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Flashcards in 473 post MT 2 Deck (81):
1

primary sensory cortex
primary motor cortex

localize and identify what and where sensory stimuli are
trigger and execute motor commands

2

what does the motor-association cortex consist of + functions?

premotor cortex-lateral surface
supplimentary motor area-superior and medial surface
involved in formulating motor programs for complex movements

3

premotor cortex functions

-involved in activating multiple mm in the limb
-most activation prior to start of movement (ie involved in planning)
-directionally specific-affects contralateral limbs

-lesions result in: inability to initiate multi-joint movements and coordinating the limb

4

supplementary motor area

-complex sequences of movements
-bilateral coordination of movement
-affects contra-lateral limbs
-affects proximal muscles directly and distal muscles indirectly via primary motor cortex
-has interhemispheric connections b/t the two sides

5

supplementary motor area lesions

-difficulty planning complex movements (apraxia)
-deficits in coupling voluntary movements with postural adjustments

6

dominant hemisphere

L parietal lobe and L hemisphere has a particular role in coordinating and planning movements-particularly w/a tool or interacting w/the environment

7

damage to which areas might result in apraxia?

motor association areas (ie supplementary or premotor)
parietal association cortex of dominant hemisphere

8

hemispatial neglect

damage to RIGHT (non dominant) parietal association cortex or frontal cortex
-inability to attend to sensory cues on the contralateral side

9

4 types of hemi-neglect

sensory
motor-intentional
combination motor and sensory
conceptual (how things are represented)

10

what is the test for hemi-neglect?

test for extinction
-motor
-tactile
touch on one side ,then both at once
-will neglect L side things, movements disappear or decrease during bilateral movements (they are attending to things on the R side)

11

conceptual neglect

two types
anosognosia-no awareness of hemi-neglect
hemiasomatognosia-no awareness of side of body-limbs "dis-owned"

12

which side would a patient have trouble dressing on if they have apraxia due to a R parietal lesion?

LEFT

13

alien hand cause

damage to corpus collosum and/or supplementary motor area of non dominant hemisphere
-hand is out of control and acts autonomously

14

what separates the lobes of the cerebellum?

primary fissure-anterior and posterior
postero-lateral fissure-separates flocculo-nodular lobe

15

functional regions of cerebellum

-vermis-down center
-intermediate-medial 1/3
-lateral-lateral 2/3
-flocculo-nodular

16

dentate nucleus

cerebellum, lateral zone

17

interposed nucleus

cerebellum, intermediate zone
-composed of globous and eboliform

18

fastigial nucleus

cerebellum, vermis and flocculonodular zones

19

what is different from the cerebrum to cerebellum about how information is carried two and from?

all info to cerebellum travels via cerebellar peduncles
cerebral peduncles go to ventral region of midbrain

20

which cerebellar peduncle carries mostly outputs?
inputs?

out-superior
in-middle and inferior

21

pontocerebellar fibers

-cortico-pontine fibers from cortex to pontine nuclei
-ponto-cerebellar fibers cross midline and enter cerebellum via middle peduncle
-efferent copy of motor commands for voluntary movement

22

spinocerebellar pathways

leg proprioceptors:via dorsal spinocerebellar tract though nucleus dorsalis of clark
arm proprioceptors: through cuneocerebellar tract via external cuneate nuclues
-ie super similar to PCML(the nuclei receive PCML inputs) but nucleus gracilis is nucleus dorsalis of clarke
via inferior cerebellar peduncle

23

vestibular inputs to cerebellum

-primary vestibular afferents plus projections from vestibular nuclei go to ipsilateral cerebellum via inferior cerebral peduncle's juxtarestiform body

24

outputs from lateral cerebellar hemispheres

fibers origionate in lateral hemispheres (involved in motor planning)
travel from dentate nucleus, axons exit through superior cerebellar peduncle, cross at midbrain and continue to contralateral thalamus
-thalamus to widespread areas of the cortex: premotor cortex, SMA, motor cortex, parietal cortex

25

which side muscles are affected by cerebellar outputs?

ipsilateral to cerebellar outputs

26

intermediate cerebellar hemiphere outputs

project to interposed nuclei
leave via superior peduncle, cross midline and project to contralateral thalamus AND red nucleus
-thalamus to ONLY motor areas of cortex, no association or learning areas (ie involved more in coordination of ongoing movements)
-influences distal limbs via the lateral cortico-spinal tract from premotor, motor, and secondary
-influences upper limbs via rubrospinal tract

27

outputs from fastigial nucleus

come from vermis
1. project to contralateral thalamus
-influence bilateral mm via ACST (trunk muscles and posture influence)
2. project to vestibular nuclei and reticular formation bilaterally
-influences balance and mm tone
-vestibular nuclei are connected via uncinate faciculus

28

where does the vermis project to directly?

