SURGICAL CONTROL OF AKINESIA IN PARKINSONS-DISEASE

Citation
F. Shima et al., SURGICAL CONTROL OF AKINESIA IN PARKINSONS-DISEASE, European neurology, 36, 1996, pp. 55-61
Citations number
24
Categorie Soggetti
Clinical Neurology",Neurosciences
Journal title
ISSN journal
00143022
Volume
36
Year of publication
1996
Supplement
1
Pages
55 - 61
Database
ISI
SICI code
0014-3022(1996)36:<55:SCOAIP>2.0.ZU;2-S
Abstract
Posteroventral pallidotomy (PVP) was carried out in 86 patients with P arkinson's disease, who presented marked bradykinesia, freezing of gai t and postural defect associated with rigidity and tremor in 82 patien ts (bradykinesia type), and similar gait and postural problems with mi nimum signs of rigidity and tremor in 4 (pure akinesia type). The ster eotactic coordinates of Leksell's device were calculated from MRI and conventional ventriculography. The final target was defined by microel ectrode techniques in the basal ganglia. The microrecording study reve aled a very high background activity in the internal pallidum in patie nts of the bradykinetic type, however, a much lower pallidal activity in patients of the pure akinesia type. Fifty-eight patients underwent unilateral PVP, and 28 underwent bilateral surgery. Following PVP, rig idity, tremor and poor reciprocal movements were significantly improve d especially in the contralateral extremities. The most dramatic findi ngs were the reversal of akinetic symptoms and wearing-off phenomena. The patients were followed up for 3-30 months (mean = 8) after surgery . Of the 82 bradykinesia type patients, good result were obtained in 4 8 (58%), fair results in 26 (32%), and minor improvement or no change in 8 (10%). In all the 4 patients of the pure akinesia type, recurrenc e of the akinetic symptoms occurred after a temporal improvement lasti ng a few days to 3 month after surgery. There was worse dysarthria in 3 patients, hemiparesis in 1 and partial motor aphasia in 1. The visua l field problem was not complicated in any patients. These findings su ggest that akinetic symptoms in PD are implicated in overactive pallid al outputs with putative GABAergic modulator by excessively inhibiting pedunculopontine nucleus activity (midbrain locomotor and posture reg ions) as well as thalamic activity. Partial interruption of the pallid al efferents eliminates the akinetic symptoms by disinhibitory effects on the target structures. The pathology of PD of the pure akinesia ty pe is supposedly in the brainstem and should be excluded from indicati on of pallidotomy.