Lecture 2 Study Questions Flashcards

1
Q

How do corticospinal tracts that control distal limb vs. axial muscles differ anatomically?

A

First, the neurons that control distal limbs primarily originate in the more lateral region of the primary motor cortex whereas the neurons that control axial muscles primarily originate more medially.

Axons that control the distal muscles travel in the lateral corticospinal tract after decussating at the medullary pyramids. After decussating, they will travel in the spinal cord and innervate motor neurons in the lateral portion of the ventral horn.

Axons that control the axial muscles travel in the anterior corticospinal tract and decussate in the spinal cord just before they synapse with lower motor neurons. Anterior corticospinal tract synapses with motor neurons in the medial ventral horn.

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2
Q

Understand the layout of dorsal and ventral roots bridging peripheral nerves and spinal cord segments.

A

Dorsal roots lie more posterior the spinal cord whereas ventral roots lie more anterior. Rootlets converge to form mixed spinal nerves outside of the CNS.

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3
Q

What are dorsal rootlets, ventral rootlets, and where are they?

A

Dorsal and ventral rootlets are branches of sensory and motor neurons that lie just outside of the spinal cord, near their respective horns.

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4
Q

Explain the anatomical reasons why the spinal cord has cervical and lumbar enlargements.

A

The spinal cord has cervical and lumbar enlargements as it must hold the gray matter for motor innervation of the arms and legs. As there is less motor innervation for the axial muscles, such enlargements are not observed in the thoracic region.

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5
Q

Describe how the paths of roots differ in cervical segments vs. progressively more distal segments.

A

In the cervical segments, spinal nerve roots exit the spinal cord transversely. As we analyze the spinal nerve roots distal to the cervical segments, we notice that the spinal nerve roots exit the spinal cord more inferiorly. This is logical as the spinal nerve roots of the lumbar and sacral segments must innervate the lower limbs which are distal to the lumbar and sacral segments.

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6
Q

Motoneurons with axons exiting via the L5 root have cell bodies in which spinal cord segments?

A

Motoneurons with axons exiting via the L5 root have their cell bodies located in the ventral horn of the spinal cord segments L4 to S1. Specifically, the cell bodies of these motoneurons are found in the anterior horn of the gray matter within this range of spinal cord segments.

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7
Q

Describe the major difference in the spinal pathways carrying pain vs. proprioceptive sensations.

A

The spinothalamic pathway is responsible for perceiving pain whereas the dorsal column medial lemniscal pathway is responsible for proprioceptive sensation. The pathways differ in where they cross the midline and where the first order neuron synapses. The spinothalamic pathway’s first order neuron immediately synapses onto a second order neuron within the dorsal horn. The spinothalamic pathway crosses the midline immediately at the spinal cord segment. The dorsal column medial lemniscal pathway’s first order neuron enters the spinal cord via the dorsal horn and then ascends ipsilaterally to synapse onto a second order neuron in the medulla. At the medullary pyramids, the DCML crosses the midline.

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8
Q

What are spinal dermatomes? Why are dermatomes clinically important when diagnosing a SCI?

A

Spinal dermatomes are sensory regions on a human that have been determined to be innervated by a specific nerve root. Clinicians assess patient sensation and, using their knowledge of spinal dermatomes, determine which spinal nerve roots have been affected after spinal cord injury.

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9
Q

What is dermatomal overlap? How is the overlap clinically evident in diagnosing cases of SCI?

A

Dermatomal overlap refers to how a sensory region can be innervated by multiple nerve roots. As such, a sensory region may still experience some sensation if only one of the nerve roots that innervate the area is affected by the injury. For example, the C6 dermatome may still have sensation from contributions of the C5 nerve root. This redundancy is a protective measure to ensure that if one spinal nerve is damaged, the area of skin it supplies doesn’t lose complete sensation.

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10
Q

Dermatomes overlap, but the territories of individual peripheral nerves don’t overlap. Why not?

A

Peripheral nerves have precise and independent innervation. Peripheral nerves combine fibres from multiple spinal nerves. The lack of redundancy facilitates targeted motor control and localized sensory perception.

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11
Q

Review the main differences in spinal and peripheral pathways of somatic vs. autonomic neurons.

