Elsevier

Biological Psychiatry

Volume 48, Issue 10, 15 November 2000, Pages 1020-1023
Biological Psychiatry

Brief report
Regional cerebral metabolism associated with anxiety symptoms in affective disorder patients

https://doi.org/10.1016/S0006-3223(00)00920-3Get rights and content

Abstract

Background: We studied the relationship between regional cerebral metabolism and the severity of anxiety in mood disorder patients, controlling for depression severity.

Methods: Fifty-two medication-free patients with unipolar or bipolar illness underwent positron emission tomography with [18F]-fluorodeoxyglucose. Hamilton Depression Rating Scale and Spielberger Anxiety-State Scale scores were obtained for the week of the scan. Analyses were performed on globally normalized images and were corrected for multiple comparisons.

Results: After covarying for depression scores, age, and gender, Spielberger Anxiety-State Scale scores correlated directly with regional cerebral metabolism in the right parahippocampal and left anterior cingulate regions, and inversely with metabolism in the cerebellum, left fusiform, left superior temporal, left angular gyrus, and left insula. In contrast, covarying for anxiety scores, age, and gender, Hamilton Depression Rating Scale scores correlated directly with regional cerebral metabolism in the bilateral medial frontal, right anterior cingulate, and right dorsolateral prefrontal cortices.

Conclusions: Comorbid anxiety symptoms are associated with specific cerebral metabolic correlates that partially overlap with those in the primary anxiety disorders and differ from those associated with depression severity.

Introduction

Patients with primary affective disorders often have prominent comorbid anxiety symptoms that impact behavior and response to treatment (McElroy et al, in press). Previous functional brain imaging studies in affective disorders have not always addressed the contribution of anxiety symptoms to the patterns of regional brain activity observed.

Several investigators have studied a variety of primary anxiety disorders as well as anxiety induced in normal subjects. The right, compared with the left, parahippocampal gyrus has been found to have increased regional cerebral blood flow and metabolism in subjects with primary anxiety disorders, i.e., panic disorder Nordahl et al 1990, Reiman et al 1984, Reiman et al 1986. Increases in regional cerebral glucose metabolism (rCMRglu) in the insular cortex, right frontal and posterior medial orbitofrontal cortices, and lenticular nucleus have been found to be associated with symptom provocation in three anxiety disorders, including obsessive-compulsive disorder (OCD), simple phobia, and posttraumatic stress disorder (PTSD) (Rauch et al 1997). Other brain areas associated with anxiety include the left inferior parietal lobe in panic disorder (Nordahl et al 1990) and secondary visual cortex, hippocampus, prefrontal and orbitofrontal cortices, temporal poles, and posterior cingulate gyrus in simple phobias (Fredrikson et al 1995). Lucey et al (1997) found decreased regional cerebral blood flow in superior frontal cortices and right caudate in both OCD and PTSD patients compared to healthy control subjects.

Studies of anxiety provoked in healthy control subjects have demonstrated increased rCMRglu in the left anterior cingulate gyrus (Chua et al 1999; Kimbrell et al 1999) left inferior frontal, temporal, and cuneus gyri (Kimbrell et al 1999), and orbitofrontal, inferior frontal, and left insula (Chua et al 1999). Kimbrell et al (1999) also showed decreased rCMRglu in right posteriotemporoparietal cortex, right superior frontal, and right medial frontal cortices with anxiety induction in these same subjects.

These findings in diverse anxiety patient populations and healthy volunteers with induction of anxiety indicate several regions of general overlap, such as frontal and temporal cortices and insula. The purpose of this study was to identify changes in rCMRglu associated with the severity of anxiety symptoms (controlling for depression severity) in patients diagnosed with an affective disorder and to differentiate these from rCMRglu associated with severity of depression. We expected to find associations between anxiety and rCMRglu in frontal, insular, and temporal areas.

Section snippets

Methods and materials

Fifty-two patients (mean age 39.8 years, SD = 12.7, range = 20–65; 23 male), with a primary affective disorder (25 unipolar, 27 bipolar), who were free of medication for at least two weeks, underwent positron emission tomography (PET) studies using [18F]-fluorodeoxyglucose (FDG) after being given a complete description of the study and giving their written informed consent. Subjects were participants in studies of treatment interventions and underwent assessments and PET scans as part of those

Results

Mean SAnx was 47.1 ± 12.7 (range = 21–74) and HAMD was 22.2 ± 9.7 (range = 3–42). There was no significant difference in SAnx or HAMD scores between unipolar and bipolar groups. SAnx and HAMD were highly correlated (r = .62, p < .0001, n = 52).

SAnx correlated directly with rCMRglu in right parahippocampal gyrus and the left anterior cingulate gyrus bordering the callosum (from Talairach coordinate Z = +16 to Z = +32) after covarying for age, gender, and HAMD scores. In the same analysis, SAnx

Discussion

Severity of anxiety symptoms in affective disorder patients was positively correlated with rCMRglu in the right parahippocampal and left anterior cingulate regions. The increase in the right parahippocampal gyrus is consistant with findings in other subject populations, such as those with panic disorder Nordahl et al 1990, Reiman et al 1984, Reiman et al 1986. Increases in rCMRglu in the left anterior cingulate gyrus converge with findings in healthy control subjects with self-induced anxiety

Acknowledgements

The support of the Theodore and Vada Stanley Foundation to T.A. Kimbrell and M.W. Willis is gratefully acknowledged.

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