Task 1

Question 1

Spianal cord

Answer 1

highway between brain & skin, joints, muscles

 Communicates with body via spinal nerves (ventral + dorsal roots

Question 2

spinal cord- dorsal root

Answer 2

toward spinal cord (afferent)

Question 3

spinal cord -ventral root

Answer 3

away from spinal cord ( effernt)

Question 4

Endoderm

Answer 4

becomes organs

Question 5

mesoderm

Answer 5

becomes bones &muscles

Question 6

ectoderm

Answer 6

becomes NS & skin

Question 7

Neurulation

Answer 7

neural plate  neural groove  neural tube + neural crest

Question 8

All neurons with cell bodies in PNS derive from

Answer 8

neural crest

Question 9

 Entire CNS develops from the

Answer 9

walls of the neural tube

Question 10

Motor levels

Answer 10

1. High- association areas & basal ganglia
2. Middle- Motor cortex & cerebellum ( basal gnglia in gazzanigga)
3. Low- brain stem & spinal cord

Question 11

High level

Answer 11

association areas of neocortex & basal ganglia

 Strategy: figure out goal of movement & the best strategy to get there; Motor plan

Question 12

Middle level

Answer 12

– motor cortex & cerebellum (& basal ganglia according to Gazzaniga – make up your minds people!)
 Tactics: concerned with the sequences of muscle contractions to smoothly & accurately achieve the strategic goal
 Translate action goals into movement instructions to lower level

Question 13

low level

Answer 13

brain stem & spinal cord
 Execution: activation of neurons that generate the goal directed movements & necessary adjustment of posture
 Motor neurons & inter neurons
 Sensory feedback is used to maintain posture, muscle length & tension before & after each voluntary movement (= adjustments

Question 14

Posterior Parietal

Answer 14

 Directs behaviour by providing spatial information

Question 15

Area 5

Answer 15

input from primary somatosensory cortical areas

Question 16

Area 7

Answer 16

input from higher order visual areas

Question 17

parietal cortex damage

Answer 17

deficits in perception& memory for spatial relationships, accurate reaching

Question 18

Apraxia

Answer 18

patients have difficulty to perform movement when asked out of context (thinking about it) but can readily perform than spontaneously in natural situations

Question 19

Contralateral neglect

Answer 19

disturbance of the ability to stimuli on the side opposite to the side of the brain damage (egocentric left) even though they can be unconsciously perceived

Question 20

Are 6

Answer 20

Sma & PMA

Question 21

Area 4

Answer 21

m1

Question 22

PFC & pareital coretx

Answer 22

together encode what actions are desired and give it on to Area 6

Question 23

Secondary Motor Areas

Answer 23

These regions include the posterior parietal cortex, the premotor cortex, and the supplementary motor area (SMA)

Question 24

Secondary Motor Areas role

Answer 24

Planning
 Convert info about what action is desired into how the actions will be carried out
 Programming of specific patterns of movement after taking general instructions from PFC
 Planning of movements yet to come (specialised for skilled, voluntary movement)
 Output to primary motor cortex
 Each has their own somatotopic map

Question 25

Supplementary motor area (SMA)

Answer 25

 Sends axons to directly innervate distal motor units  Heavily interconnected with M1/area 4  Stronger connections with PFC

Question 26

Premotor area (PMA)

Answer 26

 Primarily connects with reticulospinal neurons innervating proximal motor units

Question 27

Ideomotor Apraxia

Answer 27

rough sense of desired action but problems with proper execution

Question 28

Ideational Apraxia

Answer 28

– no clue, don’t know how to do things anymore

Question 29

Ready-set-go-idea

Answer 29

 Ready = depends on activity of parietal & PFC  Set = depends on SMA & PMA (e.g. monkey experiment: start firing on instruction stimulus & keep doing so until trigger stimulus)  Go = M1 (when movement is initiated PMA & SMA cease to fire)

Question 30

Primary motor cortex

Answer 30

Initiation Input: cerebellum through thalamus cortical areas (mostly 6) Output: spinal cord & brain stem areas involved in sensorimotor processing

Question 31

PMC rostral neurons

Answer 31

terminate on spinal interneurons

Question 32

PMC caudal neurons

Answer 32

terminate directly on alpha neurons

Question 33

Individual pyramidal cells can

Answer 33

derive multiple motor neuron pools from different muscles

Question 34

hemiplegia

Answer 34

= loss of voluntary movement on contralateral side (e.g. stroke) when primary motor cortex is damaged  Might return as spastic movements as cortical influence is removed thus no reflex control  Learned disuse can be helped with constrained-induced movement therapy

