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Andrew W. Goddard, MD; Graeme F. Mason, PhD; Ahmad Almai, MD; Douglas L. Rothman, PhD; Kevin L. Behar, PhD; Ognen A. C. Petroff, MD; Dennis S. Charney, MD; John H. Krystal, MD

Arch Gen Psychiatry. 2001;58:556-561.

Background  There is preclinical evidence and indirect clinical evidence implicating -aminobutyric acid (GABA) in the pathophysiology and treatment of human panic disorder. Specifically, deficits in GABA neuronal function have been associated with anxiogenesis, whereas enhancement of GABA function tends to be anxiolytic. Although reported peripheral GABA levels (eg, in cerebrospinal fluid and plasma) have been within reference limits in panic disorder, thus far there has been no direct assessment of brain GABA levels in this disorder. The purpose of the present work was to determine whether cortical GABA levels are abnormally low in patients with panic disorder.

Methods  Total occipital cortical GABA levels (GABA plus homocarnosine) were assessed in 14 unmedicated patients with panic disorder who did not have major depression and 14 retrospectively age- and sex-matched control subjects using spatially localized ¹H-magnetic resonance spectroscopy. All patients met DSM-IV criteria for a principal current diagnosis of panic disorder with or without agoraphobia.

Results  Patients with panic disorder had a 22% reduction in total occipital cortex GABA concentration (GABA plus homocarnosine) compared with controls. This finding was present in 12 of 14 patient-control pairs and was not solely accounted for by medication history. There were no significant correlations between occipital cortex GABA levels and measures of illness or state anxiety.

Conclusions  Panic disorder is associated with reductions in total occipital cortex GABA levels. This abnormality might contribute to the pathophysiology of panic disorder.

From the Departments of Psychiatry (Drs Goddard, Mason, Almai, and Krystal), Biomedical Engineering (Dr Mason), Internal Medicine (Dr Rothman), Radiology (Dr Rothman), and Neurology (Drs Behar and Petroff), Yale University School of Medicine, New Haven, Conn; and the National Institute of Mental Health, Rockville, Md (Dr Charney).

Corresponding author and reprints: Andrew W. Goddard, MD, Yale Anxiety Clinic, Yale Department of Psychiatry, 100 York St, Room 2J, New Haven, CT 06511 (e-mail: andrew.goddard{at}yale.edu).

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