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Movement disorders Flashcards

1
Q

The basal ganglia are involved in the _____ of movement and _____ of movement

A

The basal ganglia are involved in the initiation of movement and modulation of movement

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2
Q

The basal ganglia are a deep set of nuclear structures that receive input from the ________ _____, process it and relay it back to the ______ ____ via the ______

A

The basal ganglia are a deep set of nuclear structures that receive input from the cerebral cortex, process it and relay it back to the cerebral cortex via the thalamus

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3
Q

Basal ganglia disease can lead to too little (______) or too much (_______) movement disorders

A

Basal ganglia disease can lead to too little (hypokinetic) or too much (hyperkinetic) movement disorders

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4
Q

What are the pyramidal UMN features of movement disorder?

A

Pyramidal weakness and spasticity

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5
Q

Describe the presentation of hypokinetic movement disorders?

A 
Dystonia
Tics 
Myoclonus
Chorea 
(Tremor)
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6
Q

Describe the presentation of hyperkinetic movement disorders?

A

Rigidity, bradykinesia

= Parkinsonism, parkinsons disease

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7
Q

Where do hyperkinetic and hypokinetic movement disorders originate?

A

The basal ganglia

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8
Q

Where does ataxia originate from?

A

Cerebellum

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9
Q

What is the neurohistological hallmark of PD?

A

Lewy bodies

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10
Q

What are the motor symptoms of Parkinson’s disease?

A

Tremor
Bradykinesia
Rigidity
Postural instability

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11
Q

What are the non-motor symptoms of Parkinson’s disease?

A 
Sleep disorders
Hallucinations
Gastrointestinal dysfunction
Depression
Cognitive impairment/dementia
Anosmia
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12
Q

Loss of dopaminergic neurons from the ____ ______ region of the substantial migration- approximately __% loss of neurons (80% depletion in striatal dopamine) gives PD symptoms

A

Loss of dopaminergic neurons from the pars compacta region of the substantial migration- approximately 60% loss of neurons (80% depletion in striatal dopamine) gives PD symptoms

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13
Q

What are the two subtypes of parkinsons disease?

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/indeterminate phenotype
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14
Q

Which sub-type of parkinsons is associated with slower rate of progression and less functional disability?

A

Tremor dominant

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15
Q

What are the pre-motor/prodromal period symptoms of parkinsons?

A 
Constipation
RBD
EDS
Hyposmia
Depression
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16
Q

What are the non-motor symptoms of early stage parkinsons?

A

Pain
Fatigue
MCI

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17
Q

What are the -motor symptoms of early stage parkinsons?

A

Bradykinesia
Rigidity
Tremor

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18
Q

What are the complications of parkinsons that occur around 10 years after diagnoses?

A

Fluctiations

Dyskinesia

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19
Q

What are the late stage complications of parkinsons?

A

Psychosis

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20
Q

What are the advanced motor symptoms of parkinsons?

A

Dysphagia
Postural instability
Freezing of gait
Falls

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21
Q

What the the non-motor symptoms of unstable parkinons?

A

Urinary symptoms
Orthostatic hypotension
Dementia

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22
Q

What is essential Parkinsonism?

A

Bradykinesia and one (or more) of the following;

  • resting tremor
  • rigidity (cog-wheel or lead pipe)
  • postural instability
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23
Q

What are the additional motor features of parkinsons?

A 
Stooped, fixed posture
Dystonic postures
Hypomimia
Shuffling
Short-stepped gait (+/- festination)
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24
Q

What is lead pipe rigidity?

