Lecture 6: Descending Motor Pathways Flashcards Preview

Control Term 2 > Lecture 6: Descending Motor Pathways > Flashcards

Flashcards in Lecture 6: Descending Motor Pathways Deck (13):

What is an upper motor neuron?

Starts in CNS and synapses with either cranial nerve nucleus or in the ventral grey horn of the spinal cord.


What is a lower motor neuron?

Axons of LMNs pass from the ventral grey horn of the spinal cord (CNS) and cranial nerve motor nuclei brain stem (CNS) to muscles. From the spinal cord they will run in spinal nerves and from the brain stem they will run in cranial nerves.


What are the consequences of LMN lesions?

- Muscle wasting
- Muscle weakness/reduced power
- Hypotonia
- Absent tendon reflexes
- Fasciculation/fibrillation


What are the two types of UMN pathways?

- corticospinal (cortex to spine - spinal nerves) - corticobulbar (cortex to brainstem - cranial nerves)


What are the functions of UMNs?

- Influence LMN activity
- Modify local reflexes
- Superimpose more complex more complex patterns of movement


What happens after damage to the corticospinal tract only?

- flaccid paralysis of opposite limbs
- loss of tendon reflexes

After several days to a week motor function - - recovers but hypertonia

Long term
- Spasticity
- Hyperreflexia

Left with permanent inability to carry out fine movements of hands and feet

Other pathways appear to take over most “corticospinal” functions


Where do descending fibres for the body pass through the internal capsule?

The posterior limb.


Where do descending fibres for the face pass through the internal capsule?



What percentage of UMNs descending contralaterally?



Where do UMNs contact cell bodies of the LMNs?

Contralateral ventral grey horn


What is the corticobulbar pathway?

- Influences LMNs in cranial
nerve motor nuclei
- Fibres originate laterally
within pre-central gyrus
- Innervation of LMNs is largely
bilateral (unlike corticospinal
pathway), with one/two exceptions (facial and hypoglossal).


Describe the innervation of the hypoglossal nerve nucleus.



Why does a facial nerve lesion result in total ipsilateral face paralysis whereas internal capsule damage results in contralateral lower face paralysis?

The eyes and forehead receive innervation from both hemispheres, while the lower face only receives innervation from the contralateral hemisphere

The strictly contralateral innervation of the lower half of the face and dual innervation of the upper half of the face is critical when assessing facial weakness. Lesions that damage the motor cortex, such as acute ischemic strokes, will result in contralateral facial weakness of the lower face only, with preservation of the muscles of the upper face on both sides, due to the dual innervation of the upper face. Patients will have a weak smile, but will be able to close their eye tightly and wrinkle their forehead symmetrically. This pattern is often referred to as “central facial weakness,” because it’s caused by injury to the cerebral cortex, which is a part of the central nervous system.
Lesions that damage the facial nerve in the brainstem, or after it exits the brainstem, result in ipsilateral facial weakness involving both the upper and lower face. It doesn’t matter where the innervation is coming from; if the nerve is damaged, all the muscles on that side of the face are weak. These lesions are referred to as “peripheral lesions” because they affect the facial nerve as it exits the brainstem. Patients will be unable to wrinkle their forehead, tightly close their eye, or smile on the affected side. This distinction can aid in localizing the lesion to the appropriate place in the nervous system, thereby narrowing the differential diagnosis.