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MedCon Rehab II > COMPS:CVA Part I: Vascular Disorders in the CNS EXAM 1 > Flashcards

COMPS:CVA Part I: Vascular Disorders in the CNS EXAM 1 Flashcards

1
Q

What is CVA?

A

Sudden onset of focal neurologic deficit resulting from cerebrovascular dis.

aka stroke

aka “Brain Attack”

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2
Q

CVA epidemiology:

A
  • 4th most common cause of death
  • 610k NEW, 185k recurrent
  • ~130k deaths/yr
  • 450,000 peramanent disabled
  • $38.6bill
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3
Q

1/3 survivors of stroke sustain second stroke w/in….

A

5 yrs

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4
Q

INVERSE relationship b/w age and male/female incidence ratio meaning….

A

Men @ younger age, then as both genders age it becomes a more even relation

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5
Q

Incidence of Stroke:

A
  • 2/3 in >65yo
  • risk doubles every 10 yrs after 55yo!!!
  • prevalence: people living w/== 6 million
    • ​31% req assist
    • 20% need help walking
    • 16% long-term care
    • 71% vocationally impaired after 7yrs
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6
Q

Racial disparity overall

A

Higher in white females, black m and f, m Mexican-Am.,

age adjusted==

  1. 6 per 1000 black males, 3.6 white males
  2. 9 black females, 2.3 white females
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7
Q

Classifcations of CVA: 3

A
  • Transient Ischemic Attack or TIA
  • Reversible Ischemic Neurologic Deficit or RIND
  • CVA
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8
Q

Usually resolves w/in 24hrs

stroke s/s

A

TIA

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9
Q

Resolution >24 hrs, BUT <3wks

*spontaneous recovery

*unlikely to see these

A

Reversible Ischemic Neurologic Deficits

RIND

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10
Q

AT LEAST 3wks to resolution

*NOTE: some deficits cannot be overcome than spontaneous recovery

A

CVA

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11
Q

RISK factors CVA: NON- Modifiable

A
  • gender
  • race
  • family Hx
  • prior CVA***
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12
Q

Risk Factors CVA: Modifiable

A
  • HTN
  • smoking
  • hypERcholesteremia
  • obesity
  • T2D
  • drug abuse—-amphets/stims
  • phys. inactivity ***
  • A-Fib
  • prior CVA—-shows other probs that exist
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13
Q

Male vs. Female Diff’s CVA

A
  • Males HIGHER risk
  • LESS exposure to modifiable risk factors==> Women
    • DEC smoking and ETOH (alcohol) abuse
  • *incidence becomes MORE EQUAL ~10yrs after menopause
    • ​*protective factor for females
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14
Q

Classifications of CVA: 2

A
  • Ischemic CVA: 87% —> lack of blood flow to area
    • ​1. Thrombotic–one spot
    • 2. Embolic–moves
  • Hemorrhage: 13% —> brain bleed/rupture​
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15
Q

Thrombotic Infarction or….

A

Narrowing of tissue=== blockage

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16
Q

Atherosclerotic plaques form in this type of CVA

A

Thrombotic infarction

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17
Q

Where do Thrombotic infarctions usually form?

Common where?

A
  • Form in arteries
    • ​common @ arterial bifurcation
      • ​turbulence==> blood clots
        • can be present W/OUT s/s!!!
          • aka may be present for long pds w/out symptomology
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18
Q

Thrombotic infarction clinical presentation

A
  • “Thrombus in evolution”
    • variable clinical present. w/ uneven progression
  • s/s stroke
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19
Q

What are some common risk factors assoc’d w/ Thrombotic Infarction?

A
  • HTN
  • DM
  • Cardiac/vascular disease
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20
Q

Embolic Infarction or…

A

Artery side

debris floating in circulatory system

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21
Q

A clot from elsewhere in the body travels to the brain

this describes what type of CVA?

A

Embolic Infarction

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22
Q

This type of infarction, that comes from elsewhere in the body, typically blocks a major artery

A

Embolic Infarction

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23
Q

An Embolic Infarction will come on slowly due to what?

