SS Tracts: Nociception, Thermal Sense, and Touch (Dennis) Flashcards

1
Q

What are the different tracts of the ALS, what is their target and function?

A
  • spinothalamic (largest): target is VPL, posterior nucleus, and intralaminar nuclei in thalamus > function is awareness and gating of info to cortex
  • spinomesencephalic: target is periaqueductal gray (PAG) gray matter of midbrain > function is pain modulation by releasing NT’s
  • spinoreticular (also sends fibers to spinothalamic): target is reticular formation in brainstem > function is widespread cerebral cortex response to pain and activation of monaminergic systems
  • spinobulbar: target is brainstem nuclei > function is adaptive responses through brainstem nuclei
  • spinohypothalamic: target is hypothalamus > function is autonomic response to pain
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2
Q

What is the somaticsensory function of the ALS?

A
  • fibers that relay pain, temperature, and nondiscriminative touch, mostly from the spinothalamic tract
  • other smaller tracts that terminate in brainstem and diencephalon modulate pain and initiate responses to pain sensation
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3
Q

Where are the 1st and 2nd order neurons located in the ALS and what is the route of their axons?

A
  • ALS starts w/ free nerve endings distributed in skin, muscles, joints, blood vessels, and viscera
  • peripheral processes from the nerve endings synapse at the pseudounipolar neurons (1st order neurons) in the dorsal root ganglion
  • central processes project afferent fibers enter SC via the lateral division of the posterior root entry zone (posterior gray horn)
  • fibers ascend/descend 1-2 spinal levels in posterolateral Lissauer’s tract
  • fibers then synapse on 2nd order neurons located in the posterior horn in superficial laminae I (marginal zone), II (substantia gelatinosa), and nucleus proprius (laminae III and IV)
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4
Q

What signals does the spinothalamic pathway carry?

A
  • nondiscriminative tactile
  • innocuous thermal (temp)
  • nociceptive (pain)
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5
Q

Where does the spinothalamic tract enter the SC and what are the two possible routes it can take once entering?

A
  • afferent fibers enter posterolateral fasiculus (Lissauer’s tract)

two routes:

  1. ascending fibers synapse on 2nd order neurons of posterior horn > fibers cross midline via anterior white commissure
  2. descending fibers synapse on interneurons and moderate spinal reflexes
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6
Q

What is the somatotopic organization of the ALS?

A
  • axons from lower levels (coccygeal, sacral) of the body are found posterolaterally
  • more rostral levels are added in an anteromedial sequence

in general:

lower body > upper body

posterolateral > anteromedial

*ALS map is opposite of the posterior column’s*

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7
Q

What is the general path of the ascending spinothalamic tract?

A
  • fibers synapse on pseudounipolar neurons (1st order) in the DRG
  • afferents enter the posterolateral fasiculus > 2nd degree neurons in posterior horn
  • 2nd degree neurons cross midline at the anterior white commissure and ascend in the contralateral ALS > VPL of thalamus (few ascend in ipsilateral ALS, not clinically relevant)
  • 3rd order neurons in VPL target somatosensory cortex (somatotopic)
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8
Q

What is the general pathway of the ALS STT?

A
  1. axons enter spinal cord from spinal ganglia (1st order neurons), ascend/descend 1-2 segments in Lissauer’s tract, and then synapse in the posterior horn (2nd order neurons)
  2. axons of secondary neurons cross midline in the anterior white commissure and ascend as the anterolateral tract in the spinal cord
  3. anterolateral tract travels through caudal medulla
  4. in rostral medulla, anterolateral tract lies between inferior olivary nucleus and the nucleus of the spinal tract of the trigeminal nerve
  5. in the pons and midbrain, the anterolateral tract lies lateral to the medial lemniscus
  6. anterolateral tract terminates in the VPL of the thalamus (3rd order neurons); from the thalamus, fibers project through the IC and corona radiata to terminate in the primary somatosensory cortex (postcentral gyrus)
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9
Q
  • most of these fibers are C fibers (hot temp, dull pain), with a small amount being Aδ fibers (pin-prick pain, cold temp)
  • relay noxious and innocuous mechanical and thermal info
  • contributes to perception of dull pain and moderates behavioral and motivational changes a/w pain
  • type of pain that will keep you up at night (arthritis) because the associated dull, aching pain is relayed through the reticular formation, which alerts a large portion of the cerebral cortex of the pain
A

spinoreticular fibers

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10
Q

What is the general route of the spinoreticular tract?

