L12: Degeneration and Regeneration of Peripheral Nerves Following Trauma Flashcards

1
Q

What are the main structural components of a nerve cell (neuron)?

A

The cell body and the axon.

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2
Q

What is the primary difference between the central and peripheral nervous systems regarding injury response?

A

Peripheral nerves have the capacity to regenerate under proper conditions, while central nervous system neurons generally do not regenerate after injury.

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3
Q

What is Wallerian degeneration?

A

It is the process by which the distal segment of a damaged axon degenerates and is cleared by phagocytic cells following injury.

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4
Q

What are the three classifications of nerve injuries according to Seddon’s classification?

A

Neuropraxia, axonotmesis, and neurotmesis.

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5
Q

What is neuropraxia?

A

It is the mildest form of nerve injury, often causing temporary loss of function that fully recovers once the insult is removed.

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6
Q

What distinguishes axonotmesis from neurotmesis?

A

In axonotmesis, the axon is damaged but the connective tissue structure remains intact, allowing regeneration. In neurotmesis, both the axon and connective tissue are completely disrupted, preventing regeneration.

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7
Q

What role do glial cells play following nerve injury?

A

Glial cells, such as microglia, become activated, clear debris from the injury site, and may support axonal regeneration by forming pathways.

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8
Q

What is chromatolysis in neurons?

A

It is the process of cellular swelling and displacement of the nucleus in the neuron’s cell body, typically following axonal injury.

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9
Q

Why is trophic support from nerves important for muscles?

A

It not only provides neuronal signals for muscle contraction but also influences the biochemical and structural properties of the muscle fibers.

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10
Q

What are fibrillations, and when do they occur?

A

Fibrillations are uncontrolled muscle contractions that occur in denervated muscles shortly after nerve injury.

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11
Q

What is crush syndrome?

A

A condition resulting from massive muscle damage, leading to the release of potassium and other substances into the bloodstream, potentially causing acute renal failure.

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12
Q

What experimental finding highlighted the specificity of motor neurons to muscle fibers?

A

When type S (slow contraction) motor neurons were switched to supply type F (fast contraction) muscle fibers, the contractile properties of the muscle changed to match the neuron’s characteristics.

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13
Q

What are the layers of connective tissue in a peripheral nerve, from innermost to outermost?

A

Endoneurium, perineurium, and epineurium.

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14
Q

What is the role of the endoneurium in nerve repair?

A

It forms a connective tissue tube that helps guide regenerating axons to their target.

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15
Q

How does nerve injury affect the action potential properties of the neuron?

A

Injured neurons generate ‘injury potentials,’ which are abnormal and complex electrical signals.

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16
Q

What happens to the distal segment of a neuron after it is cut off from the cell body?

A

It loses nutritional and repair support, becomes vulnerable to phagocytosis, and undergoes Wallerian degeneration.

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17
Q

What immediate response occurs in the proximal segment of an injured axon?

A

The cell body enters a phase of increased protein synthesis to support repair, leading to chromatolysis.

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18
Q

What is the significance of the glial cell response after nerve injury?

A

Glial cells, such as microglia, clear the debris from the injury site and create an environment conducive to axon regeneration.

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19
Q

What are growth cones, and what role do they play in nerve regeneration?

A

Growth cones are structures that extend from the regenerating axon, guided by chemical signals and connective tissue tubes toward their target.

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20
Q

What is the ‘crocodile tears syndrome’?

A

It is a condition where regenerating nerves misroute and innervate the lacrimal gland instead of their original target, causing tears during eating.

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21
Q

What experimental evidence shows that motor neurons influence muscle fiber type?

A

Switching a type S motor neuron to innervate a type F muscle fiber changes the muscle fiber’s contraction properties to match the neuron’s type.

22
Q

How does neuronal injury affect synaptic inputs to the injured neuron?

A

Synaptic inputs withdraw from the injured neuron, altering interconnections and potentially impairing function.

23
Q

What are the clinical signs of muscle denervation?

A

Paralysis, fibrillations (uncontrolled contractions), and eventual muscle atrophy if not reinnervated.

24
Q

Why do CNS neurons generally fail to regenerate after injury?

A

CNS neurons lack the intrinsic growth capacity and are inhibited by the glial environment, including the presence of myelin-associated inhibitory factors.

