Corticospinal tract Flashcards
(35 cards)
Organization related to the neural control of movement
In the spinal cord and brainstem, lower motor neurons directly innervate muscle
Lower motor neurons are controlled by local circuits within spinal cord and brainstem, AND by upper motor neurons
Basal ganglia and cerebellum regulate upper motor neurons
where lower and upper motor neuron cell bodies are located
Lower motor neuron cell bodies located:
- Ventral horn of the spinal cord (IX)
- Brainstem motor nuclei
- 2 types of lower motor neurons innervate skeletal muscle: Alpha and Gamma motor neurons
Upper motor neuron cell bodies located:
- Cortex (Corticospinal)
- Cortex (Corticobulbar)
- Vestibular nuclei (Vestibulospinal)
- Superior colliculus (Tectospinal)
- Reticular formation (Reticulospinal)
- Red nucleus (Rubrospinal)
Cranial nerves having a GSE component…
have lower motor neurons in there somewhere
alpha and gamma LMNs
usually travel together, because as you are activating muscles you need to have proprioception as well (the gamma motor neuron does that)
corticobulbar is related to
our facial muscles
The LMN pools in RL IX show anatomic and functional segregation
α-MNs and γ-MNs are scattered in different LMN pools
Flexors and extensors are segregated (relatively) dorsal to ventral
Humuncular organization from axial muscles to extremeties, medial to lateral
Interneurons have different properties whether they innervate axial or limb lower motor neurons
Axial more medial, bilateral, many collaterals
Limb more lateral, unilateral, less collaterals
One LMN, many muscle fibers
A single alpha motor neuron and all the muscle fibers it innervates = “motor unit”
*increasing or decreasing the # of motor units changes the amount of force produced by a muscle
Motor units differ in the types of muscle fibers that they innervate
Slow motor units
Fast fatigable motor units
Fast fatigue-resistant motor units
slow motor units
very red, lots of myoglobin, always recruited first, basic postural muscles
fast fatigable motor units
- Larger, pale muscle fibers (few mitochondria)
- Larger Alpha motor neurons
- Large force
Easily fatigued
Brief exertions that require large forces (eg. jumping)
Fast fatigue-resistant motor units
Between slow motor units and fast fatigable motor units (aka intermediate motor units)
run / walk units
Reflex circuits and muscle tone
Muscle tone is the resting level of tension in a muscle
Allows muscle to make an optimal response to voluntary or reflexive movement by keeping them in a state of readiness to resist stretch
Lower Motor Neurons are often active in reflex pathways without any upper motor neuron involvement
Denervation causes atrophy
Denervation activates both apoptosis pathways and autophagy pathways in skeletal muscle
Muscle mass decreases rapidly Capillary supply decreases Muscle fibers degenerate, replaced by fatty and fibrous tissue Loss of contractile proteins Fibrous tissue can cause contracture
sarcopenia
In aging (sarcopenia), believed that atrophy is caused by denervation
- Muscle end plate changes in aging
- – Vacated motor end plates are innervated by collaterals of adjacent motor neurons, abnormal EMG (electromyogram) signature
- – “giant motor units” (often pathological sign)
- Reduction in LMNs from the spinal cord and periphery beginning ~ 60 yrs
- Muscle morphological changes seen in aging look like changes seen from denervation
How do we save our denervating muscle?
Improving coordination between activated muscles
More efficient innervation of the “right” combination of activating agonists and inhibiting antagonists with training
Greater discharge rates of alpha motor neurons can increase load-bearing without necessarily increasing muscle mass
Training with light loads can reduce the variability of muscle activation, specifically of slow fibers
IGF1 pathway
helps counteract the autophagy and the apoptosis going on in the muscle
It in turn activates the PI(3)K pathway and the AKT1 pathway
Typical signs of lower motor neuron damage
Paralysis or paresis
Areflexia
- Loss of muscle tone (related to areflexia)
Atrophy
- Due to denervation and disuse
Fibrillations
- Rapid twitching due to change in muscle fiber excitability denotes pathology (if an EMG picks up twitching but you dont’ feel it. More diagnostic of a LMN syndrome)
Fasciculations
- Local, small twitch due to alpha motor neuron damage
Demonstration of LMN properties: Polio and Post-Polio Syndrome
Poliomyelitis specifically affects LMNs.
- Flaccid paralysis
- Hypo/areflexia
These symptoms can disappear for a time because the vacated LMN had been compensated for (giant motor units)
In aging, these other neurons begin to degenerate/denervate skeletal muscle, so weakness is more pronounced, once again
pyramidal means
they are going to go to the medullary pyramids.
usually the pyramids are indicative of a coricospinal pathway (?)
4 brainstem pathways: extrapyramidal
Vestibular (vestibulospinal) Reticular formation (reticulospinal) Red nucleus (rubrospinal) Superior colliculus (tectospinal)
3 cortical pathways: pyramidal
Lateral corticospinal
Ventral corticospinal
Corticobulbar
Vestibulospinal tract
From lateral or medial vestibular nuclei
-Lateral: Ipsilateral, posture, antigravity, includes extensors (lower spinal cord) (specifically legs)
Medial: Ipsilateral, head position stability (cervical cord)
Medial Longitudinal Fasciculus
Tectospinal
From superior colliculus
- Decussates
- To cervical spinal cord
- Affect musculature of neck, eyes
- Postural reflexes to alarming visual stimuli, some auditory stimuli
where it decussates is not particularly important.
