Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurology > Parkinson's Disease and Parkinsonism > Flashcards

Parkinson's Disease and Parkinsonism Flashcards

1
Q

What are the pyramidal movement disorders?

A

Pyramidal weakness

Spasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the extrapyramidal hyperkinetic movement disorders?

A 
Dystonia
Tics
Myoclonus
Chorea
Tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the extrapyramidal hypokinetic (rigidity, bradykinesia) movement disorders?

A

Parkinsonism

Parkinson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the cerebellar movement disorders?

A

Ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Parkinsonian syndrome?

A

Rigidity, akinesia/bradykinesia and resting tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is dystonia?

A

Prolonged muscle spasms and abnormal postures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is chorea and ballismus?

A

Fragments of movements flow irregularly from one body segment to another causing a dance-like appearance
Ballismus: if amplitude of these movements is large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What makes up the basal ganglia?

A

Caudate nucleus, putamen, globus pallidus externa and interna, subthalamic nucleus, substantia nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does PD present with?

A

Tremor, muscular rigidity akinesia, rest tremor, gait and postural impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the subtypes of PD?

A

Tremor dominant PD (relative absence of other motor symptoms)
Non-tremor dominant PD (such as akinetic-rigid syndrome and postural instability gait disorder)
Mixed/intermediate pheynotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

With what subtype is the course and prognosis associated with a slower rate of progression and less functional disability?

A

Tremor-dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some non-motor features of PD?

A

Olfactory dysfunction, cognitive impairment, psychiatric symptoms, sleep disorders, autonomic dysfunction, pain and fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When do non-motor symptoms of PD commonly present?

A

In early PD, or before the onset of motor features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the progression of PD characterised by?

A

Worsening motor features, which initially respond well to symptomatic therapies (Honeymoon phase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the advanced stages of PD characterised by?

A

The emergency of complications related to long term symptomatic treatment, including motor and non-motor fluctuations, dyskinesia and psychosis. Treatment resistant motor and non-motor features are prominent and include axial motor symptoms such as postural instability, freezing of gait, falls, dysphagia and speech dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is rapid eye movement sleep behaviour disorder?

A

A parasomnia characterised by abnormal or disruptive behaviours (such as talking, laughing, shouting, gesturing, grabbing, punching, kicking, sitting up in bed) which occurs during REM sleep and are often related to dream enactment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is RBD diagnosed?

A

Overnight polysomnography to document the presence of REM sleep without atonia (such as sustained or intermittent muscle activity measured by EMG) and to rule out mimics (such as OSA, non-REM parasomnia, seizures)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for RBD?

A

Clonazepam or melatonin at bedtime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the pathological hallmarks of PD?

A

Loss of dopaminergic neurons within the SNpc and Lewy body pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where does neuronal loss in PD occur other than the SNpc?

A

Locus ceruleus, nucleus basalis Meynert, pedunculopontine and raphe nuclei, dorsal motor nucleus of vagus, amygdala, hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Lewy body pathology?

A

Misfolded alpha-synuclein, which is insoluble and aggregated, forms intracellular inclusions (Lewy bodies) and processes (Lewy neurites) of neurones. Present in brain, spinal cord and PNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What gross colour change can be seen in PD?

A

Loss of the normally dark black pigment in the substantia nigra and locus coeruleus. Pigment loss correlates with dopaminergic cell loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Braak staging used for?

A

Staging of Lewy body pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the M:F ratio of PD?

A

3:2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the greatest RF in PD?

A

Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the most common causes of dominant and recessive PD?

A

Mutations in LRRK2 and parkin, respectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the greatest genetic risk factor for PD?

A

Mutations in GBA, which encodes B-glucocerebrosidase, the lysosomal enzyme deficient in Gaucher’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What was the first gene to be associated with PD?

A

SNCA, which encodes the protein a-synuclein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some environmental factors which increase the risk for PD?

A 
Pesticide exposure
Prior head injury
Rural living
Beta blocker use
Agricultural occupation
Well water drinking
30
Q

What are some environmental factors which decrease the risk for PD?

A 
Tobacco smoking
Coffee drinking
NSAID use
CCB use 
Alcohol consumption
31
Q

What treatment is available for PD?

A

Symptomatic only- enhance intracerebral dopamine concentrations or stimulate dopamine receptors. Include levodopa, dopamine agonists, monoamine oxidase type B inhibitors, and amantadine

32
Q

What agents can be effective for tremor?

A

Anticholinergics, trihexyphenidyl or clozapine

33
Q

When would levodopa and dopamine agonists be used?

A

More severe symptoms

34
Q

What adverse reactions are dopamine agonists and levodopa associated with?

A

Nausea, daytime somnolence and oedema

35
Q

What psychological/neurological adverse reactions occur with dopamine agonists?

A

Impulse control disorders, hypersexuality, binge eating, compulsive spending, hallucinations (so avoid in elderly)

36
Q

What is levodopa long term sued associated with?

A

Motor complications (dyskinesia and motor fluctuations)

37
Q

What are some long term complications of dopaminergic therapies for PD?

A

Motor fluctuations, non-motor fluctuations, dyskinesia, drug induced psychosis

38
Q

What are motor fluctuations thought to result from in later disease stages?

A

The pulsatile stimulation of striatal dopamine receptors

39
Q

What are some pharmacological strategies to reduce dopamine fluctuations?

A

A dopamine agonist
MAO B inhibitor
COMT inhibitor

40
Q

What are some options for the management of complications of long term dopaminergic therapies?

A

Direct delivery of stable levodopa-carbidopa gel (duodopa) into duodenum via percutaneous endogastric gastrostomy tube attached to portable infusion pump
Subcut infusion of potent dopamine agonist, apomorphine
Non-dopaminergic treatments such as amantadine and clozapine can be helpful

41
Q

How is psychosis in PD managed?

