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Bloc J - Neuro > Oct17 M1-Basal Ganglia > Flashcards

Oct17 M1-Basal Ganglia Flashcards

1
Q

classification of movement disorders

A
  1. hypokinetic
    - PD and variants (MSA, PSP, etc.)
  2. hyperkinetic (everything else) (are usually but not always basal ganglia dz)
    - tremor
    - chorea, athetosis, ballism
    - myoclonus
    - dystonia
    - tics and stereotypy
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2
Q

bradykinesia def

A

small movements (ROM), fatigue (ROM decreasing as do the mvmt) for ANY movement (steps, voice, handwriting)

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3
Q

beats up their family + chorea = think of what dz

A

Huntington’s dz (HD).

-frontal deficiency

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4
Q

(imp) structures of the basal ganglia

A
  • caudate and putamen (forming dorsal striatum) separated by anterior limb of internal capsule
  • globus pallidus externa and interna (GPe and GPi). very close but very diff fcts.
  • substantia nigra pars compacta (SNpc). (affected in PD) (note: SN pars reticula is functionally* part of the GPe)
  • SN is in the midbrain* just lat to mamillary bodies
  • subthalamic nucleus (STN) is above SN
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5
Q

functions of the basal ganglia

A
  • circuits for modulation of movement (tone and motivation) as part of focusing actions (picking the correct ones)
  • govern output. yes or no signal (likelihood). more generally (not fine things of movement which are controlled by cortex and cerebellum)
  • not emotional**
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6
Q

what are the loops or circuits in the basal ganglia

A

diff pathways of connections

  • from SN to ventral striatum to dorsal lateral prefrontal cortex
  • from SN to premotor cortex
  • from SN to motor cortex
  • etc
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7
Q

names of the 4 main loops in the basal ganglia (which all regulate tone and motivation)

A
  • motor (move or not) (involved in hyperkinetic disorders and parkinsonism)
  • cognitive (which areas to activate? task switching and focusing priorities)
  • visual (oculomotor)
  • limbic (to act or not) (apathy (limbic loop working too much) vs impulse control (impulse disorder = limbic loop working less**)
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8
Q

main ntr in basal ganglia loops

A

dopamine

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9
Q

dopamine fct

A
  • reward ntr. is a reward prediction error signal
  • shown not to be ntr for ‘‘happy’’ bc increases before something good so more for showing ‘‘reward is coming’’
  • dopamine stops = signal to brain to not do anything, there’s nothing there
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10
Q

2 main structures controlling the motor, cognitive and limbic loops

A
  • SN (1) connects to caudate (association cortex) and putamne (motor areas)
  • SN also connects to the ventral tegmental area (2) which connects to limbic areas of the ventral striatum including the nucleus accumbens
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11
Q

SNc to putamen = what loop

A

motor (SNc to motor areas of cortex)

is a dorsal loop

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12
Q

SNc to caudate = what loop

A

cognitive (SNc to association cortex)

is a dorsal loop

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13
Q

VTA to ventral striatum = what loop

A

emotive (limbic) (VTA to ventral striatum nucleus accumbens)

  • is a ventral loop*
  • D2Rs in this loop*
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14
Q

main cause of motor sx in PD

A
  • dopamine problem bc of a lesion in SN (which controls the direct pathway which increases movement)
  • lose SN = less stim of direct pathway (loop) (D1 Rs in striatum) = less movement
  • less inhibition of indirect loop (D2 Rs in striatum) (meaning it works more intensely) (which normally inhibits movement) = less movement
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15
Q

SN charact

A
  • appears as black line on gross pathology
  • has melanin in its dopaminergic neurons
  • in Parkinson’s dz (hypokinetic), it appears lighter on gross patho bc these neurons died
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16
Q

why PD fixable

A
  • levodopa (dopamine precursor)
  • other dopamine agents
  • neurosurgery (targeting SNc and GPi)
17
Q

why dopamine works as tx for PD

A
  • mimics what SN normally does
  • inhibits the normally indirect (inhibiting) pathway = more movement
  • stim the direct (stim) pathway = more movement
18
Q

2 neurosurgical tx for PD

A
  • hole in GPi (the endpoint of both D1 and D2 pathways) which normally inhibits movement
  • hole in STN (of indirect D2 pathway) = less inhibition
19
Q

pathophgy of HD (Huntington’s dz)

