Ganong's Review of Medical Physiology, 23rd Edition

The tectospinal tract originates in the superior colliculus of
the midbrain. It projects to the contralateral cervical spinal
cord to control head and eye movements.
LATERAL BRAIN STEM PATHWAY
The main control of distal muscles arise from the lateral corticospinal
tract, but neurons within the red nucleus of the midbrain
cross the midline and project to interneurons in the
dorsolateral part of the spinal ventral horn to also influence
motor neurons that control distal limb muscles. This rubrospinal
tract excites flexor motor neurons and inhibits extensor
motor neurons. This pathway is not very prominent in
humans, but it may play a role in the posture typical of decorticate
rigidity (see below).
POSTURE-REGULATING SYSTEMS
INTEGRATION
In the intact animal, individual motor responses are submerged
in the total pattern of motor activity. When the neural axis is
transected, the activities integrated below the section are cut off,
or released, from the control of higher brain centers and often
appear to be accentuated. Release of this type, long a cardinal
principle in neurology, may be due in some situations to removal
of an inhibitory control by higher neural centers. A more important
cause of the apparent hyperactivity is loss of
differentiation of the reaction so that it no longer fits into the
broader pattern of motor activity. An additional factor may be
denervation hypersensitivity of the centers below the transection,
but the role of this component remains to be determined.
Animal experimentation has led to information on the role
of cortical and brain stem mechanisms involved in control of
voluntary movement and posture. The deficits in motor control
seen after various lesions mimic those seen in humans
with damage in the same structures.
DECEREBRATION
A complete transection of the brain stem between the superior
and inferior colliculi permits the brain stem pathways to function
independent of their input from higher brain structures.
This is called a midcollicular decerebration and is diagramed
in Figure 16–7 by the dashed line labeled A. This lesion interrupts
all input from the cortex (corticospinal and corticobulbar
tracts) and red nucleus (rubrospinal tract), primarily to
distal muscles of the extremities. The excitatory and inhibitory
reticulospinal pathways (primarily to postural extensor muscles)
remain intact. The dominance of drive from ascending
sensory pathways to the excitatory reticulospinal pathway
leads to hyperactivity in extensor muscles in all four extremities
which is called decerebrate rigidity. This resembles what
ensues after supratentorial lesions in humans cause uncal
CHAPTER 16 Control of Posture & Movement 247
herniation. Uncal herniation can occur in patients with large
tumors or a hemorrhage in the cerebral hemisphere. Figure
16–8A shows the posture typical of such a patient. Clinical
Box 16–2 describes complications related to uncal herniation.
In midcollicular decerebrate cats, section of dorsal roots to
a limb (dashed line labeled B in Figure 16–7) immediately
eliminates the hyperactivity of extensor muscles. This suggests
that decerebrate rigidity is spasticity due to facilitation of
the myotatic stretch reflex. That is, the excitatory input from
the reticulospinal pathway activates γ-motor neurons which
indirectly activate α-motor neurons (via Ia spindle afferent
activity). This is called the gamma loop.
The exact site of origin within the cerebral cortex of the fibers
that inhibit stretch reflexes is unknown. Under certain conditions,
stimulation of the anterior edge of the precentral gyrus
can cause inhibition of stretch reflexes and cortically evoked
movements. This region, which also projects to the basal ganglia,
has been named area 4s, or the suppressor strip.
There is also evidence that decerebrate rigidity leads to direct
activation of α-motor neurons. If the anterior lobe of the cerebellum
is removed in a decerebrate animal (dashed line labeled
C in Figure 16–7), extensor muscle hyperactivity is exaggerated
(decerebellate rigidity). This cut eliminates cortical inhibition
of the cerebellar fastigial nucleus and secondarily increases
excitation to vestibular nuclei. Subsequent dorsal root section
does not reverse the rigidity, thus it was due to activation of αmotor
neurons independent of the gamma loop.
DECORTICATION
Removal of the cerebral cortex (decortication; dashed line labeled
D in Figure 16–7) produces decorticate rigidity which
is characterized by flexion of the upper extremities at the elbow
and extensor hyperactivity in the lower extremities (Figure
16–8B). The flexion can be explained by rubrospinal
excitation of flexor muscles in the upper extremities; the hyperextension
of lower extremities is due to the same changes
that occur after midcollicular decerebration.
Decorticate rigidity is seen on the hemiplegic side in humans
after hemorrhages or thromboses in the internal capsule. Probably
because of their anatomy, the small arteries in the internal
capsule are especially prone to rupture or thrombotic obstruction,
so this type of decorticate rigidity is fairly common. Sixty
percent of intracerebral hemorrhages occur in the internal capsule,
as opposed to 10% in the cerebral cortex, 10% in the pons,
10% in the thalamus, and 10% in the cerebellum.
SPINAL INTEGRATION
The responses of animals and humans to spinal cord injury
(SCI) illustrate the integration of reflexes at the spinal level.
The deficits seen after SCI vary, of course, depending on the
level of the injury. Clinical Box 16–3 provides information on
long-term problems related to SCI and recent advancements
in treatment options.