Basic S & M Pathways - S

Question 1

What is the course of an affarent neuron?

Answer 1

Begins in the spinal ganglion, enters the dorsal root and courses up and/or down the SC, may give of collateral branches that terminate on interneurons

Question 2

What is the tectum comprised of? What is its job?

Answer 2

Superior and inferior colliculus

Brings in auditory and visual info

Question 3

What is the purpose of a myotactic/monosynaptic reflex?

Answer 3

To contract a muscle when it becomes stretched too far

Question 4

What is the role of the primary somesthetic cortex (S1)?

Answer 4

Plays role in the perception and discrimination of sensory stimuli

Question 5

Draw out the Fast Pain/Temp pathway.

Answer 5

See notes.

Question 6

Draw the Propioception/2-pt Tactile pathway.

Answer 6

See notes

Question 7

What are lower motor neurons (LMN), and what are the two types? What do they innervate? Where do their cell bodies exist?

Answer 7

“The final pathway”, alpha (skeletal m fibers) and gamma (intrafusal fibers)

Innervate skeletal muscle

Cell bodies exist in pools where they synapse with UMNs bringing efferent information from the brain

Question 8

What occurs when a LMN stops receiving information (upstream lesion)?

Answer 8

They become hyperactive/over-responsive

Question 9

What are the specific clinical aspects involved with lack of signals to the LMN?

Answer 9

Flaccid paralysis: muscle completely limp
Areflexia: loss of efferent reflex component
Atonia: no gamma motor nn = no muscle tone
Atrophy: muscle wasting d/t loss of muscle stimulation
Fasciculations: hypersensitive twitching

Question 10

What is Poliomyelitis? What is it’s initial onset like?

Answer 10

Viral dx that causes inflammation, vasodilation, edema, and increased macrophage activity

These cause neuronal death, specifically motor neurons of the AH and their cranial and motor nuclei

2-4 days with fever, headache, vomiting, neck stiffness, and pain in the back and limbs

Question 11

Draw the Corticospinal Pathway.

Answer 11

See notes

Question 12

A piano player is experiencing paralysis or paresis of a distal limb musculature has occurred. What has been lesioned and where?

Answer 12

A lesion of the LCST on the SAME side as the sx (ipsilateral)

Question 13

What tracts control distal limb musculature, especially precise and individualized movements of the digits?

Answer 13

LCST and RST

Question 14

A lesion of the CST RST, or an UMN is called spastic paralysis of the antigravity muscles. What are the sx that comprise this?

Answer 14

Hypertonia
Hyperreflexia
Babinski's sign (big toe extends and others fan)
Clonus (rhythmic contraction spasm)
Rigidity
Disuse atrophy

Question 15

Where do interneurons terminate? What does variability in this process provide?

Answer 15

Directly or indirectly onto a ventral/anterior horn cell

Provides means to tweak a reflex response based on the situation

Question 16

What are the 3 phases of a spinal cord injury (SCI)?

Answer 16

Phase 1: spinal shock distal to an UMN lesion, leads to: loss of voluntary urinary bladder function and sexual potency (males), suppression of spinal reflex arcs, prevents thermoregulation, quadriplegia (cervical lesion) or paraplegia (lumbar lesion), flaccid paralysis, Horner’s syndrome (lesion above T2)

Phase 2 (after weeks-months): reflexes return d/t reactivation of intrinsic circuits of SC distal to lesion, no voluntary motor control restored yet

Phase 3 (1-2 years later): affected muscle groups exhibit spasms or continued flaccidness (extensors return more frequently)

Question 17

What is spasticity? What is the facilitatory and inhibitory regions in the brainstem doing here?

Answer 17

Abnormal passive resistance to movement in ONE direction, a myotactic reflex is hyperactive d/t continual activation of gamma-motor neurons

Facilitatory region fighting passive motion with flexion, inhibitory region not activated d/t cortex dmg

Question 18

What is Rigidity?

Answer 18

Abnormal passive resistance to movement in ALL directions, continual activation of alpha-motor neurons d/t loss of inhibitory activity that stops medullary amn input