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Brief Introduction of Hypokinetic
Movement Disorders
Dr Ahmad Shahir Mawardi
Neurologist,
Neurology Department
Hospital Kuala Lumpur
26th April 2021
Movement disorder
• abnormal in initiation, implementation,
velocity, frequency or posture.
Broadly . . .
Hyperkinetic Movements
Hypokinetic Movements
• Tremor
• Tics/Tourette syndrome
• Dystonia
• Hemifacial spasm
• Ataxia
• Chorea/Balism/Athetosis
• Myoclonus
• Others
 Myokymia
 Myorhythmia
 Restless Legs
 Hyperekplekia
 Akathisia
• Parkinsonism
 Catatonia
 Psychomotor depression
 freezing Phenomenon
 Hypothyroid slowness
 Stiff muscle
Hyperkinetic
Movements
Hypokinetic
Movements
Parkinson's Disease
Davis Phinney Michael J. Fox
Muhammad Ali
Famous persons living with Parkinson's
disease
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
Drug induced Parkinsonism
• 7% of people with parkinsonism
• dopamine antagonist
• reversible
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
Prevalence of Parkinson’s disease in the Western Pacific
Region (per 100 000 population)
SY Lim et al, Parkinson’s disease in the Western Pacific Region: www.thelancet.com/neurology Published online June 4, 2019
History
• James Parkinson (11 April
1755 – 21 December 1824)
was an English surgeon,
apothecary, geologist,
palaeontologist, and political
activist.
• An Essay on the Shaking
Palsy (1817) describe
"paralysis agitans", a condition
that would later be renamed
Parkinson's disease by Jean-
Martin Charcot.
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
• Loss of
dopaminnergic
neuron in substantia
niagra
The main pathologies in
patients with clinical
Parkinson’s
disease and the
pathological progression
• Both genetic factors as well as probable
environmental factors contribute to the
risk of developing PD
• However, only 5-10% of patients have Fhx
which is why PD is usually regarded as a
sporadic condition.
What cause Parkinson's Disease?
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
Clinical presentations
• neurodegenerative disease characterized by
slowly progressive symptoms of resting tremor,
rigidity, akinesia/bradykinesia, and postural
instability.
• the second most common neurodegenerative
disease after Alzheimer disease.
• motor and non-motor symptoms
Definition
Hypokinesia: decreased amplitude of
movement
Bradykinesia: slowness of movement
Akinesia: loss of movement
* Unrelated to weakness or spasticity
Natural history of Parkinson's Disease
The Lancet
Natural History of Parkinsons
Disease
Ist
Symptoms
Loss of
Nigro-
Striatal
cells
Anosmia
3to 5 yrs
Diagnosis
ONSET
Treatment
HONEYMOON
PERIOD
4 to 6 years
MOTOR
COMPLICATIONS
Surgery
2 yrs 5
years
Cognitive
Decline
Death
1 year
6 to 7 years
Presymptomatic
stage
Postural
instability
Non Motor
complications
Gait (motor)
Face (motor)
Limbs (motor)
Suggestive Features of Idiopthic PD
• Unilateral onset
• Rest tremor present
• Progressive disorder
• Persistent asymmetry affecting the side of onset
most
• Excellent (70–100%) response to levodopa
• Severe levodopa-induced chorea
• Levodopa response for ≥ 5 years
• Clinical course of ≥ 10 years
How to make diagnosis?
• The diagnosis of PD remains clinical to this day.
• no biological marker that confirms the diagnosis
of PD.
• There are other disorders that can mimic PD and
investigations may be needed in some patients.
hallucinations are common in PD – particularly visual. sometimes this arise as an
illusory misperception from an object – a coat becomes a person – but can also
be complex, detailed and distressing.
Staging and severity
• The severity of PD is based mainly on the
clinical features.
• Hoehn and Yahr staging
• Unified Parkinson’s Disease Rating Scale
(UPDRS)
I. Mentation, Behavior and Mood
II. Activities of Daily Living
III. Motor Examination (14 components)
IV. Complications of Therapy
III. Motor Examination
III. Motor Examination
III. Motor Examination
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
Dopamine Transporter Scan ( DAT Scan)
Hot cross bun sign in MSA
Personal KinetiGraph
(PKG)
PKG
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
Treatment
• Currently no cure (or prevention)
• Motor symptoms (+ some NMS) can often be well
controlled in the earlier stages of the disease.
