Prior investigations of MST have found it to have little to no adverse neurocognitive effects. Converging evidence from virtual computer simulated models, preclinical, and clinical studies suggest that MST does not result in substantive impact on cortical or subcortical structures, which in turn allows for preservation of cognitive abilities. Data from virtual models showed that MST stimulation affected 21% of total brain volume and was limited only to grey matter. Preclinical data showed that MST had little impact on cortical areas and cognitive functions, even when administered at suprathreshold levels. The latter findings were also observed in the clinical investigations. Collectively, these data from different study methodologies provide support for the safety of MST.
The virtual and preclinical studies of MST help to explicate the underlying neurocircuitry that subserves cognitive functions, particularly memory. With the introduction of MST, experiments were able to compare the neurocognitive effects of different modalities of seizure induction, thereby discerning the between the effects of the seizure and its mode of induction (e.g. electric, magnetic). The cognitive profile associated with ECT is disorientation immediately after the treatment, and anterograde and retrograde amnesia following the treatment (Semkovska & McLoughlin, 2010
). The available data indicate that MST does not produce the same cognitive profile (see ) as ECT, which suggests that the mode of seizure induction rather than the seizure itself may be associated with adverse cognitive effects.
Comparing magnetic seizure therapy and electroconvulsive therapy effects on neurocognitive functions.
The clinical studies suggested that MST did not impact neurocognitive performance. Specifically, when administered at moderate dose (~50 Hz), patients showed quick recovery of orientation and stable or improved performance on neurocognitive measures. Even when administered at a high dose (100 Hz), patients showed rapid recovery of orientation and preservation of cognitive abilities. However, methodological variability between the clinical investigations that included different MST parameters, treatment course length, and neuropsychological measures, prevent firm conclusions. For example, in the Lisanby et al. (2003a)
study, only two MST sessions were administered at moderate dose with different coil configurations, whereas the patients in the Kayser et al. (2011)
completed 12 treatments at high dose with a twin coil. Research on ECT has found an association between stimulus dose, treatment course length, electrode configuration, and neurocognitive effects (McCall et al., 2000
; Sackeim et al., 2007
). Thus, further examination of different MST parameters and treatment algorithms is needed to evaluate the effects, if any, on neurocognitive function.
Regarding neuropsychological measures, the clinical studies included at minimum a measure of orientation, one study (Lisanby et al., 2003a
) only measured cognitive effects immediately after MST with the TEB, and two studies (Kayser et al., 2011
; Kosel et al., 2003
) utilized the TEB and additional cognitive measures to assess postictal and end of treatment effects. As such, there was limited information regarding the effects on other cognitive domains such as executive function, working memory, and processing speed which are interrelated with memory functions (Reid & Krasnegor, 1996
). Future studies should employ neurocognitive measures that assess multiple domains to comprehensively examine neurocognitive effects, are psychometrically sound with available demographic-adjusted normative scores, and have equivalent alternate forms to prevent practice effects. Also, future studies are needed to replicate and extend these early findings (e.g. effects on visuospatial reproduction) to determine the neurocognitive profile of MST, and to establish whether the profile mimics or is different than ECT.
In conclusion, the available studies that examined the neurocognitive effects of MST found it to be a cognitively safe neurotherapeutic intervention. The evidence also suggests that MST and ECT are different in terms of their seizure propogation and focality, two variables that may account for their respective differential neurocognitive effects. Further research with translational methods that combines virtual computer simulations with preclinical and clinical investigations is warranted to comprehensively characterize the neurocognitive effects on other domains such as working memory and executive function, and then to link those effects to the underlying neurocircuitry. Such investigations would aid in the development, and help to confirm and establish MST as a cognitively benign therapeutic modality to treat severe mood disorders.