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Y6 PASSMED > Neuro > Flashcards

Neuro Flashcards

1
Q

Definition of Parkinson’s

A

Progressive neurodegenerative condition cuased by degeneration of dopaminergic neruons in the substantia nigra

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2
Q

Where is the substantia nigra loacted?

A

It is a part of the basal ganglia

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3
Q

Main function of basal ganglia?

A

Motor control

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4
Q

What is the badsal ganglia?

A

Group of subcortical nuclei responsible for motor learning, executive function, behaviours and emotions

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5
Q

What is required for the functioning of input nuclei?

A

Dopamine to be released at the input nuclei
-When there is a dopamine dysfunction it can lead to movement disorders such as parkinson’s

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6
Q

What is the role of the substantia nigra?

A

Produces dopamine
-This controls muscle tone and movement
-It also plays a role in cognitive executive functions, emotional limbic activity and addiction

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7
Q

What happens to the substantia nigra in parkinson disease?

A

Neurons degenerate leading to loss of dopamine

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8
Q

What is the triad of features of parkinson disease ?

A

-Bradykinesia
-Tremor
-Rigidity

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9
Q

What is bradykineasia?

A

-Slowness of movement and speed (can also present as hesitation/halts when movements are continued)
-NOTE - movements also get smaller

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10
Q

What must you have to be considered to have Parkinson’s?

A

Bradykinesia plus either tremor or rigidity

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11
Q

How does bradykinesia present in someone with Parkinsons?

A

-Poverty of movement (hypokineasia)
-Short, shuffling steps with reduced arm swing
-Difficulty in initiating movement

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12
Q

Signs of bradykinesia?

A

-Not crossing arms and legs
-Blinking less often
-Not swinging arms when walking
-Difficulty standing up or rolling over in bed
-Freezing or pausing while moving
-Having trouble clapping hands or tapping finger

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13
Q

Tremor in parkinson’s disease?

A

-More prominent at rest, usually improves with voluntary movement
-Worse when stressed and tired
-Pill rolling tremor between thumb and index finger
-4-6 herts

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14
Q

Define lead pipe rigidity

A

Constant resistance to motion throughout the entire range of movement

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15
Q

Define cogwheel rigidity

A

Resistance that stops and starts as the limb is moved through a range of movement
-This is due to lead-pipe rigidity with tremor
-Due to superimposed tremor

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16
Q

Spascity

A

-Is a hypertonic state
-Velocity dependent
-Asymmetric
-Muscle movement are restricted in only one specific direction

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17
Q

Why does spasticity arise?

A

Due to damage of cortico reticulospinal tracts

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18
Q

Why does rigidity arise?

A

Due to dysfunction of extrapyramidal pathways

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19
Q

What is a festinating gait?

A

Rapid frequency of steps to compensate for small steps and avoid falling - this is a sign of bradykinesia

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20
Q

Other ways bradykinesia can manifest

A

-Shuffling gait
-Festinating gait
-Difficulty initiating movement
-Reduced facial movement (hypomimia)
-Small handwriting (microgrpahia)
-Flexed like posture

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21
Q

Other features of parkinson

A

-Flexed posture (postural instability) - cause falls
-Depression (40%)
-Sleep disturbances and insomnia
-Cognitive impairment and memory problems
-Fatigue
-Autonomic dysfunction (postural hypotension)
-Drooling
-Anosmia

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22
Q

How can you make tremor more pronounced when examining a patient with parkinson’s?

A

Ge the patient to do a paintbrush motion with the other hand

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23
Q

How does drug induced parkinsonism present?

A

-Rapid onset and bilateral motor symptoms
-Rigidity and rest tremors are uncommon

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24
Q

What drugs can cause drug induced parkinsonism?

A

Antipsychotics and antiemetics - they work by blocking dopamine receptors

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25
Q

What are the antiemetics that can cause drug induced parkinsonism?

A

Metoclopramide and prochlorperazine

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26
Q

What is an antiemetic that can be used in patients with parkinson’s?

A

Domperidone - does not affect the basal ganglia it selectively blocks receptors in the gut and chemoreceptor trigger zone
-Does not cross blood brain barrier

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27
Q

How is parkinson’s disease diagnosed?

A

-Diagnosed clinically but if there is difficulty in distinguishing between essential tremor and parkinson’s NICE recommend I-FP–CIT SPECT

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28
Q

What criteria to NICE recommend for clinical diagnosis of parkinson’s?

