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Carleton Neur 1203 2021 > Parkinson’s Disease > Flashcards

Parkinson’s Disease Flashcards

1
Q

What is Parkinson’s Disease?

A

• Parkinson’s disease (PD) is a long-term degenerative disorder of
the central nervous system
- Symptoms generally come on slowly, over time
- Mainly affects the motor system
- Average life expectancy following diagnosis is between 7 and 14 years
- Currently no cure for PD

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2
Q

Epidemiology of PD

A

In 2015, PD affected ~6.2 million people worldwide and resulted in about 117,400 deaths
• In Canada, ~1 in every 500 people are affected by PD - ~6,600 new cases per year
• Typically, PD occurs in people over 60 years of age - Prior to age of 50, considered young-onset PD
• Males are more often affected than females

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3
Q

Clinical Presentation – Motor Symptoms

A

Remember TRAP!
These are the most recognizable symptoms of PD:
(Resting) Tremor Rigidity
Akinesia (aka Bradykinesia) Postural instability

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4
Q

Motor Symptoms: Resting tremor

A
  • At rest!
  • Slow velocity
  • Asymmetrical
  • Tremors may affect chin, jaw, arms, legs
  • “Pill-rolling”
  • The most common presenting symptom
  • 30% of PD patients do not show tremor
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5
Q

Motor Symptoms: Rigidity

A
  • Occurs in over 90% of patients
  • Characterized by increased resistance - The “cogwheel” phenomenon
  • Increased muscle tone and contraction
  • Present through the range of passive movements of a limb
  • E.g. flexion, extension, or rotation about a joint
  • Can occur in neck, shoulders, hips, wrists, ankles - Proximally & distally
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6
Q

Motor Symptoms: Bradykinesia

A
  • The most characteristic clinical feature - Present in every single case of PD
  • Slowness in performing activities of daily living
  • Loss of spontaneous movements & gesturing
  • Monotonic and hypophonic dysarthria (speech)
  • Loss of facial expressions (hypomimia) and decreased blinking
  • Drooling
  • Reduced arm swing while walking
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7
Q

Motor Symptoms: Postural Instability

A
  • Loss of postural reflexes
  • Generally, manifestation of late stage PD
  • Can lead to impaired balance and frequent falls
  • Most common cause of falls
  • Along with freezing of gait
  • Contributes significantly to risk of hip fractures
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8
Q

Clinical Presentation – Non-Motor Symptoms

A

Psychiatric Disturbances
Autonomic Disturbances
Cognitive Impairment
Sleep Disturbances

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9
Q

Sleep Disturbances

A

Insomnia/fractured sleep

  • Narcolepsy
  • REM behavior disorder (RBD)
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10
Q

Cognitive Impairment

A
  • Executive function deficit
  • Dementia
  • Hallucinations
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11
Q

Autonomic Disturbances

A
  • Constipation
  • Sexual dysfunction
  • Orthostatic hypotension
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12
Q

Psychiatric Disturbances

A

Depression

  • Anxiety
  • Apathy
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13
Q

How does Parkinson’s Disease all happen?

A 
Let’s start with the Basal Ganglia (BG)
What is the BG?
Dorsal Striatum
Globus Pallidus
Substantia Nigra
Subthalamic Nucleus
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14
Q

Dorsal Striatum

A
  • Caudate

* Putamen

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15
Q

Globus Pallidus

A

• Externa, Gpe • Interna, Gpi

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16
Q

Substantia Nigra

A
  • Pars compacta

* Pars reticula

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17
Q

What does the BG do?

A

Sets the overall “tone” or
“motivation” for action
- Part of a system that focuses actions - Picks the correct ones
- Output of BG dictates the likelihood that movements will occur
- BG is organized into loops
- Speaks to different brain regions,
integrates information

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18
Q

BG Loops

A

Cognitive Loop
Visual/Oculomotor Loop
Affective Loop
Motor Loop

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19
Q

Motor Loop

A
  • To move or not to move?
  • Putamen, Globus Pallidus and
    Substantia Nigra
20
Q

Affective Loop

A
  • Emotional component

- Desire, apathy, impulse

21
Q

Visual/Oculomotor Loop

A

Scanning environment

- Spatial recognition

22
Q

Cognitive Loop

A
  • Turns on/off regions of frontal lobe
  • Task switching
  • Priority setting
23
Q

What happens to the BG in PD patients?

A

Main pathological characteristics of PD are cell death in the BGà Substantia Nigra

  • Up to 70% of the dopamine (DA) secreting neurons in the SN are affected
  • Leads to DA depletion in the SN and the nigrostriatal DA pathway
  • Dysfunctional motor loop of the BG
  • TRAP
24
Q

What’s Dopamine’s role?

