Lecture 4: Corticospinal Pathways and Lower Motor Neurons Flashcards
What is an Upper Motor Neuron (UMN), what tract do they utilize and where do they start/synapse?
- Influence the activity of lower motor neurons to control voluntary movement of body
- Corticospinal Tracts (AKA pyramidal) - Descending Tract
- Start in Primary Motor Cortex and end synapsing with interneurons or directly with lower motor neuron cell bodies
What is a Lower Motor Neuron; where do they start and end?
- Final Effectors of the motor systems
- Known as the “final common pathway”
- Starts at LMN motor nuclei in ventral horn of spinal cord and ends at muscle
What are the 2 types of LMN motor fibers?
- Somatic Efferent: directly innervate skeletal muscles
- Special Visceral Efferent (autonomics)
What are the LMN somatic efferent motor fibers; location of cell bodies and where do they synapse; activity influenced by?
- Directly innervate skeletal muscles
- Cell bodies in ventral horn of SC, exit in anterior root and pass into spinal nerve
- Synapse directly w/ skeletal muscle
- Activity influenced by UMN’s and segmental afferent inputs (i.e., Reflexes)
What are the LMN special visceral afferent fibers; where are the pre- an postganglionic fibers; innervate what?
- Preganglionic fibers synapse on cell bodes in peripheral visceromotor ganglion (short in sympathetic, long in parasympathetic)
- Postganglionic fibers innervate smooth muscle, cardiac muscle, and glandular epithelium
What are the 2 fiber types of somatic efferent LMN; what does each innervate?
-
Alpha - innervates skeletal muscle fibers (extrafusal)
- Voluntary, postural, and reflex motion - Gamma - innervates muscle spindles (intrafusal)
How do UMN’s control gamma neurons (fibers); what occurs if UMN control is lost?
- 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
*Muscle spindle loves to party and UMN is like the parent. When parent is away, the kids will play!
How are cell bodies of Axial, Proximal, and Distal musculature topographically arranged in LMN?
- Axial muscles - most medial
- Proximal (deltoid) muscles - medially
- Distal (fingers) muscles - laterally
Which spinal levels innervate the UE and LE’s, where are the flexors and extensors located in the ventral horn cell?
- C4-T1 for UE
- L1-S2 for LE
- Extensors located Anterior
- Flexors located Posterior
What are 5 clinical finidings associated with LMN lesions?
- Flaccid Paralysis
- Areflexia
- Atonia
- Atrophy
- Fasciculations
Damage to motor neuron and vental root of LMN will cause what problems?
Motor signs ONLY, sensation intact
Damage to nerve roots of LMN will cause what problems; what is a common example of this?
- Mixed motor and sensory (radiculopathy) - i.e., herniated disc
- Decreased sensation in specific dermatomal pattern
- Weakness in muscles innervated by the level involved
- +/- decreased DTRs depending on level
Damage to peripheral nerves (neuropathy) of LMN will cause what problems?
- Weakness in specific muscle groups
- Decreased sensation in peripheral nerve distribution
- Commonly seen in nerve entrapment
How can Polio infection lead to Poliomyelitis; what is the common clinical presentation (pattern, decreased what, sensory exam findings)?
- Poliovirus infection can lead to destruction of the ventral horn motor cell bodies
- Clinical presentation: Paresis and Paralysis in an ASYMMETRIC pattern
- Decreased or absent Tone and Reflexes
- Sensory exam almost always NORMAL
Where does the Corticospinal Tract originate and the UMN fibers descend through where?
- Originate in grey matter of precentral gyrus in the Primary Motor Cortex
- Fibers descend through:
- Internal capsule in Cerebrum
- Peduncles in midbrain*
- Anterior Pons*
- Medullary Pyramids*
85% of the fibers from the Corticospinal tract cross where; what about the other 15%?
- Cross at MEDULLARY Pyramidal Decussation at the Spinomedullary Junction
- 85% Lateral Corticospinal Tract - Crossed fibers
- 15% Anterior Corticospinal Tract - Uncrossed fibers
Damage above the Pyramidal Decussation of the Medulla leads to deficits on what side?
Damage above the crossing point = deficits on contralateral side
The lateral corticalspinal tract, consisting of 85% of the crossed fibers are located where in the spinal cord; where do these fibers synapse?
- 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
UMN fibers from the lateral corticospinal tract synapse directly on LMNs in the ventral horn and modulate what?
Influences and modulates LMN activity to control motion of body
The remaining 15% of uncrossed UMN fibers in the Anterior Corticospinal tract are found where in the spinal cord and where do they preferntially synapse?
