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OCTH 1031 > FINAL EXAM - CVA > Flashcards

FINAL EXAM - CVA Flashcards

1
Q

TIA (5)

A
  1. damage may be non-existent
  2. symptoms more focal in nature
  3. recover rapidly without permanent deficits
  4. typically last 5-20mins - severe symptoms
  5. recover with in 24 hrs.
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2
Q

TIA caused by

A

blockage, decrease period of time. Clot sits briefly, gets jostled, and moves pass

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3
Q

TIA Risk Factors Untreatable (4)

A

advanced age
african american
male
Family hx of stroke

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4
Q

TIA Risk factors (10)

A 
HTN
Atrial fib.
valve abnormalities
structural abnormalities
myocardial disease and peripheral artery disease
diabetes
Cholesterol
obesity
smoking
oral contraceptives
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5
Q

Risk factors for a TIA are the same causes as an

A

MI - cardiac output is not smooth and damages blood cells which causes them to begin to clot in circulation

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6
Q

Signs of an acute CVA -5

A
  1. sudden weakness or numbness
  2. sudden dimness or loss of vision
  3. sudden difficulty speaking or understanding speech
  4. sudden severe headache
  5. facial droop or tongue misalignment
    * Call 911 Treatment is based on time*
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7
Q

What does FAST stand for

A

Face -drooping
Arm - can they raise their arm and keep them symetrical
Speech - can person speak and understand speech
Time - Call 911

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8
Q

Diagnosis of CVA

A
  1. examination - severity; focal vs global
  2. Hx of event - sudden onset vs gradual progression
  3. Imaging - CT; MRI/MRA
  4. Ischemic (blockage) vs hemorrhagic (bleeding) - each managed differently
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9
Q

Ischemic CVA treatment

A
  1. w/in 4hrs clot busting drugs are administered - save brain tissue
  2. Resotre blood flow
  3. asprin
  4. intravenous TPA
  5. INtra-arterial TPA
  6. Mechanical Clot removal
  7. Carotid angioplasy and stenting
  8. Carotid endarterectomy - open vessel, scrape plaque out - can cause stroke (done to decrease severity b/c it’s inevitable)
  9. Maintain perfusion via higher BP (keep blood flowing)
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10
Q

Management of Ischemic - Cerebral Edema

A

larger ischemic strokes associated with cerebral edema which can increase intracranial pressure (ICP)

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11
Q

Signs of high ICP(4)

A

vomiting without nausea (no warning)
ocular palsies (one eye turns in)
altered consciousness
pupillary dilation

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12
Q

Symptoms of high ICP (2)

A
  1. headache

2. low back pain

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13
Q

Characteristics of CVA syndromes

A
  1. named according to the artery that feed the area
  2. can be parital or complete
  3. more proximal clot, closer to the heart, the greater the damage
  4. if the area has secondary supply, damage is less
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14
Q

shoulder hand syndrome

A

sensation perceived as pain with non noxious stimuli - treatable, usually goes away

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15
Q

Internal Carotid Artery - Most Common (3)

A

Clinical picture depends on the cause of ischemia (varies)
Lesions involving both MCA and ACA
Cortex supplied by MCA is most affected - UE

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16
Q

Middle Cerebral Artery (MCA) Syndrome 1

A

Contralateral hemiplegia - Damaged Right side, impaired Left side and vice versa

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17
Q

Dominant MCA CVA impact on body structures and functions

A
  1. Speech and language impairments
  2. timid
  3. hyper-aware of impairments
  4. poor processing verbal cues
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18
Q

Non-Dominant MCA CVA impact on body structures and functions

A
  1. spatial-perceptual impairments & sensory
  2. impulsive
  3. decreased insight/judgement
  4. poor processing visual cues
  5. Unaware of what they are capable of actually doing
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19
Q

Pusher syndrome (vertical orientation)

A

shift wt onto impaired side causing resistance, guard differently, difficult on therapists body

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20
Q

Anterior Cerebral Artery (ACA) Syndrome- 5

A
  1. less common
  2. has good collateral flow so damage is minimal
  3. contralateral hemiparesis and sensory loss
  4. LE more involved
  5. Abulia: delay in verbal and motor response , SLOW
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21
Q

Posterior Cerebral Artery (PCA) syndrome - 5

* Patients generally don’t survive

A
  1. prox. occulded abnormal sensation of pain, temp, proprioception
  2. completely occluded at origin- contralateral ataxia (loss of control of bodily movement)
  3. Memory issues
  4. Agnosia - decreased awareness
  5. occuleded at periphery-cortical blindness - eye fn normally, no recognition
  6. occuleded at stem-coma, decerbrate rigidity
22
Q

Posterior Cerebral Artery Syndrome - Weber’s Syndrome

*Very Rare

A

Contralateral hemiplegia & parkinsonism - not progressive live parkinson’s and may recover

23
Q

Posterior Cerebral Artery Syndrome - Claude’s Syndrome

*Very Rare

A

contralateral hemiplegia & ataxia (loss of full control of bodily movements)

24
Q

Posterior Cerebral Artery Syndrome - Hemiballismus

*Very Rare

A

flailing of extremities; not good at grading - Sit to supine; fly away from you

25
Q

Superior Cerebellar Artery (4)

A

ipsilateral
ataxia=oscillations - disoriented movement
dysmetria=inaccuracy
contralateral loss of pain/temp

26
Q

Basilar Artery - affects brainstem and pons - 5

A 
"locked in" syndrome 
unable to speak
can not move
does have eye movement
able to receive and understand speech
27
Q

