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'.