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parkinsons > parkinson's > Flashcards

parkinson's Flashcards

1
Q

Define Parkinson’s disease

A

a chronic progressive degenerative neurological disease chiefly of later life that is linked to decreased dopamine production in the substantia nigra and is marked especially by tremor of resting muscles, rigidity, slowness of movement, impaired balance, and a shuffling gait.

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2
Q

Define substantia nigra

A

part of basal ganglia located in the midbrain–required for movement and reward

Basal ganglia consists of nuclei- caudate nucleus, putamen, globus pallidus, substantia nigra - all control voluntary movements and establishing postures.
When altered as in Parkinson’s person has unwanted movements

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3
Q

Epidemiology of Parkinson’s

A

Majority of cases are idiopathic

Symptoms begin 55-60 years

1% of over 60 year olds

Males:Females 1.5:1

2nd most common neuro disorder

affects movement

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4
Q

Summarize the underlying Parkinson’s disease

A

Loss of pigmented dopaminergic neurones in substantia nigra.

Presence of Lewy bodies within pigmented neurons is characteristic.

60-80% of neurones are lost before the motor signs emerge.

As the disease progresses, components of the autonomic, limbic, and somatomotor systems become particularly badly damaged.

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5
Q

Explain the correlation of dopamine and substantia nigra

A 
Substantia nigra (motor centre) is located in the midbrain to which it projects to the caudate and putamen (Together called stiatum). They all use dopamine as a neurotransmitter to which cells in substantia nigra produce dopamine. The site of lesion in PD is the substantia nigra - degeneration of melanin containing cells. Absence of dopamine produces crippling features of PD 
Essentially loss of substantia nigra impacts the stimulation of striatum which stimulates the thalamus to stimulate the motor cortex (which feedsback to the striatum and substantia nigra). This motor circuit modulates output from the motor complex thus the imbalance of excitatory and inhibitory pathways that regulate movement- symptoms seen in PD
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6
Q

What is used to stage Parkinson’s?

A

Braak staging 1-6 correlates with clinical manifestation of the disease.

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7
Q

Causes of PD

A

Idiopathic (most common)

Toxins (Manganese, iron, MPTP, pesticides/herbicides)

Head trauma

Drug induced (antipsychotics, antiemetics, antihistamine)

Genetic (Park-1, Park-3 & Park-12) accounts for < 5%

Abnormal proteosome system

Oxygen free radicals

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8
Q

Describe the cardinal motor symptoms of PD

A

Tremor

Bradykinesia

Rigidity

Postural instability

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9
Q

Define tremor a/w PD

A

pill rolling

  • unilateral
  • rapid at rest
  • increased with stress
  • frequency of 4- 5 Hertz
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10
Q

Define bradykinesia a/w PD

A

slowness of movement

difficulty initiating voluntary movement

difficulty with sequential complex movements

decreased amplitude of movement (writing)

rapid fatigability of repetitive movements

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11
Q

Define rigidity a/w PD

A

Increased resistance of relaxed muscles to passive stretch(eg by examiner)

commonly asymmetrical

1. cogwheel (tremor and rigidity)
2. lead pipe
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12
Q

Distinguish cogwheel and leadpipe rigidity

A

Leadpipe rigidity is sustained resistance to passive stretch throughout the whole range of motion, with no fluctuations. Cogwheel rigidity is jerky resistance to passive stretch as muscles tense and relax.

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13
Q

Define postural instability

A

Balance well preserved until later stages

Shuffling gait ; poor arm swing contribute
to high falls risk

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14
Q

What are other motor clinical features a/w PD

A

Function:

  • micrographia
  • painful dystonia
  • poor bed mobility
  • difficulty with transfers
  • decreased dexterity/coordination

Face:

  • hypomimia(lack of facial expressions)
  • hypophonia- soft speech due to lack of coordination of vocal musculature
  • dysphagia/drooling

Gait:

  • shuffling
  • freezing
  • turning ‘en loc’
  • axial flexion
  • decreased arm swing
  • festination ; involuntary acceleration
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15
Q

What are the non motor clinical features of PD

A

Depression: prevalence varies (>30%)
? reactive process
? dopamine effect

Cognitive decline

  • executive dysfunction
  • dementia = 30%

Sleep disturbance

  • insomnia
  • day time solmonence/fatigue
  • vivid dreams
  • hallucinations

Sensation

  • orthostatic hypotension
  • anosmia
  • impaired proprioception
  • pain
Autonomic
urinary incontinence
weight loss
constipation 
sexual dysfunction 
sweating abnormalities
seborrhoeic dermatitis
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16
Q

