Parkinson's Disease Flashcards
What is parkinson’s disease?
Chronic, progressive movement disorder characterised by the extrapyramidal triad of bradykinesia, tremor and rigidity. Second most common neurodegenerative disease after Alzheimer’s Disease. Twice as common in men. Occurs due to loss of dopaminergic pigmented cells in the substatia nigra and build-up of Lewy bodies.
What causes parkinson’s?
Associated with loss of dopaminergic neurones – substantia nigra input to corpus striatum (Nigrostriatal pathway)
Some genetic associations
Describe in detail the triad of parkinson’s
Tremor 3-5Hz – pill rolling of thumb over finger, resting tremor and worst when stressed or tired)
Bradykinesia (slow to initiate movement, decrease in amplitude with repetition, short shuffling steps with reduced arm swing)
Hypertonia – causing shuffling gait with reduced arm swing and postural instability. Rigidity and tremor give cog wheeling, lead pipe rigidity
Describe other symptoms associated with parkinson’s
Hypophonia, reduced facial expression, micrographia (hand writing becomes smaller).
Non-motor signs such as autonomic dysfunction (postural hypotension, constipation, urinary frequency/urgency and dribbling of saliva) Sleep disturbance Cerebellar disease Pain Sphincter problems Mood changes Psychosis Dementia – associated with visual hallucinations and anxiety
How should a patient suspected of having Parkinson’s be examined?
Ask them to walk in a straight line – shuffling, pitched forward with reduced arms swing asymmetrically at first and freezing at obstacles and doors
Tapping fingers to thumb test – expect reduction in amplitude
Tapping of forehead test – blinking continues
Micrographia and copying a spiral has a characteristic look
Rapid pronation/supination to feel cogwheeling
Cerebellar signs
Signs are usually asymmetrical at first
How should a patient suspected of having Parkinson’s be investigated?
Clinical Diagnosis but must rule out other causes • Drug induced parkinson’s • Vascular Parkinson’s • Progressive supernuclear palsy • Multiple system Atrophy
Lewy bodies on autopsy is the final confirmation
DAT scan – labelled tracer showing presynaptic update dopamine which is abnormal in IPD
Describe how Levodopa is used to managed parkinson’s
Levodopa (can’t use dopamine as doesn’t cross the BBB). Levodopa combined with a dopa decarboxylase inhibitor e.g. Sinemet or Madopar. Short half-life so multiple doses given over the day. Effectiveness wanes over times, can cause SE of dyskinesia, dry mouth, anorexia, palpitations, postural hypotension, psychosis and drowsiness. Must not be stopped acutely.
Describe how dopamine agonists are used to managed parkinson’s and give examples
Dopamine Agonists such as ropinirole and pramipexole (non-ergot), rotigotine transdermal patches and apomorphine (SC) that can be given in a continuous SC injection plus rescue-pen for freezes. Cause less dyskinesis and motor complications and possible neuroprotection but less efficacy than L-DOPA can cause impulse control disorders and excessive daytime somnolence. More likely to cause hallucinations in older patients.
Describe how MAOI type B inhibitors are used to managed parkinson’s and give examples
MAOI type B inhibitors (Rasagaline, Selegiline) – inhibit the breakdown of dopamine secreted by dopaminergic neurons. Can be used alone, or for prolongsation of L-DOPA and may be neuroprotective.
Describe how COMT inhibitors are used to managed parkinson’s and give examples
COMT inhibitors (Entacapone, tolcapone (liver problems so used rarely)) – COMT involved in dopamine breakdown and so this can be used as an adjunct to Levodopa therapy. Can not be used alone.
Describe how Amantadine is used to managed parkinson’s.
Amantadine – not fully understood how it works, probably increases dopamine release and inhibits uptake at synapses. SE include ataxia, slurred speech, confusion, dizziness and livedo reticularis.
Describe how anticholinergics are used to managed parkinson’s and give examples
Anticholinergics (benhexol and orphenadrine) – used to treat drug-induced Parkinson’s rather than Parkinson’s itself. Help tremor and rigidity but no effect on bradykinesia. SE include confusion, drowsiness and the normal anticholinergic SE.
Which symptoms are anticholinergics, amantadine, MAOI type b inhibitors and COMT inhibitors used to treat?
Anticholinergic Mainly for tremor
Amantadine To control dyskinesias
MAOI inhibitors and COMT inhibitors Motor fluctuations
How can you differentiate what could be causing a tremor?
- Parkinson’s – resting, slow (3-5Hz) and typically pill rolling.
- Postural tremor – absent at rest but present when maintaining a posture e.g. worst when arms outstretched, rapid (8-12Hz), cause is usually benign essential tremor – autosomal dominant tremor of arms and/or head, supressed by alcohol. Propranolol can help. Can also be due to thyrotoxicosis or beta agonists or physiological e.g. anxiety.
- Cerebellar Syndrome – intention, past pointing and dysdiadochokinesia.
What are the Parkinson’s plus syndromes?
Group of disorders with a similar presentation to Parkinson’s disease but with extra features that differentiate them.
Progressive Supranuclear palsy
Early postural instability, vertical gaze palsy +/- fall, rigidity of trunk more than limbs, symmetrical onset, speech and swallowing problems but little tremor.
Multiple system atrophy
Early autonomic features, such as impotence and incontinence, postural hypotension, cerebellar and pyramidal signs and rigidity > tremor.
Cortico-basal degeneration
Akinetic rigidity involving one limb, cortical sensory loss (astereognosis – can’t identify an object by touching), apraxia – alien limb phenomenon – limb has a mind of its own
