Parkinson's Disease Pre Module and 101 Flashcards
(35 cards)
The common age of dx:
60 years or older
4% of all with PD are under the age of 50
What 3 conditions fall under the description of “Parkinsonism”?
PD
Progressive Supranuclear Palsy
Multiple Systems Atrophy
What type of dementia can have parkinsonian features?
Lewy Body Dementia
Progressive Supranuclear Palsy signs and symptoms
-can’t look down due to impaired eye movements
-scared appearance
-severe postural extension
-falls in the first year- typically backward
-ONSET: over age 50
** WORSE PROGNOSIS THAN PD
Multiple Systems Atrophy signs and symptoms
-dysautonomia
-parkinsonian and/or
-cerebellar syndrome-ataxia, dysarthria -orthostatic hypotension: 30mm systolic or 15mm diastolic drop
-urinary system- urinary problems usually arise from degeneration in a part of the brainstem that controls urination. Symptoms such as incontinence, leakage, urinary frequency
Cardinal Signs of PD:
rigidity
bradykinesia
resting tremor
postural instability - usually occurs later in the disease process
SUPPORTIVE CRITERIA
-unilateral onset –> then BL
-progressive course
-persistent asymmetry affecting side of onset the most
Possible non-motor signs of Parksinson’s
-cognitive impairment - attention, dual task, dementia
-pain
-depression
-hallucinations
-olfactory loss
-dysautonomia
-sleep dysfunction
-fatigue
What is required for PD diagnosis?
-cardinal signs (bradykinesia plus one other)
-pos response to dop replacement (70-100% improvement)
-type using UPDRS:
–tremor dominant form
–postural instability and gait disorder form
What is the difference between the tremor-dominant form of PD and the postural instability and gait disorder form? (UPDRS)
the PIGD form -
-more problems with instability and gait dysfunction
-more likely to have cognitive deficits
-faster decline –> need medications earlier
What are 4 common medication types for individuals with PD?
DOPAMINE REPLACEMENT: precursor to DA, levodopa crosses the BBB and converts to dopamine; Carbidopa inhibits the breakdown of levodopa peripherally
ex: Sinemet-carbidopa/levodopa (helps prevent vomiting, GI side effects),
Rytary- extended-release carbidopa/levodopa
DOP. AGONIST increases the efficiency of dopamine already in the system —> may delay starting dopamine replacement
-Pramipexole
-Ropinirole
-Rotigotine patch
-Apomorphine (rescue)
DIFFERENT ADMINISTRATIONS POSSIBLE:
-enteral through jejunum tube (duopa)
-transdermal injection
-sublingual, inhaled and nasal spray preparations being studied
COMT INHIBITORS -slows down the breakdown of dopamine
-tolcapone
-entacapone
-opicapone
MAO-B INHIBITORS- slows the breakdown of dopamine –>
-may be used early in the disease
-may have a neuroprotective effect
-rasagiline
-selegiline
Anticholinergics - bind to and block ach receptors
Adenosine A2A Receptor Antagonist
Botulinum Toxin for dystonia
Deep brain stimulation for PD:
-for medication-resistant tremor
leads go under the skin and are implanted deep into the brain –> wires go through a burr hole in the skull
the pulse generator is under the clavicle at the anterior chest wall
has the potential to decrease the amount of meds needed
LEADS GO IN:
-globus pallidus
-subthalamic nucleus
-thalamus
SE
-cog impairment, worsened balance, dysarthria
GOLD STANDARD MEASURES USED TO DESCRIBE PD
UPDRS
Hoehn and yahr
(schwab and england - not listed as gold standard)
Performance measures for PD:
freezing of gait
PDQ-39
mobility and function
look to SG for Hoehn and Yahr Classifications
look there
UPDRS CATEGORIES AND TOTAL POINTS
- mentation, behavior, mood
- ADLs
- motor examination
- complications of meds
total score: 176 points
motor subscale: 108 points
PARKSINSON’S DIAGNOSIS
-a chronic, progressive, neurodegenerative condition that often presents later in life
MUST INCLUDE:
*UKPD Brain Bank Criteria
-bradykinesia must be present plus ONE: resting tremor, rigidity, postural instability(not caused by vision, vestibular, cerebellar dysfunction)
*UPDRS parts I-IV to assess progression, medication response
*Hoehn and Yahr Staging
*Time
*Carbidopa-Levodopa trial
*Imaging - MRI (rule out structural impairment), DAT scan
*autonomic test, smell test, skin biopsy (abnormal protein in ppl with PD)
SUPPORTIVE CRITERIA:
-unilateral onset, persistent asymmetry
-responsive to levodopa
progressive
-levodopa induced dyskinesia
-prodromal symptoms (RBD, loss of smell) –> before the major signs or symptoms start
EXCLUSION
-strokes/head injuries repeated
-anti-dopaminergic agent exposure
-encephalitis
-sustained remission
-poor response to L dopa
-other neurologic signs (cerebellar signs, early dementia, supranuclear palsy)
epidemiology of PD
more in men 3:2
fastest growing neurodegenerative dod in terms of disability, prevalence, and death
RISK FACTORS
-age
-exposures- agent orange, pesticides
-reduced risk: cigarettes, caffeine
-peak: 85-89 years old
pathophysiology of PD
MACRO
-small changes macroscopically
loss of neurons in substantia nigra pars compacta (brainstem) and locus coeruleus
-the death of DA neurons in substantia nigra (basal ganglia)
-30% loss–> motor symptoms onset
-dopamine throughout the striatum is lost (basal ganglia)
MICROSCOPICALLY
alpha-synuclein protein –> aggregates into lewy bodies with mutation
Substantia nigra and connection with caudate and putamen of basal ganglia
the DA neurons of the substantia nigra project to the caudate and putamen of the striatum (BG) –> this pathway makes up the nigrostriatal pathway
Genetics of PD
the complex interaction between genetics and enviro
~15% genetic
LRRK2, GBA, PARK2, PINK1 gene
-may help to determine if someone is a candidate for DBS
COMMON MOTOR SYMPTOMS
resting tremor –> less likely essential tremor
bradykinesia –> slower, smaller movements
–decrement of movement
–interruptions/hesitations
rigidity
postural instability
decreased stride
festination- tiny steps
-FOG
-stooped posture–> camptocormia (abnormal trunk flexion), pisa syndrome (lateral flexion, stooping)
-dystonia–> toe curling, muscle cramps, big toe extension with other phalanx flexion (striatal toe)
non-motor symptoms
psychiatric–> anxiety, dep, apathy
cog impairment (at 20 years of dod –> 80% have dementia)
–PD-MCI, PD-dementia
-dysautonomia
–constipation
–urinary incontinence
–orthostatic hypotension
-dec sense of smell–> hyposmia/anosmia
-fatigue
-sialorrhea (decreased swallowing reflex –> drooling
-hypophonia, dysarthria –> quiet speech, dec muscle strength of muscles needed for speech
-pain
-sleep: insomnia, Rem sleep behavior disorder (RBD), RLS/PLMS (restless leg/periodic limb movements of sleep
ophthalmology
-convergence insufficiency
-saccadic intrusions
-eyelid opening apraxia
autonomic
-neurogenic orthostatic hypotension
- hyperhidrosis
RBD characteristics
act out dreams
can happen 10-20 years before diagnosis of the condition
Symptoms of pre-motor/prodromal period
constipation
RBD
EDS- excessive daytime
sleepiness
hyposmia
depression
