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Flashcards in Ascending Pathways Deck (34)
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31

Describe the crossing of the VSCT.

the tract first crosses in the spinal cord and then crosses a second time in the superior cerebellar peduncle and terminates in the cerebellum. Contrary to what Siegal says, we teach that the VSCT receives no peripheral input, but “samples and relays information” regarding the state of spinal cord interneurons. The important thing is that it is double crossed—and really cannot be assessed clinically.

32

Describe the VSCT - what does it sample and represent?

The ventral spinocerebellar tract
samples “interneuronal activity in the intermediate spinal gray. It represents the only afferent pathway in the mainly efferent superior cerebellar peduncle.

33

How do muscle afferents from below reach Clark's nucleus

Where does lateral cuneate pick up the slack?
How does muscle info from upper body reach lateral cuneate

How does DSCT relay muscle and golgi tendon organ info to cerebellum?

VSCT relays what kind of info? Describe its crossing.

Clark’s nucleus only exists from C8—L2.
Muscle afferents from below L3 use f. gracilis to reach Clark’s N.
The lateral cuneate nucleus picks up the slack in the medulla. Muscle info from upper body reaches the Lateral cuneate n. via f. cuneatus.
Dorsal spinocerebellar tract relays muscle spindle and golgi tendon organ info to cerebellum via inf cerebellar ped..
Ventral spinocerebellar tract relays spinal motor “interneuronal” info via superior cerebellar peducle. It is double crossed.

34

Describe Friedrich's ataxia.

Friedreich's ataxia: sclerosis of the posterior and lateral columns of the spinal cord; characterized by muscular weakness and abnormal gait; occurs in children. 


An autosomal recessive disease, usually of childhood onset, characterized pathologically by degeneration of the spinocerebellar tracts, posterior columns, and to a lesser extent the corticospinal tracts.

Clinical manifestations include GAIT ATAXIA, pes cavus, speech impairment, lateral curvature of spine, rhythmic head tremor, kyphoscoliosis, congestive heart failure (secondary to a cardiomyopathy), and lower extremity weakness. Most forms of this condition are associated with a mutation in a gene on chromosome 9, at band q13, which codes for the mitochondrial protein frataxin.