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Neuro > Disease Of The Basal Ganglia > Flashcards

Disease Of The Basal Ganglia Flashcards

1
Q

Motor disorders associated with basal ganglia dysfunction

A

Parkinson’s Disease
Huntington’s Disease
Dystonia
Gilles de la Tourette syndrome

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2
Q

Psychiatric disorders associated with basal ganglia disorder

A

OCD
ADHD

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3
Q

Secondary damage associated with basal ganglia dysfunction

A

Cerebral palsy
Wilson disease

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4
Q

Pathophysiology of Parkinson’s

A

Not enough dopamine
Detection of Lewy bodies

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5
Q

Pathophysiology of Huntington’s

A

Too much dopamine

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6
Q

Symptoms of Parkinson’s

A

Increased muscle tone
Reduced movements

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7
Q

Symptoms of Huntington’s

A

Decreased muscle tone
Overshooting movements

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8
Q

Formation of dopamine

A

L-tyrosine —> tyrosine hydroxylase
L-DOPA —> DOPA decarboxylase
Dopamine

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9
Q

Number of dopamine receptors

A

5

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10
Q

Main area damaged in Parkinson’s

A

Substantia nigra

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11
Q

How many neurons must a person lose before symptoms of Parkinson’s

A

2/3

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12
Q

Neuronal cell death in Parkinson’s

A

About 50% cell death before any symptoms

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13
Q

Main area damaged in Huntington’s

A

Caudate nucleus/ striatum

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14
Q

Lateral ventricle and Huntington’s

A

Lateral ventricles are dramatically enlarged as caudate nucleus has shrunk away

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15
Q

Parkinson’s

A

Less production of dopamine by Substantia nigra so decreases movement

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16
Q

Huntingtons

A

Reduced production of GABA by striatum so increases movement

17
Q

Main symptoms of Parkinson’s

A

Brady/Akinesia
Problems with doing up buttons, keyboard etc
Writing smaller
Walking deteriorated: Small steps, dragging one foot etc

Tremor
= At rest
May be on one side only

Rigidity
Pain
Problems with turning in bed

18
Q

Most powerful drug for Parkinson’s

A

L-DOPA (naturally occurring precursor and drug)
- aims to correct dopamine deficit

19
Q

Drug treatment of Parkinson’s

A

Drugs mostly aim at correction of dopamine deficit- L-DOPA

But:
More and more cells die
The drugs work shorter and shorter
The longer on treatment, the more likely are the patients to develop side effects, in particular dyskinesias

20
Q

Dyskinesia

A

involuntary, erratic, writhing movements of the face, arms, legs or trunk

21
Q

Deep brain Stimulation

A

Functional lesions of the Subthalamic nucleus- improvements of Parkinson’s

22
Q

What does deep brain stimulation target

A

Subthalamic nucleus

23
Q

Normal pathway in brain

A

Cortex - striatum - thalamus - cortex

Regulated. By Substantia nigra and Subthalamic nucleus

24
Q

Role of Subthalamic nucleus

A

Inhibit of motor control

25
Q

Parkinson’s pathway

A

Lack of dopamine— decreased inhibition of Subthalamic nucleus — increased inhibition of motor movements

26
Q

How does deep brain stimulation work

A

Inhibits Subthalamic nucleus— net gain of mivement

27
Q

Clinical features of Huntington’s

A

Chorea
Dementia/psychiatric illness
Personality change

28
Q

Clinical genetics of Huntington’s

A

Autosomal dominant
Fully penetrant

29
Q

Chorea

A

symptom that causes involuntary, irregular or unpredictable muscle movements. It affects your arms, legs and facial muscles

30
Q

Pharmacological treatment of Huntington’s

A

Dopamine receptor blockers = neuroleptics
-typically used for psychosis treatment

31
Q

Genetics of Huntington’s

A

40 or more triplet CAG repeats of Huntingtin gene- expansion disorder

32
Q

Normal number of triplet repeats in Huntingtin gene

A

37

33
Q

Age of onset and number of CAG repeats - Huntington’s

A

More repeats - earlier likely to develop disease

34
Q

Disease-modelling therapy- Huntington’s

A

Down regulation of mutant Huntingtin protein

Neuro (22 decks)

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