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Neuroanatomy > 473 post MT 2 > Flashcards

473 post MT 2 Flashcards

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
Q

which side muscles are affected by cerebellar outputs?

A

ipsilateral to cerebellar outputs

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26
Q

intermediate cerebellar hemiphere outputs

A

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

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27
Q

outputs from fastigial nucleus

A

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
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28
Q

where does the vermis project to directly?

A
  • inferior vermis and flocculonodular lobe cells project to vestibular nuclei ipsilaterally
  • influences balance and eye movement
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29
Q

damage to lateral vs. intermmediate cerebellar zones

A

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

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30
Q

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

A

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

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31
Q

why do young babies make more messes?

A

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

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32
Q

cerebellar intermediate hemisphere lesion symptoms

A

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)

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33
Q

tests for cerebellar symptoms

A

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
Q

midline cerebellar damage

A

ataxia of leg and trunk

  • broad, staggering gate
  • poor standing balance (from poor control of hip mm)
  • test with heel-shin while sitting
35
Q

what can cause midline cerebellar damage

A

anterior lobe syndrome from chronic alcoholism combined with poor nutrition

36
Q

flocculo-nodular lobe damage symptoms

A
  • 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
Q

5 parts of basal ganglia

A 
caudate
globus pallidus-externus and internus
-putamen
-sub-thalamic nucleus
-substantia nigra-compacta and reticulata
38
Q

caudate nucleus structure

A

follows C-shape of lateral ventricles

  • wider at the anterior head
  • has body and tail as well
39
Q

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

A

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
Q

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

A

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

41
Q

putamen

A

most lateral basal ganglia nuclei + largest

-has cellular bridges to caudate via corona radiata and internal capsule

42
Q

substantia nigra

A 
@ midbrain below subthalamic nuclei
dorsal to cerebral peduncles
has dopaminergic neurons, which stain dark
ventral part=pars reticulata
dorsal part=pars compacta
43
Q

striatum

lenticular nucleus

A

functional distinctions for basal ganglia nuclei that work together

  • caudate + putamen
  • putamen + globus pallidus
44
Q

what inputs does the striatum receive?

A

entire cerebral cortex
substantia nigra pars compacta
thalamus

45
Q

what inputs does putamen receive?

A
  • motor and somatosensory areas

- output relevant to movement

46
Q

which basal ganglia nuclei do cognitive and emotional info?

A

caudate

-via prefrontal and limbic channels

47
Q

which basal ganglia nuclei influence occularmotor function?

A

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

48
Q

direct pathway from basal ganglia

A
  • 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
Q

indirect pathway from basal ganglia

A
  • 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
Q

effect of dopamine on direct and indirect pathways

A
  • both act together normally

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

51
Q

functions of basal ganglia

A
  • “go” signal for internally-triggered movements
  • predictive control over movement-adjustments to tone/amplitude and coordination of trunk with limbs
  • *affects movements contralaterally
52
Q

what causes parkinson’s disease?

A

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
Q

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

A
  • slow progression-5-15 years

- symptoms appear after >85% of the neurons are lost

54
Q

PD symptoms

A
  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
Q

test for bradykinesia

A

-open and close finger and thumb as wide as possible

56
Q

postural instability test

A

retropullsion

  • pull backward from shoulder
  • normal response is to recover or take one step
57
Q

what seems to help some parkinsons symptoms?

A

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
Q

levadopa

A

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

59
Q

when levadopa stops managing PD symptoms

A
  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
Q

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

A

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
Q

possible new treatment for PD

A

stem cells to replace deteriorated substantia nigra cells

62
Q

huntingtons disease cause and mx

A

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
Q

chorea

A

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

64
Q

huntintons symptoms

A

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
Q

treatments for huntingtons

A
  1. anti-dopaminergic meds
  2. lesion thalamus relay nuclei
  3. deep brain stimulation (GPi)
66
Q

athetosis

A

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
Q

hemiballismus

A

excessive movements from overdrive to basal ganglia

  • circlar tendancy
  • from damage to subthalamic nuclei (typically from stroke), so direct pathway remains intact
68
Q

tourette syndrome

A

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
Q

treatment for tourettes

A

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

70
Q

reticular formation fibers

A

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

71
Q

reticular formation functions

A
  • alertness (midbrain)
  • modulating tone via RST
  • startle reflexes: from caudal pontine reticular nucleus
72
Q

startle reflex

A

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

73
Q

hyperekplexia

A

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

74
Q

what might cause absent or delayed startle reflexes?

A

progressive supranuclear palsy, dementia with lewy bodies

75
Q

treatment for hyperekplexia

A

drugs to reduce stiffness

and possibly anxiety

76
Q

anterior communicating arteries

posterior communicating fibers

A

connect the two sides of anterior cerebral arteries

connect anterior and posterior cerebral arteries

77
Q

which arteries make up the circle of willis?

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

A

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
Q

anterior cerebral artery supplies

A

superior and medial cortex from frontal to anterior parietal lobes

79
Q

posterior cerebral artery supplies

A

inferior and medial temporal lobe and occipital lobe

80
Q

middle cerebral artery supplies

where does it branch?

A
  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
Q

what symptoms would result from a middle cerebral artery occlusion?

A

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

Neuroanatomy (3 decks)

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