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parkinsons Flashcards

1
Q

parkinsons

A

progressive reduction of dopamine in the basal ganglia - leading to disorders of movement

-> loss of dopaminergic neurons froms the pars compacta region of substantia nigra
(can see this in brain (coloured) as releases melanin)

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2
Q

types of parkinsons

A

idiopathic
familial
other (non-degenerative)
- drug induced
- post-encephalic
- toxins
- trauma

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3
Q

risk factors for parkinsons

A

advancing age - greatest
fam history (esp early onset <40yrs)
males
environmental - pesticide exposure, prior head injury, RUral living, beta blocker use

genetic
- LRRK2 (AD)
- PARKIN
- Alpha-synuclein - AD, Lewy bodies

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4
Q

what harmful act can DECREASE risk of parkinsons?

A

smoking

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5
Q

basal ganglia

A

is responsible for coordinating habitual movements – walking, looking around
o Controlling voluntary movements + learning specific movement patterns

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6
Q

substantia nigra

A

produces neurotransmitter called dopamine

-> Dopamine is essential for correct functioning of the basal ganglia

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7
Q

pathophysio of parkinsons

A

reactive gliosis happens in response to dopaminergic neuron loss -> astrocyte formation

starts at brain stem + ascends up to brain
- advanced = cortical involvement
- pre-motor symptoms = just brain

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8
Q

what would be seen if mid brain was cut into sections in Parkinsons and substantia nigra visible

A

reveal loss of normal black pigment in substantia nigra + locus ceruleus (melanin reduction)

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9
Q

parkinsons triad

A

bradykinesia - slow + diminshing movements

rigidity - increased muscle tone, resistance to passive movement, “cogwheel” as you passively flex arm (gives way to small little jerks)

tremor - at rest, unilateral pill rolling

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10
Q

parkinsons motor features

A

handwriting getting smaller, shuffling gait
difficulty initiating movements - standing still to walking
diffuculty turning - having to take lots of wee steps
reduced facial movement/expressions = hypomimia

tremor worse at rest + if distracted, 4-6Hz (4-6 times a second)

reduced arm swinging
stooped posture, forward tilt
eyes move horizontally v slowly

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11
Q

non-motor symptoms of parkinsons

A

anosmia
REM sleep disorder behaviour - act out dreams, speak, move
depression, constipation

friendly hallucinations

dementia - must have parkinsons for at least 1yr prior to onset, presentation similar to DLB

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12
Q

parkinsons diagnostic criteria

A

UK PDS brain bank criteria

  1. Bradykinesia + at least one of –
    a. Muscle rigidity
    b. 4-6hz rest tremor
    c. Postural instability not causes alternate primary cause
  2. Exclusion
    a. History of stroke
  3. Supporting criteria – 3 or more
    a. Unilateral onset
    b. Rest tremor
    c. Progressive syndrome
    d. Asymmetry
    e. Excellent response to L-dopa
    f. Development of L-dopa dyskinesia
    g. Sustained L-dopa response > 5yrs
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13
Q

what can be said about tremor dominant parkinsons

A

tremor-dominant subtype being associated with slower rate of progression and less functional disability

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14
Q

neurohistological hallmark of parkinsons

A

Lewy Bodies

(pigment loss correlates with dopaminergic loss)

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15
Q

imaging for parkinsons

A

SPECT/DaT scan

normal = comma shaped
abnormal = “period” shaped

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16
Q

key medications for parkinsons

A

levodopa (with Peripheral decarboxylase inhibitors – carbidopa / benserazide)

dopamine agonists - bromocriptine, pergolide, cabergoline

SSRIs for depression
Osmotic laxatives for constipation

16
Q

key medications for parkinsons

A

levodopa (with Peripheral decarboxylase inhibitors – carbidopa / benserazide)

dopamine agonists - bromocriptine, pergolide, cabergoline

SSRIs for depression
Osmotic laxatives for constipation

17
Q

key medications for parkinsons

A

levodopa (with Peripheral decarboxylase inhibitors – carbidopa / benserazide)

dopamine agonists - bromocriptine, pergolide, cabergoline

SSRIs for depression
Osmotic laxatives for constipation

18
Q

levodopa

A

Synthetic dopamine to boost dopamine levels

Usually combined with drug that stops it being broken down before reaches brain
* Peripheral decarboxylase inhibitors – carbidopa / benserazide

