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Neuro > CVA > Flashcards

CVA Flashcards

1
Q

Definition of CVA

A

the sudden onset of neurologic signs and symptoms resulting from a disturbance of blood supply to the brain

  • may lead to temporary or permanent loss of function as a result of injury to the cerebral tissue
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2
Q

2 categories of CVA

A
  1. ischemic
    - hypoxia or decreased oxygenation to t issue and results from poor blood supply
  2. hemorrhagic
    - abnormal bleeding from rupture of cerebral vessel
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3
Q

Thrombic Ischemic CVA

A

consequence of atherosclerosis

  • lumen of artery decreases in size as plaque is deposited within vessel walls
  • blood flow through vessel is reduced and limits O2 into cerebral tissue
  • *if totally occluded=tissue will die
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4
Q

Embolic Ischemic CVA

A
  • cardiovascular disease
    ex: afib, MI or valvular disease
  • blood clot breaks away from intima or inner lining of artery and carried to brain

**if cerebral blood flow is less than 20mL/100mg per minute there is a a disruption in neurologic functioning

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5
Q

ischemic penumbra

A

transitional zone surrounding the infarcted cerebral tissue
-neurons in this area are vulnerable to injury because cerebral blood flow is decreased and is unable to support neuronal function

  • increase in glutamate levels causes an increase in calcium levels leading to catabolic enzymes and free radicals to be activated
  • leads to additional damage of cellular structures and more damage besides original site
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6
Q

intracerebral hemorrhage

A

cerebrum itself
low incidence in people less than 45 y/o

common causes:

  • vessel malformation
  • hanges in integrity of cerebral vessels from hypertension and aging
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7
Q

subarachnoid hemorrhage

A

consequence of bleeding into the subarachnoid space
primary cause is aneurysms
**berry aneurysms- congenital defect of cerebral artery in which the vessel is abnormally dilated at bifurcation

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8
Q

arteriovenous malformation

A

congenital anomalies that affect circulation in brain

  • arteries and veins communicate directly w/o conjoining capillary bed
  • blood vessels become dilated and form masses within the brain
  • causes a weakened vessel wall and causes rupture

**mostly in older generations

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9
Q

transient ischemic attacks

A

“mini strokes”
blood supply to the brain is temporarily interupted
pt. complains of neurologic dysfunction
–loss of moto,sensory or speech function
-deficits only last about 24 hours

pt. does not experience any residual brain damage or neurologic dysfunction
* recurrent TIA indicate thrombotic disease and will most likely suffer stroke

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10
Q

medical intervention

A

MD completes physical exam
Neuroimaging is performed to determine whether the CVA is a result of hemorragic or ischemic injury
-regulate BP, cerebral perfusion and intracranial pressure

**tPA: clot busting drug- if given within 3 hours of embolicc CVA can decrease effects of neurologic damageq

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11
Q

recovery from stroke

A
  • most significant recovery occurs within first 3 months after injury–after this recovery comes slower
  • movement patterns may improve for up to 2-3 years after initial injury
  • pt. who receives rehab for approximately 28 days after their stroke exhibit the greatest improvements inwalking, transfers, self-care and sphincter control
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12
Q

prevention of CVA

A

2 primary preventable risk factors

  • hypertension and heart disease
  • HTN increases risk of CVA by 4-6x

other causes: DM, cigarette smoking, hx prior CVA or TIA, race, family history,alcohol, physical inactivity,obesity, age

-education to inform society of symptoms

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13
Q

Anterior cerebral artery blood distribution

A

superior border of frontal and parietal lobes

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14
Q

anterior cerebral artery deficits

A 
contralateral weakness and sensory loss
primarily LE 
incontinence 
aphasia
memory and behavioral deficits
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15
Q

middle cerebral artery blood distribution

A

surface of the cerebral hemispheres and the deep frontal and parietal lobes

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16
Q

middle cerebral artery deficits

A

contralateral sensory loss and weakness in the face and UE
less involvement of the LE
homoymous hemianopia–visual field cuts

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17
Q

vertebrobasilar artery blood distribution

A

brain stem and cerebellum

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18
Q

vertebrobasilar artery deficits

A

cranial nerve involvment

  • diplopia
  • dysphagia
  • dysarthria
  • deafness
  • vertigo
  • ataxia
  • equilibrium disturbances
  • headaches and dizziness

**locked in syndrome can occur with this

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19
Q

posterior cerebral artery blood distribution

A

occipital and temporal lobes, thalamus, and upper brain stem

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20
Q

posterior cerebral artery deficits

A

contralateral sensory loss, thalamic pain syndrome, hmonymous hemianopia, visual agnosia and cortical blindness

