parkinson's Flashcards
Define Parkinson’s disease
a chronic progressive degenerative neurological disease chiefly of later life that is linked to decreased dopamine production in the substantia nigra and is marked especially by tremor of resting muscles, rigidity, slowness of movement, impaired balance, and a shuffling gait.
Define substantia nigra
part of basal ganglia located in the midbrain–required for movement and reward
Basal ganglia consists of nuclei- caudate nucleus, putamen, globus pallidus, substantia nigra - all control voluntary movements and establishing postures.
When altered as in Parkinson’s person has unwanted movements
Epidemiology of Parkinson’s
Majority of cases are idiopathic
Symptoms begin 55-60 years
1% of over 60 year olds
Males:Females 1.5:1
2nd most common neuro disorder
affects movement
Summarize the underlying Parkinson’s disease
Loss of pigmented dopaminergic neurones in substantia nigra.
Presence of Lewy bodies within pigmented neurons is characteristic.
60-80% of neurones are lost before the motor signs emerge.
As the disease progresses, components of the autonomic, limbic, and somatomotor systems become particularly badly damaged.
Explain the correlation of dopamine and substantia nigra
Substantia nigra (motor centre) is located in the midbrain to which it projects to the caudate and putamen (Together called stiatum). They all use dopamine as a neurotransmitter to which cells in substantia nigra produce dopamine. The site of lesion in PD is the substantia nigra - degeneration of melanin containing cells. Absence of dopamine produces crippling features of PD Essentially loss of substantia nigra impacts the stimulation of striatum which stimulates the thalamus to stimulate the motor cortex (which feedsback to the striatum and substantia nigra). This motor circuit modulates output from the motor complex thus the imbalance of excitatory and inhibitory pathways that regulate movement- symptoms seen in PD
What is used to stage Parkinson’s?
Braak staging 1-6 correlates with clinical manifestation of the disease.
Causes of PD
Idiopathic (most common)
Toxins (Manganese, iron, MPTP, pesticides/herbicides)
Head trauma
Drug induced (antipsychotics, antiemetics, antihistamine)
Genetic (Park-1, Park-3 & Park-12) accounts for < 5%
Abnormal proteosome system
Oxygen free radicals
Describe the cardinal motor symptoms of PD
Tremor
Bradykinesia
Rigidity
Postural instability
Define tremor a/w PD
pill rolling
- unilateral
- rapid at rest
- increased with stress
- frequency of 4- 5 Hertz
Define bradykinesia a/w PD
slowness of movement
difficulty initiating voluntary movement
difficulty with sequential complex movements
decreased amplitude of movement (writing)
rapid fatigability of repetitive movements
Define rigidity a/w PD
Increased resistance of relaxed muscles to passive stretch(eg by examiner)
commonly asymmetrical
1. cogwheel (tremor and rigidity) 2. lead pipe
Distinguish cogwheel and leadpipe rigidity
Leadpipe rigidity is sustained resistance to passive stretch throughout the whole range of motion, with no fluctuations. Cogwheel rigidity is jerky resistance to passive stretch as muscles tense and relax.
Define postural instability
Balance well preserved until later stages
Shuffling gait ; poor arm swing contribute
to high falls risk
What are other motor clinical features a/w PD
Function:
- micrographia
- painful dystonia
- poor bed mobility
- difficulty with transfers
- decreased dexterity/coordination
Face:
- hypomimia(lack of facial expressions)
- hypophonia- soft speech due to lack of coordination of vocal musculature
- dysphagia/drooling
Gait:
- shuffling
- freezing
- turning ‘en loc’
- axial flexion
- decreased arm swing
- festination ; involuntary acceleration
What are the non motor clinical features of PD
Depression: prevalence varies (>30%)
? reactive process
? dopamine effect
Cognitive decline
- executive dysfunction
- dementia = 30%
Sleep disturbance
- insomnia
- day time solmonence/fatigue
- vivid dreams
- hallucinations
Sensation
- orthostatic hypotension
- anosmia
- impaired proprioception
- pain
Autonomic urinary incontinence weight loss constipation sexual dysfunction sweating abnormalities seborrhoeic dermatitis
State the means of diagnosis of PD
It is a CLINICAL diagnosis
Based on Medical History & Clinical examination (triad- tremor, bradykinesia, rigidity)
NO laboratory tests
CT and MRI brain- Normal
MRI can outrule Multi-infarcts, Hydrocephalus & Wilsons (so used to exclude other diseases which may mimic PD)
PET/SPECT useful in atypical cases (but rarely needed)
Differential dx of PD
essential tremor
vascular parkinsonism
drug – Induced parkinsonism
parkinsonism in parkinson plus syndromes
Thyrotoxicosis
Outline features of Parkinson Plus syndromes
Early postural instability & dementia
These progress more quickly than IPD (worsening in first 3-5 yr)
Anti-Parkinsons medications are less effective and patients are very sensitive to neuroleptic medications/ levodopa
Autonomic features are common.
Axial > limb involvement
- multisystem atrophy
- progressive supranuclear palsy
Define multisystem atrophy
Postural Instability with falls
falls due to autonomic function of postural hypotension
Postural Hypotension
Bladder dysfunction
Pyramidal Signs
Cerebellar Signs
Define progressive supranuclear palsy
Parkinsonism (Symmetrical)
Paralysis of upward gaze
Dementia
Personality change
Speech difficulties
Principles of management of PD
educate & support
preserve function
maintain general health and fitness
treat other medical problems
What is the non pharm approach for pt with PD
PD Support Group
Physiotherapy & Occupational Therapy
SALT & Dietician & MSW
Communication with GP
Pharm tx for PD pt
Replace dopamine deficiency
Prevent dopamine breakdown
Dopamine – levodopa
Dopamine decarboxylase inhibitors(inhibit peripheral metabolism of levodopa)- carbidopa
Dopamine agonists- bromocriptine, pramipexole, ropinirole, cabergoline, apomorphine
MAOB inhibitors (prevent degredation of dopamine) – Selegiline, Rasagiline
COMT inhibitor (prevent degredation of dopamine) – Entacopone
Anticholinergics (for tremor/drooling) Procyclidine, Biperidin
Aims of pharm tx for pt w PD
Aims to control signs/symptoms for as long as possible while minimising adverse effects.
Usually provide good symptomatic control for 4-6 years. After this disability progresses.
Motor fluctuations and dyskinesias may become troublesome.
no standard algorithm - treat when function is a problem
