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Neuro 2 > Additional BG Pathologies > Flashcards

Additional BG Pathologies Flashcards

1
Q

What’s the difference between primary and secondary parkinsonisms

A

Primary is Parkinson’s
Secondary: BG damage secondary to something else

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2
Q

What’s the difference between primary and atypical parkinsonisms

A

atypical: less effective response to meds, progress faster, higher mortality than primary

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3
Q

Etiology unknown, the pathophysiology behind PSP (progressive supranuclear palsy) involves accumulation of _. protein. Among others, brainstem structures, thalamus,and _,atrophy along with astroglial cells and neurons.

A

tau; basal ganglia

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4
Q

How is PSP diagnosed? What specific MRI findings are involved? (hint: (frontal lobe, subthalamic and putamen atrophy)

A

early clinical exam is primary and onset typically in 60s
MRI: morning glory sign, hummingbird sign

morning glory
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5
Q

What is PSP commonly misdiagnosed as?

A

depression, dementia, Parkinsonisms

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6
Q

What are 5 signs and symptoms unique to PSP?

A

early gait disturbance
rocket sign and axial rigidity
pseudobulbar affect
Mona Lisa stare
loss of eye movement/lid ctrl (esp vertical)

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7
Q

How is PSP managed?

A

not really effectively managed–sometimes dopamine, botox and antidepressants

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8
Q

How is the prognosis for PSP?

A

poor- severe disability in 3-5 yrs, mortality in 5-8.

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9
Q

what serious complications may arise in PSP pts?

A

pneumonia and falls

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10
Q

Describe MSA (multiple system atrophy).

A

a rare neurodeg dx that also includes autonomic dysfunction

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11
Q

What are the two subtypes of MSA and how do they differ?

A

MSA-P (parkinsonian)
MSA-C (cerebellar)-later onset/slower progression

they are named for which s/s present first

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12
Q

How is MSA diagnosed? What specific MRI findings are involved?

A

usually in early 50s (rarely past 70s) via clinical exam
+PET, DaTscan, MRI (hot cross bun sign of pons atrophy)

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13
Q

What is MSA commonly misdiagnosed as?

A

PD> pts don’t respond to dopamine therapy

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14
Q

Etiology unknown, the pathophysiology behind multiple system atrophy involves accumulation of ____with the most involvement observed in ____ (cell type)

A

proteins in glial cells, oligodendrocytes

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15
Q

The signs & symptoms associated with premotor phase MSA are sexual dysfn, urinary incontinence, OH, and ____

A

inspiratory stridor, REM behavior

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16
Q

The signs & symptoms associated with MSA are sleep disorders, oculomotor disturbance (MSA-C), antecollis, dyskinesia, and (4)?

A

Autonomic symptoms (esp OH), symmetric PD s/s,, coat hanger pain, Pisa syndrome,

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17
Q

how is MSA managed?

A

PD meds (temp) and used w/ caution for OH effects
potentially surgical trach for feeding with later progression
symptom management

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17
Q

How is the prognosis for MSA?

A

poor-almost half are dep in 8 years w/ mortality within 5-10 years

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17
Q

what serious complications may arise in MSA pts?

A

cardiac and respiratory failure, urosepsis and sudden death

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18
Q

what s/s is rarely seen in pts with MSA?

A

cognitive deficits

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19
Q

What is the average age of onset of Corticobulbar Degeneration (CBD)?

A

60-80 years old
women> men

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20
Q

Etiology unknown, the pathophysiology behind CBD involves focal ____ and ____neuronal loss –specifically in glial cells such as ____.

A

cortical and substantia nigra lesions; astrocytes

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21
Q

An MRI image of CBD would provide the appearance of “brain shrinkage” via _____

A

over pronounced sulci

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22
Q

T/F: The Cognitive impairments related to corticobasal degeneration (Dementia, AD, FBSS) tend to present later than that of progressive supranuclear palsy.

A

False.

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23
Q

Aside from asymmetrical PD s/s, the signs & symptoms unique to CBD are visuospatial impairments, apraxia, and ____ (2)

A

myoclonus and progressive aphasia

24
Q

T/F: There is currently no cure available for CBD and treatment is largely supportive (symptom based)

A

True.

25
Q

CBD prognosis indicates an average survival of ____ years from symptom onset.

A

6-8 but there are cases of people surviving >10 years.

26
Q

_____is not a “Parkinsonism” but a BG diagnosis characterized by involuntary muscle contractions >slow, repetitive movements/ abnormal postures

A

dystonia

27
Q

the 5 classifications of dystonia are:

A

focal-1 body part
segmental (2+ continuous body parts)
multifocal (2+ noncontinuous parts)
generalized (trunk and 2+body parts)
hemi

28
Q

Dystonia is typically onset at childhood and early adulthood and the difference in presentation is that
early onset presents w/ ____while adult onset presents with ____

A

limb involvement; neck/facial involvement

29
Q

Dystonia is typically ____but can also be genetic or acquired and there aren’t any identifiable damages on imaging.