State the means of diagnosis of PD

A

It is a CLINICAL diagnosis
Based on Medical History & Clinical examination (triad- tremor, bradykinesia, rigidity)
NO laboratory tests
CT and MRI brain- Normal
MRI can outrule Multi-infarcts, Hydrocephalus & Wilsons (so used to exclude other diseases which may mimic PD)
PET/SPECT useful in atypical cases (but rarely needed)

17
Q

Differential dx of PD

A

essential tremor

vascular parkinsonism

drug – Induced parkinsonism

parkinsonism in parkinson plus syndromes

Thyrotoxicosis

18
Q

Outline features of Parkinson Plus syndromes

A

Early postural instability & dementia

These progress more quickly than IPD (worsening in first 3-5 yr)

Anti-Parkinsons medications are less effective and patients are very sensitive to neuroleptic medications/ levodopa

Autonomic features are common.

Axial > limb involvement

  • multisystem atrophy
  • progressive supranuclear palsy
19
Q

Define multisystem atrophy

A

Postural Instability with falls
falls due to autonomic function of postural hypotension

Postural Hypotension

Bladder dysfunction

Pyramidal Signs

Cerebellar Signs

20
Q

Define progressive supranuclear palsy

A

Parkinsonism (Symmetrical)

Paralysis of upward gaze

Dementia

Personality change

Speech difficulties

21
Q

Principles of management of PD

A

educate & support

preserve function

maintain general health and fitness

treat other medical problems

22
Q

What is the non pharm approach for pt with PD

A

PD Support Group

Physiotherapy & Occupational Therapy

SALT & Dietician & MSW

Communication with GP

23
Q

Pharm tx for PD pt

A

Replace dopamine deficiency
Prevent dopamine breakdown

Dopamine – levodopa
Dopamine decarboxylase inhibitors(inhibit peripheral metabolism of levodopa)- carbidopa
Dopamine agonists- bromocriptine, pramipexole, ropinirole, cabergoline, apomorphine
MAOB inhibitors (prevent degredation of dopamine) – Selegiline, Rasagiline
COMT inhibitor (prevent degredation of dopamine) – Entacopone
Anticholinergics (for tremor/drooling) Procyclidine, Biperidin

24
Q

Aims of pharm tx for pt w PD

A

Aims to control signs/symptoms for as long as possible while minimising adverse effects.

Usually provide good symptomatic control for 4-6 years. After this disability progresses.

Motor fluctuations and dyskinesias may become troublesome.

no standard algorithm - treat when function is a problem

25
Q

What is the mainstay pharm tx for PD pts

A

levodopa
most potent and effective for initial therapy >70
short term use- great benefits
-given pre meals for better absorption
given with domperidone for transient nausea
domperidone is a dopamine antagonist but cannot cross BBB thus it is used.

26
Q

A/ side effects of mainstay tx ?

A

long term use causes S/e
receptor stimulation becomes less effective

  • motor fluctuations(on/off phenomenon)
  • dyskinesias (Chorea, dystonia)
27
Q

How does one deal with motor fluctuations?

A

“Wearing off phenomenon” due to decreased response to levodopa

  1. at night - use CR nocte
  2. frequent “wearing off” between doses – add COMT inhibitor
  3. freezing episodes 

      - increase dose or frequency of levodopa
      - add COMT inhibitor, MAO-B inhibitor or dopamine agonist
      - use liquid levodopa ( fast onset )
28
Q

What is another management option for PD pts?

A

Surgery
Destruction of brain tissue to control the symptoms

Thalamotomy (thalamus) – reduces tremor

Pallidotomy (globus pallidus) – reduces tremor, rigidity, bradykinesia & dyskinesias.

Levodopa subsequently took over but surgery has since re-emerged as long term complications of levodopa have become apparent.

Has a role where drug therapy is no longer sufficient.

29
Q

What qualifies a pt for another management technique called deep brain stimulation

A

a clear diagnosis of PD
levodopa responsive patients with motor fluctuations or dyskinesias aka wearing off phenomenon
no psychiatric problems
good insight into risks/benefit of this treatment

30
Q

Features of deep brain stimulation

A

Intracerebral electrode connected to a pulse generator.

Hand held device activates the pulse generator

Leads to electrical stimulation of thalamus/globus pallidus

Resets abnormal firing patterns

Can be reversed & adjusted

It improves symptoms that formerly responded to levodopa.
Extends ‘on’ time.

Subthalamic stimulation is commonest surgical procedure which reduces dyskinesias and medication use.

Improvements maintained for up to 5 years post op

31
Q

Stages of PD

A

honeymoon period
motor complication period
late stage

parkinsons (1 decks)

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