Table 1.
Authors | Sample | Method | Result | Methodological issues | |||
---|---|---|---|---|---|---|---|
Image quality | Medication status | Control group | Duration of follow-up | ||||
Mander et al., 1987[9] | 14 patients - depressive illness | MRI before and after ECT - 6 h post to 25 h post ECT | T1 relaxation time increased immediately after ECT - but no long-term increase BBB breakdown - water influx into brain |
0.08 Tesla MRI | Not mentioned | 5 healthy controls | Last scan - 24 h post ECT |
Coffey et al., 1988[13] | 9 patients - depressive illness | MRI before and ECT - baseline and 2-3 days after full ECT course | No difference between baseline and follow-up MRI with respect to cortical atrophy, ventricle size, or white matter hyperintensity No structural changes |
1.5 Tesla | No psychotropic medication during ECT course | No control group | Last scan 2-3 days after last ECT |
Scott et al., 1990[11] | 20 patients - depressive illness | Baseline MRI and post-ECT MRI - at 25 min - 2/4/6 and 24 h post-ECT | T1 relaxation time increased immediately post-ECT - but returned to baseline within 24 h | 0.08 Tesla | Not mentioned | 5 healthy volunteers | Last scan at 24 h after ECT |
Pande et al., 1990[12] | 7 patients - depressive illness | Baseline MRI and post-ECT MRI - 1 week after ECT course | No new brain changes were found at the post-ECT scanning | 0.35 Tesla and 1.5 Tesla MRI |
Psychotropic medication discontinued 7 days prior | No control group | Last scan at 1 week post-ECT |
Coffey et al., 1991[10] | 35 patients - MDD and bipolar depression | Baseline MRI and post-ECT MRI - 2 days after and 6 months after ECT | No significant temporal changes in the total volumes of the lateral ventricles, third ventricles, frontal lobes, temporal lobes, or amygdala-hippocampal complex | 1.5 Tesla | In 26 out of 35 patients, psychotropic medications discontinued | No control group | 1st - 2 days after last ECT 2nd - 6 months after last ECT |
Diehl et al., 1994[14] | 6 patients - depressive illness | Baseline MRI and post-ECT MRI - 2 h and 30 h post-ECT | Significant post-ECT T2 relaxation time increase in the right and left thalamus and nonsignificant increase in temporal lobes T2 increase can be attributed to BBB breakdown - leading to edema |
1.5 Tesla | Psychotropic medication status not mentioned | No control group | Last imaging done 30 h after 2nd ECT |
Kunigiri et al., 2007[15] | 15 patients - depressive illness | Baseline MRI and post-ECT - 2 h after 2nd ECT | No significant increase in T2 relaxation time in MRI 2 h post-ECT | 1.5 Tesla | Psychotropic medication discontinued | No control group | Last imaging 2 h after 2nd ECT |
Szabo et al., 2007[17] | 10 patients - MDD, RDD, schizoaffective in depression | Diffusion weighted MRI after ECT - 30 min to 15 h post-ECT MRI | No obvious brain tissue changes seen immediately after ECT - even with DWI | 1.5 Tesla | Psychotropic medication status not mentioned | Six healthy elderly controls | Only one MRI imaging done - 2-15 h after ECT |
Nordanskog et al., 2010[18] | 12 patients - MDD or bipolar depression | 3 Tesla MRI 1 week prior to ECT and 1 week post-ECT | Significant increase in hippocampal volume post-ECT - both on left side and right sides and combined | 3 Tesla | Patients continued on antidepressants | No control group | Last imaging 1-week post-ECT |
Nordanskog et al., 2014[19] | 12 patients - unipolar and bipolar depression | MRI 1 week prior to ECT - A1, 1 week after ECT - A2, 6 months post-ECT - A3 and 12 months post-ECT - A4 | Significant increase in hippocampal volume at A2 which returned to baseline after 6 months. No clinical correlation between reduction in symptoms and increase in hippocampal volume | 3 Tesla | Patients continued on antidepressants | No control group | MRI scans - 1 week, 6 months and 12 months post-ECT |
Tendolkar et al., 2013[20] | 15 patients - treatment-resistant unipolar depression | MRI 1 week prior to ECT and 1 week post-ECT | Significant increase in the volume of hippocampus and amygdala post-ECT. Increase in volume not significantly correlated with treatment response | 1.5 Tesla | Psychotropic medication stopped 1 week prior to ECT | No control group | Last MRI 1 week after last ECT |
Dukart et al., 2014[21] | 3 groups - 19 with MDD, 15 with BPD 10 patients - 5 MDD + 5 BPD received ECT versus 24 patients who did not receive ECT | Patients assessed before ECT - TP1 and at 3 months post and 6 months post-ECT - TP2 and TP3. | Right unilateral ECT associated with GMV increase in the right side - hippocampus, amygdala, and anterior temporal pole and subgenual cortex ECT associated with decrease in GMV in the right prefrontal cortex. Hippocampal GMV increase and subgenual GMV increase significantly correlated with symptomatic improvement No correlation between ECT dosage and GMV changes or clinical response |
