PNS - Neurons, Types of Injury, and Classification Flashcards
Involvement of LMN results in:
Flaccid paralysis & muscle atrophy Hyporeflexia/Areflexia - muscles aren’t innervated Visible fasciculation Small, involuntary muscle contractions Myotomal pattern of weakness
Differentiation of Pathologies, neuropathy vs myopathy
Neuropathy: Disorder of the nerve (motor units stay the same but the nerve is damaged)
Myopathy: Disorder of the muscle (motor unit is smaller )
Location of peripheral nerve pathologies
Can affect any spinal nerve
-Cell bodies are located in the spinal cord
Can affect cranial nerves
-Cell bodies are located in the brainstem
In PNS diseases axons and cell body are affected, this occurs in which type of nerve fiber and progression of symptoms moves from, to
Usually affects the longest nerve fibers 1st
Result in progression of symptoms distally -> proximally
Since longest fibers are effects first the issues go from distal to proximal
Three layers of the nerve fiber from superficial to deep
Epineurium
Perineurium
Endoneurium
Mechanisms of PNS injury and which one is most common injuries that we treat (3)
1) Compression is one of the most common injuries that we treat
2) Traction
3) Transection
Traction is and types (2)
Acute: abrupt external force causing immediate loss of function from structural changes to the neural tissue
Axillary N. Palsy from a shoulder dislocation
Chronic: slow stretch causing deformation of neural tissue
Space occupying lesion (cyst, tumor, etc)
Transection is
Complete disruption of neural tissue w/ subsequent loss of function & nerve continuity - totally severs the nerve
(C5 nerve root avulsion following a MVA)
Traction injuries limit and what can you do to treat
Traction injuries limit the ability of the nerve impulse to travel down the nerve. If you can get the nerve out of an elongated position (brace) it will heal faster then it would if it was kept in the elongated position
Segmental Demyelination is and is caused by
Demyelination of segments of the nerve
The axon is intact
Is due to external compression or disease
Segmentally the axon is intact but there is a disruption with the transfer along the myelin sheath - usually from some sort of compression or disease
Wallerian Degeneration affects and types and is due to
Defined as the distal disintegration of axon & myelin – anterograde degeneration
Concurrent “Dying Back Phenomenon” – retrograde degeneration
Due to traction (stretch), transection (laceration, crush), or disease
(wallerian both axon and myelin this can lead to:
-anterograde degeneration: anterior and distal to the degeneration
or
-retrograde degeneration: proximal to the injury )
After and injury to a nerve what happens
Macrophages come in and start clearing everything out and you have a breaking down of the axon that goes to the muscle->the axon regrows and is remyelinated again and the nerve is innervated again
Explain difference between oligodendrocytes, schwann cells and the nerves they innervate
Oligodendrocytes can innervate up to 50 cells and some Schwann cells innervate up to one nerve. That means if we lose one it is okay because there are many others to help rebuild that myelin sheath
Wallerian Degeneration
begins how soon after injury and then what happens
Usually begins w/in 24 hours of injury at the distal stump
Axonal skeleton & axonal membrane disintegrate, followed by degradation of the myelin sheath
Infiltration of macrophages, assisted by Schwann cells ➡ clears the debris
Regeneration Process
of peripheral nerves when damage is not that severe
If the damage is not so severe the neurolemma (does not degenerate – remains as hollow tube that serves as “guide” for regeneration) - hollow tube that surrounds the peripheral nerve remains and allows the growth of the axon to reconnect to where it was before
Schwann cells give off NGF’s (neural growth factors) that attract axonal sprouts
Sprouts form w/in 96 hours and re-innervation occurs provided there’s no scar tissue
What happens if axonal sprouts met resistance
If resistance or barrier is met by new axonal sprouts -> they retract and form tangled masses – neuromas
If there is a resistance for example the macrophages to do not clear out the damage that well. you can hit resistance and there is a potential for the nerve not to grow back as well
What is a neuroma
tangled mass
PNS vs CNS Regeneration
Reasons CNS regeneration is slow or non-existent:
Schwann cell to axon vs. Oligodendrocyte to axon ratio
Schwann cells assist in the phagocytosis of debris - clear out path for regrowth
Oligodendrocytes do not have neurolemmas
Severity of Nerve Injury:
-Three levels of nerve injury
(how many degrees does each level have)
Neuropraxia – 1st degree
Axonotmesis – 2nd degree
Neurotmesis – 3rd, 4th, and 5th degree
Neuropraxia is
No structural change of the axon
Segmental demyelination
Transient episode of motor paralysis with little or no sensory or autonomic dysfunction
Sx generally caused by compression
(compression of the myelin sheath but no structural change to axon - segmental demyelination)
Slows/Blocks AP at site of pathology (transient the impulse can not travel down the myelin sheath but once the compression removed comes back right away)