A

UK Parkinons Disease Society Brain Bank Clincal Diagnostic Criteria

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29
Q

What is the aim of management in Parkisnons disease?

A

Controlling symptoms and minimising side effects

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30
Q

First line treatment if motor symptoms are affecting patients quality of life?

A

Levodopa

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31
Q

Mechanism of action of levodopa?

A

Levodopa is a precursor to dopamine that crosses the blood brain barrier and is then converted to dopamine (by decarboxylation) (DOPA decarboxylase)

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32
Q

What is levodopa normally given with?

A

Peripheral decarboxylase inhibitors
-These inhibit

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33
Q

Why are peripheral decarboxylase inhibitors given with Levodopa?

A

It stops the levodopa being converted into dopamine in peripheral tissues this is important for 2 reasons
1. Dopamine cannot cross BBB, so will not reach the brain and be effective
2. Peripheral dopamine can cause side effects
3. Allows a lower dose of levodopa to be used

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34
Q

What do enzyme do peripheral decarboxylase inhibitors block?

A

Peripheral DOPA decarboxylase

35
Q

What is a hallmark feature of Parkinson’s disease that causes degeneration of dopaminergic neurons?

A

alpha-synuclein aggregation - form lumps called lewy bodies

36
Q

What are the neurons damaged in parkinsons?

A

-the primary damage is to dopaminergic neurons in substantia nigra
-As disease progresses more neurons can be impacted such as noraadrenergic (hypotension) , cholinergic (dementia), serotonrgic neurons (depression), autonomic (constipation, urinary dysfunction, sexual dysfunction and temperature)

NOTE: accumulation of alpha-synuclein in other parts brain such as cortex and limbic system lead to other problems

37
Q

How does levodopa work even when dopamine neurons are depleted?

A
  1. There are residual dopaminergic neurons
  2. Non-dopaminergic cam convert levodopa
    This is why as disease progresses and there are less dopaminergic neurones the effectivness of levodopa decreases
38
Q

Give the names of peripheral decarboxylase inhibitors

A
  1. Carbidopa
  2. Benserazide
39
Q

Combination drugs with levodopa and peripheral decarboxylas einhibtors?

A

-Co-beneldopa (levodopa and benserazide) MADOPA
-Co-careldopa (levodopa and carbidopa) SINEMET

40
Q

What enzymes metabolise doapamine?

A

-Monoamine oxidase (MAO)
-Catechol-O-methyltransferase (COMT)

41
Q

What is the main side effect of levodopa?

A

Dyskinesia - this is abnormal movements due to excessive motor activity

42
Q

Give examples of dyskinesia

A

-Dystonia - excessive muscle contraction leadign to abnormal posture
-Chorea - involuntary movements that can be jerking and random
-Athetosis -involuntary twisting or writhing movments usually of fingers, hands or feet

43
Q

What other disoers that can occur due to levodopa?

A

Impulse control disorders

44
Q

What medication can be used to manage dyskinesia associated with levodopa?

A

Amantadine

45
Q

What is the first line treatment of Parkinson’s disease if motor symptoms are not affecting the patient’s quality of life?

A

-Dopamine agonists, levodopa or monoamine oxidase B (MAO-B) inhibitor

46
Q

How do dopamine agonists work?

A

They mimic dopamine stimulating dopamine receptors

47
Q

What are the types of dopamine agonists?

A

-Ergot derived (from ergot fungus) and non ergot derived

48
Q

Examples of dopamine agonists

A

-Bromocriptine (ergot)
-Cabergoline (ergot)
-Apomorphine
-Pergolide

49
Q

What is a notable effect of prolonged use of ergot dopamine agonists?

A

Pulmonary fibrosis

50
Q

How do monoamine oxidase B inhibitors work in the treatment of parkinson’s disease?

A

They inhibit MAO-BH which is the enzyme that degrades monoamines including dopamine, this increases the availability of dopamine within the brain

50
Q

What is typical use of dopamine agonists ?

A

Delay levodopa treatment and use in combination with levodopa

51
Q

Side effects of dopamine agonists?

A

Nausease, dizziness, hallucinations, sleep disturbances, impulse control disorders

52
Q

What other neurotransmitters does monoamine oxidase enzymes break down?

A

Serotonin and adrenaline however MAO-B is more specific to dopamine

53
Q

Examples of monoamine oxidase inhibitors ?

A

Selegiline
Rasagiline

54
Q

When do NICE recommend adding dopamine agonist, MAO-B inhibitor or COMT inhibitor as an adjunct in parkinson’s disease?

