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*1. Anatomical and Physiological evidence for paresis
- conscious movement from motor cortex and CST, which provide fast and direct drive to
motoneuron pools in spinal cord
- CST originates in output layer of motor cortex (layer 5)  axons through posterior limb of
internal capsule  cerebral peduncles in ventral midbrain  cross midline below pyramids
of medulla  lateral CST in spinal cord (lateral funiculus)  terminate on interneurons in
intermediate zone of spinal cord  terminate on motoneurons
- some fibers don’t cross below pyramids, but instead cross in anterior commissure of spinal
cord
Anatomy of the Upper Motor Neuron (UMN)
- LMNs receive as much as a 100,000 inputs arising from several source
- two sources include sensory and spinal cord central pattern generators (CPG)
- LMNs receive input from UMNs (traveling in the brainstem and spinal cord, corticospinal
tract (CST) is for intentional input to LMN for action)
*2. Three other tracts exist:
1. Rubrospinal tract from red nucleus to midbrain
2. Reticulospinal tract from medial/lateral reticular formation in pons/medulla;
important for activating locomotor CPG
3. Lateral vestibulospinal tract from the lateral vestibular nuclei in medulla; activate
anti-gravity muscles for postural responses
- Each brainstem nuclei receives input from motor cortex (corticobulbar)
- CST carries axons with cell bodies in motor cortex, premotor cortex, and supplementary
motor cortex ( and primary sensory cortex and postcentral gyrus to spinal cord); premotor and
supplementary motor areas are anterior to motor cortex; CST  direct input to LMNs
- lesion of CST at cortex or internal capsule (posterior limb) interrupts most outputs from
cortex; if lesion is at caudal medulla  CST damaged, but brainstem descending pathways
(corticobulbar fibers) are uninterrupted
*3.,4. - Weakness results from damage anywhere along tract from motor cortex to spinal cord
- Strength deficits following CST lesions greater for distal than proximal muscles
- LMNs supplying proximal muscles have only 1/3 of inputs from motor cortex
- LMNs supplying distal muscles (intrinsic muscles of hand) depend on motor cortex for 90%
of the inputs; this is why lesions of motor cortex have a permanent impairment on distal
(finger) movements
- The vestibulospinal, rubrospinal, and reticulospinal tracts (w/ CST) contribute relatively
equally to drive proximal motoneurons for proximal muscle control
- Distal motoneurons input mostly from CST; monosynaptic connections from motor cortex to
distal hand muscles (direct control); motor cortex has a specialized function for fine finger
movement control because:
1. Humans have skilled hand functions
2. The hand is complicated and has a flexibility of actions
This is why lesions of CST/motor cortex have a permanent impairment on distal (fine finger)
movements
5. UMN syndrome
- from spinal cord injury, multiple sclerosis, cerebral palsy, blood supply interruption to motor
cortex, internal capsule, cerebral peduncles, and brainstem motor areas
- Typical symptoms  weakness or paralysis and Babinski (dorsiflexion of toe)  2-3 weeks
later, reflexes become over exaggerated
- increased reflexes include tendon tap responses
- spasticity develops and becomes exaggerated  exaggerated response to passive stretch at a
joint; when a quick stretch is applied to a joint  joint will resist being stretched (especially a
fast stretch) and have a slowing of the imposed movement; spasticity occurs in anti-gravity
muscles (flexors of arm and extensors of leg); spasticity is unidirectional (it is not rigidity)
Immediate hyperactive reflexes
- result of a release mechanism in which normal inhibition provided by UMN is lost
- Babinski sign infers a release from inhibition; usually Babinski is suppressed
- During normal volitional movement some muscles need to be activated, but others need to be
inhibited; An individual muscle needs to be active during part of a movement and inhibited
during another part; stimulation of CST can produce inhibitory and excitatory effects on
muscles
- UMN lesion  greater loss of inhibition; less inhibitory NT, glycine, in spinal cord following
UMN lesion
- Reduced inhibition  alpha motoneurons are more excitable and respond greater to inputs,
such as sensory input; stretch input brings motoneurons to TH at lower levels  exaggerated
reflex response
Long term exaggerated reflexes and spasticity
- reflexes become increasingly exaggerated and spasticity worsens due to adaptive, local
changes in the spinal cord
Possible causes
1. Gradual changes in membrane properties of motoneurons. Intrinsic firing properties of
motoneurons altered (lower TH for firing); cells lose surface area  less channels  increased
resistance  V=IR  larger EPSP (lower TH); LMNs can become more excitable as the
become smaller; stretch reflex  motoneuron responds vigorously  exaggerated response of
spasticity
2. Denervation supersensitivity develops in post-synaptic receptors on motoneurons, which
develop sensitivity to released NT; caused by upregulation of receptors expressed in postsynapse. May occur in LMN due to a loss of CST input: increased receptors  LMN has
enhanced response when NT is released  exaggerated response
3. Collateral sprouting – new branches of intact axons innervate LMNs; other neurons
innervating same target cell grow new collaterals to synapse over old sites where the
denervated neuron made synapses
Example: Spindle afferents sprout onto vacant CST synapses  spindle afferent have more
synapses and more NT release  larger EPSP  exaggerated response to stretch