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Neuromus 3 > Atypical Parkinsonism > Flashcards

Atypical Parkinsonism Flashcards

1
Q

what is Atypical Parkinsonism

A

primary motor degenerative disease that cause sym similar to parkinsons

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2
Q

what are the AP that we talked about

A

Progressive supranuclear palsy (PSP)

Dementia with Lewy bodies

Multiple-system atrophy (MSA)

Corticobasal degeneration

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3
Q

how do we diagnosis atypical park

A

based on medical history and clinical examination

no specfic test

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4
Q

early sym of AP

A

they present similar to park

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5
Q

what are some red flags that what we are seeing is not park

A

early postural unsteadiness - abnormal posture

rapid progression

respiratory dys

emotional liability

signs of cerebellar and voluntary gaze dysfunction

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6
Q

what is Progressive Supranuclear Palsy due to

A

an adnormal collection of protien struture tau in neurons that cause the cells to die

cause is unknown for this phenomonon

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7
Q

what pop does PSP normally effect

A

60 -70

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8
Q

what specific neurons are lost with PSP

A

corticobrainstem neurons

these control voluntary eye movements and this can result in gaze palsy

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9
Q

other signs other then gaze palsy do we see with PSP

A

gait unsteady

tendancy to fall backwards

cog and phych issues - mood dys

speech and swallowing

lack of motivation

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10
Q

what is dementia with lewy bodies caused by

A

abnormal tau protein collection and alpha-synuclein proteins within neurons

cause is unknown

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11
Q

what is the second most common cause of neurodegenerative dementia

A

dementia with lewy bodies

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12
Q

dementia with lewy bodies effects what population

A

individuals ages 50 and over,

slightly more prevalent in men

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13
Q

with dementia with lewy bodies how much is the memory effects

A

memory is not disproportionately affected compared to other cognitive functions

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14
Q

Characteristic signs of dementia with lewy bodies

A

early general cog decline

visual hallucinations

postural and gait instablity

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15
Q

what are the other sym seen with dementia with lewy bodies

A

fluctuating attention/alertness,

mood changes,

sleep dysfunction,

behavioral changes,

loss of motivation,

blood pressure changes

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16
Q

what is Multiple system atrophy (MSA) caused by

A

progressive degen disease that affects the
BG
cere
autonomic system
PNS
cerebral cortex

cause is unknown

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17
Q

signs of Multiple system atrophy (MSA)

A

Akinetic/rigid syndrome

Cerebellar signs

Autonomic dysfunction

Corticospinal tract dysfunction

Decreased goal-directed cognition and difficulty with attention

Sleep dysfunction, breathing problems at night

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18
Q

Akinetic/rigid syndrome - MSA

A

slow stiff walking and balance problems

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19
Q

Cerebellar signs - MSA

A

uncoordinated speech and ataxia

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20
Q

Autonomic dysfunction - MSA

A

postural hypotension

bladder and bowel changes

abnormal respiration

decreased secretions

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21
Q

Corticospinal tract dysfunction - MSA

A

babinski

hyperreflexia

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22
Q

what is Corticobasal Degeneration caused by

A

accumulation of tau proteins in the neurons

cause is unknown

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23
Q

what is the onset for Corticobasal Degeneration

A

60-70

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24
Q

Characteristic signs of Corticobasal Degeneration

A

motor similar to park

dystonia

visuospatial and cognitive impairments

apraxia

dysphagia

speech hesitancy

myoclonus

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25
Q

what is dystonia

A

Involuntary muscle contractions that cause repetitive or twisting movements.

26
Q

what is myoclonus

A

a quick jerking movement that you can’t control

hiccups

27
Q

Corticobasal Degeneration one sided

A

it may effect one side more then the other

28
Q

Movement dysfunction meds

A

levadopa

29
Q

Dystonia meds

A

botox

30
Q

Memory/cognitive impairment meds

A

Exelon, Aricept, Razadyne, Namenda

31
Q

Hallucinations meds

A

atypical antipsychotics (Nuplazid, Clozaril, Seroquel)

32
Q

is there high-quality evidence for specific PT interventions for those with AP

A

no - it is limited

33
Q

what causes huntingtons disease

A

abnormal expansion of a gene on chromosome 4

34
Q

does the person with the abnormal gene alwats get hunt

A

no

35
Q

Child of someone with HD has what chance of having the gene

A

50%

36
Q

what is the normal age of onset for hunt

A

30 -40

37
Q

what is the life expectancy for some with hunt

A

15 -20 from onset

38
Q

Pathophysiology of hunt

A

the striadted neuron that go to the external GP in the indirect pathway are damaged

39
Q

what does damage to the striated neuro in the BG pathway do

A

since the no-go pathway is damage we get hyperkinesia

40
Q

what is hyperkinesia

A

too much movement

41
Q

what patho-wis happens with disease progression

A

more neurons are impacted

42
Q

where can neural damage occur

A

in the frontal cortex

43
Q

what are the Signs and Symptoms of HD

A

Dyskinesias

Oculomotor dysfunction

Bradykinesia

Dystonia

Myoclonus

Tics

Ataxia

Dysarthria
Dysphagia

Cognitive impairment

Personality changes, depression

44
Q

what is Dyskinesias

A

involuntary, erratic, writhing movements of the face, arms, legs or trunk.

45
Q

Chorea
Athetosis
what is the difference

A

Chorea - involuntary rapid movement s

athetosis - slow involuntary movement - worm like

46
Q

how is HD diagnosed

A

clinical assessment and genetic testing

47
Q

Medications for chorea

A

Dopamine depleting agents (Tetrabenazine)

Neuroleptic agents (Haloperidol)’

Anti-Parkinson drugs (Amantadine)

Glutamate blocker (Riluzole)

48
Q

Prioritize assessment of with HD

A

Mental status/cognition
Motor
Balance
Function

49
Q

May screen or assess in more detail
what with HD

A

Oculomotor function
Speech/swallowing
Sensory
Coordination

50
Q

what are the core outcome

A

Core outcome measures

10MWT
6MWT
ABC
5xSTS
Berg Balance Scale
FGA

51
Q

what is the Unified HD Rating Scale (UHDRS) used for

A

Used to quantify the severity of HD symptoms

52
Q

what is the Behaviours Assessment for Huntington’s Disease

A

Severity and frequency of behavioral abnormalities

53
Q

what are the best interventions for HD

A

Aerobic paired with strengthening exercise

gait training

54
Q

what is a okay intervention for HD

A

balance and breathing exercises

55
Q

what aeorbic and stregthing exercises shoudl we use for those with HD

A

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

56
Q

how should PT be for prescribing gait training

A

PTs should prescribe 1:1 gait training to improve the spatiotemporal parameters of gait

57
Q

what is Alzheimer Disease (AD)

A

Progressive neurodegenerative disease associated with build up of amyloid plaques, neurofibrillary tangles, and loss of neuronal connections in the brain

58
Q

does the risk of AD chnage with age

A

yes the risk increases

59
Q

Signs and symptoms of AD

A

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.

60
Q

exercise and AD

A

Regular exercise may delay the onset of AD in healthy older adults

Neuromus 3 (7 decks)

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