basal ganglia Flashcards

1
Q

what are the functions of the basal ganglia

A

Motor functions ( voluntary)
and non motor funcitons

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2
Q

what are examples of the motor functions that the basal ganglia controls

A

 Action selection
 Inhibition of competing movements
 Enabling motor programs

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3
Q

what are examples of non motor funcitons that the basal ganglia controls

A

 Cognition and emotion
 Reward and addiction

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4
Q

what are the pathologies of the basal ganglia

A

( movment disorders) Hypokinetic
Hyperkinetic
-Cognitive and neuropsychiatric
symptoms

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5
Q

what are the intputs to the motor cortex ( area 4)

A

 Thalamic nuclei VA & VL
 Premotor cortex (area 6)

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6
Q

how can you see intergration in the motor cortex

A
  • Cortex has subdivisions including the motor, sensory, and association cortexes.
  • From the motor cortex, there are neurons that synapse to alpha motor neurons (blue)  aka the pyramidal tracts
  • Basal ganglia receive inputs from all areas of the cortex
  • Basal ganglia then projects to the thalamic motor nuclei, VA and VL
  • VA and VL project to the motor cortex.
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7
Q

what is the basal ganglia composed of

A
  • globulis pallidus which is composed of the causdate and the putamen ( 1 nucleus)
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8
Q

what is another term of the caudate and putamen?
globulus pallidus

A
  • neostriatum
  • paleostriatum
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9
Q

what are the associated nuclei (midbrain)
- what are their recpriocal connections

A
  • Substantia nigra
    >Reciprocally connected to
    caudateputamen
    > Dopaminergic projection to striatum
  • Subthalamic nucleus
    > Reciprocally connected to globus
    pallidus
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10
Q

where is the sbstantia nigra

A
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11
Q

what is this

A

subthalmic nucleus

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12
Q

what are the symptoms of parkinsons disease

A

 Tremor at rest (“pill rolling tremor”)
 Rigidity
 Bradykinesia ( walk slowly)
 Motor blocks (“freezing”)
 Loss of postural reflexes
 Cognitive defects are common

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13
Q

what is parkinsons caused by

A
  • due to loss of dopamine in th substantia nigra, degeneration of the substantia nigra
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14
Q

what does someone with parkinsons look like

A
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15
Q

what is the biosynthetic pathway of dopamine

A

syntheitc pathway stops at DOPA in the SN

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16
Q

how can you treat parkinsons disease?
why cant you give dopamine

A
  • take L dopa which is the precusor of dopamine
  • bc of the blood brain barrier will not allow it to cross but L dopa can cross
  • the SN then converts L dopa to dopmaine
17
Q

what is huntingtons chorea
- how does it present

A

 Degeneration in caudate nucleus
 Excess movements
 Autosomal dominant ( inhertied - 50% of offspring half a likely hood of getting it )

18
Q

what does huntingtons chorea eventually affect

A
  • the prefrontal cortex
    the pt becomes degenerate
19
Q

when does huntingtons chorea present

A
  • around 50 yo
20
Q

what is the huntigintons chorea the oppoiste of how should you not treat it

A
  • parkinsons
  • DONT TREAT WITH L DOPA
21
Q

what is ballismus
- how does it present

A

 Damage in subthalamic nucleus by stroke
> typically affects half the body
 Ballistic movements
- flinging movements fof limbs and tongue

22
Q

what is athetosis
- how does it present

A

 Excess movements
 Writhing (twisting) movements

23
Q

what are some other basal ganglia disorders

A

 Dystonia
 Tics
 Tourette syndrome

24
Q

what is the role of the basal in motor function

A

 suppresses inappropriate
motor program
 Activation of direct pathway
temporarily releases one motor
program from inhibition
 Also involved in learning of motor
programs

25
Q

what is the ventral tegmental area (VTA)

A

 Dopaminergic projections to
prefrontal cortex and limbic cortex
 Selection of emotional, executive and
cognitive programs
 Dopaminergic projection to nucleus
accumbens
 Reward and addiction

26
Q

where is the ventral tegemtnal area

A