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Neurology > Parkinosn's Disease > Flashcards

Parkinosn's Disease Flashcards

1
Q

How many people in the UK are affected by Parkinson’s Disease?

A

Approximately 127,000

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2
Q

Parkinson’s Disease is the Second———–

A

most common neurodegenerative disease, after Alzheimer’s disease

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3
Q

What age are most likely to be affected by Parkinson’s?

A

Over the age of 50

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4
Q

What gender are more likely to be affected by Parkinson’s?

A

More men than women

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5
Q

Where do symptoms typically present initially?

A

On one side

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6
Q

What is heterogeneous Parkinson’s?

A

considerable variability seen in terms of symptoms and rate of progression

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7
Q

What is progressive Parkinson’s?

A

no cure, but symptoms managed primarily through medication and therapy

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8
Q

Who published the first medical description of Parkinson’s and when?

A

James Parkinson in 1817

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9
Q

What is secondary parkinsonism?

A

Drug induced, vascular

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10
Q

What is Parkinson’s-Plus Syndromes (Atypical Variants)

A

Multiple System Atrophy (MSA) Progressive Supranuclear Palsy (PSP)
Corticobasal Degeneration (CBD)

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11
Q

What does idiopathic mean?

A

Exact cause is unknown

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12
Q

How is diagnosis made?

A

through individuals’ clinical presentation, physical examination and medical history
• SPECT scan may be carried out
• There is currently no ‘test’ for Parkinson’s Disease
• Positive response to levodopa suggestive of Parkinson’s Disease

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13
Q

What are Cardinal Symptoms of Parkinson’s disease?

A

Tremor
Rigidity
Bradykinesia
Postural Instability

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14
Q

What are some other symptoms?

A 
Masked face 
Dysarthria 
Gait disturbance 
Micrographics 
Dysphagia 
Depression 
Anxiety 
Apathy 
Attention deficit 
Sleep disorders 
Autonomic symptoms 
Gastrointestinal symptoms 
Sensory symptoms 
Fatigue 
Dementia 
Hallucinations
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15
Q

What leads to Parkinson’s disease long before motor symptoms become evident?

A

Pathological process

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16
Q

What are the 3 phases?

A

Preclinical
Promotor
Motor Parkinson’s Disease

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17
Q

What is the preclinical phase?

A

no clinical symptoms, but pathology assumed to be
present

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18
Q

What is the premotor phase?

A

Early symptoms

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19
Q

What is the motor Parkinson’s disease?

A

manifestation of classic motor and non-motor symptoms

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20
Q

What can promotor characteristics include?

A

• Olfactory (smell) deficit
• Sleep disorders
• Constipation
• Mood changes

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21
Q

What can premotor symptoms have potential use for?

A

Clinical bioamarkers

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22
Q

What other biomarkers have been identified?

A

Potential neuroimaging, genetic and neurochemical

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23
Q

What is dopamine in relations to the neuropathology of Parkinson’s?

A

Dopamine - loss of dopamine producing neurons
Typically, there is a 70- 80% reduction in dopamine production by the time of diagnosis

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24
Q

What is lewy body pathology in terms of neuropathology in terms of Parkinson’s?

A

abnormal aggregates (clumps) of alpha- synuclein protein

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25
Q

What is dopamine?

A

A neurotransmitter

26
Q

How many dopaminergic pathways are there?

A

4

27
Q

In Parkinson’s when is the loss of dopamine producing neurons is most profound?

A

within the Substantia Nigra Pars Compacta (SNc) – the origin of the nigrostriatal pathway.

28
Q

Dopaminergic neurons are also lost in where?

A

Ventral Tegmental Area (VTA)

29
Q

What are the basal ganglia?

A

are a collection of subcortical, grey matter structures, deep within the brain

30
Q

What are the main structures of the basal ganglia?

A

Striatum
- Caudate nucleus, putamen and accumbens nucleus • Globus Pallidus (GP)
- Internal (GPi) and external (GPe)
• Substantia Nigra (SN)
-Pars reticulata (SNr) and Pars compacta (SNc)
• Subthalamic Nucleus (STN)

31
Q

What is the role of the basal ganglia?

