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parkinsons disease lecture Flashcards

1
Q

what structures make up the basal ganglia?

A

striatum - ie the caudate + putamen
globus pallidus
subthalamic nucleus
substantia nigra

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2
Q

which is more superior (in terms of anatomical position), the subthalamic nucleus or the substantia nigra?

A

the subthlamic nucleus

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3
Q

what circuits are the basal ganglia involved in?

A

motor circuit
limbic
oculomotor

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4
Q

name some illnesses associated with BG dysfunction

A 
parkinson's 
Huntington's
dystonia
Gilles de la tourette syndrome 
OCD
ADHD
cerebral palsy
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5
Q

what is rigidity?

A

a feature of extrapyramidal disease - involves increased tone in the muscles across the whole range of movement

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6
Q

What is spasticity?

A

a feature of an UMN lesion ie a pyramidal tract disease - feel the increased tone more on flexion than extension

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7
Q

Give examples of a condition where spasticity is seen

A

stroke
MND
MS

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8
Q

give an example of a condition where rigidity is seen?

A

parkinson’s

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9
Q

how much dopamine is there in parkinson’s?

A

not enough dopamine

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10
Q

how much dopamine is there in huntingtons?

A

too much dopamine

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11
Q

how are muscle tone and movements affected in parkinson’s?

A

increased muscle tone

reduced movements

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12
Q

how are muscle tone and movements affected in huntington’s

A

decreased muscle tone

overshooting movements

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13
Q

describe the dopamine synthesis pathway

A 
L-tyrosine
L-DOPA
dopamine
norepinephrine 
epinephrine
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14
Q

what is L-tyrosine?

A

an essential amino acid

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15
Q

where is dopamine stored?

A

in presynaptic vesicles

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16
Q

which brain structure produces dopamine?

A

substantia nigra

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17
Q

where is dopamine transported to?

A

transported to the striatum from the substantia nigra

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18
Q

describe the pathophysiology of parkinson’s disease

A

loss of dopaminergic neurones in the substantia nigra (where dopamine is created).
so there is a reduction in dopamine levels
degeneration of the nigrostriatal tract (the path of neurones from the substantia nigra to the striatum)
surviving neurones of the substantia nigra contain cytoplasmic inclusions = Lewy bodies
the motor pathway: cortex - BG - thalamus - cortex - movement is amplified by stimulatory signals from the substantia nigra and dopamine and this is lost in parkinsons so there is reduced movement
also the substantia nigra normally inhibits the inhibitory impulses of movement of the subthalamic nucleus
but as the substantia nigra is damaged, then it can no longer inhibit the sub thalamic nucleus so the subthalamic nucleus inhibits movements further

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19
Q

what are the 3 cardinal features of PD?

A

brady/akinesia
tremor
rigidity

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20
Q

how does brady/akinesia present?

A

problems with doing up buttons
writing smaller = micrographia
festinating gait - small steps, dragging one foot
actions are initiated with effort - difficult to get out of a chair and difficult to start walking

21
Q

what type of tremor is seen in parkinson’s?

A

resting tremor

22
Q

what symptoms does rigidity give?

A

pain

problems turning in bed

23
Q

what management options are there for parkinson’s?

A

dopamine receptor agonists - Levodopa - a naturally occurring precursor of dopamine (prodrug)
enzyme inhibitors eg COMT inhibitors and MAO inhibitors
deep brain stimulation = electrodes put into sub thalamic nucleus

24
Q

how does deep brain stimulation work?

A

it inhibits the inhibitory impulses of movement coming from the substantia nigra, so addressed on of the pathways that has gone wrong and increases movement

25
Q

whare the ‘hardware’ dyskinesias?

A

Parkinson’s

Huntington’s

26
Q

what are the ‘software’ dyskinesias?

A

essential tremor
dystonia
Tourette

27
Q

what type of tremor is seen in essential tremor?

A

action tremor

28
Q

what type of tremor is seen in intention tremor?

A

cerebellar disease

29
Q

what is the order of assessing tremor?

A
  1. rest tremor
  2. action tremor
  3. intention tremor
30
Q

what distribution is essential tremor?

A

symmetrical

31
Q

do pts with parkinsons have weakness?

A

no

32
Q

EXAM: what are the 2 pathological features seen in parkinsons?

A
  1. intracytoplasmic inclusion bodies

2. loss of neuromelanin containing dopaminergic neurones in the substantia nigra

33
Q

what are the causative factors for parkinsons?

A

inhertied factors including susceptibility factors and parkinson genes
oxidative stress
mitochondrial dysfunction
risk factors and toxins from the environment

34
Q

what are the motor complications of late stage PD?

A

wearing off - the drugs work shorter and shorter
on-dyskinesias - hyperkinetic, choreiform movements when drugs work
off-dyskinesias - fixed, painful dystonic posturing, typically of feet when the drugs don’t work
freezing - unpredictable loss of mobility

35
Q

which is the most powerful drug we have for PD?

A

levodopa

36
Q

what is the first-line drug treatment for PD pts under 60?

A

DA agonists such as ropinirole and pramipexole

37
Q

what are the different preparations of levodopa?

A

dispersible levodopa - kick start in the morning
standard release - day time medication
slow release - helps through the night

38
Q

what are the other features of PD apart from parkinsosns?

A

depression
psychiatric disorders eg phobias, anxiety disorders, hallucinations
dementia
autonomic problems - constipation, increased urinary frequency

39
Q

what should not be present at the beginning of PD?

A

incontinence
dementia
symmetry
early falls

40
Q

what is normal pressure hydrocephalus?

A 
a syndrome of enlarged lateral ventricles in elderly pts with a clinical triad of: 
- gait apraxia 
- dementia 
- urinary incontinence 
there is intermittently raised ICP
41
Q

how is normal pressure hydrocephalus corrected?

A

ventriculoperitoneal shunting of CSF (from the ventricles to the peritoneal cavity)

42
Q

How does essential present?

A

ACTION tremor
gradual worsening
no rest tremor, no increased tone and no problem with fine finger movements

43
Q

how do we treat essential tremor?

A

beta blockers are first line
primidone
gabapentin

44
Q

how does cerebellar ataxia present?

A
  • slowly progressive walking problems
  • deterioration of fine finger movements
  • slurred speech
  • broad based gait
  • intention tremor
  • normal tone ie no rigidity
  • clumsy
45
Q

how does cerebellar ataxia compare to PD?

A
  • slurred speech - doesn’t happen in PD
  • broad based gait - narrow based in PD
  • intention tremor - rest tremor in DP
  • normal tone ie no rigidity
  • clumsy - no clumsy in PD, but have bradykinesia ie decreasing amplitude of fine finger movements
46
Q

what is seen on imaging of a pt with cerebellar ataxia?

A

cerebellar atrophy

47
Q

what is dystonia?

A

a syndrome of sustained muscle contraction, frequently causing twisting and repetitive movements as well as abnormal posture

48
Q

what treatments are there for HD?

A

neuroleptics (antipsychotics) are used to treat are used to treat the chorea and psychosis

Neuro (9 decks)

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