Module 7 - Lecture 4 - Clinical Conditions Affecting the PNS Flashcards
What are the main concepts of a peripheral nerve?
- What does it contain?
- What is it bound within?
- What information does it carry?
Peripheral nerves are bundles of axons of a bunch of individual neurons and surrounded by connective tissue layers.
- What does it contain? It contains both motor efferent and sensory afferents.
- What is it bound within? It is surrounded by the epineurium which is the dense outer layer of connective tissue supporting the nerve.
- What information does it carry? Motor and sensory nerves
How does the spinal nerves split when entering the spinal cord and what root contains what information?
The mixed spinal nerve contains mixed information until after enters the intervertebral foramen. At this point the spinal nerve splits into 2 roots as it enters the spinal cord:
- Dorsal Root = purely afferent sensory information
- Ventral Root= purely efferent motor information
What parts of the nervous system is responsible for myotomes and dermatomes?
Dermatomes signify the transfer of sensory information from a specific dorsal root of the spinal cord to the mixed Spinal nerve.
Myotomes signify the transfer of motor information from a specific ventral root of the spinal cord to the mixed Spinal nerve
*** - Regions of sensory AFFERENT information if it is a DERMATOME (that information that is being carried in the dorsal root of the particular spinal nerve) has a unique area of skin that it innervates. That allows for specific testing to see potentially what spinal nerve is damaged.
The idea of a MYOTOME, the particular muscles that have motor EFFERENT that is being sent to this ventral root.
What is the general formation, and separation of a plexus (spinal nerve, to trunk to a terminal branch) and speculate what “information” it might carry?
Spinal nerves from various levels converge and bundle together to form the trunks of a Plexus. These trunks then diverge to create terminal nerves with information from multiple spinal nerves. These terminal nerves then innervate very specific muscles or regions of skin of the region distal to said plexus. This causes the area to become very compartmentalized in regards to its innervation. A plexus typically contains both sensory and motor information.
For an appendicular nerve (ie median or femoral) what information does it contain, and what it innervates? Compare and contrast this with the spinal nerves.
An Appendicular nerve innervates very specific muscles or regions of the skin of the region distal to a plexus. For example, the Median nerve has a motor function for muscles in a specific area whereas the medial cutaneous nerve has a sensory function for a specific area of skin on the forearm. This is different from spinal nerves in that a very specific area of the limb is affected
What are the three names (specific and common) for 3 nerve injuries?
- Neurapraxia = Focal demyelination = Demyelination of the myelin in an area.
- Axonotmesis = Nerve crush injury . Denervation of the muscle fiber
- Neurotmesis = Severed/lacerated neuron. Nerve degenerates.
What is neurapraxia?
- Focal myelin injury
- Conduction block
Focal Demyelination = NEURAPRAXIA = Represents that some patch’s of myelin sheath along the axon are starting to deteriorate –> in these areas this will slow down the passive conductance… OR in severe cases or in cases where there might be local inflammation, this may in fact prevent/block conductance of AP propagation.
What is axonotmesis?
- Axonal injury
- Conduction block
- Denervation
Nerve crush = ANONOTMESIS = this injury can vary in severity. But in a severe state, if the axon is crushed and knowing the metabolic properties (the ability to form enzymes) is all occurring within the cell body. If the axon is to lose the connexion to the cell body, the axon might actually degenerate = WALLERIAN DEGENERATION. So in severe cases this axon can be fully compromised and no information can be propagated to it. Now, this muscle fiber that used to be connected to the lower motor neuron has lost its innervation –> DENERVATION of the muscle fiber.
What is neurotmesis?
- Injury to the axon and supporting connective tissue.
Nerve laceration = NEUROTMESIS = the cell body and the axon connected to it –> that can survive!!! However, any axon that was distal to the cell body has now lost the ability to generate enzymes, and it will degenerate. This prevents AP to propagate to the next step.
What are the key differences between upper and lower motor neuron syndrome?
UMNS:
- Weakness because you may not be able to excite the respective LMN.
- Hyperreflexia because the LMN do not have their descending inhibition. Can also lead to abnormal cutaneous reflexes and spasticity of the LMN.
LMNS:
- Hyporeflexia and hypotonia because muscle can’t be excited.
- Weakness and muscle wasting because muscle can’t be excited.
Name the 6 neurophysiological pathway dysfunctions that could lead to “weakness”.
- Spinal cord injury
- Motor neuron
- Spinal Nerve
- Peripheral Nerve
- Neuromuscular junction
- Muscle fiber
Name an example of each 6 neurophysiological pathway dysfunctions that could lead to “weakness”.
