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Allergy History
No known food or drug allergy
Family History
Vital signs:
Findings are confined to the left upper and lower limb which suggests
upper motor neuron lesion with hypertonia more on the left side,
reduced power and brisk reflexes.
Bradykinesia
Short shuffling gait
Stooped posture
Reduced arm swing
Difficulty to initiate gait
Turning “en bloc”
Case Summary
Mr R, a 70 year old gentleman with underlying
Hypertension, Dyslipidemia and Asymmetrical
Parkinson’s Disease presented with 2 days
history of weakness of left lower limb and left
facial asymmetry. Physical examination
showed findings suggestive of Upper Motor
Neuron Lesion involving left upper and lower
limb with involvement of Facial Nerve.
Investigation
• Full blood count
-anemia (compromise recovery especially in ischemic stroke)
-polycythemia
-thrombocytopenia (antiphospholipid syndrome)
• Random blood glucose (stroke can increase blood glucose)
• Renal profile
-common complication of stroke
-dehydration may lead to hyphotension and compromise the blood supply to
ischemic area
• Fasting serum lipid
• UFEME
• Ecg (atrial fibrillation)
• CT Brain (to exclude hemorrhage lesion)
• MRI brain (differentiate hemorrhage and ischemic lesion)
FBC
Flag Test Results Units Range
White Cell Count 8.9 x10^9/L 4.1 – 11.4
Red Cell Count 5.2 x10^12/L 4.5 – 6.0
Hemoglobin 15.2 g/dL 13.5 – 17.4
- Hematocrit 45.7 % 40.1 – 50.6
Mean Cell Volume 87.4 fl 80.6 – 95.5
MCH 29.1 pg 26.9 – 32.3
MCHC 33.3 g/dL 31.9 – 35.3
RDW 13.3 % 12.0 – 14.8
Platelet 259 x10^3/L 150 - 410
+ Neutrophils 6.7 x10^9/L 3.9 – 7.1
Eosinophils 0.1 x10^9/L 0.0 – 0.8
Basophils 0.0 x10^9/L 0.0 – 0.1
Lymphocytes 2.4 x10^9/L 1.8 – 4.8
Monocytes 0.8 x10^9/L 0.4 – 1.1
Nucleated Red Blood Cells 0 x10^9/L 1. – 0.1
Fasting blood sugar: 5.6mmol/L
HBA1c : 5.4%
Fasting serum lipid:
B. Intraarterial thrombolysis
– Major stroke of <6 hours duration
– Option for selected patient
– Due to occlusion of the middle cerebral artery, internal carotid and carotid terminus who are not
suitable for intravenous rt-pa.
Non-motor features
● Anosmia, sensory disturbance
● Mood disorders (depression)
● Orthostatic hypotension
● Cognitive impairment
Physical Examination
● Nervous System Examination
○ Cranial Nerves - hyposmia, myerson’s sign
■ impaired vertical eye movements → Progressive supranuclear palsy
■ Impaired horizontal eye movements → multiple system atrophy
○ Tone - cogwheel rigidity
○ Motor and Sensory
■ Bradykinesia
■ Tremor - worsens when distracted with mental tasks
○ Reflex
■ Asymmetry, up-going Babinski test → vascular parkinsonism
■ Up-going toe → multiple system atrophy
○ Coordination - finger-nose test, ataxia → multiple system atrophy
○ Gait and balance
■ Freezing of gait, shuffling gait, reduced arm swing, limitations in turning
■ Timed Up and Go test, Pull test
Physical Examination
● Mental State Examination or MMSE
○ cognitive impairment, dementia
○ depression
● Speech - hypophonia
● Function
○ Micrographia
○ Fine motor functioning - undo buttons
● Others
○ Blood pressure measurement (sitting and standing reading)
○ other cerebellar signs
INVESTIGATION
• No lab test; diagnosis is made by recognizing
physical signs and distinguish Idiopathic
Parkinson Disease from other Parkinsonian
disease.
• Dopamine transporter (DAT)
- PET or SPECT scan to assess the extent of
nigrostriatal dopaminergic cell loss.
• MRI
- Usually normal and not necessary in typical case.
Management
A) Pharmacological therapy
-Levodopa
-Dopamine agonist
-MAO-B Inhibitors
-COMT Inhibitors
-Anticholinergics
-Amantadine
B) Nonpharmacologic therapy
-Education
-Nutrition
-Exercise
-Support
C) Surgical therapy
-Deep brain stimulation
1) Levodopa
- a natural chemical that passes into brain and converted into dopamine
- combine with dopa-decarboxylase inhibitor- Benserazide or Carbidopa to prevent premature
conversion to dopamine outside your brain (reduce the side effects like nausea and hypotension)
Example: 50 mg of L-dopa (e.g. co-careldopa 62.5 mg) three times daily, increasing after 1 week to
100 mg three times daily is a typical starting dose
2) Dopamine Agonist
- mimic dopamine effects in brain
- used as mono therapy or in combination with levodopa in less than 65 years old
Example: Bromocriptine
- Non-ergot DAs (Example: Pramipexole and ropinirole or rotigotine via transdermal patch) are used
in preference to ergot-derived drugs, which may be associated with fibrotic reactions including
cardiac valvular fibrosis
5) Anticholinergics
-may help tremor and a little on akinesia but are now rarely used as can
may cause confusion
-side effects such as impaired memory, confusion, hallucinations, constipation, dry
mouth and impaired urination.
Example: trihexyphenidyl hydrochloride or benztropine
6) Amantadine
- to provide short-term relief of symptoms of mild, early-stage Parkinson's disease.
- also given with carbidopa-levodopa therapy during the later stages of Parkinson's
disease to control involuntary movements (dyskinesias) induced by carbidopa-levodopa.
- side effects may include a purple mottling of the skin, ankle swelling or
hallucinations.
Deep brain stimulation (DBS)
-Stereotactic insertion of electrodes into the brain (usually under age 70) with disabling
dyskinesias and motor fuctuations not adequately controlled with medical therapy.
-The electrodes are connected to a generator implanted in your chest near your collarbone
that sends electrical pulses to your brain and may reduce your Parkinson's disease
symptoms
Targets include:
b) Globus pallidus – improves dyskinesia but levodopa still required for motor symptoms