behavior, which means
that the behavior is egosyntonic; in some cases, negative feelings of guilt,
remorse or shame when the act is over. All of these characteristics are
recognizable in the pathological gambler.
(2) Because of
the high incidence of depression throughout the life of pathological gamblers,
up to 75% reported in some studies, many authors consider that pathological
gambling could be a form of affective disorder
(McCormick et al., 1984; Linden et al., 1986; Roy et al., 1988a; Cusack et al.,
1993; Sullivan et al., 1994). Supporting this hypothesis is the fact that there
is high comorbidity between pathological gambling and alcoholism (also related
to affective disorders), and a higher frequency of affective disorders in first
degree relatives of pathological gamblers. Additional evidence in support of
this hypothesis are the high incidence of suicidal attempts found in this
population (Saiz-Ruiz & López-Ibor, 1983; McCormick et al., 1984; Sullivan
et al., 1994) and the high scores found in scales that measure depression (Glen,
1979; McCormick et al., 1987; Blaszczynski & McConaghy, 1988; Saiz-Ruiz et
al., 1992). Contrary to the idea that pathological gambling is a form of mood
disorder is the idea that in many cases the affective disorders observed in
pathological gamblers are not primary, but constitute a secondary reaction to
the negative consequences of gambling (Saiz-Ruiz & López-Ibor, 1983; Taber
et al., 1987a; Ramírez et al., 1988; Saiz-Ruiz et al., 1992; Sullivan et al.,
1994; Thorson et al., 1994; Moreno et al., 1995). Additionally, some studies
have not found significant differences in the frequency of affective disorders
in first degree relatives of pathological gamblers and the general population
(Thorson et al., 1994; Ibáñez, 1997).
(3) Some authors
consider that pathological gambling is best understood as an
obsessive-compulsive spectrum of disorder. In this context, the term
obsessive-compulsive spectrum disorder is used to describe a group of disorders
with pathophysiological similarities that also share genetic and biological
mechanisms. Patients with spectrum-related disorders show an intense desire to
perform a specific behavior preceded by unpleasant feelings and physiological
activation, all of which are relieved when the behavior is performed (Hantouche
& Merckaert, 1991; Hollander, Skodol & Oldham, 1996; Cartwright et al.,
1998). In addition, it has been noted that patients with pathological gambling
report a repetitive thought related to gambling that they cannot remove from
their minds, which leads them to gamble against their will, especially in
advanced phases of the disorder (Lesieur, 1979).
Authors who
oppose this view argue that the idea of gambling and the gambling behavior in
itself, although not its consequences, are egosyntonic for the patients in all
phases of the disorder, in contrast to what happens in the obsessive-compulsive
spectrum disorders, where the behavior is consistently egodystonic (Moreno,
1991; APA, 1994; Ibáñez, 1997). Furthermore, pathological gamblers do not show
the excessive doubt characteristic of obsessive-compulsive patients (Rasmussen
& Eisen, 1992). Moreover, compulsive behaviors include increased evasive
behavior, risk aversion and anticipatory anxiety, all of which are not observed
in the behavior of pathological gamblers.
(4) A fourth
model views pathological gambling as a non-pharmacological addiction. The common
elements to all kinds of addiction are an intense desire to satisfy a need, loss
of control over the substance or behavior, symptoms of abstinence and tolerance,
thoughts about the use of the substance and performance of the behavior despite
its adverse consequences (OMS, 1993). All of these elements are present in
pathological gambling. Gamblers' intense longing to bet is equivalent to the
cravings experienced by substance abusers, even a study by Castellani and Rugle
(1995) found that gamblers had more difficulties resisting the cravings than
substance abusers. Moreover, evidence suggests that up to a third of
pathological gamblers experience withdrawal symptoms such as irritability,
psychomotor agitation, difficulties for concentration and other somatic
complaints (Wray et al., 1981; Dickerson, 1989). Gamblers also experience the
equivalent of tolerance when they need to increase the frequency of bets or the
amount of money spent in order to obtain the desired excitation. Furthermore,
pathological gamblers become progressively preoccupied and involved in
gambling-related activities at the cost of abandoning other sources of pleasure
and enjoyment (Lesieur, 1979), and despite the negative domestic, professional,
financial and social consequences of their behavior (McCormick & Ramirez,
1988; Bland et al., 1993).
