Parkinson’s Disease

On my first firm this year, there was an elderly lady on the ward with Parkinson’s Disease. One of the F1s asked me to put in a cannula but there was no way I was going to attempt to put in my first ever cannula on a lady with such a large resting tremor in both arms. No way. So, I got Josh, my firm partner, to do it. He didn’t manage it, but he gave it a fair shot.

I can’t actually remember what she was in hospital for; it was unrelated to her Parkinson’s but what I do remember, and what also contributed to my not wanting to put a cannula in, was her overbearing relatives.

These kind of relatives are a doctor’s nightmare, especially for the F1s that interact with the patients daily. These relatives are concerned, pushy, want to be informed about everything, ask lots of questions and sometimes question decisions. I mean, there was no way I was going to put a cannula with both her daughters breathing down my neck. And then, when the F1 asked the patient about her tremor, just to make conversation and assess her level of consciousness, from behind the curtain, a daughter barges in, absolutely horrified, “she has Parkinson’s doctor!”, sounding appalled at the fact that he did not already know her medical background (he did).

But you know what, despite the nightmare these relatives present to the staff caring for patients- and sometimes you do need to politely tell relatives to step outside- their loved ones are in hospital, and they are worried and anxious, and they just want them to be well and get the best possible care. And that’s exactly the sort of daughter I would want to be looking out for me when my time comes, and the kind of daughter I hope that I will be to my parents (but maybe tone it done a notch).

Well that turned emotional really fast….

 Parkinson’s Disease

Definition: Parkinsonism; a cardinal triad of tremor, rigidity and bradykinesia; without a known cause is referred to as Idiopathic Parkinson’s Disease, or simply, Parkinson’s Disease (PD)- a neurodegenerative disease.

Aetiology/ risk factors:

Image result for parkinson's disease pathology-Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurones in the substantia nigra pars compacta of the midbrain, which project to the striatum (caudate nucleus and putamen).

-Surviving neurones often contain eosinophilic cytoplasmic inclusions (Lewy bodies). Patients only symptomatic after > 70% neuronal loss.

-The cause is usually idiopathic (not known) in Parkinson’s Disease, but there are other causes of Parkinsonism.

Causes of Parkinsonism: drugs- neuroleptics (e.g. for schizophrenia), metoclopramide (anti-emetic), prochlorperazine (anti-psychotic, anti-emetic)

Rarely- trauma/ boxing (e.g. Muhammad Ali), post-encephalopathy, manganese or copper toxicity (Wilson’s disease), HIV, vascular insults (e.g. basal ganglia or midbrain strokes)

There are familial forms of Parkinson’s Disease.

Epidemiology:  Prevalence: 0.6% at 60-64 years, 3.5% at 85-89 years (Europe)

-Typical age of onset = 65 years

Symptoms: insidious onset

-tremor at rest, usually noticed in hands

-stiffness and slowness of movements

-difficulty initiating movements e.g. getting out of chair

-frequent falls

-smaller hand writing (micrographia)

Image result for parkinson's micrographia

Non-motor symptoms:

reduced sense of smell


-frequency/ urgency

-dribbling of saliva


-visual hallucinations, dementia (later on in disease)

-poor sleep (REM sleep disorders), insomnia

-mental slowness


Cardinal triad

-tremor- worse at rest, often ‘pill-rolling’ of thumb over fingers (4-6 cycles/sec), one side usually worse. Decreased on action or flexed posture.

-rigidity/increased tone- lead pipe rigidity of muscle tone with superimposed  tremor gives ‘cogwheel rigidity’ (jerky resistance to passive movement).

-bradykinesia/hypokinesia- slow initiating movement, and slow, low amplitude excursions in repetitive actions e.g. if you ask them to make a ‘chatter box’ hand sign, they will move their hand very slowly and they will not move their thumb apart from the rest of their fingers very far.

