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PARKINSONISM Flashcards

1
Q

Role of BASAL GANGLIA

A
  • initiation of movements
  • modulation of movement
    (relays info recieved from the cerebral cortex BACK to the cerebral cortex)
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2
Q

What occurs with basal ganglial disease?

A
  • HYPOKINETIC or HYPERkinetic movement disorders
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3
Q

DIsease of the corticospinal/pyradmidal tract results in __________ and ______

A
  • SPASTICITY
  • PYRAMIDAL weakness

(UMN fts)

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4
Q

Disease of the cerebellum results in ________

A

ATAXIA

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5
Q

Disease of Basal Ganglia

A
  1. Hyperkinetic MD (dystonia/ Tics/ myoclonus/ chorea/ tremor)
  2. Hypokinetic MD
    - parkinsonism
    - parkinson’s disease
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6
Q

Pathological hallmark of parkinson’s?

A
  • loss of dark pigment in the substantia nigra and locus ceruleus
  • pigment loss correlates with dopaminergic cell loss
  • LEWY bodies on histology
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7
Q

Loss of how many percent of dopaminergic neurones is requires for symptoms to become clinically apparent.

A

50-60% of neurones from the PARS COMPACTA of the SUBSTANTIA nigra

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8
Q

What are lewy bodies

A
  • misfolded a-synuclein : insoluble and aggregated will form intracellular inclusions
  • —LEWY bodies may also be seen in spinal cord and the peripheral nervous system
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9
Q

What are the motor symptoms of parkinson’s?

A

Tremor
Rigidity
Bradykinesia

postural instability

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10
Q

Non-motor symptoms of Parkinson’s?

A
  • sleep d.o
  • hallucinations
  • GI dysfxn
  • depression
  • cognitive impairment/ dementia
  • anosmia
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11
Q

According to BRAAK staging of LEWY pathology what are the first abnormalities seen?

A
  • olfactory bulb

- enteric nervous system

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12
Q

What are the 2 subtypes of PD?

Which subtype has a small rate of progression?

A
  1. Tremor Dominant (relative absence of the other motor symptoms) —SLOWER progression (less functional dysability)
  2. Non-tremor dominant PD (akinetic-rigid syndrome and postural instability gait d.o)
  3. MIXED
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13
Q

Name a few prodromal symptoms of PD?

A
  • constipation
  • REM sleep Behavious d.o
  • EDS/ HYPOSMIA/ DEPRESSIOn
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14
Q

What are additional fts which help in dx of PD?

A
  • Bradykinesia AND one or MORE of the following: RESTING tremor, rigidity, postural instability
  • ADDITIONAL motor fts (STOOPED, fixed posture, DYSTONIC postures, hypomimia, shuffling, short-stepped gait
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15
Q

To confirm dx of parkinson’s, what should the pts NOT present with?

A
  • esrly onset bulbar problems, hallucinations, dementia, preferential involv. of lower limbs
  • prominent eye movement
  • intrusive early autonomic problems
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16
Q

If dx tests are needed, what invx are available?

A
  • structural brain imaging

- SPECT (DaTSCAN)

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17
Q

What is seen on DaTSCAN to confirm PD dx?

A
  • period-shaped
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18
Q

What may be ddx for parkisons?

A
  • MPTP exposure
  • NEGATIVE response to large doses of levodopa (malabsorpt. excluded)
  • babinski sign
  • cerebellar signs
  • supranuclear gaze palsy
  • cerebral tumor/ communicating hydrocephalus on MRI/CT
  • early autonomic involvement
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19
Q

What must be ruled out when considering postural instability as a PD sign?

A
  • should not be caused by primary visual, cerebellar, vestibular, proprioceptive dysfxn
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20
Q

Who is most likely to get PD?

A
  • men
  • of advancing age
  • w. FAMILY HX
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21
Q

What suggests genetic cause of PD?

A
  • early onset (< 40 y.o)
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22
Q

What gives rise to idiopathic PD?

