Neurophysiological correlates of bradykinesia in Parkinson’s disease

Abstract

Many neurophysiological abnormalities have been described in the primary motor cortex of patients with Parkinson's disease. However, it is unclear whether there is any relationship between them and bradykinesia, one of the cardinal motor features of the condition. In the present study we aimed to investigate whether objective measures of bradykinesia in Parkinson's disease have any relationship with neurophysiological measures in primary motor cortex as assessed by means of transcranial magnetic stimulation techniques. Twenty-two patients with Parkinson's disease and 18 healthy subjects were enrolled. Objective measurements of repetitive finger tapping (amplitude, speed and decrement) were obtained using a motion analysis system. The excitability of primary motor cortex was assessed by recording the input/output curve of the motor-evoked potentials and using a conditioning-test paradigm for the assessment of short-interval intracortical inhibition and facilitation. Plasticity-like mechanisms in primary motor cortex were indexed according to the amplitude changes in motor-evoked potentials after the paired associative stimulation protocol. Patients were assessed in two sessions, i.e. OFF and ON medication. A canonical correlation analysis was used to test for relationships between the kinematic and neurophysiological variables. Patients with Parkinson's disease tapped more slowly and with smaller amplitude than normal, and displayed decrement as tapping progressed. They also had steeper input/output curves, reduced short-interval intracortical inhibition and a reduced response to the paired associative stimulation protocol. Within the patient group, bradykinesia features correlated with the slope of the input/output curve and the after-effects of the paired associative stimulation protocol. Although dopaminergic therapy improved movement kinematics as well as neurophysiological measures, there was no relationship between them. In conclusion, neurophysiological changes in primary motor cortex relate to bradykinesia in patients with Parkinson's disease, although other mechanisms sensitive to dopamine levels must also play a role.

Impairment of Motor Function Correlates with Neurometabolite and Brain Iron Alterations in Parkinson’s Disease

“…MDS-UPDRS3 scores strongly discriminated PD patients from controls. In contrast, differences in fine motor tests were less pronounced although PD patients displayed larger amplitudes and lower tapping speed than controls in line with other investigations [32,33]. In a large cohort of healthy subjects, we have demonstrated that age is a strong determinant of dexterity [11].…”

Dual-Site Transcranial Magnetic Stimulation for the Treatment of Parkinson's Disease

“…Furthermore, studies using PAS found that synaptic plasticity may be deficient in the absence of dopaminergic medication in the motor cortex of patients with PD (49, 50). This has been recently shown to correlate with motor performance and be in part reversible by dopamine replacement (51), suggesting not only a pathophysiological link between plasticity and dopamine availability, but also between motor cortical plasticity and akinesia in PD. The human STN receives dopaminergic projections from midbrain dopamine neurons (52).…”

Effects of Transcranial Alternating Current Stimulation on Repetitive Finger Movements in Healthy Humans

“…Finally, repetitive finger tapping is one of the tests most commonly used in the clinical assessment of patients with parkinsonian syndromes. Namely, specific kinematic abnormalities of finger tapping, that is, the amplitude decrement (also known as the sequence effect) are hallmarks of PD [ 25 – 28 ]. Thus, a better knowledge of the effectiveness of tACS on motor control is essential for future studies in pathological conditions [ 29 ].…”