PD: presentation, diagnosis, exam Flashcards
Parkinson’s Disease
neurodegenerative disorder of subcortical gray matter in the basal ganglia
dopamine loss causes loss of inhibitory control of indirect loop and excitatory control over direct loop results in decreased movement
highest incidence among caucasians, males, and in early to mid 60s
PD cardinal signs (TRAP)
Tremor (resting): diminishes w/ effort, increase w/ stress/fatigue
Rigidity: not velocity dependent, common in trunk, extremities and neck
Akinesia/bradykinesia: correlates best with severity of loss of dopamine
Postural instability: not common early in diagnosis
Movement symptoms of PD
- resting tremor
- rigidity
- bradykinesia
- postural instability (later on)
- micrographia (handwriting getting smaller over time)
- festinating gait
- freezing
- soft speech
- masked face
- Sialorrhea (drooling) and dysphagia (motor function)
non-movement symptoms of PD
- anosmia
- anxiety
- apathy
- bone health
- breathing difficulty
- cognitive changes
- constipation and nausea
- dysautonomia
- fatigue
- hallucinations
- pain & sensory disturbances
- sleep disorders
T/F there is NO diagnostic test for PD
True
- based on clinical exam
- gold standard: neurological exam at autopsy
- no biological marker that confirms diagnosis
Supportive criteria for diagnosing PD
Clear & dramatic response to dopamine therapy
Levodopa-induced dyskinesia (not unique to PD)
Resting tremor of a limb
Diagnostic testing: loss of olfaction & abnormal cardiac MIBG scintigraphy
9 absolute exclusions for diagnosing PD
- unequivocal cerebellar abnormalities
- downward vertical supranuclear gaze palsy
- Frontotemporal dementia (w/in first 5 yrs)
- parkinsonism restricted to lower limbs longer than 3 yrs
- treatment with dopamine receptor blocker (drug induced PD)
- absence of response to levodopa
- unequivocal cortical sensory loss
- normal functional neuroimaging of dopaminergic system
- documentation of alternative condition know to produce parkinsonism & plausibly connected symptoms
PD prognosis
Progressive disease with no cure
- shift from unilateral to bilateral involvement
- increasing rigidity and postural flexion
- increasingly limited mobility and increasing need for assistance
- eventually w/c and/or bed-bound
- cause of death usually pneumonia
PD: Stage zero
no signs of disease
PD: stage 1
unilateral symptoms- tremor, stiffness, slowed movement
PD: stage 1.5
unilateral symptoms plus ataxial involvement- postural problems
PD: stage 2
mild bilateral involvement & minor sxs: swallow, talk, and decreased facial expression
PD: stage 2.5
bilateral involvement, recovers on pull test
PD: stage 3
bilateral involvement worsened. Postural instability noticed. Person is still independent
PD: stage 4
Severe disability, able to walk or stand unassisted, but will need help with ADL
PD: stage 5
person confined to w/c or bed; needs total assistance
common early presentation of PD
tremor micrographia slowness with ADLs voice changes (soft speech) difficulty maneuvering in bed lack of arm swing with gait dragging the foot with walking
common presentation of PD after 5 years
motor fluctuations: wearing off, on-off phenomena, narrowing therapeutic window
loss of postural control; retropulsion
gait freezing and festination
cognitive changes
medication side effects: dyskinesia, dystonia
Primary objective of medical management of PD
maximize control over the “target” signs and symptoms
patient’s therapeutic response to any individual drug may change over time and requires regular visits and frequent communication between the medical team, the patient, and caregiver to maintain the best management of the disease with the fewest side effects possible
Advantage and mechanism of Carbidopa/Levodopa
Dopamine agonists
COMT inhibitors
MAO inhibitors
Anticholinergic agents
- most effective; prolongs capacity to perform ADLs
- works by copying actions of dopamine in the brain
- inhibits enzyme responsible for metabolism of levodopa
- slow metabolism of dopamine
- used for treatment of tremor in younger patients
History questions during exam
PMH/co-morbidities symptom onset medications: dosing schedule, time of last dose, on/off periods falls home set-up and current daily activities equipment social support primary complaint and current symptoms current exercise regimen
MSK exam
ROM - rigidity -posture assessment -limited cervical and trunk rotation -hip flexor tightness (thomas test) Strength -generally should be WNL -5x sit to stand: >16 secs correlated with fall risk
Coordination observations
movements bradykinetic, small, fatigue with repetition
no dysmetria
dyskinesia
Sensory exam
Pain:
-MSK
-central neuropathic
Oculomotor and visual:
-visuoperceptual deficits
-abnormalities atypical in early stages of idiopathic PD
-impaired/bradykinetic saccades in late stages
Olfactory disturbances
-odor detection, discrimination, identification
Proprioception:
-decreased sensory integration: joint position sense, postural orientation
-decreased kinesthetic awareness: larger limb displacement required in order to detect movement