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PARKINSONISM

History of Presenting Illness

History was obtained both from patient and the


caregiver (the wife) since patient had slurred
speech.
Mr R, a 70-year-old Malay, retired project
manager with underlying

1. Hypertension for 13 years


2. Dyslipidemia for 13 years
3. Asymmetrical Parkinsonism for 2 years
Mr R presented to the A&E department with
complaints of bilateral lower limb weakness
more on the left side and left sided facial
asymmetry with multiple history of falls at
home 1 day prior to admission.
Bilateral lower limb weakness
- More on left leg than right
- Noticed in the morning while buying breakfast at a stall
- Was still able to ambulate until he had worsening
weakness which resulted in multiple history of falls and
sustained bruises on right dorsum of hand, elbow and
lower back. There was trauma to his head once whereby
he fell backwards hitting his head but with no external
bleeding.
- There was also left facial asymmetry with slurring of
speech which occurred concurrently with the weakness.
- He also complained of dysphagia at home associated
with drooling of saliva.
- There was reduced oral intake due to dysphagia.
- Denied any loss of sensation over upper and
lower limb.
- No urinary or bowel incontinence
- No headache, blurring of vision, nausea and
vomiting prior to episode of weakness (TRO
hemiplegic migraine and space occupying lesion)
- There was no abnormal involuntary movements
or seizures.
- Patient denied having any hypoglycemic
symptoms such as sweating, dizziness and
presyncopal attack.
- He also denied having diarrhea or abdominal pain
and recent URTI symptoms such as cough and
sore throat, preceding the weakness to suggest
GBS.
- There was no shortness of breath, cough and
fever to suggest aspiration pneumonia.
- There was no chest pain, chest discomfort,
palpitation and sweating to suggest concurrent
acute coronary syndrome.
- He denied having any loss of weight or loss of
appetite.
He was only brought to the A&E in the next
morning by his wife because patient refused
to be admitted thinking that it was not serious
and only came the next day after consulting
the family friend.
Past medical history
1. Hypertension for 13 years
- Diagnosed at private clinic during routine medical
check up.
- Unsure of BP reading at diagnosis.
- Previously on T.Felodipine and now changed to
Perindopril 4 mg OD due to lower limb edema 2⁰ to
CCB.
- He is not on regular home BP monitoring but during
last follow up BP reading was 120/70 mmHg.
- He is compliant to his medications.
2. Dyslipidemia for 13 years
- Diagnosed at Private clinic with high
Triglyceride and LDL.
- Currently, on T. Lovastatin 40 mg ON.
- Compliant to medications.
3. Asymmetrical Parkinsonism
- Incidentally diagnosed 2 years ago after being seen in Klinik Primer during
follow up.
- Complained of numbness in toes, noticed to be slow in doing daily
activities such as bathing, buttoning his shirt.
- He also had stooped posture and noticed that he tend to lean towards
right side during Friday prayers.
- He also had a change in gait and found to have rigidity and tightness in
hamstring while walking, and has difficulty to initiate walking.
- He was then referred to Neurology PPUKM and diagnosed to have
Asymmetrical Parkinson’s Disease.
- He is on Levodopa 200 mg/Benserazide 50 mg BD (Madopar) and
Pramipexole dihydrochloride 0.375 mg ER 1 OD.
- He is also on monthly physiotherapy for the past 2 months and group
physiotherapy 3 monthly.
- Despite medications and physiotherapy, his symptoms are worsening over
the past 2 years. He also has on and off constipation for past 2 years but
not on any medications.
- He was ADL independent and able to drive and do his daily activities.
Past surgical History
Nil

Allergy History
No known food or drug allergy
Family History

- Strong family history of DM, Ischemic Heart disease and


Hypertension.
- Patient’s father passed away due to old age and mother passed away
due to complications of DM and HTN.
- Almost all siblings have IHD, DM and HTN. His eldest sister passed
away due to cervical cancer and his 2nd sister passed away due to
eclampsia during delivery.
Social History
• Retiree, previously worked as a Project Manager
(retired 15 years ago)
• Staying with wife, daughter and wife’s younger
sister.
• Has one daughter only
• Staying at a double-storey house in Taman
Melawati, Cheras.
• Financially stable
• Non smoker and does not consume alcohol.
Physical Examination
Patient was alert, conscious, GCS: 15/15, lying on a 45⁰
bed, with a nasogastric tube inserted and a IV cannula
inserted on the right dorsum of hand. He was not on
respiratory distress.

