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Functional Neuroanatomy > Task 1 > Flashcards

Task 1 Flashcards

1
Q

Spianal cord

A

highway between brain & skin, joints, muscles

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

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2
Q

spinal cord- dorsal root

A

toward spinal cord (afferent)

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3
Q

spinal cord -ventral root

A

away from spinal cord ( effernt)

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4
Q

Endoderm

A

becomes organs

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5
Q

mesoderm

A

becomes bones &muscles

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6
Q

ectoderm

A

becomes NS & skin

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7
Q

Neurulation

A

neural plate  neural groove  neural tube + neural crest

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8
Q

All neurons with cell bodies in PNS derive from

A

neural crest

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9
Q

 Entire CNS develops from the

A

walls of the neural tube

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10
Q

Motor levels

A
  1. High- association areas & basal ganglia
  2. Middle- Motor cortex & cerebellum ( basal gnglia in gazzanigga)
  3. Low- brain stem & spinal cord
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11
Q

High level

A

association areas of neocortex & basal ganglia

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

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12
Q

Middle level

A

– 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

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13
Q

low level

A

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

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14
Q

Posterior Parietal

A

 Directs behaviour by providing spatial information

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15
Q

Area 5

A

input from primary somatosensory cortical areas

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16
Q

Area 7

A

input from higher order visual areas

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17
Q

parietal cortex damage

A

deficits in perception& memory for spatial relationships, accurate reaching

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18
Q

Apraxia

A

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

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19
Q

Contralateral neglect

A

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

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20
Q

Are 6

A

Sma & PMA

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21
Q

Area 4

A

m1

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22
Q

PFC & pareital coretx

A

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

23
Q

Secondary Motor Areas

A

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

24
Q

Secondary Motor Areas role

A

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

25
Q

Supplementary motor area (SMA)

A

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

26
Q

Premotor area (PMA)

A

 Primarily connects with reticulospinal neurons innervating proximal motor units

27
Q

Ideomotor Apraxia

A

rough sense of desired action but problems with proper execution

28
Q

Ideational Apraxia

A

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

29
Q

Ready-set-go-idea

A

 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)

30
Q

Primary motor cortex

A

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

31
Q

PMC rostral neurons

A

terminate on spinal interneurons

32
Q

PMC caudal neurons

A

terminate directly on alpha neurons

33
Q

Individual pyramidal cells can

A

derive multiple motor neuron pools from different muscles

34
Q

hemiplegia

A

= 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

35
Q

Cells encode force & direction of movement by

A

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

36
Q

cerebellum

A

 Output: brainstem nuclei & cortex via thalamus

 Input & output from & to cortex cross over so ipsilateral organisation

37
Q

Vestibulocerebellum

A

to brainstem vestibular nuclei

 Balance & coordination of eye movement with body movement

38
Q

Spinocerebellum

A

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

39
Q

Neocerebellum

A

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

40
Q

Basal Ganglia

A

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

41
Q

the somatic ns

A

controls skeletal musles contractions

42
Q

The automatoic ns

A

automatic regulation or smooth uscle , cardiac muscle

43
Q

action

A

 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

44
Q

Spinal interneurons

A

– 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

45
Q

Gamma motor neurons

A

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

46
Q

Alpha motor neurons

A

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

47
Q

Amyotrophic Lateral Sclerosis (ALS)

A

 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

48
Q

Duchenne Muscular Dystrophy

A

 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!)

49
Q

Myasthenia Gravis

A

 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)

50
Q

Non-primary motor areas

A

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

51
Q

All premotor areas have

A

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

52
Q

Primary motor area

A

 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)

53
Q

rostral dorsal premotor area

A

strong connections with PFC

 Selects responses based on arbitrary spatial cues

54
Q

Caudal dorsal premotor araes

A

strong connections with M1

 Influences generation of movements

Functional Neuroanatomy (5 decks)

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