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Cortical motor reorganization in akinetic patients with Parkinson's disease
A functional MRI study
U. Sabatini1,5, K. Boulanouar1, N. Fabre1,2, F. Martin1, C. Carel1,2, C. Colonnese5, L. Bozzao5, I. Berry1,3, J. L. Montastruc4, F. Chollet1,2 and O. Rascol1,4
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.
Brain, Vol. 123, No. 2, 394-403, February 2000
http://brain.oxfordjournals.org/cgi/...full/123/2/394
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Motor task
The activation paradigm consisted of a sequential movement performed with the right hand. This sequential task had been chosen among several others, according to preliminary fMRI data from our laboratory, because it induces a clear activation signal in areas known to be involved in both motor programming and motor execution. To perform this task, the subjects had to (i) make finger-to-thumb opposition movements in the specified order of the index, middle, ring and little finger; (ii) open and clench the fist twice; (iii) complete finger-to-thumb oppositions in the opposite order (i.e. little, ring, middle and index finger); (iv) open and clench the fist twice again; and finally (v) repeat the same series of movements during the 30 s of data acquisition. This was intentionally a more complex and cognitively demanding task than generally used in previously published SPECT and PET studies performed in patients with Parkinson's disease.
Conclusions
The present fMRI neuroimaging study shows that the subcortical putaminal dopamine deficit which characterizes Parkinson's disease disorganizes the cortical motor pathways in a complex way.
It induces a focal `underactivation' restricted to the rostral SMA and DLPC, possibly responsible for the patients' akinesia. It also induces an abnormal pattern of `overactivation' in most of the other known motor cortical areas, including the caudal SMA, the anterior cingulate cortex, the lateral premotor, the primary sensorimotor and the parietal cortices.
This reorganization, which involves parallel-acting multiple motor areas, can be seen as an attempt at motor recovery.
The general aspect of this reorganization resembles what has been described previously with PET in other motor diseases, such as paresis induced by acute stroke (Chollet et al., 1991Go; Weiller, 1995Go; Chollet and Weiller, 1997). It is also interesting to compare the present results with those reported in patients with cerebellar degeneration (Wessel et al., 1995Go). The pattern of motor activation in this last condition appeared to be the opposite to what we observed in Parkinson's disease: several areas of the lateral motor circuit, including the lateral premotor cortex and the lobus parietalis inferior, were less activated in the cerebellar patients than in the normal controls, probably as a result of defective cerebellar inputs, while, in contrast, other premotor systems, including the SMA, were used more heavily in the cerebellar patients than in the controls. It is thus tempting to speculate that these phenomena illustrate the capacity of the adult human brain for functional plasticity in compensating for one motor circuit deficit by recruiting another parallel one. The exact mechanisms of these phenomena remain to be understood.
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It is hypothesised that bradykinesia is not simply a compensation for defective preparatory processes, but may reflect a defective internal cue in PD which disrupts and impairs the outflow of motor responses.
http://www.springerlink.com/content/l1wkju7393q363tn/