Search

In the past decade, we have witnessed the emergence of pharmacological treatments for pathological gambling with some success but many question marks. We aimed to explore pharmacological treatments that have been previously explored with some success, with the intent of comparing their efficacy and pave the way to larger placebo-controlled trials.

SUMMARY Major depressive disorder is a mood disorder characterized by both severe affective and neurovegetative symptoms together. It is a common disorder seen in a quarter of consecutively admitted depressed patients and is often associated with severe symptomatology, increased suicide risk, poor acute response to antidepressants and poor acute and long-term treatment outcome. The question of the optimal duration of pharmacotherapy in order to prevent relapse and improve the long-term (i.e., 5-year) outcome is a focus of current investigation. This article will review currently recommended treatment strategies for the acute, continuation and maintenance phases of therapy. In particular, it will address the role of newer-generation antidepressants, the use of mood stabilizers and indications for electroconvulsive therapy. Other possible treatment strategies such as transcranial magnetic stimulation, vagus nerve stimulation, deep brain stimulation and glucocorticoid receptor antagonists will be discussed.

Pathological gambling (PG) is a relatively common and highly disabling impulse control disorder. A range of psychotherapeutic agents including selective serotonin reuptake inhibitors, antiepileptic drugs, and opioid antagonists are shown to be effective in the short-term treatment of PG. The use of a wide range of pharmacological treatments for PG is consistent with the observation that PG shares features of obsessive-compulsive spectrum disorders, impulse control disorders, and addictive disorders. The aim of the study is to assess the rate of relapse in treatment-responder pathological gamblers after discontinuation of the active treatment.

Psychotic major depressive disorder (MDD) is a mood disorder characterized by severe affective and neurovegetative symptoms together with the presence of delusions and/or hallucinations. It is a common disorder seen in a quarter of consecutively admitted depressed patients and is often associated with severe symptomatology, increased suicide risk, poor acute response to antidepressants and poor acute and long-term treatment outcome. It is possible that poor response in psychotic depression is caused by the fact that we have yet to identify the most efficacious treatment protocol for psychotic MDD. Multiple studies have shown that modifications in the treatment paradigm may increase treatment efficacy in psychotic MDD. It has been generally accepted that, during the acute treatment phase, antidepressant–antipsychotic drug combination therapy is more effective than either treatment alone, although this strategy has recently been challenged. The question of the optimal duration of pharmacotherapy in order to prevent relapse and improve long-term (i.e., 5-year) outcome is a focus of current investigation. This article will review currently recommended treatment strategies for the acute, continuation and maintenance phases of therapy. In particular, it will address the role of newer-generation antidepressants, the role of second-generation antipsychotics, the use of mood stabilizers and indications for electroconvulsive therapy. Other possible treatment strategies such as transcranial magnetic stimulation, vagus nerve stimulation, deep-brain stimulation and glucocorticoid receptor antagonists will be discussed. Current recommendations for the prevention of relapse and improvement of long-term outcome will be reviewed.

Pathological gambling (PG) is a relatively common and highly disabling impulse control disorder. A range of psychotheraputic agents, including selective serotonin reuptake inhibitors, mood stabilizers, and opioid antagonists, has been shown to be effective in the treatment of PG. The use of selective serotonin reuptake inhibitors and opioid antagonists for PG is consistent with the observation that PG shares features of both the obsessive-compulsive spectrum disorders and addictive disorders. The aim of the study is to compare the effectiveness of sustained-release bupropion versus naltrexone in the treatment of PG.

Background: Pathologic gambling (PG) is a prevalent and disabling impulse-control disorder. Recent studies have consistently demonstrated that PG patients respond well to treatment with selective serotonin reuptake inhibiters (SSRIs), mood stabilizers and opioid antagonists. These findings have supported the observation that PG is strongly associated with mood disorders, obsessive––compulsive spectrum disorders, panic disorder and addictive disorders. The aim of the study was to show the effectiveness of bupropion sustained release in PG.Methods: A total of 16  male PGs who had failed two previous trials of SSRI pharmacotherapy were enrolled in the study and were treated with bupropion sustained release for 12  weeks. A comprehensive psychiatric diagnostic evaluation was performed on all patients at baseline, and patients were screened for symptoms of gambling, depression and anxiety using the South Oaks Gambling Screen, the Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale and the Clinical Global Impression-Impovement Scale. In addition, the patients completed self-report questionnaires concerning their demographic status.Results: Most patients responded well to bupropion treatment. A total of 12 out of 16 subjects completed the 12-week treatment program. Treatment response was determined by the level of gambling behavior reported by subjects at the 12-week visit. Full remission of gambling behavior was defined as the absence of gambling behavior for a period of 1  week prior to the follow-up visit. A total of nine out of the 12 completers reported full remission, and three completers had partial remission.Conclusion: Bupropion SR could be effective in the treatment of pathologic gamblers who are SSRI nonresponders.

