Cerebrospinal fluid corticotropin-releasing factor concentrations in patients with anxiety disorders and normal comparison subjects

Fossey, Mark D.; Lydiard, R. Bruce; Ballenger, James C.; Laraia, Michele; Bissette, Garth; Nemeroff, Charles B.

doi:10.1016/0006-3223(95)00197-2

Cited by 76 publications

(32 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although it could also be argued that PD subjects, who score higher on measures of stress reactivity such as neuroticism, are more sensitive than other subjects to the psychological stress of lumbar puncture. Mean CRF concentration in the PD group (39.9727.8 pg/ml) was comparable to those reported previously in clinical populations with depression (Carpenter et al, 2004), anxiety disorder (Fossey et al, 1996), acute alcohol withdrawal (Adinoff et al, 1996), schizophrenia (Nishino et al, 1998), in PTSD with and without psychosis (Sautter et al, 2003), and as measured by serial sampling in PTSD (Baker et al, 1999). It is of interest that CRF values in our normal controls (27.1713.2 pg/ml) are comparable to those reported by Carpenter et al (2004) (24.978.6 pg/ml).…”

Section: Discussionsupporting

confidence: 85%

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

Lee

Gollan

Kasckow

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

This cross-sectional investigation tests the relationship between the level of self-reported childhood parental care and cerebrospinal fluid (CSF) corticotropin-releasing factor (CRF) concentration in adults with and without personality disorder (PD). Based on preclinical models of the lasting effect of post-natal parental care on central CRF function, the primary hypothesis was that childhood parental care, as reflected by the parental bonding inventory (PBI) care and involvement subscale, is inversely correlated with adult CSF CRF levels. The sample includes cerebrospinal fluid CRF samples from 19 subjects who were included in a previously published report on the relationship between CRF level and Childhood Trauma Questionnaire score. Parental bonding was measured retrospectively with the PBI in 54 medication-free male and female subjects, 37 of whom were diagnosed with a DSM-IV PD, 17 of whom were normal controls free of Axis I and II psychopathology. CSF CRF level as measured by lumbar puncture was entered into a model as the dependent variable, with the independent variables of PBI Parental Care and Involvement, diagnostic category, age, and gender. The model predicting CSF CRF level was significant, with PBI parental care and involvement negatively correlated with CSF CRF level. PD subjects with higher than median PBI parental care and involvement score had significantly lower CSF CRF levels than both normal controls and PD subjects with lower than median PBI parental care and involvement. Higher levels of self-report parental care predict lower CSF CRF levels in PD subjects, consistent with a beneficial effect of parental care on decreased stress reactivity, and consistent with previous reports in humans. The cross-sectional design of the study, however, limits causal inferences.

show abstract

Section: Discussionsupporting

confidence: 85%

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

Lee

Gollan

Kasckow

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Initial investigations of CRF dysregulation, as measured by CSF concentrations, in anxiety disorders have been mostly negative, with GAD and panic disorder patients exhibiting no difference from controls (Banki et al, 1992;Fossey et al, 1996;Jolkkonen et al, 1993). The lack of differences in CRF concentrations in CSF does not negate the possibility of CRF aberrations contributing to these disorders, however (Arborelius et al, 1999).…”

Section: Anxietymentioning

confidence: 99%

“…CSF CRF levels have been reported to be increased in Tourette's syndrome and in some but not all studies in obsessive-compulsive disorder (Altemus et al, 1992;Chappell et al, 1996;Fossey et al, 1996), with no clear correlation to depression or anxiety symptom severity reported (Chappell et al, 1996). Conversely, CRF content is reduced in the brains of Parkinson's disease and Huntington's disease patients, with reciprocal increases in receptor expression (for a review, see .…”

Section: Role Of Crf In Affective and Anxiety Disorders Depressionmentioning

confidence: 99%

“…OCD, although sharing some features with the other anxiety disorders, is thought (though this is controversial, Bartz and Hollander, 2006) to have a substantially different neurobiology (e.g., neural circuitry). For ease of presentation, we have decided not to further discuss OCD in this manuscript.Initial investigations of CRF dysregulation, as measured by CSF concentrations, in anxiety disorders have been mostly negative, with GAD and panic disorder patients exhibiting no difference from controls (Banki et al, 1992;Fossey et al, 1996;Jolkkonen et al, 1993). The lack of differences in CRF concentrations in CSF does not negate the possibility of CRF aberrations contributing to these disorders, however (Arborelius et al, 1999).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Risbrough

