Control of Body Movement
command inputs from descending pathways. This was dem-
onstrated in classical experiments involving animals with their
cerebrums surgically separated from their spinal cords just
above the brainstem. Though sensory perception and volun-
tary movement were completely absent, when suspended in
a position that brought the limbs into contact with a tread-
mill, normal walking and running actions were initiated by
afferent inputs arising from contact with the moving surface.
This demonstrates that afferent inputs and spinal cord neu-
ral networks contribute substantially to the coordination of
Under normal conditions, neural activation occurs in
the cerebral cortex, cerebellum, and brainstem as well as in the
spinal cord during locomotion. Moreover, middle and higher
levels of the motor control hierarchy are necessary for postural
control, voluntary override commands (like breaking stride to
jump over a puddle), and adaptations to the environment (like
walking across a stream on unevenly spaced stepping stones).
The fact that damage to even small areas can cause marked
disturbances in gait attests to the ultimate importance of the
sensorimotor cortex.
Center of
Figure 10–14
Postural changes with stepping. (a) Normal standing posture. The
center of gravity falls directly between the two feet. (b) As the left
foot is raised, the whole body leans to the right so that the center of
gravity shifts over the right foot.
A number of disorders of motor control were discussed
earlier in this chapter (Parkinson’s disease, cerebellar disease,
upper motor neuron disorders). We now return to a disease
that was alluded to in the introduction to this chapter, and
which demonstrates the importance of the balance between
excitatory and inhibitory circuits in controlling motor
Tetanus is a neurological disorder that results from a decrease
of the inhibitory input to alpha motor neurons. It occurs
when spores of the soil bacterium
Clostridium tetani
invade a poorly oxygenated wound. Proliferation of the
bacterium under anaerobic conditions induces it to secrete a
neurotoxin that specifi cally targets inhibitory interneurons in
the brainstem and spinal cord. Blockage of neurotransmitter
release from these interneurons allows the normal excitatory
inputs to dominate control of the alpha motor neurons, and
the result is high-frequency action potential fi ring that causes
increased muscle tone and spasms.
Because the toxin attacks interneurons by traveling
backward along the axons of alpha motor neurons, muscles
with short motor neurons are affected fi rst. Muscles of the
head fall into this category, in particular those that move the
jaw. The jaw rigidly clamps shut, because the muscles that
close it are much stronger than those that open it. Appearance
of this symptom early in the disease process explains the
common name of this condition,
Treatment for tetanus includes: (1) administering
antibiotics to kill the bacteria, (2) injecting antibodies that
bind the toxin (tetanus immune globulin, or TIG),
(3) providing drugs to relax and/or paralyze spastic muscles,
and (4) mechanically ventilating the lungs, to maintain air
fl ow despite spastic or paralyzed respiratory muscles. With
prompt treatment, approximately 90 percent of patients with
tetanus make a complete recovery within a few months.
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