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Download MBBS Physiology Presentations 70 Type Of Nerve Fibers Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Physiology 70 Type Of Nerve Fibers PPT-Powerpoint Presentations and lecture notes

This post was last modified on 08 April 2022

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Objectives

Should be able to describe,

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I. Types of injuries
I . Responses of nerve injury in

CNS and PNS
End Organs (e.g. Muscles)

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I I. Factors that effect nerve regeneration

Nerve injury may occur due to :

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? Obstruction of the blood flow
? Toxic substances
? Pressure over the fibre- crushing of the

fibre

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? Transection of the fibre
Classification of nerve injuries

(Seddon Classification)

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1. Neuropraxia

2. Axonotmesis

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3. Neurotmesis

Neuropraxia

? Injuries due to pressure

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? Local conduction block only
? This is the mildest for of nerve injury. Mild, blunt

blows, including some low-velocity missile injuries

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close to the nerve

? Recovery takes place without wallerian

degeneration.

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? Pressure over the fibre- short period -

Obstruction of the blood flow, hypoxia

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? The axon is not destroyed mild

demyelination looses the function for a

short period ,conduction block.returns

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within few hrs ? few wks
Axonotmesis

? Usually traction injury

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? Endoneurial tubes are intact

Axonotmesis

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? Severe pressure over the fibre- long period

? endoneurium is intact

? Repair of function 18 months

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Endoneurium

? Each nerve fibre is

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covered by

endoneurium

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? Endoneurium is interrupted
? Epineurium and perineurium are intact
? Recovery is slow
? Neurotmesis

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Each fasciculus is covered by

Perineurium

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Epineurium

Whole nerve is covered by a sheath
Degenerative changes

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- axonotmesis- Wallerian degeneration

? Changes in cell body
? Changes in axon

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Changes in cell body

1. Cellular edema
2. Chromatolysis starts near axon hillock.

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(Dispersion of Nissl fine granules -Cytoplasmic

RNA)

3. Moving of nucleus to periphery

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Changes in axon

1. Degeneration process

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a. Distal segment

? Swelling and fragmentation of axon &

branches called wallerian degeneration

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? Debris digested by Schwann cells and

tissue macrophages

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b. Proximal segment

? Degenerate til first node of Ranvier


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2.Regeneration process

? Schwann cells rapidly proliferate and forms

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parallel cords within basement membrane

? Endoneurial sheath and contained cords of

Schwann cells called band fiber

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? The band fiber extends from first node of Ranvier

in proximal segment up to end organ.

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? When there is gap in the injury site

Schwann cell wil form the codes and bridge

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the gap if only endoneurial tube is intact.



(In CNS microglial cells phagocytosed the

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debris and astrocytes form a scar and no

band fiber

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formation

? So regeneration of PNS depends on endoneurial

tubes and Schwann cells

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? Multiple sprouts arise from proximal axon and cross

the gap through the codes of Schwann cell and

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enter in to distal segment.


But only one filament wil persist

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and grows and reach the end organ.

? When axon reaches end organ Schwann

cells begin to lay down the myelin sheath.

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? It starts from injury site and spread distally.
? The time may be months to complete the

process depending on the severity of injury

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Recovery- reappearance of Nissl gran: due

to Protein synthesis


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Reduction of edema



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Repositioning of nucleus

Recovered peripheral nerve may not

be that efficient compare with the

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original nerve.

Why?

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1.Reduced conduction velocity



(Axon that reaches end organ wil have 80%

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original diameter)

2.Muscle control wil be less precise
(Innervation of more muscle fibers)

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No nerve regeneration in Central nervous

system as in PNS.
Why?

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1. Absence of endoneurial tubes
2. Failure of oligodendrocytes to serve as in

the same manner as schwann cells in PNS

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3. Laying down of scar tissue by active

astrocytes cells

4. Absence of nerve growth factors, or

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5. Production of nerve inhibitory factors in CNS

Changes of end organs supplies by the

nerve

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A. Loss of function

B. Denervation hypersensitivity

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(supersensitivity)

Loss of function

1. Skeletal muscles ? atrophy

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2. Sensory loss -cutaneous

3. Vasomotor-loss of sympathetic control

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impaired blood supply.

4. Sudomotor ?loss of sweating & skin become

dry

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5. Trophic changes

Local tissue changes due to:


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Nutrition/blood supply

Disuse & Loss of sensation

(E.g. in nail, bone)

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Denervation hypersensitivity

(Supersensitivity)

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Hypersensitivity of end organs supplied by

denervated nerve due to increase response to

neurotransmitter

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Denervation hypersensitivity can occur in;

? Skeletal muscles

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Fine irregular contraction of individual fibers

called fibril ation.

? smooth muscles

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? Exocrine glands except sweat glands



This is due to :

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1. Receptor up regulation in end Organs
2. Increase neurotransmitter levels at the site due to

reduce uptake by the nerve

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The factors that effect regeneration

? Type of injury
Gap between nerve ends

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Distance to cell body

(Worse with proximal injuries)

Damage to adjacent tissue

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Presence of foreign bodies
? Ischaemia &Infections
? Delay between injury and repair
? After care

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