-inferior vermis and flocculonodular lobe cells project to vestibular nuclei ipsilaterally
-influences balance and eye movement

29

damage to lateral vs. intermmediate cerebellar zones

lateral: more effect in planning of movements, less on coordination
-intermediate: if damage is in the anterior lobe vermis, the trunk will be affected
-posterior lobe vermis has no body representation

30

what is the cerebellum's main function on terms of movement?

comparator
compares efferent info (corollary discharge) to ascending afferent feedback, finds errors, and projects to motor areas for corrections

31

why do young babies make more messes?

their cerebellum is not myelinated and their coordination is poor
-also happens when there's damage

32

cerebellar intermediate hemisphere lesion symptoms

ipsilateral symptoms
1. pendular reflexes
2. ataxia involving
-dysrythmia-abnormal timing of movement
-dysmetria-abnormal amplitude of movement
-intention tremor (during movement)
dysdiadochokinesia-difficulty with alternating movements (angonist-antagonist)
-dysarthria-poor rhythm and flow of speech (sound drunken)

33

tests for cerebellar symptoms

dysrythmia-tap foot (can't keep time)
dysmetria-open and close hand or finger to nose: becomes irregular/always undershooting and overshooting
dysdadochokinesia-flip palm up and down

34

midline cerebellar damage

ataxia of leg and trunk
-broad, staggering gate
-poor standing balance (from poor control of hip mm)
-test with heel-shin while sitting

35

what can cause midline cerebellar damage

anterior lobe syndrome from chronic alcoholism combined with poor nutrition

36

flocculo-nodular lobe damage symptoms

-unstable standing and walking (normal leg movements when seated)
-deficits only when balance is involved
-difficulty w/visual tracking of moving objects, multiple corrections in eye movements
-inability to suppress VOR (nystagmus while moving head instead of eyes moving with head)

37

5 parts of basal ganglia

caudate
globus pallidus-externus and internus
-putamen
-sub-thalamic nucleus
-substantia nigra-compacta and reticulata

38

caudate nucleus structure

follows C-shape of lateral ventricles
-wider at the anterior head
-has body and tail as well

39

which structures of the basal ganglia are medial to the internal capsule?

caudate**
thalamus
amygdala

the two sides of the lateral ventrical C's are basically touching at the midline until they get more posterior, then the bottom part of the C wraps around more laterally

40

which structures of the basal ganglia are lateral to the internal capsule?

putamen
globus pallidus
GPe-more lateral
GPi-closest to internal capsule

41

putamen

most lateral basal ganglia nuclei + largest
-has cellular bridges to caudate via corona radiata and internal capsule

42

substantia nigra

@ midbrain below subthalamic nuclei
dorsal to cerebral peduncles
has dopaminergic neurons, which stain dark
ventral part=pars reticulata
dorsal part=pars compacta

43

striatum
lenticular nucleus

functional distinctions for basal ganglia nuclei that work together
-caudate + putamen
-putamen + globus pallidus

44

what inputs does the striatum receive?

entire cerebral cortex
substantia nigra pars compacta
thalamus

45

what inputs does putamen receive?

-motor and somatosensory areas
-output relevant to movement

46

which basal ganglia nuclei do cognitive and emotional info?

caudate
-via prefrontal and limbic channels

47

which basal ganglia nuclei influence occularmotor function?

cortical areas controlling eye movement and those from somatosensory cortex go to caudate

48

direct pathway from basal ganglia

-acts to increase thalamic output to cerebral cortex
-striatum inhibits GPi
-GPi has inhibitory influence on thalamus
-net effect=excitation of thalamus and cortex
***globus palidus externus is bypassed

49

indirect pathway from basal ganglia

-striatum has inhibitory influence on GPe, which inhibits subthalamic
-less inhibition on subthalamic means it excites GPi
-GPi inhibits thalamus
-net effect=inhibition of thalamus

50

effect of dopamine on direct and indirect pathways

-both act together normally
-dopamine is the modulator, it excites striatal neurons for direct pathways and inhibits those for indirect

51

functions of basal ganglia

-"go" signal for internally-triggered movements
-predictive control over movement-adjustments to tone/amplitude and coordination of trunk with limbs
**affects movements contralaterally

52

what causes parkinson's disease?

unknown cause-10% thought to have geneti contributor, other causes might be environmental or viral factors
-degeneration of dopaminergic receptors in substantia nigra pars compacta

53

why is parkinson's often diagnosed late in the progression of the disease?

