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NSB Lectures > Parkinson's + drug therapy of basal ganglia disorders > Flashcards

Parkinson's + drug therapy of basal ganglia disorders Flashcards

1
Q

What are some common clinical features of Parkinson’s disease?

A

Tremor
Rigidity
Bradykinesia (slowness of movements)
Postural abnormalities
Reduced arm swing
Unilateral symptoms at onset
Shuffling, festinating gait (small steps, suddenly speed up)
Microphagia (small handwriting)
Anosmia (lack of smell)
Falls

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2
Q

Which area of the brain does Parkinson’s affect?

A

The basal ganglia

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3
Q

What does the basal ganglia consist of?

A

Caudate nucleus
Putamen
Globus pallidus
Substantia nigra
Subthalamic nucleus

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4
Q
A
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5
Q

Where is the basal ganglia located?

A

In the forebrain and midbrain

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6
Q

What is the function of the basal ganglia?

A

Control of movement and motor learning

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7
Q

What does the neostriatum comprise of?

A

Caudate nucleus and putamen

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8
Q

Which parts of the basal ganglia are anatomically and functionally close to the neostriatum?

A

Substantia nigra
Subthalamic nucleus

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9
Q

What are the two regions in the substantia nigra?

A

Pars compacta
Pars reticulata

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10
Q

What structure is connected to the tail of the caudate nucleus?

A

Amygdala

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11
Q

The basal ganglia primarily receives afferent information from which area of the brain?

A

Cerebral cortex

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12
Q

Afferent information from the somatosensory cortex and the primary motor cortex is sent to which area of the basal ganglia?

A

Putamen

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13
Q

Where do the afferent fibres sent to the caudate nucleus originate from?

A

Frontal and prefrontal cortices
Parietal association cortex

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14
Q

Efferent pathways from the basal ganglia back to the cortex are direct and indirect. What do these pathways influence?

A

Motor functions

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15
Q

Which sex is Parkinson’s disease more common in?

A

Male

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16
Q

Parkinson’s disease is the result of losing dopamine containing neurons in which part of the brain?

A

Pars compacta of the substantia nigra.

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17
Q

Which distinguishing feature of Parkinson’s disease is present in neurons?

A

Lewy bodies

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18
Q

What causes Parkinson’s disease?

A

No definitive cause - some links to genetics and environmental toxins

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19
Q

What are Lewy bodies?

A

Abnormal aggregations/clumping of the protein alpha-synuclein.

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20
Q

In Parkinson’s disease, which part of the brain are Lewy bodies located, and how is this different to dementia with lewy bodies?

A

PD - LB just in substantial nigra
Dementia with LB - LB all throughout cerebral cortex

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21
Q

If someone with Parkinson’s disease develops dementia within a year of their Parkinsonian symptoms developing, would they have PD with dementia or dementia with lewy bodies?

A

Dementia with Lewy bodies if <1 year
>1 year could be PD with dementia

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22
Q

Why is the substantial nigra dark and what happens to this in Parkinson’s disease?

A

It’s dark because it’s a major area for dopamine production and dopamine expresses neuromelanin (structurally related to melanin. Very pigmented)
In PD - Dopamine + therefore melanin granules lost so SN becomes more pale.

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23
Q

Do symptoms in Parkinson’s disease occur when only a few dopamine neurons have been lost in the substantial nigra?

A

No - takes about 70-80% loss for symptoms to occur.

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24
Q

What does dementia with Lewy bodies initially present with?

A

Cognitive impairment
In PD - tremor, rigidity and bradykinesia usually first.

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25
Q

Why is treating Lewy body dementia with anti-parkinsonian treatments and neuroleptics difficult?

A

Anti-parkinsonian treatments can make hallucinations and confusion worse.
Neuroleptics can make extra-pyramidal symptoms worse (involuntary movements)

26
Q

What is myoclonus and which neurological condition can this be present in?

A

Involuntary twitching/jerking of muscles
Lewy body dementia

27
Q

What is the gold standard drug treatment for Parkinson’s disease?

A

Levodopa - dopaminergic amino acid

28
Q

What is the MOA of levodopa?

A

Passes through BBB as the pre-cursor of dopamine. Converted to dopamine in brain, and replenishes dopamine in the neostriatum.

29
Q

What is the MOA of Carbidopa and benserazide?

A

Dopamine-decarboxylase inhibitor
Inhibits peripheral conversion of L-dopa to dopamine.
Instead increases the amount of L-dopa available to the brain tissue to then be converted to dopamine.

30
Q

Which medications containing L-dopa and a dopamine decarboxylase inhibitor are more commonly used in Parkinson’s disease?

A

Co-careldopa (sinemet) - L-dopa and carbidopa
Co-beneldopa (Madopar) - L-dopa and benserazide

31
Q

What are the adverse affects of Levodopa?

A

Postural hypotension
>7 years, motor fluctuations - on-off phenomenon (mobile 1 min, ‘off’ the next)
Tardive dyskinesia - hyperkinetic involuntary movements (writing around, very poorly controlled)
Neuro-psychiatric complications - confusion, hallucinations, psychosis

32
Q

What is the first line treatment for Parkinson’s disease for someone under 60?

A

Dopamine agonist - directly stimulate dopaminergic receptors to produce dopamine.
Ropinirole, rotigotine patch, Pramipexole

33
Q

What are some adverse effects of dopamine agonists?

A

Postural hypotension
GI disturbances
Dopamine dysregulation syndrome/impulsive control disorders - compulsive gambling, hyper sexuality.
Excessive daytime sleepiness

34
Q

Which dopamine agonist is particularly effective in the treatment or tremor and depression?

