SC Corticospinal Pathways/LMN Flashcards
Descending pathways control voluntary motion and consist of what 2 types of neurons?
Upper motor neurons (UMN)
Lower motor neurons (LMN)
Function of UMNs
Influence lower motor neurons to control voluntary body movements
What tracts do UMNs run in?
Corticospinal tracts (aka Pyramidal tracts)
UMNs begin their course in gray matter of _____ gyrus which is the primary motor cortex
Precentral
From the precentral gyrus, what is the order of UMNs descent?
Precentral gyrus Internal capsule in cerebrum Peduncles in midbrain Anterior pons Medullary pyramids
85% of UMN fibers cross at the pyramidal decussation at the _____ junction
The crossed fibers run in the ____ tract while the 15% of uncrossed fibers run in the _____ tract
Spinomedullary
Lateral corticospinal; anterior corticospinal
The lateral corticospinal tract (crossed UMNs) is located in the posterior half of the _____ ____ of the spinal cord; UMNs in this tract synapse at ______ or with ________
Lateral funiculus; interneurons; LMN cell bodies in ventral horn
The anterior corticospinal tract (uncrossed UMNs) continues in the _____ ____ of the spinal cord. These UMNs preferentially synapse with nuclei of _________
Anterior funiculus; axial skeletal muscle
T/F: isolated damage to the anterior corticospinal tract does not lead to any obvious signs/symptoms
True (bc only 15% of the UMN fibers are in this tract)
Signs/symptoms of UMN lesion
Spastic paralysis/paresis
Hypertonia
Hyperreflexia
Clonus
Rigidity
Disuse atrophy
(+) Babinskis
Define clonus
Rapid series of alternating muscle contractions in response to sudden stretch
Difference between rigidity and spasticity
Rigidity = non-velocity dependent increase in resistance to passive motion in ALL directions
Spasticity = velocity-dependent increase in resistance to passive movement, typically in specific direction
What is the + babinskis sign seen with UMN lesion?
Upward extension of hallux and fanning of toes when plantar surface of foot is stroked
Other characteristics of UMN damage in terms of distribution of paralysis, DTR changes, and specific reflexes
Paralyzes movements in hemiplegic, quadruplegic, or paraplegic distribution, not just individual muscles
Hyperactive DTRs
Absent abdominal cremasteric reflexes
Causes of UMN lesions/damage
Strokes
Spinal cord trauma
How would you localize UMN lesions based on location of decussation?
Lesions above decussation —> contralateral signs/symptoms at and below level of lesion
Lesions below decussation —> ipsilateral signs/symptoms at and below the level of lesion
Define function of LMNs
Final effectors of motor system (final common pathway)
LMNs start at lower motor neuron motor nuclei in the ____ horn of the SC, then synapse directly in ____
Ventral; skeletal m
2 types of LMN fibers
Somatic efferent = directly innervate skeletal m.
Special visceral efferent=motor innervation to muscles of pharyngeal arches including CN V, VII, IX, X, and ???
Somatic efferent LMNs have cell bodies in ventral horn of SC, exit via anterior root and pass into spinal nerve. Their activity is influenced by UMNs and segmental afferent inputs (reflexes)
What are the 2 types of somatic efferent LMN fibers?
Alpha (extrafusal) = innervates skeletal muscle fibers; voluntary, postural, and reflex motion
Gamma (intrafusal) = innervates muscle spindles; sensitivity and activity reflex threshold adjusted by UMNs
Topographic arrangement of LMN cell bodies in ventral horn of SC — what is the location of axial muscles vs. proximal muscles vs. distal muscles?
Axial muscles most medially
Distal musculature laterally
Proximal muscles located between axial and distal muscles
Topographic arrangement of LMN cell bodies in ventral horn of SC — which levels innervate extremities? Flexors vs. extensors?
C4-T1 and L1-S2 innervate extremities
Extensors are located more anterior
Flexors are located more posterior
Symptoms of LMN lesions
Flaccid paralysis Areflexia Atonia Atrophy Fasciculations
The areflexia seen with LMN lesion is d/t absence of the _____ component of reflex arc
Efferent
The atonia seen with LMN lesions is d/t loss of ____ motor neuron activity leading to loss of tone
Gamma
Why do fasciculations occur with lesions to LMNs?
