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
Superior Cerebellar Artery (4)
ipsilateral ataxia=oscillations - disoriented movement dysmetria=inaccuracy contralateral loss of pain/temp
26
Basilar Artery - affects brainstem and pons - 5
``` "locked in" syndrome unable to speak can not move does have eye movement able to receive and understand speech ```
27
Anterior Inferior Cerebellar Artery - 8
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
Vertebral and Post. Inf. Cerebellar Artery Syndrome -2
1. vestibular | 2. ataxia
29
Vertebral and Post. Inf. Cerebellar Artery Syndrome: Wallenberg's Syndrome (3)
1. vertigo and nausea 2. ipsilateral ataxia 3. dysphagias
30
Intracerebral Hemorrhage (ICH) (4)
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
Symptoms of ICH (3)
1. headache 2. Seizure 3. Altered Consciousness
32
ICH treatment (5)
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
ICH Syndromes - Putamen (most common) -3
contralateral sensorimotor deficit pupillary abnormalities visual field loss
34
ICH Syndromes - Thalamus (4)
1. sensory loss 2. some motor deficits 3. oculomotor dysfunction 4. in dominant hemisphere - apraxia - can't produce voluntary movement on demand
35
ICH Syndromes - Cerebellum (3)
1. ataxia 2. nausea 3. dizziness
36
ICH Syndromes - Pons (all motor tracts go through the pons) 4
1. coma 2. quadperesis 3. unreactive pupils 4. contralateral sensory and motor symptoms
37
Subdural Hemorrhage (4)
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
Common Clinical Manifestation of Stroke: sensory and or motor changes (6)
1. hemiparesis = weakness 2. hemiplegia = paralysis 3. spasticity = hyperactive stretch reflex 4. flaccidity 5. synergies - abnormal co activation of muscle
39
hypertonicity
spasticity
40
Common Clinical Manifestation of Stroke: Flaccidity (4)
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
Common Clinical Manifestation of Stroke: Synergies
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
UE Flexion Synery in MCA stroke presents as
``` elevation retraction abduction elbow flexion supination radial deviation wrist and finger flexion ```
43
LE extension Synergy in ACA stroke presnets as
``` hip extension adduction IR knee extension planter flexion inversion toe flexion ```
44
Brunnstrom Stages of Recovery (7)
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
CVA impact on body str. and fn : perceptual impairments - 3
1. visual inattention/neglect 2. sensory inattention/neglect (oral commands opposite ear) 3. motor neglect
46
CVA impact on body str. and fn : Coordination deficits -3
1. ataxia 2. dysmetria 3. dysdiadodyskinesia (rapid change of movement)
47
CVA impact on body str. and fn : Visual system - 2
1. hemianopsia - peripheral on one side nasal block on other side 2. visual manifestation can prove where occlusion was in visual tract
48
CVA impact on body str. and fn : Mental functions (2)
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
CVA impact on body str. and fn : Voice and Speech -4
1. Communication deficits (dominant) 2. Dysarthria (motor) 3. Aphasia (cognitive) - receptive, expressive, global 4. Swallowing impairments - dysphagia
50
Secondary complications of Stroke -6
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
Functional Prognosis after CVA -6
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