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Parkinsons Flashcards

1
Q

pathology in parkinsons

A

loss of pigmente dopaminergic cells of the zona compacta of the substantia nigra. in the remaining neurones there are cytoplasmic inclusions - Lewy bodies.

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2
Q

what are Lewy bodies?

A

lewy bodies are spherical eosinophilic cytoplasmic inclusions, primary composed of alpha-synuclein. two morphological types: classical (brainstem) and the cortical LEwy body

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3
Q

the 4 main classical features of Parkinsons

and generally early features

A

resting tremor
rigidity (lead pip + cogwheeling)
bradykinesia

Postural instability

Stiffness, difficulty with fine movement - writing, buttoning, fatigue.

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4
Q

what is the typical onset of parkinsons?

A

typically features begin asymmetrically and generally upper limbs are first.
daily fluctuation in severity

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5
Q

Non-motor features of PD

A
  1. Sense of smell reduced
  2. Constipation
  3. Visual hallucinations
  4. Frequency/urgency
  5. Dribbling of saliva
  6. Depression & dementia
  7. Insomnia
  8. Postural Hypotension
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6
Q

epidemiology

A

Typical age at onset: 65yrs. Prevalence: 0.6% at 60–64yrs; 3.5% at 85–89yrs (Europe).

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7
Q

neurological findings of PD

A

Hypertonia, rigidity, bradykinesia (test: tap fingers, tap foot, clap rotating hand) soft and monotonous speech, reduced blinking frequency, dysarthria, lack of sweating, micrographia.
Features are worse with concurrent activity: eg waving the right arm when assessing for hypertonia in the left

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8
Q

hOW to exagerate PD features on examination?

A

With concurrent activity eg arm waving whilst examining the other arm

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9
Q

gait in PD

A 
Narrow base
slow initiation
shortened stride length
slow turns
lack of arm swing
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10
Q

daignostic features suggesting idiopathic parkinsons disease

A

asymmetrical onset

good therapeutic response to L-dopa

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11
Q

DDx for parkinsonism

A
  1. Parkinson’s disease
  2. Cerebellar dysfunction
  3. Dementia with Lewy bodies
  4. Drug-induced (antipsychotics)
  5. Normal-pressure hydrocephalus
  6. CVA or space occupying lesion affecting basal ganglia
  7. Post-encephalitis
  8. Wilson’s disease
  9. Parkinsons-plus syndromes:
    a. progressive supranuclear palsy,
    b. multisystem atrophy: Shy-Drager syndrome,
    c. corticobasal degeneration
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12
Q

what is shy-drager syndrome?

A

Multiple-system atrophy (MSA) is a degenerative neurological disorder.

Aka olivopontocerebellar atrophy and striatonigral degeneration

Features: varying degrees of parkinsonism autonomic failure, cerebellar dysfunction and pyramidal signs

This cell degeneration causes problems with movement, balance, and other autonomic functions of the body such as bladder control or blood-pressure regulation.

The cause of MSA is unknown and no specific risk factors have been identified.

Around 55% of cases occur in men, with typical age of onset in the late 50s to early 60s.

MSA often presents with some of the same symptoms as Parkinson’s disease. However MSA patients generally show minimal if any response to the dopamine medications used for Parkinsons.

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13
Q

What are Parkinson-plusconditions?

A 
Parkinson-plus conditions are neurodegenerative conditions with parkinsonian characteristics but with additional features that help distinguish from the idiopathic PD. 
progressive supranuclear palsy, 
multisystem atrophy (shy-drager), 
Lewy body dementia.
cortico-basal degeneration 
vascular parkinsonism
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14
Q

progressive supranuclear palsy features

A

Most common Parkinson-plus syndrome

Involves multiple neurotransmitter pathways.

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15
Q

what are parkinson’s plus signs?

A

Poor response to levodopa
Marked symmetry of sings in the early stages
Early onset of dementia
Early onset of postural instability and falls
Early onset of hallucinations
Early onset of Sx of autonomic dysfunction, ie postural hypotension
Pyramidal signs
Cerebellar signs
Oscular signs – gaze palsies, nuystagmus

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16
Q

TX for Parkinsons

A

Management: MDT – neurologist, physiotherapist, OT, specialist nurse, SALT
Levodopa
Other meds:
dopamine agonists – eg ropinirole
anticholinergics – eg trihexyphenidyl useful for tremor
MAO-B inhibitor - eg selegiline
COMT inhibitors – eg entacapone, help decrease immobility by shortening the off time associated with L-dopa
Apomorphine – parenteral dopamine agonist.
Surgery: deep brain stimulation when meds fail

17
Q

Anticholinergic drugs examples

A

benzhexol, benzatropine

18
Q

rationale for anticholinergics

A

Rationale:
loss of DA dis‐inhibits striatal cholinergic interneurones →

□↑ striatal ACh levels →

□Activation of muscarinic ACh receptors in striatum □Further ↑ overactivity of indirect pathway

→□ Contributes to symptoms of tremor

19
Q

SE of anticholinergic

A

 central:confusion, mood changes Peripheral: constipation, blurred vision, dry mouth

20
Q

effectiveness of anticholinergics

A

 Muscarinic antagonists are v effective against tremor (~30% patients) ◊ useful if sialorrhoea is a problem
 Minimal effect against bradykinesia and rigidity

21
Q

Dopaminergic drugs mechanisms to increase availability and reduce destruction

A

□Levo DOPA or L –DOPA: Natural DA precursor which, unlike DA, can cross BBB
●BUT L‐DOPA is ~90% converted by DDC in intestinal wall →
□Co‐administered with peripherally‐acting DDC inhibitors
 Carbidopa ( as Sinemet) or benserazide (as Madopar)
● L‐DOPA is ~5% metabolised by plasma Catechol O‐Methyl Transferase
 COMT inhibitor, entacapone, may be used as adjunct
● Ensure majority of L‐DOPA enters brain unchanged
● Conversion by DDC (inside DA (and 5‐HT?) neurones) produces DA

22
Q

can Dopamine cross BBB?