Background: Despite the previously accepted notion that panic disorder (PD) is rare in the elderly, recent data have shown that late-life PD may be more common than previously thought. Paroxetine is a selective serotonergic reuptake inhibitor which has had clear efficacy in the treatment of PD in the general adult population. In this study we aimed to examine the treatment outcome of paroxetine pharmacotherapy for late-life PD. Method: In this long-term naturalistic follow-up study, a group of 61 elderly (aged 59 years or older) PD patients were compared with a group of 95 younger (aged between 18  and 59 years) PD patients in terms of treatment response to paroxetine pharmacotherapy. The two groups were followed during both the initial short-term treatment phase (first 3 months) and throughout long-term (month 4––12) maintenance treatment. The two groups were also compared for side effects of paroxetine therapy. Results: No differences were found between the two patient groups in terms of response rate, side effects and tolerability of drug treatment. Conclusions: The use of paroxetine for the treatment of late-life PD appears to be both beneficial and well tolerated. Further controlled studies are needed to confirm these preliminary results.

Panic disorder is one of the most common anxiety disorders and has a lifetime prevalence of 3–5%. Panic attacks can begin at any age, but commonly have their onset in early adulthood between the ages of 20 and 40 years. Naturalistic data has shown that panic disorder has a chronic and relapsing course. Panic disorder is reported to be associated with an increased risk of suicidal behavior and comorbid psychiatric diagnoses such as depression and substance abuse. Currently, recommended treatment modalities for panic disorder include the use of antidepressant pharmacotherapy and/or cognitive behavioral therapy. Paroxetine is unique among the selective serotonin reuptake inhibitors since, in addition to its effect on the CNS serotonergic neurotransmission, it also has mild noradrenergic properties demonstrated to be effective in the treatment of anxiety disorders and depression. Paroxetine treatment has the potential to cause weight gain and sexual dysfunction, primarily anorgasmia and ejaculatory dysfunction for the long term. In the short-term, treatment causes nausea, gastrointestinal disturbances, irritability, headaches and eating and sleeping difficulties. Paroxetine is an example of an selective serotonin reuptake inhibitor agent, which has been well studied in the treatment of panic disorder and is efficacious and well-tolerated. Paroxetine pharmacotherapy has been recommended to be continued for 1 year as specified in the treatment guidelines set by the American Psychiatric Association in the treatment of panic disorder.

Objectives:Kleptomania, defined by DSM-IV as the inability to resist the impulse to steal objects which are not needed for personal use or for their monetary value, may reflect a form of obsessive-compulsive spectrum disorder and/or affective spectrum disorder. Methods:Twenty-one kleptomanic patients and 57 first-degree relatives completed a semistructured DSM-IV-based interview and questionnaires. Questionnaires are: the HDRS-17 (the Hamilton Rating Scale for Depression), the HARS (Hamilton Rating Scale for Anxiety), the Y-BOCS (Yale-Brown Obsessive Compulsive Scale), the YMRS (Young Mania Rating Scale). The two groups were compared to demographically matched normal controls (n = 64). Results: We found a high prevalence of affective and anxiety disorders in our sample of kleptomanic patients and their first-degree relatives. In addition, the scores on the HDRS, HARS, and Y-BOCS were significantly higher in the study group than in the control group. Conclusions:Our finding of a high prevalence of psychiatric comorbidity in kleptomanic patients could lead to the development of new treatment strategies for this disorder. Furthermore, the pattern of psychiatric disorders seen in the first-degree relatives can lead to new insights about the nosology and etiopathology of kleptomania.

Since its introduction to the clinical realm in 1985, transcranial magnetic stimulation (TMS) has rapidly developed into a tool for exploring central nervous system function in both health and disease. The antidepressant effects of TMS were initially observed in 1993. Since then, a solid body of evidence has accumulated suggesting antidepressant effects for both slow TMS (sTMS) and repetitive TMS (rTMS). This review is divided into four parts. First, it addresses the basic concepts governing TMS, and then, second, it discusses the technical parameters involved in administering TMS. Knowledge of these parameters is necessary for understanding how TMS is administered, and how manipulation of the technique impacts on the results obtained. Third, we review the most relevant studies on the antidepressant effects of sTMS and rTMS published to date. Finally, we discuss cortical excitability and how the understanding of this basic neurophysiological function of cortical neurons can be used for monitoring the effects of TMS. In our discussion, we conclude that the time has arrived for TMS to be offered to depressed patients as a treatment.

Background: Schizo phreni form dis or der (SFD) has an un clear di ag nos tic and prog nos tic status within the psy chotic spec trum.Method: We stud ied 36 in pa tients ad mit ted to our ward be tween 1983 and 1993 due to SFD. The pa tients were con tacted an av er age of 12 years af ter in dex hos pi tali za tion, and we noted the course of their ill ness, as well as their pres ent di ag no sis.Results: Of the sam ple, 84% had ad di tional, mostly psy chotic, epi sodes dur ing the follow-up, and 70% had di ag no ses in the schizo phrenic spec trum (that is, schizo phre nia and schizoaf fec tive dis or der). A sur vival analy sis re vealed that con fu sion and the pres ence of at least 2 good prog nos tic fac tors (GPF) at in dex hos pi tali za tion pre dicted bet ter out come.Conclusions: SFD seems to be an early mani fes ta tion of schizo phre nia. Only a few of those sam pled did not ex pe ri ence ad di tional re lapses—a pes si mis tic find ing at 12-year follow- up. The find ings of this study ac cord with DSM- IV cri te ria and the lit era ture regard ing the long- term prog no sis of SFD and the im por tance of the GPF.