A
  • susceptible genes+ env. triggers+ AGE
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23
Q

Name a few env. triggers.

A
  • pesticide and manganese exposure
  • prior head injury
  • rural living
  • beta-blocker use
  • well water drinking & agricultural job
  • mining, welding jobs
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24
Q

What reduces the risk?

A
  • tobacco smoking
  • coffee drinking
  • alcohol
  • calcium channel blocker
  • NSAID use
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25
Q

How many genes are involved in PD?

A
  • mutations in 11 genes
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26
Q

Name 2 important monogentic forms of PD?

A
  • LRRK2

- PARKIN

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27
Q

How to treat bradykinesia and rigidity seen in severe PD?

A
  • symptomatic rx
  • dopaminergic rx alleviates motor symptoms
  • —-levodopa
  • —-MAO B-inhibitors
28
Q

What is given to treat tremor?

A
  • anticholinergic drugs (clozapine/ trihexyphenidyl)
29
Q

What are the s.e one gets from use of dopamine agonists?

A
  • nausea
  • daytime somnolence
  • edema
  • impulse control d.o (gambling/hypersexuality/bingeating )
  • HALLUCINATIONS
30
Q

What is seen with long term use of levodopa?

A
  • a.w motor complications

- (dyskinesia and motor fluctuations)

31
Q

Summary of long-term complications of levodopa?

A
  • Motor Fluctuations
  • Non-motor fluctuations
  • Dyskinesia
  • drug-induced PSYCHOSIS
32
Q

What is seen with drug-induced psychosis (levodopa) ]?

A
  • visual (more commone)
  • less common= non-visual (tactile/auditory/olfactory)
  • illusions
  • delusions (paranois)
33
Q

What is dyskinesia?

A
  • involuntary choreiform/ dystonic movements

- occurs when levodopa is at peak dose

34
Q

What can be given to treat REM sleep behav. d.o?

A
  • benzodiazepine

CLONAZEPAM

35
Q

What is given to treat dementia ?

A
  • ACh-E inhibitor

RIVASTIGMINE

36
Q

What is given to treat psychosis?

A

atypical antipsychotics= quetiapine and CLOZAPINE

37
Q

How to manage PD?

A
  • have a good care-taker system involved
  • MDT
  • non-oral therapies can be considered (DUODOPA- direct delivery through gastrostomy tube/ deep brain stimulation/ continuous apomorphine infusion)
38
Q

What is the use of apomorphine injection?

A
  • reduces the “off” time
39
Q

How is bradykinesia tested?

A
  • ask pt to perform repetitive movement —-it will shows the slowness of movement with progressive LOSS of amplitude
40
Q

What are other form of bradykinesia apart from the usual movement d.o?

A
  • hypomimia
  • hypophonia
  • micrographia
41
Q

Does rest tremor of PD vanish with active movement?

A

YES

- reappears when hands are held outstretched

42
Q

Most common resting tremor?

A
  • pinr-rolling

- finger flexion-extension/ adbuction-adduction

43
Q

How to distinguish rigidity from spasticity (seen in UMN) ?

A
  • resistance is felt through out full range of passive movement
  • NO increase in rigidity with higher speed (in PD rigidity)
    = COGWHEEL rigidity
44
Q

Festination is often seen in PD. What is it?

A
  • very fast succession of steps and difficulties stopping
45
Q

Describe the PD gait.

A
  • slow
  • narrow base
  • short, shuffling steps
  • decr. arm swinging
46
Q

Parkinsonism affecting the lower limbs predominantly, is called______. It presents with other _______

A
  • VASCULAR Parkinsonism

- shows other brain vascular lesions like (spasticity/ hemiparesis/ pseudobulbar palsy)

47
Q

What sets vascular parkinsonism apart from PD?

A
  • resting tremor is UNCOMMON
  • poor levodopa response
  • structural brain scanning helps
48
Q

What are the fts like in drug-induced parkinsonism?