Other findings
in favor of this hypothesis are the high comorbidity found between pathological
gambling and other addictive disorders, especially alcoholism; the family
history of addictions found in pathological gamblers; the tendency to relapse;
and, the positive response of pathological gamblers to psychological treatment
modalities used for other addictions (Ibáñez, 1997).
(5) Finally, it
is also possible that pathological gambling may not be an homogeneous entity
that fits only into one of the models mentioned above, but rather a mixed group
with different subtypes that share certain characteristics. In order to confirm
or reject the existence of such subgroups and define their particularities,
future research should assess phenomenological aspects of gambling behaviors
such as the choice of the gambling setting and activity, the motivations to
gamble, and the mood present during gambling or triggered by it. Studies of the
natural history of the disorder, possible differential treatment response, and
underlying neurobiological differences can further help in the definition of
these subtypes.
Along with the
existence of different conceptualizations of pathological gambling, a number of
biological and psychological theories have been presented to explain the
etiology of pathological gambling. The biological theories have focused on the
intervention of neurotransmitters’ systems in pathological gambling. The
psychological explanations arise from different psychological orientations,
including psychoanalysis, behavioral psychology or cognitive psychology.
Phenomenological similarities between pathological gambling and other
impulse control disorders have led to a search of serotonergic abnormalities in
pathological gamblers. Serotonin dysfunction has been frequently shown to be
associated to other impulsive behaviors such as fire-setting, violent offenses
and violent suicide. Impulsivity implies a deficit in cerebral inhibition, which
is partly mediated by serotonergic pathways (Carlton & Manowitz, 1987;
Linnoila, 1990; Jacobs, 1991).
Because platelet monoamine oxidase (MAO) activity is believed to be a
good indicator of serotonergic systems, Blanco et al. (1996) compared platelet
MAO activity in 27 male pathological gamblers and 27 controls matched for age,
gender and tobacco consumption. Platelet MAO activity was significantly lower
for the patients than for the comparison subjects, suggesting that pathological
gamblers have a deficit in their serotonergic function.
In further support of the hypothesis of a serotonergic deficit in
pathological gamblers, another study has found an allele variant of a
polymorphism in the MAO-A gene in a group of 31 severe pathological gamblers
(Ibáñez et al., 2000). In contrast, the same study found that the gene for
MAO-B did not have a different allele distribution in patients and controls,
suggesting that low levels of MAO-B activity in pathological gamblers are not
determined by the gene for MAO-B, although they may be mediated through genes
that modulate the expression of the MAO-B gene.
Moreno et al. (1991) administered IV clomipramine to 8 pathological
gamblers and 8 healty volunteers matched for gender and age. Pathological
gamblers had lower baseline prolactin levels and blunted prolactin levels at 60
minutes post-CMI infusion compared with controls, suggesting decreased serotonin
transporter binding acitivity in pathological gamblers.
In a subsequent study, DeCaria et al. (1996) compared prolactin
response to a single dose of m-CPP between pathological gamblers and matched
controls. They found that pathological gamblers showed increased changes in
prolactine in contrast with the controls, and a positive correlation between
changes in prolactin and gambling severity. These findings suggest an
hypersensitivity of 5-HT postsynaptic receptor in pathological gamblers.
Central norepinephrine is involved in the physiological functions
associated with arousal and impulse control. A study by Roy et al. (1988b, 1989)
points to an implication of the NE system in the pathophysiology of pathological
gambling related to arousal. They found an increase of CSF MHPG, plasma MHPG,
urinary NE and vanillymandelic acid in pathological gamblers. Furthermore, they
found a significant correlation between these indexes of noradrenergic
functioning and the scores on the extraversion scale of the Eysenck Personality
Questionnaire. This study suggests that pathological gamblers may have a
functional disturbance of their noradrenergic system that could be reflected in
their personality.