-slow progression-5-15 years
-symptoms appear after >85% of the neurons are lost

54

PD symptoms

1. bradykinesia-small, slow movements
-hands, feet, and some eye movements, and speech
2. resting tremor, decreases with voluntary movement
3. rigidity-lead pipe or cog-wheel type
4. postural instability and unsteady gait-last symptom to appear

5. expressionless face
6. micrographia-small writing
7. difficulting turning
8. freezing
9. diminished arm swing and shuffling gait while walking

55

test for bradykinesia

-open and close finger and thumb as wide as possible

56

postural instability test

retropullsion
-pull backward from shoulder
-normal response is to recover or take one step

57

what seems to help some parkinsons symptoms?

extra sensory stimuli
-eg something to step over can overcome freezing
-walking is particularly affected, other locomotor patterns might not be
-eg a patient who can't walk might be able to ride a bike

58

levadopa

replacement dopamine
can cross BBB
on/off swings caused by sensitization over time

59

when levadopa stops managing PD symptoms

1. surgical removal of basal ganglia (globus pallidus if there's freezing and rigidity type symptoms, thalamus (relay inputs) if there's more tremor)
-collateral damage possible + irreversible
2. deep brain stimulation
-"lesion" basal ganglia using magnetic stimulation and a pacemaker under clavicle
-can be modulated over course of disease

60

which parkinson's symptom is NOT improved by any of the treatments?
what does that mean?

postural instability
meaning there's an issue in another system causing it
-they have induced parkinson's symptoms (with drugs) in monkeys and this did not result in postural instability
-possibly cholinergic neurons are also affected

61

possible new treatment for PD

stem cells to replace deteriorated substantia nigra cells

62

huntingtons disease cause and mx

genetic-autosomal dominant gene-50% if one parent has it
-onset is at 30-50 years old-after people typically have kids and pass it on
-visible degeneration of striatal cells in caudate and putamen
(lateral ventricles look ballooned out on scans)

63

chorea

frequent, non-rhythmic, involuntary, writhing, or jerky movements

64

huntintons symptoms

dystonia-abnormal sustained postures due to excessive drive to a muscle
-abnormal eye movement
-dementia
-depression, anxiety, O-C disorder
**indirect pathway mostly affected leading to hyperkinetic responses and excessive movements

65

treatments for huntingtons

1. anti-dopaminergic meds
2. lesion thalamus relay nuclei
3. deep brain stimulation (GPi)

66

athetosis

in b/t dystonia and excessive unwanted movements
-involves slow, unwanted, and possibly freezing movements in distal limbs (fingers)
-usually caused by a stroke

67

hemiballismus

excessive movements from overdrive to basal ganglia
-circlar tendancy
-from damage to subthalamic nuclei (typically from stroke), so direct pathway remains intact

68

tourette syndrome

affects striatal cells/receptors
-possibly due to hypersensitivity to dopamine
-genetic component
4:1 males to females
-involuntary motor and vocal tics, vary with stress and concentration

69

treatment for tourettes

no cure
psychotherapy for social aspects
-dopamine blockers
-deep brain stimulation

70

reticular formation fibers

ascending: to all parts of the brain (from midbrain)
descending: to reticulo-spinal tract from pons and medulla

71

reticular formation functions

-alertness (midbrain)
-modulating tone via RST
-startle reflexes: from caudal pontine reticular nucleus

72

startle reflex

evoked by sudden and intense sensory stimuli (not smell or taste)
-eyes close, arms raise, joints flex

73

hyperekplexia

exaggerated startle reflex, early, continuous, and non-habituating
major (genetic) and minor forms)
-major form involves stiffness (stiff-baby syndrome present from birth)

74

what might cause absent or delayed startle reflexes?

progressive supranuclear palsy, dementia with lewy bodies

75

treatment for hyperekplexia

drugs to reduce stiffness
and possibly anxiety

76

anterior communicating arteries
posterior communicating fibers

connect the two sides of anterior cerebral arteries
connect anterior and posterior cerebral arteries

77

which arteries make up the circle of willis?
where do the arteries that make up the circle of willis lie?

post. cerebral, anterior cerebral, and post. and anterior communicating fibers
they lie in subarachnoid space, smaller branches punch through pia to supply regions of the brain

78

anterior cerebral artery supplies

superior and medial cortex from frontal to anterior parietal lobes

79

posterior cerebral artery supplies

inferior and medial temporal lobe and occipital lobe

80

middle cerebral artery supplies
where does it branch?

1. superior division: lateral aspect of frontal lobe and anterior parietal lobe
2. inferior: superior and lateral temporal lobe and posterior parietal cortex
3. deep branch: body of caudate and most of lentiform, thalamus

branches in sylvian fissure

81

what symptoms would result from a middle cerebral artery occlusion?

upper MN symptoms lateral aspects of motor cortex (not legs)