The aim of this study was to compare, retrospectively the value of chr
onic bilateral stimulation of the internal globus pallidus (GPi) and t
he subthalamic nucleus (STN) in patients with young onset Parkinson's
disease. We selected 13 consecutive patients with similar characterist
ics at the rime of surgery: age at onset <40 years, disabling motor fl
uctuations (Hoehn and Yahr stage 4 or 5 in off-drug phases) and levodo
pa-induced dyskinesias (LID). Eight patients were operated on in the S
TN and five in the GPi. The Unified Parkinson's Disease Rating Scale (
UPDRS), timed motor tests and a LID scale were compared in on-and off-
drug conditions before surgery and 6 months after surgery on stimulati
on using the chronic electrical parameters found to improve best the m
otor stare of the individual patient, without adverse effects. In off-
drug phases, the motor score of the UPDRS was improved by 71% with STN
stimulation and by 39% with GPi stimulation on average. This differen
ce was statistically significant (P < 0.05). Whereas rigidity and trem
or showed good improvement in both groups, the decrease in the akinesi
a score pl,ns more pronounced in the STN group. In the STN group, the
improvement of all motor symptoms was very close, or equal, to the bes
t levodopa response. Thus the levodopa test was predictive of outcome.
The improvement in off-drug period motor handicap allowed a decrease
in the levodopa-equivalent dose only in the STN group (-56%). The volt
age, frequency and pulse width used for chronic stimulation were lower
in the STN group. In the on-drug phases,there was a marked improvemen
t in LID in the GPI group, as measured by the dyskinesias score during
an acute levodopa rest, whereas there was only a small decrease in th
e STN group (P < 0.05). However; in the long term, the reduction of le
vodopa dosage in the STN group led to an indirect reduction of LID sim
ilar to that in the GPi group during activities of everyday life. In c
onclusion, the overall results favour the neurosurgical treatment of P
arkinson's disease by stimulating the STN rather than the GPi.