Theta burst stimulation over the primary motor cortex does not induce cortical plasticity in Parkinson’s disease

Eggers, Carsten; Fink, Gereon R.; Nowak, Dennis A.

doi:10.1007/s00415-010-5597-1

Cited by 56 publications

(46 citation statements)

References 30 publications

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“…Interestingly, the first dose of l -DOPA failed to modulate the plasticity in these patients and there was no significant difference between the more and less affected sides. Deficient iTBS induced LTP-like plasticity in PD was observed in other studies (58, 60, 61). In one study (60) following facilitatory iTBS, neither the medication state (ON and OFF), disease severity nor the presence of LID had any effect on this lack of potentiation, suggesting that the reduced M1 plasticity in PD is unrelated to dopaminergic therapy, disease severity, and the developments of LID.…”

Section: M1 Plasticity Studies In Pdsupporting

confidence: 83%

“…Similarly, instead of potentiation, iTBS produced no change in excitability in eight patients ON dopaminergic drugs (61). In another study (58), inhibitory cTBS on M1 did not change in M1 excitability in PD patients. Another study (64) demonstrated altered plasticity in both early and late stages of PD and different effects of dopaminergic medications at different stages of the disease.…”

Section: M1 Plasticity Studies In Pdmentioning

confidence: 86%

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Motor Cortical Plasticity in Parkinson’s Disease

Udupa¹,

Chen²

2013

Front. Neurol.

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In Parkinson’s disease (PD), there are alterations of the basal ganglia (BG) thalamocortical networks, primarily due to degeneration of nigrostriatal dopaminergic neurons. These changes in subcortical networks lead to plastic changes in primary motor cortex (M1), which mediates cortical motor output and is a potential target for treatment of PD. Studies investigating the motor cortical plasticity using non-invasive transcranial magnetic stimulation (TMS) have found altered plasticity in PD, but there are inconsistencies among these studies. This is likely because plasticity depends on many factors such as the extent of dopaminergic loss and disease severity, response to dopaminergic replacement therapies, development of l-DOPA-induced dyskinesias (LID), the plasticity protocol used, medication, and stimulation status in patients treated with deep brain stimulation (DBS). The influences of LID and DBS on BG and M1 plasticity have been explored in animal models and in PD patients. In addition, many other factors such age, genetic factors (e.g., brain derived neurotropic factor and other neurotransmitters or receptors polymorphism), emotional state, time of the day, physical fitness have been documented to play role in the extent of plasticity induced by TMS in human studies. In this review, we summarize the studies that investigated M1 plasticity in PD and demonstrate how these afore-mentioned factors affect motor cortical plasticity in PD. We conclude that it is important to consider the clinical, demographic, and technical factors that influence various plasticity protocols while developing these protocols as diagnostic or prognostic tools in PD. We also discuss how the modulation of cortical excitability and the plasticity with these non-invasive brain stimulation techniques facilitate the understanding of the pathophysiology of PD and help design potential therapeutic possibilities in this disorder.

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Section: M1 Plasticity Studies In Pdsupporting

confidence: 83%

Section: M1 Plasticity Studies In Pdmentioning

confidence: 86%

Motor Cortical Plasticity in Parkinson’s Disease

Udupa¹,

Chen²

2013

Front. Neurol.

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“…Similarly to what observed with PAS, TBS protocols failed to induce plasticity in patients with PD in most studies (12, 13). Suppa et al (13) tested the effects of intermittent theta-burst stimulation (iTBS), a technique used to induce LTP-like plasticity in M1, in patients with PD, OFF and ON dopaminergic therapy, with and without l -DOPA -induced dyskinesias (LIDs).…”

Section: Tbs Protocolsupporting

confidence: 58%

Do Studies on Cortical Plasticity Provide a Rationale for Using Non-Invasive Brain Stimulation as a Treatment for Parkinson’s Disease Patients?

Koch

2013

Front. Neurol.

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Animal models of Parkinson’s disease (PD) have shown that key mechanisms of cortical plasticity such as long-term potentiation (LTP) and long-term depression (LTD) can be impaired by the PD pathology. In humans protocols of non-invasive brain stimulation, such as paired associative stimulation (PAS) and theta-burst stimulation (TBS), can be used to investigate cortical plasticity of the primary motor cortex. Through the amplitude of the motor evoked potential these transcranial magnetic stimulation methods allow to measure both LTP-like and LTD-like mechanisms of cortical plasticity. So far these protocols have reported some controversial findings when tested in PD patients. While various studies described evidence for reduced LTP- and LTD-like plasticity, others showed different results, demonstrating increased LTP-like and normal LTD-like plasticity. Recent evidence provided support to the hypothesis that these different patterns of cortical plasticity likely depend on the stage of the disease and on the concomitant administration of l-DOPA. However, it is still unclear how and if these altered mechanisms of cortical plasticity can be taken as a reliable model to build appropriate protocols aimed at treating PD symptoms by applying repetitive sessions of repetitive TMS (rTMS) or transcranial direct current stimulation (tDCS). The current article will provide an up-to-date overview of these issues together with some reflections on future studies in the field.

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“…Our sample size is within the range of other TBS publications in Parkinson's disease (Eggers et al, 2010;Huang et al, 2011b) and Dystonia (Huang et al, 2010), but our findings need to be confirmed in larger samples. In this context, one should note that despite the observed differences in plasticity responses between both groups, larger sample sizes are needed to explain the exact directions and the underlying mechanisms.…”

Section: Limitationsmentioning

confidence: 42%