Deep brain stimulation,La stimulation cérébrale profonde dans la maladie de Parkinson

V. Fraix, P. Pollak, S. Chabardes, C. Ardouin, A. Koudsie, A. Benazzouz, P. Krack, A. Batir, J.-F. Le Bas, A.-L. Benabid
Revue Neurologique. 2004-05-01; 160(5): 511-521
DOI: 10.1016/s0035-3787(04)70980-7

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1. Rev Neurol (Paris). 2004 May;160(5 Pt 1):511-21. doi:
10.1016/s0035-3787(04)70980-7.

[Deep brain stimulation].

[Article in French]

Fraix V(1), Pollak P, Chabardes S, Ardouin C, Koudsie A, Benazzouz A, Krack P,
Batir A, Le Bas JF, Benabid AL.

Author information:
(1)Département de Neurologie, Centre Hospitalier Universitaire de Grenoble,
Grenoble.

The present renewal of the surgical treatment of Parkinson’s disease, almost
abandoned for twenty Years, arises from two main reasons. The first is the
better understanding of the functional organization of the basal ganglia. It was
demonstrated in animal models of Parkinson’s disease that the loss of
dopaminergic neurons within the substantia nigra, at the origin of the striatal
dopaminergic defect, induces an overactivity of the excitatory glutamatergic
subthalamo-internal pallidum pathway. The decrease in this hyperactivity might
lead to an improvement in the pakinsonian symptoms. The second reason is the
improvement in stereotactic neurosurgery in relation with the progress in
neuroimaging techniques and with intraoperative electrophysiological
microrecordings and stimulations, which help determine the location of the deep
brain targets. In the 1970s chronic deep brain stimulation in humans was applied
to the sensory nucleus of the thalamus for the treatment of intractable pain. In
1987, Benabid and colleagues suggested high frequency stimulation of the ventral
intermediate nucleus of the thalamus in order to treat drug-resistant tremors
and to avoid the adverse effects of thalamotomies. How deep brain stimulation
works is not well known but it has been hypothetized that it could change the
neuronal activities and thus avoid disease-related abnormal neuronal discharges.
Potential candidates for deep brain stimulation are selected according to
exclusion and inclusion criteria. Surgery can be applied to patients in good
general and mental health, neither depressive nor demented and who are severely
disabled despite all available drug therapies but still responsive to levodopa.
The first session of surgery consists in the location of the target by
ventriculography and/or brain MRI. The electrodes are implanted during the
second session. The last session consists in the implantation of the
neurostimulator. The ventral intermediate nucleus of the thalamus was the first
target in which chronic deep brain stimulation electrodes were implanted in
order to alleviate tremor. This technique can be applied bilaterally without the
adverse effects of bilateral thalamotomies. Like pallidotomy, internal globus
pallidum stimulation has a dramatic beneficial effect on levodopa-induced
dyskinesia but its effects on the parkinsonian triad are less constant and
opposite motor effects are sometimes observed in relation with the stimulated
contact. The inconstant results, perhaps related to the complexity of the
structure led to the development of subthalamic nucleus stimulation. The
alleviation of motor fluctuations and the improvement in all motor symptoms
allows a significant decrease in levodopa daily dose and in levodopa-induced
dyskinesia. Presently, deep brain stimulation is a fashionable neurosurgical
technique to treat Parkinson’s disease. Subthalamic nucleus stimulation seems to
be the most suitable target to control the parkinsonian triad and the motor
fluctuations. Because of the possible adverse effects it must be reserved for
disabled parkinsonian patients. No large randomized study comparing different
targets and different neurosurgical techniques has been performed yet. Such
studies, including cost benefit studies would be useful to assess the respective
value of these different techniques.

DOI: 10.1016/s0035-3787(04)70980-7
PMID: 15269668 [Indexed for MEDLINE]

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