Basic mechanism of magnetic human cerebellar stimulation and its clinical application

Ugawa, Y.

Rinsho Shinkeigaku 49(10): 621-628

2009


ISSN/ISBN: 0009-918X
DOI: 10.5692/clinicalneurol.49.621
Accession: 068510655

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Abstract
I here summarize the history of cerebellar stimulation experiments in humans and give some caution to use this stimulation method. In clinical evaluation, we consider the cerebellum as a kind of computer to get information from the peripheral structures and also higher motor cortical centers including the primary motor cortex (M1) and send a cerebellar command to M1 after computation of much information. We study functions of the cerebello-afferent and cerebello-efferent connections using cerebellar stimulation and differentiate these pathways dysfunction. We first activated the cerebellum using electrical stimulation. The most effective position, effective current direction and the interval of conditioning and test stimuli suggested that the observed effect might be produced by some cerebellar structures activation. Studies of cerebellar ataxia patients and other disorders supported the idea that the suppression is produced by the inhibition of dentato-thalamo-cortical pathway by Purkinje cell activation. In patients with a lesion at cerebellar hemisphere, dentate nucleus, superior cerebellar peduncle, motor thalamus, the suppression effect was not evoked. In contrast, the suppression was normally elicited in patients with a lesion at pontine nucleus, middle cerebellar peduncle even though they had clinically definite ataxia. Normal suppression was evoked in patients with non-cerebellar ataxia (sensory ataxia due to paraneoplastic syndrome, tabes dorsalis, ataxic sensory neuropathy). Based on these results, we concluded that the cerebellar electrical stimulation method was useful to differentiate cerebellar ataxia due to cerebellar efferent pathways lesions from other cerebellar ataxia and non-cerebellar ataxia. We demonstrated that magnetic stimulation over the cerebellum using a double-cone coil can produce the same effect as those elicited by electrical cerebellar stimulation. These all results supported the proposal that the magnetic stimulation over the cerebellum can enable us to differentiate the cerebellar efferent ataxia from other cerebellar ataxia and non-cerebellar ataxia. A recent paper has cautioned us to conclude the observed phenomenon to be produced by cerebellar activation after exclusion of several other factors as stated in the original paper. The most serious factor to exclude is the antidromic activation of the corticospinal tracts by the cerebellar stimulation conditioning stimulus. To exclude this possibility, it is important how to measure the threshold of the corticospinal tracts. We recommend that we should use rectified EMG recordings when determining it. In summary, I conclude that the cerebellar magnetic stimulation is a good tool for physiological differentiation of cerebellar ataxia mechanisms in ataxic patients. At a current stage, I recommend a conservative method mentioned in the editorial paper for magnetic cerebellar stimulation.