Reticulospinal tract

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This tract originates in the medullary reticular formation, mainly from the nucleus gigantocellularis (meaning very large cells, see Figure 42A, Figure 42B, and Figure 67C). The tract descends more laterally in the spinal cord than the pontine pathway, and is thus named the lateral reticulo-spinal tract (see Figure 68 and Figure 69); some of the fibers are crossed. The tract lies beside the lateral vestib-ulo-spinal pathway.

The pathway also has its greatest influence on axial musculature. This part of the reticular formation is functionally the reticular extensor inhibitory area, opposite to that of the pontine reticular formation. This area depends for its normal activity on influences coming from the cerebral cortex.

Neurological Neuroanatomy

The location of the tract in the brainstem is shown at the cross-sectional levels of the mid-pons, the lower pons, the mid-medulla, and cervical and lumbar spinal cord levels, intermingled with other tracts in the white matter of the spinal cord (see Figure 68 and Figure 69).

Clinical Aspect: Spasticity

A lesion destroying the cortico-bulbar fibers, an upper motor neuron lesion, results in an increase in the tone of the extensor/anti-gravity muscles, which develops over a period of days. This increase in tone, called spasticity, tested by passive flexion and extension of a limb, is velocity dependent, meaning that the joint of the limb has to be moved quickly. It is the anti-gravity muscles that are affected in spasticity; in humans, for reasons that are difficult to explain, these muscles are the flexors of the upper limb and the extensors of the lower limb. There is also an increase in responsiveness of the stretch reflex, called hyperreflexia, as tested using the deep tendon reflex, DTR (discussed with Figure 44), which also develops over a period of several days.

There are two hypotheses for the increase in the stretch (monosynaptic) reflex responsiveness:

• Denervation supersensitivity: One possibility is a change of the level of responsivity of the neurotransmitter receptors of the motor neurons themselves caused by the loss of the descending input, leading to an increase in excitability.

• Collateral sprouting: Another possibility is that axons adjacent to an area that has lost syn-aptic input will sprout branches and occupy the vacated synaptic sites of the lost descending fibers. In this case, the sprouting is thought to be of the incoming muscle afferents (called 1A afferents, from the muscle spindles).

There is experimental evidence (in animals) for both mechanisms. Spasticity and hyperreflexia usually occur in the same patient. Another feature accompanying hyperre-flexia is clonus. This can be elicited by grasping the foot and jerking the ankle upward; in a person with hyperre-flexia, the response is a short burst of flexion-extension responses of the ankle, which the tester can feel and which also can be seen.

Lesions involving parts of the motor areas of the cerebral cortex, large lesions of the white matter of the hemispheres or of the posterior limb of the internal capsule, and certain lesions of the upper brainstem all may lead to a similar clinical state in which a patient is paralyzed or has marked weakness, with spasticity and hyperreflexia (with or without clonus) on the contralateral side some days after the time of the damage. The cortico-spinal tract would also be involved in most of these lesions, with loss of voluntary motor control, and with the appearance of the Babinski sign in most cases immediately after the lesion (see Introduction to this section).

A similar situation occurs following large lesions of the spinal cord in which all the descending motor pathways are disrupted, both voluntary and nonvoluntary. Destruction of the whole cord would lead to paralysis below the level of the lesion (paraplegia), bilateral spas-ticity, and hyperreflexia (usually with clonus), a severely debilitating state.

It is most important to distinguish this state from that seen in a Parkinsonian patient who has a change of muscle tone called rigidity (discussed with Figure 24), with no change in reflex responsiveness and a normal plantar response.

This state should be contrasted with a lower motor neuron lesion of the anterior horn cell, with hypotonia and hyporeflexia as well as weakness (e.g., polio, discussed with Figure 44).

Reticulospinal Tract

FIGURE 49B: Medullary (Lateral) Reticulo-Spinal Tract

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