• Mask like facies, monotonous speech, dyskinesias
• Upper limbs
• Resting tremors which disappears with use
• Bradykinesia (thumb to finger, rotate wrist and “twinkle stars”
• Leadpipe rigidity and cogwheeling
• Acute dystonia or alien limb syndrome
• Pronator drift and cerebellar signs
• Palmomental reflex, grasp reflex
• Eye movements, vertical Doll’s if vertical gaze impaired
• Close eyes for blepharospasm
• Feel for seborrhea
• Look for KF rings
• Count 1-20
• Unbutton shirt, write, cap a pen, comb his hair
• Gait – typical parkinsonian gait; also rule out gait apraxia
• Speech if not done
• Postural BP
Sir, this elderly gentleman has Parkinsonism with mask like, expressionless facies. He
has asymmetrical resting tremor of the right hand with characteristic pill rolling
movements of the thumb that disappears with use of the hand. There is also presence of
bradykinesia with leadpipe rigidity at the elbows and cogwheeling at the wrist.
Movement of the contralateral upper limb accentuates these features.
There is presence of seborrhea and Myerson’s sign or the glabella tap sign is positive.
He has difficulty initiating his gait and has a stooped posture associated with shuffling
gait with festination and lack of normal arm swing. He also turns in numbers. His gait is
not apraxic and he is not on any urinary catheter to suggest NPH.
Functionally he is able to walk unaided and can perform keyturning movements and
unbutton his short unaided.
There is no evidence of dyskinesias which can result as a result of L-dopa therapy.
He dose not have features suggesting presence of Parkinson-plus syndrome. There is no
evidence of Progressive Supranuclear Palsy such as impairment of the vertical gaze,
blepharospasm or frontal lobe signs such as palmomental reflex and the grasp reflex.
There are also no cerebellar signs to suggest multisystem atrophy. There is also no
evidence of corticobasal ganglia degeneration such as dystonic arm or alien limb
In summary, this patient has Parkinsonism most likely due to Parkinson’s disease and
relative preservation of his function; there is no evidence of dyskinesia currently to
suggest side effects of L-dopa therapy.
What is Parkinson’s disease?
It is a progressive neurodegenerative disorder associated with degeneration of the
dopaminergic nigrostriatal neurons.
Dx clinically with 2 out of 3 signs comprising of resting tremors (3-5Hz),
bradykinesia and rigidity. The 4th
sign of postural instability occurs later in the course of
What are the causes of Parkinsonism?
1. Parkinson’s disease
2. Parkinson-plus syndromes
3. Drugs (Neuroleptics, antiemetics, MPTP- 1 methyl 4 phenyl 1,2,3,6
4. Anoxic brain damage ( Post cardiac arrest, Manganese, CO)
5. Post encephalitis ( encephalitis lethargica or von Economo’s disease)
6. Tumor such as giant frontal meningioma
What are the pathologic findings in Parkinson’s disease?
• Loss of pigmented dopaminergic neurons in the substantia nigra
• Presence of Lewy Bodies (eosinophilic cytoplasmic inclusions)
What are the Parkinson-plus syndromes?
• Progressive supranuclear palsy (most common) (frontal lobe) (3)
• Vertical gaze palsy
• Downgaze affected first, then upgaze, then horizontal
• Can be overcome by vertical Doll’s
• Other features such as blepharospam and slow pursuit or saccadic eye
• Postural instability and axial rigidity with falls early in the course of the disease
• Frontal lobe signs
• Multiple sytem atrophy (Cerebellar)
• MSA-P = Parkinsonism features
• MSA-C = Cerebellar features
• Features (3)
• Cerebellar signs
• Autonomic features – orthostatic hypotension, urinary dysfn and erectile dysfn
• Corticospinal signs – hyperreflexia and extensor plantar response
• Corticobasalganglionic degeneration (frontoparietal lobe)
• 2 features
• Limb apraxia or alien limb syndrome
• Parkinsonism-dementia-ALS complex
• Diffuse Lewy Body disease (Parkinsonism, dementia and neuropsychiatry)
What is the significance of diagnosing Parkinson Plus syndrome?
• Poorer prognosis
• Poor response to L-dopa therapy
What are the features that suggest that patient may have Parkinson plus syndromes?
• Early onset of dementia
• Presence of hallucination or psychosis
• Early onset of postural instability
• Truncal symptoms more prominent than appendicular symptoms
• Marked symmetry of signs early in the stage of the disease
• Lack of response to levo-dopa therapy in the early stage of the disease
• Presence of symptoms and signs suggestive of Parkinson-plus syndromes.
What are the stages of Parkinson’s disease?
Staged via the Hohen and Yahr staging system comprising of 5 stages:
• Stage 1 – symptoms and signs unilateral and mild
• Stage 2 – Bilateral and minimal disability
• Stage 3 – Generalised dysfunction with sig bradykinesia and gait impairment
• Stage 4 – Rigid and bradykinesia, severe symptoms with limited walking
• Stage 5 – Completely invalid and requires nursing care
How would you investigate?
• Brain scan to rule out
• Multi-infarct syndromes
• Frontal meningiomas
• Parkinson-plus syndrome
• MSA – atrophy of the cerebellum, brainstem
• PSP – Atrophy and hyperintensity of the midbrain and red nucleus
• CBGD – Frontoparietal cortical atrophy
• If patient is young, ie<50, rule Wilson’s disease
• Slit-lamp examination
• Serum ceruloplasmin and 24Hr Urinary Copper
How would you manage?
• Multidisciplinary approach
• Education and counselling, PT/OT/ST
• Dopamine agonist, eg pramipexole or ropinirole
• Early in the course of the disease or younger patients
• Delay onset of motor fluctuations and dyskinesias
• Nausea, orthostatic hypotension, hallucinations or somnolence, edema
• L-dopa therapy (usually combined with a peripheral decarboxylase inhibitor)
• Should be used if there is disability
• Never used in patients with melanoma
• Peak dose dyskinesia and end of dose rigidity
• Nausea, orthostatic hypotension, hallucinations
• Tremors – anticholinergic (dry eyes and mouth, urinary retention, arrhythmia), e.g.
arcane or benztropine.
• Rigidity – beside Dopa and D agonist, can use MAO-B inhibitors or amantadine
(cognitive side effects)
• COMT inhibitors (diarrhea and hepatotoxicity)
• Lesion surgery – thalomotomy (tremors) and pallidotomy (for all features)
• Deep brain stimulation (for all features especially tremors)
How would you manage dyskinesia?
• Peak dose dyskinesia
• Reduce the dose and increased frequency
• Add on COMT inhibitors i.e. entacapone which increases half life of L-dopa
• Initiating with dopamine agonist and adding on L-dopa therapy resulted in less
• End of dose
• Increase dose, frequency
• Switch to CR formulations
• Add DA, MAO-B inhibitors, COMT inhibitors
What is the prognosis?
• Some will have mild while other will have severe symptoms
• Some will be troubled mainly with tremors, other by rigidity and bradykinesia
What is the abbreviated mental test?
• Use as a screening for possible dementia in the elderly
• A score of less than 6 warrants further assessment
• Remember this address – 42 West Street
• Time (nearest hour)
• Recognition of 2 persons
• Prime Minister of UK
• First Year of WW1 (1914-1918)
• Count backwards 20 to 1