COMPS:CVA Part I: Vascular Disorders in the CNS EXAM 1 Flashcards
(120 cards)
1
Q
What is CVA?
A
Sudden onset of focal neurologic deficit resulting from cerebrovascular dis.
aka stroke
aka “Brain Attack”
2
Q
CVA epidemiology:
A
- 4th most common cause of death
- 610k NEW, 185k recurrent
- ~130k deaths/yr
- 450,000 peramanent disabled
- $38.6bill
3
Q
1/3 survivors of stroke sustain second stroke w/in….
A
5 yrs
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
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
6
Q
Racial disparity overall
A
Higher in white females, black m and f, m Mexican-Am.,
age adjusted==
- 6 per 1000 black males, 3.6 white males
- 9 black females, 2.3 white females
7
Q
Classifcations of CVA: 3
A
- Transient Ischemic Attack or TIA
- Reversible Ischemic Neurologic Deficit or RIND
- CVA
8
Q
Usually resolves w/in 24hrs
stroke s/s
A
TIA
9
Q
Resolution >24 hrs, BUT <3wks
*spontaneous recovery
*unlikely to see these
A
Reversible Ischemic Neurologic Deficits
RIND
10
Q
AT LEAST 3wks to resolution
*NOTE: some deficits cannot be overcome than spontaneous recovery
A
CVA
11
Q
RISK factors CVA: NON- Modifiable
A
- gender
- race
- family Hx
- prior CVA***
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
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
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
15
Q
Thrombotic Infarction or….
A
Narrowing of tissue=== blockage
16
Q
Atherosclerotic plaques form in this type of CVA
A
Thrombotic infarction
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
- can be present W/OUT s/s!!!
-
turbulence==> blood clots
-
common @ arterial bifurcation
18
Q
Thrombotic infarction clinical presentation
A
- “Thrombus in evolution”
- variable clinical present. w/ uneven progression
- s/s stroke
19
Q
What are some common risk factors assoc’d w/ Thrombotic Infarction?
A
- HTN
- DM
- Cardiac/vascular disease
20
Q
Embolic Infarction or…
A
Artery side
debris floating in circulatory system
21
Q
A clot from elsewhere in the body travels to the brain
this describes what type of CVA?
A
Embolic Infarction
22
Q
This type of infarction, that comes from elsewhere in the body, typically blocks a major artery
A
Embolic Infarction
23
Q
An Embolic Infarction will come on slowly due to what?
A
Collateral blood supply not being established
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
25
Risk factors assoc'd w/ Embolic infarction
* 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
26
Hemorrhagic CVA or
Too much blood flow
## Footnote
**Bleeding into brain tissue**
27
Bleeding into the brain tissue OR
## Footnote
**arterial blood flow INTO brain cavity**
Hemorrhage
\***exact mech. unknown\***
28
There are 3 things Hemorrhage is **most commonly due to:**
* Ruptured **saccular aneurysm**
* **aka blood breaks thru weakened wall**
* HTN
* Arteriovenous malformation present @ birth
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Mortality rate **Ischemic CVA**
## Footnote
**pay attention to this!!!**
8-12% w/in 1st month
30
Mortality rate **Hemorrhagic CVA**
**pay attention to this**
37-38% w/in 1st month
31
So... which type of CVA has a HIGHER mortality rate **w/in the 1st month?**
Hemorrhagic!!!
32
Overall death rate 50%
Stats....
* 48.1 white males
* **74.9 black males**
* 47.2 white females
* **65.5 black females**
33
When does **survivability approach normal w/ CVA?**
~18 mos post CVA
34
Deficits in **thrombotic/embolic CVAs** dictated by this?
Location of the blockage
35
W/ thrombic/embolic CVA...which artery is MOST freq involved?
MCA
\*no more supply==no function
36
Characteristic s/s of Thrombic/Embolic CVA assoc'd w/.....
Occlusion of **specific vessels**
37
Ischemic Syndromes to Consider.....