Spinal cord injury –> spinal cord lesion
Motor neuron –> Lou Gehrig’s disease
Spinal Nerve –> Guillain-Barre Syndrome
Peripheral Nerve –> Guillain-Barre Syndrome
Neuromuscular junction –> Myasthenia Gravis
Muscle fiber –> Muscular Dystrophy
Which of the 6 neurophysiological pathway dysfunctions that could lead to “weakness” have sensory deficits?
Spinal cord injury –> spinal cord lesion –> SENSORY SYMPTOMS
Motor neuron –> Lou Gehrig’s disease –> NO SENSORY INVOLVEMENT
Spinal Nerve –> Guillain-Barre Syndrome –> SENSORY SYMPTOMS = associated sensory symptoms in the same distribution - dermatome
Peripheral Nerve –> Guillain-Barre Syndrome –> SENSORY INVOLVEMENT = Sensory loss in the distribution of the affected nerves
Neuromuscular junction –> Myasthenia Gravis –> NO SENSORY SYMPTOMS
Muscle fiber –> Muscular Dystrophy –> NO SENSORY SYMPTOMS
What is the common presentation of spinal cord injury?
What is the common presentation of motor neuron injury?
What is the common presentation of ALS?
KEY CONCEPT = There are fewer motor units that are innervating the muscle fibers = the muscles get weak and waste away and an individual may have fatigue.
What is the common presentation of a spinal nerve injury?
What is the common presentation of a peripheral nerve injury?
What is the common presentation of the neuromuscular junction injury?
What is the common presentation of a muscle injury?
What is the common presentation of GBS?
What is the common presentation of MG?
What is the common presentation of MD?
How does nerve conduction testing change in latency (speed) and amplitude with axonal loss?
***Axonal Loss: Decrease amplitude due to axon loss, Speed remains unchanged.
Axonal loss = what would happen if we had a certain crush/cut that impaired some but not all of the axons within the neuron, we would expect that there are fewer axons in this recording area and the amplitude would decrease. Because it is just loss of axon and no features that are impairing the myelin or the passive conduction properties of AP propagation… you would still expect the time of which the signal would get to different points along the nerve would NOT be compromised.
How does nerve conduction testing change in latency (speed) and amplitude with generalized myelin injury?
*** Generalized Myelin injury: Amplitude remains unchanged, speed is slowed due to myelin loss.
C = Generalized myelin injury = very systematic that all of the axons contained within a nerve are injured, what you would expect is a general flowing. The idea that the AP may not be able to propagate as quickly and it requires the generation of more AP to continually boost its signal to send it along the nerve.
How does nerve conduction testing change in latency (speed) and amplitude with focal demyelination?
***Focal Demyelination: Speed Slowed and Amplitude decreased because of the arrival of the signals.
D = Focal demyelination = A nerve actually contains a variety of axons, some but not ALL may be undergoing demyelination. What would happen is that if you had focal demyelination is not only would you have a general slowing down but the rate at which any individual axon containing that information and how much it is slowing down could be different from one axon to another. What would happen then is you would have a diminished amplitude in the recorded electrode site but it is not because you have fewer axons excited or propagating their AP but the time at which they arrived at the recording electrode is now separating in time. –> THAT SEPERATION in AP arriving makes it as though the amplitude is reduced.
What happens with nerve conduction testing in individuals with MG?
With MG, the antibodies build up with repeated contraction!!!
- With electric diagnostic studies can do repetitive nerve stimulation…
○ Normal = expect that every time we excite the axon you would get excitation of the muscle fibers and the synaptic transmission would occur reliably.
○ Myasthenia Gravis –> with this repetitive nerve stimulation the antibodies will build up more and more… = with each excitation event more antibodies would build up and prevents the receptor from opening up its ion channel and the subsequent excitation of the muscle fiber gets lower and lower as fewer muscle fibers get activated by the AP being sent from the axon.
What happens with nerve conduction testing in individuals with MD?
Nerve conduction studies with muscular dystrophy…
- What happens is some of the muscle when the fibers are wasting away, they may randomly elicit some excitation –> these fibrillations as the muscle is starting to break down.
- The amplitude would decrease in size as fewer fibers are excited as we would activate a signal motor unit.
Eventually, the muscle fiber would not be able to record any AP –> in the advance stages of MD this nerve conduction study becomes “electrically silent” because you have non connective fat and connective tissue in the area.
