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00000 Neurology > 435 Parkinson's Disease > Flashcards

435 Parkinson's Disease Flashcards

1
Q

2nd most common age-related neurodegenerative disease (exceeded only by AD)

A

PD

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2
Q

Mean age of onset of PD

A

60 years old

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3
Q

Classic features of PD (4)

A
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4
Q

hallmarks of PD (pathologically)

A
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5
Q

What is BRAAK Staging

A
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6
Q

Examples of OTHER MOTOR FEATURES of PD (mga non -cardinal motor features)

A
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7
Q

Examples of NONMOTOR features of PD

A
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8
Q

percentage of PD occuring sporadically

A

85-90%

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9
Q

only known cause of PD

A

Gene mutations

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10
Q

4 common gene mutations in PD

A
  • Alpha-synuclein (SNCA)
  • GBA
  • LRRK2
  • PINK1/ Parkin
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11
Q

HLA gene associated with PD

A

Class II HLA gene DRB1

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12
Q

NO environmental factor has yet been proven to cause or contribute to PD . True or false

A

True

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13
Q

Relationship of PD to Calcium pacing

A

With aging, dopamine neurons switch from sodium to calcium pacing through calcium channels

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14
Q

Genes associated with classical PD vs early onset PD vs parkinsonism

A
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15
Q

First PD-linked gene mutation

A

Alpha-synuclein (SNCA)

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16
Q

Most intensely investigated gene mutation has in PD

A

Alpha-synuclein (SNCA)

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17
Q

Differentiate SNCA disease from nongenetic PD in terms of disease onset

A

Earlier age of disease onset than in nongenetic PD

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18
Q

Differentiate SNCA disease from nongenetic PD in terms of progression of sx

A

Faster progression of motor signs that are mostly levodopa-responsive

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19
Q

Differentiate SNCA disease from nongenetic PD in terms of occurrence of motor fluctuations

A

Early occurrence of motor fluctuations

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20
Q

constitutes the major component of Lewy bodies

A

SNCA

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21
Q

ost important risk factor in terms of effect size for the development of PD

A

GBA gene

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22
Q

GBA gene encodes for what enzyme

A

glucocerebrosidase (Gcase)

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23
Q

function of glucocerebrosidase (Gcase) (2)

A
  • promotes lysosomal function
  • Enhances the clearance of misfolded proteins like SNCA
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24
Q

ASSOCIATION OF GBA AND SNCA

A
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25
Q

most common variant of LRRK2 mutation

A

p.G2019S

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26
Q

p.G2019S is associated with what gene mutation

A

LRRK2

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27
Q

This symptoms is a useful diagnosti clue for LRRK2 mutation

A

leg tremor

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28
Q

Can block toxicity associated with LRRK2 mutation

A

kinase inhibitors

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29
Q

Mutation that is the major cause of autosomal recessive and early-onset PD

A

Parkin mutations

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30
Q

Parkin and PINK1 mutations are commonly complicated by what symptomq

A

Dystonia

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31
Q

Neurodegeneration in Parkin and PINK1 mutations are usually restricted to what areas of the brain (2)

A

restricted to SNc and LC

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32
Q

Lewy bodies are typically present in Parkin and PINK1 mutations. True or false

A

Lewy bodies typically absent

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33
Q

Explanation for pathologic findings in Parkin and PINK1 mutations

A

impairerd ubiquination of damaged proteins

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34
Q

Refers to group pf neurodegenerative conditions that are usually assoc with MORE WIDESPREAD pathology than found in PD

A

Atypical Parkinsonism

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35
Q

relationship of atpyical parkinsonism and speech/gait

A
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36
Q

relationship of atpyical parkinsonism and rest tremor

A
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37
Q

relationship of atpyical parkinsonism and levodopa response

A
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38
Q

clinical course of atypical parkinsonism

A
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39
Q

4 types of atypical parkinsonism

A
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40
Q

why is neuroimaging not helpful in atypical parkinsonism

A

Because striatal dopamine depletion can be seen in both PD and atypical parkinsonism

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41
Q

Role of metabolic imaging in atypical parkinsonism

A
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42
Q

Combination of atypical parkinsonian features AND CEREBELLAR and AUTONOMIC features