A

Pramipexole

35
Q

What are monoamine oxidase B inhibitors and why are they used earlier in Parkinson’s disease?

A

Selective inhibitor of MAO-B - blockade of central dopamine metabolism.
Evidence if used early in disease, it prolongs the time before L-dopa or dopamine agonist is required.
Also used as an adjunctive to l-dopa to prevent end of dose deterioration.
Radagiline
Selegaline - cardiac side effects

36
Q

What is the MOA of COMT inhibitors and why is this used in Parkinsons?

A

Inhibits COMT (an enzyme). COMT blocks dopamine metabolism.
It extends L-dopa’s benefits so given combined.
Entacapone - combined with co-careldopa = stalevo

37
Q

What is the role of Amantadine in Parkinsons?

A

It’s an antiviral agent that has an anti-parkinsonian effect.
Reduces the severity of L-dopa induce dyskinesias.

38
Q

What is deep brain stimulation and what is it used for?

A

Used in complex or late stage PD to treat/control motor symptoms.
Electrodes implanted into globus pallidus or subthalamic nuclei.
Indicated in on/off fluctuations and/or L-dopa induced dyskinesias (If more than 30% of time in these states).
Long-lasting
For subthalamic nuclei DBS - particularly useful to improve depression, apathy, reduced verbal fluency and executive function.

39
Q

Which SC dopamine agonist can be given as a ‘rescue medication’ in conjunction with l-dopa?

A

Apomorphine
Lasts around 40 minutes.
To help with dyskinesia.
SE’s: sleepy, hallucinations, impulse behaviours, hypotension, cardiac disorders.

40
Q

Which medication can be given via a continuous intestinal infusion for Parkinson’s?

A

Duodopa
Combination of l-dopa and carbidopa.
Usually given if other medications have not controlled symptoms, to reduced motor fluctuations and improve QOL.

41
Q

Which condition of the nervous system shares similarities with Parkinson’s disease, but has synuclein inclusions in the glia, affecting the ANS?

A

Multiple system atrophy (MSA)

42
Q

Neurofibrillary triangles within neurones occur in which parkinsonian like syndrome?
What are the symptoms of this?

A

Progressive suprenuclear palsy (PSP)
Early falls, failure of vertical eye movements, dysarthria, dysplasia, cognitive impairment.

43
Q

What are the main five hyperkinetic disorders?

A

Chorea
Dystonia
Tremors
Tics
Myoclonus

44
Q

What are tics?

A

Sudden movements or sounds that occur at irregular intervals.
Can be suppressed.
Worse with anxiety and fatigue.
Reduced by distraction and concentration.

45
Q

When does Giles de la Tourette’s syndrome typically present?

A

Around 7 or early adulthood

46
Q

Is Giles de Tourette’s syndrome more common in males or females?

A

Males

47
Q

What conditions is Giles de la Tourette’s associated with?

A

ADHD
OCD
Anxiety

48
Q

Rapid, irregular dance like movements that flow randomly from one body region to another is called what?

A

Chorea

49
Q

Which progressive disorder is chorea prominent in?

A

Huntington’s disease

50
Q

Is Huntington’s disease autosomal dominant or autosomal recessive?

A

Autosomal dominant

51
Q

What is Huntington’s disease caused by?

A

Expanded CAG trinucleotide repeated on Ch4.
>37 of the repeats = HD
<30 of the repeats is normal

52
Q

What is Huntington’s disease caused by?

A

Expanded CAG trinucleotide repeated on Ch4.
>37 of the repeats = HD
<30 of the repeats is normal

53
Q

Huntington’s disease is associated with atrophy in which areas of the brain?

A

Caudate nucleus
Putamen
Globus pallidus
Some cerebral atrophy

54
Q

Aside from Huntington’s disease, what are some other causes of chorea?

A

Vascular problems
Sydenham’s or rheumatic chorea
Systemic lupus erythematous
Auto-immune encephalitis
Toxoplasmosis (HIV)

55
Q

What is dystonia and what happens in the brain to make it occur?

A

Abnormal twisting posture - may be associated with jerky tremor.
Cause not fully understood.
Suggested links to abnormal activity in the motor cortex, supplementary motor areas, cerebellum and BG.
Dystonia can be caused by blocking dopamine receptors + some dystonia’s are levodopa responsive = supports that dystonia is related to abnormal dopaminergic activity.

56
Q

What can cause dystonia?

A

Stroke
Brain injury
Encephalitis
Parkinson’s
Huntington’s
Antipsychotics

57
Q

A benign essential tremor is different to the tremor seen in Parkinson’s disease. What causes this tremor?

A

GABAergic dysfunction in the cerebellum

58
Q

What types of drugs can treat hyperkinetic movement disorders?

A

Dopamine receptor blocking agents (Haloperidol, Chlorpromazine, Primozide, Risperidone)
Dopamine depleting agents (Tetrabenazine, reserpine)
Atypical anti-psychotics (Clozapine, Olanzapine, Aripiprazole).

59
Q

What brain activity are tics associated with?

A

Increased dopaminergic activity in the basal ganglia.
Abnormality in cortico-striato-thalamocortical circuits.
Thought to be disinhibition of excitatory neurons in the thalamus, resulting in hyperexcitability of cortical motor areas.

60
Q

What non medication therapies can be used in the treatment of Parkinson’s disease?

A

Physiotherapy
Tai chi
Pilates

NSB Lectures (48 decks)

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