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AIM - The Brain > Basal Ganglia > Flashcards

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
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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

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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 vis 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
Q

secondary causes of Parkinsonism

A
  • toxins (MPTP, manganse)
  • postcephalitic parkinsonism
  • dopamine blocker/depleter drugs (antipsychotics, antiemetics)
26
Q

if there is a subacute onset of Parkinson’s, think of ____________

A

if there is a subacute onset of Parkinson’s, think of MEDICATIONS that block/deplete dopamine

27
Q

epidemiology of Huntington’s (prevalence, onset)

A

2-10 per 100,000 worldwide

  • onset: middle/later stages of life
  • relentless progression (dead w/i 10-15 years of symptom onset)
28
Q

genetics of Huntington’s

A
  • 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
Q

clinical features of Huntington’s

A

Movement disorder

  • chorea
  • Parkinsonism (late/juvenile cases)

Dementia

Psychiatric

  • depression
  • psychosis
30
Q

pathology of Huntington’s disease

A

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
Q

neuronal loss and gliosis in striatum causes

A

neuronal loss and gliosis in striatum causes ATROPHY

32
Q

early sign of chorea?

A

difficulty systaining tongue protrusion

33
Q

treatment of Huntington’s

A

-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
Q

tremor

A

oscillatory movements

-alcohol may help reduce

35
Q

hemiballismus

A
  • violent, flailing movements

- can be caused by hyperglycemia

36
Q

myoclonus

A

-rapid, jerky movements

37
Q

dystonia

A

-involuntary contractions

38
Q

tics

A
  • semivoluntary
  • stereotyped movements
  • uniquely human
  • can be supressed (but uncomfortable to do so)
39
Q

effect of striatum on GPe

A

striatum INHIBITS GPe

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

40
Q

effect of GPe on STN

A

GPe INHIBITS STN

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

41
Q

effect of STN on GPi

A

STN STIMULATES GPi

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

42
Q

effect of GPi on thalamus

A

GPi INHIBITS thalamus

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

43
Q

effect of thalamus on cortex

A

thalamus STIMULATES cortex

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

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