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Neurology 1- M2 > 09 09 2014 Basal Ganglion > Flashcards

09 09 2014 Basal Ganglion Flashcards

1
Q

What is the basal Ganglia

A

cluster of nuclei in the cerebrum, diencephalon, and midbrain that function together to facilitate or inhibit behaviors and actions.

-play large role in movement (also play a role in emotion and cognition and eye movement)

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2
Q

Basal Ganglia loops

  • loop?
  • What does it help in?
A

Cortex-Cortex

  • -Motor cortex sends signal to striatum.
  • Striatum sends output to Globus pallidus.
  • Internal Globus pallidus sends signal to VA/VL
  • VA/VL (thalamus) sends signal back to cortex

Facilitates motor cortical areas – turns up excitability

  1. initiates movement
  2. sequencing movement
  3. automaticity
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3
Q

What happens when there is a lesion in the basal ganglia

A

Increase or decrease in movement

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4
Q

Dopamine modulates actions in the basal ganglia, limbic system and prefrontal cortex through which pathways?

A
  1. Nigrostriatal pathway (aka mesostriatal) – dopaminergic neurons that control of movements. Projects to caudate and putamen. Defect = parkinson’s disease ( Basal ganglia)
  2. Mesolimbic pathwy – dopminergic neurons that regulate the reward pathway. Defects = schizophrenia (positive symptoms) and/or depression
    (Limbic system)
  3. Mesocortical pathway- working memory. Defects may play a role in Schizophrenia (negative symptoms), hypokinesia seen in Parkinson’s.
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5
Q

Mechanisms of VA/VL

A

Excites motor complex by increasing motor output

-Glutamate

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6
Q

Internal Global Pallidus

A

provides tonic inhibition to VA/VL

-GABA

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7
Q

Disinhibition vs. Excitation

A

Disinhibition: inhibition of internal globes pallid us cause more excitation of VA/VL to cortex

Excitation: Internal Globus Pallidus gets excited via input. It leads to more inhibition of VA/VL –> less signals sent to motor cortex

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8
Q

Who excites GPi and who inhibits GPi?

A
  • Subthalamic nucleus excites GPi – causing inhibition of cortex and movement
  • Striatum inhibits GPi – causing more excitation of cortex and movement.
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9
Q

What would happen to the frequency of movement if there was a lesion in the sub thalamic nucleus?

A

produce too much movement (contralateral hemiballismus – wild flinging movement)

-Subthalamic nucleus excites GPi – causes damping of VA/VL and cortex signals.

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10
Q

Direct pathway (loop)

A

Facilitiates movement

-disinhibition of GPi (from striatum) that increases activation of VA/VL

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11
Q

Indirect pathway (loop)

A

Inhibits unwanted movement

-disinhibition of subthalamic nucleus – increases GPi = decrease VA/VL signaling

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12
Q

The effect of dopamine to both the direct and indirect pathway ( general)

A

Dopamine facilities movement! Increase signaling from VA/VL to motor cortex

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13
Q

How/ what is the mechanism by which dopamine increases signaling to motor cortex (via VA/VL) via direct ?

A
  • dopamine from substance nigra pars compactus binds to DA1 receptors in Striatum (excitatory). They inhibit GPi (downstream)
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14
Q

How/ what is the mechanism by which dopamine increases signaling to motor cortex (via VA/VL) via the indirect pathway?

A

Dopamine neurons from substance nigra target D2 receptors (inhibitory) on striatum (putamen) . Inhibits sub thalamic nucleus which therefore also inhibits GPi stimulation.

Releases VA/VL from inhibition

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15
Q

Acetylcholine is present in the striatum. In what pathway does it have an effect and what is the effect?

A

ACh is in striatum and is most effective in indirect pathway.

It excites the indirect pathway –> tends to inhibit movement.

Anticholinergics are effective if you want more movement in Parkinson’s disease

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16
Q

hypokinesia

A

too little movement

“negative symptoms”

17
Q

Hyperkinesia

A

too much movement

“positive symptoms”

18
Q

Dyskinesia

A

abnormal movement

19
Q

If there is a lesion in basal ganglia, where will the effects be seen– ipsilateral or contralateral?