List the major ones?
https://accessphysiotherapy.mhmedical.com/ViewLarge.aspx?figid=120048160&gbosContainerID=0&gbosid=0&groupID=0§ionId=120048133
* MCA
* upper
* lower
* ACA
* IC
* PCA
* prox/central
* peripheral
* Vertebral
* Basilar
* Cerebellar: SCA, AICA
* COMPLETE
38
Thrombic/Embolic CVAs may be ______ or ______ meaning\_\_\_\_\_\_\_
Partial
Complete
\*some areas may survive
39
More damage is found in thrombic/embolic CVAs with what type of lesions?
Central lesions/Prox lesions
40
Greater collateral circulation====\>
LESS extensive damage
41
Ischemic CVAs are rarely fatal.... BUT
They damage tissue which can lead to **inflammation**
42
Other secondary effects of an Ischemic CVA
Cerebral edema
\*potentially fatal
43
Explain the sequela of **Cerebral edema...**
* **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**
44
In secondary effects w/ an Ischemic CVA....careful observation is req'd to monitor BS signs
what are some examples of these?
1. Conjugate gaze palsy
2. Ipsilateral CN 5 or CN 7 weakness
\*BOTH are NON-normal BS function
45
Pharmacological tx's used to manage **inflammation in brain**
* Steroids
* Corticosteroids
* Dexamethasone
* Prednisone
* NSAIDs
46
Hemorrhagic CVAs are named in terms of what?
Location of the **hematoma**
## Footnote
**ex's include**
**Subdural, epidural, etc..**
47
Hemorrhagic CVAs are further **localized in relation to the \_\_\_\_\_\_\_\_\_\_**
* Tentorium Cerebelli---\> thickening of **dura mater** separates CB from cerebellum
* **Supratentorial== ABOVE**
* **Infratentorial== BELOW**
48
ICH or....
Intracranial Hemorrhage
49
2 Subdivisions of a **Supratentorial (above tentorium cerebelli) Hemorrhagic CVA**
1. Lobar
2. Deep
50
Supratentorial ICH: **Lobar**
* involves the **hemispheres**
* **MOST often due to**
* Trauma
* diasthesis (predisposition to hemorrhage)
* hyperanticoagulation (over-treated)
* amyloid angiopathy (weakening of blood vessel wall)
51
Supratentorial ICH: **Deep**
* Involves **midbrain structures**
* **putamen**
* **thalamus**
* **caudate**
52
Infratentorial ICH involves what?
BS or Cb
53
What is MOST FREQ'LY INVOLVED w/ ICH ?
BG
Thalamus
70%
54
Three other structures involved w/ ICH other than most freq BG and thalamus?
1. Cerebral white matter
2. BS
3. Cb
55
Prognosis:
Recovery from ICH is BETTER why?
Lesions are characterized by **compression, NOT tissue destruction**
56
Prognosis:
Damage occurring w/ ICH due to:
Rapid accumulation of blood, which displaces adjacent tissues
\***best prognosis IF fluid reabsorbed BEFORE causing ischemia**
57
So... in general...
Prognosis for **early survival** is WORSE w/ hemorrhagic stroke vs. ischemic.....BUT......
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
Lacunar CVA aka
several small strokes
\*MOSTLY @ end point of the circ. system where **arteris and venous capillary systems meet**
59
Lacunar strokes have characteristics of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Ischemic AND hemorrhagic CVA
\*MOSTLY ischemic character.
60
Where do Lacunar strokes usually occur?
Deep white matter of the brain
61
Lacunar CVA occurs in deep white matter of the brain
why here?