A
  • 1st order afferents enter SC through posterolateral fasiculus
  • 2nd order neurons located in the posterior gray horn in the laminae II and III join contralateral ALS by crossing over AWC
  • 3rd order neurons are located in reticular formation
  • fibers relayed to thalamus (intralaminar and posterior group nuclei)
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11
Q

What is the blood supply to the ALS and what would lesions of these vessels result in?

A
  • blood supply originates from arterial vasocorona via sulcal branches of the anterior spinal artery
  • occlusion/lesions result in patchy loss of nociceptive, thermal, and touch over the contralateral side of the body, about two spinal segments below the lesion
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12
Q
  • SCI that produces bilateral, total loss of all motor and sensory function at/below the level of injury
A

complete SCI

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13
Q
  • SCI injury to the motor and pain/temp pathways in the anterior SC
  • patients still have propriception and sensation
A

anterior cord syndrome

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14
Q
  • SCI to the center of the cord or anterior white commissure
  • causes loss of pain/temp pathways w/ deficits relative to the size of the lesion
A

*central cord syndrome*

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15
Q
  • SCI where individuals may have motor and sensory deficits due to roots containing both types of nerves
  • location of deficits depends on distribution of nerve root involved
A

injuries to spinal nerve root

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16
Q
  • SCI that is transient and generally resolves within 1-2 days
  • produces neurological symptoms including numbness, tingling, electric shock-like sensations, and burning in the extremities
A

spinal contusions

17
Q
  • combination of sensory and motor deficits due to damage to ALS, PCMLS, and CST pathways
  • contralateral deficits involve ALS and are approx 2 segments below lesion
  • ipsilateral deficits involve PCML at/below level of lesion and CST dependent on level of lesion
A

Brown-Séquard syndrome

18
Q

What are the contralateral deficits of Brown-Séquard syndrome?

A
  • loss of nociceptive and thermal sensations a/w ALS
  • occurs approx 2 segments below level of lesion
19
Q

What are the ipsilateral deficits associated with Brown-Séquard syndrome?

A
  • loss of discriminative tactile vibratory, and position sense (PCMLS), at/below the level of lesion
  • paralysis of the trunk and extremity (CST), dependent on level of lesion
20
Q
  • condition involving cystic cavitation of central regions of SC, typically develops between C3-T2
  • syrinx enlarges due to fluid accumulation > surrounding neural tissue destroyed
  • initial damage is to ALS fibers in AWC, usually progresses to anterior horn causing motor deficits
  • deficits present in distinct cape-like pattern: loss of pain and temp bilat over arms/shoulders; weakness, atrophy, and fasciculations of muscles of hands
A

syringomyelia

21
Q
  • lesion location: lateral medulla
  • syndrome:
  • deficits:
  • vascular territory:
A

- lesion location: lateral medulla

  • syndrome: lateral medullary syndrome (aka PICA syndrome or Wallenburg syndrome)
  • deficits: contralateral loss of pain and thermal sensation (body)
  • vascular territory: occlusion of posterior inferior cerebellar A.; occlusion of vertebral artery at the origin of the PICA, blocking the PICA flow
22
Q
  • lesion location: lateral pons
  • syndrome:
  • deficits:
  • vascular territory:
A

- lesion location: lateral pons

  • syndrome: lateral pontine syndrome
  • deficits: contralateral loss of pain and thermal sensation (body)
  • vascular territory: occlusion of long circumferential branches of basilar A. and branches of anterior inferior cerebellar A. or superior cerebellar A.
23
Q

What is the nucleus of the trigeminal nerve that is involved in pain, temp, and nondiscriminative touch?

A

spinal trigeminal nucleus

(3 parts: pars caudalis, pars oralis, and pars interpolaris)

24
Q

What is the general path of the spinal trigeminal tract?

A

(SGN runs from obex in pons > C2/C3)

  • pain/temp signals relayed to 1st order neurons located in the trigeminal nucleus
  • primary trigeminal afferents descend to 2nd order neurons located in the spinal trigeminal nucleus (caudal brainstem)
  • tract extends caudally to about 3rd cervical segment and becomes continuous w/ Lissauer’s tract in the upper cervical cord
  • 2nd order neurons cross midline and ascend as anterior trigeminothalamic tract
  • 3rd order neurons of contralateral VPM (thalamus) target somatosensory cortex
25
Q

What is the purpose of SGN descending to the 3rd cervical segment when the primary afferents enter around the midpons area?

