Parkinson's disease

Question 1

how is a clinical diagnosis of idiopathic parkinson’s disease made?

Answer 1

• using the Brain Bank criteria, and is based on:
• bradykinesia-slowness of voluntary movements, and reduced automatic movements, also seen as as progressive reduction in amplitude of repetitive movements
• muscular rigidity (lead pipe, cog wheel)
• resting tremor, low velocity, ‘pill rolling’, abolished by movement
• postural instability
• gait abnormality-forward flexed shuffling gait with reduced arm swing, and turning en-bloc-part. associated with falls

symptoms classically asymmetrical at presentation, but progress to involve both sides of the body, with side of onset characteristically affected worse

Question 2

examples of rating scales used in parkinson’s disease assessment?

Answer 2

• Hoehn and Yahr

- UPDRS-unified parkinson’s disease rating scale-objectively rate motor symptoms

Question 3

examples of parkinsonian plus syndromes?

Answer 3

• progressive supranuclear palsy (PSP)
• multi system atrophy (MSA)
• corticobasal degeneration (CBD)
• vascular (arteriosclerotic)

Question 4

what is a glabellar tap?

Answer 4

this is a primitive reflex where the eyes shut if person tapped lightly between the eyebrows, but may normally be overcome rapidly so pt soon fails to blink
however, in some pts reflex cannot be overcome e.g. in parkinson’s

Question 5

how does the tremor of idiopathic parkinson’s differ from that of benign essential tremor?

Answer 5

essential tremor: tremor is there all the time, not just at rest
bilateral tremor, usually affects both upper limbs
postural tremor-worse when arms are outstretched
improved by alcohol and rest
most common cause of head tremor (titubation)

essential tremor=autosomal dominant condition

Question 6

management of essential tremor?

Answer 6

propranolol 1st line

primidone

Question 7

causes of drug-induced parkinsonism?

Answer 7

drugs which block dopamine receptors or reduce the storage of dopamine:
prochlorperazine-typical antipsychotic, also used for N+V and labyrinthine disorders e.g. acute attacks of menieres disease-tinnitus, fluctuating SN deafness and episodic vertigo lasting mins-hrs
other 1st generation antipsychotics e.g. haloperidol
metoclopramide

px classically bilateral and rapid onset of motor symptoms, with rigidity and rest tremor uncommon

Question 8

causes of parkinsonism (classic triad of bradykinesia, rigidity and resting tremor)?

Answer 8

• idiopathic parkinson’s disease
• parkinson’s plus syndromes
• multiple cerebral infarcts
• post-encephalitis
• wilson’s disease
• drug-induced
• toxin-induced e.g. MPTP, manganese, Cu (Wilson’s)
• trauma (pugilistic encephalopathy)

Question 9

peak age of parkinson’s disease onset?

Answer 9

55-65yrs

Question 10

how might the resting tremor of parkinsons be made more apparent?

Answer 10

asking pt to concentrate on something

Question 11

how can the rigidity of parkinson’s be made more apparent?

Answer 11

get the pt to perform an action in the opposite limb e.g. moving arm up and down then drawing a circle
=contralateral synkinesis

Question 12

what is the most likely diagnosis if a pt has parkinsonism worse in the leg than arms with a prominent gait abnormality and pyramidal signs?

Answer 12

vascular parkinsonism

Question 13

non-motor symptoms of parkinson’s?

Answer 13

hyposmia or anosmia-may be present for many years before onset of motor symptoms
depression
dementia
visual hallucinations
mild urinary frequency and urgency
dribbling saliva
REM behavioural sleep disorder

Question 14

LT problems in parkinson’s patients following L-DOPA treatment for around 5-10 years?

Answer 14

motor fluctuations:
-on-off fluctuations-rapid and unpredicatable fluctuations between on and off periods, and wearing off of the treatment before next dose is due (end of dose fading)
-dyskinesias during ‘on’ phase
-axial problems not respond to tment:
balance, speech and gait disturbance that don’t respond to tment, problems thought to be related to axonal degeneration outside SN where dopamine not the NT, can try and help with physio, OT and SALT
parkinson’s disease dementia:
-dementia occurring more than 1 yr after PD diagnosis.

