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66 Cards in this Set

  • Front
  • Back
What structures are considered higher motor structures?
cortex, cerebellum, and basal ganglia
What structures are considered lower motor control structures?
Spinal cord & brainstem
What are higher motor structures and what is their function?
planning of voluntary actions
What are lower motor structures and what is their function?
Spinal Cord, Brainstem

Execution of movements, automatic movements
What are some examples of automatic movements?
Postural control, respiration, reflexes
What are the 3 major descending motor pathways?
Ventromedial brainstem pathway
Lateral brainstem pathway
Corticospinal pathway
From what nuclei does the ventromedial brainstem pathway arise & what are the individual tracts called?
Superior colliculus (midbrain) --> Tectospinal tract
Reticular formation (Pons/Medulla) --> Reticulospinal tract
Vestibular nuclei (Medulla) --> Vestibulospinal tract
What muscles are targeted by the tracts of the ventromedial brainstem pathway?
Axial (trunk) muscles

Especially activates the extensors
From what nucleus does the lateral brainstem pathway arise and what is its tract called?
Red nucleus --> Rubrospinal tract
What muscles are targeted by the lateral brainstem pathway?
Proximal and girdle muscles (upper limb)

Especially activates the flexors
From where does the corticospinal pathway originate and what is its tract called?
Cerebral cortex and corticospinal tract
What runs along with the rostral corticospinal tract?
Corticobulbar tract
From where does the corticobulbar tract originate and what is its target?
Cerebral cortex --> Cranial motor nuclei in the brainstem
What functions are mediated by the tectospinal tract and superior colliculus?
Coordination of eye and head movements
What functions are mediated by the ventromedial pathway?
Balance and posture
The corticospinal and corticobulbar tracts are considered what types of tracts?
Pyramidal tracts
Which are the extrapyramidal tracts?
Rubrospinal Tract (Lateral Brainstem Path)

Tectospinal, Vestibulospinal, Reticulospinal Tracts (Ventromedial Path)
Which tracts do not decussate?
Reticulospinal and Vestibulospinal Tracts
What path does the corticospinal tract run from cerebral cortex to the spinal cord?
Cerebral cortex --> Internal Capsule --> Cerebral peduncles --> Medullary Pyramids --> Decussate at the Spinomedullary Jxn --> Lateral funiculus of the spinal cord
Where do corticobulbar fibers decussate?
At the level of the cranial nerve nuclei that they innervate
What functions are mediated by the corticospinal pathway?
Voluntary movements, fine, precise, skilled actions
What muscles do corticospinal fibers target?
Widely distributed, overlapping the projections of the ventromedial and lateral brainstem pathways

*Also target the distal limbs (legs, hands)*
Onto what neurons do corticospinal fibers terminate?
Mostly interneurons in the intermediate, ventral gray

Fibers targeting distal muscles terminate *directly* on motor neurons (e.g. finger muscles)
What is an upper motor neuron?
A neuron whose axon descends in one of the descending pathways
What is a lower motor neuron?
A neuron that projects directly to a muscle (e.g. cranial nerve motor neuron)

alpha motor neuron
How prevalent are individual tract lesions?
Not prevalent - usually all are damaged; expect a compilation of signs to present
Name the upper motor neuron signs (aka. long tract signs)
Paresis without atrophy (unless from disuse)
Groups of muscles affected
No fibrillations or fasciculations
Spasticity (after weeks)
Babinski sign

*Clinical signs are contralateral to the lesion, unless lesion is bilateral*
What is paresis?
What is plegia?
How would you expect a patient to present if he/she has a limited cortical or corticospinal tract lesion?
Individual movements of limbs and trunk preserved, but with diminished speed, agility, and power

Paresis and clumsiness of hand movements ("clumsy hand syndrome")

*Clinical signs are contralateral to the lesion, unless lesion is bilateral*
What is spasticity?
Hyperreflexia, hypertonia (especially in antigravity mm)
When does spasticity occur?
Only occurs with lesions in the CNS (*not seen in peripheral neuropathy*)

Manifests weeks after damage to long motor tracts
Immediately after upper motor neuron damage, what clinical finding could confuse your diagnosis?
Pt will present initially with hypotonia and hyporeflexia, which counters an expected presentation of spasticity
What is clonus?
rhythmic, repetitive, involuntary muscle contractions due to sudden stretching of the muscle

Indicative of upper motor neuron damage - CNS failing to inhibit contractions
What does a positive Babinski sign indicate?
Damage specifically to the corticospinal tract
What other clinical test will reveal corticospinal tract damage?
Failure in rapid hand movement test
What is decerebrate rigidity and what is its cause?
Caused by midbrain lesions

Lower brainstem and spinal cord receive no input from forebrain and midbrain, leaving the vestibulospinal and reticulospinal tracts unregulated
How does decerebrate rigidity present clinically?
Person has a posture of exaggerated extension of all four limbs because axial extensors activated by vestibulospinal/reticulospinal tracts, proximal extensors activated by lesion to rubrospinal tract, and distal extensors activated by lesion to corticospinal tract

All four limbs extended
What is decorticate rigidity and what is its cause?
Caused by large scale lesions to the cerebral cortex

Lateral brainstem pathway left intact, providing a net flexor drive to the upper limbs
What is the clinical presentation of decorticate rigidity?
Arms can flex, legs cannot
What is the clinical presentation of damage to all three descending pathways?
Death :(
What are some causes of decerebrate rigidity?
syringobulbia - formation of a syrinx (cystic cavity) around the 4th ventricle

syringomyelia - formation of a syrinx around the central canal of the spinal cord

midbrain tumor

midbrain stroke (basilar)
Explain the pathology of locked-in syndrome
Caused by bilateral ventral pontine lesions (e.g. basilar infarct), resulting:

- bilateral transection of long descending cortical fibers (quadraplegia)
- damage to CN VI, VII, IX, X, XII (no horizontal eye mvmt, facial mvmt, speech)
What functions are left intact in a person with locked-in syndrome?
vertical eye movements and blinking (CN III)
What functions are generated by the primary motor cortex?
Skilled, voluntary, finely graded movement

Direction, speed, and amplitude of movement
What is the function of supplementary motor cortex (area 6)?
Motor planning
From where does the motor cortex (areas 4, 6) receive inputs?
VL Thalamus (basal ganglia, cerebellum)
Somatic Sensory Cortex
Parietal Association cortex
Brainstem & Basal Forebrain
What is the function of the parietal association cortex?
receive inputs from auditory somatosensory, higher visual, prefrontal cortical areas
To where does the motor cortex send its outputs?
Cortico-striatal projection to Basal ganglia
Cortico-ponto-cerebellar projection to Pons
Descending motor pathways (3)
VL Thalamus
Parietal Association cortex
Somatic Sensory cortex
A patient comes into the ED presenting with bilateral leg weakness. What are potential causes of this presentation?
Damage along the falx cerebri:
- Meningeal tumor on the medial surface of the cerebral hemispheres
- Infarct of an ACA branch

Spinal Cord Injury (more likely):
- Herniated disk
Damage to what structure is the most likely cause for paresis of both arms and/or legs?
Spinal cord
Lesions to what area causes apraxias?
Supplementary Motor Area (medial of area 6)

Pre-motor Area (lateral part of area 6)

Posterior Parietal Cortex
What is an apraxia?
*Loss of the ability to perform a pre-learned task,* even though:

The request or command is understood
Pt is willing to perform the task
The muscles needed to perform the task are intact
Pt does not have sensory loss
A supranuclear lesion to CN VII nucleus cause will what clinical presentation?
Will interrupt all the corticobulbar input to the muscles of the LOWER HALF of the face

Only the upper part of the face can still be voluntarily activated by the remaining ipsilateral corticobulbar projection
A nuclear lesion to CN VII nucleus will cause what clinical presentation?
Paresis or plegia of the entire face because nucleus cannot register stimulus from ipsilateral nor contralateral corticobulbar fibers
An infranuclear lesion with respect to the CN VII nucleus will cause what clinical presentation?
Paresis or plegia of the entire face because axons traveling to the face are damaged
Which artery supplies the area of the motor cortex projecting to the face, arm, and hands?
Middle cerebral artery (MCA)
Which artery supplies the part of the motor cortex projecting to the foot and legs?
Anterior cerebral artery (ACA)
Which structures does the basilar artery and/or its branches supply?
Cerebral peduncles, midbrain tegmentum, pons (pontine arteries), cerebellum (AICA)
What is the blood supply for the medulla?
Vertebrals and vertebro-basilar junction
What is the blood supply for the spinal cord
Anterior and posterior spinal arteries?
From where do the anterior and posterior spinal arteries receive their blood supply?
Primarily from vertebral arteries; also from various branches of the aorta
From where does the internal capsule receive its blood supply?
Middle cerebral artery
From where do the basal ganglia receive their blood supply?
Middle cerebral artery
What is the peri-Rolandic cortex?
Synonymous with the sensory-motor cortex; all of the cortical areas involved in motor control
How can the cortex control its own sensory input?
Via the corticospinal axons that originate in the parietal sensory cortex and project to sensory relay structures (dorsal horn/dorsal column nuclei)