Unit 3 - lower motor neurons

motor unit

motor neuron, its axon, and all the muscle fibers it innervates

upper motor neuron

originate in motor cortex and synapse onto LMNs

lower motor neuron

directly innervate skeletal muscles

motor system receives input from

many structures and systems like sensory feedback and extrapyramidal structures

corticospinal tract

main path driving muscles of the body

corticobulbar/corticobrainstem tract

drives muscles of the face

LMNs found in the spinal cord

located in ventral horn of spinal cord and control myotomes

LMNs found in brainstem motor nuclei

CN 3-12, innervate muscles

LMNs are known as the

final common pathway in the control of movement (final snip of information from nervous system to the muscle)

LMN need

input

LMN structure is

multipolar, many sources converge

LMNs have interneuons that

are excitatory or inhibitory

LMN reflexive inputs

spinal (deep tendon) or supraspinal (from brain) reflexes

LMNs have descending control for

voluntary movement and muscle tone

in the spinal cord, lower motor neurons are primarily located in the

ventral horn of gray matter

if a movement is reflexive

the afferent signal never reaches the cortex to become aware of the sensation and voluntarily move

lower motor neurons can be found in

the brainstem or spinal cord

alpha LMN

innervate extrafusal fibers, large, fast, myelinated axons

alpha LMN activate to

cause a muscle contraction

gamma LMN innervate

intrafusal fibers in the muscle spindle, smaller myelinated axon

gamma LMN modulate

how sensitive the muscle spindles are, keep them taut to trigger contractions with stretch

alpha and gamma LMN cell bodies are in

ventral horn

LMN diseases include

trauma, demyelination, infection, chronic neuropathy, radiculopathy or PNS injury like neurpraxia, axonotmesis, neurotmesis

signs/symptoms of LMN disease

decreased/loss of stretch reflexes, weakness/paralysis, decreased resistance to passive movement and muscle tone, fasciculation and fibrillations, denervation atrophy

damage to LMN results in denervation by

muscular atrophy from disuse, and eventual muscle replaced by fat and connective tissue

denervation atrophy

muscle cells need innervation by LMN, remain viable for a year but eventually die off, other trophic changes will occur (protein/gene expression changes cause remaining muscles to shrink)

fibrillation

spontaneous brief contraction of individual muscle fibers, not visible, and always abnormal/pathologic (ALS can cause these)

fasciculation

involuntary twitching of whole motor unit, visible, non-pathologic or pathologic

nonpathologic causes of fasciculation

anxiety, stress, caffeine

pathologic cause of fasciculation

demyelination and ectopic foci causing abnormal action potentials in axon, hyperexctiability of MNs

polio is a

disease of LMN - collateral sprouting tries to compensate but unable to support - less MN for the fiber causes atrophy and deformities

UMNs innervate

LMNs to produce voluntary control

UMN cell bodies are

primarily in primary motor cortex