A 
DA neurons in the SN form strong connections with the dorsal striatum, globus pallidus and the motor cortex
- These are excitatory connections - Dorsal striatum (motor) has dense
expression of (D1 and D2) dopamine receptors - DA is main driver of motor cortex activation
There are a number of compensatory mechanisms that can mask early symptoms of PD
25
Q

Noradrenergic

A
  • Urinary frequency

- Erectile dysfunction

26
Q

Serotonergic

A
  • Sleep disturbances

- REM Behavioral disorder

27
Q

Cholinergic

A
  • Constipation
28
Q

Understanding PD progression

A

There are 4 stages

29
Q

Stage 1 of PD

A

Olfactory bulb

Dorsal motor nucleus

30
Q

Stage 2 of PD

A

Locus coeruleus

31
Q

Stage 3 of PD

A

Substantia nigra

32
Q

Stage 4 of PD

A

Cortex

33
Q

PD progression Neuronal cell loss

A

Subtle, non-motor symptoms

34
Q

PD progression 5 years

A

Diagnosis

First clinical symptoms appear when around 70% of neurons are lost

35
Q

PD progression 10 years

A

Neuronal cell loss continues

Symptoms Progress

Wearing off phenomena
Random fluctuations

36
Q

PD progression 15 years

A

Severe presynaptic cell loss

Decreasing response to L-dopa

37
Q

What Causes Cell Death in PD?

A

PD is mostly idiopathic we don’t know what causes it!

Environmental

Genetic

38
Q

Environmental PD

A
  • Toxins and/or pollutants (e.g. insecticides, herbicides) - Head injuries (e.g. boxing)
  • Infections (e.g. encephalitis, syphilis)
  • Side effects of drugs (e.g. MPTP)
  • Injury (e.g. stroke, lesions)
39
Q

Genetic

A
  • Typically early onset (>50) PD is associated with genetic factors
  • 15% of individuals with PD have a first-degree relative with the disease
  • 5% – 10% of PD cases are known to occur because of mutation in one of several specific genes
  • SNCA,encodesalpha-synuclein
  • Genetic testing for some of the genes is possible, but
    interpretation is difficult
40
Q

Lewy bodies

A

Both genetic and environment lead to Lewy bodies
Affected neurons show presence of Lewy Bodies
• Abnormal aggregates of the alpha-synuclein protein that develop inside neurons
- Pathological alpha-synuclein acts as a template that corrupts normal alpha-synuclein
- Leads to spherical masses located in the cytoplasm
- Displace other cell components
• Can be identified under the microscope
- Appear in the olfactory bulb, medulla oblongata, pontine
tegmentum
- As disease progresses, substantia nigra, midbrain, basal forebrain and finally neocortex
• Leads to apoptosis of affected neurons
- Signs of programmed cell death are evident

41
Q

Current Treatment Options

A

Levodopa (L-DOPA)

COMT Inhibitors & MAO-B Inhibitors

DopamineAgonists

Non-PharmacologicalTreatment

42
Q

Levodopa (L-DOPA)

A
  • Precursor to dopamine
  • Only 5-10% crosses BBB
  • Improvement (temporarily) in motor symptoms
  • Long-term, leads to involuntary movements called dyskinesias, hallucinations, agitation
  • Fluctuations occur and patient will cycle through phases with good responses to medication and poor responses to medication
43
Q

COMT Inhibitors & MAO-B Inhibitors

A

Catechol-O-Methyltransferase (COMT) and monoamine oxidase (MAO) B are enzymes that degrades dopamine

  • Can be used to compliment L-DOPA in early stages
  • Modest symptomatic relief when used alone
44
Q

DopamineAgonists

A
  • Bind to DA receptor, and reduce motor symptoms of PD
  • Less effective than L-DOPA, but can be used in early stages
  • Side effects include hallucinations, insomnia, nausea, constipation, impulse control issues
45
Q

Non-PharmacologicalTreatment

A
  • Education, support, exercise, nutrition
46
Q

Management through surgery

A

Deep Brain Stimulation (DBS)

Stem Cell Treatment

47
Q

Stem Cell Treatment

A
  • Healthy DA cells can be plugged into the SN
  • Many obstacles in the way before this is a mainstream treatment option
    • Healthy DA cells can be plugged into the SN
  • Many obstacles in the way before this is a mainstream treatment option

Carleton Neur 1203 2021 (16 decks)

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