2. Basal Ganglia Flashcards

1
Q

basal ganglia

A
  • group of structures affecting motor control, cognitive function, and affective function
  • motor: normal function is to control level of excitatory drive to cortex, level changes during movement and may be permanently altered from disease
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2
Q

basal ganglia in the brain

A
  • striatum: caudate and putamen
  • globus pallidus
  • associated structures:
    • diencephalon: motor thalamus, subthalamic nucleus
    • midbrain (mesencephalon):
      • substantia nigra (black substance; neurons are dopaminergic)
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3
Q

movement diseases/disorders involving basal ganglia

A

+ too much excitation: involuntary movements
- too little excitation: slowness (bradykinesia) or absence (akinesia) of voluntary movement

ex: parkinson’s, tourette’s, restless leg syndrome, tardive dyskinesia, tardive dystonia, dystonias (abnormal tone and posture), huntington’s disease (involuntary movement)

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4
Q

parkinson’s disease

A
  • usually but not always in elderly
  • neurodegenerative disease
  • age of onset: 60+
  • 55 men/45 women
  • slow progressive disease
  • can have substantia nigra
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5
Q

substantia nigra in PD

A
  • degeneration (death) of neurons of SN, loss of dopaminergic neurons –> loss of dopaminergic input to the caudate and putamen
  • cause unknown (possibly genetic, environmental, postinfectious PD)
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6
Q

PD symptoms

A
  • motor, affective (depression), cognitive (dementia)
    motor:
  • tremor (at rest, hands, mouth; disappears when movement is initiated)
  • bradykinesia (slowness of movement)
  • akinesia (absence of movement, esp self-initiated movement and “associated movements”; swinging arms when walking, loss of facial expression)
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7
Q

PD treatments

A
  • medical: I-dopa (precursor of dopamine to help with symptoms temporarily)
  • surgical: lesion in pathway (destroy axons to alleviate symptoms)
  • DBS: deep brain stimulation (electrodes implanted in brain, subthalamic nucleus, pacemaker-like device); eliminates abnormal signals to cortex
  • experimental: tissue/stem cell implants
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8
Q

MPTP

A
  • drug that was synthesized by mistake trying to imitate heroin
  • causes substantia nigra degeneration and Parkinson’s symptoms
  • used to induce PD in animals and test treatments
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9
Q

true or false: dopamine is only found in substantia nigra

A

false: several other cell groups synthesize and release dopamine
- it is a transmitter in multiple structures and functional systems (ex: reward system)

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10
Q

true or false: several disorders are attributed to dopamine dysfunction, either too much or too little dopaminergic activity

A

true (transmitter, receptors, and transporters can be affected)

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11
Q

dopamine acts on dopamine __, of which there are multiple types (__-__) and they have different distributions in the brain

A

receptors, D1-D5

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12
Q

dopamine in schizophrenia

A
  • too much dopaminergic action in frontal lobes
  • treatment: “neuroleptics” (dopamine receptor blockers)
  • longterm use of neuroleptics can result in irreversible movement disorders (tardive dyskinesia or tardive dystonia)
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13
Q

atypical antipsychotics

A
  • affect only subsets of dopamine receptors (those in cortex thought to mediate schizophrenia, NOT those for movement in striatum)
  • does not cause tardive dyskinesia
  • may cause other medical problems like weight gain or diabetes
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14
Q

tourette’s syndrome

A
  • movement disorder (tic - brief involuntary movement)
  • can suppress tics for short period of time
  • age 3-9, occurs with ADHD, may be misdiagnosed as behavioral
  • male 3:1
  • symptoms may resolve by late adolescence
  • clear hereditary component but no gene disorder
  • too much dopaminergic activity in motor pathways (serotonin and norepinephrine)
  • treated with dopamine receptor blockers (haldol)
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15
Q

restless leg syndrome (RLS)

A
  • both sensory and motor symptoms
  • uncomfortable sensations that are relieved by moving legs
  • worst at night, disrupts sleep (sleep and movement disorder)
  • more common in women
  • cause unknown, maybe too little dopamine
  • genetic contribution
  • basal ganglia/dopamine disorder
  • treated with dopaminergic drugs and dopamine precursors
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16
Q

how does cocaine increase dopamine levels

A

by blocking the dopamine transporter
- action of dopamine at a synapse is terminated by its reuptake into the presynaptic cell by a “transporter”, which repackages dopamine for release later

17
Q

ADHD/ADD

A
  • 1/10-20 children
  • functional dopamine deficiency, probably in frontal cortex
  • difficulty paying attention, impulse control, hyperactivity
  • symptoms may continue into adulthood
  • behavioral diagnosis, lots of variability
18
Q

ADHD/ADD treatment

A
  • ritalin (methylphenidate) or adderall (amphetamine)
  • increase dopamine levels
  • ritalin acts on dopamine transporter
  • adderall increases the release of dopamine and norepinephrine
19
Q

huntington’s disease (huntington’s chorea)

A
  • degeneration of cells in striatum, NOT dopamine disorder
  • genetic, autosomal dominant, can be tested for
  • age 30-50
  • progressive and fatal
  • changes in voluntary movement, emergence of involuntary movement, loss of cognitive function (dementia) and changes in affective function (depression)
20
Q

progressive supranuclear palsy (PSP)

A
  • loss of cells in substantia nigra and degeneration of neurons in other structures of brainstem and cerebellum
  • not responsive to dopaminergic drugs