Week 2.5 Flashcards
final common pathway
contains LMNs and peripheral mechanism mediating all motor activity
-includes CN’s and spinal nerves
direct activation pathway
UMN system and also known as pyramidal tract or direct motor system
-two divisions (corticobulbar tract-CNs)
(corticospinal tract- spinal nerves)
indirect activation pathway
also known as extrapyramidal tract or indirect motor system and is the source of input for LMNs
-mediates subconscious automatic muscle activities
control circuits
do not have direct contact with LMNs (final common pathway)
-coordinates and controls movements by integrating sensory information
-sensory and basal ganglia
what are extrafusal muscle fibers
contractile elements of skeletal muscles
motor unit
motor neuron + all the muscle fibers it innervates
innervation ratio
number of muscle fibers innervated by a single motor neuron
effects of damage to final common pathway
-prevents normal activation of muscle fibers
-may lead to weakness or paresis. If muscle is deprived of inout from all of its LMNs it results in paralysis
-flaccid dysarthria (many will experience fasciculations)
what happens with paralysis as a result of damage to LMNs
muscle atrophy (losing bulk)
fasciculations (brief, localized twitches to muscle fibers)
reduced muscle tone
hyporeflexia (reduced reflexes)
fibrillations
primary motor cortex
top of pyramidal tract and main launching motor platform for direct motor system
direct activation pathway
-responsible for conscious, skilled, voluntary movements
-contain corticobulbar (to brainstem) and corticospinal tracts
-fibers are arranged in a fanlike mass of fibers (corona radiate) and then this converges into internal capsule
effects of damage to direct pathway
weakness not as bad as LMN damage, but decreased muscle tone due to UMN innervations are bilateral
-result in dysarthria
unilateral: weakness on other side of body and may be hyporeflexia or reflexes are preserved
bilateral: involves both direct and indirect pathways
UMN innervation of trigeminal (V), facial (VII) upper face, glossopharyngeal (IX), vagus (X), and accessory (XI)
bilateral
-won’t lose all function if weakness is on one side (50% from left and 50% from right)
UMN innervation for lower facial and hypoglossal (XII)
contralateral
-ex: damage to left UMN, you see right side of tongue will be impacted and face
lower motor neuron lesion
paralysis of ipsilateral upper and lower facial musculature (unable to raise eyebrows or smile on side of lesion)
upper motor neuron lesion
paralysis of contralateral lower facial musculature (unable to smile on both sides, but can raise eyebrows)
what is a major sign of paralysis for UMN lesions
if the wrinkle is not present
indirect activation pathway
country road to direct pathways
-responsible for mediating reflexes and other automatic movements
-maintaining posture
-facilitating direct pathway
effects of damage to indirect pathway
hyperreflexia and spasticity
-hyperadduction of vocal folds (mild if unilateral but severe if bilateral)
-impact on speech (spasticity will slow speech, spastic dysarthria with bilateral UMN lesion and unilateral if damage is one side)
decorticate rigidity
damage above midbrain to corticoreticular fibers (descending pathways can be disinhibited resulting in increase extension of tone of legs and increase of flexion tone of arms
decerebrate rigidity
damage at level of midbrain and resulting in excitation of all extensor muscles
neural control circuits
in charge of integration and control of movements
-basal ganglia and cerebellar control circuits (regulate UMNs and through that, communicate with LMNs)
cerebellar control circuits
1) flocculonodular lobe: connections to vestibular system
function: modulate equilibrium, eye movement
2) body: mid portion (vermis), anterior and posterior lobes
function: proprioception, coordinati skilled, sequential voluntary movements
effects of cerebellar damage: flocculonodular lesions
truncal ataxia (inability to stand or sit without swaying or falling, gait disturbances)