A

contralateral

  • basal ganglia is sitting right next to motor complex.
  • -regulates pathway on same side so of course it affects the opposite side of the body.
20
Q

Negative symptoms of Basal Ganglia disease

A

Parkinson’s disease

  • Akinesia (no movement)
  • Bradykinesia (slow movement)
  • Decreased postural adjustments
  • Hypokinesai (decreased amplitude of movements
    - handwriting gets smaller
21
Q

Positive symptoms of Basal Ganglia disease

A

-rigidity

  • dystonia-increased muscle tone in isolated muscles
    - limbs to bend/twist
    - head turned to one side (CN 11)
  • athetosis: slow, writhe ring movements in lips, hands, and fingers. Patients cannot maintain fixed position.
  • chorea: continuous rapid movements of face, tonuge, and limbs. Most common with Huntingont’s
  • Hemiballismus – violent, involuntary flailing movements
  • Tics
  • Tardive dyskinesia : from antipsychotic or antiemetic drugs- causes dyskinesia
  • Tremor–
  • Prakinson’s: 3-5 hz at rest: hands and arms. beginning unilaterally.
  • Essential tremor:5-8 Hz : everywhere. Usually bilaterally.– basal ganglia

-Myoclonus: sudden rapid muscular jerks – whole body. damage = basal ganglia, cerebellum and cortex.

22
Q

what are the 4 parallel basal ganglia pathways

A
  1. motor
  2. Oculomotor – abnormal eye movements
  3. Cognition (prefrontal)
  4. Emotions (limbic)
23
Q

What are two diseases that result from damage to basal ganglia

A
  1. Huntington’s Chorea

2. Parkinson’s disease

24
Q

Huntington’s Chorea

what is it?
onset?
Prognosis?
Treatment?

A

Autosomal dominant neurodegenerative disorder with cell loss in caudate and putamen.

onset = 40s-50s

progressive and degenerative

Median survival = 15 years

treated with drugs that decrease dopamine.

25
Q

Major symptoms with huntington’s chorea

A
  1. chorea: rapid movements of face, tongue, limbs.
  2. dementia (cognitive impairment)
  3. psychiatric manifestations
    - anxiety
    - moodiness
    - OCD
    - Impulsiveness
26
Q

What basal ganglia pathway does Huntington’s disease affect?

A

Indirect pathway

-cell death of caudate and putamen causes loss of inhibition of sub thalamus. Subthalamus is inhibited so stimulation of GPi is lost.

VA/VL is released from inhibition

= increase in movement

27
Q

Cardinal symptoms of PD

A

BEGIN UNILATERALLY

  • Bradykinesia
  • resting tumor (pill rolling motion)
  • rigidity
  • postural instibilty
28
Q

Other motor symptoms of parkinson’s

A
  • Masked facies (hypomimia)– no emotional feeback.
  • Festination gait – a shuffle that starts out slowly and then increases in speed.
  • stooped posture
  • freezing
  • difficulty turing in bed.
29
Q

What are some non-motor symptoms?

A

symptoms can spread across systems. May develop dementias and other cognitive/behavioral disorders

30
Q

what are some treatment options of PD

A
  1. pharmaceutical (look at pharm lecture for PD)
  2. Surgical lesions
    • Thalamus : young unilateral tremor and no rigidity or bradykinesai.
    • Globus pallidus (internal) for tremor and rigidity
  3. Deep-brain stimulation
    - GPi
    - Subthalamic nucleus
    - Thalamus.
31
Q

How does deep brain stimulation work?

A
  1. normalizes outputs

2. blocks action potential

32
Q

What is the more common neuroprotective treatment?

A

Exercise

-neuroprotective AND neurorestorative (after lesions)

33
Q

Parkinson’s plus syndromes

A
  1. lack of resting tremor
  2. symmetrical symptoms
  3. Early postural instability
  4. Lack of response to dopamine
  5. Progressive supranuclear palsy– above CN nuclei. Affects rostral brain.

Neurology 1- M2 (22 decks)

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