A

Dopamine canNOT cross BBB, but L-DOpa, which is its natural precursor) can

23
Q

what converts L-dopa into DA?

A

dopa decarboxylase DDC

24
Q

where is DDC present and what is the implicayion + ways around it

A

in intestinal wall, 90% of L-dopa is converted there into DA. L-dopa coadministered with peripherally acting DDC inhibitors (carbidopa, benserazide)

25
Q

The effects (and fate) of L Dopa administration on the brain:

A

L DOPA with benserazide/ carbidopa raises striates DA levels ○Activity normalised in direct (D1) and indirect (D2) circuits;
○ Improves rigidity, bradykinesia, facial expression, speech and handwriting in ~80% patients

26
Q

Acute SE of LDOP

A

□Nausea – due to remaining peripheral DA-R activation → □Peripheral DA receptor antagonist domperidone given as adjunct
□ Postural hypotension (esp. in patients on antihypertensive drugs)
□Psychological – hallucinations, confusion, insomnia, nightmares

27
Q

peripheral DA receptor antagonis NAME and function

A

domperidone, to prevent nausea from remaining dopaine receptor activation peripherally

28
Q

chronic SE of LDOPA`

A

within 2 years of starting the drug 1/3 patients develop
1)motor fluctuations (‘on-off’ effect and wearing off)
○Rapid fluctuations in clinical state. Freezing may last min or hours.
□Related to plasma fluctuations in L-DOPA? (entacapone help?)
□Related to ltd. storage of dopamine as degeneration progresses?
2) Levodopa-induced dyskinesia (LID)
○Excess, hyperkinetic involuntary movements (choreic or dystonic).
□ Face and limbs mostly affected. □Occur at peak dose or at beginning and end of dose. □Mechanism uncertain. Related to dose and disease severity. □ Thalamocortical feedback is increased above normal.
□Amantadine (NMDA-type glutamate receptor blocker) only drug offering relief

29
Q

dopamine agonists examples

A

bromocriptine, lysuride, ropinirole, pramipexole

30
Q

dopamine agonists effects

A

○Produce effects mainly through activation of striatal D2 receptors ○Not affected by progressive neurodegeneration

○Longer half‐life so, less plasma fluctuation, less “on‐off” effect & reduced incidence of dyskinesia

31
Q

side effects of dopamine agonists

A

▼ Acute SE – as for L‐DOPA ▼Chronic SE lessened

32
Q

dopamine agonist use indicati

A

○ Often as first line treatment in the younger BUT less effective than L‐DOPA in relieving symptoms, so L‐dopa needed eventually
□ Used as adjuncts to lower L‐DOPA dose when L‐DOPA required
○Alternative routes of drug administration
to circumvent dyskinesia: Rotigotine (dopamine agonist) patch effective in early PD;
Duo-Dopa: intraduodenal infusion of L-DOPA (no sc formulation)

33
Q

MAO-B inhibitors

example and reason for indication o

A

selegiline
● Monoamine oxidase B (MAO‐B) is principal route of DA metabolism in DA rich brain regions

● MAO‐B inhibitors block DA metabolism ● Often used as an adjunct to lower L‐DOPA dose required

● May be used as monotherapy in early stage PD

34
Q

MAOB inhibitor side effects

A

SE: Unlike non‐selective MAO inhibitors, selegiline does not inhibit peripheral tyramine metabolism so NO cheese reaction.

35
Q

Surgical g Approaches to treating PD

A 
Neuroablative Surgery (“otomy”)
Deep Brain Stimulation (DBS)
36
Q 
Neuroablative Surgery (“otomy”)
mechanism and types
A

● Very popular prior to L‐DOPA ● Now used in medically‐refractory patients only
● A stereotaxic thermolytic lesion (uni‐ or bi‐lateral) is made in part of basal ganglia motor loop to restore normal thalamocortical feedback.
Thalamotomy (tremor‐dominant cases)
 Pallidotomy (improves rigidity & bradykinesia)
 Subthalamotomy (improves rigidity, bradykinesia and LIDs)

37
Q

disadvantages of ablative therapy

A

• Irreversible • Risk of visual impairment (if optic tract damaged); intracerebral haemorrhage; mild speech & cognitive impairment

38
Q

DBS mechanism and advantages

A

● High frequency stimulation to ‘switch off’ or normalise firing of motor loop nuclei
● Mechanism likely involves depolarising block of nerve conduction
● Subthalamic nucleus (STN) – preferred region
● Advantage over lesioning as procedure is REVERSIBLE & graded
● Improved imaging technology now means surgery can be performed confidently with patient under anaesthesia.
●Patient controls stimulation using a pacemaker attached via wires implanted under skin to the indwelling electrode

39
Q

Failings of current treat

A
  • Only treat some of the symptoms ₋ Postural imbalance left unaffected
  • Side effects ₋Very disabling in some cases ; dyskinesia
  • Do not address the progressive degeneration

NOP (24 decks)

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