Basal Ganglia Flashcards

1
Q

structures of basal ganglia

A
  • striatum
  • globus pallidus (interna/externa)
  • subthalamic nucleus
  • substantia nigra

all paired, subcortical structures

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2
Q

striatum - structures, input, blood supply

A
  • Caudate nucleus, putamen
  • receive input from cortex
  • branches from ACA and MCA (medial/lateral striate arteries)
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3
Q

globus pallidus - output, blood supply

A
  • main output to thalamus

- branches of ICA and MCA (anterior choroidal a, lateral striate aa.)

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4
Q

subthalamic nucleus - blood supply, which pathway is it part of?

A
  • key component of INDIRECT pathway

- branches of PCA and PCOM

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5
Q

substantia nigra - structures, regulator of what?, blood supply

A
  • pars compacta (DA), pars reticula (output to thalamus)
  • key inhibitor/activator of striatal activity
  • blood supply: branches of PCA and PCOM
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6
Q

common area of hemorrhage?

A

basal ganglia

-very susceptible vessels

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7
Q

functions of extrapyramidal motor system

A
  • facilitates voluntary movement (initiates movement– gas)

- attenuates involuntary movements (prevents unwanted movements – brake)

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8
Q

neurotransmitters involved with basal ganglia

A
  • glutamate (excitatory)
  • GABA (inhibitory)
  • dopamine (excitatory or inhibitory)
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9
Q

direct pathway of basal ganglia

A

NET ACTIVATION of cortex

  • stepping on the gas
  • facilitates movements

striatum (-) –> GPi (-) –> thalamus (+) –> cortex

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10
Q

effect of dopamine on direct pathway of basal ganglia

A

STRONGER NET ACTIVATION of cortex

-substantia nigra activates striatum, leading to further activation

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11
Q

indirect pathway of basal ganglia

A
  • NET INHIBITION of cortex
  • hitting the brakes

striatum (-) –> GPe (-) –> STN (+) –> GPi (-) –> thalamus (+) –> cortex

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12
Q

effect of dopamine on indirect pathway of basal ganglia

A

NET ACTIVATION of cortex

  • lifts breaks
  • substantia nigra inhibits the striatum, thus inhibiting the inhibition
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13
Q

synthesis of dopamine

A

tyrosine –[tyrosine hydroxylase]–> L-Dopa –> dopamine –> norepinephrine

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14
Q

four cardinal features of hypokinetic disorders

A

“Parkinsonism”

1) BRADYKINESIA (required)
2) resting tremor
3) rigidity
4) postural instability

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15
Q

symptoms of hyperkinetic disorders

A
  • tremors (rhythmic, oscillatory)
  • hemiballismus (violent, flailing)
  • myoclonus (rapid, jerk like)
  • chorea (random, purposeless)
  • dystonia (abnormal co-contraction of muscles)
  • tics (stereotypic movements, supressible)
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16
Q

epidemiology of Parkinson’s disease (incidence, onset)

A
  • 1-3% of population above age 60%
  • onset: 55-60 years
  • most idiopathic
17
Q

Parkinson’s disease is a result of a loss of which cells?

A

Parkinson’s is a result of a loss of DOPAMINE cells in the SUBSTANTIA NIGRA

18
Q

Parkinson’s affects which basal ganglia pathway?

A

DIRECT PATHWAY

  • less dopamine is available to activate the direct pathway
  • leads to a NET DEACTIVATION of the cortex
19
Q

features of Parkinson’s disease

A

2+ symptoms:

  • bradykinesia (required)
  • resting tremor
  • rigidity
  • postural instability (late finding)

Asymmetry of symptoms
Functional neuroimaging

20
Q

Lewy body

A

characteristic histologic symptom of Parkinson’s

  • intracytoplasmic collections
  • in the cortex, substantia nigra, olfactory bulbs (widespread)
21
Q

SPECT (DaTscan)

A
  • tracer absorbed into striatum
  • shows uptake of dopamine
  • lack of tracer = lack of dopamine transport = lack of dopamine
22
Q

Tx for Parkinsons

A
  • dopaminergic medications
  • –carbidopa/levodopa
  • –dopamine agonists
  • –prolong dopamine via MAO/COMT inhibitors
  • surgery
  • –lesioning treatment (GP)
  • –deep brain stimulation (GP or STN)
23
Q

lesioning treatment

A
  • for Parkinson’s
  • outdated
  • lesion the globus palatus to alleviate inhibition of thalamus
24
Q

deep brain stimulation

A
  • Tx for Parkinson’s
  • implant stimulator to inhibit target
  • ADJUSTABLE
25
secondary causes of Parkinsonism
- toxins (MPTP, manganse) - postcephalitic parkinsonism - dopamine blocker/depleter drugs (antipsychotics, antiemetics)
26
if there is a subacute onset of Parkinson's, think of ____________
if there is a subacute onset of Parkinson's, think of MEDICATIONS that block/deplete dopamine
27
epidemiology of Huntington's (prevalence, onset)
2-10 per 100,000 worldwide - onset: middle/later stages of life - relentless progression (dead w/i 10-15 years of symptom onset)
28
genetics of Huntington's
- autosomal dominant - chromosome 4 - mutation in Huntingtin protein - CAG repeat: more repeats = more severe - anticipation: gets worse with more generations - paternal inheritance increases severity
29
clinical features of Huntington's
Movement disorder - chorea - Parkinsonism (late/juvenile cases) Dementia Psychiatric - depression - psychosis
30
pathology of Huntington's disease
Neuronal loss and gliosis in striatum --> atrophy - early disease: shift to direct pathway causes chorea - late disease: both pathways involved causes Parkinsonism Neuronal loss in cortex -cognitive and psychiatric symptoms
31
neuronal loss and gliosis in striatum causes
neuronal loss and gliosis in striatum causes ATROPHY
32
early sign of chorea?
difficulty systaining tongue protrusion
33
treatment of Huntington's
-mainly supportive (nothing to alter/stop disease) Treat chorea - dopamine receptor blockers (antipsychotics) - dopamine deleting agents - benzodiazepines Neuropsychiatric Support Nutrition (to sustain movements) Genetic counseling
34
tremor
oscillatory movements | -alcohol may help reduce
35
hemiballismus
- violent, flailing movements | - can be caused by hyperglycemia
36
myoclonus
-rapid, jerky movements
37
dystonia
-involuntary contractions
38
tics
- semivoluntary - stereotyped movements - uniquely human - can be supressed (but uncomfortable to do so)