Estudio mediante estimulación magnética transcraneal de las cortezas somatosensorial primaria y parietal posterior en la enfermedad de Parkinson

Résumé

Abstract parkinson¿s disease (pd) is the second most common neurodegenerative disease after alzheimer¿s disease. The loss of dopaminergic neurons within the substantia nigra pars compacta leads to the degeneration of the dopaminergic nigrosgtriatal pathway. This degeneration produces a functional impairment of the basal ganglia circuit and the cerebral cortex. Paired-pulse protocols of transcranial magnetic stimulation (tms) can be used to study intracortical circuits and intercortical connections of different cortical areas with the motor cortex. These protocols allow us to evaluate the modulatory effect of a first magnetic stimulus in the effect of a second magnetic stimulus at different interstimuli intervals between them. Tms investigations with pd patients have shown different intracortical circuit impairment within the primary motor cortex (m1), as well as in the connectivity of different cortical areas with m1. The objective of the present study was evaluate, using tms, intracortical circuits in the primary somatosensory cortex (s1) and the connectivity between the posterior parietal cortex (ppc) and ipsilateral m1 in pd patients and their modulation by dopaminergic treatment. To study s1, a paired-pulse tms protocol was used and both stimuli were delivered over s1. To study ipsilateral ppc to m1 connectivity, a similar protocol was used but this time using two different coils to each stimulus. The first magnetic stimulus was delivered over the ppc and the second magnetic stimulus was delivered over m1 using a different coil. The results obtained in this study showed that in pd there are not a impairment of s1 intracortical circuits, but that these circuits are affected by the presence of dopaminergic treatment in pd patients. On the other hand, there is a ppc to m1 connectivity impairment in pd patients that is partially improved by the dopaminergic treatment. This impairment was related to bradykinesia observed in pd studied patients. Overall, these results demonstrate that in pd there is a functional cortical impairment involving more tan m1 area, thus providing new knowledge in the pathophysiological process of pd.