Elsevier

Biological Psychiatry

Volume 62, Issue 11, 1 December 2007, Pages 1258-1264
Biological Psychiatry

Original Article
5-HT1A Receptor Binding in Temporal Lobe Epilepsy Patients With and Without Major Depression

https://doi.org/10.1016/j.biopsych.2007.02.015Get rights and content

Background

Major depressive disorder (MDD) is the most common comorbid psychiatric condition associated with temporal lobe epilepsy (TLE). Preclinical and clinical studies suggest that 5-HT1A receptors play a role in the pathophysiology of both TLE and MDD. There is preliminary evidence for an association between decreased 5-HT1A receptor binding in limbic brain areas and affective symptoms in TLE patients. The objective of this study was to compare 5-HT1A receptor binding between TLE patients with and without MDD. For the first time, 5-HT1A receptor binding was measured in a sample large enough to permit sensitive comparisons between TLE patients with and without comorbid MDD diagnosed by clinical and structured psychiatric interviews.

Methods

Thirty-seven epilepsy patients with temporal lobe foci confirmed by ictal video-electroencephalogram (EEG) monitoring were recruited from the Clinical Epilepsy Section, National Institute of Neurological Disorders and Stroke. We performed interictal positron emission tomography scanning, with [18F]FCWAY, a fluorinated derivative of WAY100635, on a GE Medical Systems (Waukesha, Wisconsin) Advance scanner with continuous EEG monitoring. The 5-HT1A receptor binding was estimated by partial volume-corrected [18F]FCWAY V/f1 values.

Results

In addition to decreased 5-HT1A receptor binding in the epileptic focus itself, comorbid MDD was associated with a significantly more pronounced reduction in 5-HT1A receptor binding in TLE patients, extending into non-lesional limbic brain areas outside the epileptic focus. Focus side and the presence of mesial temporal sclerosis were not associated with the presence of comorbid depression.

Conclusions

Reductions in 5-HT1A receptor binding might help elucidate the neurobiological mechanisms underlying the TLE–MDD comorbidity.

Section snippets

Sample and Clinical Assessments

Thirty-seven patients with TLE were recruited from the Clinical Epilepsy Section, National Institute of Neurologic Disorders and Stroke, National Institutes of Health (NIH), where they were evaluated for refractory TLE. Fourteen had been included in a previous study (26). Patients had clinical interviews and physical examination by board-certified neurologists. Seizure onset was localized with ictal scalp video-electroencephalogram (EEG); only patients with complex partial seizures of temporal

Results

Table 1 shows demographic and clinical characteristics of TLE patients with and without MDD. There were no differences in any demographic factors, but the MDD group did have higher depression scores.

Average f1 values were .12 (SD = .04) in TLE patients without MDD and .12 (SD = .03) in TLE patients with MDD. Table 2 shows [18F]FCWAY V/f1 values in TLE patients with and without MDD. Analysis of variance revealed that the effect of diagnostic group on V/f1 was statistically significant across all

Discussion

The TLE patients with and without comorbid MDD did not differ regarding age, gender, prevalence of MTS, and epileptic focus side. After Bonferroni-correction, TLE patients with comorbid MDD had lower [18F]FCWAY V/f1 values in the anterior cingulate, right hippocampus, and medial and superior temporal lobe. In addition, we found a group × laterality effect in the hippocampus: reduced values associated with comorbid MDD were mainly found on the right side. Gender, age, current major depressive

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    The authors do not have conflicts of interest, neither financial nor otherwise, and they do not have any conflicts to disclose.

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