**Tiny arterioles** are vulnerable to **hypertensive hemorrhage** OR the **vessel may thicken or thrombose**
62
3 general syndromes assoc'd w/ Lacunar CVA
1. Pure motor
2. Facial weakness
3. Pure sensory
63
Lacunar CVA: **pure motor syndrome**
PLIC
\*paralysis on that side
64
Lacunar CVA: **Facial weakness**
Internal Cap--ant. limb
65
Lacunar CVA: **pure sensory**
Posterolateral thalamus
66
Prognosis Lacunar CVA generally GOOD
Much smaller strokes
67
Medical Tx of Ischemic CVA: **blood pressure mgmt**
* 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
Medical Tx Ischemic CVA: **Antiocoagulation Tx**
* **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
Medical Tx of Ischemic CVA: **Thrombolytic agents**
## Footnote
**\*\*recent**
* 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
Medical TX Ischemic CVA: **Nimodipine**
## Footnote
**what is this?**
* 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
Medical Tx Ischemic CVA: **Corticosteroids**
## Footnote
**ex's**
* Dexamethasone
* DEC cerebral edema
* treats **post-event inflamm.**
72
Sx mgmt Ischemic CVA: **Carotid Endarterectomy**
* \*\*Tx of choice for people w/ **TIA**
* **narrow the lumen of carotid aa.**
* **\*\*\* can dislodge a clot==\> MORE Sx**
73
Sx mgmt Ischemic CVA: **Posterior fossa decompression**
## Footnote
**\*can be life saving!!!**
* Performed in case **of potentially fatal BS compression**
74
Medical intervention for **Ruptured Aneurysm**
**2 things we DEFINITELY want to do:**
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
Medical intervention for Ruptured Aneurysm: **If pt is Comatose:**
1. treat shock
2. maint. airway and O2 flow
3. monitor blood gases, blood, CT, spinal fluid
4. tube feeding
76
What is the Tx of choice for **ruptured aneurysm?**
Surgery
\*esp if not yet bursted
77
In regards to sx interventions of ruptured aneurysms, **pre-op mgmt of what is important?**
1. recurrent hemorrhage
2. vasospasm
78
Sx's for Ruptured aneurysm can be: 3 things
1. **Embolization** w/ glue or coils
2. radiosurgery
3. clipping of the **neck** of the aneurysm
79
2\* issues assoc'd w/ Hemorrhagic CVA
* hypERtonia
* seizures
* Resp involvement
* PNA
* trauma
* thrombophlebitis
* pain
* CRPS/RSD--\> **shoulder-hand syndrome**
* **spares arm/forearm**
80
Initial improvements of hemorrhagic CVA include **reduction of**
cerebral edema===improved function
81
initial improvements of hemorrhagic CVA include **absorption of**
damaged tissue
82
initial improvements of hemorrhagic CVA include **improved local**
vascular flow==collateral circ.
83
initial improvements of hemorrhagic CVA include **damaged areas of brain are....**
Circumvented
\*new tracks--\> **neuroplasticity**
84
Functional Recovery of CVA: 2 Mechanisms
1. Collateral sprouting
2. Unmasking of neural pathways
\*regen and reorganization\*
85
this mechanism is when **nearby neurons go to damaged paths to rekindle lost connections**
Collateral sprouting
86
AKA **silent synapses**
## Footnote
**presence of a pathway NOT recently used but now being utilized**
Unmasking of neural paths.
\*regen/reorganization
87
Recovery process for CVA has 3 stages:
1. Acute
2. Active
3. Adapt to personal environment
88
**Acute** recovery stage
w/in first few weeks
act. lvl LOW
healing
medically stable===GOAL
89
**Active** stage of recovery process
PT!!!
train to get back to PLOF
90
**Adaptation** recovery process stage:
back home
learn to operate independently w/in environment
more well-defined
can and can't do's
91
In terms of recovery w/ stroke...**it was previously believed to be COMPLETE following 3-6mos**
Accelerated recovery w/in first few wks-mos after then **plataeus**
## Footnote
**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
Predictors of recovery:
Motor recovery may **continue after 6 mos**
* 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
Predictor of recovery....
Initial return of UE when?
* Initial return UE mvmt in **first 2 wks**
* ****POSS. of full arm recovery and vice versa
94
predictors of recovery:
absence of grip strength by....
