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Block 5; Week 3 > Parkinson's & Huntington's Disease-Farbman > Flashcards

Parkinson's & Huntington's Disease-Farbman Flashcards

1
Q

What are movement disorders? What causes them? What are the 2 types?

A

impaired voluntary movement
Causes: NOT cerebellum, but they ARE related to basal ganglia.
2 types: hypokinetic & hyperkinetic

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2
Q

What is another term for slowed movements/hypokinesias? What is an example of a type of movement in this category?

A

aka bradykinesia

Ex: Parkinsonian

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3
Q

What are some examples of hyperkinesia movement types?

A 
tremor
chorea
athetosis
dystonia
tics
ballismus
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4
Q

What are the motor features of parkinsonism?

A

tremor
rigidity
bradykinesia
postural instability

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5
Q

What is the pathological basis of parkinsonism?

A

dysfunction of the substantia nigra

this affects the production of dopamine

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6
Q

What are some causes of Parkinsonism?

A

antipsychotic drugs
postencephalitis
toxic agents
MOST COMMON-Parkinson’s Disease

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7
Q

How can antipsychotic drugs cause Parkinsonism?

A

they reduce the amount of dopamine available chemically

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8
Q

How can post encephalitis cause Parkinsonism?

A

this damages the nigrostriatal system

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9
Q

Which types of toxic agents can cause Parkinsonism?

A

Manganese

MPTP

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10
Q

The first account of Parkinson’s disease in 1817 described it how?

A

a condition w/ a resting tremor & a festinating gait

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11
Q

What is the mean onset age of Parkinson’s?

A

63

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12
Q

What is the male to female ratio for Parkinson’s?

A

3:2

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13
Q

What is the prevalence of Parkinson’s? How many new cases are there annually?

A

160/100K

50K new cases annually

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14
Q

What do lab values show for Parkinson’s patients?

A

they are normal!

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15
Q

How does a diseased substantia nigra look in a Parkinson’s patient? How do lewy bodies appear in patients?

A

substantia nigra will appear whiter b/c deprived of melanocytes & some neurons destroyed (less dopamine)
lewy bodies appear with a dark ring of melanocytes around them.

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16
Q

Describe the resting tremor of a Parkinson’s patient.

A

it is at 5 tremors/s (hz)
pill rolling action
asymmetric-if symmetric think abnormal PD or drugs

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17
Q

Describe the rigidity seen with Parkinson’s patients.

A

they exhibit increased resistance to passive movements

the often show cog wheeling

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18
Q

What all is involved in the bradykinesia of Parkinson’s patients?

A

you will often see an armswing b/c there is a loss of automatic movements
masked facies (loss of expression)
festinating gait
freezing in position

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19
Q

What is a festinating gait?

A

this is a type of gait in which it looks like you are almost falling as soon as you start walking.

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20
Q

What types of postural instability features will you notice w/ Parkinson’s patients?

A

they will have difficulty rising from a chair (esp if they have their arms folded across their chest)
they wills start falling backwards if you tap them (good thing to check)

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21
Q

Do Parkinson’s patients experience a tremor when they are moving or when they are at rest?

A

When they are at rest. Cerebellum-intention, during movement. The tremor for PD patients kind of goes away when they are moving.

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22
Q

While Parkinson’s is largely a clinical diagnosis & you may have to just wait to see how the medication works…what are the imaging options that are available?

A

SPECT scan-shows the dopamine NT in the brain

PET scan-only used in research

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23
Q

Why can’t you just give a Parkinson’s patient dopamine directly?

A

b/c it wouldn’t be able to cross the BBB

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24
Q

What form of dopamine does work w/ PD patients?

A

LevoDOPA-can cross the BBB & be converted into dopamine.

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25
Q

T/F Parkinson’s medications slow the destruction of the substantia nigra neurons.

A

FALSE> they do not cure the disease. They only lessen the symptoms.

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26
Q

Aside from levodopa, what are other PD meds?

A

dopamine agonists
MAOB inhibitors: prevent the breakdown of dopamine
COMT inhibitors: prevent the breakdown of dopamine
Anti-Cholinergics: restore the ACH: Dopamine balance.

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27
Q

When should a surgical option be considered for Parkinson’s patients? What does this help treat?

A

only as a last resort
will only help those patients that are responsive to dopamine medications.
helps: rigidity, tremors, dyskinesia
doesn’t help: postural instability

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28
Q

What is the main surgical option available to Parkinson’s patients?

A

deep brain stimulation at the substantia nigra or GPi

install pack in the right chest & the wires are only 7 mm long.

29
Q

What are symptoms that can precede a diagnosis of Parkinson’s?

A

anosmia (loss of smell)
constipation
REM sleep behavior disorder (kicking during REM)

30
Q

Aside from the hallmarks of PD, what are some other symptoms that may be present?

A

depression
orthostatic hypotension
dementia

31
Q

What is the Braak hypothesis? What is the significance of its 6 stages?

A

neuronal damage begins to occur in the first stage of Braak in certain areas of the brain. As you progress to the later stages, the damage becomes worse even tho it mostly stays in the same centers of the brain.
Stages 3 & 4: What we think of as Parkinson’s
Stages 5 & 6: When we hit the cortex

32
Q

What is the most common movement disorder?

A

Essential tremor

33
Q

What is essential tremor?

A

a hyperkinetic movement disorder that is mainly located in the arms & neck
we don’t know what causes it
alcohol makes it better

34
Q

How is essential tremor different from Parkinson’s tremors?

A

Essential is faster, bilateral, an action tremor (not resting), responds to alcohol
*Parkinson’s rarely hits the neck-most common spot of essential tremor

35
Q

What is athetosis?

