Anatomy seminar 7.1 topic 6

By: Evalda Vasconcelos Tavares, gr.34

Reactions of neurons to injury

The adult central nervous system has the lowest regenerative capacity of all organ systems.

Injuries to axons and axon bundles were once thought

to result in neuronal death and irreversible losses of function.

We now know that neurons have the capacity to

remodel and restructure their projections and synaptic connections.

INTRO

Neurons may be injured physically or by disease processes.

Interneurons are likely to suffer total destruction Injury to a large neuron ,may result in either in

destruction if body is effected or in regeneration if axon is effected

INJURY

All neurons react similiarly

Differences - functional mechanisms and especially, the extent and speed of process

RESPONSE TO INJURY

Neuropraxia- (demyelination) reversible conduction block. Axon and endoneurium still intact, myelin is compressed. Eg. radial nerve compression

Axonotmesis-(demyelination+axon loss) endoneurium is intact.Eg. crach injuries and fractures.

Neurotomisis-( MOST SEVERE) as axonotmesis+ involvement of endoneurium, epineurium, and perineurium.

CLASSIFICATION OF NERVE INJURY

CLASSIFICATION

CELLS

Myelin forming cells: (myelin important for conduction). oligodendroglia in CNS Schwann cells in PNS. oligodendrocytes (CNS) are inhibitory to axon

regrowth in adult CNS regeneration; Schwann cells (PNS) are supportive, as a growth

surface and releaser of growth factors. Astroglia development: supports axon growth and cell migration; mature: important for ion flux, synaptic function, blood-brain barrier injury: accumulate in scar, release excess matrix; inhibit axon growth?

Microglia (resting) and macrophages (active) cells of immune system, similar to monocytes. injury: help or hinder? ….not well-understood

Chromatolysis Nissl substances or RER dissolute and a decrease in

cytoplasmatic basophilia. Nucleus assumes an eccentric position and the whole

body swells The closer the injury is to the body the more severe

the swelling

Transneuronal degeneration Occurs in neuronal bodies that have been deprived of

their input or output  This can be either anterograde or retrograde

WHAT HAPPENS TO THE CELL BODY?

CHROMATOLYSIS

TRANSNEURAL DEGENERATION

Axon doesnt last long after separation from the body, phagocytes remove bits of the axon and myelin

Wallerian degeneration occurs in both PNS and  CNS. Distal ends of the

chopped off neuron will degenerate. Prior to degeneration, distal axon stumps tend to

remain electrically excitable. The axonal degeneration is followed by degradation of

the myelin sheath and infiltration by macrophages

WHAT HAPPENS TO THE AXON?

Axons grow 2-4 mm/day used clinically to estimate time to recovery of function.

Each axon divides into many filamentous branches known as growth cone.

Axons grow within the endoneurium (connective tissue sheath) along channels formed by Schwann cells. Schwann cells make laminin (growth-supportive extracellular matrix) and nerve growth factor which stimulates axon regeneration

Optimal regeneration requires nerve sheath to be intact if axons grow outside sheath can form neuromas

AXONAL REGENERATION IN PERIPHERAL NERVES

Reactive astrocytes form a 'glial scar' near the injury site that could block axon regeneration. [deposits of chondroitan sulfate proteoglycans (CSPGs) in the ECM shown t collapse growth cone.]

Emigration of monocytes from bloodvessels form

reactive microglia, the resting macroglia also transform into phagocytes.

CNS myelin inhibits axon growth, has several

molecules that inhibit axon growth: Nogo-A , Myelin-associated glycoprotein (MAG), etc

AXONAL REGENERATION IN CNS

The regeneration is not perfect, far from it, often the final outcome is only limited.

A deficit of 25% of nerve function is reported even with ideal surgery repair. Eg. nerve grafts

NEUROREGENERATION

Functional recovery involves the taking over of the functions of damaged neurons by neurons that remain intact. The reorganization of connections within the brain is known as plasticity.

PLASTICITY OF NEURAL CONNECTIONS

http://mcloonlab.neuroscience.umn.edu/4100/Lectures/lecture%2038.pdf

https://tigger.uic.edu/classes/anat/anat403/Lectures/lecture20_09.htm#Questions

http://en.wikipedia.org/wiki/Nerve_injury

Video: https://www.youtube.com/watch?v=OKr-9WJTHME

SOURCES

THANK YOU