A

Motor control
•Learning
•Cognitive functions
•Emotions

32
Q

What is the putamen linked with?

A

motor control (as well as being associated with habit learning)

33
Q

What is the caudate linked with?

A

eye movements and cognitive functions

34
Q

What is the ventral striatum linked with?

A

The limbic system (emotional behaviour)

35
Q

What is the input structure?

A

mainly the Striatum (caudate, putamen and accumbens nucleus)
oReceives projections from the cerebral cortex, brainstem and thalamus
o Input also received through the Subthalamic Nucleus (STN)

36
Q

What are the output structures?

A

globus pallidus interna (GPi) and the substantia nigra pars reticulata (SNr).
oProjects initially to the thalamus and brainstem
oThalamus projects principally to widespread areas of the frontal lobe

37
Q

What is the direct pathway?

A

Cortex Striatum GPi/SNr Thalamus

38
Q

What is an indirect pathway?

A

Cortex striatum GPi Thalamus

39
Q

What is a hyper direct pathway?

A

Cortex subthalamic Nucleus Thalamus

40
Q

Are D1 receptors excitatory or inhibitory?

A

Excitatory

41
Q

What does activation of D1 receptors result in?

A

increased activity of the direct pathway

42
Q

Are d2 receptors excitatory or inhibitory?

A

Inhibitory

43
Q

What does activation of D2 receptors result in?

A

Decreased activity of the indirect pathway

44
Q

Reduction in dopamine=?

A

• Reduction in activation from direct pathway
• Increase in inhibition from indirect pathway
Overall = turning down of “Go” and turning up of “NoGo”

45
Q

What does previous evidence toward the classical model of the basal ganglia indicate?

A

that the direct and indirect pathways may be more intertwined than previously thought, both structurally and functionally

46
Q

What other neurotransmitter systems are also implicated in PD?

A 
Cholinergic 
Serotonergic 
Adernergic 
Glutamatergic 
GABAergic
47
Q

What evidence is there proving that the cerebellum also contributes to the clinical symptoms seen in PD?

A

Reciprocal connections evident between the basal ganglia and cerebellum
Some indication of structural changes in the cerebellum in Parkinson’s Disease

48
Q

Where do Lewy bodies and Lewy Neurites Present?

A

SNc
nervous system
Abnormal aggregates (clumps) of alpha-synuclein protein

49
Q

What has been proposed that lewy body pathology progresses in?

A

a predictable pattern, divided by Braak and colleagues into 6 stages
• Proposed to begin in structures of the lower brainstem and the olfactory system

50
Q

What are the 4 ‘Pathways’ stages?

A

Diagnosed
• Maintenance

• Complex
• Palliative

51
Q

What is an example of a dopamine agonists?

A

Ropinrole

52
Q

What is an example of a Levodopa?

A

Sinemet

53
Q

What is an example of an enzyme inhibitor and what do they do?

A

Prevent breakdown of dopamine

MAO-B inhibitor

54
Q

What side fears come from increased dopamine?

A

Hallucinations

55
Q

What side affects are caused by Levodopa?

A

Choreic movements
• Abnormal, purposeless involuntary movements
• Dystonic movements
• Muscles tighten, involuntarily (sustained contractions)

56
Q

When is deep brain stimulation considered?

A

if side effects of medication are large, or medication no longer working as effectively

57
Q

What is a deep brain stimulation?

A

Electrodes placed in specific brain area are connected to a pulse generator
• Electrical impulses sent to the brain when generator turned on
• Bilateral or Unilateral

58
Q

What are the two types of deep brain stimulation?

A

STN or GPi

59
Q

What is the other surgical option beside deep Brian stimulation

A

Lesioning

60
Q

How is dysarthria characterised in PD?

A

Characterised by mono-pitch and mono-loudness, reduced stress, imprecise consonants, short rushes of speech, variable rate, harsh and breathy voice and pitch disturbances

61
Q

How is language affected by PD?

A

Link with cognitive changes and dysarthria

Neurology (8 decks)

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