A

Collateral blood supply not being established

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24
Q

The impact and symptoms of an Embolic Infarction

A

IMMEDIATE IMPACT bc NO collateral blood flow

Think of “shutting off faucet”

s/s vary if the clot moves

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25
Q

Risk factors assoc’d w/ Embolic infarction

A
  • Afib
    • stagnation of blood w/in atrium
    • clot can break loose into Carotid circ.
  • DVT
    • embolism can break loose from the DVT and NOT cause stroke
    • can lodge into pulmonary system
  • Bacterial infection
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26
Q

Hemorrhagic CVA or

A

Too much blood flow

Bleeding into brain tissue

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27
Q

Bleeding into the brain tissue OR

arterial blood flow INTO brain cavity

A

Hemorrhage

*exact mech. unknown*

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28
Q

There are 3 things Hemorrhage is most commonly due to:

A
  • Ruptured saccular aneurysm
    • ​aka blood breaks thru weakened wall
  • HTN
  • Arteriovenous malformation present @ birth
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29
Q

Mortality rate Ischemic CVA

pay attention to this!!!

A

8-12% w/in 1st month

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30
Q

Mortality rate Hemorrhagic CVA

pay attention to this

A

37-38% w/in 1st month

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31
Q

So… which type of CVA has a HIGHER mortality rate w/in the 1st month?

A

Hemorrhagic!!!

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32
Q

Overall death rate 50%

Stats….

A
  • 48.1 white males
  • 74.9 black males
  • 47.2 white females
  • 65.5 black females
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33
Q

When does survivability approach normal w/ CVA?

A

~18 mos post CVA

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34
Q

Deficits in thrombotic/embolic CVAs dictated by this?

A

Location of the blockage

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35
Q

W/ thrombic/embolic CVA…which artery is MOST freq involved?

A

MCA

*no more supply==no function

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36
Q

Characteristic s/s of Thrombic/Embolic CVA assoc’d w/…..

A

Occlusion of specific vessels

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37
Q

Ischemic Syndromes to Consider…..

List the major ones?

https://accessphysiotherapy.mhmedical.com/ViewLarge.aspx?figid=120048160&gbosContainerID=0&gbosid=0&groupID=0&sectionId=120048133

A
  • MCA
    • upper
    • lower
  • ACA
  • IC
  • PCA
    • prox/central
    • peripheral
  • Vertebral
  • Basilar
    • Cerebellar: SCA, AICA
    • COMPLETE
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38
Q

Thrombic/Embolic CVAs may be ______ or ______ meaning_______

A

Partial

Complete

*some areas may survive

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39
Q

More damage is found in thrombic/embolic CVAs with what type of lesions?

A

Central lesions/Prox lesions

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40
Q

Greater collateral circulation====>

A

LESS extensive damage

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41
Q

Ischemic CVAs are rarely fatal…. BUT

A

They damage tissue which can lead to inflammation

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42
Q

Other secondary effects of an Ischemic CVA

A

Cerebral edema

*potentially fatal

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43
Q

Explain the sequela of Cerebral edema…

A
  • Osmolality INCs w/ ischemia
    • ​moving fluid INTO brain to restore normal osmotic press.
      • ​happens shortly w/in occlusion
  • mins after occlusion peaks in 3-4 days
  • causes INC ICP==> severe 2* damage to Cb/BS
    • ​brain can herniate thru foramen magnum
  • monitor all BS signs
    • ​conjugate gaze palsy
    • ipsilateral CN5 or CN7 weakness
      • ​NON-norm BS function
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44
Q

In secondary effects w/ an Ischemic CVA….careful observation is req’d to monitor BS signs

what are some examples of these?

A
  1. Conjugate gaze palsy
  2. Ipsilateral CN 5 or CN 7 weakness

*BOTH are NON-normal BS function

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45
Q

Pharmacological tx’s used to manage inflammation in brain

A
  • Steroids
  • Corticosteroids
  • Dexamethasone
  • Prednisone
  • NSAIDs
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46
Q

Hemorrhagic CVAs are named in terms of what?

A

Location of the hematoma

ex’s include

Subdural, epidural, etc..

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47
Q

Hemorrhagic CVAs are further localized in relation to the __________

A
  • Tentorium Cerebelli—> thickening of dura mater separates CB from cerebellum
    • Supratentorial== ABOVE
    • Infratentorial== BELOW
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48
Q

ICH or….