Using growth hormone (GH) response to clonidine, an alpha-2 adrenergic
agonist, as a form of assessment of central noradrenergic function, DeCaria et
al. (1997) compared a group of five pathological gamblers with eight healthy
volunteers on GH response to clonidine. They found an increased response of
pathological gamblers compared to controls. In addition, severity of gambling
behavior correlated with the magnitude of clonidine-induced GH response,
suggesting an involvement of the noradrenergic system in the etiology of
pathological gambling.
A growing body of literature relates the dopaminergic system to reward
mechanisms and addictive behaviors (Wise, 1987). It has been hypothesized that
some individuals may have deficits in dopaminergic transmission in the brain,
which would lead them to experience generalized feelings of discomfort. These
subjects would engage in activities or would use substances in an attempt to
increase and normalize dopaminergic transmission (Sunderwirth & Milkman,
1991).
Based on the
conceptualization of pathological gambling as a behavioral addiction, some
authors have sought to investigate dopaminergic function in pathological
gamblers. Roy et al. (1988b) failed to find significant differences in plasma,
urinary and dopamine CSF between pathological gamblers and controls. However,
more recently, in a study with ten pathological gamblers and seven controls
matched for height and weight, Bergh et al. (1997) found that pathological
gamblers had a decrease in dopamine in the CSF and an increase in dopamine
metabolites compared to healthy volunteers. These findings suggest an increased
release of dopamine in pathological gamblers. An explanation of the difference
in the results obtained by these two studies is unclear and points to the need
to perform more studies on the dopaminergic system of pathological gamblers.
The first people to offer an explanation for pathological gambling was
the psychoanalysts. Von Hattingberg conducted the first study of pathological
gambling in 1914. He proposed that pathological gamblers had a fixation in the
anal phase of development which explained the compulsive and masochistic traits
in their personality. Pathological gamblers eroticize the tension and fear
involved in gambling.
The work of von Hattingberg was further elaborated by Freud and Bergler
who have largely influenced later psychoanalytic work on this topic. In his
paper “Dostoyevski and Parricide”, Freud (1928) suggests that pathological
gambling is a form of addiction related to the Oedipus complex. The individual
gambles as a substitute for masturbation. Also gambling constitutes a way of
punishment that secondarily becomes a pleasurable activity. Thus, Freud suggests
masochistic component to pathological gambling. For Bergler (1957), pathological
gambling is also masochistic and related to the Oedipus complex, but he
emphasizes the relationship with authority figures as the origin of guilt.
More recently Rosenthal (1986) has suggested that pathological gambling
may be more closely related to the preoedipal than to the oedipal phase of
development. According to him, pathological gamblers tend to have narcissistic
personality traits. Omnipotence and negation are then the defense mechanisms
that explain the gambler’s belief in his capacities to win beyond any rational
thought.
Behavioral
theory views pathological gambling as a learned behavior acquired through a
process of reinforcement. However, there is disagreement about the reinforcing
element in pathological gambling.
Some authors
consider that the occasional economic gains in a pathological gambler are a
strong reinforcement, at least in the initial stages of the disorder (Morán,
1970). It has been shown that variability and unpredictability of reinforcements
strengthens learned behavior (Skinner, 1953). Gambling is characterized by such
an intermittent schedule of rewards, thus theoretically fostering the
reinforcement of the gambling behavior. Supporting the hypothesis of economic
gains as the most important reinforcement in this disorder is the fact that
almost half of the gamblers report a significant monetary gain in the initial
phase of their disorder that could act as a trigger for it. (Custer, 1982;
Custer, 1984; Custer & Milt, 1985).
