Atypical Parkinsonism Flashcards
what is Atypical Parkinsonism
primary motor degenerative disease that cause sym similar to parkinsons
what are the AP that we talked about
Progressive supranuclear palsy (PSP)
Dementia with Lewy bodies
Multiple-system atrophy (MSA)
Corticobasal degeneration
how do we diagnosis atypical park
based on medical history and clinical examination
no specfic test
early sym of AP
they present similar to park
what are some red flags that what we are seeing is not park
early postural unsteadiness - abnormal posture
rapid progression
respiratory dys
emotional liability
signs of cerebellar and voluntary gaze dysfunction
what is Progressive Supranuclear Palsy due to
an adnormal collection of protien struture tau in neurons that cause the cells to die
cause is unknown for this phenomonon
what pop does PSP normally effect
60 -70
what specific neurons are lost with PSP
corticobrainstem neurons
these control voluntary eye movements and this can result in gaze palsy
other signs other then gaze palsy do we see with PSP
gait unsteady
tendancy to fall backwards
cog and phych issues - mood dys
speech and swallowing
lack of motivation
what is dementia with lewy bodies caused by
abnormal tau protein collection and alpha-synuclein proteins within neurons
cause is unknown
what is the second most common cause of neurodegenerative dementia
dementia with lewy bodies
dementia with lewy bodies effects what population
individuals ages 50 and over,
slightly more prevalent in men
with dementia with lewy bodies how much is the memory effects
memory is not disproportionately affected compared to other cognitive functions
Characteristic signs of dementia with lewy bodies
early general cog decline
visual hallucinations
postural and gait instablity
what are the other sym seen with dementia with lewy bodies
fluctuating attention/alertness,
mood changes,
sleep dysfunction,
behavioral changes,
loss of motivation,
blood pressure changes
what is Multiple system atrophy (MSA) caused by
progressive degen disease that affects the
BG
cere
autonomic system
PNS
cerebral cortex
cause is unknown
signs of Multiple system atrophy (MSA)
Akinetic/rigid syndrome
Cerebellar signs
Autonomic dysfunction
Corticospinal tract dysfunction
Decreased goal-directed cognition and difficulty with attention
Sleep dysfunction, breathing problems at night
Akinetic/rigid syndrome - MSA
slow stiff walking and balance problems
Cerebellar signs - MSA
uncoordinated speech and ataxia
Autonomic dysfunction - MSA
postural hypotension
bladder and bowel changes
abnormal respiration
decreased secretions
Corticospinal tract dysfunction - MSA
babinski
hyperreflexia
what is Corticobasal Degeneration caused by
accumulation of tau proteins in the neurons
cause is unknown
what is the onset for Corticobasal Degeneration
60-70
Characteristic signs of Corticobasal Degeneration
motor similar to park
dystonia
visuospatial and cognitive impairments
apraxia
dysphagia
speech hesitancy
myoclonus
what is dystonia
Involuntary muscle contractions that cause repetitive or twisting movements.
what is myoclonus
a quick jerking movement that you can’t control
hiccups
Corticobasal Degeneration one sided
it may effect one side more then the other
Movement dysfunction meds
levadopa
Dystonia meds
botox
Memory/cognitive impairment meds
Exelon, Aricept, Razadyne, Namenda
Hallucinations meds
atypical antipsychotics (Nuplazid, Clozaril, Seroquel)
is there high-quality evidence for specific PT interventions for those with AP
no - it is limited
what causes huntingtons disease
abnormal expansion of a gene on chromosome 4
does the person with the abnormal gene alwats get hunt
no
Child of someone with HD has what chance of having the gene
50%
what is the normal age of onset for hunt
30 -40
what is the life expectancy for some with hunt
15 -20 from onset
Pathophysiology of hunt
the striadted neuron that go to the external GP in the indirect pathway are damaged
what does damage to the striated neuro in the BG pathway do
since the no-go pathway is damage we get hyperkinesia
what is hyperkinesia
too much movement
what patho-wis happens with disease progression
more neurons are impacted
where can neural damage occur
in the frontal cortex
what are the Signs and Symptoms of HD
Dyskinesias
Oculomotor dysfunction
Bradykinesia
Dystonia
Myoclonus
Tics
Ataxia
Dysarthria
Dysphagia
Cognitive impairment
Personality changes, depression
what is Dyskinesias
involuntary, erratic, writhing movements of the face, arms, legs or trunk.
Chorea
Athetosis
what is the difference
Chorea - involuntary rapid movement s
athetosis - slow involuntary movement - worm like
how is HD diagnosed
clinical assessment and genetic testing
Medications for chorea
Dopamine depleting agents (Tetrabenazine)
Neuroleptic agents (Haloperidol)’
Anti-Parkinson drugs (Amantadine)
Glutamate blocker (Riluzole)
Prioritize assessment of with HD
Mental status/cognition
Motor
Balance
Function
May screen or assess in more detail
what with HD
Oculomotor function
Speech/swallowing
Sensory
Coordination
what are the core outcome
Core outcome measures
10MWT
6MWT
ABC
5xSTS
Berg Balance Scale
FGA
what is the Unified HD Rating Scale (UHDRS) used for
Used to quantify the severity of HD symptoms
what is the Behaviours Assessment for Huntington’s Disease
Severity and frequency of behavioral abnormalities
what are the best interventions for HD
Aerobic paired with strengthening exercise
gait training
what is a okay intervention for HD
balance and breathing exercises
what aeorbic and stregthing exercises shoudl we use for those with HD
mod intensoty aeoribc (50-90) max heart rate
paired with
strengthening at least 3x per week
for a min of 12 weeks to improve fitness and stablization
how should PT be for prescribing gait training
PTs should prescribe 1:1 gait training to improve the spatiotemporal parameters of gait
what is Alzheimer Disease (AD)
Progressive neurodegenerative disease associated with build up of amyloid plaques, neurofibrillary tangles, and loss of neuronal connections in the brain
does the risk of AD chnage with age
yes the risk increases
Signs and symptoms of AD
Memory changes that disrupt daily life.
Difficulty making decisions, especially in planning or solving problems.
Difficulty completing familiar tasks.
Confusion about time and/or place.
Trouble understanding visual images, or the way things fit together (spatial relationships).
Finding the right words to say when speaking or writing.
Misplacing items and losing the ability to retrace your steps.
Poor or decreased judgment about safety.
Withdrawal from work or social activities.
Changes in mood or personality.
exercise and AD
Regular exercise may delay the onset of AD in healthy older adults