- Continue in the anterior funiculus of the SC
- Preferntially synapse and terminates to nuclei of axial skeletal muscles
Isolated damage to the Anterior Corticospinal Tract usually results in?
Typically doesn’t result in obvious signs, becasue this only accounts for 15% of the fibers which went uncrossed.
What are 7 common clinical presentations of UMN lesions?
1) Spastic Paralysis/Paresis: is velocity dependent increase resistance to passive movement, in specific direction
2) Hypertonia: increased resting muscle tone due to loss of inhibition
3) Hyperreflexia: increase in reflex due to loss of inhibition
4) Clonus: rapid series of alternating muscle contractions in response to sudden stress
5) Rigidity: is non-velocity dependent increase in resistance to passive motion in ALL directions
6) Disuse Atrophy: decreased muscle, less severe than LMN
7) (+) Babinskis: upward (extension) motion of the hallux when plantar surface of the foot is stroked
What is the difference between Spastic Paralysis/Paresis and Rigidity?
Spastic Paralysis: is velocity dependent increase resistance to passive movement, typically in specific direction
Rigidity: is NON-velocity dependent increase resistance to passive movement in ALL directions
*BOTH can be present at same time, but they are NOT the same. Signs of UMN lesion
What are common causes of lesions to the Corticospinal Tract?
- Cerebrovascular Accidents (strokes)
- Spinal Cord Trauma
When localizing a lesion of the Corticospinal Tract what will be seen if above the decussation and what if below the decussation?
Above: will be contralateral signs and symptoms at, and below level of lesion
Below: will be ipsilateral signs and symptoms at, and below the level of lesion
Lesions to the motor cortex of corticospinal tract by the ACA and MCA will effect what parts of body?
- ACA: contralateral LE>UE
- MCA: contralateral face and UE >LE
Occlusion or lesion to the Lentricular Strate A., will affect what part of the corticospinal tract and ultimately lead to?
- Posterior limb of internal capsule
- Face = LE = UE
- Contralateral complete hemiparesis
Spinal cord injuries intially present with what? What occurs over time depending on level and severity of lesion?
- Initially present with Spinal Shock
- LMN signs and sx’s lasting about 1 wk - 2 mo.
- Tone and reflexes return leading to spastic paresis depending on level of lesion (severity of sx’s depend on extend of damage to SC)
- Can be unilateral or bilateral
What is Cerebral Palsy, what causes it and when does it present?
- Group of disorders of the CNS characterized by aberrant control of movment or posture
- Caused by: neonatal stroke, prenatal circulatory disturbances, congenital infections, brain maldevelopment, perinatal asphyxia
- Present early in life and NOT result of progressive or degenerative disease
What is Spastic Cerebral Palsy; what are signs and symptoms; what are 3 subtypes?
- Most common subtype of CP
- Presentation: Spasticity, Hyperreflexia, Clonus, Babinskis
Subtypes:
1) Spastic Hemiplegia: only one side affected
2) Spastic Diplegia: LEs affected with little to no UE involved
3) Spastic Quadriplegia: all limbs affected, children are often severely handicapped; increased risk of complications
Amyotrophic Lateral Sclerosis may be due to a defect in; what are the clinical features of this disease?
- Pathophysiology unknown, may be defect in glutamate metabolism
- Asymmetric MIX of UMN and LMN signs
- UMN: degeneration of motor neurons in the primary motor cortex as well as axons throughout corticospinal/corticobulbar tracts (weakness, hyperreflexia and spasticity)
- LMN: degeneration of Ventral horn cells (weakness, atrophy, fasciculations)
What is the extrapyramidal Pontine Reticular pathway used for?
Activates antigravity reflexes in erect position
What is the extrapyramidal Medullary reticulospinal pathway used for; how is it related to reflex hypersensitivity in UMN damage?
- Mediate cortical control of reflexes
- Inhibits postural or flexor reflexes that may interfere with execution of voluntary motor activity
- UMN damage –> loss of reflex inhibition —> Reflex Hypersensitivty –> UMN signs
What is the extrapyramidal Rubrospinal tract used for; originates where?
- Mediated voluntary motion, most notably flexor movement of the arms
- Originates in Red nucleus of midbrain (small in humans)
What is the extrapyramidal Tectospinal tract used for; originates where?
- Coordinates movement of head with eyes
- Originates in Superior colliculus
What is the extrapyramidal Vestibulospinal tract used for; originates where?
- Maintains posture against gravity, most notably, trunk and UE/LE extensors
- Originates in vestibular cortex