A

MSA multiple system atrophy

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43
Q

2 clinical syndromes of MSA (multiple system atrophy)

A
  • MSA-p (parkinsonian)
  • MSA-c (cerebellar)
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44
Q

usual autonomic disturbance in MSA multiple system atrophy

A

orthostatic hypotension

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45
Q

What type of atypical parkinsonims:
Degeneration of the SNc, striatum, cerebellum, and inferior olivary nuclei

A

MSA multiple system atrophy

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46
Q

What type of atypical parkinsonims:
With characteristic glial cytoplasmic inclusions (GCIs)

A

MSA multiple system atrophy

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47
Q

What type of atypical parkinsonims:
Pathologic iron accumulation in the striatum (T2weighted)

A

MSA multiple system atrophy

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48
Q

What type of atypical parkinsonims:
MRI showing putaminal rim

A

MSA-p

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49
Q

What type of atypical parkinsonims:
MRI showing Pontine “ hot cross bun” sign

A

MSA-c

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50
Q

What is putaminal rim

A
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51
Q

What is Pontine “ hot cross bun” sign

A
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52
Q

What type of atypical parkinsonism…:
no established Gene mutation

A

MSA multiple system atrophy

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53
Q

Parkinsonism with
* Slow ocular saccades
* Eyelid apraxia
* Restricted vertical eye movements with particular impairment of downward gaze

A

PSP - progressive supranuclear palsy

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54
Q

What type of atypical parkinsonism:
Hyperextension of the neck with early gait disturbance and falls

A

PSP - progressive supranuclear palsy

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55
Q

2 clinical forms of PSP - progressive supranuclear palsy

A
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56
Q

differentiate Parkinson form vs Richardson form in terms of response to levodopa

A
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57
Q

What type of atypical parkinsonism:
MRI : hummingbird sign

A

PSP - progressive supranuclear palsy

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58
Q

What is hummingbird sign

A

MRI finding showing Atrophy of the midbrain with relative preservation of the pons on midsagittal images (seen in PSA)

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59
Q

What type of atypical parkinsonism:
degeneration of the SNc, striatum, STN, midline thalamic nuclei, and pallidum

A

PSP - progressive supranuclear palsy

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60
Q

What type of atypical parkinsonism:
(+) mutation for MAPT gene which encodes tau protein

A

PSP - progressive supranuclear palsy

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61
Q

TAU protein is seen in which type of atypical parkinsonism

A

both PSP and CBS

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62
Q

What type of atypical parkinsonism:
Asymmetric dystonic contractions and clumsiness of one hand

A

CBS - corticobasal syndrome

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63
Q

What type of atypical parkinsonism:
alien limb phenomenon

A

CBS - corticobasal syndrome

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64
Q

What is alien limb phenomenon

A

Limb assumes a position in space without the patient being aware of its location or recognizing that the limb belongs to them

Seen in CBS

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65
Q

MRI findings of corticobasal syndrome

A
  • Asymmetric cortical atrophy
  • May not be obvious to casual inspection
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66
Q

PAtho findings of Corticobasal syndrome

A
  • Achromatic neuronal degeneration with tau deposits
  • may overlap with PSP pathologically
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67
Q

“Historical” diagnosis of PD

A

PD diagnosed based on presence of 2 out of 3 parkinsonian features ( tremor, rigidity, bradykinesia)

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68
Q

UK Brain Bank Criteria for diagnosis of PD

A
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69
Q

MDS Clinical Diagnostic Criteria for Parkinson’s disease —- CLinicially PROBABLE PD

A
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70
Q

MDS Clinical Diagnostic Criteria for Parkinson’s disease —- Clinically ESTABLISHED PD

A
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71
Q

Major input region of basal ganglia

A
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72
Q

Major output region of basal ganglia

A
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73
Q

Part of basal ganglia which Provides inhibitory (GABAergic) tone to thalamic and brainstem neurons

A
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74
Q

Effect of decreased vs increased activity of GPi

A
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75
Q

Pathophy of parkinsonism based from Fig 435-5

A
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76
Q

Pathophy of dyskinesia based from Fig 435-5

A
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77
Q

Mainstay of therapy for PD / GOLD standard

A

Levodopa

78
Q

Most effective symptomatic treatment for PD

A

LEvodopa

79
Q

Levodopa is Routinely given in combination with what type of drug

A

PERIPHERAL DECARBOXYLASE INHIBITOR

80
Q

Role of PERIPHERAL DECARBOXYLASE INHIBITOR

A

To prevent peripheral metabolism of levodopa to dopamine

81
Q

Primary source of disability in PD (2)