A

these are movements that are slow, sinous, writhing

can be generalized or specific to a particular part of the body

36
Q

What is dystonia? What are the different types of dystonia?

A

these movements are so sustained that they appear to be abnormal postures

  • *can have focal dystonia in violinists or golfers
  • *can have general dystonia as a disease
  • *dystonia is a symptom too, of Parkinson’s
37
Q

What is the treatment for dystonia?

A

botox for focal dystonia

deep brain stimulation for general dystonia

38
Q

What are tics? Are they common? Can you suppress them?

A

rapid, purposeless movements; repetitive
super common (affect up to 20% of children, you outgrow them)
you can suppress them for a while, but then they come back

39
Q

What is the clinical definition of Tourrette syndrome?

A

motor & vocal tics

40
Q

Do people with tics do them in their sleep?

A

no, unless you have palatoclonus. hear clinic of soft palate in the middle of the night.

41
Q

What is hemiballismus? Do they resolve?

A

these are violent movements involving proximal muscles

often resolve spontaneously

42
Q

What usu causes hemiballismus? What condition is it sometimes confused with?

A

a stroke in the contralateral subthalamic nucleus

sometimes confused with chorea

43
Q

What is chorea?

A

irregular unpredictable jerky movement

spreads from one part of the body to another in random sequence

44
Q

What are the possible causes of chorea?

A

Huntington’s disease
Drug induced
Syndenham’s Chorea

45
Q

What is syndenham’s chorea? Which age group is this most common in?

A

this mainly occurs in children
this is chorea from a complication of Group A Hemolytic Streptococcal Infections
**if you have this & then recover, can recur during pregnancy

46
Q

In 1872, A Long Island Physician, George Huntington described Huntington’s disease. What were his 3 hallmarks of the disease?

A
  1. hereditary
  2. tendency to insanity & suicide
  3. becomes grave only in later adult life
47
Q

What is the mean age of onset of Huntington’s disease? When you have the young variant of it which additional symptoms do you see?

A

mean age of onset: 40

Younger get rigidity & akinesia

48
Q

What are the results/symptoms of Huntington’s disease?

A 
caudate atrophy
chorea
speech disturbances
falls
cognitive & psychiatric problems
49
Q

What type of genetic disease is Huntington’s?

A

fully penetrant autosomal dominant disorder

demonstrates anticipation, though

50
Q

Which chromosome are the Huntington’s genes found on?

A

short arm of chromosome 4

CAG repeats are found there

51
Q

If you have less than 26 CAG repeats…what is your classification? Do you have Huntington’s disease?

A

Normal, no disease.

52
Q

If you have between 27 & 35 CAG repeats…what is your classification? Do you have Huntington’s disease?

A

Intermediate classification.

No disease.

53
Q

If you have between 36 & 39 CAG repeats…what is your classification? Do you have Huntington’s disease?

A

Classification: Not fully penetrant.

Maybe get the disease

54
Q

If you have over 40 CAG repeats…what is your classification? Do you have Huntington’s disease?

A

Fully penetrant.

You have the disease.

55
Q

Although Huntington’s disease is difficult to treat b/c of its progressive & neurodegenerative nature…how can you treat the chorea?

A

with neuroleptics

can treat with tetrabenazine (a dopamine depleter)

56
Q

How many Huntington’s patients experience psychiatric problems?

A

50%-depression
30%-major depressive episode
10%-mania
suicide more common than in other depressed patients

57
Q

What are some of the cognitive problems experienced by Huntington’s patients?

A

apathy
impulsivity
executive dysfunction

58
Q

T/F There are many approved medications to treat a wide array of movement disorders.

A

False. Only really for Parkinson’s.

59
Q

What are the symptoms of Wilson’s disease?

A

Hepatic: jaundice, varices, spider angiomas
Neurological: tremors, Parkinsonism, chorea, dystonia, dysarthria
Psychiatric

60
Q

What is the Kayser-Fleischer ring?

A

this is a ring of accumulated copper around the iris.

61
Q

What causes the symptoms of Wilson’s disease?

A

abnormal metabolism of copper

toxic buildup of free copper

62
Q

How can you diagnose Wilson’s disease?

A
  • Gold standard: 24 hr urinary screen of copper (elevated about 100 micrograms) in WD
  • ceruloplasmin will be low
  • Liver biopsy may be helpful
  • Gene test difficult unless you know a family member w/ the condition
  • MRI-will show hyper intensities of the bilateral thalamus & putamen on T2 images
  • Midbrain shows face of panda
63
Q

What does it mean that the MRI of a WD patient would show the face of a panda in the midbrain?

A

high signal in tegmentum
normal red nucleus
**these are the things that make the face

64
Q

What are the genetics of WD?

A

aut recessive
error in ATP7B gene
a bunch of different genes could cause the problem

65
Q

Why would an acetylcholine esterase inhibitor help with tics?

A

b/c it raises your ACh levels & helps with the ACh/Dopamine seesaw so that you aren’t as hyperkinetic.

66
Q

Can you use something that reduces dopamine levels to deal with hyperkinetic movement disorders like WD?

A

Sorta, you can use atypical antipsychotics that will reduce dopamine levels
Side Effects: weight gain, fatigue, irritability

67
Q

What are some of the difficulties that patients with Huntington’s disease might have at work?

A

they may have trouble planning & multitasking

68
Q

What is the significance of a Huntington’s disease patient not being able to do the tap no tap test well?

A

this shows disinhibition of the frontal lobe

Block 5; Week 3 (9 decks)

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