Oct17 M2,3-Movement disorders Flashcards
(35 cards)
3 synucleinopathies
- PD (Parkinson’s dz)
- DLB (Dementia with Lewy bodies)
- MSA (multiple system atrophy)
3 tau-opathies
- CBD (corticobasal degeneration)
- PSP (progressive supranuclear palsy)
- AD (Alzheimer’s dz)
classif of symptoms of Parkinson’s
- cardinal motor symptoms (are the TRAP sx of parkinsonism)
- important non-motor sx
TRAP sx of parkinsonism
- tremor at rest
- rigidity
- bradykinesia (A for akinesia)
- postural instability
non motor sx of PD
- psychiatric disturbance
- autonomic disturbance
- cognitive impairment
- sleep disturbance
how PD is dx
- need 2 or more symptoms
- one of these HAS to be bradykinesia
- 3 things that make it more likely to be PD than a parkinsonism variant of PD: asymmetry, tremor, response to levodopa*
charact of the rest tremor of parkinsonism and PD
- at rest (as opposed to tremor when hold something which is NOT worrisome)
- 3-5 Hz
- asymmetrical (one side)
- typically the pill rolling tremor of the hand but can affect chin, jaw, arms, legs
- 30% of PD pts = no rest tremor
charact of the bradykinesia of parkinsonism and PD
- charact. of PD
- slowness in activities and reaction time
- lack of facial expression (hypomimia) and less blinking
- slow movement
- monotonous and hypophonic speech
- reduced arm swing
- loss of spontaneous movement and gesturing
charact of the rigidity in parkinsonism and PD
- in >90% of PD pts
- increased resistance + cog-wheeling (catch)
- is caused by an underlying tremor causing interruption in the tone
- detected by doing a slow movement (velocity independent) whereas spasticity is a quick catch that is velocity dependent (need quick movement)
- to catch rigidity, slow mvmt at wrist, elbow, ankle
- proximal and distal
charact of postural instability of parkinsonism and PD
- late in PD progression so now a minor criteria
- caused by loss of postural reflexes
- is the most common cause of falls and contributes significantly to the risk of hip fractures (along with freezing gait of PD).
- Freezing gait = PD gait = small, slow, shuffling steps + back and neck bent forward. is also called festinations which means hurrying small steps forward to keep balance
- postural instability assessed by the pull test (3+ steps backwards = abnormal)
- early = red flag
some helpful clinical findings in PD dx
- masked face, reduced eye blink
- change in voice
- trouble arising from chair
- difficulty turning in bed
- trouble buttoning shirt
- flexed posture with loss of arm swing
- sialorrhea (drooling) (bc don’t swallow as frequently)
- change in handwriting (micrographia specifically meaning amplitude of the writing wanes as they are writing)
direction of spread of PD in the brain
caudal to rostral
stage 1 PD charact
- still pre-motor phase of dz
- olfactory bulb + dorsal motor nucleus of the vagus
- related to viscera
- main sx = changed smell and constipation*
stage 2 PD charact
- still pre motor phase of the dz
- locus ceruleus
- LC = a brainstem region imp for arousal, mood, sleep
- main sx = sleep disorders (REM behavior disorders) years before PD*
stage 3 PD charact
- now motor phase
- SN affected
- main sx = rest tremor and bradykinesia*
stage 4 PD charact
- in motor phase of the dz
- cortex now affected
- main sx = cognitive impairment, hallucinations*
premotor sx of PD
- hyposmia (change in smell)
- REM sleep behaviour disorder (acting out dreams, moving, kicking)
- excessive daytime sleepiness
- anxiety or depression
- constipation
- erectile dysfunction
- once have motor PD, can help for dx*
clinical and pathological correlations in HD
- between time 0 and 5 years: neuronal cell loss leading to subtle, non motor sx
- 5 yrs: 70% of dopaminergic neurons are lost = get diagnosis bc first clinical sx appear
- 10 yrs: neuronal cell loss continues and sx progress (wearing off phenomena and + random fluctuations)
- 15+ years: severe presynaptic cell loss leading to decreasing response to L-dopa
theory of PD dx based on diff types of sx
dopaminergic neurons loss in SN in PD CORRESPONDS (but DOESN’T mean causes) to premotor sx crossing threshold to dx much earlier than motor sx crossing threshold for dx
non-motor sx in PD
- autonomic (constipation, urinary frequency, sexual dysfunction, orthostatic hypotension)
- sleep (insomnia and fractured sleep, REM Behaviour disorder)
- neuropsychiatric (depression, anxiety, apathy)
- cognitive (dementia, hallucinations)
- other (pain) = rare
what explains the non-motor sx in PD
degeneration of other ntr pathways
- noradrenergic
- serotonergic
- cholinergic
typical presentation for PD
- 1 year hx of tremor in right arm at rest
- loss of dexterity
- slowness of gait
- anxiety
- constipation
- mild cogwheel rigidity and bradykinesia in RUE and RLE
- normal power all limbs
- slow to rise from chair
- loss of arm swing on R when walking
for how long are the PD sx unilateral
stay unilateral for 5 years. after that, become bilateral
-if stay unilateral > 5 yrs = check for focal lesion
some neuro exam (PE) tests in PD
- finger taping: see small ampltiude waning + hesitating (bradykinesia)
- hand opening and closing, pronation supination, finger taping = to check for the bradykinesia
- gait = stiff leg + arm not swinging
- pull back test 3 steps+