Neuro: Lecture 8- Corticospinal

Question 1

Describe in detail the structure and function of the corticospinal tract.

Answer 1

1. Begins In pre central gyrus with 2 nuclei, one for axial muscles and one for the limb muscles
2. Descend into the internal capsule ➡into the brain stem ➡
3. At medulla 90% decussate (these are fibres that innervate the limbs)
   The axial fibres don’t decussate here
4. After leaving the brainstem the 2 fibres will run down the corticospinsl tract (anterior and lateral?
5. When they get to their level, the fibres of the anterior corticospinsl tract decussate through the anterior white commissure, before synapsing info the anterior horn of grey matter

A lesion anywhere between anterior horn and muscles would be a LMN lesion

2 neuron pathway

• Everyone’s drinking (motor) at Pres (pre central gyrus)
• everyone gets into the car (internal capsule)
• they drove for a while but lu (lateral fibres) need to throw up, so she gets out of car and crosses the road and throws up in an Egyptian restaurant (decussation at pyramids). 90% of Lus stomach contexts came out that day (90% fibres decussate)
• the rest of the car keeps driving till they reach their destination. (Corticospinsl tracts)
• when they get there they have to cross the raging white river to get into the bar (anterior white commisure)

Question 2

Describe how voluntary movement occurs

Answer 2

The primary motor pathway is the corticospinal tract

• the tract is crossed so that the left hemisphere controls movement on right half of body
• motor pathways consists of upper and lower motor neuron
• upper motor neurons originate in the pre central gyrus, decussate the medulla, descend in the lateral column of the spinal cord
• terminates on lower motor neurons in ventral horn
• lower motor neurone exit the CNS and innervate skeletal muscles via peripheral NS

Question 3

Give me a neuroanatomical description of a voluntary knee extension

Answer 3

• The cell body of the upper motor neurone is located in the pre central gyrus
• the axon decussates through the internal capsule, decussates in the medulla
• decsends through the lateral column of the spinal cord and terminates in the ventral horn
• cell body of the lower motor neurone is located in the ventral horn
• axon exits the CNS via ventral rootlets of spinal nerves and innervates skeletal muscles via peripheral nerves
• skeletal muscles contract to produce the force to extend the knee

Question 4

What would happen if there was a lesion of the left corticospinal tract (at the level of the cortex) produces what impairment?

Answer 4

Corticol damage to the left corticospinal tract causes upper motor neurone signs on the right face and body (arm, leg, and trunk, contralateral). Stroke is the most common cause of supra spinal damage to the corticospinal tract.

Behvaioural Tract lesions
-damage to the corticospinal tract, prior to decussation produces UMN signs and symptoms to the contralateral face and body
UMN signs:
-weakness (spastic paralysis)
-hyperreflexia (+ Babinski, clonus)- why? coz there is normally a neurone that stops the reflex after it happens but its damaged
-hypertonia: mpaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition.[2] These consequences result in abnormally increased muscle tone of symptomatic muscles

• Impairment is seen in the contralateral face coz CN 7 is crossed and the contralateral body because the UMN decussated in the medulla
• impairment is generalised to all body parts below the lesion level because the lateral corticospinal tracts is an efferent pathway

Question 5

Lesion of the right lateral corticospinal tract produces what impairment?

Behavioural explanation?

Neuroanatomical explanation

Answer 5

Damage to the right lateral corticospinal tract causes UMN signs and symptoms in the right (ipsilateral) side of the body, generalized below the lesion level.

Impairment is ipsilateral because the pathway decussated in the medulla. Impairment is generalized below the lesion level because it is an efferent pathway. The lateral corticospinal tract exists only at the level of the spinal cord.

Behavioural Explanation:
Damage to the lateral corticospinal tract, after to the decussation, produces ipsilateral UMN signs and symptoms, generalized below the lesion level.
Because the lesion involves UMNs that have already decussated, impairment is ipsilateral to the lesion. Impairment is generalized to all body parts below the
lesion level because
the lateral corticospinal
tract is an efferent
pathway.

Question 6

Lesion of the right ventral horn at L2-L4 produces what impairment?
behavioural explanation

Neuroanatomical explanation

Answer 6

Lesion of the right ventral horn at L2-4 produces LMN signs (weakness and atrophy) of the right hip flexion, adduction, and knee extension muscles.

Lesion of the ventral horn will damage the cell bodies of LMNs. L2-4 is the origin of femoral and obturator nerves which innervate the muscles of hip flexion, adduction, and knee extension. Because LMNs are uncrossed the impairment will be seen ipsilateral to the lesion.

Question 7

Case study
In the emergency room the patient’s wife reports her husband had a sudden onset slurring of speech, inability to stand from a chair because of the inability to accept body weight onto his right leg, and the inability to feed himself or drink with his right hand. On examination the right side of his face was hypotonic, he was drooling from the drooping right corner of his mouth, and he had lost the nasal labial fold on the right.

Damage to what system(s) is causing this patient’s problems?

Answer 7

Lesion of the left corticospinal tract above the level of the brainstem.

Lesion of the left corticospinal tract, prior to the decussation (corticobulbar tract): removed cortical input to cranial nerves serving the face which are crossed (hypotonia and drooping of right face with drooling).
Lesion of the left corticospinal tract, after the decussation: removal of cortical input to cervical (inability to feed himself or drink with his right hand) and lumbar regions of the cord (inability to stand from a chair because of the inability to accept body weight onto his right leg).
Pathophysiology: stroke involving the perfusion territory of the left middle cerebral artery (primary motor and sensory cortical areas).

Behavioural Explanation:
Damage to the corticospinal tract, prior to the decussation, produces UMN signs and symptoms to the contralateral face and contralateral body.

UMN signs:
Weakness (Spastic paralysis)
Hyperreflexia (+ Babinski, clonus)
Hypertonia

Neuoranatomical explanation
Impairment is seen in the contralateral face because the cranial nerves serving the face are crossed.
Impairment is seen in the contralateral body because the UMN decussated in the medulla.
Impairment is generalized to all body parts below the lesion level because the lateral corticospinal tract is an efferent pathway.

Question 8

Case 2
Imaging report: The CT image reveals a mass producing impingement of the lateral region of the right lateral column of the spinal cord at L1.

What signs and symptoms would be expected from this lesion?

Answer 8

A mass impinging the right lateral column at L1 would affect the lateral corticospinal tract. The size of the mass will determine the extent of damage. The lesion will produce UMN signs in the right leg from L1 down involving all leg muscles from the hip flexors down. If the lesion is complete, there will be paralysis. If the lesion is incomplete there will be paresis. In addition to weakness (paralysis or paresis), there will be hyperreflexia and hypertonia.

Common causes include penetrating injuries, lateral compression from tumors, and MS. 
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Ipsilateral upper motor neurons signs
generalized below the lesion level
	UMN signs
		Weakness (Spastic paralysis)
		Hyperreflexia (+ Babinski, clonus)
		Hypertonia