Motor Pathways Flashcards
Lower Motor Neurons: Inputs
- come from three hierarchal sources:
1. Reflex pathways- produce stereotyped movements in response to specific stimuli
2. Pattern generators - interneuron groups produce movement combos (grasping)
- simple, repetitive movements (e.g. walking, breathing).
3. Descending Upper motor neuron pathways - allow higher brain regions to control motor activity
- minute posture adjustments to goal-directed movements.
- produce stereotyped movements in response to specific stimuli
Lower Motor Neurons: Location
-α-motor neurons: neurons w/ axons directly innervating muscle
-Found in ventral horn of spinal cord gray matter
*and in certain cranial nerve nuclei in the brainstem
-Axons exit spinal cord in the ventral roots
*travel w/ spinal nerves to skeletal muscle.
The axons of brainstem LMNs course with cranial nerves to innervate skeletal muscle of head & neck.
Lower Motor Neurons: Convergence on single LMN
- Multiple excitatory & inhibitory inputs converge on a single LMN
- Firing rate of LMN determined by spatial & temporal integration of inputs.
- All motor commands are conveyed to the muscles by LMNs:
- “final common pathway” for motor control
Lower Motor Neurons: Somatotopic Organization
- somatotopically organized in the ventral horn of the spinal cord
- LMNs innervating the trunk & proximal muscles of extremities:
- located in medial ventral horn.
- LMNs that innervate the distal muscles of the limbs
- located in the lateral part of the ventral horn.
Upper Motor Neurons: Location
- neurons in the cerebral cortex/brainstem
- axons form tracts that descend to the spinal cord
- influence the activity of LMNs
Upper Motor Neurons: Function
- Descending pathways control the activity of LMNs
- directly
- Indirect via interneurons of reflexes & simple pattern generators
- Descending motor pathways:
- medial and lateral descending systems
lesion of lower motor neurons
- denervates skeletal muscle.
- produces flaccid paralysis of the affected muscle(s)
- flaccid b/c denervated muscle can’t receive signals to contract
- Flaccidity is characterized by
- reduced muscle tone (hypotonia).
- reduced or absent myotatic reflex.
- rapid atrophy of the affected muscle(s)
lesion of upper motor neurons
- clinically means lesion of the neurons or axons of the LCST
- produces spastic paralysis of the affected muscles.
- The lesion does not denervate skeletal muscle
- LMNs from damaged UMNs still connected to muscle(s).
- w/o control from UMNs, LMNs have enhanced reflex activity.
- Increased LMN activity produces spasticity in affected muscle(s).
- Spasticity is characterized by
- increased resting muscle tone (hypertonia).
- increased resistance to passive movement.
- hyperactive myotatic reflexes (hyperreflexia).
- return of primitive reflex normally inhibited by supraspinal input
- Ex. Babinski sign
- slow muscle atrophy due to disuse
- can be minimized with physical therapy
Lateral Descending Motor System
- 2 crossed tracts: fibers cross before reaching the spinal cord
- descend on the contralateral side
- In the spinal cord, the tracts course in the lateral funiculus
- Axons synapse directly or via an interneuron on LMNs in the lateral portion of the ventral horn
- innervate the distal muscles of the limbs
- Interneurons associated w/ the lateral descending system have short axons
- communicate w/ a small number of LMNs.
- allows lateral descending system to control individual muscles.
- Function: controls fine, skilled movements of distal limb muscles
Medial Descending Motor System
- Tracts course in the anterior funiculus of the spinal cord
- Axons synapse directly or via an interneuron on LMNs in the medial portion of the ventral horn
- innervate the axial (trunk & neck) and proximal limb muscles.
- Interneurons have long axons that span several cord segments
- project to both sides
- control movements involving groups of muscles on both sides
- regardless of tracts being crossed, uncrossed or bilateral
- Unilateral lesions do not produce obvious neurological deficits.
- Function: controls axial & proximal musculature
- maintain posture and balance.
Lateral Corticospinal Tract (LCST): Origin
- Neurons giving rise to the corticospinal tract are located in the cerebral cortex
- primary motor cortex (>50% of corticospinal fibers arise here)
- premotor and supplementary motor cortex
- somatosensory cortex.
Lateral Corticospinal Tract (LCST): Course
- fibers descend ipsilaterally thru the forebrain & brainstem.
- Fibers course in the:
- corona radiata (white matter below the cerebral cortex)
- posterior limb of the internal capsule
- crus cerebri of the midbrain (middle 1/3)
- basilar pons
- medullary pyramids.
