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YEAR 4 NEURO > Parkisons disease and Parkinsonism > Flashcards

Parkisons disease and Parkinsonism Flashcards

1
Q

What is parkisons disease?

A

Progressive neurodegenerative disorder caused by degeneration of dopaminergic neurons in substantia nigra

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2
Q

What are the triad of symptoms in Parkinsons disease?

A

Bradykinesia, tremor and rigidity
(also get postural instability)
Motor symptoms usually asymmetrical

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3
Q

Describe the bradykinesia associated with Parkisons

A

Poverty of movement also seen
Short shuffling steps with reduced arm swinging
Difficulty initiating movement

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4
Q

What are the non-motor features of Parkisons disease?

A

Mood changes- depression most commonly, dementia, psychosis
REM sleep behaviour disorder
Sweating
Drooling of saliva
Micrographia
Mask like face
Olfactory loss
autonomic failure e.g. postural hypotension

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5
Q

Describe the Parkisonian tremor?

A

Most marked at rest, 3-5Hz
Worse when stressed or tired, improves with voluntary movement
Typically ‘pill-rolling’

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6
Q

Describe the rigidity in Parkisons disease?

A

Lead pipe
Cogwheel, due to superimposed tremor

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7
Q

How do you diagnose Parkisons Disease?

A

1) Based on clinical features:
Bradykinesia + at least one of muscular rigidity, 4-6Hz rest tremor, postural instability (not caused by primary visual, vestibular, cerebellar or propiocepetive dysfunction)

2) Exclude other causes of parkisoniasm

3) 3 or more of the following needed (plus step 1)
Unilateral onset
Rest tremor present
Progressive disorder
Persistent asymmetry
Excellent response to Levodopa
Clin course of 10 years or more
Levodopa response for 5 years or more

NOTE: structural neuro imaging in normal

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8
Q

Outline the pathology of Parkinsons disease?

A

Neurodegneration
Lewy body in the substania nigra with alpha synuclein
Loss of pigment in the substania nigra- 50% of pigment loss–> symptoms, increased turnover
Reduced Dopamine

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9
Q

What medication is first line in Parkisons if the patients motor symptoms are affecting their QOL?

A

Co-careldopa (Levodopa + peripheral dopamine decarboxylase)

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10
Q

Why do we give LevpDopa instead of dopamine?

A

Dopamine cannot cross the blood brain barrier

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11
Q

MOA of levodopa?

A

Taken up by dopaminergic cells in substantia nigra and converted to dopamine.

If their are less dopaminergic cells–> less reliable affect of Levodopa

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12
Q

What do we need to prescribe along with levodopa?

A

A peripheral DOPA decarboxylase inhibitor (so it doesn’t get broken down before it reached the BBB) e.g co-careldopa (Brand name: sinemet) or Co-beneldopa (madopar)

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13
Q

Benefits of prescribing co-careldopa/co-beneldopa instead of just LevoDopa?

A

Reduced dose required
Reduced side effects
Increase L-DOPA reaching brain

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14
Q

Advantages of Co-careldopa?

A

Highly efficacious
Low side effects

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15
Q

Side effects of Levodopa?

A

Dry mouth
psychosis
tachycardia
nausea/anorexia
hypotension

Note side effects are reduced as L-dopa administered as co-careldopa

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16
Q

Disadvantages of Levodopa?

A

Precursor so needs enzyme conversion
Long term leads to loss in efficacy, involuntary movement, on and off- variations in motor performance

17
Q

When do you use dopamine receptor agonists?

A

De novo therapy
Add on therapy

18
Q

What are the risks of ergot-derived dopamine receptor agonists?

A

Associated with pulmonary, retroperitoneal and cardiac fibrosis, Pts should have an Echocardiogram, ESR, creatinine and CXR before treatment and pts need to be closely monitored

19
Q

Advantages of dopamine receptor agonists?

A

Direct actings
less motor complications
Possible neuroprotection

20
Q

Disadvantages of dopamine receptor agonists?

A

Less efficacy than L-dopa
Impulse control disorders
Excessive daytime somnolence
More likely than Ldopa to cause hallucinations in some pts

21
Q

What are features of impulse control disorders?

A

Pathological gambling
hyper-sexuality
compulsive shopping
desire to increase dosage
punding

22
Q

Side effects of dopamine receptor agonists?

A

Sedation
hallucinations
confusion
nausea
hypotension
Impulse control disorders

23
Q

What is the role of monoamine oxidase-B in dopamine metabolism?

A

Metabolises dopamine

From Google:
* Monoamine oxidase-B (MAO-B) is an enzyme in the body that breaks down several chemicals in the brain, including dopamine

24
Q

Examples of dopamine receptor agonists?

A

bromocriptine, ropinirole, cabergoline, apomorphine
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline

25
Q

What are Monoamine oxidase B inhibitors?

A

MAOB inhibitors enhance dopamine by preventing breakdown

26
Q

Examples of MAOB inhibitors?

A

Selegiline
Rasagaline

27
Q

What is the role of MAOB inhibitors?

A

Can be used alone
Prolong the actionn of L-DOPA
smooths out the motor response
May be neuroprotective

28
Q

What is Catechol-O-Methyl Transferase (COMT) inhibitors?

A

COMT is an enzyme that is involved in breakdown of dopamine so COMT inhibitors reduce the peripheral breakdown of L-dopa

29
Q

When are COMT inhibitors used?

A

Adjunct to L-dopa therapy as it reduced symptoms wearing off

30
Q

What is the role of anticholinergics in parkisons treatment?

A

Block cholinergic receptors
Now used more to treat drug induced Parkinsonism
Help tremor and rigidity
e.g procyclidine, benzotropine, trihexyphenidyl

31
Q

Side effects of anticholinergics in Parkisons

A

Confusion
drowsiness
usual anticholinergic side effects

32
Q

What is the role of surgery in Parkisons disease?

A

Carried out stereotactically
Of value in specific cases: dopamine responsive, significant side effects with L-dopa, no psychiatric illness

33
Q

Causes of parkisonism?

A

Parkisons disease
Drug-induced e.g antipsychotics, metoclopramide
Wilsons disease
post- encephalitis
Progressive suprenuclear palsy

34
Q

How to exam a pt with suspected IDP (idiopathic parkisons disease)?

A

WALK:
Gait? Shuffling and forward flexed in IPD with turning on block and asymmetric arm swings.
In advanced cases, pts may have a Festination gait–>patient falls forward and uses legs to catch up with the rest of the body (as the problem is with initiating movement)

RIGIDITY:
Lead pipe- at the elbow–>resistance throughout
Cogwheel- hold at wrist and move it up slowly (feels like a cogwheel), must do this SLOW as you need to go slower than the tremor
Micrographia- as them to write something and it will get smaller

BRADYKINESIA:
Asymmetric
Ask pt to touch fingers to thumb–> cannot maintain amplitude (so they do tiny movements)
Can ask pt to tap their hand/ foot–> unable to maintain rhythm

TREMOR:
Asymmetric low frequency tremor marked at rest and abolished when moving. Usually pill- rolling tremor

35
Q

What can cause a tremor?

A

IPD
benign essential tremor
cerebellar dysfunction
drugs e.g. salbutamol, amiophylline, antipsychotics, lithium, sodium valporate
alcohol

36
Q

What should you be thinking about when seeing a pt with a tremor?

A

Worse with rest or movement?
Is it high frequency or low frequency
Is it symmetrical or asymmetrical

37
Q

Features of inherited tremor?

A

Fhx- usually present later on in life
symmetrical
improves with a tiny bit of alcohol
high frequency

YEAR 4 NEURO (37 decks)

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