A

falls and dementia

82
Q

Main reason for hospitalization and nursing home placement (2)

A

falls and dementia

83
Q

Acute dopaminergic side effects of levodopa (3)

A

Nausea , Vomiting , Orthostatic hypotension

84
Q

first thing to do if there is occurrence of acute dopaminergic side effects with use of levodopa

A
85
Q

next things to do if there is persistence of acute dopaminergic side effects with use of levodopa after doing the first line action (3)

A
86
Q

How does dyskinesia develop with levodopa use

A

CURRENTLY, it is now thought that dyskinesia results from alteration in the GPi/SNr neuronal firing pattern and not simply the firing frequency alone

This leads to transmission of misinformation from pallidum to thalamus/cortex leading to dyskinesia

87
Q

dyskinesia with levodopa use most likely occurs in this subset of population (4)

A
  • Younger individuals
  • Women
  • Those using higher doses of levodopa
  • Those with more severe disease
88
Q

Difference between ON vs OFF episodes

A
89
Q

What is on-off phenomenon

A
90
Q

What is wearing off effect

A
91
Q

What is peak-dose dyskinesia

A
92
Q

What is diphasic dyskinesia

A
93
Q

Consist of transient stereotypic rhythmic movements that predominantly involve the lower extremities asymmetrically

A
94
Q

treatment for diphasic dyskinesia

A
95
Q

How to Minimize risk of developing motor complications in px using levodopa (2)

A
  • Using the lowest dose of levodopa that provides satisfactory benefit
  • Use of polypharmacy
96
Q

Location of absorption of levodopa

A

Duodenum

97
Q

Px craving for levodopa and take frequent and unnecessary doses in an addictive manner

A

Dopamine dysregulation syndrome

98
Q

Purposeless, stereotyped behaviors like the assembly or disassembly or collection and sorting of objects

A

Punding

99
Q

LEVODOPA has neither beneficial nor deleterious effect on disease progression. True or False

A

TRUE. LEVODOPA has neither beneficial nor deleterious effect on disease progression. It is used solely to provide symptomatic relief balanced by the risk of causing motor complications and other side effects

100
Q

PET or SPECT findings in PD

A

Shows REDUCED and ASYMMETRIC uptake of striatal dopaminergic biomarkers particularly in the posterior putamen with relative sparing of the caudate nucleus

These findings reflect the degeneration of nigrostriatal dopaminergic neurons and the loss of their striatal terminals

101
Q

Most common genetic association with PD

A

Genetic variants of GBA (glucocerebrocidase)

102
Q

Responsible for 1% of typical sporadic cases of PD

A

Genetic variants of LRRK2 gene

103
Q

Most common cause of secondary parkinsonism

A

Neuroleptics (dopamine-blocking agents)

104
Q

Region of basal ganglia affected by carbon monoxide

A
105
Q

Region of basal ganglia affected by manganese

A
106
Q

Region of basal ganglia affected by stroke or tumor

A
107
Q

Disease that Results from mutation in the GTP-cyclohydrolase 1 gene

A

Dopa-responsive dystonia

108
Q

Should be considered in patients <20 years old who present with parkinsonism particularly if there are dystonic features

A

Dopa-responsive dystonia

109
Q

Can be prevented with the use of copper chelators

A

Wilson’s disease

110
Q

Has Westphal variant (juvenile form)

A

Huntington’s disease

111
Q

Formerly known as Hallervorden-Spatz disease

A

PANK-associated neurodegeneration

112
Q

Neurodegenerartive disorder assoc with parkinsonism that is associated with brain iron accumulation

A

PANK-associated neurodegeneration

113
Q

Alternative diagnosis to consider if there is:
early speech and gait impairment (no tremor, no motor asymmetry, with early falls

A
114
Q

Alternative diagnosis to consider if there is:
exposure to neuroleptics

A
115
Q

Alternative diagnosis to consider if there is:
onset prior to 40 years old (3)

