Bales: Pain and temp-trunk and limb sensation Flashcards

1
Q

What is the pathway for somatic pain and temperature from the limbs and trunk currently referred to as?

A

Anterolateral system (ALS)

(used to be called spinothalamic (lateral) but it was decided that pain and temp also travel with crude touch so they both make up ALS now)

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2
Q

What are the 2 pain and temp fibers?

A

A δ for temperature and faster pain (lightly myelinated) and C for temperature and slower pain (unmyelinated)

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3
Q

What do the primary afferents for limb and trunk pain and temp do at entry to the spinal cord?

A

form short ascending and descending collaterals that pass up or down 1-2 segments before entering the dorsal horn gray matter of the spinal cord.

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4
Q

What is the dorsolateral tract of Lissauer?

A

is mostly a short-fibered 2-way tract formed by the cumulative effect of all the pain & temperature branches

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5
Q

Where do 1st order axons of pain and temp synapse (mostly)?

A

in laminae I (marginal zone) and II (substantia gelatinosa) of dorsal horn gray matter

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6
Q

Where do fibers decussate for pain and temp?

A

2nd order pain and temp fibers (spinothalamic tracts) decussate in the ventral white commissure (at the level of entry)

then collect anterolaterally as the ALS internal to the ventral spinocerebellar tract

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7
Q

Where do the second order neurons of ALS synapse? (what other tract synapses here?)

A

ALS courses in the lateral tegmentum of the brainstem and synapses on 3rd order neurons in the ventral posterior lateral nucleus (VPL) of the thalamus

(same synapse as the DCML)

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8
Q

What is ALS a part of?

A

lateral funiculus

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9
Q

What would a lesion of the ventral white commissure cause?

A

bilateral loss of pain and temperature at the levels affected

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10
Q

What is syringomyelia? What can it lead to?

A

central canal expansion

may compress the ventral white commissure
Syringomyelia often starts in the cervical region and includes multiple spinal levels; the result is a capelike distribution of pain & temperature loss

because it is slowly enlarging, symptoms might go unnoticed until the pt burns something because of a loss of pain reflexes

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11
Q

How is ALS somatotopically organized?

A

Fibers are added from outside (more lateral) to inside (more medial)

leg more lateral; arm more medial

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12
Q

What structure does ALS converge with in the pons?

A

The lateral end of the medial lemniscus

A lesion here could affect BOTH

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13
Q

What is the PLIC somatotopy for pain and temp?

A

the same for touch and proprioception (except contralateral to the side the sensation was on)

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14
Q

What would a lesion of ALS fibers from the cord to the cortex produce?

A

loss of contralateral pain and touch below the lesion

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15
Q

What would unilateral lesion of the dorsal horn produce?

A

ipsilateral loss of pain and temp at the lesioned levels only

difficult to test–> might go unnoticed

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16
Q

What would Brown-sequard syndrome (spinal cord hemisection) lead to?

A

ipsilateral loss of touch and conscious proprioception (DC-ML) and contralateral loss of pain and temp (ALS)

17
Q

What could arise as a result of an anterior spinal a. infarction at T9?

A

loss of pain and temp below T9

18
Q

What is the descending pain modulation projection? How does this work?

A
  • supraspinal neurons (originate above the spinal cord) operate via descending pathways to inhibit the dorsal horn pain pathway (produce analgesia)
  • Periaqueductal gray (PAG) neurons are stimulated by ascending ALS spinomesencephalic input. –> these PAG neurons have opioid receptors that bind to the internal opioids and project serotinergic axons to the nucleus raphe magnus (NRM)
  • NRM then projects serotinergic axons in the lateral funiculus to the region of the 1st order pain synapses in the dorsal horn to directly inhibit the ascending pain fibers
  • NRM also stimulates inhibitory interneurons that inhibit the ascending pain fibers via opioid transmitters.
19
Q

How can visceral pain be interpreted?

A

primary afferent nociceptive “c” fibers enter the dorsal horn and can synapse on either:

  1. 2nd order neurons which enter the ALS–> referred pain
  2. an alternate nociceptive pathway: involves 2nd order neurons in the intermediate gray near the central canal that will ascend in the dorsal calumn, parallel to the DC-ML pathway to the VPL thalamus
20
Q

What are 2 ways that analgesia can be produced?

A
  1. morphine acting on the opioid receptors

2. electrical stimulation of PAG and NRM.