Control of Muscle Tone;
Posture, Balance and Walking
Edwin E. Gilliam, Ph.D., R.N., University of Arizona, Department of
Physiology, Psio 418: Physiology for Engineers
LECTURE OBJECTIVES
1. Transection at what levels of the central nervous system is responsible
for decorticat and decerebrate posturing ??
2. What are the four tract used in the maintenance of posture and spatial
orientation ??
3. What area of the brain is responsible for turning on the signal for
locomotion and where do the patterns for locomotion originate ?
Maintenance of Upright Posture and Balance
The maintenance of an upright posture involves postural reflexes
which include the stretch reflex and the crossed-extensor reflex which have
already been discussed. Along with the maintenance of upright posture is
the maintenance of balance which is a complex process in the human because
of our tall height, which must be balance over the feet which is a small
area (See Figure 12.14 in Vander). Adding to the difficulty of maintaining
balance and posture is our high center of gravity, centered over the hips.
The postural reflexes are aided by afferent sensory information from
the eyes, the vestibular apparatus, and the somatic receptors
and the efferent response is to the skeletal muscles after integration in
the brainstem and spinal cord. Control of posture involves active muscular
resistance to displacement of the body. The crossed-extensor reflex is one
example of a postural reflex. As one leg is flexed, the other is extended
to support the added weight of the body. In addition, the positions of various
parts of the body are shifted to move the center of gravity over the single,
weight-bearing leg. This shift in the center of gravity is important in
the stepping mechanism of locomotion.
Figure 1. Pathways responsible for the maintenance of posture and
their effect on muscles of flexion and extension. Structures in the brainstem,
the red nucleus, pontine and medullary reticular formation,
vestibular nuclei, and superior colliculus, are are responsible
for the control of posture and spatial orientation.
Pathways for the maintenance of posture include the:
A. Rubrospinal Tract: Originates in the red nucleus. Fibers
project to interneurons in the spinal which excite motoneurons of flexor
muscles and inhibit motoneurons of extensor muscles to release the body
from a postural stance.
B. Pontine (Medial) Reticulospinal Tract: Originates in the reticulospinal
tracts of the pons and has a greater excitatory effect on extensor than
on flexor motoneurons, thus allowing for an erect posture.
C. Medullary (Lateral) Reticulospinal Tract: This pathway originates
in the medullary reticular formation and terminates on interneurons in
the spinal cord. This tract has the opposite effect of the pontine reticulospinal
tract in that it strongly inhibits extensors.
D. Lateral Vestibulospinal Tract: This tract originates in the
lateral vestibular nucleus (Dieter's nucleus) and projects to motoneurons
and interneurons. Stimulation of cells in the nucleus produces a powerful
excitation of extensors and inhibition of flexors. This tract plays
an important role in the control of antigravity muscles and the maintenance
of posture.
Brainstem Control of Posture:
Transections at different levels of the brainstem have been used to demonstrate
the importance of brainstem centers in the control of posture. Isolation
of centers below the transection from central influences above, reveals
the regulatory functions of the intact centers.
A. Spinal Transection
If the spinal cord is cut three events begin to happen.
1. Complete loss of voluntary movements. This results from the interruption
of descending pathways from motor centers located in the brain and higher
centers. Following spinal transection, there is a total paralysis of
all muscles below the level of the lesion.
2. Loss of conscious sensation below the level of the lesion. Sensory
information from the body regions below the transection cannot reach higher
centers and those regions appear to be anesthetized.
3. Initial loss of reflexes. Immediately following transection, the
sudden loss of tonic background facilitation provided by descending pathways
results in a loss of muscle tone and the limbs become flaccid. The animal
can no longer stand and stretch reflexes are absent. A high spinal transection
(above C3) interrupts the innervation to the respiratory muscles and a
respirator is required. If the cut were to occur around C7, sympathetic
tone to the heart would decrease, bradycardia and hypotension result.
The loss of reflexes, flaccid limbs, bradycardia and hypotension are
called spinal shock. This condition may last for one to two weeks
up to several months before they recover.
B. Decerebrate Rigidity (Mid-Collicular Transection):
Two brainstem centers that are important for the maintenance of muscle
tone in antigravity muscles (the extensors) are the pontine reticular
formation (medial reticulospinal tract) and Dieter's nucleus (lateral
vestibulospinal tract). Both centers have an excitatory influence on
extensor muscles. Stimulation of cells in the pontine reticular formation
has a very powerful excitatory effect on extensors, but its activity is
normally inhibited by central (cortical) projections. If
the spinal cord is cut above the level of the pontine reticular formation,
(mid-collicular), the inhibitory influence is removed and there
is an exaggerated activation of muscle tone in the extensors (antigravity
muscles). This produces a rigid posture which is referred to as decerebrate
rigidity. In patients with this condition, the arms and legs are extended,
the back is arched, the head is dorsiflexed, and the feet are pointed with
the toes curled. This stiff posture does not permit the joints to bend
and the body is capable of standing upright. This is very different from
spinal transection, where extensor muscle tone is abolished and the body
becomes limp.
