cholecystokinin and Phobic-Disorders

Although Social Phobia has been recognised for centuries in comparison with other anxiety disorders, relatively little work has been done to understand its neural basis. The present review attempts to redress this balance by giving an overview of the current state of knowledge in this disorder. By putting together data from the treatment responses to specific agents, the effects of chemical challenges which have been used in other anxiety disorders and by reviewing data on central and peripheral neurotransmitter and endochrine abnormalities, it is possible to begin to generate some potentially testable theories of aetiology and mechanisms. Finally, we review the potential use of neuroimaging techniques to better detail the brain circuits and possibly neurotransmitters involved in social phobia, showing some of our preliminary work using (15)O water blood flow PET activation studies to determine the brain circuits in which metabolism is changed during the experience of social anxiety.

Topics: Brain; Caffeine; Carbon Dioxide; Cholecystokinin; Epinephrine; Female; Flumazenil; Human Growth Hormone; Humans; Hypothalamo-Hypophyseal System; Lactic Acid; Male; Neurotransmitter Agents; Panic Disorder; Phobic Disorders; Pituitary-Adrenal System; Thyroid Gland; Tomography, Emission-Computed; Tomography, Emission-Computed, Single-Photon

The neurobiology of social anxiety disorder is poorly understood, although preliminary research has suggested several possible biological abnormalities. Challenge studies have demonstrated that subjects with social anxiety disorder have a sensitivity to carbon dioxide, cholecystokinin, and caffeine somewhere between that of panic disorder patients and normal controls. Serotonergic pathways may play a role in social anxiety disorder, as shown by the clinical effectiveness of selective serotonin reuptake inhibitors, plus fenfluramine and m-chlorophenylpiperazine challenge studies. Dopaminergic function and striatal dopamine uptake appear to be reduced in social anxiety disorder. There is also evidence for cardiovascular and adrenergic abnormalities. Recently, positron emission tomography has begun to identify brain regions that appear to be uniquely activated in this condition. These results offer the promise of an understanding of the brain mechanisms of social anxiety disorder, but much further research is needed to fully elucidate the neurobiological cause(s) that exist.

Topics: Animals; Brain; Caffeine; Carbon Dioxide; Cholecystokinin; Dopamine; Fear; Fenfluramine; Humans; Panic Disorder; Paroxetine; Phobic Disorders; Piperazines; Rats; Ritanserin; Selective Serotonin Reuptake Inhibitors; Serotonin; Tomography, Emission-Computed

Current knowledge of the neurobiology of social anxiety and social phobia is reviewed within the framework of chemical models of anxiety. Preliminary evidence for noradrenergic, serotonergic, and adenosinergic systems in the neurobiology of social phobia is presented and discussed within the context of medical model versus continuum theories of anxiety. The clinical and theoretical implications of a hypothesized linkage between anxiety disorders and hypothalamic-growth hormone dysfunction are presented. The author recommends that additional research strategies be developed to examine growth patterns and the function of growth hormone and other growth factors in children and adults with anxiety disorders; moreover, the rationale for additional longitudinal investigations of children with growth hormone deficiency short stature and psychosocial short stature is presented. It is hypothesized that individuals with growth hormone deficiency may be at high risk for the development of anxiety disorders.

Topics: Adenosine; Adrenal Glands; Anxiety Disorders; Cholecystokinin; Comorbidity; Dexamethasone; Dopamine; Growth Disorders; Growth Hormone; Humans; Hydrocortisone; Norepinephrine; Phobic Disorders; Serotonin; Thyroid Gland