UMNL vs LMNL

Question 1

Upper motor neuron lesions

Answer 1

2 tracts:
– corticospinal tract (cortex–>spinal cord, anterior grey horn)

– corticobulbar tract (cortex–>bulb of the brainstem)
—- when there is damage to the corticobulbar tract, its called a pseudo bulbar palsy

Upper motor neurons start within the motor areas of the cerebral cortex.
– the corticospinal will move from the cerebral cortex and give off their axons to the spinal cord, which can then be send to musculoskeletal muscles as a lower motor neuron

– the corticobulbar will move from the cerebral cortex and give its axons to specific cranial nerve nuclei located in the pons and the medulla

Question 2

Lower motor neuron lesions

Answer 2

2 start points:
– anterior grey horn- skeletal muscles
– cranial nerve nuclei:
—- CN5- muscles of mastication
—- CN7- muscles of facial expression
—- Nucleus ambiguous- CN9, CN10, CN11 (pharynx, larynx all muscles for speech and articulations)
—- CN12- muscles of tongue

Lower motor neurons are the end points of the upper motor neurons (corticospinal and corticobulbar)

Question 3

Causes of upper motor neuron lesions

Answer 3

Stroke

Demyelinating disease:
– MS
– Fredericks ataxia
– B12 deficiency

Amyotrophic lateral sclerosis

Question 4

Causes of lower motor neuron lesions

Answer 4

Damage to anterior grey horns:
– polio
– West Nile virus
– spinal muscular atrophy

Damage to axon itself:
– cauda equina syndrome (herniated disc)
– piriformis syndrome
– peripheral neuropathy (neuropraxia, axonotmesis, neurotmesis)
—- can be caused by diabetes (diabetic neuropathy)

Damage to axon terminal:
– botulism
– ALS can also damage lower motor neurons

Question 5

Symptoms differentiating upper vs lower motor neuron lesions

Answer 5

Upper motor neuron lesions:
– weakness
– disuse atrophy (unable to activate the nerve, leading to a disuse atrophy)
– no fasciculations
– hyperreflexia
– hypertonia

Lower motor neuron lesions:
– weakness
– atrophy
– fasciculations
– hyporeflexia
– hypotonia