A

Both somatic neurons and autonomic neurons have afferents that enter the dorsal horn of the spinal cord. From here, they synapse onto interneurons within the spinal cord. The interneurons synapse onto efferents of the somatic and autonomic pathways. Beginning here is where they differ. Somatic efferents travel directly to their target skeletal muscle. Autonomic efferents from the spinal cord synapse onto another efferent within the autonomic ganglia chain. This efferent exits the autonomic ganglia chain and acts on the autonomic smooth muscle.

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12
Q

Review the spinal and para-spinal pathways in the sympathetic vs. parasympathetic systems.

A

Sympathetic systems
- Preganglionic neurons (first order) are in the lateral horn of the spinal cord in the thoracolumbar region. Exit the spinal cord through the ventral root of the corresponding spinal nerve then synapse onto the chain of sympathetic ganglia.
- Postganglionic neurons (second order) project directly onto visceral organs (heart, liver,intestines, kidneys)
- Some preganglionic fibres do not synapse onto the sympathetic chain ganglia and travel via the splanchnic nerve. They innervate smooth muscles in blood vessels, cardiac muscles, sweat glands, and smooth muscles of the bronchi. The splanchnic nerve carries afferent and efferent visceral fibers.

Parasympathetic systems
- Preganglionic neurons originate from the brainstem or in the sacral spinal cord (S2-S4). The axons of preganglionic neurons exit via cranial nerve CN III, CN VII, CN IX, CN X.
- Post ganglionic neurons are located in the ganglia close to the target organ.
- The axons of the sacral spinal cord (S2-S4) are sent through the pelvic splanchnic nerves to innervate the lower parts of the digestive system.

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13
Q

What are the typical acute neurological consequences of spinal cord injuries?

A

Spinal shock: transitory suspension of function and reflexes (areflexia) below the level of injury - can cause severe bradycardia and hypotension due to unopposed parasympathetic outflow through the intact vagal nerve.
- Flaccid paralysis of all muscles below the level of SCI (if complete transection)
- Loss of sensation at and below the level of SCI
- If incomplete, there can be some remaining motor and sensory connectivity

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14
Q

What are the typical chronic neurological consequences of spinal cord injuries?

A

If SCI occurs above splanchnic sympathetic outflow (T5-T6), autonomic dysreflexia is observed in the chronic phase after spinal shock resolution.

Noxious stimuli below the level of injury will trigger a massive reflex sympathetic discharge. There will be a severe rise in blood pressure below the level of injury that will not be corrected by the parasympathetic system due to injury. However, baroreceptors in the carotid sinus and aortic arch will detect the blood pressure and activate the parasympathetic nervous system. Due to the spinal cord injury, the parasympathetic signals will only affect the areas above the level of injury. This is why the individual experiences bradycardia and flushing but hypertension below the level of injury.

The individual will also experience hyperreflexia which is stronger than normal reflexes. They may observe hyperreflexia and a positive Babinski sign (big toe extension). Spasticity will also be observed. Paraesthesia below the level of SCI if incomplete are possible.

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15
Q

If a SCI is “above C4, breathe no more”. Explain why.

A

The phrenic nerve arises mainly from the C4 spinal cord segment, with contributions from C3 and C5. It innervates the diaphragm, which is the major muscle involved in respiration. A spinal cord injury above C4 will result in the diaphragm losing its ability to contract, leading to the inability to breathe effectively on one’s own.

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16
Q

What are the reasons for differences in acute vs. chronic consequences of spinal cord injuries?

A

Overtime, the surviving fibres sprout collaterals to take over sites vacated by transected axons. There is an increase in afferent input and thus an increase in gain in stretch reflexes. This leads to tremors with sensory input. This is the reason why spasticity is observed.

SCI also result in reduced excitability in the interneurons that modulate spinal reflex pathways. As such, the interneurons are less likely to inhibit the antagonist muscle and hyperreflexia can be observed.

17
Q

Why do increasing numbers of quadriplegic individuals have incomplete injuries nowadays?

A

Advancements in health care have resulted in the increased preservation of function in those with spinal cord injuries. This includes better immobilization and stabilization techniques immediately after spinal cord injuries. Additionally, medical care (surgical, steroid, rehabilitation, patient education), has also advanced. This results in increased patient independence and ability.

18
Q

What nerve fibers comprise a motor nerve?

A

Myelinated efferent fibres. Somatic motor fibres innervate skeletal muscles. Autonomic motor fibers innervate involuntary muscles.