A

Intracranial Hemorrhage

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49
Q

2 Subdivisions of a Supratentorial (above tentorium cerebelli) Hemorrhagic CVA

A
  1. Lobar
  2. Deep
50
Q

Supratentorial ICH: Lobar

A
  • involves the hemispheres
  • MOST often due to
    • Trauma
    • diasthesis (predisposition to hemorrhage)
    • hyperanticoagulation (over-treated)
    • amyloid angiopathy (weakening of blood vessel wall)
51
Q

Supratentorial ICH: Deep

A
  • Involves midbrain structures
    • ​putamen
    • thalamus
    • caudate
52
Q

Infratentorial ICH involves what?

53
Q

What is MOST FREQ’LY INVOLVED w/ ICH ?

A

BG

Thalamus

70%

54
Q

Three other structures involved w/ ICH other than most freq BG and thalamus?

A
  1. Cerebral white matter
  2. BS
  3. Cb
55
Q

Prognosis:

Recovery from ICH is BETTER why?

A

Lesions are characterized by compression, NOT tissue destruction

56
Q

Prognosis:

Damage occurring w/ ICH due to:

A

Rapid accumulation of blood, which displaces adjacent tissues

*best prognosis IF fluid reabsorbed BEFORE causing ischemia

57
Q

So… in general…

Prognosis for early survival is WORSE w/ hemorrhagic stroke vs. ischemic…..BUT……

A

For those who survive a Hemorrhagic stroke….

prognosis for recovery from the stroke is BETTER for someone w/ hemorrhagic stroke vs. ischemic

this is because of the MOI

basically….ischemic strokes lead to tissue destruction

58
Q

Lacunar CVA aka

A

several small strokes

*MOSTLY @ end point of the circ. system where arteris and venous capillary systems meet

59
Q

Lacunar strokes have characteristics of ________________

A

Ischemic AND hemorrhagic CVA

*MOSTLY ischemic character.

60
Q

Where do Lacunar strokes usually occur?

A

Deep white matter of the brain

61
Q

Lacunar CVA occurs in deep white matter of the brain

why here?

A

Tiny arterioles are vulnerable to hypertensive hemorrhage OR the vessel may thicken or thrombose

62
Q

3 general syndromes assoc’d w/ Lacunar CVA

A
  1. Pure motor
  2. Facial weakness
  3. Pure sensory
63
Q

Lacunar CVA: pure motor syndrome

A

PLIC

*paralysis on that side

64
Q

Lacunar CVA: Facial weakness

A

Internal Cap–ant. limb

65
Q

Lacunar CVA: pure sensory

A

Posterolateral thalamus

66
Q

Prognosis Lacunar CVA generally GOOD

A

Much smaller strokes

67
Q

Medical Tx of Ischemic CVA: blood pressure mgmt

A
  • Lowered if >180/120
    • limits hypoperfusion
    • NOTE: you may maintain this to limit the hypoperfusion which can make the stroke WORSE
    • BP can be kept HIGHER after an ischemic stroke
  • Horiz. pos for few days post CVA
    • ​limtd to bedside PROM
    • bedside mob. beneficial!!!
68
Q

Medical Tx Ischemic CVA: Antiocoagulation Tx

A
  • Typ first line of defense!!!
    • ​Coumadin (Warfarin) OR aspirin used preventatively (A-fib)
  • used acutely w/ ischemic stroke
    • DEC occurence
  • Danger of conversion to a hemorrhagic CVA…
    • ​blood flow stops—> aa clot can break down–> incd pressure
  • Prothrombin times closely monitored
69
Q

Medical Tx of Ischemic CVA: Thrombolytic agents

**recent

A
  • Streptokinase, TPA (Tissue Plasminogen Activator)
    • must be admin’d w/in 6hrs of onset
      • ​risk of conversion
    • breaks up thrombus to restore circ.
    • danger of conversion to hemorrhagic CVA
  • THIS IS WHY IT IS ALWAYS GOOD TO KNOW THE EXACT TIME OF THE STROKE!!!
70
Q

Medical TX Ischemic CVA: Nimodipine

what is this?

