Week 2.5

Question 1

final common pathway

Answer 1

contains LMNs and peripheral mechanism mediating all motor activity
-includes CN’s and spinal nerves

Question 2

direct activation pathway

Answer 2

UMN system and also known as pyramidal tract or direct motor system
-two divisions (corticobulbar tract-CNs)
(corticospinal tract- spinal nerves)

Question 3

indirect activation pathway

Answer 3

also known as extrapyramidal tract or indirect motor system and is the source of input for LMNs
-mediates subconscious automatic muscle activities

Question 4

control circuits

Answer 4

do not have direct contact with LMNs (final common pathway)
-coordinates and controls movements by integrating sensory information
-sensory and basal ganglia

Question 5

what are extrafusal muscle fibers

Answer 5

contractile elements of skeletal muscles

Question 6

motor unit

Answer 6

motor neuron + all the muscle fibers it innervates

Question 7

innervation ratio

Answer 7

number of muscle fibers innervated by a single motor neuron

Question 8

effects of damage to final common pathway

Answer 8

-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)

Question 9

what happens with paralysis as a result of damage to LMNs

Answer 9

muscle atrophy (losing bulk)
fasciculations (brief, localized twitches to muscle fibers)
reduced muscle tone
hyporeflexia (reduced reflexes)
fibrillations

Question 10

primary motor cortex

Answer 10

top of pyramidal tract and main launching motor platform for direct motor system

Question 11

direct activation pathway

Answer 11

-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

Question 12

effects of damage to direct pathway

Answer 12

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

Question 13

UMN innervation of trigeminal (V), facial (VII) upper face, glossopharyngeal (IX), vagus (X), and accessory (XI)

Answer 13

bilateral
-won’t lose all function if weakness is on one side (50% from left and 50% from right)

Question 14

UMN innervation for lower facial and hypoglossal (XII)

Answer 14

contralateral
-ex: damage to left UMN, you see right side of tongue will be impacted and face

Question 15

lower motor neuron lesion

Answer 15

paralysis of ipsilateral upper and lower facial musculature (unable to raise eyebrows or smile on side of lesion)

Question 16

upper motor neuron lesion

Answer 16

paralysis of contralateral lower facial musculature (unable to smile on both sides, but can raise eyebrows)

Question 17

what is a major sign of paralysis for UMN lesions

Answer 17

if the wrinkle is not present

Question 18

indirect activation pathway

Answer 18

country road to direct pathways
-responsible for mediating reflexes and other automatic movements
-maintaining posture
-facilitating direct pathway

Question 19

effects of damage to indirect pathway

Answer 19

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)

Question 20

decorticate rigidity

Answer 20

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

Question 21

decerebrate rigidity

Answer 21

damage at level of midbrain and resulting in excitation of all extensor muscles

Question 22

neural control circuits

Answer 22

in charge of integration and control of movements
-basal ganglia and cerebellar control circuits (regulate UMNs and through that, communicate with LMNs)

Question 23

cerebellar control circuits

Answer 23

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

Question 24

effects of cerebellar damage: flocculonodular lesions

Answer 24

truncal ataxia (inability to stand or sit without swaying or falling, gait disturbances)

Question 25

effects of cerebellar damage: vermis lesions

Answer 25

gait ataxia

Question 26

effects of cerebellar damage: lateral cerebellar hemisphere lesions

Answer 26

intention tremor and incoordination which is reflected in dysmetria, dyssynergy, or decomposition of movement, and dysdiodokinesia

Question 27

effects of cerebellar damage: on speech

Answer 27

incoordination and hypotonia

Question 28

incoordination test

Answer 28

ask patient to touch their finger and nose (they can’t do with cerebellar damage)
-difficulty with monosyllables and syllables (papa, tata, kaka, pataka)

Question 29

basal ganglia circuits

Answer 29

have cognitive, affective, and motor control functions
-motor: opening gates to intended movements (initiation) and closing gates to unwanted movements (inhibition) preventing lock up of movements

Question 30

effects of basal ganglia damage

Answer 30

-reduced mobility or hypokinesia (related to damage of substantial nigra or blockage of dopamine receptors)
-slowness, stiffness, initiated and stopped with difficulty

-involuntary movements or hyperkinesia (excessive activity in dopaminergic nerve fibers, reducing circuit’s dampening effect
-chorea, athetosis, dystonia