Lecture 9: Control Of Movement

Front 1

rostral to central sulcus is___caudal is__

Back 1

primary motor cortex, primary somat cortex

Front 2

motor cortex organized in terms of particular movements and prolonged stimulation makes

Back 2

complex movements

Front 3

primary motor cortex (M1) major input of ___signals and major output of these signals is to ____motor pathway to initiate movement. M1 also receives info from

Back 3

cortical sensorimotor,descending,somatosensory cortex

Front 4

SMA (supplemental motor area) located on medial surface, while premotor complex more lateral surface. SMA and premotor cortex receive sensory info from (2)

Back 4

parietal and temporal lobes

Front 5

SMA involved in the

Back 5

learning sequences of movement

Front 6

monkeys with SMA lesions unable to

Back 6

perform two seq response (push in lever and turn it)

Front 7

muscimol

Back 7

GABA agonist inhibits neural activity, used in SMA inactivity experiment

Front 8

SMA and pre SMA (rostral to SMA) involved in

Back 8

desire to move. if stimulated provoke urge to move

Front 9

premotor complex involved in (2), The movements can be guided by (2) info

Back 9

-learning and executing complex movements guided by sensory info
-non-arbitrary-->to reach for object need visual info
-arbitrary--> natural,nothing directing action example waving to taxi,movements guided that not related to them

Front 10

monkeys with premotor inactivation able to

Back 10

move hand toward non-arbitrary stimulus but not able to make previously learnt movement in response to arbitrary

Front 11

humans with premotor damage can make

Back 11

several different movements in response to spatial cues but cant make movement in response to arbitrary visual/auditory or tactile stimulus

Front 12

mirror neurons in monkey brains found in ___cortex (area F5)
they fire when:
play role in:
activated by:
help us:

Back 12

-ventral premotor
-preform action or when observe same action by another monkey or human
-ability to imitate movements of others
-sounds indicating occurence of familiar action
-understand action of others and intentions

Front 13

apraxia and 4 types

Back 13

-caused by damage to left or right frontal or parietal lobe
-trouble imitating movements
-limb,oral,apraxic agraphia,constructional

Front 14

what is limb apraxia, assessment, three type of lesions to cause it

Back 14

-problem with moving arms,hands,fingers
-asking people to imitate hand gestures ("pretend to turn imaginary key" see messed up motion, real key okay)
-anterior corpus callosum, motor cortex in left frontal lobe, intraparrietal sulcus of left parietal lobe

Front 15

oral apraxia

Back 15

problems with muscles in speech

Front 16

apraxic agraphia

Back 16

problem writing

Front 17

constructional apraxia and lesion causing it

Back 17

problem drawing/constructing object, unable to perceive/imagine geometrical, difficulty with tasks involving spatial perception/navigation (reading maps)

Front 18

basal ganglia mainly made up of (2), receive most input from (4) major outputs (4)

Back 18

-caudate putamen and globus pallidus
-cerebral cortex,primary motor cortex/somatosensory and substantia nigra (dopamine neuron cell bodies)
-primary motor cortex,SMA,premotor area,motor nuclei of brainstem

Front 19

substantia nigra-->caudate putamen-->thalamus-->cortex-->movement then cycles around. What happens when damage caudate and two diseases. If damage substantia

Back 19

-involuntary movements (hyperkinetic), unwanted choreiform (writhing/twitching)
-huntingtons,tourettes
-hypokinetic,difficulty moving,example Parkinsons

Front 20

GPi influences

Back 20

thalamic projections which modulates size/force of movement made from cortex (GPi-->thalamus-->cortex)

Front 21

direct pathway on GPi, indirect pathway on GPi

Back 21

direct=putamen to GPi
indirect=subthalamic nuclei to GPi

Front 22

theres two pathways affecting movement inhibitory and excitatory
if activity in inhibitory path higher than excitatory, if activity in excitatory higher than inhibitory then

Back 22

-GPi inhibited and thalamus can excite cortex
-GPi excited, inhibits thalamus =less input to cortex

Front 23

Parkinsons disease

Back 23

-neurodegenerative, basal ganglia disorder
-muscular rigidity,slowness
-imbalance of direct/indirect pathway
-indirect show decrease in inhibitory output due to decrease dopaminergic input to caudate
-treatment=L-DOPA,lesion to GPi maybe
-cortex basically inhibited

Front 24

too much dopamine stimulation via L DOPA =__(2)
and it doesnt work forever since

Back 24

-involuntary movement/posture(dyskinesia/dystonia)
-dopamine neurons decline and symptoms worsen

Front 25

Hungtingtons Chorea

Back 25

-genetic
-basal ganglia disorder
-uncontrollable movements,jerky
-degeneration of caudate=decrease of inhibition by GABA neurons of caudate affect indirect pathway
-no treatment

Front 26

cerebellum

Back 26

-outputs to every motor structure of brain
-half of all neurons in NS here
-damage=jerky uncoordinated movements
-keep track of timing of movements or adjusting movements to maintain accuracy