Movement Disorders ShortNote
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JMJ Movement Disorders JMJ IDIOPATHIC PARKINSON’S DISEASE (PD) SYMPTOMS AND SIGNS Prodromal premotor symptoms Motor symptoms Anosmia (90%)- olfactory bulb is one of the first structure to be affected Depression / anxiety (50%) Aches and pains REM sleep behavior disorder Autonomic features- urinary urgency, hypotension Constipation Restless leg syndrome Tremor Rigidity Akinasia Postural and gait disturbance RISK FACTORS Age – more than 70 years Gender – male Environmental factors – Rural living Drinking well water Pesticide exposure High oxidative stress Non-smoker Genetic factors- usually non-familial PATHOLOGY 1. Presence of neuronal inclusions (Lewy bodies) 2. Loss of dopaminergic neurons – pars compacta of substantia nigra in the midbrain The extent of nigrostriatal dopaminergic cell loss correlates with the degree of akinasia AKINASIA Cardinal clinical feature of PD Main cause of disability Difficulty initiating movement Upper limb usually affect first Almost always unilateral for the first years Rapid dexterous movements are impaired causing difficulty in writing (micrographia) Facial immobility- mask like semblance of depression Spontaneous blinking diminished – serpentine stare TREMOR Present in 70% of patients Almost always starts in fingers and hands Initially unilateral Spreading later to the legs on the same side Then the opposite arm Present at rest Reduces or stops completely when the hand is in motion “pill-rolling” Tremor made worse by emotion or stress
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Transcript of Movement Disorders ShortNote
JMJ Movement Disorders JMJ
IDIOPATHIC PARKINSON’S DISEASE (PD)
SYMPTOMS AND SIGNS Prodromal premotor symptoms
Motor symptoms
Anosmia (90%)- olfactory bulb is one of the first structure to be affected
Depression / anxiety (50%) Aches and pains REM sleep behavior disorder Autonomic features- urinary urgency,
hypotension Constipation Restless leg syndrome
Tremor Rigidity Akinasia Postural and gait disturbance
RISK FACTORS
Age – more than 70 years Gender – male Environmental factors –
Rural living Drinking well water Pesticide exposure High oxidative stress Non-smoker
Genetic factors- usually non-familial
PATHOLOGY
1. Presence of neuronal inclusions (Lewy bodies)
2. Loss of dopaminergic neurons – pars compacta of substantia nigra in the midbrain
The extent of nigrostriatal dopaminergic cell loss correlates with the degree of akinasia
AKINASIA
Cardinal clinical feature of PD Main cause of disability Difficulty initiating movement Upper limb usually affect first Almost always unilateral for the first
years Rapid dexterous movements are impaired
causing difficulty in writing (micrographia) Facial immobility- mask like semblance of
depression Spontaneous blinking diminished –
serpentine stare
TREMOR
Present in 70% of patients Almost always starts in fingers and hands Initially unilateral Spreading later to the legs on the same side Then the opposite arm Present at rest Reduces or stops completely when the hand
is in motion “pill-rolling” Tremor made worse by emotion or stress
JMJ Movement Disorders JMJ
RIGIDITY
Sign rather than a symptom Stiffness on passive limb movement, Present throughout the range of movement
- “lead-pipe” Is not dependent on speed of movement
When stiffness occurs with tremor-
ratchet-like jerkiness is felt – Cog-Wheel rigidity
POSURAL AND GAIT CHANGES
Stooping posture is characteristic Gait gradually becomes
o Shuffling o Small stride length o Slow turns o Freezing o Reduced arm swelling
Postural stability deteriorated – leading to fall
SPEECH AND SWALLOWING
Speech become quite, indistinct and flat Drooling – present Swallowing difficulty is late Can lead to aspiration pneumonia
COGNITIVE AND PSYCHIATRIC CHANGES
Cognitive impairment Dementia Visual hallucinations on treatment Psychosis – not uncommon Depression is common
DIAGNOSIS
No laboratory test Diagnosis is made by physical signs MRI – normal Dopamine transporter (DaT) imaging –
assess the extent of nigrostriatal cell loss
TREATMENT
Dopamine replacement with levodopa or a dopamine agonist – improves motor symptoms
Non motor symptoms – depression, constipation, pain and sleep disorders (Quality of life)
JMJ Movement Disorders JMJ
TREATMENT LEVODOPA DOPAMINE AGONIST
Most effective treatment Combine with a dopa decarboxylase inhibitor
Can combine with levodopa As initial monotherapy in younger patients with
mild to moderate impairment Less well tolerated Effective than levodopa
OTHER DRUGS USED IN PD
SELEGILINE
5-10 mg daily Mono amine oxidase B inhibitor Reduced catabolism of dopamine in
brain RASAGILINE
AMANTIDINE
Modest anti-parkinsonism drug Mainly used to improve dyskinesia
in advanced disease
ANTICHOLINERGICS
May help tremor Rarely used in PD except in
younger patients High doses cause confusion in
older patients
APOMORPHINE
Potent, short acting Administrated SC Used in advanced PD
MANAGEMENT OF PD
1. Dose fractionation of levodopa – a. increasing dose frequency
2. Addition of COMT inhibitor entacapone to prolong duration of action. 3. Slow release levodopa –
a. mostly used in overnight symptoms as absorption is erratic and difficult to predict, so limiting effectiveness in control of daytime symptoms
4. Avoiding protein-rich meals (which impair levodopa absorption) and taking doses at least 40 minutes prior to meals
5. Apomorphine continuous SC infusion 6. Deep brain stimulation and L-dopa intestinal gel
DEEP BRAIN STIMULATION (DBS)
Usually under 70 years Stereotactic insertion of electrodes
into brain Selected patients with dyskinesia and
motor fluctuations not adequately controlled with medical therapy
L-DOPA INTESTINAL GEL INFUSION
Infusion into small intestine via a jejunostomy To selected patients with severe motor
complications At present – used where apomorphine or DBS
contraindicated
JMJ Movement Disorders JMJ
TISSUE TRANSPLANTATION
Transplantation of embryonic mesencephalic dopaminergic cells directly into the putamen
PHYSIOTHERAPY, OT AND PHYSICAL AIDS
To reduced disability, speech and swallowing problems and falls
