This pathway is very important in that it provides a link between the vestibular influences (i.e., gravity and balance) and the control of axial musculature, via the spinal cord. The main function is to provide corrective muscle activity when the body (and head) tilt or change orientation in space (activation of the vestibular system, CN VIII, see Figure 8B).
This tract originates in the lateral vestibular nucleus, which is located in the lower pontine region (see next illustration and Figure 66C). The nucleus is found at the lateral edge of the fourth ventricle and is characterized by extremely large neurons. (This nucleus is also called Dei-ter's nucleus in some texts and the large neurons are often called by the same name.)
The lateral vestibular nucleus receives its major inputs from the vestibular system and from the cerebellum; there is no cerebral cortical input. This tract descends through the medulla and traverses the entire spinal cord in the ventral white matter (see Figure 68 and Figure 69). It does not decussate. The fibers terminate in the medial portion of the anterior horn, namely on those motor cells that control the axial musculature (see Figure 44).
Functionally, this pathway increases extensor muscle tone and activates extensor muscles. It is easier to think of these muscles as anti-gravity muscles in a four-legged animal; in humans, one must translate these muscles in functional terms, which are the flexors of the upper extremity and the extensors of the lower extremity.
The same cross-sectional levels have been used as with the reticular formation, starting at the mid-pons. The vestibular nuclei are found at the lower pontine level and are seen through the mid-medulla; the tract descends throughout the spinal cord, as seen at cervical and lumbar levels. In the spinal cord the tract is positioned anteriorly, just in front of the ventral horn (see Figure 68 and Figure 69) and innervates the medial group of motor nuclei.
A lesion of this pathway would occur with spinal cord injuries and this would be one of the "upper motor neuron" pathways involved, leading to spasticity and hyperreflexia.
Decorticate rigidity: Humans with severe lesions of the cerebral hemispheres but whose brainstem circuitry is intact often exhibit a postural state known as decorticate rigidity. In this condition, there is a state of flexion of the forearm and extension of the legs.
Decerebrate Rigidity: Humans with massive cerebral trauma, anoxic damage, or midbrain destructive lesions exhibit a postural state in which all four limbs are rigidly extended. The back is arched and this may be so severe as to cause a posture known as opisthotonus, in which the person is supported by the back of the neck and the heels.
Physiologically, these conditions are not related to Parkinsonian rigidity but to the abnormal state of spastic-ity (see discussion with the previous illustration). The postulated mechanism involves the relative influence of the pontine and medullary reticular formations, along with the vestibulo-spinal pathway, with and without the input from the cerebral cortex.
FIGURE 50: Lateral Vestibulo-Spinal Tract
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