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Fig. 13.3: Basal ganglia during a lack of dopamine (Parkinson's disease). Key nu-
clei and their synaptic paths including excitatory (
gray line
), inhibitory (
dark line
),
and dopaminergic (
gray perforated line, dark perforated line
) paths are shown.
Dark-colored
nuclei signify diminished activity while
bright-colored
regions sig-
nify heightened activity. This figure is modified from the figures reported by Gur-
ney et al. [56] to emphasize changes due to dopamine depletion as described by
Delong [31].
13.4.1 Treatments
The treatment for early stage Parkinson's disease typically consists of the admin-
istration of levodopa (L-DOPA) orally. L-DOPA crosses the blood-brain barrier
where it is converted into dopamine, thus restoring some of the movement capabili-
ties to the patient. However, side effects that may emerge are dyskinesia (difficulty
performing voluntary movements), depression, and psychotic episodes in some pa-
tients [28, 110].
Surgical procedures that have been used in the past as a treatment for advanced
stage Parkinson's disease include pallidotomy, thalamotomy, and subthalamotomy
[55]. In these procedures, functional MRI imaging techniques detect the location
of specific nuclei in the brain of the patient. Following this, stereotactic surgical
techniques are employed for the placement of electrodes at the target location. Next,
electrode recordings are analyzed to achieve a more precise placement [59]. Finally,
high temperatures
80
o
C
or electric currents are applied to cause destruction of
cells (known as lesioning) in the STN or GPi.
The success of pallidotomies is hypothesized to be due to a reduction of activity
in the GPi that is caused by the administrated (or artificially placed) lesions [84].
Furthermore, lesioning the STN with a subthalamotomy has a similar effect in the
GPi because of the excitatory neuronal paths from the STN to the GPi [3]. Thus,
lesions in the GPi simulate the inhibitory input to the STN and GPi that would
otherwise be present under physiological conditions (see Figs. 13.2 and 13.3).
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