5. Where is the primary motor cortex found?
a. in the cerebellum
b. in the occipital lobe of the cerebrum
c. between the somatosensory cortex and the premotor area of
d. in the ventral horn of the spinal cord
e. just posterior to the parietal lobe assocation cortex
True or False
6. Neurons in the primary motor cortex of the right cerebral
hemisphere mainly control muscles on the left side of the body.
7. Patients with upper motor neuron disorders generally have
reduced muscle tone and ﬂ accid paralysis.
8. Neurons descending in the corticospinal pathway control
mainly trunk musculature and postural reﬂ exes, whereas
neurons of the brainstem pathways control ﬁ ne motor
movements of the distal extremities.
9. In patients with Parkinson’s disease, an excess of dopamine
from neurons of the substantia nigra causes intention tremors
when the person performs voluntary movements.
10. The disease tetanus results when a bacterial toxin blocks the
release of inhibitory neurotransmitter.
Chapter 10 Quantitative and Thought Questions
(Answers appear in Appendix A.)
1. What changes would occur in the knee jerk reﬂ ex after
destruction of the gamma motor neurons?
2. What changes would occur in the knee jerk reﬂ ex after
destruction of the alpha motor neurons?
3. Draw a cross section of the spinal cord and a portion of the
thigh (similar to Figure 10–6) and “wire up” and activate the
neurons so the leg becomes a stiff pillar; that is, so the knee
does not bend.
4. We have said that hypertonia is usually considered a sign of
disease of the descending motor pathways. How might it also
result from abnormal function of the alpha motor neurons?
5. What neurotransmitters/receptors might be effective targets for
drugs used to prevent the muscle spasms characteristic of the
Chapter 10 Answers to Physiological Inquiries
Recall that when chloride channels are opened,
a neuron is inhibited from depolarizing to threshold (see
Figure 6–29 and accompanying text). Thus, the neurons of
the spinal cord that release glycine are inhibitory interneurons.
By speciﬁ cally blocking glycine receptors, strychnine shifts
the balance of inputs to motor neurons in favor of excitatory
interneurons, resulting in excessive excitation. Poisoning
victims experience excessive and uncontrollable muscle
contractions body-wide, and when the respiratory muscles are
affected, asphyxiation can occur. These symptoms are similar to
those observed in the disease state tetanus, which is described
at the end of this chapter.
Tendons are stretched more by actively
contracting muscles than when muscles are passively
stretched (see Figure 10–7). Thus, during very intense
contractions that have the potential to cause injury, Golgi
tendon organs are strongly activated. The resulting high-
frequency action potentials arriving in the spinal cord
stimulate interneurons that inhibit motor neurons to the
muscle associated with that tendon, thus reducing the force
and protecting the muscle.
When a region of the brain is deprived of oxygen
and nutrients for even a short time, it often results in a
stroke—neuronal cell death (see Chapter 6, section D). Because
the right primary motor cortex was damaged in this case, the
patient would have impaired motor function on the left side
of the body. Given the midline location of the lesion, the leg
would be most affected (see Figure 10–11).