Cortical motor reorganization in akinetic patients with Parkinson's disease

Abstract

Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies. Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex. These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex. These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.

Role of hyperactive cerebellum and motor cortex in Parkinson's disease

“…The finding that the motor cortex is hyperactive extends previous studies in PD patients on sequential movements (Sabatini et al, 2000;Thobois et al, 2000), and single joystick movements (Haslinger et al, 2001). In contrast, using fMRI Buhmann and colleagues (2003) found that in drug naïve PD patients the primary motor cortex was hypoactive during an auditory-paced random finger opposition task, and the activation increased after L-dopa intake.…”

“…Our first goal was to replicate previous findings that the putamen is hypoactive in PD (Jahanshahi et al, 1995), and the ipsilateral cerebellum (Rascol et al, 1997;Wu and Hallett, 2005) and motor cortex (Haslinger et al, 2001;Sabatini et al, 2000;Thobois et al, 2000) are hyperactive in PD. The first hypothesis is that this pattern of hypoand hyperactivation is not task specific and occurs during both automatic rhythmic movements (900 ms) and cognitively controlled discrete movements (2400 ms).…”

“…This model is supported by brain imaging studies showing reduced regional cerebral blood flow (rCBF) and reduced blood oxygenation level dependent (BOLD) activation in the basal ganglia, and in cortical regions such as the supplementary motor area (SMA) and dorsolateral prefrontal cortex (DLPFC) (Buhmann et al, 2003;Dirnberger et al, 2005;Jahanshahi et al, 1995;Playford et al, 1993;Samuel et al, 1997;Thobois et al, 2004). On the other hand, brain imaging studies in PD patients using a variety of motor tasks have found hyperactivation in the primary motor cortex (Haslinger et al, 2001;Sabatini et al, 2000;Thobois et al, 2000) and the cerebellum (Rascol et al, 1997;Wu and Hallett, 2005). Hyperactivation in PD patients has been suggested as a strategy of the central nervous system to compensate for the defective function in the basal ganglia (Ceballos-Baumann, 2003;Rascol et al, 1997;Sabatini et al, 2000;Thobois et al, 2000;Thobois et al, 2004;Wu and Hallett, 2005), although the direct support for this hypothesis has been tentative.…”

“…On the other hand, brain imaging studies in PD patients using a variety of motor tasks have found hyperactivation in the primary motor cortex (Haslinger et al, 2001;Sabatini et al, 2000;Thobois et al, 2000) and the cerebellum (Rascol et al, 1997;Wu and Hallett, 2005). Hyperactivation in PD patients has been suggested as a strategy of the central nervous system to compensate for the defective function in the basal ganglia (Ceballos-Baumann, 2003;Rascol et al, 1997;Sabatini et al, 2000;Thobois et al, 2000;Thobois et al, 2004;Wu and Hallett, 2005), although the direct support for this hypothesis has been tentative. Alternatively, it has been argued that hyperactivation could be related to specific signs of the disease such as rigidity (Kleine et al, 2001;Pierantozzi et al, 2001;Ridding et al, 1995).…”

Loss of gait control assessed by cognitive-motor dual-tasks: pros and cons in detecting people at risk of developing Alzheimer’s and Parkinson’s diseases

“…Unfortunately, the exact compensatory mechanisms underlying gait disorders in the prodromal phase of PD remain unclear. Previous studies examining manual motor performance proposed the following mechanisms: (i) an increased activity in lateral premotor and parietal areas as well as in the anterior cingulate cortex to counterbalance defective striatofrontal motor circuits (Samuel et al 1997;Sabatini et al 2000;Buhmann et al 2005), (ii) an increase in corticostriatal excitatory input to the basal ganglia (Wu et al 2015), and (iii) the use of extrastriatal areas, such as executive attention control and more B'voluntary^brain activity efforts to execute movements usually performed automatically in healthy people (Wu et al 2015).…”