Anterior Inferior Cerebellar Artery - 8

A
  1. ipsil. deafness
  2. facial weakness
  3. verigo
  4. nausea
  5. vomiting
  6. nystagmus -eyes make repetitive, uncontrolled movements, often resulting in reduced vision
  7. ataxia
  8. contralateral loss of pain/temp
28
Q

Vertebral and Post. Inf. Cerebellar Artery Syndrome -2

A
  1. vestibular

2. ataxia

29
Q

Vertebral and Post. Inf. Cerebellar Artery Syndrome: Wallenberg’s Syndrome (3)

A
  1. vertigo and nausea
  2. ipsilateral ataxia
  3. dysphagias
30
Q

Intracerebral Hemorrhage (ICH) (4)

A
  1. bleeding from an arterial source into the brain NOT caused by trauma
  2. Typically due to anomaly of blood vessel or changes caused by HTN
  3. HTN single most important modifiable risk factor
  4. Sx’s occur gradually
31
Q

Symptoms of ICH (3)

A
  1. headache
  2. Seizure
  3. Altered Consciousness
32
Q

ICH treatment (5)

A
  1. Surgically repair vessel by clipping or coiling
  2. AVM (genetic anomally) removal
  3. Discontinue blood thinners
  4. Lower BP aggressively (less blood until arteries repair)
  5. monitor for and treat cerebral edema
33
Q

ICH Syndromes - Putamen (most common) -3

A

contralateral sensorimotor deficit
pupillary abnormalities
visual field loss

34
Q

ICH Syndromes - Thalamus (4)

A
  1. sensory loss
  2. some motor deficits
  3. oculomotor dysfunction
  4. in dominant hemisphere - apraxia - can’t produce voluntary movement on demand
35
Q

ICH Syndromes - Cerebellum (3)

A
  1. ataxia
  2. nausea
  3. dizziness
36
Q

ICH Syndromes - Pons (all motor tracts go through the pons) 4

A
  1. coma
  2. quadperesis
  3. unreactive pupils
  4. contralateral sensory and motor symptoms
37
Q

Subdural Hemorrhage (4)

A
  1. tearing of bridging veins between the brain surface and dural sinus
  2. accumulation of blood in dural space
  3. leads to compression of brain tissue
  4. spontaneous
38
Q

Common Clinical Manifestation of Stroke: sensory and or motor changes (6)

A
  1. hemiparesis = weakness
  2. hemiplegia = paralysis
  3. spasticity = hyperactive stretch reflex
  4. flaccidity
  5. synergies - abnormal co activation of muscle
39
Q

hypertonicity

A

spasticity

40
Q

Common Clinical Manifestation of Stroke: Flaccidity (4)

A
  1. immediately after a CVA (Stage 1)
  2. complete absence of muscle tone
  3. most common in UE
  4. Longer pt is flacid the less recovery
  5. be aware of dislocation
41
Q

Common Clinical Manifestation of Stroke: Synergies

A
  1. abnormal co activation of muscle groups related to active movement
  2. proximal loading/activation
  3. only seen when in AROM
    Ex. shoulder loaded in flexion = contraction of elbow, wrist - All muscles fire at the same time = synergistic
42
Q

UE Flexion Synery in MCA stroke presents as

A 
elevation
retraction
abduction
elbow flexion
supination
radial deviation
wrist and finger flexion
43
Q

LE extension Synergy in ACA stroke presnets as

A 
hip extension
adduction
IR
knee extension
planter flexion
inversion
toe flexion
44
Q

Brunnstrom Stages of Recovery (7)

A

Stage I- Flaccidity - no resting muscle tone early after stroke, usually resolves
Stage II - Spasticity and Synergies emerge
Stage III - voluntary control of synergies; spasticity increases
Stage IV - movements in synergy will dominate; movements out of synergy emerge, spasticity decreases
Stage V - Dominance of synergies decrease, isolated movement increases, spasticity decreases
Stage VI - no spasticity, isolated movement dominates, coordination emerges
Stage VII - Normal

45
Q

CVA impact on body str. and fn : perceptual impairments - 3

A
  1. visual inattention/neglect
  2. sensory inattention/neglect (oral commands opposite ear)
  3. motor neglect
46
Q

CVA impact on body str. and fn : Coordination deficits -3

A
  1. ataxia
  2. dysmetria
  3. dysdiadodyskinesia (rapid change of movement)
47
Q

CVA impact on body str. and fn : Visual system - 2

A
  1. hemianopsia - peripheral on one side nasal block on other side
  2. visual manifestation can prove where occlusion was in visual tract
48
Q

CVA impact on body str. and fn : Mental functions (2)

A
  1. depression - pt will fn at a low level, needs to be managed for success
  2. Cognitive behavioral impairments: impulsivity (SAFETY), anosognosia (lack of awareness), decreased drive
49
Q

CVA impact on body str. and fn : Voice and Speech -4

A
  1. Communication deficits (dominant)
  2. Dysarthria (motor)
  3. Aphasia (cognitive) - receptive, expressive, global
  4. Swallowing impairments - dysphagia
50
Q

Secondary complications of Stroke -6

A
  1. deconditioning with increases the risk for CAD and DM
  2. Loss of ROM = contractures
  3. Incontinence = UTI
  4. Pneumonia
  5. DVT = Pulmonary emboli
  6. Pressure ulcers
51
Q

Functional Prognosis after CVA -6

A
  1. younger better than older
  2. married better than non-married
  3. employed better than not employed
  4. dominant better than non-dominant
  5. cognitively intact better than impaired
  6. DM, CAD, HTN

OCTH 1031 (22 decks)

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