Effects of right unilateral electroconvulsive therapy on motor cortical excitability in depressive patients

Bajbouj, Malek; Lang, Undine E.; Niehaus, L.; Hellen, Florence; Heuser, Isabella; Neu, Peter

doi:10.1016/j.jpsychires.2005.07.002

Cited by 79 publications

(44 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…8 In addition, alterations in motor cortical excitability by different antidepressant interventions had been reported by several groups. 9,10 In line with these findings, we previously showed an increase in cortical inhibition after ECT 11 and repetitive TMS of the left dorsolateral prefrontal cortex. 12 To further elucidate possible common effects of different antidepressant stimulation techniques, the present investigation was undertaken to explore the effects of VNS on motor cortical excitability by noninvasive TMS in patients with unipolar major depression.…”

supporting

confidence: 76%

“…19 Our data are in line with neurophysiological studies showing increased motor cortical inhibition in patients with major depression after ECT. 11 Consistent with these findings, brain imaging studies using proton magnetic resonance spectroscopy demonstrated an increase of GABA concentrations in patients with depression after different antidepressant treatments. 20,21 Finally, in support of this view, there is indirect evidence from magnetic resonance spectroscopy 22 and TMS of the motor cortex 23 that patients with major depression have decreased GABA concentrations and motor cortical inhibition, respectively.…”

Section: Discussionsupporting

confidence: 56%

See 1 more Smart Citation

Motor Cortex Excitability After Vagus Nerve Stimulation in Major Depression

Bajbouj¹,

Gallinat²,

Lang³

et al. 2007

Journal of Clinical Psychopharmacology

View full text Add to dashboard Cite

Recent data suggest that inhibitory pathways may be involved in the pathophysiology of depression and in the mode of action of some antidepressant interventions. The aim of the present study was to test whether vagus nerve stimulation (VNS) can affect motor cortex excitability. Measures of motor cortical excitability were probed by using single-pulse and paired-pulse transcranial magnetic stimulation at baseline, after 10 weeks of left VNS, and additionally, in an on-off paradigm in 10 patients with treatment-resistant unipolar depression. Ten weeks of VNS was associated with a selective and pronounced increase in intracortical inhibition, whereas no changes occurred in the on-off paradigm. These results suggest that VNS is capable of changing motor cortical excitability in patients with depression.

show abstract

supporting

confidence: 76%

Section: Discussionsupporting

confidence: 56%

Motor Cortex Excitability After Vagus Nerve Stimulation in Major Depression

Bajbouj¹,

Gallinat²,

Lang³

et al. 2007

Journal of Clinical Psychopharmacology

View full text Add to dashboard Cite

show abstract

“…Along with other promising hypotheses (Nestler et al, 2002), an emerging line of clinical evidence seems to be consolidated into yet another concept. Cortical excitability is shown to be increased in depressives (Bajbouj et al, 2006b) and normalized by treatments with transcranial magnetic stimulation (TMS; Bajbouj et al, 2005) or electroconvulsive therapy (ECT; Bajbouj et al, 2006a). These reports indicate an association between cortical excitability and depression, although other data on patients' brain activity, based on cerebral blood flow or glucose metabolism, do not necessarily agree with a generalized increase in cortical excitability (Paus and Barrett, 2004).…”

Section: Introductionmentioning

confidence: 99%

Increase in Cortical Pyramidal Cell Excitability Accompanies Depression-Like Behavior in Mice: A Transcranial Magnetic Stimulation Study

Sun¹,

Wang²,

Wang³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

Clinical evidence suggests that cortical excitability is increased in depressives. We investigated its cellular basis in a mouse model of depression. In a modified version of forced swimming (FS), mice were initially forced to swim for 5 consecutive days and then were treated daily with repetitive transcranial magnetic stimulation (rTMS) or sham treatment for the following 4 weeks without swimming. On day 2 through day 5, the mice manifested depression-like behaviors. The next and last FS was performed 4 weeks later, which revealed a 4 week maintenance of depression-like behavior in the sham mice. In slices from the sham controls, excitability in cingulate cortex pyramidal cells was elevated in terms of membrane potential and frequencies of spikes evoked by current injection. Depolarized resting potential was shown to depend on suppression of large conductance calcium-activated potassium (BK) channels. This BK channel suppression was confirmed by measuring spike width, which depends on BK channels. Chronic rTMS treatment during the 4 week period significantly reduced the depression-like behavior. In slices obtained from the rTMS mice, normal excitability and BK channel activity were recovered. Expression of a scaffold protein Homer1a was reduced by the FS and reversed by rTMS in the cingulate cortex. Similar recovery in the same behavioral, electrophysiological, and biochemical features was observed after chronic imipramine treatment. The present study demonstrated that manifestation and disappearance of depression-like behavior are in parallel with increase and decrease in cortical neuronal excitability in mice and suggested that regulation of BK channels by Homer1a is involved in this parallelism.

show abstract

“…Authors showed an up-regulation of the GABA-B receptors in the brain of rats after ECT sessions and an increase of the brain GABA rates as well as an increased activity of the GABA-B after treatment with ECT in humans [20][21][22][23][24]. However, a single session of ECT does not increase CSP 23 while several ECT increase CSP (24), a finding consistent with GABAergic activity of ECT.…”

Section: Discussionmentioning

confidence: 86%