Most effective Mx for symptoms but becomes less effective over time

19
Q

side effects of levodopa

A
  • Postural hypotension – give midodrine if bad
  • Dry mouth, anorexia, palpitations
  • End of dose wearing off – worse symptoms at end of dosage interval
  • Greatest symptomatic benefit but longterm is assoc with motor complications
  • When dose too high, can develop dyskinesias (abnormal movement assoc with excessive motor activity) examples –
    o Dystonia – where excessive muscle contraction leads to abnormal postures or exaggerated movements
    o Chorea – abnormal involuntary movements that can be jerking + random
    o Athetosis – involuntary twisting or writhing movements usually in fingers, hands or feet
20
Q

side effects of levodopa

A
  • Postural hypotension – give midodrine if bad
  • Dry mouth, anorexia, palpitations
  • End of dose wearing off – worse symptoms at end of dosage interval
  • Greatest symptomatic benefit but longterm is assoc with motor complications
  • When dose too high, can develop dyskinesias (abnormal movement assoc with excessive motor activity) examples –
    o Dystonia – where excessive muscle contraction leads to abnormal postures or exaggerated movements
    o Chorea – abnormal involuntary movements that can be jerking + random
    o Athetosis – involuntary twisting or writhing movements usually in fingers, hands or feet
21
Q

4 main parkinson plus syndromes

A

progressive supranuclear palsy
multiple system atrophy
cortico-basal degeneration
Lewy body dementia

all present with parkinsonism (resting tremor, rigitidy + bradykinesia) plus additional symptoms

22
Q

progressive supranuclear palsy

A

parkinsonism + vertical gaze palsy - dysfunction of muslce involved in looking upwards

impairment of vertical gaze - down worse than up
-> may complain of difficulty reading or descending stairs

bradykinesia prominent - broadbased stiff gait, falls

tend to present with a more symmetric + tremor negative parkinsonism

23
Q

multiple system atrophy

A

rare condition where neurons of multiple system in brain degenerate
affects basal ganglia + other areas
- degen of basal ganglia -> parkinsonism
- degen in others -> autonomic + cerebellar dysfunction

autonomic dysfunction
- postural hypotension, constipation
- sexual dysfunction, abnormal sweating

cerebellar dysfucntion -> ataxia

24
Q

cortico-basal degeneration

A

parkinsonism plus spontaneous activity by an affected limb, or akinetic rigidity of that limb - “alien hand syndrome”

  • Patients sometimes present with apraxia - the inability to conceptulise movement i.e. description of not being able to follow instructions, but being able to do them automatically
25
Q

Lewy body dementia

A

progressive/FLUCTUATING cognitive decline with assoc symptoms of visual hallucinations, delusions, disorders of REM sleep

typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms

26
Q

drug induced parkinsonism

A

dopamine-blocking or depleting drugs, esp neuroleptics (except clozapine), induce parkinsonism or worsen symtpoms

antimuscarinic drugs reduce these symptoms, although tardive dyskinesia may be made worse

27
Q

Wilsons disease

A

autosomal recessive, characterised by excessive copper deposition in tissues, younger onset 10-25yrs (<50y/o)

hepatitis
basal ganglia degeneration
speech, psychiatric problems
chorea, dementia, parkinsonism
blue nails
Kayser-Fleischer rings - green/brown ring round iris

28
Q

management of Wilsons

A

penicillamine

neuro (26 decks)

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