• Can be divided into:
– Pharmacological (oral,non-oral)
– Non-pharmacological
Pharmacological therapy
• Levodopa remains the most effective
medication.
– disadvantage: motor fluctuations, especially
dyskinesias.
www.thelancet.com/neurology Vol 14 June 2015
Sites of Action of
Anti-PD Drugs
62
2. (Other) Drugs available
Dispersible Madopar
• Properties and AE: same as Madopar
• Pharmacokinetic : time to peak concentrations
tends to be shorter, less interindividual variability
in absorption parameters
• Administration: to be dispersed in 25-50 ml of
water. The tablets disintegrate completely,
producing a milky-white dispersion
Rasagiline
Safinamide
Tolpicapone
Epicapone
Non-oral therapy
1. deep brain stimulation (DBS)
2. apomorphine infusion
3. jejunal L-dopa infusion
Advanced therapy
costs
1. Deep Brain Stimulation (DBS)
RM 120-130K (10 -15 years)
2. Apomorphine infusion (KPK)
RM70-100K per year + consumables.
However company has issues to
register the consumable items.
3. Jejunal L-dopa
infusion
£16K / RM 88K
Deep Brain Stimulation
• Main indication : Parkinson's Disease
• Mainly to control : Motor symptoms
(bradykinesia,rigidity, tremor) also reported
to improve some non-motor symptoms
Criteria for DBS based on Movement
Disorders Society (MDS)
• PD
• motor complications: –fluctuations–severe
dyskinesias
• tremor
• refractory to optimal medical treatment
• important enough (severity/duration) to
justify surgical risk
• Intolerance to dopaminergic drugs
DBS for PD
Inclusion Criteria
1. Diagnosis by UKPDSBB criteria
2. Good Levodopa response (improvement >30% of motor
component in UPDRS)
3. Disabling symptoms
4. Normal cognition
5. Realistic expectation and good family support
6. Access & commitment to programming stimulation
*age < 70 yrs
DBS for PD
Exclusion Criteria:
1. Minimal / Absent response to Levodopa
2. Atypical Parkinsonism / Secondary Parkinsonism
3. Poor functional state while “ON”
4. Significant cognitive dysfunction
5. Untreated depression / psychiatric disease
Other assessment
 MMSE/MOCA
 UPDRS
 DRS-2 (Dyskinesia Rating scale)
 GCSI (Gastroparesis Cardinal Symptom Index )
 QUIP ( Parkinson's Disease Impulsive-Compulsive Disorders
Questionnaire )
 MADRS (Montgomery and Asberg Depression Rating Scale )
 Euro QoL (Euro Quality of Life)
 DQ-39
BS Stimulation of the Subthalamic Nucleus (STN).
•In 2 large randomized 6-mth trials versus best medical treatment,
 UPDRS motor scores improved by 54% for STN and 28% for STN or
pallidal stimulation.
• A meta-analysis showed:
 an average improvement of 53% .
 Levodopa-equivalent dosage could be reduced by 50–60%.
 UPDRS motor scores were still improved after 5 years, although
deteriorated compared with 1 year after surgery (Class III ).
 Dyskinesias were reduced by 54%.
 OFF time improved from 6.2 to 2h or 5.7 to 3.4h versus no
change in the medical group
The German Parkinson Study Group, Neurostimulation Section. N Engl J Med 2006;
Weaver et al, JAMA 2009; 301: 63–73.
Complications
Bilateral DBS STN versus Gpi in
advanced PD
Dutch NSTAPS study :
No significant difference in primary outcome
between STN vs Gpi.
Bilateral STN DBS and Gpi DBS are both
efficacious
(Lancet Neurology 2013)
Paul Krack, Deep Brain Stimulation in Movement Disorders: From Experimental
Surgery to Evidence-Based Therapy, Movement Disorders, 2019
Outline
1.Epidemiology
2.Aetiology
3.Clinical presentations
4.Investigations
5.Treatments available
6.Prognosis
World Health Organization Estimated
Deaths 2012
Treatment of Advanced Parkinson Disease and Related Disorders
Janis M. Miyasaki, MD, MEd, FRCPC, FAAN, Continuum (Minneap Minn)
2016;22(4):1104–1116.
Thank you

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