A
  • symmetrical
  • coarse postural tremor
  • presence of other drug induced d.o (orolingual dyskinesias- face and mouth involvement, tardive dystonia, akathisia- restlessness )
  • note series of events (sx after drug exposure?/ improvment with drug halt)
49
Q

How is essential tremor distinct from PD tremor?

A
  • NOT seen at rest
  • SYMMETRIC, POSTURAL or kinetic tremor (with high freq.)
  • Autosomal dominant inheritance with mean onset of 15 years
  • —alcohol responsiveness
  • HEAD tremor (mild)
50
Q

What is a common cause of degen. parkinsonism? When is it seen?

A
  • MULTI-SYSTEM ATROPHY

- 60-70 Y.O

51
Q

What is the triad of Multi-system atrophy>

A
  1. Dystautonomia
  2. Cerebellar fts
  3. Parkinsonism
52
Q

What is seen on MRI of Multisystem Atrophy?

A
  • cerebellar and pontine atrophy (HOT CROSS BUN)

- —-hypertense rim around PUTAMEN in T2 seq.

53
Q

Which gaze palsy may also be a.w Parkinsonism?

A
  • Progressive Supranuclear Palsy
    (vertical gaze palsy+ STARING+gait problems+ RETROCOLLIS- head tilted back+ Frontal-subcortical cognitive decline+ pseudobulbar sx+ parkinsonism )
54
Q

What genetic manifestation results in FXTAS?

And its course?

A
  • those with abnormal no. of CGG repeats in the FMR1 gene

- LATE-onset and SLOW Progression

55
Q

What are the CORE sx of Fragile X-tremor Ataxia Syndrome?

A

cerebellar GAIT ataxia+ postural/intention tremor+dysautonomia+ cog. decline of FRONTAL type and PERIPHERAL neuropathy

56
Q

In women FXTAS is a.w with what other conditions?

A
  • Premature Ovarian FAILURE

- MENOPAUSE

57
Q

What is seen on MRI of FXTAS?

A
  • MRI T2 hyperintensities in the MIDDLE cerebellar peduncles (MCP)
58
Q

Which parkinson associated conditions have POOR/NO response to Levodopa?

A
  • No response: Progressive Supranuclear Palsy and Vascular Parkinsonism
  • short-lived resp. to Levodopa in 1/3 of pts. in Multisystem atrophy
59
Q

What investigations can be done for PD?

A
  • r.o treatable probs of Asthenia (Hypothyroidism and anemia)
  • PET with fluoro-dopa ($$)
  • DATSPECT
  • POSITIVE levodopa challenge (s.c apomoprhine _ genetic testing
60
Q

How useful is dopamine functional imaging to distinguish PD from other parkinsonism?

A
  • UNABLE to distinguish PD from other degen. parkinsonism

—imaging should be NORMAL in ESSENTIAL tremor, dystonic tremor and psychogenic parkinsonism

61
Q

What signs should not be seen in a pt to diagnose PD?

A
  • ABSENT sensory, pyramidal and cerebellar signs
  • NO OTHER movement d.os
  • gaze palsies should NOT be present
62
Q

What are the non -motor sx of PD? Early and late?

A

EARLY:

  • hyposmia
  • REM sleep d.o
  • constipation
  • depression

LATE: dementia and hallucinations

63
Q

When does dementia set in?

A

> 80% of pts, sets in after 20 years

64
Q

How is depression a.w PD managed?

A

TCA (desipramine/ nortriptyline)
SSRIs (citalopram/ paroxetine/ sertraline)
—–EXTENDED release formulation of VENLAFAXINE

65
Q

What surgcial rx are available for PD ?

A

DEEP BRAIN stimulation targeting SUBTHALAMIC nucleus or GLOBUS pallidus internus

  • for rx of motor symptoms
66
Q

What are the other signs of Multisystem Atrophy?

A
  • Antecollis
  • dysarthria/ dysphonia
  • inspiratory sighing
  • OROFACIAL dystonia
  • babinski sign
  • generalised HYPERREFLEXIA

NEUROLOGY (36 decks)

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