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21
Q

laclunar infarcts

A

deep regions of the brain-internal capsule, basal ganglia and pons

common in individuals with HTN and DM

clinical findings: contralateral weakness, sensory loss, ataxia and dysarthria

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22
Q

parietal CVA

A

clinical findings

  • inattention or neglect for involved side of body
  • impaired perception of vertical, visual, spatial and topographic relationships , motor perservation
  • *one of the parietal lobes affected
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23
Q

Thalamic Pain Syndrome

A

occurs after infarction or hemorrhage in the lateral thalamus, posterior limb of the internal capsule or the parietal lobe

  • pt. experiences intolerable burning pain and sensory perservation
  • sensation of stimulus remains long after the stimulus has been removed or terminated
  • pt. percieves the sensation as noxious and exaggerated
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24
Q

Pusher Syndrome

A
  • right or left posterolateral thalamus
  • actively push or lean toward their hemiplegic side and are at increased risk of balance deficits
  • passively correct posture with resistance
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25
Q

what do patients present with: Pusher Syndrome

A

cervical rotation and lateral trunk flexion

absent or significantly impaired tactile and kinesthetic awareness
visual deficits
truncal asymmetries
increased WB on the left during sitting activities
resistance in response to attempts to equalize WB
difficulties w/ transfers as the pt. pushes backward and away with right(uninvolved) extremities

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26
Q

flaccidity

A

no voluntary or reflex activity is present in the involved extremity

-initally a pt. will have flaccidity or low tone

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27
Q

Spasticity

A

motor disorder characterized by exaggerated DTR and increased muscle tone

  • increased resistance to passive stretching
  • hypertonicity occurs from abnormal processing of the afferent input after the stimulus reaches the spinal cord
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28
Q

synergy

A

group of muscles that work together to provide patterns of movement

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29
Q

7 stages of Brunnstrom

A
  1. flaccidity
  2. spasticity begins to develop
  3. spasticity increases and reaches peak
  4. spasticity begins to decline
  5. spasticity continues to decline
  6. spasticity essentially absent
  7. return to normal function
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30
Q
  1. flaccidity
A

no voluntary or reflex acitivity is present in involved extremity

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31
Q
  1. spasticity begins to develop
A

synergy patterns begin to devlop

some of the synergy patterns may appear with associated reactions

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32
Q
  1. spasticity increases and reaches its peak
A

movement synergies of the involved upper or lower extremity can be performed voluntarily

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33
Q
  1. spasticity begins to decrease
A

deviation from the movement synergies is possible

limited combinations of movement may be evident

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34
Q
  1. spasiticty continues to decrease
A

movement synergies are less dominant

more complex combinations of movement are possible

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35
Q
  1. spasticity essentially absent
A

isolated movements and combinations of movements are evident

coordination deficits may be present with rapid activities

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36
Q

7 return to normal function

A

return of fine motor skills

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37
Q

Brunnstrom stages of recover

A

pts. can plataue at any stage

each patient progresses through stages at different rates

pt. passes through all of the stages and that no stage is skipped but may not get through all stages

may not start at stage 1 or end at stage 7

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38
Q

Brunnstrom UE FLEX and EXT

A 
flex:
scap retraction or elevation
shoulder ER 
shoulder abd 90
elbow flex
forearm supination
wrist and finger flexion
ext:
scap protraction
shoulder IR
shoulder ADD 
full elbow ext
forearm prontation
wrist ext and finger flexion
39
Q

Brunstromm synergy LE flex and ext

A 
Flex:
hip flex, abd, er
knee flex 90
ankle DF and inversion
toe ext
Ext:
hip ext, add, IR 
knee ext
ankle PF and inversion
toe flexion
40
Q

motor planning deficits

A

most frequently in pts. with left hemisphere involvement

APRAXIA: pts. can exhibit difficulty in performing purposeful movements, although no sensory or motor impairments

  • -unable to remember the steps to achieve this movement goal
  • affects ADLs
41
Q

sensory impairments

A
  • parietal lobe affected
  • may lose tactile or proprioceptive capabilities
  • partial impairments more common than total impairment
  • may lose their sense of vertical
42
Q

communication impairments

A

infarcts in the frontal and temporal lobes lead to communication deficits

APHASIA: acquired communication disorder casued by brain damage and is characterized by impairment of language comprehension, oral epression and use of symbols to communicate ideas

