Maeda et al (Reference Maeda, Keenan and Pascual-Leone2000) have succeeded in demonstrating the interhemispheric asymmetry of motor cortical excitability in major depression, using transcranial magnetic stimulation (TMS). This is an important finding that raises questions not only about the pathophysiology of major depression, but also about the state or trait nature of the results.
In discussing possible explanations for this functional asymmetry the authors consider the activity of inhibitory interneurons between cortical output cells, as proposed by Wasserman et al (Reference Wasserman, Samii and Mercuri1996), but it is not clear whether this mechanism is thought to act within the hemisphere being stimulated. The role of transcallosal inhibitory mechanisms has been demonstrated in schizophrenia (Reference Davey, Puri and LewisDavey et al, 1997; Reference Boroojerdi, Töpper and FoltysBoroojerdi et al, 1999) and is likely to be relevant to understanding asymmetrical motor thresholds in depression. In support of this view, Menkes et al (Reference Menkes, Bodnar and Ballesteros1999) hypothesised that depression is associated with decreased left hemisphere excitability with respect to the right hemisphere. They successfully showed that inhibitory low-frequency repetitive TMS applied to the right frontal lobe produced a significant anti-depressant effect, in contrast to exciting the left frontal lobe by means of fast-frequency repetitive TMS, the antidepressant effects of which have been known for some years.
Furthermore, Maeda et al report mean motor thresholds in the depression group of 41.13% for the left hemisphere and 37.63% for the right hemisphere, and in the healthy group of 48.29% for the left hemisphere and 52.7% for the right hemisphere. This gives a mean motor threshold of 39.38% for the depression group and 50.50% for the controls, which suggests important differences in both absolute threshold and laterality between the groups. Any changes to either of these parameters in subjects recovered from depression, and possibly in their first-degree relatives, not only promises new insights into the pathophysiology of depression, but also may provide clues about the most elusive object, a biological marker for depression.
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