Question 15

where in the nervous system in the problem in parkinson’s disease?

Answer 15

basal ganglia: substantia nigra pars compacta-degeneration of dopaminergic neurones causing reduction of dopamine in the striatum, lewy bodies (alpha synuclein proteins) also form here.

Question 16

typical features of parkinson’s disease dementia?

Answer 16

limb parkinsonism
visual hallucinations
frequent fluctuations in lucidity

can tx some of symptoms with antypical antipsychotics e.g. quetiapine, which are effective at reducing symptoms whilst not worsening the features of parkinson’s disease.

Question 17

complications of parkinson’s disease?

Answer 17

falls
aspiration pneumonia
poor nutrition
bed sores
infections
contractures
bowel and bladder disorders
pain-dystonia, akathisia, primary and central neuropathic pain

Question 18

parkinson’s disease prognosis?

Answer 18

variable
some patients follow relatively benign course, others develop severe disability more quickly
younger age of onset tend to have shorter life spans
slowly progressive disease with mean duration of 15 years.

Question 19

driving advice in parkinson’s?

Answer 19

pt should inform DVLA of diagnosis and insurers

Question 20

investigations necessary before treatment with non-ergot derived dopamine agonist (although rarely used now)?

Answer 20

ESR
renal function
CXR

non-ergot derived e.g. cabergoline assoc. with risk of fibrotic reactions

Question 21

how can dyskinesias assoc. with LT L-DOPA treatment be managed?

Answer 21

if occurring at peak dose try to reduce each dose of L-DOPA but make it more frequent so total daily dose remains the same
add on LA dopamine agonist
may try slow release or liquid L-DOPA
surgery may be needed

if happen at beginning or end of dose ca try soluble L-DOPA before meals, or add a COMT inhibitor.

Question 22

what is acute akinesia?

Answer 22

also known as parkinson’s crisis
this is a rare but life-threatening complication of the disease with a sudden worsening of motor symptoms and severe akinesia
can be triggered by infection, GI disease, changes in treatment and surgery
often needs hosp admission

Question 23

why must patients be warned about driving and operating machinery if taking a dopamine agonist e.g. ropinerole, or rotigotine patch?

Answer 23

patients can fall asleep suddenly so must be wary of feeling drowsy and being unsafe to drive

Question 24

most common psychiatric problem in patient with PD?

Answer 24

depression

Question 25

when does PD become clinically apparent?

Answer 25

not until more than 50% of dopaminergic cell activity in the substantia nigra has been lost

Question 26

risk associated with abrupt withdrawal of levodopa treatment?

Answer 26

neuroleptic malignant syndrome:
characterised by muscualar rigidity, pyrexia, altered mental status, autonomic dysfunction-pallor, tachcardia, fluctuating BP, tremor, incontinence, excessive sweating/salivation.

Question 27

results of investigations for neuroleptic malignant syndrome?

Answer 27

• FBC-often leukocytosis
• U+Es-maybe AKI, acidosis
• ABG
• clotting studies
• urine-myoglobinuria, drugs
• low Ca2+
• LFTs-raised transaminases
• raised LDH
• CK-raised
• CXR, cultures if suspect sepsis
• CT/MRI
• LP-raised protein, may be indicated to rule out differentials e.g. meningitis-pyrexia, altered mental status

Question 28

management of neuroleptic malignant syndrome?

Answer 28

• A to E assessment, protect airway, may need ventilation and circulatory support
• IV fluids-rehydration
• reduce temperature-antipyretics, cooling devices
• reduce agitation-IV BZDs
• alkalinisation of urine and dialysis often needed if rhabdomyolysis and AKI

Question 29

causes of mortality in neuroleptic malignant syndrome?

Answer 29

• respiratory failure
• cardiac arrhythmias
• CVS collapse
• AKI
• DIC