4) Corticospinal Pathways and Lower Motor Neurons Flashcards
Differentiate upper and lower motor neurons.
Upper motor neurons influence lower motor neurons to control voluntary movements of the body (run in pyramidal/corticospinal tracts)
Lower motor neurons are the final effectors, starts at LMN motor nuclei in ventral horn of spinal cord and ends at muscle
Differentiate somatic efferent from special visceral efferent motor fibers.
Somatic Efferent - Directly innervate skeletal muscles
Preganglionic fiber synapse on cell bodies in peripheral visceromotor ganglion, they’re short in sympathetic, long in parasympathetic
What are the two different types of somatic efferent LMN? What does each one do?
Alpha - innervates skeletal muscle fibers (extrafusal) – Voluntary, postural, and reflex motion
Gamma - innervates muscle spindles (intrafusal) – UMNs adjusts sensitivity and activity of Gamma neurons, thus adjusting threshold of muscle spindle to influence reflex. Activity dependent – If UMN control is lost, Muscle spindle becomes more sensitive -> UMN signs and symptoms
How are the ventral horns specifically arranged? (What type of musculature at which parts)
Topographic arrangement of LMN cell bodies – Axial Muscles -most medial – Proximal musculature medially – Distal Musculature laterally
C4-T1 and L1-S2 levels innervate extremities: – Extensors Anterior – Flexors Posterior
Lower motor lesions can lead to several things such as:
Flaccid paralysis, areflexia, atonia, atrophy, and fasciculations… define these
Flaccid Paralysis- Muscle completely limp with inability to contract
Areflexia- absence of efferent component of the reflex arc
Atonia- Loss of Gamma motor neuron activity leading to loss of tone
Atrophy- Loss of stimulation to muscle fibers leading to denervation atrophic changes
Fasciculations-Denervation leading to increased sensitivity of motor end plates causing “twitching
Polio virus can lead to what?
Describe polio
Can lead to destruction of the ventral horn motor cell bodies (motor bodies)
Pathogenesis – 90-95% infections are asymptomatic – 4-8% develop short viral syndrome- 2-4 days
Fever, myalgia, HAs, etc – .1% develop paralytic polio
Clinical Presentation- Paresis and Paralysis in an Asymmetric pattern – Decreased or absent Tone and Reflexes – Sensory exam almost always Normal
Treatment- Supportive- prevention gold standard (vaccine)
Describe the path of the corticospinal tract.
Originates in grey matter of precentral gyrus of primary motor cortex.
Fibers descend through, Internal capsule in Cerebrum – Peduncles in midbrain – Anterior Pons – Medullary Pyramids
85% of fibers cross at the spinomedullary junction… lateral corticospinal tract crosses, anterior does not.
Describe the lateral corticospinal tract.
85% of corticospinal tract, crossed fibers. Located in Posterior half of the lateral funiculus of the spinal cord. Terminates at synapses with interneurons or directly on LMNs in the ventral horn
Influences and modulates LMN activity to control motion of the body
Describe the anterior corticospinal tract.
Remaining 15% uncrossed fibers that continue in the anterior funiculus of the spinal cord. Preferentially synapse and terminates to nuclei of axial skeletal muscles
Isolated damage typically doesn’t result in obvious signs
Upper motor neuron lesion can lead to the following clinical presentations.
Define: Spastic paralysis, hypertonia, hyperreflexia, clonus, rigidity, disuse atrophy, Babinskis
Spastic Paralysis/Paresis- Velocity dependent increase resistance to passive movement, typically in a specific direction
Hypertonia-Increased resting muscle tone due to loss of inhibition from corticospinal tract
Hyperreflexia- Increase in reflex due to loss of inhibition from corticospinal tract
Clonus-Rapid series of alternating muscle contractions in response to sudden stretch
Rigidity-Non-velocity dependent increase in resistance to passive motion in ALL directions
Disuse Atrophy- decreased muscle, less severe than LMN
(+) Babinksis-Upward (extension) motion of the hallux when plantar surface of the foot is stroked
Two common causes of lesion to the corticospinal tract
Cerebrovascular accidents (strokes)
Spinal cord trauma
When trying to localize the lesion in the tract, describe the presentation when the lesion is above decussation vs. when it is below
Above decussation- contralateral signs and symptoms at, and below level of lesion. Below- ipsilateral signs and symptoms at, and below level of lesion
Blood supply to the motor cortex is supplied by the anterior cerebral and middle cerebral arteries, clinically what happens when each is compromised?
ACA- contralateral LE>UE
MCA- Contralateral face and UE>LE
What is spinal shock?
LMN damage that lasts from about 1 wk to 2 months
Symptoms vary greatly dependent on damage to spinal cord.
What is cerebral palsy? What is it caused by?
Definition- Group of disorders of the CNS characterized by aberrant control of movement or posture – Present since early in life and NOT result of progressive or degenerative disease. Clinical presentation based on area of CNS affected
Causes- Neonatal stroke, prenatal circulatory disturbances, congenital infections, brain maldevelopment, Perinatal asphyxia