A
  • Ca+ channel antagonist
    • ​Neuroprotective
      • ​Given w/in 12hrs of ischemic CVA
        • DEC mortality and morbidity in 65+ yrs of age
          • reduces risk/disability amt
71
Q

Medical Tx Ischemic CVA: Corticosteroids

ex’s

A
  • Dexamethasone
    • DEC cerebral edema
    • treats post-event inflamm.
72
Q

Sx mgmt Ischemic CVA: Carotid Endarterectomy

A
  • **Tx of choice for people w/ TIA
    • ​narrow the lumen of carotid aa.
  • *** can dislodge a clot==> MORE Sx
73
Q

Sx mgmt Ischemic CVA: Posterior fossa decompression

*can be life saving!!!

A
  • Performed in case of potentially fatal BS compression
74
Q

Medical intervention for Ruptured Aneurysm

2 things we DEFINITELY want to do:

A
  1. DEC arterial blood pressure (can be KEPT LOW)
  2. Bed rest

**NOTE: if we LOWER arterial blood pressure==> LESS spewing of blood==LESS bleeding after hemorrhagic stroke

75
Q

Medical intervention for Ruptured Aneurysm: If pt is Comatose:

A
  1. treat shock
  2. maint. airway and O2 flow
  3. monitor blood gases, blood, CT, spinal fluid
  4. tube feeding
76
Q

What is the Tx of choice for ruptured aneurysm?

A

Surgery

*esp if not yet bursted

77
Q

In regards to sx interventions of ruptured aneurysms, pre-op mgmt of what is important?

A
  1. recurrent hemorrhage
  2. vasospasm
78
Q

Sx’s for Ruptured aneurysm can be: 3 things

A
  1. Embolization w/ glue or coils
  2. radiosurgery
  3. clipping of the neck of the aneurysm
79
Q

2* issues assoc’d w/ Hemorrhagic CVA

A
  • hypERtonia
  • seizures
  • Resp involvement
    • PNA
  • trauma
  • thrombophlebitis
  • pain
  • CRPS/RSD–> shoulder-hand syndrome
    • ​spares arm/forearm
80
Q

Initial improvements of hemorrhagic CVA include reduction of

A

cerebral edema===improved function

81
Q

initial improvements of hemorrhagic CVA include absorption of

A

damaged tissue

82
Q

initial improvements of hemorrhagic CVA include improved local

A

vascular flow==collateral circ.

83
Q

initial improvements of hemorrhagic CVA include damaged areas of brain are….

A

Circumvented

*new tracks–> neuroplasticity

84
Q

Functional Recovery of CVA: 2 Mechanisms

A
  1. Collateral sprouting
  2. Unmasking of neural pathways

*regen and reorganization*

85
Q

this mechanism is when nearby neurons go to damaged paths to rekindle lost connections

A

Collateral sprouting

86
Q

AKA silent synapses

presence of a pathway NOT recently used but now being utilized

A

Unmasking of neural paths.

*regen/reorganization

87
Q

Recovery process for CVA has 3 stages:

A
  1. Acute
  2. Active
  3. Adapt to personal environment
88
Q

Acute recovery stage

A

w/in first few weeks

act. lvl LOW

healing

medically stable===GOAL

89
Q

Active stage of recovery process

A

PT!!!

train to get back to PLOF

90
Q

Adaptation recovery process stage:

A

back home

learn to operate independently w/in environment

more well-defined

can and can’t do’s

91
Q

In terms of recovery w/ stroke…it was previously believed to be COMPLETE following 3-6mos

A

Accelerated recovery w/in first few wks-mos after then plataeus

THIS IS NOT TRUE

You CAN keep making improvements

current research—may cont. mos to yrs

person must have willingness to make change happen!!

92
Q

Predictors of recovery:

Motor recovery may continue after 6 mos

A
  • Functional status remains constant
  • 86% variance in 6month recovery PREDICTABLE @ 1 MONTH
    • ​Basically….we can predict how they’ll be @ 6mos at 1 month
93
Q

Predictor of recovery….

Initial return of UE when?

A
  • Initial return UE mvmt in first 2 wks
    • ​POSS. of full arm recovery and vice versa
94
Q

predictors of recovery:

absence of grip strength by….