A

If symptoms continue despite optimal levodopa use or patient has developed dyskinesia

55
Q

What are the common adverse effects with levodopa?

A

-Dry mouth
-Anorexia
-Palpitations
-Postural hypotension
-Psychosis

56
Q

Describe on and off period

A

-On is when medications are acting and patient is moving freely
-Off is when medications wear off

57
Q

How does COMT inhibitor work in treatment of parkinson’s disease?

A

COMT is an enzyme involved in breakdown of dopamine COMT inhibitors slow the breakdown of levodopa in the brain extending the effective duration of levodopa

58
Q

Example of COMT inhibitor

A

Entacapone

59
Q

When are antimuscarinics used in parkinsons?

A

These are more helpful in drug-induced parkinsonism
-Help tremor and rigidity
-Block cholinergic receptors

60
Q

What are patients at risk of if medication used to treat PD is not taken in/absorbed?

A

Acute akinesia or neuroleptic malignant syndrome

61
Q

Name four kinds of parkinson plus syndromes?

A

1.Multiple system atrophy
2. Dementia with Lewy body
3. Progressive supranuclear palsy
4. Corticobasal degeneration

62
Q

Describe multiple system atrophy

A

-Parkinson plus syndrome
-Various neurons in the brain degenerate
-Degeneration of neurons in the basal ganglia leads to parkinson’s symptoms
-Degeneration in other areas leads to autonomic dysfunction and cerebellar dysfunction

63
Q

Name signs that are more specific to cerebellar dysfunction

A

1.Ataxia
2.Dysmetria
3. Intention tremor
4. Dysdiadochokineasia
5. Nystagmus (horizontal)
6. Rebound phenomenon
7. Pendulkar reflexes
8. Wide based staggerign gait

64
Q

Define ataxia

A

Cerebellar dysfunction involving uncoordinated movement - drunken or clumsyt appearance

65
Q

Define dysmetria

A

-Control range of movements
-May overshoot (hypermetria) or undershoot (hypometria) when reaching for an object

66
Q

How does an intention tremor differ to other types of tremors ?

A

Worse with purposeful movements and worsens when hand or limb approaches target

67
Q

Define dysdiachokinesia

A

The ability to perform rapid alternating movements - specific motor sign of cerebellar dysfunction

68
Q

How is nystagmus in cerebellar dysfunction different to other kinds of nystagmus?

A

Horizontal more common and occurs when the eye moves away from central line of site

69
Q

Describe pendular reflexes

A

Instead of a single reflexive movement in cerebellar dysfunction there can be multiple oscillation or “pendulum-like movements after a reflex is triggered)

70
Q

What are the symptoms associated with dementia with lewy bodies?

A

-Visual hallucination
-Delusions
-Rem sleep
-Fluctuating consciousness

71
Q

Progressive supranuclear palsy vs parkinsons disease?

A

-Parkinson’s symptoms but more symmetrical and postural instability
-Ocular symptoms also occur (brainstem)
-Dementia

72
Q

Define apraxia

A

Neurological disorder characterised by the inability to perform learned purposeful movements or tasks

73
Q

Why does apraxia occur?

A

Due to damage of areas of the brain that are involved in planning and executing movements - left parietal lobe and frontal lobe

74
Q

Corticobasal degeneration vs PD?

A

-Impacts cortex and basal ganglia
-Apraxia and alien limb (dystonia)

75
Q

What medication can be considered if sleepiness persists with mediation treatment of PD?

A

Modafinil however first you should review medication

76
Q

What should you do if orthostatic hypotenison develops?

A

Look for causes and midodrine can be considered

77
Q

Define benign essential tremor

A

-Common disorder associated with older age
-Often hereditary - autosomal dominant

78
Q

Where is tremor most notable?

A

In the hands but can cause head tremor (titubation), jaw tremor and vocal tremor

79
Q

Features of BET

A

-Fine tremor (6-12hz)
-Symmetricla
-More prominent with voluntary movement
-Worse when stressed, tired or after caffeine
-Improved with alcohol
-Absent in sleep

80
Q

How is BET diagnosed?

A

Clinically after excluding other causes such as PD, MS, Huntingtons, hyperthyroidism, fever alcohol withdrawal, caffeien, drug indcued

81
Q

How is BET managed?

A

-Can manage symptoms using propranolol
-Primidone can be used

82
Q

What is a common consequence of subarachnoid haemorrhage?

A

syndrome of inappropriate antidiuretic hormone secretion (SIADH)

83
Q
A

Y6 PASSMED (8 decks)

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