Premium
Depression in Temporal Lobe Epilepsy Surgery Patients: An FDG‐PET Study
Author(s) -
Salzberg Michael,
Taher Taufik,
Davie Michael,
Carne Ross,
Hicks Rodney J.,
Cook Mark,
Murphy Michael,
Vinton Anita,
O'Brien Terrence J.
Publication year - 2006
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2006.00860.x
Subject(s) - temporal lobe , depression (economics) , statistical parametric mapping , epilepsy , frontal lobe , orbitofrontal cortex , epilepsy surgery , psychology , voxel , medicine , radiology , psychiatry , magnetic resonance imaging , prefrontal cortex , cognition , economics , macroeconomics
Summary: Purpose: Depression is common in temporal lobe epilepsy (TLE) and after temporal lobectomy, and its etiology is obscure. In nonepileptic depression (including depression associated with other neurologic disorders), a consistent PET imaging finding is frontal lobe hypometabolism. Many TLE patients have hypometabolism involving frontal regions. Thus in data available from routine clinical assessments in an epilepsy surgery unit, we tested the hypothesis that the pattern of hypometabolism, particularly in the frontal lobe, may be associated with the depression seen in patients with TLE and TLE surgery. Methods: We studied 23 medically refractory TLE patients who underwent anterior temporal lobectomy and who had preoperative FDG‐PET scanning. All patients had pre‐ and postoperative psychiatric assessment. By using statistical parametric mapping (SPM‐99), patterns of hypometabolism were compared between patients who had a preoperative history of depression (n = 9) versus those who did not (n = 14) and between those in whom postoperative depression developed (n = 13) versus those in whom it did not (n = 10). A significant region of hypometabolism was set at p < 0.001 for a cluster of ≥20 contiguous voxels. Results: Patients with a history of depression at any time preoperatively showed focal hypometabolism in ipsilateral orbitofrontal cortex compared with those who did not ( t = 4.64; p < 0.001). Patients in whom depression developed postoperatively also showed hypometabolism in the ipsilateral orbitofrontal region ( t = 5.10; p < 0.001). Conclusions: Although this study is methodologically limited, and other explanations merit consideration, orbitofrontal cortex dysfunction, already implicated in the pathophysiology of nonepileptic depression, may also be relevant to the depression of TLE and temporal lobectomy.