Parkinson's disease Flashcards
(38 cards)
define parkinsons
Parkinsonism: a syndrome manifested by part or all of symptoms of resting tremor, bradykinesia, and rigidity (with resulting postural instability)
Parkinson’s disease is a specific chronic progressive neurodegenerative disease with features of Parkinsonism
Key factor: loss of dopamine-producing cells in basal ganglia
First described by James Parkinson in 1817
No cure
aetiology
Characteristic feature: degeneration of dopamine-producing cells in substantia nigra pars compacta of the basal ganglia
Unknown cause
Environmental factors + genetic predisposition
Cellular mechanisms: Oxidative stress, premature apoptosis, loss of neurotrophic factors, glutamate toxicity, mitochoncrial dysfunction, inflammation
differential diagnosis
secondary Parkinsonism
Parkinson’s plus syndrome
epidemiology
2nd most common neurodegenerative disease (after Alzheimer’s) Incidence rises steeply with age Most common over age 60 1% of people over age 60 4% over age 80 5-10% onset age 20-50 (young onset PD) Higher incidence in Causasians M:F 1.5:1 slightly more common in men 1.2 million people in Europe affected
secondary Parkinsonism
Multiple possible causes: Toxins Carbon monoxide, manganese Structural brain damage Tumour, trauma, hydrocephalus Drugs Neuroleptic drugs, dopamine-depleting agents Infections Post-encephalitis, AIDS, Creutzfeldt-Jakob Disease
parkinson’s plus syndrome
Idiopathic
Includes other syndromes:
Progressive supranuclear palsy (PSP) Multiple system atrophy (MSA) Corticobasal degeneration (CBD) Dementia with Lewy Bodies (DLB)
Beyond the scope of this lecture
diagnostic criteria
No single laboratory test
(Pathological diagnosis based on Lewy bodies in basal ganglia)
Diagnosis based on clinical exam and presence of 2 out of 3 cardinal symptoms of resting tremor, bradykinesia and rigidity
+ Absence of other cause of Parkinsonism
+ Absence of upper motor neurone signs
+ Response to levodopa (clinical improvement 4-8 weeks)
must be given by a neurologist
basal ganglia
Many proposed function Not all related to movement Different nuclei of BG make loop Info from pre motor cortex Impulse to striatum Made up of caudate and putamen Take in signal first Message to output nuclei Output then to thalamus Ventral anterior and ventral lateral nuclei Series of inhibitory loops
Motor plan of body – postural stability plan for standing
To walk – turn off postural control mechanisms and turn on step mechanisms
BG give automatic mechanism ensuring good amplitude movement at the right time
Walking – don’t think about step length
No dopamine – too inhibitied steps are too small
BG not functioning in park –have to use other ways to achieve good movement
excitatory pathways Glutamate Inhibitory pathways GABA Modulatory pathways Dopamine
clinical features
Three cardinal symptoms:
Resting tremor
Bradykinesia
Rigidity
Leading to:
Postural instability and impaired balance reactions
Gait impairment (shuffling, freezing)
Plus many other symptoms and signs
resting tremor
Often first symptom noticed
Occurs at rest, diminishes when hands moved
Frequency 4-6 Hz (slow)
Hands affected first, then legs, chin, mouth, tongue
Often unilateral, may progress to other side
Characteristic: flexion of fingers, rotation of
wrist joint (“pill-rolling”)
bradykinesia
Slowness of movement
Difficulty with repetitive automatic tasks, e.g. writing, walking, playing music
Limbs have decreased amplitude on all movement tasks
Manifestations:
Micrographia
Shuffling gait
Hyphonia
Tests: finger tap tests - tap finger on table at certain amplitude
hand open / close, heel tapping
speaking - quiet tone
feature of the Parkinson’s disease
postural instability
Combined effect of rigidity and bradykinesia
Loss of postural reflexes: anticipatory adjustments and righting reactions
Festination in gait
Also associated with freezing
freezing gait
Sudden inability or hesitancy in moving
limbs during gait
Most commonly in gait initiation and
turns
Once freezing is overcome, movement might be normal (“thawing”)
Falls can occur during freezing episodes
FOG = freezing of gait
non-motor symptoms
Neuropsychiatric: cognitive impairment, depression, anxiety, psychosis (late stage)
Sleep disturbance
Autonomic dysfunctions: hypotension, urinary dysfunction, sweating
Gastrointenstinal: drooling, dysphagia, nausea, constipation
Sensory: olfactory disturbance, pain, paresthesia
Other: fatigue, weight changes
Non-motor and cognitive symptoms indicate that PD is not just a disease of the basal ganglia, but that cortical functions are also impaired
impairments in execute functioning
Internal control of attention
Set shifting: changing attention between one or more stimuli
Planning
Conflict resolution
Concentration
Retaining and using information
Dual task performance
Decision-making (considering advantages and disadvantages of options)
Social interaction (understanding others’ intentions, desires and humour)
Consider the implications for physiotherapy.
imaging
MRI and CT no useful
PET studies demonstrate reduced uptake in striatum SPECT can quantitatively measure dopamine in basal ganglia
medical management
The goal is to replace Dopamine (DA)
Levodopa = precursor of DA
Converts to DA once it crosses BBB by dopa decarboyxlase (DDC)
Combined with DDC inhibitors to prevent conversion in peripheral tissues
Sinemet = levodopa + carbidopa Madopar = levodopa + benserazide
Gradual introduction of L-Dopa
Maintenance dose 300-600 mg / day
Marked improvement in rigidity and tremor
Less improvement in gait
Side effects
Gastrointestinal Cardiovascular Psychiatric
Half life = 1.5 hours
Best effect after 20-30 mins, can last 8 hours
problems with L-dopa
Effectiveness decreases over time
“End-of-dose” deterioration: worsening of motor symptoms before next dose due
Morning dystonia, nocturnal akinesia
Dyskinesias emerge in 50% after 5 years
other medication
Dopamine agonists Apomorphine, rigotine, pramipexole More side effects than L-dopa Delay dyskinesias COMT inhibitors Catecholamine-O-Methyltransferase Adjunctive with L-dopa Monoamine Oxidase B Inhibitors Anticholingergics Amantadine
surgical treatment
Considered where limits of medication are reached: worsening, non-responsive symptoms
Neurosurgical options: Thalamotomy Pallidotomy
Deep brain stimulation (DBS)
assessment
observation Posture Speech, saliva management Tremor Facial expression
posture and gait Flexion
Shuffling
Freezing
TUG
movement
tone
ROM
strength
gait feature
Slowness of movement Difficulty with gait initiation Temporal-spatial changes: Uneven step lengths Slow speed Reduced cadence Increased double support time Kinematic changes: Flexed hips and knees Reduced angular displacement hips / knees / ankles Reduced arm swing Reduced foot clearance
destination
freezing
falls
PD symptoms affected by
Constipation Illness / surgery Stress episode Dehydration Withdrawal / medication change / non compliance Use of contraindicated medications (neuroleptics) Depression Pain Anxiety, panic attacks Poor sleep
goals of physio
maximise
independence
safety
function
maintain or improve Prevent deconditioning
Maintain strength
Manage bradykinesia, rigidity Reduce falls
Maintain flexibility
Optimise gait
Improve gross motor coordination Maintain balance