Longitudinal MRS studies of pediatric bipolar disorder and youth at risk for bipolar disorder
Study | Sample | Methods (Device/FS/TR/TE/Sequence) | Region-of-Interest Voxel Size and Location | Findings |
---|---|---|---|---|
Davanzo et al, 200178 | 11 Patients with BD mania, medicated (n = 9), unmedicated (n = 2), (mean age, 11.4 yr), | Signaa/1.5T/3000/30/PRESS | 8 mL in the anterior cingulate cortex | ↓ mIns/tCre was associated with acute lithium treatment (P = .047); |
↓ mIns/tCre in lithium responders (P < .012); | ||||
mIns/tCre was not significantly different in lithium nonresponders (P < .655); | ||||
NAA/tCre was the metabolite least affected by lithium | ||||
Treatment with lithium for 1 week (mean lithium level = 0.64 mEq/L), | ||||
Scans obtained at baseline and day 7 | ||||
DelBello et al, 200681 | 19 Unmedicated manic or mixed patients with BD treated with olanzapine, 10–20 mg/day for 4 weeks, | Signa/1.5T/2000/35/PRESS | 8 mL in the medial ventral prefrontal cortex, | ↑ tChol in medial ventral prefrontal cortex (P = .0001) associated with olanzapine treatment; |
(mean age, 14.7 yr), | 8 mL in the left and right ventral lateral prefrontal cortices, | ↑ baseline tChol in the medial ventral prefrontal cortex associated with remission at 4 weeks (P = .001); | ||
10 healthy volunteers, (mean age, 15 yr), | Scans obtained at baseline, day 7, and day 28 | ↑ NAA for 4 weeks in the medial ventral prefrontal cortex in olanzapine remitters (n = 11) vs ↓ NAA in nonremitters (n = 8) (P = .006); | ||
↑ NAA for 4 weeks was associated with reduction in YMRS scores (r = 0.68; P = .004) | ||||
Patel et al, 200679 | 28 Unmedicated depressed patients with BD, (mean age, 15.5 yr), | Signa/1.5T/2000/35/PRESS | 8 mL in the medial prefrontal cortex, | mIns in medial prefrontal cortex did not significantly differ among baseline, day 7, or day 42; |
8 mL in the left and right lateral prefrontal cortices, | ↓ baseline mIns in medial prefrontal cortex in lithium remitters (n = 8) vs non-remitters (n = 20) (P = .003) | |||
Treatment with lithium for 42 days, titrated to serum levels of 1.0–1.2 mEq/L | Scans obtained at baseline, day 7, and day 42 | |||
Chang et al, 200983 | 10 Offspring of BD parents with mood symptoms but not BD, medicated (n = 3), unmedicated (n = 7), (mean age, 11.3 yr), | Signa/3T/2000/35/ PRESS | 8 mL in the left and right dorsolateral prefrontal cortices, | No significant difference in NAA in the left (P = .88) or right (P = .13) dorsolateral prefrontal cortex associated with 12 weeks of divalproex treatment; |
Scans obtained at baseline and 12 weeks | Effect size for decreased NAA = 0.94 for the right dorsolateral prefrontal cortex; | |||
Exploratory analyses showed no significant differences in tChol or mIns | ||||
Treatment with divalproex for 12 weeks; mean serum VPA level = 82 μg/mL | ||||
Strawn et al, 201276 | 25 Unmedicated manic or mixed patients with BD (mean age, 14.5), | Varianb/4T/3000/23/PRESS | 8 mL in the anterior cingulate cortex (gray matter), | ↓ Glx at baseline in the left ventrolateral prefrontal cortex in treatment remitters (P = .01); |
8 mL in left and right ventrolateral prefrontal cortices (white matter), | In divalproex treatment remitters, change in Glu in the left ventrolateral prefrontal cortex correlated with change in YMRS score (r = 0.82; P = .03) | |||
Treatment with divalproex for 28 days, titrated to a serum VPA level of 85–125 μg/mL | Scans obtained at baseline, day 7, and day 28 | |||
Chang et al, 201282 | 26 Unmedicated depressed patients with BD, | Signa/3T/2000/26/ PRESS | 8 mL in the anterior cingulate cortex, | ↓ Posttreatment mIns in the ACC in quetiapine responders (5 of 16 patients); |
Treatment with either quetiapine (n = 16) or placebo (n = 10) for 8 weeks, | and | 8 mL in the left dorsolateral prefrontal cortex, | no significant change in NAA between the quetiapine and placebo groups | |
(mean age, 15.6 yr) | Varian/4T/2000/26/PRESS | 8 mL in the right dorsolateral prefrontal cortex |