To evaluate the prevalence of suicidal behavior in patients with panic disorder (PD) and to study the role of alexithymia (AL), an affect component, as a predictor of suicidal behavior in PD, we compared 42 patients with PD with or without agoraphobia with 24 healthy controls with regards to depression, AL and suicide risk. Only 5% of the PD patients reported previous suicide attempts. A higher frequency of positive AL (score > 73) was found among the PD patients (39% v4% among the controls). PD patients had a higher suicide risk and AL as compared to controls, but only the increased suicide risk reached statistical significance. AL subjects had higher suicide risk scores as compared to non-AL subjects. Significant correlations were found between the AL score and suicide risk, although the most significant correlation was, as expected, between the depression level and the suicide risk. A low rate of previous suicide attempts was found in the PD group, perhaps reflecting the low comorbidity in our sample. We suggest that AL may have a role in the causation of suicidal behavior in PD patients, although further studies should re-examine this issue with larger samples.

The objective of this study was to determine the efficacy of pindolol as an augmentor of fluoxetine in treatment-resistant panic disorder (PD). Twenty-five outpatients having PD with or without agoraphobia were included. These patients had not responded to two different trials with antidepressants and an 8-week trial of fluoxetine 20 mg/day. Treatment-resistant PD was defined as a less than 20% reduction in score on the Panic Self-Questionnaire (number of attacks per week) (PSQ) and the Clinical Anxiety Scale With Panic Attacks (CAS+PA). These patients continued to receive fluoxetine 20 mg/day and were randomly assigned to additionally receive either pindolol (2.5 mg three times daily) or placebo for the following 4 weeks. Evaluations were performed weekly using the Hamilton Rating Scale for Anxiety, the Hamilton Rating Scale for Depression (HAM-D), the CAS+PA, the NIMH Anxiety Scale, the PSQ, and the Clinical Global Impression Scale. The data were analyzed using a repeated-measures analysis of variance (ANOVA) and a t-test for independent samples. Patients treated with the combination of pindolol and fluoxetine (N = 13) demonstrated a significant improvement over the patients treated with fluoxetine and placebo on all rating scales, with the exception of HAM-D. The statistical differences were shown using the repeated-measures ANOVA (baseline, week 2, week 4) and also with t-tests from the second week of the trial. These preliminary results demonstrate that pindolol has an augmenting effect on fluoxetine in patients with treatment-resistant PD.

Electroconvulsive therapy (ECT) is considered to be one of the most effective treatments for patients with major depression and persistent psychosis. Seizure characteristics probably determine the therapeutic effect of ECT; as a consequence, short seizures are accepted as one of the factors of poor outcome. During most ECT courses seizure threshold increases and seizure duration decreases. Methylxanthine preparations, caffeine, and theophylline have been used to prolong seizure duration. The use of aminophylline, more readily available than caffeine, has not been well documented. The objective of this study was to test the effects of aminophylline on seizure length. Fourteen drug-free patients with diagnoses of affective disorder or psychotic episode receiving ECT participated in this study. Seizure length was assessed clinically and per EEG. Statistical comparisons were done using paired ttests. A significant increase (p < 0.04) in seizure length was achieved and maintained on three subsequent treatments with aminophylline. No adverse events were noted from the addition of aminophylline.

Labetalol, a combined α- and β-adrenergic blocker is often used to attenuate the transient increases in heart rate and blood pressure that accompany electroconvulsive therapy (ECT). It has been suggested that labetalol should not be administered during ECT without the protection provided by anticholinergic medications, because of its potential severe bradycardic effects. We present our experience with 32 patients from all age groups who received labetalol without anticholinergic treatment during ECT. None of the patients demonstrated adverse bradycardic effects. We conclude that administration of labetalol during ECT does not routinely require premedication with anticholinergic drugs and does not lengthen asystole.

Transcranial magnetic stimulation (TMS) applied over the motor cortex depolarizes neurons and leads to motor-evoked potentials (MEP). To assess cortico-spinal excitability we compared the motor threshold (MT) and the averaged MEP amplitude generated by TMS in patients with major depression (MD) and matched controls. Nineteen patients, who where participants in a protocol comparing the antidepressant effects of rTMS with those of ECT, and thirteen age- and gender-matched normal controls were studied. MT was similar between patients and normal controls. The MEP amplitude response was significantly increased by rTMS, however, the magnitude of the response was similar in patients and normal controls. Correlations between the averaged MEP amplitude and age revealed that older subjects demonstrated significantly lower responses at all time-points. We conclude that cortico-spinal excitability is increased following rTMS, however, differences between patients and normal controls were not apparent with the paradigm used.