Muscles are denervated, causing motor endplates to increase their sensitivity, and any small amounts of ACh floating around can cause slight contraction at the muscle
Other characteristics of LMN lesions in terms of paralysis distribution and DTR changes
Paralyzes individual muscles or sets of muscles in root of peripheral nerve distribution
Hypoactive or absent DTRs
Different types of damage to LMNs can cause different symptoms, what results from damage to motor neurons in ventral root vs. damage to nerve roots themselves vs. damage to entire peripheral nerve?
Damage to motor neurons in ventral root —> motor signs ONLY, sensation intact
Damage to nerve roots themselves —> mixed motor and sensory = radiculopathy
Damage to peripheral nerve —> weakness in specific muscle groups + decreased sensation in peripheral nerve distribution = neuropathy
Primary example of damage to LMN motor neurons in ventral root
Poliomyelitis
Poliovirus leads to destruction of ventral horn motor cell bodies
Clinical presentation = paresis and paralysis in asymmetric pattern, decreased or absent tone and reflexes, sensory exam almost always normal
Signs/symptoms of damage to LMN nerve roots themselves
Mixed motor and sensory = radiculopathy
Decreased sensation in dermatomal pattern
Weakness in muscles innervated by level involved
+/- decreased DTRs depending on level
Localizing lesions to the corticospinal tract, specifically the motor cortex, can be done using the homunculus, as well as the arterial supply. What changes would you see with an anterior cerebral artery infarct vs. middle cerebral artery infarct?
ACA —> contralateral LE > UE
MCA —> contralateral face and UE > LE
Localizing lesions to the corticospinal tract, specifically the posterior limb of the internal capsule, can be done using the arterial supply of this area. What is the arterial supply and what effect would damage to this artery have?
Lenticular striate artery; damage —> face, LE, and UE affected, causing contralateral complete hemiparesis
Localizing lesions to the corticospinal tract after a spinal cord injury can be difficult. The patient initially presents with spinal shock, with ______ motor neuron signs/symptoms lasting from about 1 week to 2 months. Tone and reflexes later return, leading to _____ motor neuron symptoms like spastic paresis depending on area of lesion. These can be unilateral or bilateral
lower; upper
Group of disorders of the CNS characterized by aberrant control of movement/posture present since early in life and NOT the result of progressive or degenerative disease
Cerebral palsy
Subtypes of CP and corresponding brain area affected
Spastic = cerebral cortex Dyskinetic = basal ganglia Ataxic = cerebellum Mixed = multiple areas
Causes of CP
Neonatal stroke Prenatal circulatory disturbance Congenital infection Brain maldevelopment Perinatal asphyxia
Most common subtype of CP and symptoms
Spastic — spasticity, hyperreflexia, clonus, babinskis sign
Subtypes of spastic CP
Spastic hemiplegia = one side affected
Spastic diplegia = LEs affected with little to no UE involvement
Spastic quadruplegia = all limbs affected
Rapidly progressive disease with asymmetric mix of UMN and LMN signs; pathophysiology unknown
Amyotrophic lateral sclerosis (ALS)
Describe UMN and LMN involvement in ALS
UMN = degeneration of motor neurons in primary motor cortex + axons throughout corticospinal/corticobulbar tracts; causes weakness, hyperreflexia, spasticity
LMN = degeneration of ventral horn cells; causes weakness, atrophy, fasciculations
Besides the corticospinal tract, what are 4 other descending (extrapyramidal) motor tracts?
Reticulospinal tract
Rubrospinal tract
Tectospinal tract
Vestibulospinal tract
The reticulospinal tract operates through which 2 motor pathways?
Pontine reticular pathway = activates antigravity reflexes in erect position
Medullary reticulospinal pathway = mediates cortical control of reflexes (inhibits postural or flexor reflexes that may interfere with voluntary motor activity)
Which extrapyramidal motor tract mediates voluntary motion, most notably flexor movements of the arms, and originates in the red nucleus of the midbrain?
Rubrospinal tract
[note: small in humans]
Which extrapyramidal motor tract coordinates movement of the head with eyes and originates in the superior colliculus?
Tectospinal tract
Which extrapyramidal motor tract maintains posture against gravity, most notably the trunk and UE/LE extensors, and originates in the vestibular cortex?
Vestibulospinal tract
