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473 post MT 2 Flashcards

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1
Q

primary sensory cortex

primary motor cortex

A

localize and identify what and where sensory stimuli are

trigger and execute motor commands

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2
Q

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

A

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

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3
Q

premotor cortex functions

A
  • 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

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4
Q

supplementary motor area

A
  • 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
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5
Q

supplementary motor area lesions

A
  • difficulty planning complex movements (apraxia)

- deficits in coupling voluntary movements with postural adjustments

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6
Q

dominant hemisphere

A

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

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7
Q

damage to which areas might result in apraxia?

A

motor association areas (ie supplementary or premotor)

parietal association cortex of dominant hemisphere

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8
Q

hemispatial neglect

A

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

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9
Q

4 types of hemi-neglect

A

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

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10
Q

what is the test for hemi-neglect?

A 
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)
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11
Q

conceptual neglect

A

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

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12
Q

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

A

LEFT

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13
Q

alien hand cause

A

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

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14
Q

what separates the lobes of the cerebellum?

A

primary fissure-anterior and posterior

postero-lateral fissure-separates flocculo-nodular lobe

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15
Q

functional regions of cerebellum

A
  • vermis-down center
  • intermediate-medial 1/3
  • lateral-lateral 2/3
  • flocculo-nodular
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16
Q

dentate nucleus

A

cerebellum, lateral zone

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17
Q

interposed nucleus

A

cerebellum, intermediate zone

-composed of globous and eboliform

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18
Q

fastigial nucleus

A

cerebellum, vermis and flocculonodular zones

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19
Q

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

A

all info to cerebellum travels via cerebellar peduncles

cerebral peduncles go to ventral region of midbrain

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20
Q

which cerebellar peduncle carries mostly outputs?

inputs?

A

out-superior

in-middle and inferior

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21
Q

pontocerebellar fibers

A
  • 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
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22
Q

spinocerebellar pathways

A

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

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23
Q

vestibular inputs to cerebellum

A

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

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24
Q

outputs from lateral cerebellar hemispheres

A

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

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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)

Neuroanatomy (3 decks)

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