A

This allows the SGN fibers to meet and mix w/ C2/C3 fibers which provide somatosensory innervation to regions of the posterior head.

This prevents gapping in innervation from C2/C3 and the trigeminal N.

26
Q

What is the somatotopic organization of the spinal trigeminal nucleus?

A

STN organized in two planes:

  1. anterior > posterior
    - face is inverted, opthalmic (V1) dermatome is anterior in the STN and mandibular (V3) dermatome is posterior
  2. rostral > caudal
    - fibers from circumoral/intraoral zones terminate rostrally, near obex; fibers of midcheek region target middle segments of STN; fibers of lateral edges of face target caudal regions down to C2/C3
27
Q
  • damage to spinal trigeminal tract leads to this type of sensory loss
  • more caudal lesion > spares oral region, but affects posterior and lateral boundaries of face
  • more rostral lesion (into brainstem) > sensory loss that is increasingly anterior and converges on mouth
  • trigeminal fibers ending in cervical cord overlap spinal fibers that innervate C1 and C2 dermatomes, allows for smooth transition of cutaneous info from posterior head (spinal) w/ cutaneous anterior face/head (brainstem)
A

onion-peel sensory loss

28
Q

What is the difference between anatomical vs. clinical orientation?

A
  • anatomical: based on anatomical images; ophthalmic is inferior, mandibular is superior; posterior structures are up on the page and anterior structures are down
  • clinical: relevant to evaluating neuroimaging and identifying lesions; opthalmic is superior, mandibular is inferior; posterior structures are down and anterior structures are up
29
Q
  • PNS lesion that causes anesthesia and loss of general sensations in the trigeminal dermatomes
  • paralysis of the muscles of mastication and loss of ipsilateral afferent limb of corneal reflex
A

unilateral trigeminal nerve/nuclei lesion

30
Q
  • CNS lesion causing unilateral destruction of trigeminal nerve and CST in the pons
  • ipsilateral trigeminal anesthesia and paralysis of muscles of mastication, and contralateral spastic hemiplegia
A

alternating trigeminal hemiplegia

31
Q

What deficits arise from lateral medullary syndrome?

(LMS: occlusion of posterior inferior cerebellar artery (PICA) or branches of PICA)

A
  • Contralateral loss of pain and thermal sense on body (ALS)
  • Ipsilateral loss of pain and thermal sense on face and in the oral cavity (Spinal trigeminal tract/nucleus)
  • Dysphagia, soft palate paralysis, hoarseness, diminished gag reflex (Nucleus ambiguus, roots CNIX/X)
  • Ipsilateral Horner syndrome (miosis, ptosis, anhidrosis, flushing of face) (Hypothalamospinal fibers)
  • Nausea, diplopia, tendency to fall to ipsilateral side, nystagmus, vertigo (vestibular nuclei)
  • Ataxia to the ipsilateral side (restiform body, spinocerebellar fibers)
32
Q

What are the deficits a/w lateral pontine syndrome?

(LPS: occlusion of long circumferential branches of basilar A., and branches of anterior inferior cerebellar A. or superior cerebellar A.)

A

deficit > structure damage causing deficit

  • Ataxia, unsteady gait, fall toward side of lesion > Middle and superior cerebellar peduncles (caudal and rostral levels)
  • Vertigo, nausea, nystagmus, deafness, tinnitus, vomiting (at caudal levels) > Vestibular and cochlear nerves and nuclei
  • Ipsilateral paralysis of facial muscles > Facial motor nucleus (caudal levels)
  • Ipsilateral paralysis of masticatory muscles > Trigeminal motor nucleus (midpontine levels)
  • Ipsilateral Horner syndrome > Descending hypothalamospinal fibers
  • Ipsilateral loss of pain and thermal sense from face > Spinal trigeminal tract and nucleus
  • Contralateral loss of pain and thermal sense from UE, trunk, and LE > Anterolateral system
  • Paralysis of conjugate horizontal gaze > Paramedian pontine reticular formation (mid to caudal levels)
33
Q
  • medulla: vascular territories of spinal trigeminal nucleus and spinal trigeminal tract
A
34
Q
  • pons: vascular territories of mesencephalic and principal sensory nuclei
A
35
Q
  • midbrain: vascular territories of mesencephalic and principal sensory nuclei
A