High frequency extradural motor cortex stimulation transiently improves axial symptoms in a patient with Parkinson's disease

Abstract

In a primate model of Parkinson's disease (PD), the benefit of extradural motor cortex stimulation (EMCS) was associated with high-frequency stimulation (130 Hz), whereas no significant motor improvement was achieved at 10 Hz or intermediate frequencies of stimulation. We report the case of a 72-year-old female patient affected by severe PD who underwent bilateral EMCS. In baseline med-off condition the patient was unable to arise from a chair and to stand without assistance. Stimulation at 3 and 60 Hz failed to provide any improvement of symptoms, whereas, when stimulating at 130 Hz, axial akinesia and walking improved consistently: the patient, in med-off condition, was able to arise from chair and to walk without assistance. The patient underwent two brain 99mTc- Ethylcysteinate Dimer-SPECT studies: semiquantitative and Statistical Parametric Mapping revealed that the regional cerebral perfusion was significantly increased in the supplementary motor area during stimulation at 130 Hz. After five months, the benefit of EMCS gradually disappeared.

Which one is more effective in Parkinson's disease? stimulating the motor cortex or the basal ganglia?

“…This observation is consistent with the increase in rate of thalamic relay nucleus due to STN-DBS. Finally, it has been observed that MCS improves Parkinson's motor signs [16][17][18][19][20][21]. This observation is consistent with increase in the rate of thalamic relay nucleus due to MCS.…”

Electrical Stimulation of Primary Motor Cortex for Parkinson's Syndrome

“…Indeed, ECD SPECT data demonstrated a resting state reduction of neuronal activity in motor cortical areas during EMCS (Cilia et al, 2008). Finally, functional neuroimaging studies showed a significant increase of cerebral perfusion in the SMA and the DLPFC in STIM-ON condition Fasano et al, 2008;Tani et al, 2007). The SMA and the DLPFC are known to be under-active in patients with PD, probably underlying bradykinesia (Haslinger et al, 2001;Jahanshahi et al, 1995;Rascol et al, 1992), and these cortical metabolic abnormalities can be reversed by antiparkinsonian therapies such as dopaminergic treatment (Jenkins et al, 1992), pallidotomy (Grafton et al, 1995), STN-DBS (Limousin et al, 1997) or GPi-DBS (Fukuda et al, 2001).…”

“…Most of EMCS studies did not find significant mean changes between stimulation-on and stimulation-off in UPDRS part II and III (Cilia et al, 2008;Gutierrez et al, 2009;Strafella et al, 2007). On the other hand, motor evaluation in individual patients revealed clinical improvement during stimulation in comparison to STIM-OFF condition (Cilia et al, 2008;Fasano et al, 2008;Gutierrez et al, 2009;Strafella et al, 2007;Tani et al, 2007). These published data must be interpreted very cautiously, because they are from open labelled studies that involved only small numbers of patients from a few centres.…”

“…The latency of the clinical effects of high-frequency STN-DBS is also known to vary from one type of parkinsonian motor symptoms to another with short latency benefit (less than 1 min) observed for rigidity and tremor and longer time delay (a few minutes, up to a few days) observed for other symptoms such as bradykinesia and akinesia (Krack et al, 2002). As discussed by others, the delays of clinical benefits observed with EMCS may be due to synaptic plasticity, long-term potentiation, long-term depression, expression of secondary messengers or polarization of brain tissue Krack et al, 2002;Priori and Lefaucheur, 2007), and the immediate effects may be due to the dual effect -imposing a specific pattern of activity and suppress abnormal, disease-associated rhythmicity of oscillation in corticobasal gangliacortical circuit (Brown, 2006;Fasano et al, 2008;Garcia et al, 2003;Priori and Lefaucheur, 2007). Studies of rTMS of M1 reveal that PD is associated with excess excitability or reduced inhibition at the M1 (Cantello et al, 2002), and rigidity and tremor might be caused by hyperactivity of the M1 (Haslinger et al, 2001;Rodriguez-Oroz et al, 2009).…”

Chronic motor cortex stimulation in patients with advanced Parkinson’s disease and effects on striatal dopaminergic transmission as assessed by 123I-FP-CIT SPECT

“…Therefore, this technique has been recently applied as a minimally invasive treatment for patients with advanced PD who refused or are not eligible to undergo DBS [5,[9][10][11][30][31][32][33]. Although some researchers did not find significant clinical improvement in PD patients [13][14][15], different groups have reported beneficial effects of EMCS on PD symptoms (tremor, rigidity, motor dexterity, bradykinesia, posture, gait and freezing) as well as the reduction of dopaminergic therapy [33,34]. The mechanisms of action of EMCS are still poorly understood, and any hypothesis is speculative.…”