24 days
\*correlated to no recovery of arm function @ 3mos
95
Predictors of recovery...
based on these things we can tell how recovery will go
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
Outcomes w/ CVA:
* **Framingham Heart Study**
* ****GOOD chance functional recovery
* rehab IS effective
* age NOT a factor in outcome
97
Neurological findings CVA usually impacted by: 3 things
1. size of lesion
2. location of lesion (remember **central/prox==worse)**
3. Amt collateral blood flow (**more collateral==less severe)**
98
Neuro. Findings CVA: **Unilateral deficits**
## Footnote
**cause?**
Carotid vascular system
99
Neuro findings CVA: **Bilateral deficits**
## Footnote
**cause?**
Vascular supply to the **basilar system**
100
Organization of the brain
Homonculus!!!
101
**CNS response to injury**
usually starts w/ initial\_\_\_\_\_\_\_\_\_\_
THEN evolves over time into \_\_\_\_\_\_\_\_\_
* **Initial flaccid paralysis/hypOreflexia**
* **Neural Shock**
* **THEN evolves into UMN syndrome**
* **Spastic paralysis**
* **hypERreflexia**
102
best imaging for strokes and why?
CT
bleeding
103
S/S **Cortical CVA (6)**
* Hemiplegia (1/2 body)
* Sensory dysf.
* Aphasias (lang. dysf.)
* Dysarthria
* trouble articulating words/mouth
* visual field deficits
* cognitive impairments
104
Initial Dx CVA:
* Hx of events?
* timing is important!!!
* remember they can admin drugs w/in 6hrs or 12hrs!!!
* PMH?
* Risk factors?
* Dx tests
105
Initial Dx of CVA: **Dx Tests**
* Confirm CVA/kind
* cause, location, extent
* eval complications
* **assess risk of recurrent CVA**
106
GOLD STANDARD Dx test for CVA
\*esp **Hemorrhagic**
CT of brain
107
Other Dx tests for CVA
1. ECG/ECHO
2. coagulation studies
3. Blood count
4. Blood GLU
108
More Dx Tests CVA
* MRI---$$$
* Cerebral arteriography
* CSF exam--\> lumbar puncture
* Carotid bruits--\> **checks turbulent sounds**
* Cartoid doppler--\> **checks occlusion**
109
Carotid bruits vs. Carotid doppler
Bruits checks **turbulent sounds**
Doppler checks for **occlusion**
110
Delivery of care post CVA comes down to these things :
1. team mbrs
2. types rehab settings
3. considerations
4. who makes decisions?
\***Other medical team members involved as well!!!**
111
3 Screening methods for rehab:
1. ID pts who will benefit from PT
2. approp setting for after
3. ID probs that need Tx
112
Benefit inpatient rehab
specialty units
\*stroke units
113
Acute care:
* coordinate services b/w team mbrs
* diagnostic, acute mgmt, prevention + rehab services
* **Research:**
* ****reduced mortality
* improved **functional outcomes in specialized stroke units**
114
Acute Care priorities
1. control life-threatening probs
2. prevent recurrent stroke
3. prevent complications
4. mng. gen health
5. mobilize + resume self-care
115
Life threatening problems that occur **Post-CVA**
* 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
Preventing Complications post-CVA
* If **Dysphagia... (swallow problem)**
* **prevent aspiration (food down wrong pipe)**
* Maint. skin integrity
* prevent **falls**
* **manage bladder function**
117
Early mobilization (by PT) for post-CVAs
what are some bennies???
* **Prevents** DVT/decubitus ulcers (pressure sores)
* **Prevents** contractures, PNA, atrophy/bone wasting
* osteoporosis
118
Early mobilization is GREAT, but what are some **Precautions?**
* if **coma/stupor**
* if **progressing neuro signs----getting worse**
* if **unstable vitals**
* if **severe orthostasis**
119
Pt Education involved w/ Post-CVA
* Acute care process/med. mgmt/team
* discharge plan?
* effects and prognosis of CVA?
* pot. complications?
120
