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Flashcards in Ascending Pathways Deck (34):
1

Describe the 3 main types of information relayed through the dorsal column pathway.

functional unit?

2 point discrimination (stereognosis)
vibration sense (with a tuning fork)
proprioception (position sense due to the conscious perception of muscle spindle and golgi tendon receptors)

GSA

(an afferent pathway relaying info about 2 point discrimination, position sense, and vibration. It is a 3 neuron (or axon) pathway --receptor to medulla, medulla to thalamus, thalamus to cortex. Enters the dorsal horn via medial divison)

2

What receptors do the dorsal columns mainly use?

Pacinian corpuscles, Meissner’s Corpuscles, Merkel’s Disks, and joint receptors.

3

Describe the fasciculus gracilis and fasiculus cuneatus.
Where do they exist? What do they contain?

The fasciculus gracilis exists at all levels of the spinal cord and contains long ascending fibers from the lower limbs (shown in red).

The fasciculus cuneatus exists in thoracic (T) segments above T6 (T1–T6) and cervical (C) segments (C1–C8) and contains long ascending fibers from the upper limbs (shown in blue).

4

Describe the axons of second-order neurons (neuron II) in the nucleus gracilis and cuneatus.

What kind of fibers do they travel as?
Where do they cross? What do they form?

The axons of second-order neurons (neuron II) in the nucleus gracilis and cuneatus travel as internal arcuate fibers and cross in the midline to form the medial lemniscus, which ascends through the medulla, pons, and midbrain and terminates in the contralateral ventral posterolateral nucleus of the thalamus.

5

Describe the axons of third-order neurons. Where do they travel and terminate?

Axons of third-order neurons (neuron III) in the thalamus travel in the internal capsule and terminate in the sensorimotor cerebral cortex.

6

What are head pain and position carried by?

head pain and position are carried by the trigeminal nerve complex

7

Where does first order axon from upper limb synapse? (dorsal column pathway)

How do sensory fibers from upper extremity get to nucleus cuneatus?

First order axon from upper limb synapses in nucleus cuneatus.

Sensory fibers from the upper extremity will use the fasciculus cuneatus to get to the nucleus cuneatus.

First order fibers from the leg use fasciculus gracilus (think gracilis—muscle in leg) to get to nucleus gracilus.

Faciculus gracilus is medial to fasciculus cuneatus—think medial—gracilus----MG (a small car just ran over your foot)

8

Describe second order axons of dorsal column pathway - where they begin, cross, and synapse.

Second order axon begins in nucleus cuneatus, crosses the midline, travels in a fiber bundle known as the medial lemniscus, and finally synapses on neurons in the VPL

(When the 2nd order axons cross the midline to pile up and form the medial lemniscus, they are called internal arcuate fibers. Fibers of the medial lemniscus then synapse on the ventral posterior lateral nucleus of the thalamus)

9

Describe third order axons of dorsal column pathway.

Third order axons synapse on the post central gyrus of the sensory cortex of the parietal lobe

(Finally 3rd order axons reach consciousness by synapsing on area 312 of the post central gyrus.)

10

Where does DCP info reach? What would cutting the tract in the cord result in?

Remember DCP info reaches the OPPOSITE cortex. Cutting the tract in the cord results in ipsilateral loss---ie deficits on same side of cord as lesion----while a stroke of the right cortex will wipe out vibration sense—etc-- on the left side of the body.

11

Describe the location of key sensory or ascending tracts in the spinal cord.

See slide 15.

Remember fasciculus gracilus is medial—MG—like the little car—fasciculus cuneatus does not exist below t6

12

Describe Rhomberg sign/Tabes dorsalis.

When is it positive?
How do you test it?
What kind of patients have a positive Romberg's sign
What is there damage to?

Syphilis destroys the dorsal columns and DRG’s

Romberg's sign is positive if patient requires vision to stand steadily
-patient is asked to stand with feet together. If patient is steady with eyes open but unsteady with eyes closed then there are signs of Rombergism.

Positive in patients with sensory ataxia and negative in cerebellar ataxia.

13

Describe the Spinothalamic tract.

(classic pain pathway)
Nucleus Proprius is the origin of the STT
Pain and temp receptors in skin relay info via lateral division of dorsal root to nucleus proprius.

14

What is the origin of the STT?

Nucleus proprius in dorsal horn—the true origin of the spinothalamic tract.

"proper sensory nucleus"
receives many sensory inputs
contains many interneurons
contains "tract cells" that project contralaterally as STT
all cord levels

15

Where do fibers from nucleus proprius go? (STT)

Fibers from nucleus proprius cross the midline in the anterior commissure of the spinal cord and “pile up” in the lateral and part of the anterior funiculus.

16

What will cutting STT in cord affect?

will affect pain on opposite side of body

17

Where does STT synapse? Then where is it relayed?

The STT then synapses in the VPL---from there it it is relayed to area 312-

18

How do the peripheral processes of DRG cells end? What will the central processes of these DRG synapse with?

 The peripheral processes of these dorsal root ganglion cells end as receptors sensing pain, temperature, and simple tactile sensations. The central processes of these dorsal root ganglion cells synapse with the neurons of the nucleus proprius.

19

Describe the axons of second and third order neurons in regards to the STT.

The axons of these second-order neurons cross via the anterior white commissure, enter the contralateral white matter, ascend in the lateral funiculus, and synapse on third-order neurons located in the ventral posterolateral nucleus of the thalamus. The axons of third-order neurons project to the primary sensory cortex.

20

What can happen in syringomyelia?