25
Q

What is the functional impact of axonotmesis compared to neurotmesis?

A

Axonotmesis allows for potential regeneration and functional recovery, while neurotmesis often leads to permanent loss of function due to complete nerve disruption.

26
Q

What is a neuroma, and how does it relate to nerve injury?

A

A neuroma is a growth or swelling at the end of a severed nerve, often a result of failed or incomplete regeneration.

27
Q

What is the role of the myelin sheath in axonal regeneration?

A

The myelin sheath provides structural support and chemical signals that guide regenerating axons along their original pathways.

28
Q

What causes crush syndrome in patients with muscle injuries?

A

The release of intracellular potassium and other substances into the bloodstream overwhelms the renal system, leading to acute renal failure.

29
Q

What are the two major systems of effector neural pathways?

A

The somatic nervous system and the autonomic nervous system.

30
Q

What is the primary function of the somatic nervous system?

A

It controls voluntary actions through skeletal muscle innervation.

31
Q

What is the main function of the autonomic nervous system?

A

It regulates involuntary functions, such as smooth muscle activity and glandular secretions.

32
Q

Why is the distinction between the central and peripheral nervous systems important in nerve injury studies?

A

The peripheral nervous system has regenerative capacity, while the central nervous system does not.

33
Q

What are the main types of insults that can cause nerve injury?

A

Lacerations, crushing injuries, and environmental disturbances affecting neuronal function.

34
Q

How does the depth of a nerve injury influence the severity of dysfunction?

A

Greater depth, such as reaching the axon itself, results in more severe dysfunction and a longer recovery process.

35
Q

What is the main consequence of severing a peripheral axon?

A

The axon is divided into proximal and distal segments, with the distal segment undergoing Wallerian degeneration.

36
Q

How does nerve injury affect intracellular fluid and the surrounding environment?

A

Intracellular fluid leaks from the damaged axon, disrupting the surrounding environment and aggravating the injury.

37
Q

What happens to the presynaptic terminal shortly after neuronal injury?

A

Synaptic inputs are withdrawn, leading to immediate disruption of inter-neuronal communication.

38
Q

How do activated glial cells assist after nerve injury?

A

They clear debris, secrete factors that guide regenerating axons, and help create a conducive environment for regeneration.

39
Q

What are injury potentials, and why are they significant?

A

Injury potentials are abnormal electrical signals produced by damaged neurons, indicating the extent of injury.

40
Q

What histological change characterizes chromatolysis?

A

The cell body swells, the nucleus is displaced to the periphery, and the Nissl substance becomes dispersed or disappears.

41
Q

How does the proximal segment of an axon respond to injury?

A

It initiates repair processes, including axon sprouting, to attempt regeneration.

42
Q

What factors determine whether a regenerating axon successfully reinnervates its target?

A

The integrity of connective tissue tubes (endoneurium, perineurium, epineurium) and the presence of supportive chemical signals.

43
Q

What is the primary outcome of neurotmesis without surgical repair?

A

Permanent loss of function due to the complete disruption of axons and connective tissue pathways.

44
Q

Why does denervated muscle eventually die without reinnervation?

A

Muscle fibers rely on trophic support from their nerve supply to maintain their structure and function.

45
Q

What is the role of microglia during the degeneration of the distal axon segment?

A

Microglia act as phagocytes, digesting the degenerating axon and clearing debris.

46
Q

How does axon regeneration speed vary?

A

Regeneration typically progresses at a rate of about 1 millimeter per day under optimal conditions.

47
Q

What are fasciculations, and what do they indicate?

A

Fasciculations are spontaneous contractions of denervated muscle fibers, signaling nerve injury.

48
Q

What experimental technique revealed the role of trophic factors in muscle-nerve interactions?

A

Switching motor neurons between type S and type F muscle fibers demonstrated changes in muscle contractile properties based on neuronal input.

49
Q

What is the result of improper reinnervation of target tissues?

A

Misrouted nerve fibers may lead to abnormal functions, such as the crocodile tears syndrome.

50
Q

How does acute muscle damage in crush injuries contribute to systemic failure?

A

It releases potassium and other substances, potentially leading to crush syndrome and acute renal failure.