C. Decorticate Rigidity (Transection of the corticospinal fibers
or internal capsule)
Interruption of the corticospinal tract (with the brainstem circuitry
intact) produces decorticate rigidity. In this condition the extensors
of the legs and the flexors of the arms contract steadily. One reason for
this is that the rubrospinal tract in humans only projects as far as the
cervical cord and may counteract vestibulospinal facilitation of arm but
not leg extensors.
Figure 2. Example of decorticate posturing (A) and decerebrate
(B) posturing. Decorticate posturing results from interruption of
the corticospinal tracts (with the brainstem centers intact). Decerebrate
posturing results from a lesionabove the level of the pontine reticular
formation (mid-collicular). (Adapted from Thelen et al. Critical Care
Nursing. 2nd ed. St. Louis: Mosby-Year Book, 1994).
Locomotion
Figure 3. This figure shows that locomotion in vertebrates is initiated
in the brainstem and generated by spinal cord circuits interacting with
sensory signals. (Adapted from S. Grillner. Neural control of vertebrate
locomotion-central mechanisms and reflex interaction with special reference
to the cat. Barnes and Gladden (Eds). Feedback and Motor Control in Invertebrates
and Vertebrates. London: Croom Helm, 1985)
CONTROL AND INITIATION OF LOCOMOTION BY SUPRASPINAL STRUCTURES
Cortex and Diencephalon: Goal-Directed Behavior In vertebrates,
locomotion can be performed in the absence of the cerebral cortex.
Decorticate cats spontaneously initiate locomotion, and it is difficult
for a naive observer to identify any clear deficit in their motor behavior.
This means that the goal-directed aspect of locomotion is retained when
only the basal ganglia and other diencephalic structures remain intact.
However, under ordinary conditions, the cortex is important for fine control,
as in walking along a horizontal ladder.
The descending command signals for locomotion are thought to originate
in the midbrain mesencephalic locomotor region. This area projects
to regions of the reticular formation in the pons and medulla that are important
in the "switiching on" and sustaining the spinal cord stepping
circuitry. This area in turn projects to the spinal cord. The mesencephalic
locomotion region (ML) was first demonstrated in the mid 1950's. The ML
has been identified in different mammals (primate, cat and rat) and in reptiles.
Stimulation of the mesencephalic locomotion region produces stepping
in cats, however the stimulation does not have to have a temporal pattern;
the electrical stimulation can be a constant-rate train of pulses. A tonic
descending activation is all that is needed for the pattern generator to
produce a rhythmic output. Stronger stimulation leads to a faster rhythm
(walking to trotting to galloping).
Spinal Circuits Generate Rhythmic Locomotor Patterns
Spinal circuits act as central pattern generators, producing a well-differentiated
and functional motor output for stepping. To do this they transected
the lower thoracic cord of a cat, isolating the part of the spinal cord
that controls the hindlimbs from descending signals. Under these conditions
the spinal animal will walk on a moving treadmill with a near normal stepping
pattern, although the cat does require external support for balance. The
overall stepping pattern consists of a rhythmic alternation between contractions
of flexor and extensor muscles. The swing phase of locomotion (foot is off
the ground) is generally controlled by contraction of flexor muscles, and
the stance phase (foot is planted and the leg is extended relative to the
body) is controlled by contraction of extensors. As locomotor patterns have
been seen on cats whose spinal cord were transected at 1-2 weeks of age,
it appears the central pattern generators are built into the architecture
of the spinal circuitry.
There are individual pattern generators for each limb. If one
hind limb is prevented from moving on the treadmill, the other limb continues
stepping normally. Thus the pattern generator for each limb can act independently
of the other pattern generators. In normal locomotion the pattern generators
for each limb are coupled to one another. When a cat walks on a treadmill,
the movements of the left and right hindlimb are exactly out of phase with
each other so that while one is flexing the other is extending. Increasing
the speed of the treadmill dramatically shifts the coupling between the
limbs, as the animal changes from walking to trotting to galloping; the
hindlimbs are in phase with each other; they flex and extend together. Thus,
independent but connected pattern generators provide for flexibility in
interlimb coordination.
In summary, the spinal cord is capable of generating more than
just stereotypical reflex stepping movements. The spinal cord can and does
make 'decisions' regarding the activation sequences of muscle groups
that are appropriate for the proprioceptive information received during
a given phase of the step cycle. For example, the CPG network in the spinal
cord can make purposeful decisions that tend to optimize locomotion when
the condition under which locomotion is occurring suddenly changes. Also,
it appears the mammalian spinal cord can be taught to walk, i.e. rhythmic
training of the hindlimbs results in improved locomotion capabilities. So
it appears that the spinal cord can "learn" and probably
'forget'.
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