A

24 days

*correlated to no recovery of arm function @ 3mos

95
Q

Predictors of recovery…

based on these things we can tell how recovery will go

A
  1. motor recovery may cont. after 6mos
  2. initial return of UE mvmt in first 2 wks
  3. absence of grip strength by 24 days
96
Q

Outcomes w/ CVA:

A
  • Framingham Heart Study
    • ​GOOD chance functional recovery
    • rehab IS effective
    • age NOT a factor in outcome
97
Q

Neurological findings CVA usually impacted by: 3 things

A
  1. size of lesion
  2. location of lesion (remember central/prox==worse)
  3. Amt collateral blood flow (more collateral==less severe)
98
Q

Neuro. Findings CVA: Unilateral deficits

cause?

A

Carotid vascular system

99
Q

Neuro findings CVA: Bilateral deficits

cause?

A

Vascular supply to the basilar system

100
Q

Organization of the brain

A

Homonculus!!!

101
Q

CNS response to injury

usually starts w/ initial__________

THEN evolves over time into _________

A
  • Initial flaccid paralysis/hypOreflexia
    • ​Neural Shock
  • THEN evolves into UMN syndrome
    • ​Spastic paralysis
    • hypERreflexia
102
Q

best imaging for strokes and why?

A

CT

bleeding

103
Q

S/S Cortical CVA (6)

A
  • Hemiplegia (1/2 body)
  • Sensory dysf.
  • Aphasias (lang. dysf.)
  • Dysarthria
    • trouble articulating words/mouth
  • visual field deficits
  • cognitive impairments
104
Q

Initial Dx CVA:

A
  • Hx of events?
    • timing is important!!!
    • remember they can admin drugs w/in 6hrs or 12hrs!!!
  • PMH?
  • Risk factors?
  • Dx tests
105
Q

Initial Dx of CVA: Dx Tests

A
  • Confirm CVA/kind
  • cause, location, extent
  • eval complications
  • assess risk of recurrent CVA
106
Q

GOLD STANDARD Dx test for CVA

*esp Hemorrhagic

A

CT of brain

107
Q

Other Dx tests for CVA

A
  1. ECG/ECHO
  2. coagulation studies
  3. Blood count
  4. Blood GLU
108
Q

More Dx Tests CVA

A
  • MRI—$$$
  • Cerebral arteriography
  • CSF exam–> lumbar puncture
  • Carotid bruits–> checks turbulent sounds
  • Cartoid doppler–> checks occlusion
109
Q

Carotid bruits vs. Carotid doppler

A

Bruits checks turbulent sounds

Doppler checks for occlusion

110
Q

Delivery of care post CVA comes down to these things :

A
  1. team mbrs
  2. types rehab settings
  3. considerations
  4. who makes decisions?

*Other medical team members involved as well!!!

111
Q

3 Screening methods for rehab:

A
  1. ID pts who will benefit from PT
  2. approp setting for after
  3. ID probs that need Tx
112
Q

Benefit inpatient rehab

A

specialty units

*stroke units

113
Q

Acute care:

A
  • coordinate services b/w team mbrs
  • diagnostic, acute mgmt, prevention + rehab services
  • Research:
    • ​reduced mortality
    • improved functional outcomes in specialized stroke units
114
Q

Acute Care priorities

A
  1. control life-threatening probs
  2. prevent recurrent stroke
  3. prevent complications
  4. mng. gen health
  5. mobilize + resume self-care
115
Q

Life threatening problems that occur Post-CVA

A
  • procedures to prevent recurrent stroke and maint. life
    • ​bed rest/monitor vitals/bed mobs
  • High BP: need to lower gradually if poss
    • risk of hypOperfusion w/ dec’d BP
    • Med. stable vs unstable—-> monitor this!!!
116
Q

Preventing Complications post-CVA

A
  • If Dysphagia… (swallow problem)
    • ​prevent aspiration (food down wrong pipe)
  • Maint. skin integrity
  • prevent falls
  • manage bladder function
117
Q

Early mobilization (by PT) for post-CVAs

what are some bennies???

A
  • Prevents DVT/decubitus ulcers (pressure sores)
  • Prevents contractures, PNA, atrophy/bone wasting
    • osteoporosis
118
Q

Early mobilization is GREAT, but what are some Precautions?

A
  • if coma/stupor
  • if progressing neuro signs—-getting worse
  • if unstable vitals
  • if severe orthostasis
119
Q

Pt Education involved w/ Post-CVA

A
  • Acute care process/med. mgmt/team
  • discharge plan?
  • effects and prognosis of CVA?
  • pot. complications?

MedCon Rehab II (5 decks)

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