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Neuro > Movement disorders > Flashcards

Movement disorders Flashcards

1
Q

Where in the brain is the substantia nigra?

A

Midbrain

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2
Q

What are the 2 parts of the striatum?

A

Caudate and Putamen

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3
Q

What is the globus pallidus also known as?

A

Pallidum

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4
Q

Which parts of the brain are heavily involved in movement disorders and why?

A

The SN, striatum, pallidum, and subthalamic nuclei

Control movement via thalamo-cortical projections

Affected = movement disorders

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5
Q

Which disease becomes very similar to Lewy Body Dementia later in the disease?

A

Parkinson’s (eventually it starts to affect the parietal lobe)

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6
Q

What degenerates in PD?

A

Dopaminergic neurons in the SN degenerate

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7
Q

What does too little dopamine cause?

A

Hypokinesia (Bradykinetic, akinetic)

Too little movement

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8
Q

What does too much dopamine cause?

A

Hyperkinetsia (Dyskinetic)

Too much movement

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9
Q

What effect does dopamine replacement have on patient life expectancies?

A

Dramatically increases the life expectancy

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10
Q

What diseases are treated with dopamine blockers?

A

Schizophrenia

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11
Q

What are the side effects of dopamine blockers?

A

Parkinsonian-like symptoms

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12
Q

People used to believe PD wasn’t genetic.

What happened to change that?

A

1997

An autosomal dominant family with alpha synuclein mutation developed Parkinson

Alpha synuclein was discovered to be a hallmark of PD

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13
Q

Describe the pattern of dopaminergic neuron loss in PD

A

Progressive and asymmetric

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14
Q

What are the symptoms of PD?

A
  • Stiffness of arm/shoulder
  • Tremor
  • Handwriting/micrographia
  • Repetitive tasks gets slower on repeating
  • Generalised slowing down
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15
Q

What are signs of PD?

A
  • Bradykinesia
  • Cogwheel rigidity
  • Gait disorder
  • Rest tremor
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16
Q

What percentage of people with PD have a tremor?

A

50%

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17
Q

How do you treat PD?

A
  1. Explanation of diagnosis, nurse specialist, patient support groups Physiotherapy, occupational therapy, SALT (speech and language therapy)
Drug treatments:
L-dopa
Dopamine agonist
Amantadine
COMT inhibitor
MAO-B inhibitor
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18
Q

What is the mechanism of action of amantadine?

A

Not well understood

An increase in synthesis and release of dopamine, with perhaps some inhibition of dopamine uptake

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19
Q

Name 2 L-DOPA drugs

A

Co-Careldopa and Co-Beneldopa

both have L-DOPA and Carbidopa

20
Q

Name 3 dopamine agonists

A

Ropinirolee
Pramipexole
Pergolide

21
Q

Name a COMT inhibitor

A

Entacapone

22
Q

Name 2 MAO-B inhibitors

A

Rasagaline and Selegeline

23
Q

What are the non-motor complications of treatment for PD?

A
  • Nausea
  • Postural hypotension
  • Fatigue
24
Q

What are the motor complications of PD treament?

A
  • Dyskinesias due to supersensitivity
  • On/off fluctuations
  • Wearing off
25
Q

How does Parkinson’s progress?

A

Starts with motor symptoms, can go to dementia and then cause hallucinations partially due to the treatment

26
Q

What is Braak’s hypothesis?

A

Sporadic PD is caused by a pathogen that enters the bodyviathe nasal cavity

This is swallowed and reaches the gut, initiating Lewy pathology (LP) in the nose and the digestive tract

It is suggested that Parkinson’s spreads from the periphery upwards (ascending theory)

27
Q

Map out ascending progression of PD

A

SN –> temporal cortex –> frontal and parietal cortices

28
Q

What are the prodromal symptoms of PD?

A

Cognitive: Frontal-executive impairment

Affective: Depression, anxiety, decreased novelty seeking

Sleep: REM behaviour disturbance

Autonomic: constipation

Special senses: loss of sense of smell

29
Q

What causes the prodromal constipation in PD?

A

Affects neurons in gut and in brainstem that controls the autonomic NS

30
Q

What are the NINDS criteria for possible symptoms of progressive supranuclear palsy?

A

Vertical supranuclear gaze palsy (loss of ability to look up and down)

Falls or the tendency to fall in the first year of symptoms

31
Q

What are useful clues to suggest someone has supranuclear palsy?

A

Frontalis over-activity

Impaired verbal fluency without bvFTD

Decreased blink rate

Erect posture with ambling gait

Falls with retained postural reflexes

32
Q

What is seen in the histology of someone with supranuclear palsy?

A

Tau tangles and tufted astrocytes

33
Q

What is supranuclear palsy usually misdiagnosed as?

A

Parkinson’s (it’s actually a parkinson’s plus condition)

34
Q

What are the diagnostic criteria for multiple system atrophy?

A

Autonomic failure –> urinary incontinence (ED for men)

Postural hypertension

Poorly L-DOPA responsive parkinsonism or cerebellar syndrome

35
Q

What is cerebellar syndrome?

A

Gait ataxia with cerebral dysarthria (difficulty speaking)

Limb ataxia

Cerebellar oculomotor dysfunction

36
Q

What are clinical features of multiple system atrophy?

A

Poly-mini-myoclonus

Action tremor

Incontinence

“Strangulated” dysarthria -problem with speech and swallowing

REM sleep behavioural disorders

Postural hypotension - black out when standing up

Cerebellar eye signs

Cranial-cervical dyskinesia/dystonia

37
Q

Which disorder is identical to multiple system atrophy in the early stages?

A

PD

38
Q

What are cerebellar eye sings?

A

Flutter, lack of coordinationn, instability of gaze, “dancing eyes” etc.

39
Q

What part of the nervous system does multiple system ataxia affect?

A

The autonomic nervous system

40
Q

What is muscle atonia?

A

It is how your muscles (except for respiratory muscles and eyes) get paralyzed in REM sleep.

41
Q

What is a possible prodromal symptom of multiple system ataxia?

A

REM sleep and behavioural disturbances

42
Q

What can you see in MSA histology?

A

Synuclein deposits

Especially in glial cells

43
Q

What are the symptoms of cortico-basal degeneration?

A

Limb apraxia

Asymmetric stiffness

Dystonia

Action myoclonus

Cortical sensory loss

Eye movement apraxia

Oro-buccal apraxia
(alien limb)

44
Q

What is cortico-basal degeneration often misdiagnosed as?

A

PD or stroke

45
Q

How is cortico-basal degeneration different from PD?

A

Doesn’t affect the substantia nigra, it affects the cortex

Causes people to have a useless limb

Doesn’t involve memory problems early on

46
Q

What is the age of onset for corticobasal degeneration?

A

50 or over

47
Q

Do MSA, CBD and PSP respond well to L-DOPA?

A

No, because the down stream receptors/neurons are not there

Neuro (23 decks)

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