19
Q

What nerve fibers comprise a sensory nerve?

A

Somatic afferent fibres send information to the CNS regarding skin, temperature, vibration, and proprioception. Visceral sensory afferent nerves (enteroreceptors) innervate smooth and cardiac muscles.

20
Q

Review the anatomical location of dorsal root ganglia and what this means in terms of differences in the peripheral axon and the central axon of sensory afferent neurons.

A

Dorsal root ganglia reside within the peripheral nervous system just outside the dorsal horn. The peripheral axon extends from the sensory receptors in the skin, muscles, or organs to the cell body in the DRG. It transmits sensory information such as pain, temperature, touch, and proprioception from the peripheral tissues to the DRG.

The central axon extends from the DRG cell body into the dorsal horn of the spinal cord and it transmits the sensory information from the DRG to the CNS where it can be processed and integrated.
Peripheral axons are generally longer as they must reach from the periphery to the DRG, sometimes over long distances, depending on the location of the sensory receptors (e.g., toes vs. hands). Central axons are shorter as they travel directly from the DRG to the spinal cord.
Peripheral axons have a higher regenerative capacity compared to central axons. If damaged, peripheral nerves can often regenerate and reinnervate target tissues, whereas central axons have a limited ability to regenerate due to the inhibitory environment in the CNS.

21
Q

What are the ipsilateral and contralateral signs of a complete SC hemi-section at T5?

A
  • Weakness or paralysis distal to T5 on ipsilateral side
    • T6 is approximately level with bottom of sternum
    • Corticospinal tract affected
  • Loss of proprioception, vibration, and fine touch below T5 on ipsilateral side
    • Dorsal column medial lemniscus is affected
  • Loss of pain and temperature below T5 on contralateral side
    • Spinothalamic tract affected
22
Q

How have leg stretch reflexes changed in the next few days after a thoracic level SC vs after several months?

A

Initially, the individual suffers from spinal shock which is complete loss of reflexes (areflexia) and flaccid paralysis of muscles.

Overtime, the surviving fibres sprout collaterals to take over sites vacated by transected axons. There is an increase in afferent input and thus an increase in gain in stretch reflexes. This leads to tremors with sensory input. This is the reason why spasticity is observed.

SCI result in reduced excitability in the interneurons that modulate spinal reflex pathways. As such, the interneurons are less likely to inhibit the antagonist muscle and hyperreflexia can be observed. Clonus, rhythmic muscle oscillations, can be observed

23
Q

How does autonomic regulation change after a spinal cord injury at C5? SCI at T5? SCI at L5?

A

C5: Complete loss of sympathetic control as it originates from spinal segments T1 - L2
- Hypotension, bradycardia, dysregulated blood pressure response (autonomic dysreflexia)
- loss of control of the uterus, bladder, genitalia.

T5:
- Acute: loss of function below the level of injury
- Chronic: autonomic dysreflexia
- Noxious stimuli below the level of injury will result in extreme sympathetic discharge including peripheral vasoconstriction below level of injury. This will result in hypertension.
- Baroreceptors will sense hypertension and activate the parasympathetic nervous system resulting in vasodilation of vessels above the level of injury (including face → flushing) and bradycardia. However, severe hypertension will still persist below the level of injury.
- loss of control of the uterus, bladder, genitalia.

L5: loss of parasympathetic control of the uterus, bladder, genitalia due to splanchnic nerve affected

24
Q

How is the control of bladder and bowel functions changed after a SCI? Why?

A

Loss of bladder control and bowel function as it is denervated. Inability to retain urine, and fecal matter or the inability to excrete it depending on the level of injury. Loss of sensation in the area can lead to festering infections. Urinary tract infections, kidney damage and bowel impaction can occur.

25
Q

Why are persons with SCI affected by sudden changes in body temperature and associated events?

A

This is because they lack the ability to regulate their temperature appropriately through the autonomic nervous system. The blood vessels cannot constrict or dilate properly leading to difficulty releasing excess body heat and conserving body heat. Below the level of SCI, sweating is impaired and so is the ability to shiver as they have lost motor control in those areas.

Sudden changes in body temperature can trigger autonomic dysreflexia if the SCI is at or above T6. Bradycardia and vasodilation and excessive sweating above the level of injury will occur. This can result in face flushing and a pounding headache. This can also cause fainting if the heart rate is too low