Other authors
suggest that the true reinforcement in pathological gambling is not an external
factor such as economic gains but an internal one. Brown (1986) has suggested
that some form of arousal or excitement, either autonomic or cortical, plays a
major role in the development and maintenance of gambling behavior. Each
individual has an optimum level of arousal at which he feels best. Particularly
when the environment is insufficiently stimulating for the individual, he seeks
levels of stimulation that maintain his optimum level of arousal. Gambling has
the power of changing this arousal level.
Blaszczynski et
al. (1986) and McConaghy et al.
(1988) have postulated that what is essential in the etiology of pathological
gambling is the "behavior completion mechanism". According to this
theory, once a behavior becomes a habit, any stimulus associated to that
behavior, either internal or external, creates a need in the subject to perform
that behavior, so that if it is not completed the subject experiences an intense
feeling of discomfort. The reinforcement would then be the avoidance of these
negative physiological states, instead of the achievement of some pleasurable
state.
In a similar
line of thought, Hand (1998) suggests that pathological gamblers engage in this
behavior in order to avoid or reduce unbearable mental states. However, in his
model, these negative mental states arise, not as a result of the behavior
completion mechanism, but as a consequence of environmental distress, coping
deficits, psychiatric disorders or other daily-life problems in the individual.
If the subject stops gambling, the negative mental state will arise again, and
the subject is thus forced to engage in the behavior repeatedly.
Some authors
emphasize the role of cognitive distortions in the development and maintenance
of pathological gambling. Gambling creates the illusion of control in the
subject and the perception that one is capable of controlling the results. At
the same time, subjects develop a series of irrational thoughts related to
gambling that lead them to make false inferences regarding their possibilities
to obtain positive results, and to distort the meaning of the outcome of the
gambling.
Regular gamblers
have more irrational thoughts than occasional gamblers and therefore, they
engage in more risky behaviors (Gaboury & Ladouceur, 1989). When the
individual wins, his beliefs about his chances of winning again and about the
role of good luck are reinforced. Losses are interpreted as a sign of an
imminent gain because the bad luck has to end at some point. Supporting this
idea, a study found that 60% of gamblers risk more money after having lost
instead of after having won (Leopard, 1978).
Another
distorted thought is related to the assessment of the results. Gamblers tend to
remember and overestimate their gains, and they tend to forget, underestimate or
rationalize their losses (Ladouceur et al., 1987). It is possible that these
kinds of distortions explain the histories of initial gains, prior to the onset
of the disorder, described by many patients.
The growth of
the information available to professionals and the lay public about pathological
gambling, and the increasing recognition of the negative consequences that this
disorder brings for the lives of those who suffer from it, has made evident the
urgency to find effective treatment options. Based on the different
conceptualizations of pathological gambling, a number of treatment strategies
have been tried in this population. Nevertheless, the treatment research in
pathological gambling is still very scarce and there is no agreement about the
relative efficacy of one form of treatment over others.
The selective serotonin reuptake inhibitors (SSRI) have been used in
studies in which pathological gambling was thought to be a form of
obsessive-compulsive disorder. Their use is based in the positive response of
patients with diagnosis of obsessive-compulsive disorder to treatment with
serotonin reuptake inhibitors.
Clomipramine, a triclycic antidepressant with a predominantly
serotonergic mechanism of action, has been effective in a placebo controlled
double-blind single-case study (Hollander et al., 1992). The patient had a
history of twelve years as a pathological gambler. Treatment started with a dose
of 25 mg. of clomipramine a day, and the dose was increased gradually up to 125
mg. a day. The patient stopped gambling during the third week of treatment and,
except for a short relapse in week 17, her gambling behavior continued in
remission for an additional 28 weeks, with a daily dose of 175 mg. of
clomipramine.