43
Q

brocas aphasia

A

expressive disorder

44
Q

wernickes aphasis

A

receptive disorder

45
Q

global aphasia

A

both expressive and receptive

46
Q

dysarthria

A

difficulty articulating words as a result of weakness and inability to control the muscles associated with speech production

47
Q

emotional lability

A

difficulty controlling emotions

common in pts. with R. hemisphere infarcts

48
Q

orofacial deficits

A

brain stem or midbrain affected
inability to smile frown or initate other expressions
ability to use body language affected
inadequate lip closure
difficulty swallowing - Dysphagia
poor coordination btw. eating and breathing-aspiration issues

49
Q

respiratory impairments

A

lung expansion is decreased because of a lack of control of the muscles of respiration-diaphragm

hemiparesis of the diaphragm or external in
intercostal muscles may be apparent and can affect individuals ability to expand lungs
-decrease in vital capacity–by 30-40%

50
Q

visual deficits

A

most common form of sensory loss with hemipelgia

lesion affects the eye, optic radiation or visual cortex

poor eyesight, diplopia, homonymous hemianopia, damage to visual cortex or retinal damage

51
Q

reflex activity

A

primitive spinal an brain stem reflexes may re-appear following a stroke

  • spinal level reflexes result in overt movement
  • DTR’s may be altered
  • brainstem reflexes
  • associated reflexes

**need to educate pts. families that these are involuntary

52
Q

bowel and bladder dysfunction

A

incontinence may be seen initially secondary to muscle paralysis or inadequate sensory stimulation to the bladder
-early WB activities through either bridging or standing activities can assist the pt. with regaining bladder control

53
Q

most common spinal reflexes seen with CVA pts

A

flexor withdrawl
cross extension
startle
grasp

54
Q

FIM-functional independence measure

A

measures physical, psychological and social function
-specific items include: self-care, transfers, locomotion,communication and cognition
7pt scale:
-1 =total assist
7=independent

55
Q

Fugl-Meyer Assessment

A

used to quantify motor functioning following a stroke

  • can be used to analyze the efficacy of treatment interventions provided
  • evaluates PROM, light tough, proprioception, motor function, balance
56
Q

oral management of spasticity

A

baclofen, valium

  • system, decrease CNS activity, promote lethargy
  • dantrium is less likely to cause lethargy or cognitive changes
57
Q

injections for spasticity

A

botulinum toxin type A-botox
injected directly into the spastic muscle, producing selective muscle weakness
can last 3-6 months

58
Q

pump for spasticity

A

implanted into the abdominal cavity and a catheter administers the baclofen directly into the subarachnoid space and then acts directly onto muscle

59
Q

Complex regional pain syndrome CRPS

A

result from Upper Motor Neuron injury

characterized by pain, autonomic nervous system signs and symptoms, edema, movement disorders, weakness and atrophy

60
Q

Stage 1 of CRPS

A 
begins immediately after the injury
can last 3-6 months 
S&S: 
-burning and aching pain
-edema
-warm
-red skin
-accelerated hair and nail growth
61
Q

Stage 2 of CRPS

A 
onset btw. 3-6 months
duration of 6 months
S&S:
-continuous aching and burning pain
-edema leading to joint stiffness
-thin, brittle nails 
-thin and cool skin
-osteoporosis
62
Q

Stage 3 of CRPS

A

begins 6-12 months after onset and may last years
S&S:
-irreversible
-atrophic changes to skin as well as contractures

63
Q

treatment of CRPS

A

based on prevention and encouragement of active functional use of hand
-elevation, compression, loading the limb through WB and contrast baths

64
Q

what causes increase risk of thrombophlebitis

A

decreased effciency of the calf muscle pump

65
Q

acute care and PT

A

2-4 days in hospital
PTA may or may not be involved in acute care
once pt. medically stable-> positoning, pt. education, skin checks, bed mobility, transfer training

66
Q

cardiopulmonary retraining

A

work on diaphragmatic strengthening and thoracic expansion w. inhalation

67
Q

positioning a patient

A

position patient out of characteristic synergy patterns assist in stimulating motor function, increases sensory awareness, improves respiratory and oromotor function, assists w. maintaining normal ROM in the neck, trunk and extremities