Image result for parkinson's patient bradykinesia hand

-reduced blink rate (so, no stare-offs)

-monotonous, soft, hypophonic speech; expressionless face- hypomimesis (and no poker)

-frontalis overactivation (furrowing of the brow)

Gait: reduced arm swing, festinating gait with small shuffling steps and stooped posture, freezing at obstacles and doors

Image result for parkinson gait
Here’s a good clip of the gait

-postural instability- falls easily with little pressure from the front or back


-poor executive functioning

-impaired olfaction on formal testing

Parkinson’s-plus syndromes:

Progressive supranuclear palsy/ Steele-Richardson-Olszewski syndrome = early postural instability + vertical gaze palsy +/- falls, rigidity of trunk > in limbs, speech and swallowing problems, little tremor

Multiple system atrophy = early autonomic features e.g. impotence/ incontinence, postural hypotension; cerebellar + pyramidal signs (e.g. reduced power, hyper-reflexia, Babinski’s sign); rigidity > tremor

Lewy body dementia = fluctuating cognition with visual hallucinations and early dementia

Cortico-basal degeneration = akinetic rigidity involving one limb, cortical sensory loss (e.g. Astereognosis-inability to identify an object by touch), apraxia, ‘alien hand syndrome’

Vascular parkinsonism = pyramidal signs (legs) e.g. in diabetic/ hypertensive patient who falls or has gait problems e.g. ataxia


-Diagnosis is clinical.

Levodopa trial

Blood- serum caeruloplasmin to exclude Wilson’s

CT/MRI brain- to exclude other causes of gait decline e.g. hydrocephalus, vascular disease

-Dopamine transporter scintigraphy (DAT-scan): reduction in striatum and putamen. May be necessary for distinguishing from essential tremor.

Image result for DAT scan


Multi-disciplinary team approach: GP, neurologist, PD nurse, social worker, carers, physiotherapist, occupational therapist

-Respite care in advanced disease (break for carers)

-Assess disability and cognition objectively and regularly e.g. by Unified PD Rating Scale (UPDRS)

Postural exercises can help


Levodopa + dopa-decarboxylase inhibitor =

-Madopar (co-beneldopa = benserazide + levodopa)

-or Sinemet (co-careldopa = carbidopa+ levodopa)

S/E of levodopa = short-term: nausea, vomiting; long term: dyskinesias, painful dystonias, response fluctuations e.g. unpredictable ‘off’ freezing and pronounced end-of-dose reduced response, psychosis, visual hallucinations

(dopamine induced dyskinesias develop over 5-10 years)

Dopamine agonistsRopinirole, pramipexole

   –Rotigotine (transdermal patches)

   –Amantadine- for drug induced dyskinesias in late PDS

S/E = drowsiness, nausea, hallucinations, compulsive behaviour

  -Older ergot-derived DA agonists- bromocriptine, cabergoline, pergolide- are not favoured as they can cause heart valvulopathy and serosal fibrosis

Apomorphine- potent DA agonist used with continuous SC infusion to even out end-of-dose effects, or as a rescue pen for sudden ‘off’ freezing. (S/E = injection site ulcers)

bromocriptine, cabergoline- allow L-DOPA to be started later or at lower dose

MOA-B inhibitorsSelegiline, Rasagiline

Alternative to DA agonists in early PD. Both allow levodopa to be started later, or at a lower dose.

S/E = postural hypotension, atrial fibrillation

COMT Inhibitorsentacapone, tolcapone

May lessen the ‘off’ time in those with end-of-dose wearing off.

S/E = tolcapone may cause severe hepatic complications (monitor LFTs)

Anticholinergics- benzhexol, orphenadrine

Help tremor, but cause confusion in elderly.

S/E = dry mouth, dizziness, reduce vision, urinary retention, increased pulse, anxiety, confusion, excitement, hallucinations, insomnia, memory impairment

Depression: try SSRIs or psychological therapy

Psychosis: distinguish drug-induced psychosis from disease progression. Consider reducing dopamine agonist doses (drug induced) or try atypical anti-psychotics e.g. quetiapine, olanzapine (progression).

Deep brain stimulation may help those who are partly dopamine responsive

Surgical ablation of overactive basal ganglia circuits


-Parkinson’s dementia

-Psychosis, depression (disease progression or drug side effects)

-Autonomic dysfunction

-Death (usually from pneumonia or PE)

-Side effects of treatment

Prognosis: incurable and progressive, but amenable to palliation. Rate of progression variable. Optimal treatment can delay impact of disability by 5-10 years.

References: Rapid Medicine, Cheese & Onion

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