Control of Body Movement
307
Parkinson’s Disease
In
Parkinson’s disease,
the input to the basal nuclei is dimin-
ished, the interplay of the facilitory and inhibitory circuits is
unbalanced, and activation of the motor cortex (via the basal
nuclei-thalamus limb of the circuit just mentioned) is reduced.
Clinically, Parkinson’s disease is characterized by a reduced
amount of movement
(akinesia),
slow movements
(bradyki-
nesia),
muscular rigidity, and a tremor at rest. Other motor
and nonmotor abnormalities may also be present. For exam-
ple, a common set of symptoms includes a change in facial
expression resulting in a masklike, unemotional appearance,
a shuffl ing gait with loss of arm swing, and a stooped and
unstable posture.
Although the symptoms of Parkinson’s disease refl ect
inadequate functioning of the basal nuclei, a major part of the
initial defect arises in neurons of the
substantia nigra
(“black
substance”), a brainstem nucleus that gets its name from the
dark pigment in its cells. These neurons normally project
to the basal nuclei, where they release dopamine from their
axon terminals. The substantia nigra neurons degenerate in
Parkinson’s disease, and the amount of dopamine they deliver
to the basal nuclei is reduced. This decreases the subsequent
activation of the sensorimotor cortex.
The drugs used to treat Parkinson’s disease are all designed
to restore dopamine activity in the basal nuclei, and fall into
three main categories: (1) agonists of dopamine receptors,
(2) inhibitors of the enzymes that metabolize dopamine at
synapses, and (3) precursors of dopamine itself. The most
widely prescribed drug is
Levodopa (L-dopa),
which falls
into the third category. L-dopa enters the bloodstream,
crosses the blood-brain barrier, and is converted to dopamine
(dopamine itself is not used as medication because it cannot
cross the blood-brain barrier, and it has many systemic side
effects). The newly formed dopamine activates receptors in
the basal nuclei and improves the symptoms of the disease.
Other therapies include the lesioning (destruction) of over-
active areas of the basal nuclei, or deep-brain stimulation of
underactive areas. The latter is accomplished with surgically
implanted electrodes connected to an electric pulse genera-
tor resembling a cardiac artifi cial pacemaker (Chapter 12).
Still highly controversial is the transplantation of cells derived
from various sources into the basal nuclei, including fetal
cells, cells that have been genetically engineered, or cells taken
from dopamine-secreting tissues in the patient’s own body. In
most cases, the injected cells are neurons, but more recently,
undifferentiated embryonic stem cells have shown the ability
to begin producing dopamine when injected into damaged
areas of the brain. Regardless of their source, the implanted
cells have shown some promise in reversing the symptoms of
Parkinson’s disease.
Cerebellum
The cerebellum is behind the brainstem (see Figure 10–2a).
It infl uences posture and movement indirectly by means of
input to brainstem nuclei and (by way of the thalamus) to
regions of the sensorimotor cortex that give rise to pathways
that descend to the motor neurons. The cerebellum receives
information both from the sensorimotor cortex (relayed via
brainstem nuclei) and from the vestibular system, eyes, ears,
skin, muscles, joints, and tendons—that is, from some of the
very receptors that movement affects.
One role of the cerebellum in motor functioning is to
provide timing signals to the cerebral cortex and spinal cord for
precise execution of the different phases of a motor program, in
particular the timing of the agonist/antagonist components of
a movement. It also helps coordinate movements that involve
several joints and stores the memories of these movements so
they are easily achieved the next time they are tried.
The cerebellum also participates in planning move-
ments—integrating information about the nature of an intended
movement with information about the surrounding space.
The cerebellum then provides this as a feedforward signal to
the brain areas responsible for refi ning the motor program.
Moreover, during the course of the movement, the cerebellum
compares information about what the muscles
should
be doing
with information about what they actually
are
doing. If a dis-
crepancy develops between the intended movement and the
actual one, the cerebellum sends an error signal to the motor
cortex and subcortical centers to correct the ongoing program.
The role of the cerebellum in programming movements
can best be appreciated when seeing its absence in individuals
with
cerebellar disease
.
They typically cannot perform limb
or eye movements smoothly, but move with a tremor—a so-
called
intention tremor
that increases as a movement nears
its fi nal destination. (Note that this differs from patients with
Parkinson’s disease, who have a tremor while at rest.) People
with cerebellar disease also cannot start or stop movements
quickly or easily, and they cannot combine the movements of
several joints into a single smooth, coordinated motion. The
role of the cerebellum in the precision and timing of movements
can be appreciated when you consider the complex tasks it helps
us accomplish. For example, a tennis player sees a ball fl y over
the net, anticipates its fl ight path, runs along an intersecting
path, and swings the racquet through an arc that will intercept
the ball with the speed and force required to return it to the
other side of the court. People with cerebellar damage cannot
achieve this level of coordinated, precise, learned movement.
Unstable posture and awkward gait are two other symp-
toms characteristic of cerebellar disease. For example, people
with cerebellar damage walk with their feet wide apart, and
they have such diffi culty maintaining balance that their gait
appears drunken. Visual input helps compensate for some of
the loss of motor coordination—patients can stand on one
foot with eyes open, but not closed. A fi nal symptom involves
diffi culty in learning new motor skills. Individuals with cere-
bellar disease fi nd it hard to modify movements in response to
new situations. Unlike damage to areas of sensorimotor cor-
tex, cerebellar damage does not cause paralysis or weakness.
Finally, there is growing evidence that, in addition to
its motor functions, the human cerebellum may also par-
ticipate in higher cognitive activity. Though making up only
one-tenth of the brain’s volume, the cerebellum contains at
least half of the total neurons. Anatomists have determined
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