Vital signs:

BP: 201/104 mmHg


PR: 74 bpm, good pulse volume and regular rhythm
Temperature: 37⁰C
RR: 16 breaths/min
On peripheral examination, no clubbing, no
stigmata of IE, no peripheral cyanosis and CR
was less than 2 seconds. There were bruises
on the right dorsum of hand and elbow.
Patient was not pale and was not jaundiced.
Oral hygiene was good and hydration status
was fair. There was obvious left facial
asymmetry seen.
Heart: JVP not raised, no carotid bruit. No thrills
and parasternal heaves. Apex beat was at 5th
left intercostal space at midclavicular line,
S1S2 heard with no murmurs, no pedal
edema.
Lungs: Clear with no added sounds.
Abdomen: Soft, non tender
Upper Limb Lower Limb
Right Left Right Left
Tone Cog wheel Cog wheel Hypertonia Hypertonia
rigidity rigidity (> (> on left)
on left)
Nervous system:
Power Shoulder, elbow, wrist: Hip, Knee, Ankle:

5/5 4/5 5/5 4/5


Reflex 2+ Brisk 2+ Brisk
Babinski Downgoing Downgoing
Clonus Absent Absent
Sensation Intact Intact

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.

Gait: Not able to assess because patient was still weak.

Patient had reduced blinking of eyes. Otherwise, patient had no resting


tremors and glabellar tap was negative. Patient had no dysadiodyskinesia
Cranial Nerve Examination
• Partial ptosis of right eye, otherwise pupils
measured 3 cm bilaterally, and were reactive to
light.
• There was no nystagmus or diplopia.
• Other findings are confined to left facial nerve:
– Left facial asymmetry
– Loss of left nasolabial fold, no loss of wrinkles on
forehead bilaterally.
– Orbicularis oculi, frontalis, buccinator and oricularis
oris muscles are affected on the left side.
Others:
If patient was able to walk, expect to see:

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:

Results Reference values


Triglyceride 0.87 <1.7mmol/L
Total cholesterol 6.88 <5.18mmol/L
HDL 2.56 >1.2mmol/L
LDL 3.92 <3.8mmol/L
UFEME
Flag Test Result Range
Urine glucose Negative
Urine protein Negative
SG 1.005 1.015 – 1.025
UpH 7 4.8 – 7.4
Leucocyte Negative
Nitrite Negative
Ketones 1.5 mmol/L
Urobilinogen Negative
Bilirubin Negative
Blood 25 ul
ECG
ECG
• Rate 75 bpm
• Regular rhythm
• Narrow QRS complex
• Sinus rhythm
CT Brain
CT Brain
Findings:
No intracranial bleed
There is an ill-defined hypodensity noted at the right corona radiate extending to
the right external capsule in keeping with recent infarct.
Well defined old lacunar infarct noted at the anterior limb of the left internal
capsule.
No midline shift
Ventricles and CSF spaces are prominent in keeping with age related cerebral
atrophy.
Basal cisterns are not effaced.
Mucosal thickening within the bilateral ethmoid, maxillary and sphenoid sinuses.
The rest of the visualized paranasal sinuses and mastoid air cells are clear.
No skull abnormality.
Management of stroke
Aim of management
1. ABC of emergency (resuscitation)
2. To prevent complication of stroke
3. Reperfusion
4. Rehabilitation
5. To prevent resubsequent stroke.
1. Resuscitation 2. To prevent complication of stroke

• Ensure adequate oxygen • Ryles tube insertion


supply (patient has dysphagia and
• Monitoring of vital signs (BP, to prevent aspiration)
HR, spO2, Temperature • T. Aspirin 300mg stat ->
• Blood glucose 150 mg OD
• Intravenous fluid • T. Amlodipine 5mg stat ->
• Input/output chart 0D
3. Reperfusion therapy
A. Intravenous thrombolysis with rt-pa (alteplase)
– Within 48 hours of onset of ischemic stroke
– Intravenous rt-pa (0.9mg/kg, maximum 90mg) with 10% of the dose given as a bolus followed by a
60 minute infusion, is recommended within 4.5 hours of onset of ischemic stroke.