1.5 Tesla | Psychotropic medication continued | 21 healthy controls | Last MRI 6 months after the last ECT\comment: unilateral ECT - 2.5 times ST administered - not an adequate ECT dosage as per RCPsych Guidelines |
Abbott et al., 2014[22] | 19 patients - MDD | Patients scanned twice - within 2 days of starting ECT and 5 days after completion of ECT | Right and left hippocampal volume significantly reduced in pre-ECT patients compared to controls Significant increase in hippocampal volume and hippocampal connectivity in ECT responders Right and left hippocampal volumes and connectivity not significantly different between post-ECT responders and healthy controls Increase in hippocampal connectivity correlated with symptom improvement but not so for increase in hippocampal volume |
3 Tesla MRI - structural and functional imaging done | Psychotropic medication continued | Twelve healthy controls included - scanned once | Last imaging done 5 days after completion of ECT course |
Lyden et al., 2014[23] | 20 patients with RDD - presently severe depression | Patients imaged thrice - pre-ECT, 48 h post- first ECT, and after completion of course of ECT | Significant increase in FA and decrease in RD were shown in the anterior cingulum, the forceps minor, and left SLF between pre- and post-ECT groups - suggesting increased fiber integrity in the dorsal fronto-limbic pathway Longitudinal white matter changes were associated with improved clinical response |
3 Tesla MRI | Psychotropic medication discontinued | 28 healthy controls included - imaged once | Within 1 week of completion of ECT course |
Bouckaert et al., 2016[24] | 28 patients - MDD, age>55 | MRI done - 1 week pre-ECT and 1 week post-ECT | Significant GMV changes only on the side of stimulation in the right unilateral ECT along with a lack of correlation between GMV change and clinical improvement |
3 Tesla MRI | Psychotropic medication continued in some patients | No control group | 1 week after last ECT in the ECT course |
Ota et al., 2015[25] | 15 patients with MDD | MRI done roughly 1 week pre-ECT and 1 week post-ECT | Significant increase in volume in bilateral inferior temporal cortices, hippocampi and para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus post-ECT in total patient group ROI analysis of hippocampal - Amygdala complex: significant increase in volume in the right hippocampus and right amygdala and trend level increase in left amygdala |
1.5 Tesla MRI | Psychotropic medication continued in all patients | No control group | 1 week after the last ECT |
Zeng et al., 2015[26] | 24 patients with first-episode MDD | DTI study - patients scanned 1 day before ECT and 1 week after 8 ECTs | Significant reorganization in eight anatomical connections/connectomes - Limbic structure, frontal and temporal lobes - pre- and post-ECT Connection changes between amygdala and para-hippocampus correlated with depressive symptom reduction |
3 Tesla MRI | Psychotropic medication continued | No control group | Last MRI 1 week after the last ECT |
van Eijndhoven et al., 2016[27] | 23 treatment resistant MDD patients - 19 completed study | Patients imaged 1 week before starting ECT and 1 week after completion of ECT - to assess cortical thickness | Large bilateral clusters of increased cortical thickness after ECT treatment - involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex post-ECT | 1.5 Tesla MRI | Psychotropic medication stopped 1 week before beginning ECT | 22 healthy controls - 16 completed study | Last MRI 1 week after completion last ECT |
Bouckaert et al., 2016[28] | Cohort of 66 MDD patients - 23 remained at the end of 6 months | Imaging done at 1 week before ECT - T0, after 6th ECT - T1, 1 week (T2), 4 weeks (T3) and 6 months (T4) post-ECT Serum BDNF - sBDNF measured at T0, T1, T2, T3, T4 MADRS at T0, T1, T2, T3, T4 |
ECT induces a significant increase in hippocampal volume - but this does not show correlation with improvement in depressive symptoms. The hippocampal volume increase appears to be transient - returning to the baseline after 6 months - though not accompanied by relapse of depression. Hippcampal volume increase in unrelated to the sBDNF levels. Further, the improvement in depressive symptoms showed no correlation to the sBDNF levels | 3 Tesla MRI | Psychotropic medication continued | No control group | Last MRI done at 6 months after ECT (but of the original 66 only 23 remained at 6 months) |