A

main problem in HD = frontal degeneration
selective degeneration of indirect pathway (D2). D1 is working fine
-result = move more
-mvmts are excessive and unforced
-center-surround system (fact of having 2 systems) for focusing mvmts stopped working

20
Q

dyskinesia def

A

abnormal mvmt

21
Q

PD patient moving too much, what might be the cause

A

got a dose of meds that was too high

22
Q

tx of HD (chorea and dyskinesia)

A
  • dopamine blockade (neuroleptics, dopamine depletors)

* note chorea is the least of the pts problems*

23
Q

consequence of dopamine agonist dose being too high in a PD pt

A

on top of the motor benefits and better mood, pt starts spending, hypersexuality, etc. becomes excessive

  • dopamine agonist fixed the SNc (dorsal loops)
  • dopamine agonist stimulated the D2Rs in the ventral loop (VTA to ventral striatum) = this loop became excessive
24
Q

consequence of suddenly stopping meds in a PD pt

A

severe depression (apathy, anhedonia, nothing is worth it, suicidal)

25
Q

tremors cause

A

problem in the normal suppression of tremor loops in the brain

  • tremors come early in dz and don’t progress
  • cog-wheeling = a tremor that you feel. is a rigidity tremor. you feel it by first relaxing the pt and then moving them
26
Q

newer classif of neurodegenerative dz

A

based on proteins deposited (doesn’t always mean this proteins are the killer though)

  • amyloidopathies (AD)
  • Tau-opathies (Atypical Parkinsonism (PSP, CBD, FTD = frontal basal dementias, etc.) + AD)
  • TDP-43opathies = ALS
  • others (like Huntingtonopathy?)
  • synucleinopathy (PD, dementia with Lewy bodies, multiple system atrophy). note PD also has Lewy bodies = synuclei inclusions.
27
Q

PD easily described pathophgy

A

premature aging of some areas of the brain

28
Q

synucleinopathy def

A

premature protein deposition dz (alpha synuclein is what makes up Lewy bodies)

29
Q

stages of PD (Braak model)

A
  • stage 1 (dorsal motor nucleus of vagus + olfactory tract)
  • stage 2 (after dz marches up to brainstem) (coerulus and sub-ceruleus complex which have fcts in sleep and mood): sleep and mood problems
  • stage 3 (SNpc): motor sx
  • stages 4-6: broader involvement. to reach stage 4 = synuclein reached the cortex
30
Q

implications of Braak model

A
  • PD is not a dz of the dopamine and the SNpc
  • non motor features are the greatest determinants of QoL in PD
  • PD starts with non motor features
31
Q

strongest predictor of PD

A

REM sleep behavior disorder
-98% of pts with that get PD (half of people with REM sleep behavior disorder get PD first, other half get DLB (dementia with Lewy bodies) first and then the two dz overlap)

32
Q

lifetime risk of PD

A

2% (1 in 50). 3% if add DLB

33
Q

RFs for PD

A
  • male
  • pesticides
  • non coffee use and non smoking (diff motivational system)
  • not much heredity (twin studies = almost no diff)
34
Q

main genes in PD that are related to heredity

A
  • LRRK2 (inflammation). Ashkenaji Jews and North African Berbers
  • GBA (heterozygous stage). French Canadian population (nasty young onset PD)
  • then the rest is autosomal recessive genes which are probbaly mitochondrial (pesticides affect mts)
35
Q

how did they discover the idea that PD can be caught from environment

A
  • bc of the two areas affected at stage 1
  • but mostly of case reports of pt dying 14 years after fetal transplant (so caught PD from environment, wasn’t intrinsic)
36
Q

most recent discoveries in PD pathophgy

A
  • most imp thing is oligomers leading to synuclein inclusions
  • synuclein spreads along nerve connections (and nerves connected together die together)
  • synuclein is a normal abundant protein in the brain but fct unknown
  • prion-like things (oligomers) turn normal synuclein into abnormal synucleins to make them aggregate
  • if try to inject synuclein, will end up finding more synuclein in dz than injected
  • ability to intervene is possibly in immunotherapy
37
Q

core features of PD

A
  • bradykinesia
  • rigidity
  • rest tremor
  • many non-motor symptoms
  • synuclein-mediated degeneration
  • dysfunction of basal ganglia loops (as part of the general dz)

Bloc J - Neuro (60 decks)

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