A

Constant resistance throughout passive movement

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25
What is cogwheel rigidity?
A superimposed clicking resistance, which is attributed to underlying tremor
26
How is a parkinsons diagnosis confirmed?
Parkinsonism No alternative explanation Dopamine responsivenedd
27
What should PD patients not present with
Early onset bulbar problems, dementia and hallucinations, preferential involvement of Lower limbs Prominent eye movement disorder Intrusive early autonomic problems
28
What scans can be helpful in parkinsons disease?
Structural brain imaging and SPECT (DaTSCAN) can be helpful
29
Men are ___ times more likely to develop parkinsons
Men are 1.5 times more likely to develop parkinsons
30
What are the risk factors for PD?
- Advancing age - Positive family history- especially if onset <40 - Male gender - Environmental factors - Genetics
31
What decreases the risk of PD?
``` Tobacco smoking Coffee drinking NSAID use Alcohol consumption CCB use ```
32
What increases your risk of PD?
``` Pesticide exposure Prior head injury Living rurally Beta Blocker use Well water drinking ```
33
What is the most clinically relevant pathogenic mutation for PD
Autosomal dominant- LRRK2 | Autosomal recessive- PARKIN
34
How do symptomatic treatments for PD work?
By enhancing intracerebral dopamine concentrations or stimulating dopamine receptors
35
What are the symptomatic drugs for parkinsons?
Levodopa Dopamine agonists Monoamine oxidase type b inhibitors Amantadine
36
Bradykinesia and rigidity respond reliably to ________ treatment in early disease
Bradykinesia and rigidity respond reliably to dopaminergic treatment in early disease
37
MAO B inhibitors are ______ effective, ____ and ______ _____ are needed for more severe treatment
MAO B inhibitors are moderately effective, levodopa and dopamine agonists are needed for more severe treatment
38
Tremor is inconsistency responsive to treatment with dopamine and so may require
Anticholinergic agents, trihexyphenidyl, clozapine
39
What are dopamine agonists and levodopa associated with?
Nausea, daytime somnolence and oedema
40
When do impulse control disorders, including; pathological gambling, hyper sexuality, binge eating, compulsive spending occur?
With dopamine agonists
41
When should dopamine agonists be avoided?
If there is a history of addiction, OCD or compulsive personality. Avoided in elderly who have congitive impairment- can cause hallucinations
42
What is longterm use of levodopa associated with?
motor complications (dyskinesia and motor fluctuations)
43
What are motor fluctuations?
Alterations between periods of good motor symptom control (on time) and periods of reduced motor symptom control (off time)
44
What are non-motor fluctuations?
Alterations between periods of good non-motor symptom control and periods of reduced non-motor symptom control
45
What is dyskinesia?
Involuntary choreiform or dystonic movements
46
When does dyskinesia occur most frequently?
When levodopa concentrations are at their maximum (peak dose)
47
What is biphasic dyskinesia?
Involuntary movements that develop at the beginning or the end of a levodopa dose
48
What is drug induced psychosis?
Hallucinations include minor phenomena, such as the sense of presence or passage hallucinations, but also well-formed visual and less-commonly non-visual (tactile, auditory, olfactory) hallucinations. Other psychotic features might include illusions and delusions (often with paranoia)
49
What are some non oral therapies for PD?
Deep brain stimulation, DUODOPA, continuous apomorphine infusion
50
Define bradykinesia
Slowness of movement with progressive loss of amplitude or speed during attempted rapid alternating movement of body segments
51
How can bradykinesia be assessed?
Ask the patient to perform some repetitive movements as quickly and widely as possibly (opening and closing the hand, foot tapping) OR Global assessment of spontaneous movements of the patient (standing up)
52
What is micrographia
Progressively smaller handwriting
53
When does a parkinsonian tremor dissapear?
With active movement
54
What is the most distinguishing resting tremor in PD?
Poll-rolling type
55
In clinical practice when is tremor best observed?
When patient is focused on a particular task (counting back from 100)
56
What is ridity?
Increased muscle tone felt during examination by passive movement
57
What distinguishes rigidity from spasticity?
It doesn't increase with higher mobilising speed
58
Describe parkinsonian gait
- Slow, occurs at narrow base with short, shuffling steps - Decreased arm swing - Slow turning with multiple small steps - Freezing - Festination
59
Describe the investigations required for PD diagnosis?
- Rule out treatable conditions of asthenia (hypothyroidism, anaemia) - structural brain imaging - possible dopamine functional imaging - positive levodopa (or s.c. apomorphine) challenge - genetic testing
60
What is dopamine functional imaging
PET with fluoro-dopa (limited availability and high cost) Dopamine transporter imaging with single photon emission CT (DAT- SPECT)
61
Describe vascular parkinsonism
Affects predominantly lower limbs Rest tremor is uncommon Other signs of vascular lesions might be present (spasticity, hemiparesis, pseudo bulbar palsy)
62
Vascular Parkinsonism will have a poor ______ response
Vascular Parkinsonism will have a poor levodopa response
63
What will guide the diagnosis of vascular Parkinsonism?
Structural brain imaging
64
Describe the presentation of of drug induced parkinsonism
Symmetrical parkinsonism Coarse postural tremor Presence of other drug induced disorders - orolingual dyskinesias, tardive dystonia, akathisia
65
Describe essential tremor
Symmetric, postural or kinetic tremor with higher frequency (up to 12Hz) Infrequently observed at rest Often autosomal dominant inheritance with mean onset of 15 years Alcohol responsiveness Head tremor- if present- mild
66
What is the core triad of multi system atrophy?
Dysautonomia, cerebellar features and Parkinsonism
67
Multi system atrophy is a common cause of degenerative _______, the age of onset is in late __ or __ decade.
Multi system atrophy is a common cause of degenerative Parkinsonism, the age of onset is in late 6th or 7th decade.
68
What features are suggestive of multi system atrophy?
- severe dysarthria or dysphonia, marked antecollis, inspiratory signing, orofacial dystonia
69
What may you see on an MRI of multi system atrophy?
Cerebellar and pontine atrophy (hot cross bun sign, or hyper intense rim surrounding the putamen in T2 weighted sequence)
70
What is progressive supra nuclear palsy?
Symmetric akinetc-rigid syndrome with predominantly axial involvement
71
Describe the presentation of progressive supra nuclear palsy
- Gait and balance impairment - vertical gaze supranuclear palsy - pseudo bulbar symptoms - retrocollis - continuous activity of the frontal muscle with eyes wide open (staring) - frontal-subcortical cognitive deficits - some patients may present with Parkinsonism Not usually a tremor
72
does progressive supranucelar palsy respond to levodopa?
No
73
What are the core symptoms of fragile X-tremor ataxia syndrome (FXTAS)
Cerebellar gait ataxia, postural/intention tremor, variably Parkinsonism, dysautonomia, cognitive decline of frontal type, and peripheral neuropathy
74
How does FTAX present on MRI?
MRI with T2 hyperintensities in the middle cerebellar peduncles (MCP sign)
75
What are motor fluctuations and dyskinesias thought to result from?
Pulsatile stimulation of striatal dopamine receptors in later disease stages
76
Pharmacological strategies to reduce dopamine fluctuations include the additions of;
A dopamine agonist Monoamine oxidase type b receptor Catechol-o-methyltransferase
77
What might cholinesterase inhibitors such as rivastigmine be used for in PD?
Visual hallucinations and delusions in PD patients with dementia
78
What does serotonin 5-HT inverse agonists primavanserin do?
Reduces positive psychotic symptoms
79
Late stage dementia in PD is treated with?
Rivastigmine
80
What are the surgical treatments for PD?
Deep brain stimulation for treating motor symptoms/complications is well established targeting either the subthalamic nucleus or globes pallidus internus

Neurology (41 decks)

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