Test: Physiology of Nerve- 2 - NEET PG MCQ

In neurapraxia, the axon remains intact; however, only a local injury to the myelin takes place, resulting in a conduction block.

In axonotmesis, both the axon and the myelin sheath are disrupted, yet the connective tissue remains undamaged.

Motor march: Following recovery from axonotmesis, the proximal muscles tend to regain function before the distal ones.

• This recovery progresses from proximal to distal.
• Motor march is observed in cases where Wallerian degeneration takes place.

In neurapraxia, the restoration of motor functions in both proximal and distal muscle groups happens simultaneously.

As the initial portion of the axon possesses the greatest concentration of voltage-sensitive Na⁺ channels, it consequently has the lowest threshold for initiating an action potential.

Synaptic conduction is primarily orthodromic due to several reasons:

• Dendrites cannot be depolarised, which limits the direction of impulse flow.
• After an area is repolarised, it cannot be depolarised again immediately.
• The strength of an antidromic impulse is generally weaker.
• The chemical mediator is mainly found in the presynaptic terminal, ensuring effective transmission.

In a natural context, impulses travel in a single direction, specifically from synaptic junctions or receptors along axons to their endpoints. This type of conduction is referred to as orthodromic.

Conversely, conduction that occurs in the opposite direction is known as antidromic.

• They are found throughout the cell body and in large dendrites.
• However, Nissl bodies are absent in the axon.

Irreversible damage takes place if there is an absence of O₂ for more than 5 minutes.

Acute and chronic hypoxias are linked to a decrease in nerve conduction velocity, the generation of neuronal action potentials, and axonal transport. In central neurons, the diminished excitability of nerve cells during hypoxia is mainly due to an increase in K⁺ conductance.

Therefore, hypoxia also impacts action potentials. However, in comparison to other assertions, it may serve as the answer.

It continues to be in a relative refractory phase.

Accommodation describes a gradual rise in threshold due to extended periods of slowly increasing sub-threshold nerve depolarisation, which is a result of sodium channel inactivation.

Adaptation occurs when a supra-threshold (not sub-threshold) stimulus remains constant for several minutes, without any alteration in position or amplitude (not slowly increasing). In this case, the neural response decreases and the sensation is diminished, a phenomenon known as receptor adaptation.

Examine the rate of ascent (slope) of the stimulus. A gradually increasing stimulus leads to accommodation, resulting in a reduced likelihood of action potential (AP) generation.

• Graph A: Most effective stimuli for generating AP (rapidly increasing stimuli, eliminating the possibility of Na channel accommodation).
• Graph B: Least effective stimuli for generating AP from the given options (slowest rising stimuli, thus increasing the chance of Na channel accommodation).

Check the rate of rise (slope) of stimulus. Slowly rising stimulus produces accommodation, so chance of AP development is less.
Graph A: Best stimuli to produce AP (rapidly rising stimuli, no chance of Na channel accommodation).
Graph B: Least effective stimuli to produce AP, among the options provided (slowest rising stimuli among the provided options, so chance of Na channel accommodation).

Patients experiencing paresthesias (unusual sensations such as burning or tingling) typically have a diminished ability to perceive cutaneous sensations (like pain and temperature). This is often due to the selective impairment of the small myelinated fibres responsible for transmitting these sensations.

• Paresthesia fundamentally involves the pain fibres, which are myelinated (Aδ).
• It is important to remember that A fibres are particularly vulnerable to pressure, although this does not equate to paresthesia.

Superficial pain is associated with A delta fibers. In contrast, visceral pain and deep pain are linked to C fibers. This likely arises from a relative shortage of Aδ nerve fibers in deeper tissues, resulting in minimal rapid, sharp pain.

Spike durations are as follows:

• C: 2 ms
• B: 1.2 ms
• A: 0.4 to 0.5 ms