Hostname: page-component-cd9895bd7-gxg78 Total loading time: 0 Render date: 2024-12-23T03:29:23.048Z Has data issue: false hasContentIssue false

LS-01. Satellite symposium: Bridging the gap between schizophrenia and mood disorders

Published online by Cambridge University Press:  16 April 2020

Abstract

Type
Interdisciplinary
Copyright
Copyright © European Psychiatric Association 2005

LS-01-01

Biological basis of schizophrenia, bipolar disorder and mood disorder

A. Weizman. Geha Psychiatric Hospital Research Unit, Petah Tiqva, Israel

Objective: Advanced review of the biochemistry and genetics of different psychiatric disorders and how they overlap.

Abstract: Neuroanatomical, neurobiochemical and genetic abnormalities are common in psychiatric disease and have been observed in all major types of psychiatric illnesses, including depression, bipolar disorder, schizophrenia, and a variety of anxiety disorders such as social phobia and panic disorder. There is a considerable overlap in abnormal neurochemical processes between them and genetic linkage has also been observed between psychiatric diseases such as bipolar disorder and schizophrenia (long arm of chromosome 13 and 22) suggesting that there is a shared genetic predisposition to have both disorders. [1] Linkage studies have identified multiple potential genetic abnormalities such as the t( 1:11) translocation associated with DISC 1, which has been linked to schizophrenia, schizoaffective disorder, recurrent major depression, and bipolar disorder. [2] Functional imaging using signal transduction and functional magnetic resonance imaging are further enhancing our understanding of the neurobiology of psychiatric disease (i.e. glycogen synthase kinase- 3 in bipolar disorder).

Conclusion: There is considerable neurochemical and genetic overlap between schizophrenia, bipolar disorder, and mood disorders suggesting that pharmacological agents that modulate shared pathways may be effective treatments for this group of psychiatric disorders.

LS-01-02

Clinical overlaps in schizophrenia, bipolar disorder and mood disorders

S. Potkin. USA

Objective: Demonstrate the clinical overlap between

schizophrenia, bipolar disorder, and mood disorders.

Abstract: There is considerable symptom overlap in patients with these psychiatric disorders such that for the prescribing psychiatrist, identifying the underlying morbidity is not always straightforward. Acute symptom control is required in all patients with mood stabilization and in some cases control of cognitive impairment. The major psychiatric disorders often exhibit various degrees of co-morbid depression and anxiety, which can lead to significant morbidity as well as occasional mortality. For instance, anxiety disorder is a common co-morbidity found with bipolar disorder. Some of this clinical overlap may derive from shared neurochemical, genetic, and neuroanatomical abnormalities. For example, there is some evidence that social phobia may be localized to abnormalities in the amygdaloid-hippocampal region of the brain. [1] Given the clinical overlaps, psychiatrists need to

bridge the gaps in their perception and treatment of these complex disease syndromes. In bipolar disorder, schizophrenia, and mood disorders, multiple studies have documented the important contribution of both genetics and environmental factors in contributing to the expression of these disease states.

Conclusion: Schizophrenia, bipolar disorder, and mood disorders share many clinical features that relate in part to genetic and environmental factors. Such similarities have profound implications for current as well as future psychiatric pharmacotherapy.

LS-01-03

Advancing the treatment of psychiatric disorders

W. Fleischhacker. Psychiatrische Univers.-Klinik Innsbruck, Innsbruck, Austria

Objective: Review the latest developments in antipsychotic treatment.

Abstract: The development of antipsychotic medications will be reviewed and data on the safety and efficacy of these treatment options presented. Antipsychotic treatment has evolved from early antipsychotics such as chlorpromazine and haloperidol with their limited efficacy and poor side-effect profile to the introduction of the first-generation antipsychotic, clozapine. Newer second-generation antipsychotics with improved efficacy or better tolerability have been introduced and the latest have advantages over earlier antipsychotics. New second-generation antipsychotics with improved efficacy or better tolerability have been introduced and have some advantages over previously licensed drugs, especially with regard to safety. These additions allow psychiatrists to treat the full spectrum of schizophrenia, which in addition to positive symptoms also includes negative symptoms, depression, cognitive dysfunction, and improvement in quality of life. Recent data demonstrate the importance of newer second-generation antipsychotics in the management of bipolar disorder in both acute and long-term treatment for mania, depression and anxiety. The most recendy introduced new second-generation andpsychotics provide the psychiatrist with better tolerability profiles and minimal metabolic side-effects (minimal weight gain, low risk of developing diabetes, no elevation of prolactin and minimal effects on lipid profile).

Conclusion: New second-generation antipsychotics are becoming increasingly better tolerated and effective. Their efficacy is dependent on multiple factors. Given the impact of these new second-generation antipsychotics on the treatment of psychiatric disorders, psychiatrists should expect a new standard of care for treatment.

References

Gershon, ESBadner, JA.Progress toward discovery of susceptibility genes for bipolar manic-depressive illness and schizophrenia. CNS Spectr. 2001;6:965-8.10.1017/S1092852900001073CrossRefGoogle Scholar
Blackwood, DH.Muir, WJ.Clinical phenotypes associated with DISC 1. a candidate gene for schizophrenia. Neurotox Res. 2004;6;35-41.10.1007/BF03033294CrossRefGoogle Scholar
Tillfors, M.Why do some individuals develop social phobia? A review with emphasis on the neurobiological influences. Nord J Psychiatry. 2004;58:267-76.10.1080/08039480410005774CrossRefGoogle ScholarPubMed
Submit a response

Comments

No Comments have been published for this article.