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.

C. Endovascular mechanical thrombectomy


– <8 hours duration in slected patient with major stroke syndrome
– Ineligible for or failing intravenous thrombolysis.
4. Rehabilitation
• To refer physiotherapy, speech therapy, occupational
therapy
• Refer dietitian
• Turn patient every 2 hours (mobilization)

5. Prevent resubsequent stroke


• Pharmacological (antiplatelet, anticoagulant,
antihypertensive, statin)
• Lifestyle modification
Management of the patient in the
1. T. Plavix 75 mg OD (clopidogrel)ward
2. Cardiprin 100mg OD
3. Increase Medopar to 125mg TDS
4. Ryle’s tube feeding
5. Intravenous fluid 30ml of normal saline for 24 hours
6. Strict I/O chart
7. Dextrostix monitoring QID
8. Monitoring vital signs. If temperature spikes, to start antibiotic and septic
workup.
9. For echocardiogram and carotid doppler as outpatient
10. Continue old medication
11. Refer physiotherapy, dietitian and neurology
PARKINSON’S DISEASE
PARKINSONISM
● Parkinson’s Disease
● Atypical Parkinsonism
○ Multiple-system Atrophy (MSA) - cerebellar /
parkinson type
○ Progressive supranuclear palsy
Corticobasal ganglionic degeneration
○ Frontotemporal dementia

Harrison’s Principle of International Medicine 19th Edition (2015); vol.2 p2609-2613


● Secondary Parkinsonism
○ Drug-induced - antipsychotics (fluphenazine,
haloperidol, clozapine, quetiapine)
○ Toxin-induced - carbon monoxide, cyanide, carbon
disulphide
○ Infection - viral encephalitis, creutzfeldt-jakob
disease
○ Tumour
○ Liver failure
● Other Neurodegenerative Disorders
○ Wilson’s disease
○ Huntington’s disease
○ Alzheimer’s disease with parkinsonism
PARKINSON’S DISEASE
● First described in 1817 by James Parkinson
● Affects 1-2 per 1000 of the population (less
common in Asian)
● Mean age of onset is 60 years - prevalence
increases with age
● Degeneration of dopaminergic neurons in
substantia nigra

Harrison’s Principle of International Medicine 19th Edition (2015); vol.2 p2609-2613


Epidemiology of Parkinson's Disease, Journal of Neural Transmission, Volume 124, Issue 8, Pages 901-905
doi: 10.1007/s00702-017-1686-y
Cardinal features:
1. Resting tremor
2. Rigidity
3. Bradykinesia
4. Gait impairment / Postural instability
Pathophysiology of Parkinson’s
Disease
Normal
Parkinson’s
Disease
Clinical Signs of
Parkinson’s
Disease
Motor features
● Micrographia
● Hypomimia (poker face)
● Hypophonia
● Reduced eye blinking
● Dysphagia

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

3) Monoamine oxidase B inhibitors


- inhibits the catabolism of dopamine in the brain by inhibiting the brain enzyme monoamine
oxidase B (MAO-B) which metabolizes brain dopamine.
- side effects may include nausea or insomnia.
Example: Selegiline 5–10 mg once daily or Rasagiline
4) Catechol-O-methyltransferase (COMT) inhibitors
-mildly prolongs the effect of levodopa therapy by blocking an enzyme that breaks
down dopamine.
-side effects increased risk of involuntary movements (dyskinesias) and diarrhoea
Example: Entacapone
- Tolcapone (Tasmar) is rarely prescribed due to a risk of serious liver damage and liver
failure.

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:

a) Subthalamic nucleus – response similar to levodopa with reduction in dyskinesia

b) Globus pallidus – improves dyskinesia but levodopa still required for motor symptoms

c) Thalamus – for tremor only.


COMPLICATION
• Increase risk of fall due to instability
• Cognitive problem involving thinking and memory
- Dementia, confusion
• Anxiety, depression
• Wearing off
- During wearing off, symptoms of Pakinson return
or worsen before the next dose of levadopa is due.

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