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. Author manuscript; available in PMC: 2010 Apr 22.
Published in final edited form as: Neurosci Biobehav Rev. 2009 Jan 21;33(5):699–771. doi: 10.1016/j.neubiorev.2009.01.004

Table 21.

Functional Anatomical Studies of the Ventro-Medial Prefrontal Cortex in BD.

Study Sample Age Method Age of
Onset
Illness
Duration/#
Episodes
Family
History
of
Illness
Clinical Status at
Testing
Medication Status Comorbidity Findings Brodmann
Map/Stereotaxic
Coordinates
(Drevets et al 1997) 21 BD
21 HC
35±8.2
34±8.2
1.5T
1mm slice
ROI
NR NR Yes Depressed Cohort not treated for 4 weeks prior to scans NR Decreased metabolism of L sgACC in BD group. 1; 25; −6
(Blumberg et al 2000) 11 BD 33.4±11.6 15O-H2O NR 14.2±14.9 (manic)
12.0±5.6 (euthymic)
NR 5 manic BD; 6 euthymic MS, AP, AD, BZ No comorbid axis I or II conditions. Substance abuse taking place > 5 years previously was allowed. Manic patients had greater rCBF in R ventral ACC than remitted subjects BA 32
10; 26; −8
(Ketter et al 2001) 43 BD I + II (treatment resistant)
43 HC
37.5±10.6
38.1±10.4
18 F-FDG 18.8±9.9 18.3±10.4 NR Depressed, mildly depressed + euthymic Unmedicated for 2+ weeks NR Decreased metabolism of L middle frontal and inferior frontal gyri in depressed BD patients only. Global cerebral metabolism decreased in depressed BD too. BA 9 + 44
No coordinates given
(Drevets et al 2002a) 20 MDD
14 HC
36±10
34±9.1
18 F-FDG NR NR NR Depressed Patients medication free for 3+ weeks prior to study. No other psychiatric disorders or substance abuse Reduced baseline metabolism of L sgACC PFC in MDD NR
(Dunn et al 2002) 27 BD 36.7±11.3 18 F-FDG 18.0±9.9 26.7±14.6 NR Mildly to severely depressed Unmedicated for 2+ weeks No active substance abuse, eating disorder, OCD, dementia, medical illness Anhedonia associated with greater metabolism of R sgACC 10; 42; −4
(Kegeles et al 2003) 19 (14 MDD, 5 BD)
10 HC
36±11
39±19
18 F-FDG NR NR Yes Depressed BZ discontinued 24 hours before study in 12 cases. 7 subjects on BZ. Patients free of other medication for 2+ weeks. 3 panic disorder, 2 dysthymia, 1 each with social phobia, simple phobia, anorexia + PTSD. No medical illness Lower metabolic activity of the R pregenual ACC in MDD. BA 32
4; 34; −12
(Kruger et al 2003) 11 depressed BD
9 remitted BD
43±9
38±12
15O-H2O Voxel-wise 22±6 8±3 (dep episodes)
3±2 (manic episodes)
8±5 (dep episodes)
3±2 (manic episodes)
NR Depressed/Remitted MS No axis I or II disorders. No substance abusers BL decreases in rCBF to ventral medial PFC after sadness induction in both BD groups In remitted group increased rCBF to dorsal anterior cingulate – BA24a: 10; 20; 24. Decreased rCBF to orbitomedial and ventromedial cortex – BA 11:
6; 42; −10
14; 46; −20
20; 62; −4
−18; 54; 10
−14; 64; 0
In depressed group: decreased orbitomedial and ventromedial rCBF:
8; 56; −6
4; 58; 9
(Lennox et al 2004) 10 BD
12 HC
37.3±12.8
32.6±10.7
fMRI
3T
voxel-wise
NR NR NR Manic 8 Lith, 7 MS, 3 haloperidol, 4 olanzapine NR BD patients had attenuated BL activation of sgACC in response to sad faces −2; 20; −14
BA25
(Bauer et al 2005) 10 BD I
10 HC
39.3±7.8
35.0±9.3
18 F-FDG NR 20.4±7.0 NR Depressed AD + MS No psychosis Higher activity in R sgACC which decreased with treatment. 8; 24; −6
(Haldane et al 2007) 8 BD I 42.1±11.8 fMRI
1.5T
7mm (0.7mm gap)
23.1±5.6 10.1±6.5 episodes NR Mildly depressed Lamotrigine No alcohol or substance abuse, significant medical or neurological disorder, treatment resistance, suicide attempts, axis I comorbidity Greater activation of L medial frontal gyrus + R ACC in response to angry faces after lamotrigine therapy relative to baseline. BA 10
−4; 46; 10
BA 32/24
10; 36; 6
(Mah et al 2007) 13 BD II
18 HC
43.0±8.4
39.0±8.0
18 F-FDG 20±10.5 22.9±12 NR Depressed Lithium No substance abuse within 90 days, substance dependence within 5 years. No current psychotic features. 1 OCD, 1 eating disorder Increased metabolism of R pregenual ACC in BD. 12; 47; 5