Depping et al., 2017[29] | 12 ECT-naïve patients with treatment-resistant MDD and 16 healthy controls | Patients imaged 5 days prior to ECT and 8 days post-ECT. Right unilateral ECT administered | At baseline, MDD patients showed increased GMV of right cerebellar area VIIIa and left cerebellar area VIIb compared to healthy controls Post-ECT patients exhibited increased GMV in left cerebellar area VIIa crus I Cerebellar volume increase following ECT was associated with HAMD score reduction |
3 Tesla MRI | Psychotropic medication were continued | 16 healthy controls | Last MRI 8 days after completion of course of ECT |
Joshi et al., 2016[30] | 43 patients in severe depression - MDD (n - 35) and bipolar disorder (n - 7) | Patients assessed at three time points - 24 h before ECT - T1, 24 h after 3rd ECT - T2, within 1 week of completing ECT - T3 | Hippocampal and amygdalar volume were significantly lesser in pre-ECT patients compared to healthy controls and also that there was a significant increase in the volume of bilateral hippocampus and amygdala post-ECT Significant correlation between increase in hippocampal and amygdalar volume and reduction in HAMD |
3 Tesla MRI | Psychotropic medication discontinued | 32 healthy controls imaged twice | Last MRI within 1 week of last ECT |
Pirnia et al., 2016[16] | Patients with MDD or BPAD currently severe depression - 41 enrolled - 29 completed | Patients imaged at three time points - T1 - baseline before ECT, T2 - 48 h after 2nd ECT, T3 - within 1 week of completing ECT | Pair-wise comparisons at T1 and T3 showed significant changes in the bilateral ACC, right para - hippocampal gyrus, superior temporal gyrus, and temporal pole ROI analysis showed significant increase in cortical thickness post-ECT in ACC, para hippocampal, entorhinal, superior temporal, inferior temporal, and fusiform cortex Significant correlation between increase in cortical thickness in the fusiform, superior, inferior temporal cortex and reduction in clinical symptoms |
3 Tesla MRI | Psychotropic medication discontinued | 29 healthy controls | Last MRI within 1 week of last ECT |
Wade et al., 2016[31] | 53 patients in severe depression - unipolar or bipolar selected - 34 completed all assessments | Patients assessed at three time points - T1 before ECT, T2 - 48 h after 2nd ECT and T3 - 1 week after last ECT | At baseline - nucleus acumbens and pallidum volume significantly reduced in patients. Volume increase of putamen during course of ECT. Differential response of nucleus acumbens and caudate nucleus to ECT in responders and nonresponders. Patient’s responsiveness to ECT predicted with 89% accuracy using machine learning techniques | 3 Tesla MRI | Psychotropic medication discontinued prior to starting ECT | 33 healthy controls - controls assessed at two time points: 4 - 6 weeks apart | Last MRI 1 week after last ECT |
Wolf et al., 2016[32] | 21 ECT-naïve patients - 12 with MDD and 9 with schizophrenia | Patients imaged twice - within 5 days prior to the first ECT session and 6-8 days after last ECT | ECT leads to increase in structural network strength in MPFC and MTL networks in MDD - but no correlation with clinical improvement In schizophrenia patients with depression - significant difference post-ECT in two networks - DLPFC and MTL network with significant correlation between clinical improvement and the increase in strength of the DLPFC network |
3 Tesla MRI | Psychotropic medication continued | 21 healthy controls | Last MRI 8 days after last ECT |
Qiu et al., 2016[14] | 12 patients - Unipolar depression and 15 matched controls | Imaging 1 day pre- and post-ECT. | Comparison between pre- and post-ECT data showed increase in GMV in bilateral hippocampus and amygdala Analysis of fMRI data indicated baseline functional differences between healthy controls and MDD patients with functional changes occurring in MDD patients post-ECT - though not returning to full normalcy |
3 Tesla MRI | Psychotropic medication discontinued | 15 healthy controls | Last MRI 1 day after the 8th ECT in a series of 12 ECTs |
MDD – Major depressive disorder; RDD – Recurrent depressive disorder; BPD – Borderline personality disorder; ECTs – Electroconvulsive therapies; BPAD – Bipolar affective disorder; MRI – Magnetic resonance imaging; BDNF – Brain-derived neurotrophic factor; sBDNF – Serum BDNF; DTI – Diffusion tensor imaging; fMRI – Functional MRI; BBB – Blood–brain barrier; DWI – Diffusion-weighted imaging; GMV – Gray matter volume; FA – Fractional anisotropy; RD – Radial diffusivity; SLF – Superior longitudinal fasciculus; HAMD – Hamilton Depression Rating Scale; ACC – Anterior cingulate cortex; MPFC – Medial prefrontal cortex; MTL – Medial temporal lobe; DLPFC – Dorsolateral prefrontal cortex; ST – Seizure Threshold; ROI – Region of Interest