In syringomyelia a vacuole, hole, or tube (syrinx) form in or near the central canal. It can grow and eventually transect the cord.

21

How are the fibers of STT organized and what are the implications for this?

The fibers of the STT are organized such that sacral fibers are most lateral—and thus are the last to be destroyed by a syrinx (sacral sparing of pain and temp)

The syrinx wipes out the spinothalamic fibers that are crossing at the level of the lesion. Fibers are spared above and below the lesion such that one gets a “vested’ loss of sensation. (Vested loss----of course if the syrinx gets big enough total loss of sensation and paralysis may occur.)

22

Describe brown-squared injury.

Cord injury destroys DCP input ipsilaterally below lesion---but STT input on the contralateral side below the lesion.

proprioception is lost on side of lesion, pain and temp lost on side opposite lesion

(Yet a stroke of one hemisphere would wipe out both the STT and DCP on the opposite side---remember both cross—STT in cord---DCP in medulla.)

23

Describe the medial lemniscus and posterior columns.

medial lemniscus: crossed secondary sensory axons

posterior columns: uncrossed primary sensory axons

24

Describe a stroke of lateral medulla.

A stroke of the lateral medulla occurs when blood flow is interrupted in either the vertebral artery or posterior inferior cerebellar artery (PICA). With a lack of blood flow, the neurons and tracts that compose the lateral medulla die and give rise to the signs and symptoms discussed below.

25

Describe what lateral medullary stroke can give rise to.

gives rise to a stereotypical pattern of symptoms known collectively as Wallenberg syndrome.
-Pain and temperature sensation from the opposite side of the body, and the same side of the face are affected. This is secondary to interruption of the spinothalamic and yet uncrossed spinal trigeminal tracts.
-The descending sympathetic fibers, which are in close proximity to the spinothalamic tract, are also interrupted. This leads to a "Horner's syndrome",
Patient's also present with ataxia (ie: a loss of muscle coordination) because the spino-cerebellar connections are destroyed.
Nausea, vomiting, vertigo, and nystagmus
These symptoms are attributable to the death of neurons in the vestibular nuclei.
Injury to the neurons that compose the nucleus ambiguus leads to difficulty swallowing (secondary to paralysis of the pharyngeal muscles) and difficulty speaking (secondary to paralysis of the muscles that control the larynx).

26

Describe the spinocerebellar tracts (DSCT and VSCT)

unconscious proprioception. reside in lateral funiculus and use Clark’s nucleus--

Dorsal Spinocerebellar tract arises from Clark's nucleus (C8-L2)
relays muscle stretch

Ventral Spinocerebellar Tract- from dorsal horn and intermediate gray (rexed V-VIII)
relays info of spinal motor centers- reflexes, interneurons?

27

Describe nucleus dorsalis.

"clark's nucleus"
homologous to the lateral (accessory) cuneate
nucleus in the medulla
receives muscle spindle information
projects ipsilaterally to the cerebellum as the dorsal spinocerebellar tract

28

Describe the dorsal (posterior) spinocerebellar tract pathway.

The dorsal (posterior) spinocerebellar tract. The peripheral processes of the first-order neurons (located in the dorsal root ganglion) innervate mainly muscle spindles and, to a lesser extent, Golgi tendon organs (located at the junction of the muscle and tendon). The central processes of these sensory neurons project to the nucleus dorsalis of Clarke that extends from C8 to L2. Axons of neurons located in the dorsal nucleus of Clarke ascend ipsilaterally (i.e., the tract is uncrossed), reach the inferior cerebellar peduncle (restiform body) in the medulla, and terminate ipsilaterally in the cerebellar vermis of the anterior lobe. Although the nucleus dorsalis of Clarke receives afferents from all parts of the body (C8–L2) except the head and neck, functionally it transmits information about muscle spindle and tendon afferents from the ipsilateral caudal aspect of the body and legs. In so doing, this tract provides the cerebellum with information about the status of individual muscles as well as groups of muscles (e.g., how long each muscle is, how fast each muscle is moving, and how much tension is on each muscle). The individual is not aware of this information going to the cerebellum (nonconscious proprioception). With this information, the cerebellum is enabled to coordinate and integrate neural signals controlling movement of individual lower limb muscles and posture. Damage to the dorsal spinocerebellar tract results in the loss of nonconscious proprioception and coordination ipsilateral to the lesion.

29

Describe the cuneocerebellar tract pathway.

The cuneocerebellar tract--It should be recalled that the nucleus dorsalis of Clarke is not present in the spinal segments rostral to C8. Therefore, afferent fibers entering the spinal cord rostral to this level ascend ipsilaterally in the fasciculus cuneatus and project to neurons located in the accessory cuneate nucleus of the lower medulla. Neurons located in this nucleus then give rise to the cuneocerebellar tract, which is functionally related to the upper limb, conveying nonconscious proprioception. (Recall that the dorsal spinocerebellar tract is functionally related to the lower limb.) The fibers in this tract then terminate in the cerebellar cortex.

30

Describe the DSCT. What happens above C8? What direction are both tracts?

—The DSCT brings mostly trunk and lower limb info about unconscious proprioception ipsilaterally to the cerebellum. Incoming dorsal root sensory fibers synapse on Clark’s nucleus and second order fibers ascend in the dorsal lateral edge of the lateral funiculus. Here they synapse on the same side in the cerebellum Above C8 there is no Clark’s nucleus—so incoming upper limb, unconscious spindle info synapses on the tiny lateral cuneate nucleus—then joins the DSCT and synapses in the cerebellum-----both tracts are ipsilateral—cerebellar injury signs are ipsilateral.

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.