A
116
Q

Alternative diagnosis to consider if there is:
liver disease (2)

A
117
Q

Alternative diagnosis to consider if there is:
diplopia, impaired vertical gaze

A
118
Q

Alternative diagnosis to consider if there is:
poor or no response to an adequate trial of levodopa (2)

A
119
Q

Alternative diagnosis to consider if there is:
dementia as first or early feature

A
120
Q

Alternative diagnosis to consider if there is:
prominenty orthostatic hypotension

A
121
Q

Alternative diagnosis to consider if there is:
prominent cerebellar signs

A
122
Q

Alternative diagnosis to consider if there is:
slow saccades with impaired downward gaze

A
123
Q

Alternative diagnosis to consider if there is:
high frequency 6-10Hz symmetric postural tremor with a prominent kinetic component

A
124
Q

Unlike levodopa,
they do not require metabolic conversion
and Do not undergo oxidative metabolism

A

Dopamine agonists

125
Q

Adverse effects
Unwanted sleep episodes
Impulse-control disorder

A

dopamine agonists

126
Q

That is why some doctors initiate this type of drug in YOUNGER patients who are more prone to develop motor complications because they are less prone to dyskinesia

A

Dopamine agonists

127
Q

Side effect of dopamine agonists (ergot derivates)

A
128
Q

Non-ergot dopamine agonists (3)

A
129
Q

How to administer the following dopamine agonists :
* Ronipinirole
* Pramipexole
* Rotigotine
* Apomorphine

A
130
Q

Dopamine agonist with efficacy comparanble with Levodopa

A
131
Q

Careful while driving . Should not drive when tired when using this drug class

A

Dopamine agonists

132
Q

Leg edema as chronic side effect of this drug class

A

Dopamine agonist

133
Q

Drug class that blocks central dopamine metabolism

A

MAO-B inhibitor

134
Q

Examples of MAO-B inhibitors (3)

A

Selegiline, Rasagiline, Safinamide

135
Q

2 drugs that….
Provide antiparkinsonian benefits when used as monotherapy in early disease

Reduce “off” time when used as adjunct to levodopa

A

Selegiline and Rasagiline

136
Q

Relatively selective suicide inhibitors of the MAO-B isoform of the enzyme

A

Selegiline and Rasagiline

137
Q

Inhibition of MAO-A isoform prevents metabolism of tyramine in the gut leading to a potentially fatal hypertensive reaction

A

Cheese effect

138
Q

Reversible MAO-B inhibitor

A

Safinamide

139
Q

Also acts on SODIUM CHANNELS and inhibit glutamine release

Potential to provide antiparkinsonian as well as anti dyskinetic effect

A

Safinamide

140
Q

What STUDY:
Selegiline significantly delayed the time till the emergence of disability necessitating the introduction of levodopa

A
141
Q

What STUDY:
Early treatment with RASAGILINE 1mg/d provided benefits that could not be achieved when treatment with same drug was initiated at a later time point

A
142
Q
  • Increase the elimination half life of levodopa and enhances it brain availability
  • Reduces “off” time
  • Prolongs “on” time
A

COMT INHBITORS

143
Q

Metabolizes levodopa in the peripehery

A

Catechol-O-methlytransferase (COMT) enzyme

144
Q

Examples of COMT inhibitors (3)

A
145
Q

COMT inhibitor that has fatal hepatic toxicity

A
146
Q

most effective COMT inhibitor

A
147
Q

COMT inhibitors that cause severe diarrhea

A
148
Q

Stalevo is a combination of what 3 drugs

A
149
Q

differentiate the 3 COMT inhibitors in terms of timing and frequency of administration

A
150
Q

Urine discoloration is seen in what PD drug class

A

COMT inhibitors

151
Q

Drug class that decreases the excessive activation of the indirect pathway in PD

A

Adenosine A2A receptor antagonists

152
Q

Drug class that:
* Restores the balance in the basal ganglia -thalamocortical circuit
* Providing a dopaminergic effect without the need to increase levodopa doses

A

Adenosine A2A receptor antagonists (Istradefylline)

153
Q

Only Adenosine A2A receptor antagonist that is approved for use

A

Istradefylline

154
Q

Drinking coffee is associated with reduced frequency of PD . True or False

A

True. Coffee is A2a antagonist

155
Q

Introduced initially as antiviral agent but noticed to have antiparkinsonian effect (due to NMDA receptor antagonism effect)