A

idiopathic

30
Q

what are the 4 common initial s/s of dystonia? (hint: 3 in foot, 1 in hand). Generally speaking these may lead to contracture.

A

foot: cramping, toe drag, and/or excessive inversion @ swing

hand: cramping while writing

31
Q

what are the effects of eyelid and neck/trunk dystonias?

A

eyelid: excessive blinking
neck/trunk: postural abnormality

32
Q

T/F: Dystonia can be circumstantial and only impact specific movements.

A

true

33
Q

What are the 4 pharmacologic treatment options for dystonia and which have the highest success rate?

A

Botox
but also anticholinergics, GABAergic and dopaminergic agents have mixed reviews.

34
Q

___,___, ____,and____ are surgical intervention options for dystonia that aren’t usually a go-to due to invasiveness. Of them___is the most common.

A

Deep Brain stimulation, thalamotomy, pallidotomy, and anterior cervical rhizotomy

DBS

35
Q

_____has no direct mortality prognosis or commonly fatal secondary complications

A

Dystonia

36
Q

_____is a drug induced dx that involves uncontrolled stiff and jerky movements of the face/body. The primary culprits are____ and ______

A

tardive dyskinesia; amphetamine/meth/haloperidol and phenothiazines (for schizophrenia)

37
Q

risk factors for TD are the amount/long term use of the drug, drug. abuse, and __(3 demographic RFs)

A

age >55, women>men, race (Black and Asian)

38
Q

TD is dx via clinical exam and med review. Its treated via Deutetrabenzine, Valbenzine or ____

A

Cessation!

39
Q

Huntington’s Disease is a ____autosomal trait that results in ___activity of basal nuclei.

A

Dominant
hyper-

40
Q

The pathophysiology of Huntington’s involves severe loss of neurons in the ___ and putamen, among other lobes, that resembles ______on imaging.

A

caudate,
dilation of lateral ventricles

41
Q

In HD, the indirect “no-go” pathway is hit first causing ______. Next, the direct “go” pathway is hit and we see more widespread loss and s/s similar to ____

A

disinhibition of thalamus (runnin amuck)

PD

42
Q

HD is characterized by unique s/s including mood changes, cognitive impairment (including dementia and OCD) , and ____(3)

A

choreiform movements, motor impersistence, and PD s/s in later stages.

43
Q

Pharmacologic treatment for Huntington’s is typically introduced when ….

A

chorea interferes w/ fn

44
Q

How is the prognosis for Huntington’s?

A

mortality: 15-25 after onset
causes: often respiratory failure, suicide common

45
Q

Our treatment plan for PSP and MSA would likely favor (compensation/remediation). Additionally, emphasisis should be placed on maintaining (distal/proximal) strength, stretch and positioning.

A

compensation, proximal

46
Q

PT treatment considerations for dystonia and chorea
can be remembered as R.I.S.C.S. This stands for____

A

-relaxation techniques (may refer to psych)
-ID triggers and tricks
-Serial casting for severe cases
-Cog and Sensory training

47
Q

T/F Conservative treatment (PT) using postural ctrl, balance reactions and biofeedback are typically the first line of defense for tardive dyskinesias.

A

False. We can do these things and should if the damage is permanent. But stopping the causative drugs is the first-step.

48
Q

neck extensors, ____ and muscles of the hand/feet are common areas of weakness in people with HD.

A

postural trunk muscles

49
Q

Early stage HD exercise recs include:

A

aerobic exercise, strengthening, stretch/ROM, coordination and advanced balance activity

50
Q

Middle/Late stage HD exercise recs include:

A

shorter and more frequent activity bouts

salient practice of functional activity

Fall prevention

51
Q

In addition to characteristic s/s of the dx, these common gait deviations make HD patients more of a fall risk (and hence can direct your treatment):

A

-narrow BOS
-variable step length
- frequent/drastic trunk displacement
-difficulty w/ dual tasks

52
Q

What are the major problems associated with early stage HD?

A

chorea
gait
balance/flexibility
fine motor

53
Q

What are the major problems associated with middle stage HD?

A

early stage +
falls
joint hypomobility
weak postural stabilizers

54
Q

What are the major problems associated with late stage HD?

A

previous stages +
overall mobility
respiratory limitations (pneumonia risk)

55
Q

Dysphagia is a common s/s in these dx: (4)

A

PSP
MSA
CBD
HD

56
Q

Dystonia/Ataxia are common s/s in:

A

All of them!
HD
TD
dystonia
CBD
MSA
PSP

57
Q

What makes up the clinical triad of fronto-behavioral-spatial syndrome

A

Executive dysfunction, behavioral/personality changes, Visio spatial deficits

58
Q

Infection/ post-encephalitis, atherosclerosis, and _____ are common etiologies behind secondary Parkinsonisms.

A

toxicity/ drugs

Neuro 2 (8 decks)

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