Module 8 - Lecture 5 - Repair and Compensation in the PNS Flashcards
What are the names of the 3 common axon injuries and their common name.
Axonotmesis (nerve crush injury)
Neurotmesis (laceration or cut injury)
Neurapraxia (focal demyelination)
What is the first phase of a traumatic axon injury (ie Cut or large crush) and what happens?
Macrophages enter and digest the remaining axon.
*In the area distal from the lesion, the remaining axon that is there would rapidly begin to degenerate. The macrophages would come to clear up the dead tissue (axon that no longer has the ability to have enzymes).
How do Schwann cells assist in axon growth?
Phase 2: axon develops a growth cone, and grows towards the specialized target as laid out by Schwann cells. They secrete trophic signals that promote growth and tropic signals that provide direction & framework.
What is the distinction between neurotrophic factors and neurotropic factors?
Trophic promotes growth at all, tropic factors provide direction and a framework for such growth to ensure its occurring in the right location.
How do cell adhesion molecules on Schwann cells and extra cellular matrix (epineurium) act as a local “target”? Is this neurotrophic or neurotropic?
CAM’s are neurotropic, they provide a target for the axons to grow towards whereas the neurotrophic signals initiate growth.
Understand the distinction between crush and cut injuries = Which one is more likely to have Wallerian degeneration? Which has a better recovery and why?
Which one is more likely to have Wallerian degeneration?
Cut, where there are severed axons, macrophages will enter to decompose the tissue.
Which has a better recovery and why?
Crush, easier for re-propogation to occur, as there isn’t severed, connections still made, guiding repair. Schwann cell framework is less disrupted. Damage distally guides regenerating proximal axon. (trophic factors)
What is the concept of re-apposition surgery? How does it improve axon regrowth?
Re-aligns axon and soma, in severed nerves, helps to provide the distal target more accurately for axonal repair. However, this is not an exact science, and axons may project to multiple distal targets (imprecise surgery) without adequate trophic signals.
Approximately how quickly an axon re-grows (per day)?
1mm per day. Or 1 inch/month
What is a limitation of axon re-growth and what conditions may result in higher imprecision (cut vs crush?, surgery vs no surgery?, distance to nearest “local target?”)
Cut provides more imprecision, as axon can sprout to multiple targets, surgery would help to improve this by realigning the nerves, but with multiple neurons in a nerve this is still imprecise, motor/sensory function would take significant time to resolve (as seen in Head case). Polyneuronal innervation = axon projects to too many synapses.
How do activity and experience can improve recovery from an axon injury?
Engaging the motor system we can train and make sense of new connectivity following injury. This improves action potential propagation, and ability to interpret sensory/motor signals/commands (happens intrinsically). Takes advantage of “plastic changes” (strengthens needed synapses, and removes unneeded.
Understand the concepts of axon collateralization. What is the impact on single motor unit size? What is the impact on a compound motor unit action potential (M-wave)?
The impact on single motor unit size:
single motor units get larger, as 1 LMN innervated more MF’s…. this occurs as a result of lost LMN, another one picks up the slack, and reinnervated denervated MF’s.
The impact on a compound motor unit action potential (M-wave):
M-wave stays constant, (relative preservation), because more MF’s innervated by a healthy LMN/MU.
however, there is a finite number of MF’s that can be innervated by 1 MU, therefore in the ‘very’ old we see decrease in M-wave.
What can axon collateralization can compensate for and how it impacts “function” like strength?
Strength is maintained but lost quicker with age, or pathology, as there are less LMN’s, so the loss of any exponentially decreases strength relative to a healthy/normal individual.
What is the limitation of axon collateralization (ie when does it stop working)?
Something like polio, where MU degeneration is prevalent, there is exponential muscle wasting and loss of strength. MU collateralization can be saturated, and MU can no longer pick up extra MF’s.
Additionally with age in someone who already has large MU’s from injury or pathology, would exponentially lose strength, and muscle capability, often results in premature death, or inability to care for oneself.
