Parkinson's Flashcards
Causes of Parkinson’s
2 Types
Parkinson’s Disease is Primary atrophy of substantial nigra
Parkinsonism - secondary due to drugs, toxins, other disease
Environmental
Pesticides
Define parkinson’s
Complex disorder involving motor impairment and deficits in behaviour, cognition and daily function
Age of onset and incidences of Parkinson’s
Adults 45-60 yr
> Males
early onset 60 yr old. increases with age.
Pathogenesis of Parkinson’s
Depletion of dopaminergic neurone in sustantia nigra and presence of alpha synuclein and other protein inclusions in nigral cells. It is thought that environmental or genetic factors alter the α-synuclein protein, rendering it toxic and leading to Lewy body formation within the nigral cells. Lewy bodies are also found in the basal ganglia, brain- stem and cortex, and increase with disease progression. PD is recognised as a synucleinopathy alongside multiple system atrophy and dementia with Lewy bodies. The loss of dopaminergic neurotransmission is responsible for many of the clinical features.
Examination findings of parkinson’s
Classic features - Tremor, rigidity and bradykinesia.
GI - diminished facial expression, stooped posture, fine falling resting tremors, speech monotonous, soft, faint, repetition of end of world.
Gait - Festinating gait, slow to rise from chair, stuffing, slow to initiate and difficulty stopping, lack of normal arm swing.
Vital - may have orthostatic hypotension.
Hand - examine Tremor – asymmetrical resting tremor (may reduce with finger nose testing [faster tremor may develop])
Tapping – tap fingers in turn on table with both hands at once
Twidling – rotate hands around one another in front of the body
Both will be slow and clumsy
Cogweel rigidity at wrists and elbows
Face
Tibulation (tremor) of head, sweating of brow
Lack facial expression, reduced blinking, dribbling saliva.
Glabellar tap – tap mid forehead – patient continues to blink
EOM movement – weakness upward gaze
Writing
Micrographia
Sometimes Dementia - if arises within
Describe the progression of Parkinson’s
Premotor
Motor
Non Motor
Diagnostic criteria of parkinson’s
Inclusion criteria Bradykinesia - everything speech, gait. And at least one of the followings Muscular rigidity 4-6 Hz rest tremor Postural instability not caused by visual/cerebellar dysfunction Supportive criteria 3 or more required for definite diagnosis unilateral onset rest tremor Progressive disorder 70-100% response to levodopa severe levodopa induced dyskinesias Levodopa response ≧5 years Disease course ≧ 10 years
Ix of parkinson’s
CT scan/MRI to rule out structural lesions
Single photon emission CT (SPECT scans) - Nirgrostriatal degeneration
Salivary gland biopsy may Dx PD.
Exclusion criteria for parkinson’s disease
History of repeated strokes, repeated head injury, or definite encephalitis –Babinski sign
Neuroleptic treatment at onset of symptoms –Drug induced Parkinson’s disease
Poor response to laevodopa –Supranuclear gaze palsy or Multi system atrophy
Essential tremors
Early, severe dementia
Cerebral tumor or hydrocephalus on computed tomography (CT) –CT/MRI to rule out structural lesions
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure
Treatment for Parkinson’s
Education and explanation Drugs aim is to correct dopamine deficiency and/or block cholinergic excess in brain- 1st line L-Dope/Carbidopa/benzariside Non pharmacological treatment MDT in PD Refer to Neurologiest Geriatric specialist OT - wheelie walkers, walking sticks Physiology Parkinson Nurse - Education and support Parkinsons Queensland Inc
Characteristics of L Dopa
Counters Bradykinesia Start low and inc slowly Titrate to efficacy ≈200-600mg Give with Carbidopa Immediate release More rapid onset = Shorter duration of benefit Controlled release= Longer duration of benefit SEs- nausea,dizziness,somnolence
Characteristics of a Dopa agonist
Effective monotherapy or adjunctive Less symptomatic benefit than levodopa Start low and increase slowly Pramipexole 1.5mg-4.5mg/d Ropinirole 9.0-24mg/d Rotigitine 4.0-6.0mg/d SEs nausea,dizziness,impulsive behaviour disorders (must warn them as they may get up and go gamble all their money)
Non drug treatment of Parkinson’s
Deep brain stimulation
Pacemakers that develop stimulates to Substagia nigra to reduce tremor. Indicated if erratic and disabling responses to prolongedL-dopa therapy
Compare Parkinson’s to cerebellar disease
Parkinson is bilateral but can start either side where cerebellar can be either.
Parkinson is resting tremor where cerebellar in intentional tremor. Progression in parkinson is slow where in cerebellar is usually sudden. Parkinson’s is persistent and not curable where cerebellar can be curable or persistent.
Classic triad parkinson’s
Resting tremor, rigidity, and bradykinesia and postural instability (loss of postural reflexes
Symptoms of parkinson’s
Hx of falls
reduced sense of smell is one of the first symptoms
Changes in cognition, behaviour or mood
Ask about drugs that inhibit dopamine.
Drugs used in parkinson’s disease
L-Dopa/carbidopa/benzariside
Dopa agonists. This and L-Dopa are the main ones used in combination.
MAO-B inhibitors
Amantadine -
Apomorphine - Non ergot derivatives Dopamine agonists
Anticholinergics, don’t use in elderly
Anticholinesterases: Rivastigmine
Dosing frequency
Daily fluctuations in wearing off. May need to give regular doses e.g. 4-6 a day.
Symptoms in the premotor stage of parkinson’s
REM sleep abnormalities - By 10-15years
Constipation - Predate PD by 10years
Hyposmia-early symptoms
Depression 28%-36%
Symptoms in the motor stage of parkinson’s
Predictable complications - wearing off/off period dystonia and Peak dose dyskinesia
Unpredictable complications - On-off response or Dosing failure
Freezing
Symptoms of Non motor stage of parkinson’s
Psychosis =Hallucinations - Lewy body dementia, impulsive compulsive disorder - side effect of drugs
Cognitive problems = Lewi body dementia, PD/alzheimerdiseases, PD/Dementia
sleep/wake abnormalities
