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Neurology > Movement disorders > Flashcards

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
Q

What is cogwheel rigidity?

A

A superimposed clicking resistance, which is attributed to underlying tremor

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26
Q

How is a parkinsons diagnosis confirmed?

A

Parkinsonism
No alternative explanation
Dopamine responsivenedd

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27
Q

What should PD patients not present with

A

Early onset bulbar problems, dementia and hallucinations, preferential involvement of Lower limbs

Prominent eye movement disorder

Intrusive early autonomic problems

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28
Q

What scans can be helpful in parkinsons disease?

A

Structural brain imaging and SPECT (DaTSCAN) can be helpful

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29
Q

Men are ___ times more likely to develop parkinsons

A

Men are 1.5 times more likely to develop parkinsons

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30
Q

What are the risk factors for PD?

A
  • Advancing age
  • Positive family history- especially if onset <40
  • Male gender
  • Environmental factors
  • Genetics
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31
Q

What decreases the risk of PD?

A 
Tobacco smoking
Coffee drinking
NSAID use
Alcohol consumption
CCB use
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32
Q

What increases your risk of PD?

A 
Pesticide exposure
Prior head injury
Living rurally
Beta Blocker use
Well water drinking
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33
Q

What is the most clinically relevant pathogenic mutation for PD

A

Autosomal dominant- LRRK2

Autosomal recessive- PARKIN

34
Q

How do symptomatic treatments for PD work?

A

By enhancing intracerebral dopamine concentrations or stimulating dopamine receptors

35
Q

What are the symptomatic drugs for parkinsons?

A

Levodopa
Dopamine agonists
Monoamine oxidase type b inhibitors
Amantadine

36
Q

Bradykinesia and rigidity respond reliably to ________ treatment in early disease

A

Bradykinesia and rigidity respond reliably to dopaminergic treatment in early disease

37
Q

MAO B inhibitors are ______ effective, ____ and ______ _____ are needed for more severe treatment

A

MAO B inhibitors are moderately effective, levodopa and dopamine agonists are needed for more severe treatment

38
Q

Tremor is inconsistency responsive to treatment with dopamine and so may require

A

Anticholinergic agents, trihexyphenidyl, clozapine

39
Q

What are dopamine agonists and levodopa associated with?

A

Nausea, daytime somnolence and oedema

40
Q

When do impulse control disorders, including; pathological gambling, hyper sexuality, binge eating, compulsive spending occur?

A

With dopamine agonists

41
Q

When should dopamine agonists be avoided?

A

If there is a history of addiction, OCD or compulsive personality.
Avoided in elderly who have congitive impairment- can cause hallucinations

42
Q

What is longterm use of levodopa associated with?

A

motor complications (dyskinesia and motor fluctuations)

43
Q

What are motor fluctuations?

A

Alterations between periods of good motor symptom control (on time) and periods of reduced motor symptom control (off time)

44
Q

What are non-motor fluctuations?

A

Alterations between periods of good non-motor symptom control and periods of reduced non-motor symptom control

45
Q

What is dyskinesia?

A

Involuntary choreiform or dystonic movements

46
Q

When does dyskinesia occur most frequently?

A

When levodopa concentrations are at their maximum (peak dose)

47
Q

What is biphasic dyskinesia?

A

Involuntary movements that develop at the beginning or the end of a levodopa dose

48
Q

What is drug induced psychosis?

A

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
Q

What are some non oral therapies for PD?

A

Deep brain stimulation, DUODOPA, continuous apomorphine infusion

50
Q

Define bradykinesia

A

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

51
Q

How can bradykinesia be assessed?

A

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
Q

What is micrographia

A

Progressively smaller handwriting

53
Q

When does a parkinsonian tremor dissapear?

A

With active movement

54
Q

What is the most distinguishing resting tremor in PD?

A

Poll-rolling type

55
Q

In clinical practice when is tremor best observed?

A

When patient is focused on a particular task (counting back from 100)

56
Q

What is ridity?

A

Increased muscle tone felt during examination by passive movement

57
Q

What distinguishes rigidity from spasticity?

A

It doesn’t increase with higher mobilising speed

58
Q

Describe parkinsonian gait

A
  • Slow, occurs at narrow base with short, shuffling steps
  • Decreased arm swing
  • Slow turning with multiple small steps
  • Freezing
  • Festination
59
Q

Describe the investigations required for PD diagnosis?

A
  • 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
Q

What is dopamine functional imaging

A

PET with fluoro-dopa (limited availability and high cost)

Dopamine transporter imaging with single photon emission CT (DAT- SPECT)

61
Q

Describe vascular parkinsonism

A

Affects predominantly lower limbs

Rest tremor is uncommon

Other signs of vascular lesions might be present (spasticity, hemiparesis, pseudo bulbar palsy)

62
Q

Vascular Parkinsonism will have a poor ______ response

A

Vascular Parkinsonism will have a poor levodopa response

63
Q

What will guide the diagnosis of vascular Parkinsonism?

A

Structural brain imaging

64
Q

Describe the presentation of of drug induced parkinsonism

A

Symmetrical parkinsonism
Coarse postural tremor
Presence of other drug induced disorders
- orolingual dyskinesias, tardive dystonia, akathisia

65
Q

Describe essential tremor

A

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
Q

What is the core triad of multi system atrophy?

A

Dysautonomia, cerebellar features and Parkinsonism

67
Q

Multi system atrophy is a common cause of degenerative _______, the age of onset is in late __ or __ decade.

A

Multi system atrophy is a common cause of degenerative Parkinsonism, the age of onset is in late 6th or 7th decade.

68
Q

What features are suggestive of multi system atrophy?

A
  • severe dysarthria or dysphonia, marked antecollis, inspiratory signing, orofacial dystonia
69
Q

What may you see on an MRI of multi system atrophy?

A

Cerebellar and pontine atrophy (hot cross bun sign, or hyper intense rim surrounding the putamen in T2 weighted sequence)

70
Q

What is progressive supra nuclear palsy?

A

Symmetric akinetc-rigid syndrome with predominantly axial involvement

71
Q

Describe the presentation of progressive supra nuclear palsy

A
  • 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
Q

does progressive supranucelar palsy respond to levodopa?

A

No

73
Q

What are the core symptoms of fragile X-tremor ataxia syndrome (FXTAS)

A

Cerebellar gait ataxia, postural/intention tremor, variably Parkinsonism, dysautonomia, cognitive decline of frontal type, and peripheral neuropathy

74
Q

How does FTAX present on MRI?

A

MRI with T2 hyperintensities in the middle cerebellar peduncles (MCP sign)

75
Q

What are motor fluctuations and dyskinesias thought to result from?

A

Pulsatile stimulation of striatal dopamine receptors in later disease stages

76
Q

Pharmacological strategies to reduce dopamine fluctuations include the additions of;

A

A dopamine agonist
Monoamine oxidase type b receptor
Catechol-o-methyltransferase

77
Q

What might cholinesterase inhibitors such as rivastigmine be used for in PD?

A

Visual hallucinations and delusions in PD patients with dementia

78
Q

What does serotonin 5-HT inverse agonists primavanserin do?

A

Reduces positive psychotic symptoms

79
Q

Late stage dementia in PD is treated with?

A

Rivastigmine

80
Q

What are the surgical treatments for PD?

A

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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