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P A R T 4
Drugs acting on the central and peripheral nervous systems
Treatment
At this time, there is no treatment that arrests the neuron
degeneration of Parkinson’s disease and the eventual
decline in the person’s function. Surgical procedures
involving the basal ganglia have been tried with varying
success at prolonging the degeneration caused by this
disease. Drug therapy remains the primary treatment.
Therapy is aimed at restoring the balance between
the declining levels of dopamine, which has an inhibit
ory effect on the neurons in the basal ganglia, and the
now-dominant cholinergic neurons, which are excitat
ory. This may help to reduce the signs and symptoms
of parkinsonism and restore normal function for a time
(Figure 24.2).
Total management of care in individuals with Parkin
son’s disease presents a challenge. People should be
encouraged to be as active as possible, to perform exer-
cises to prevent the development of skeletal deformities
and to attend to their care as long as they can. Both the
person and their family need instruction about follow
ing drug protocols and monitoring adverse effects, as
well as encouragement and support for coping with the
progressive nature of the disease (Box 24.1). Because of
the degenerative effects of this disease, individuals may
experience episodes of depression or emotional upset.
Psychological support, as well as physical support, is a
crucial aspect of care.
■■
Parkinson’s disease is a progressive nervous system
disease characterised by tremors, changes in posture
and gait and a mask-like facial expression.
KEY POINTS
■■
The loss of dopamine-secreting cells results in a loss
of the inhibitory dopamine effect and is thought to be
responsible for Parkinson’s disease.
DOPAMINERGIC AGENTS
Dopaminergics
—drugs that increase the effects of
dopamine at receptor sites—have been proven to be even
more effective thananticholinergics in the treatment of par-
kinsonism (see Table 24.1). Dopaminergic agents include
amantadine (
Symmetrel
), apomorphine (
Apomine
),
bromocriptine (
Parlodel
), cabergoline (
Bergoline
),
carbidopa–levodopa (
Sinemet
), levodopa-benserazide
(
Madopar
), levodopa-carbidopa-entacapone (
Stalevo
),
pergolide (
Permax
), pramipexole (
Sifrol
), ropinirole
(
Appese
,
Repreve
) and rotigotine (
Neupro
) (not available
in New Zealand).
Therapeutic actions and indications
Dopamine does not cross the blood–brain barrier.
Therefore, other drugs that act like dopamine or
increase dopamine concentrations indirectly must be
used to increase dopamine levels in the substantia nigra
or to directly stimulate the dopamine receptors in that
area. This action helps to restore the balance between
the inhibitory and stimulating neurons. Dopaminergic
agents are effective as long as enough intact neurons
remain in the substantia nigra to respond to increased
levels of dopamine. After the neural degeneration has
progressed beyond a certain point, these agents are no
longer effective.
The dopaminergics are indicated for the relief of the
signs and symptoms of idiopathic Parkinson’s disease
INHIBITION
STIMULATION
Type 1 drugs
Type 2 drugs
Basal ganglia cells
A. Increase dopamine concentration
levodopa
Anticholinergic drugs
block stimulant
benztropine
biperiden
benzhexol
B. Increases dopamine release
amantadine
rasagiline
C. Stimulate dopamine receptors
apomorphine
bromocriptine
pramipexole
ropinirole
cabergoline
pergolide
rotigotine
FIGURE 24.2
Drug therapy in treating
Parkinson’s disease is aimed at
achieving a balance between the
stimulating cholinergic effects and
the inhibitory effects of dopamine
in the basal ganglia. Type 1 drugs
affect dopamine and are inhibitory.
Type 2 drugs block cholinergic effects,
preventing stimulation.