Question 35

Cells encode force & direction of movement by

Answer 35

means of population coding  Each cell has a tuning curve  Activity of each cell represents a direction vector (direction that’s best for the cell)  length of the vector shows how active that cell was during movement  get population vector by averaging the vectors of the different directions (so each cell basically votes  Direction of movement depends on the average of votes  The larger the population of neurons the finer the possible control

Question 36

cerebellum

Answer 36

 Output: brainstem nuclei & cortex via thalamus |  Input & output from & to cortex cross over so ipsilateral organisation

Question 37

Vestibulocerebellum

Answer 37

to brainstem vestibular nuclei |  Balance & coordination of eye movement with body movement

Question 38

Spinocerebellum

Answer 38

input from vision, auditory & proprioceptive system and output to descending systems (extrapyramidal)  Motor execution & balance

Question 39

Neocerebellum

Answer 39

– input from parietal & PFC, output to motor areas  Motor planning  Lesion: ataxia = problem with coordination of distal limb movements (+ intention tremor)

Question 40

Basal Ganglia

Answer 40

 Input received by striatum  Output from globus palladius & part of the substantia nigra  To thalamus to motor regions  Initiation

Question 41

the somatic ns

Answer 41

controls skeletal musles contractions

Question 42

The automatoic ns

Answer 42

automatic regulation or smooth uscle , cardiac muscle

Question 43

action

Answer 43

 Neurons become input from muscle spindles that inform them about how stretched the muscle is  Muscle spindle  dorsal root  motor neuron in spinal cord  Stretch reflex: sudden stretch directly activates motor neuron

Question 44

Spinal interneurons

Answer 44

– integration of sensory feedback with motor commands resulting in voluntary movement  Input from descending motor fibres that originate from cortex & afferent sensory nerves  Output to motor neurons

Question 45

Gamma motor neurons

Answer 45

sense & regulate length of the muscle fibres (proprioceptive system)

Question 46

Alpha motor neurons

Answer 46

innervate muscle fibres & provide physical basis for translating nerve signals into muscles

Question 47

Amyotrophic Lateral Sclerosis (ALS)

Answer 47

 Muscle weakness and atrophy  Degeneration of large alpha motor neurons & large neurons of motor cortex that innervate those  Other neurons of CNS are spared thus cognitive functions & intelligence are unchanged  Possible causes  Genetic mutation affecting enzyme superoxide dismutase: normally reduces toxic superoxide radicals (by-product of metabolism)  radical build up especially in cells that are metabolically very active  Excitotoxicity: elevated levels of glutamate and/or defective glutamate transporter lead to overstimulation resulting in cell death  Treatment  Riluzole – block glutamate release but can only slow progress by a few months

Question 48

Duchenne Muscular Dystrophy

Answer 48

 Progressive weakness & deterioration of muscle in boys (typically don’t survive past age 30)  Passed on from mothers  Causes  Defective region on X chromosome encoding dystrophin (= cytoskeletal protein) that contributes to cytoskeleton lying just under the sarcolemma in muscles  lack mRNA  Secondary changes in contractile apparatus  Becker muscular dystrophy (milder form): only a portion of mRNA is altered  Treatment  Gene therapy: replace defective gene by either sending a virus that carries the gene or by transplanting stem cells (very promising in mice!)

Question 49

Myasthenia Gravis

Answer 49

 Weakness & fatigability of voluntary muscles (typically including facial expression)  Severity fluctuates even over the course of a day  Can be fatal when respiration is compromised  Causes  Autoimmune disease: system generates antibodies against own receptors  bind & interfere with normal actions  degenerative changes  less effective ACh release at neuromuscular junction  Treatment  Drugs inhibiting reuptake (but leads to desensitisation)  Suppression of immune system (drugs/ removal of thymus gland)

Question 50

Non-primary motor areas

Answer 50

all areas in the frontal lobe that can influence motor output at the level of M1 & the spinal cord

Question 51

All premotor areas have

Answer 51

weak direct influence on the spinal motor neurons & the majority of their neurons terminate in the intermediate zone of the spinal cord

Question 52

Primary motor area

Answer 52

 Direct influence on lateral motor-nuclei in spinal cord  Connected to fewer cortical structures than the premotor areas (TMS modulated less regions than when applied to premotor areas)

Question 53

rostral dorsal premotor area

Answer 53

strong connections with PFC |  Selects responses based on arbitrary spatial cues

Question 54

Caudal dorsal premotor araes

Answer 54

strong connections with M1 |  Influences generation of movements