A

Amantadine

156
Q

Role of amantadine in early vs late PD

A
157
Q

ONLY oral agent able to reduce dyskinesia WITHOUT worsening parkinsonian features

A
158
Q

SIDE EFFECTS
* Cognitive impairment
* Livedo reticularis
* Weight gain
* Withdrawal-like symptoms (hence should be discontinued gradually)

A

Amantadine

159
Q

PD drug class whose Major clinical effect is addressing tremors

A

CENTRAL-ACTING ANTICHOLINERGICS
Example: Benztropine and Trihexypenidyl

160
Q

SIDE EFFECTS particularly in the elderly
* Urinary dysfunction
* Glaucoma
* Cognitive impairment

A

CENTRAL-ACTING ANTICHOLINERGICS
Example: Benztropine and Trihexypenidyl

161
Q

An anticonvulsant which also has antiparkinsonian effect

A

Zonisamide

162
Q

ON-DEMAND THERAPIES FOR “OFF” PERIODS (3)

A
  • Inhaled Levodopa
  • SQ Apomorphine
  • SL Apomorphine
163
Q

indication for Deep brain stimulation (2)

A

Primarily indicated for px
* who suffer disability resulting from levodopa-induced motor complications
* With severe tremors

164
Q

Simulates the effects of a lesion without needing to make a brain lesion

A

Deep Brain Stimulation

165
Q

parts of basal ganglia targeted by deep brain stimulation (2)

A

Targets STN or GPi

166
Q

stimulation of what part of basal ganglia is assoc with decreased frequency of depression

A

GPi

167
Q
  • Persists after lowering or even stopping levodopa
  • Postulated to be related to suboptimal release of dopamine from grafted cells leading to a sustained form of diphasic dyskinesia
A

GRAFT-INDUCED DYSKINESIA

168
Q

2 examples of proteins that enhance neuronal growth and restore function to damaged neurons

A

Trophic factors : GDNF (glial-derived neurotrophic factor) and Neurturin

169
Q

virus most often used in gene therapy for PD

A

AAV2 virus

170
Q

Difference between gene therapy and gene delivery

A
171
Q

Drug that may be helpful for both PD motor features and depression

A

Pramipexole

172
Q

Harbinger of developing dementia

A

PSychosis

173
Q

Drugs for anxiety in PD

A

Short-acting benzodiazepines

174
Q

severe side effect of clozapine

A

agranulocytosis

175
Q

differs from other atypical neuroleptics in that it is also an inverse agonist of the serotonin receptor

A

Pimavanserin

176
Q

In contrast to AD, this disease primarily affects executive functions and attention with relative sparing of language, memory, and calculation domains

A

Dementia in PD (PDD)

177
Q

if dementia precedes, develops, coincident with, or occurs within 1 yea

A

DLB (not PDD)

178
Q
  • Drugs used to treat PD can worsen cognitive function. They are discontinued in the following sequence
A
179
Q

what to give if PD px develops sexual dysfunction

A

Sildenafil or Tadalafil

180
Q

What to give if PD px develops sleep disturbancews

A

Clonazepam 0.5 to 1mg at bedtime

181
Q

EXERCISE - generally recommended for ALL PD patients .. True or False

A

True

182
Q

Major cause of falling

A

Freezing

183
Q

Treatment of FREEZING during ON vs OFF periods

A
184
Q

Dopamine terminal degeneration
May be complete within ________years of diagnosis

A

4 years

185
Q

Premotor features of PD (3)

A

Constipation, RBD, anosmia

186
Q

Met all 3 prespecified primary endpoints consistent with a disease-modifying effect

A

Rasagiline 1mg per day

187
Q

ideal subsets of population wherein levodopa, MAO B inhibitor, or Dopamine agonist should be started

A
188
Q

Only drug that has been demonstrated to TREAT dyskinesia WITHOUT worsening parkinsonism

A

Amantadine

189
Q

What is Duodopa

A

Continuous intraintestinal infusion of levodopa/carbidopa intestinal gel

190
Q

Drug Associated with skin nodules

A

Apomorphine continuous infusion

00000 Neurology (3 decks)

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