A

Clozapine (be aware of idiosyncratic adverse drug reactions and agranulocytosis)
Quetiapine

42
Q

What might reduce visual hallucinations and delusions in PD patients with dementia?

A

Cholinesterase inhibitors, such as rivastigmine

43
Q

What is depression associated with PD treated with?

A

Antidepressants: tricyclics preferably, SSRIs, extended release formulation of venlafaxine, a serotonin and norepinephrine reuptake inhibitor and the dopamine agonist pramipexole

44
Q

What is late stage dementia in PD treated with?

A

Rivastigmine

45
Q

What are the motor symptoms of PD?

A

Bradykinesia
Rest tremor
Rigidity
Postural and gait impairment

46
Q

What is Bradykinesia?

A

Slowness of movement with progressive loss of amplitude or speed during attempted raid alternating movement of body segments

47
Q

What is hypomimia?

A

Decreased facial expression and eye blinking

48
Q

What is micographia?

A

Progressively smaller handwriting

49
Q

How is a rest tremor described?

A

Rhythmic oscillatory involuntary movement of affected body part at rest
Vanishes with active movement

50
Q

At what frequency is a rest tremor?

A

Low to mid range (3-6Hz) with variable amplitude

51
Q

Where can the tremor effect people in PD?

A

Upper limbs, lower limbs, jaw, tongue

Not head

52
Q

How is rigidity described?

A

Increased muscle tone felt during examination by passive movement
Resistance felt throughout full movement
No increase with higher mobilising speed

53
Q

What is a positive Froment’s manoeuvre?

A

Rigidity increased in examined body segment by voluntary movement of other body parts

54
Q

How is postural and gait impairment described?

A

Stooped posture owing to impaired postural reflexes -in some cases camptocormia
Slow gait, occurs at narrow base with short, shuffling steps

55
Q

What is festination?

A

Very fast succession of steps and difficulties stopping

56
Q

What investigations are required for PD?

A

Rule out treatable conditions of asthenia (hypothyroidism, anaemia)
Structural brain imaging
Possible dopamine functional imaging: PET with fluoro-dopa, Dopamine transporter imaging with single photon emission (DAT-SPECT)
(Dopamine imaging unable to distinguish PD from other causes of Parkinsonism)
Positive levodopa challenge
Genetic testing

57
Q

What are some red flags in PD diagnosis?

A 
Absence of asymmetry of symptoms
Severe axial or lower limb involvement
Frequent falls
Fast progression
Eye movement disorder
Tics, myclonus, chorea
Pyramidal/cerebellar dysfunction
Bulbar/psuedobulbar features
Parietal associative sensory disturances
Apraxia
Severe cognitive deterioration or psychosis
Marked autonomic dysfunction
-ve levodopa challenge
58
Q

What is vascular parkinsonism?

A

Parkinsonism affects predominantly lower limbs
Rest tremor uncommon
Other signs of brain vascular lesions might be present
Poor levodopa response
Structural brain imaging will guide diagnosis

59
Q

What will be seen in Drug induced Parkinsonism?

A

Symmetrical
Course postural tremor
Presence of other drug induced disorders: orolingual dyskinesias, tardive dystonia, akathisia
Series of events is important
Improvement/resolution within few months of complete drug withdrawal

60
Q

What distinguishes essential tremor with tremulous PD?

A

Symmetric, postural or kinetic tremor with higher frequency
Infrequent at rest
Often AD inheritance with mean onset of 15y
Alcohol responsiveness
Head tremor- if present, mild

61
Q

Describe multi system atrophy

A

Common cause of degenerative Parkinsonism
Age of onset late 6th/7th decades
Core triad of dysautonomia, cerebellar features, and Parkinsonism

62
Q

What are some features of multi system atrophy?

A

Jerky postural tremor, pyramidal signs (generalised hyperflexia and extensor plantar responses)
Suboptimal and shortlived levodopa response in 1/3
Dysarthria or dysphonia, marked antecollis inspiratory sighing, orofacial dystonia

63
Q

What may an MRI show in multi system atrophy?

A

Cerebellar and pontine atrophy (hot cross bun sign, or hyperintense rim surrounding putamen in T2-weighted sequences)

64
Q

What is progressive supranuclear palsy?

A

Symmetric akinetic-rigid syndrome with predominantly axial involvement

65
Q

What are the features of progressive supranuclear palsy?

A 
Gait and balance impairment (early falls)
Tremor infrequent in patients
Vertical gaze supranuclear palsy
Pseudobulbar symptoms
Retrocollis
Continuous activity of frontalis muscle with eyes wide open
Frontal-subcortical cognitive deficits
No levodopa response
Some patients may have Parkinsonism
66
Q

What is fragile X-tremor ataxia syndrome?

A

Late-­‐onset (>50 years) neurodegenerative disorder in pts with an abnormal number of CGG repeats in the FMR1 gene, in the premutation range (55-­‐200)

67
Q

What are the core symptoms of FXTAS?

A

Core symptoms include cerebellar gait ataxia, postural / intention tremor, variably Parkinsonism, dysautonomia, cognitive decline of frontal type, and peripheral neuropathy

68
Q

What is the progression in FXTAS?

A

Slow

69
Q

What symptoms of FXTAS are seen in females with permutation (x-lined inheritance)?

A

Milder symptoms, often premature ovarian failure and menopause

70
Q

What MRI findings are seen in FXTAS?

A

T2 hyperintensities in the middle cerebellar peduncles (MCP sign)

71
Q

How is FXTAS confirmed?

A

Molecular testing

72
Q

What may children of FXTAS permutation carriers have?

A

Classical fragile X syndrome

Neurology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions