motor organization

Question 1

organization of motor systems

Answer 1

primary motor cortex (precentral)
secondary motor cortex (premotor)
teritary cortex (prefrontal division)

Question 2

primary motor cortex

Answer 2

connects with cerebellum, basal ganglia, thalamus, secondary motor cortex
- lesions are area specific

Question 3

secondary /supplemental motor area

Answer 3

secondary: integration of motor skills and learned motor programs
supplemental: arousal level, initiating responses
- face motor area: organization and patterning of speech

Question 4

prefrontal areas

Answer 4

pathways to basal ganglia, thalamus, brainstem reticular formation
- attends, integrates, formulates and executes activity
damage - difficulties in voluntary action, movement initiiation and executive dysfunctions

Question 5

spinal horn

Answer 5

dorsal (posterior) - sensory processing

ventral (anterior) - motor neurons

Question 6

upper motor neuorns

Answer 6

carry motor system output from the cortex to lower motor neurons in the BS and spinal cord

Question 7

lower motor neurons

Answer 7

synapse with upper motor nuerons in BS or spinal cord and project to peripheral muscles

Question 8

lateral corticospinal tract

Answer 8

• motor pathway in NS
• controls movements in the extremities
• UMN originate in M1 and synapse on ventral horn of spinal cord

Question 9

corticobulbar tract

Answer 9

projects from cortex to brain stem

Question 10

anterior corticospinal tract

Answer 10

ipsilateral- information from the trunks

Question 11

corticospinal fibers

Answer 11

85% decassation at pyramid (lateral)

15% remain ipsilateral (anterior)

Question 12

babinskis sign

Answer 12

normal- toes flex down when scraped
extensor plantar response- toes fan up
- means cortex was affected

Question 13

im/probable locations of unilateral face, arm and leg paralysis with no sensory deficits

Answer 13

improbable: cortex because sensory involvement would be present, spinal cord because face would not be involved, LMN because face arm and leg on same side
probable: corticospinal and corticobulbar tract fibers below cortex and above medulla
side: contralateral to paralysis because above pyrimidal decussation

Question 14

im/probable locations of unilateral face, arm & leg paralysis with sensory deficits

Answer 14

imporable: spinal cord and medulla because face is involved, LMN because face is involved
probable: entire primary motor cortex or corticospinal tract fiber below cortex above medulla
side: contralateral to paralysis (above pyramidial decussation)

Question 15

im/probable location unilateral arm & leg paralysis

Answer 15

improbable: LMN: arm and leg on same side of body required, CS b/w M1 and medula: face would be involved
probable: M1 if sensation is affected, CSC b/w medulla and c5 of cervical
side: if M1- contralateral because above decussation
if spinal cord- ipsilateral because below decussation

Question 16

im/probable location of unilateral face and arm paralysis

Answer 16

probable: lower homonculus (assume sensory)
imporable: internal capsule would affect legs

Question 17

corpus striatum

Answer 17

caudate nucleus + putamen

Question 18

lenticular nucleus

Answer 18

globus pallidus + putamen

Question 19

direct pathway

Answer 19

Glu from cortex excites striatum
+ DA (d1) inputs from SNc
Ach excites synapses with GABA in GPi
GABA inhibits GPi releasing it from inhibition of thalamus
thalamus can now excite cortex –> movement
(-1)(-1) = + 1

Question 20

indirect pathway

Answer 20

Glu from cortex excites striatum
- DA (d2) inputs from SNc
Ach excites synapses with GABA, ENK in GPe
GPe is released from inhibiting STN
STN can then excite GPi which inhibits thalamus from stimulating cortex –> inhibition of movement
(-1)(-1)(+1)(-1) = (-1)

Question 21

2 classes of disorders of basal ganglia

Answer 21

hypokinetic: less movement - parkinsons
hyperkinetic: excess movement - huntingtons

Question 22

parkinsons disease characteristics

Answer 22

second most common neurogenarative disorder and most common motor disorder

• associated with mutations
  symptoms: difficulty initiating movement, slowness, stiffness, shaking at rest

Question 23

cause of parkinsons

Answer 23

degeneration and loss of dopamine producing neurons in STN

- formation of Lewy bodies

Question 24

parkinsons basal ganglai effects

Answer 24

direct: loss of DA neurons:
- not as much excitation to GABA
GABA doesnt release inhibition of GPi enough
GPi inhibits thalamus –> inhibition of movement
indirect: loss of DA neurons
- striatum has too much excitation because it doesnt receive inhibition from DA
- results in too much excitation from thalamus to cortex and unwanted movements

Question 25

huntingtons characteristics

Answer 25

hyper kinetic: excessive movement
- common CAG repeat on huntington gene genetic disorder (more repeats)
- if one parent has disorder than 50% of siblings will carry
onset around 35-50 years

Question 26

symptoms of huntingtons disease

Answer 26

quick and jerkey involuntary movements, rigidity
mental: loss of ability to concentrate, decreased ability to perform daily tasks, deteroation of judgement and memory, depression, dementia

Question 27

neuropathology of huntingtons

Answer 27

dysfunciton and death of neurons in striatumm, cortex, hypothalamus

Question 28

huntingtons basal ganglia

Answer 28

direct: loss of GABAergic leads to overinhibition of the thalamus and less movement produced
indirect: loss of GABAergic neurons leads to overactivation of the thalamus and hyperkinesia