More recently, Hollander et al. (1998) assessed the efficacy of
fluvoxamine in the treatment of pathological gambling. 16 patients with a
diagnosis of pathological gambling entered an 8-week single-blind placebo
lead-in phase. Six dropped out while receiving placebo, and ten patients, six
men and four women, completed the 8 weeks of treatment with fluvoxamine. The
average dose at the end of the study was 220 mg. a day of fluvoxamine. Seven of
the ten patients that finished the
study were considered responders: they had greater than 25% decreases in their
gambling behavior scores on the pathological gambling modification of the
Yale-Brown Obsessive-Compulsive Scale, and their CGI scores were very much
improved or much improved. The seven responders were found to be abstinent by
the end of the trial according to patient report, clinician and patient ratings,
and information from other informants.
Lithium, a presynaptic agonist, has been used in a variety of
pathologies. Also, the presence of mood disorders’ symptoms coupled with
excitability and impulsivity has been a common link found in patients whose
treatment with lithium was most effective. It has been hypothesized that in the
case of pathological gambling the excitement for winning is bigger than the
prize in itself. Furthermore, a risky situation increases the excitement. This
intense combination of feelings of confidence, enthusiasm, fear and guilt seems
to lead the patient to repeat the gambling behavior.
Based on these observations, Moskowitz (1980) used lithium in three
patients. One of them has a history of ten years as a pathological gambler. The
patient had periods when he played for long hours and felt confident and
optimistic, alternating with periods when he stopped gambling and felt guilty
and depressed. Treatment started with 600 mg. of lithium three times a day.
After two weeks of treatment the patient reported a calming effect and for many
months he was less willing to risk his money. At the same time, he improved his
economic situation. At the follow-up, the patient continued to be stable.
Another patient showed a similar pattern of gambling: phases of optimism and
increased gambling were followed by phases of low mood and less gambling
activity. Treatment in this case started also with a dose of 600 mg. of lithium
three times daily. After one year the gambling periods decreased, the patient
was able to maintain a job and his economic situation improved substantially.
During the next one year and a half period of treatment improvement was moderate
(Moskowitz, 1980).
Lithium seems to be effective in the treatment of pathological
gambling, especially when there is comorbidity with a bipolar disorder.
Nevertheless, it is necessary to do more research with lithium because the data
obtained to date comes from small samples, and also because it is difficult to
distinguish whether the improvement is specific for pathological gambling or is
due to a successful treatment of a comorbid mood disorder.
Carbamazepine has also been tried as a treatment for pathological
gambling due to its effectiveness as a mood stabilizer. Haller and Hinterhuber
(1994) studied the efficacy of carbamazepine in a patient with a history of 16
years of pathological gambling. They used a double-blind, placebo-controlled
design. Prior to this study the patient had been on behavioral therapy,
psychoanalysis and Gamblers Anonymous but did not obtain positive results. On
week 12 of the placebo phase of treatment there were no improvements according
to the information obtained from the patient and measures of psychopathology and
social functioning. The treatment phase with
carbamazepine then began. The initial dose was 200 mg. daily, and it was
gradually increased to a dose of 600 mg. daily. The patient stopped gambling in
the second week of this phase of the treatment and the disorder stayed in
complete remission for 30 more months with the same dose of carbamazepine.
Some preliminary reports suggest that pathological gambling may have a
favorable response to naltrexone, an opioid antagonist. Although naltrexone was
initially used for the treatment of opioid dependence, recently some studies
show its usefulness in the treatment of other addictive behaviors (O'Malley et
al., 1992; Volpicelli et al., 1992).
Naltrexone inhibits the transmission of dopamine in the nucleus
acumbens, and modulates the dopaminergic paths that seem to be implicated in the
etiology of addictions. Based on the purported alteration of dopanergic
transmission in pathological gambling, Turón et al. (1990) used naltrexone in a
study with 30 pathological gamblers. They found that 56% remained in abstinence
after ten months of treatment with this substance.
A case report by Kim (1998), also suggests that naltrexone may be
useful in the treatment of pathological gambling. The patient was a 55 year-old
male pathological gambler. Treatment started with 50 mg. of naltrexone daily
during two weeks, after which the patient reported no changes in his symptoms.
The dose was changed to 100 mg. daily and after a few days the patient’s
interest towards gambling and his gambling behavior completely disappeared. The
patient continued in abstinence during the nine months of treatment.
