4 Pain and Temperature - A Flashcards

1
Q

Name 2 main tracts that are motor and descending pathways?

A
  1. Pyramidal tracts
  2. Extrapyramidal tracts
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2
Q

What are the sub-tracts of Pyramidal tracts? (2)

A
  1. Lateral corticospinal tract
  2. Anterior corticospinal tract
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3
Q

What are the sub-tracts of Extrapyramidal tracts? (4)

A
  1. Rubrospinal tract
  2. Reticulospinal tract
  3. Olivospinal tract
  4. Vestibulospinal tract
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4
Q

Name the 3 main tracts of sensory and ascending (afferent) pathways?

A
  1. Dorsal Column Medial Lemniscus System
  2. Spinocerebellar tracts
  3. Anterolateral system
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5
Q

What are the sub-tracts of Dorsal Column Medial Lemniscus system? (2)

A
  1. Gracile fasciculus
  2. Cuneate fasciculus
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6
Q

What are the sub-tracts of the Spinocerebellar tracts? (2)

A
  1. Posterior spinocerebellar tract
  2. Anterior spinocerebellar tract
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7
Q

What are the sub-tracts of the Anterolateral system? (2)

A
  1. Lateral spinothalamic tract
  2. Anterior spinothalamic tract
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8
Q

What pathway are rapid, sharp, pricking, precise localized pain and temperature conveyed via?

A

direct spinothalamic (“fast” pain) pathway

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9
Q

What are the two types of fibers that are part of the direct spinothalamic (“fast” pain) pathway?

A
  1. A-delta fibers
  2. C fibers
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10
Q

Describe A-delta fibers.

A

myelinated with conduction rate (5-30 m/s)

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11
Q

Describe C fibers.

A

unmyelinated with conduction rate (0.5-2 m/s)

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12
Q

How are burning, throbbing, dull, aching, diffuse pain AND crude touch/pressure conveyed via?

A

indirect spinothalamic system (“slow” pain pathway)

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13
Q

What fibers make up the indirect spinothalamic system (“slow” pain pathway)?

A

C fibers

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14
Q

Describe the direct spinothalamic (“fast” pain) pathway.

A

receptor –> spinal cord –> lateral thalamus –> somatosensory cortices

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15
Q

Describe the indirect spinothalamic system (“slow” pain pathway).

A

receptor –> spinal cord –> reticular formation –> medial thalamus –> cingulate, frontal, limbic cortices

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16
Q

Primary neurons of the direct spinothalamic (“fast” pain) pathway start where?

A
  1. peripheral pain/temperature receptors.
17
Q

Primary neurons of the direct spinothalamic (“fast” pain) pathway enter the spinal cord where ascend/descend via what tract?

A
  1. Fibers enter the spinal cord through the dorsal root ganglion and ascend/descend (1-2 segments) in the posterolateral fasciculus (Lissauer’s tract)
18
Q

Primary neurons of the direct spinothalamic (“fast” pain) pathway terminate on 2nd order neurons where?

A
  1. Fibers then synapse on the secondary neurons in the substantia gelatinosa and some synapse in the nucleus proprius
19
Q

Secondary neurons of the direct spinothalamic (“fast” pain) pathway start where and cross via ___ to enter which part of the anteriolateral/spinothalamic tract?

A
  1. the substantia gelatinosa/(nucleus proprius) cross in the anterior white commissure (AWC) and ascend in the Lateral spinothalamic Tract (LSTT) of the contralateral anterolateral funiculus
20
Q

Secondary neurons of the direct spinothalamic (“fast” pain) pathway organize themselves how in the LSTT?

A
  1. Somatotopic lamination of the Lateral Spinothalamic Tract (LSTT).
    * Sacral* levels enter the tract first and are located in the posterolateral aspect of the tract
    * Cervical* levels enter the tract last and are located in the anteromedial aspect of the tract
21
Q

Secondary neurons of the direct spinothalamic (“fast” pain) ascend through spinal cord via what tract(s) and terminate where?

A
  1. In the medulla, the Lateral Spinothalamic Tract (LSTT) joins with the Ventral Spinothalamic Tract (VSTT) and spinotectal tract to form the spinal lemniscus (SL). The SL terminates in the Ventral Posterior Lateral (VPL) nucleus of the dorsal thalamus
22
Q

Tertiary neurons of the direct spinothalamic (“fast” pain) pathway start where?

A
  1. Neurons located in the ventral posterior lateral nucleus (VPL) of the dorsal thalamus.

The VPL nucleus receives sensory information from the contralateral body via the spinal lemniscus.

23
Q

Tertiary neurons of the direct spinothalamic (“fast” pain) pathway travel through what structure and terminate where?