Stein

2006

Hormones and Behavior

211

139

View full text Add to dashboard Cite

Anxiety disorders are a group of mental disorders that include generalized anxiety disorder (GAD), panic disorder, phobic disorders (e.g., specific phobias, agoraphobia, social phobia) and posttraumatic stress disorder (PTSD). Anxiety disorders are among the most common of all mental disorders and, when coupled with an awareness of the disability and reduced quality of life they convey, they must be recognized as a serious public health problem. Over 20 years of preclinical studies point to a role for the CRF system in anxiety and stress responses. Clinical studies have supported a model of CRF dysfunction in depression and more recently a potential contribution to specific anxiety disorders (i.e., panic disorder and PTSD). Much work remains in both the clinical and preclinical fields to inform models of CRF function and its contribution to anxiety. First, we will review the current findings of CRF and HPA axis abnormalities in anxiety disorders. Second, we will discuss startle reflex measures as a tool for translational research to determine the role of the CRF system in development and maintenance of clinical anxiety. KeywordsCRH; CRF; Posttraumatic stress disorder; Anxiety; Panic disorder; Startle Overview of CRF neuroendocrine effects and its effects on G-protein-coupled receptorsCorticotropin releasing factor (CRF; also termed "CRH" for corticotropin releasing hormone) was first described in Science by Vale et al. (1981). They reported the discovery of a hypothesized hypothalamic factor, CRF, a 41 amino acid peptide which selectively and potently activated pituitary corticotropin (or adrenal corticotropin releasing hormone, ACTH) secretion. They predicted that this peptide could be "a key signal in mediating and integrating an organism's endocrine, visceral and behavioral response to stress" (Vale et al., 1981(Vale et al., p. 1397). More than 20 years of subsequent animal research and clinical studies have confirmed this hypothesis, supporting a role for CRF, and its more recently discovered ligand family Urocortin 1, 2 and 3, in anxiety and stress responses Reyes et al., 2001;Spina et al., 1996). In this review, we will focus on the current state of knowledge of CRF system dysregulation in clinical anxiety and discuss future avenues of translational research on the role of CRF in startle phenotypes observed in some anxiety disorders. CRF mediation of the neuroendocrine response to stressIn response to stress, CRF is released from the median eminence of the hypothalamus, where it subsequently binds to receptors at the anterior pituitary and increases ACTH release into the * Corresponding author. 8950 Villa La Jolla Drive, Suite B-218, La Jolla, CA 92037, USA. E-mail address: mstein@ucsd.edu (M.B. Stein). bloodstream. ACTH consequently acts at the adrenal cortex to facilitate release of glucocorticoids such as cortisol. This system, known as the hypothalamic-pituitary-adrenal axis (HPA), is an important component of the response to stress and has been shown to be dysregulated in both anxiety and de...

show abstract

“…Moreover, genetic predisposition, early life events and other environmental or epistatic phenomena might be of importance in the individual interaction between stressors and the activity of CRH neurocircuits Wilson and Hayward, 2005). As CRH concentrations in the cerebrospinal fluid of panic disorder patients were found to be normal (Fossey et al, 1996), there is more likely an imbalance of central CRH pathways not in general but only in distinct brain areas, which are involved in the endogenous network of fear such as the hippocampus and the amygdala (Gorman et al, 2000). Although there is a similar peripherally measurable response to CRH in panic and depressed patients, the central mechanisms leading to these clinical conditions might be different.…”

Section: Hpa System Regulation In Panic Disorder and Depressionmentioning

confidence: 98%

Regulation of the Hypothalamic–Pituitary–Adrenocortical System in Patients with Panic Disorder

Erhardt

Ising

Unschuld

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

Anxiety and depressive disorders are among the most common psychiatric disorders with a high number of hospital admissions and a lifetime prevalence of up to 25%. So far, the pathophysiological mechanisms for anxiety disorders remain to be found. Preclinical studies suggest that changes in hypothalamic-pituitary-adrenocortical (HPA) system function are causally related to the expression of anxietyrelated behavior. The findings on HPA system function in patients with anxiety disorders are, however, heterogeneous. Both hypo-and hyperresponsiveness of HPA response in various anxiety disorders under different experimental conditions were found. In order to characterize putative case/control differences in HPA system function, we performed a Dex-CRH test, a widely used test to pick up changes in HPA system regulation with high sensitivity, in 30 patients with panic disorder, 35 patients with major depressive episode and in 30 controls individually matched for ethnicity, age and gender. The results indicate a similar dysregulation of the HPA system response in the Dex-CRH test in both patient groups. This finding further underlines the hypothesis that both, depression and panic disorder, share impaired HPA system regulation, supporting the notion that the impairment is involved in the pathophysiology of these clinical conditions. However, differences in the suppression effects and psychopathological correlation patterns between depressed and panic patients suggest different biological mechanisms of HPA system dysregulation in both disorders.

show abstract

Cerebrospinal fluid corticotropin-releasing factor concentrations in patients with anxiety disorders and normal comparison subjects

Cited by 76 publications

References 28 publications

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

CSF Corticotropin-Releasing Factor in Personality Disorder: Relationship with Self-Reported Parental Care

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Regulation of the Hypothalamic–Pituitary–Adrenocortical System in Patients with Panic Disorder

Contact Info

Product

Resources

About