Bergler (1957) was one of the first authors to report a successful
treatment of pathological gambling through psychoanalytic psychotherapy. From a
total number of 60 patients, he reported that 14 had improved with
psychoanalysis. However, little information is available about the other 46
patients, suggesting that psychoanalysis may be of benefit to only a minority of
pathological gamblers. Other authors have observed positive results with the use
of psychoanalysis or psychoanalytic psychotherapy in some case studies. However,
it is difficult to assess the degree of efficacy of these types of treatment due
to methodological problems, such as lack of randomization and comparison groups,
the indequate use of assessment tools, and the lack of long-term follow-up
studies (Allcock, 1986).
The types of
treatment used initially for pathological gambling, based on behavioral
theories, were aversive conditioning through the use of electric shocks (Barker
& Miller, 1968; Koller, 1972), response prevention (Symes & Nicki, 1997)
and imaginary desensitization (McConaghy et al., 1983). These studies showed a
significant decrease in the impulse to gamble and the corresponding behavior in
the patients, achieving complete abstinence in some cases. However, these
studies used small sample sizes and lacked valid and reliable tools to assess
the outcomes.
At present, from
a psychological perspective, theories that combine behavioral and cognitive
findings are the dominant models as an explanation of the etiology of
pathological gambling (Sharpe & Tarrier, 1993). Bujold et al. (1994)
reported the successful application of cognitive-behavioral therapies using
cognitive restructuring strategies, problem-solving, social skills training and
relapse-prevention in three pathological gamblers. Patients became abstinent
after four weeks of treatment and the results were maintained during the
nine-month follow-up. In another study, these researchers (Sylvain et al., 1997)
assigned 29 pathological gamblers randomly to manual-guided treatment or a
waiting list control group. From the 14 patients that completed the study,
twelve were considered responders, while only one out of 15 in the control group
responded to the treatment. After a twelve-month follow-up, eight patients from
the active treatment group were still improved.
Gamblers
Anonymous, a self-help group modeled after Alcoholics Anonymous, is the most
widely used treatment option for pathological gambling. It emphasizes confession
to a group of peers in order to attain total abstinence, and it offers
financial, legal and vocational assistance. Nevertheless, its efficacy when it
is used exclusively has not been established. The information available suggests
that only 10-30% of patients that attend a meeting ever return. Moreover, from
those who continue the treatment, only 8% remain abstinent after one year and 7%
do so for longer than two years (Stewart & Brown, 1988).
There is
some evidence suggesting that the combination of Gamblers Anonymous with some
type of professional treatment leads to better results. Lesieur and Blume (1991)
studied the response of patients to treatment in an inpatient program that
combined multimodal individual and group psychotherapy. Attendance to Gamblers
Anonymous was strongly encouraged. From the 124 participants, 72 were contacted
between 6 and 14 months after being discharged, and 64% of them continued to be
abstinent.
Other studies
also encourage the notion of combining treatments in order to obtain better
outcomes. Russo et al. (1984) studied the outcome of patients who received
individual and group psychotherapy, and attended Gamblers Anonymous at the same
time in an inpatient program. 55% of the patients were abstinent. Another study
by Taber et al. (1987b) similarly found that 56% of a total of 57 hospitalized
patients were abstinent.
Pathological gambling is a growing public health problem with
psychological, familial, financial, and legal consequences. The available
literature suggests that both biological and psychological factors play a role
in the etiology of pathological gambling, and that further research on its
competing conceptualizations is needed to clarify its place in the psychiatric
nosology.
There are currently no standard treatments for pathological gambling.
However, both cognitive-behavioral approaches and medications have obtained
promising results. In addition, referral to GA and Gam-Anon may assist some
gamblers and their families, although GA participation alone may not be
sufficient for most patients. As public awareness and interest of policy-makers
about the severity and consequences of pathological gambling continues to grow,
psychiatrists will benefit from an increased understanding of the phenomenology
and treatment of pathological gambling.
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