- Corss at the spinomedullary junction (90% of fibers)
- pass dorsolaterally
- Forms the lateral corticospinal tract.
- Fibers that don’t cross continue down ipsilaterally as anterior corticospinal tract
- LCST descends in the lateral funiculus of the spinal cord
Lateral Corticospinal Tract (LCST): Termination
LMNs & interneurons in the lateral part of the ventral horn at all levels of the spinal cord.
Lateral Corticospinal Tract (LCST): Function
Mediates fine movements of the distal limbs (skilled voluntary movements.)
Anterior Corticospinal Tract (ACST)
- Same origin and initial course as the LCST
- 1˚ motor cortex, premotor cortex and somatosensory cortex
- Course:
- LCST & ACST descend in ipsilateral:
- corona radiata
- internal capsule
- crus cerebri
- basilar pons
- pyramids.
- tracts are indistinguishable
- referred to collectively as the corticospinal tract
- At spinomedullay junction, 10% of the fibers don’t cross midline.
- The non-crossing fibers continue descending ipsilaterally in the anterior funiculus as the ACST
Rubrospinal Tract (RST)
- part of the lateral descending system.
- originates in the red nucleus of the midbrain.
- Course:
- Fibers cross at their site of origin in the midbrain.
- descends in the lateral funiculus, close to the LCST.
- It extends only to cervical spinal cord levels.
- Function: facilitates activity of LMNs of the upper limb flexors.
- lesions of RST are not associated w/ clinical motor deficits
- B/c the RST’s functions are also carried out by the LCST.
Vestibulospinal Tracts
- Two vestibulospinal tracts arise in the vestibular nuclei of the upper medulla and pons
- descend in the anterior funiculus of the spinal cord.
- Lateral Vestibulospinal Tract
- part of the medial descending system
- facilitates extensor muscles of the upper & lower limbs.
- important for maintaining balance–
- righting reflex: vestibular system detects that one is falling.
- Medial Vestibulospinal Tract
- extends only to the cervical spinal cord.
- coordinates head movts w/ eye movts when changing gaze
Reticulospinal Tracts
- Two reticulospinal tracts originate in the reticular formation of pons & medulla
- descend in the anterior funiculus.
- Pontine reticulospinal tract
- facilitates axial & proximal muscles for posture & adjustments.
- may contribute to locomotor control.
- Medullary Reticulospinal Tract
- inhibitory influence on axial and proximal limb musculature.
- may be involved in producing muscle atonia during sleep.
Lesion to Corticospinal tract above the pontomedullary junction
- before the decussation of the LCST fibers
- UMN signs will be observed on the contralateral side of the body. Examples:
- Primary motor cortex
- Medial hemisphere- weakness of contralateral lower limb
- lateral aspect-weak contralateral upper limb, trunk & lower face
- Posterior limb of internal capsule, crus cerebri or basilar pons-
- weakness of entire contralateral body & lower face
- Medullary pyramid- weakness of contralateral body
- face is spared
lesion of the LCST in the spinal cord
- UMN clinical signs on ipsilateral side of the body
- muscles innervated by segments below the lesion
- Damage to LCST in cervical cord- affects ipsilateral upper limb, trunk and lower limb
- Damage to LCST in upper lumbar cord- affects ipsilateral lower limb
Poliomyelitis
- caused by a neurotrophic virus
- paralytic polio (<1% of infections)
- the virus damages lower motor neurons; rarely symmetrically.
- causes rapid-onset, usually asymmetric weakness, muscle atrophy, loss of muscle tone & myotatic reflexes
- sensory loss is rare.
- Disease can affect CN motor nuclei and/or phrenic nerve nuclei
- weakness of facial musculature & breathing difficulty
Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease)
- although rare, is the most common motor neuron disease
- occurs most frequently in males over age 50.
- Pathology:
- Progressive, bilat degeneration of upper & lower motor neurons
- Typically present with weakness and both UMN & LMN signs
- Sensory and mental status exam are typically normal.
- LMN signs: muscle wasting (atrophy), fasciculations
- UMN signs: increased tone, hyperreflexia, Babinski sign
- Sensory and mental status exam are typically normal
- Eye muscles are typically spared as the disease progresses.
Decerebrate rigidity:
- caused by transection of brainstem near pons/midbrain junction
- disrupts almost all of the descending UMN pathways
- spares the LVST since the lateral vestibular nucleus is located in the upper medulla/lower pons.
- characterized by exaggerated extensor posturing of limbs, due to the unopposed action of the LVST.