A
  1. Tertiary axons leave the VPL nucleus as thalamic radiations which course through the posterior limb of the internal capsule, and the corona radiata and terminate in the primary somesthetic cortex (postcentral gyrus).
24
Q

Primary neurons of the indirect spinothalamic (“slow” diffuse pain) pathway start and end where? [Step 1]

A

Primary fibers are unmyelinated, type C fibers with a very slow conduction rate (0.5-2.0 m/s)

It enters the spinal cord and bifurcates either ascend/descend 1-2 segments in the posterolateral fasciculus (Lissaur’s tract). Throughout its course, the primary fibers synapses with the nucleus proprius (lamina IV). [This is the part that’s different from direct pathway, which would synapse with substantia gelatinosa]

25
Q

Secondary neurons of the indirect spinothalamic (“slow” diffuse pain) pathway start and end where? [Step 2/3]

A

Secondary fibers from the nucleus proprius course bilaterally in fasciculus proprius. (CLINICALLY IMPORTANT)

Slow pain information from the nucleus proprius may ascend to the thalamus as spinoreticular fibers. The fasciculus proprius is part of a diffuse neuronal net called the reticular formation, which surrounds the gray matter of the spinal cord and extends rostrally through the core of the brainstem to the thalamus.

26
Q

Spinoreticular fibers (of indirect pathway) terminate in reticular formation of the ______ (3 areas) on both sides of the brain.

A
  1. brainstem
  2. hypothalamus
  3. centromedian nucleus of the dorsal thalamus
27
Q

The projections through the reticular formation (indirect pathway) function in the ______ of the organism in response to nociceptive input.

A

arousal

28
Q

Projections (indirect pathway) to the hypothalamus and the limbic cortex function in the _____ (3) aspects of pain.

A
  1. autonomic
  2. reflex
  3. emotional
29
Q

Why clinically, do unilateral lesions of the spinoreticular fibers (indirect pathway) do not result in significant sensory deficits?

A

Because it is bilaterally and too diffuse to be affected by unilateral lesions. Incomplete transections may allow spinoreticular fibers to get around lesion via intact portion of the fasciulus proprius. This is the basis of persistent pain.

30
Q

Loss of sensation for pain/temperature at L1 and below on the right. Where is the lesion?

A

Lesion is 1-2 segments above on the contralateral side (T10-11)

Just spinothalamic tract lesion only!

31
Q

Describe what you would see with a patient with Brown-Sequard Syndrome.

A

HEMISECTION OF SPINAL CORD

  • Loss of Pain and temp from contralateral side of body
  • complete loss of pain and temperature sensation 1-2 levels below level of lesion (Lissauer’s tract)
  • Loss of Discriminative touch and conscious proprioception on ipsilateral side below
  • ipsilateral loss of ALL sensation at level
  • motor loss
32
Q

What is Syringomyelia?

A

Formation of fluid filled cyst (syrinx) within the spinal cord (within central canal), most common C8-T1

  • Pain and temperature affected

Anterior white commissure (2nd order fibers of spinothalamic tract affected)

  • Results in bilateral loss of pain/temperature sensation in shawl or cape-like distribution
  • Motor also lost if the cyst expands into anterior horn
33
Q

Describe the normal bladder reflex.

A

Mechanoreceptors in bladder wall (detrusor muscle) are stretched when bladder fills. Impulses are sent to S2-S4 via visceral afferent innervation (pelvic nerve) and enter the dorsal root to synapse on visceral afferent nucleus. Interneurons convey stimulus to sacral autonomic nucleus. Visceral efferent neurons from SAN will cause the detrusor to contract and internal sphincter to relax.

Signals also sent from visceral afferents to pontine micturition center (PMC) which can override the micturition reflex OR increase the reflex depending on current situation (is it okay to urinate?)

When micturition is desired, PMC increases impulses via pelvic nerve (efferent) causing contraction of detrusor muscle. Also, somatic innervation via pudendal nerve to external sphincter is inhibited causing relaxation and micturition.

34
Q

What lesions cause Atonic Bladder

A

dorsal roots of S2-S4

35
Q

What is seen clinically due to Atonic Bladder.

A

(Remember lesions at dorsal roots of S2-S4)

Micturition reflex contraction cannot occur if the sensory nerve fibers from the bladder to the spinal cord are destroyed, thereby preventing transmission of stretch signals from the bladder

Instead of emptying periodically, the bladder fills to capacity and overflows a few drops at a time through the urethra. This is known as overflow incontinence.

36
Q

What is the disease process called for a large, dilated, flaccid bladder and increased bladder capacity. Voluntary voiding is possible, but incomplete.

Causes: crush injury to sacral region, diseases (e.g., Syphilis, damage to dorsal horn/dorsal columns)

A

ATONIC BLADDER

37
Q

What spinal cord damage is seen with reflex/automatic bladder?

A

Spinal cord damage above the sacral region (S2)

38
Q

Can micturition reflexes still occur with reflex/automatic bladder and are they still controlled by the brain?

A

Typical micturition reflexes can still occur, but they are no longer controlled by the brain.

39
Q

Describe what is seen with patients with Reflex/Automatic Bladder.

A

During first few days to several weeks after damage to cord has occurred, micturition reflexes are suppressed due to “spinal shock” from sudden loss of impulses from the brainstem and cerebrum (patients require catheterization)

Micturition reflex returns and unannounced emptying occurs