  • minimizes risk of deformities and potential pressure sores
  • pt. should be alternately placed on back, involved and uninvolved sides
68
Q

neurodevelopmental treatment approach NDT

A

developed by Bobaths

common therapeutic intervention for pts. with hemiplegia

  • initially worked with children with CP
  • -movements were elicited by peripheral stimuli and primitive reflexes that resulted in abnormal movements

goal of PT was to facilitate normal motor patterns

  • treatment approach emphasis’ pts. postural reflex mechanism
  • intact postural reflex mechanism implies that the pt. has normal muscle tone and is able to grade and regulate movements and after injury to the CNS would be impaired

Goal of treatment shifted: facilitation of normal postural control mechanism

69
Q

NDT treatment goals

A 
head and trunk control
midline orientation
pts. ability to shift weight over BOS
static and dynamic balance
distal control of extremities
70
Q

NDT handling

A

control and guide the patient’s motor performance through the use of sensory facilitation applied at key points of control
-influencing a patient’s tone and abnormal movement patterns by using key points of control

  • proximal key points such as the shoulder and pelvic girdles are the most important points from which to influence postural alignment and tone
  • use ofm ore distal key points affect movements of the trunk
  • once tone is more normal, the therapist superimposes normal movements and postures within context of the functional activity
  • therapist withdraw assistance as pt. learns to control movements
71
Q

NDT principles of guiding or placing -8

A 
visual observation
tactile observation or feel
use of key points of control
open handed approach
move slowly
preperation
give "feel" for movement
communication
72
Q

normal alignment of trunk and limbs SEATED

A 
weight evenly distributed over ischial tuberosities
normal curves of spine
neck at midline over shoulders
shoulders aligned over pelvis
knees and feet inline with hip 
knee slightly lower than hip
forearm pronated
hand lower than elbow
neutral wrist
stable scap against thorax and neutral
73
Q

normal STANDING position

A 
neutral pelvis
normal spine curves
neck and head in midline
shoulder aligned over pelvis
knees and feet in line with hip
knees exteneded but not locked
stable scap 
foot WB on entire plantar surface
74
Q

Rolling supine to prone

A 
head flexion
cervical spine-flexion
clavicle-retraction
scap-protraction
UE: flexion and adduction across midline
thoracic spine:flexion
Lumbar-flexion
LE: flexion and adduction across midline
75
Q

Supine to Sit

A 
cervical spine: flexion
Clavicle:retraction
Scap: protraction
abdominal mus: concentric contraction
thoracic spine: flexion
Lumbar Spine: flexion w/ posterior pelvic tilt
hip: flexion
76
Q

Sit to stand

A

cervical spine: extension
clavical: protraction
Scapula: retraction
UE: shoulder forward
thoracic spine: extension
abdominal muscle: inital concentric then eccentric
lumbar spine: inital flexion followed with extension
pelvis: ant. and superior translation –anterior pelvic tilt
LE: extension of hips and knees

77
Q

Facilitation of lumbar exentsion

A

concentric lumbar extensors and isometric abdominals

KEY POINT:

  • trunk extensors
  • symmetrical and directly on the paravertebrals
  • above the sacrum in the lumbar region
  • forward and up

KEY POINT:

  • clavicle, sternum and true ribs
  • on clavicles or slightly below the clavicles
  • symmetrical on clavicles to protract and on sternum and ribs to elevate
  • movement is up and back
78
Q

Facilitation of thoracic extension

A

concentric thoracic extensors
isometric abdominals

TRUNK EXTENSORS:

  • symmetrical and directly on the paravertebrals and ribs
  • below inferior angles of the scapula and in the thoracic region
  • movement is down and towards ischial tuberosities

Clavicle, Sternum and true ribs:
-on clavicles or slightly below clavicles
-symmetrical on clavicles to protract and sternum and ribs to elevate
movement is up and back

79
Q

Neck and Head control facilitation

A

use your back hand and arm to facilitate cervical extension

-use front hand to support patients jaw and facilitate cervical extension/retraction

80
Q

dominant synergy component following CVA-UE

A

shoulder adduction
elbow flexion
forearm pronation
wrist and finger flexion

81
Q

Dominant synergy component following CVA-LE

A

hip flexion and adduction
knee extension
ankle plantar flexion

82
Q

raimiste’s phenomenon:

A

-supine–> resisted hip adduction of the noninvolved
LE will facilitate hip adduction of the involved LE
-heavily resisted hip abduction of noninvolved LE may faciliate hip abduction of involved LE

83
Q

souque’s Phenomenon

A

stim: flexion/abduction of involved UE above 90
Response: extension of the thumb or fingers

84
Q

Brunnstrom stages 1-3 goals UE

A
  • maintain ROM
  • develop tension
  • develop voluntary control within synergies
  1. -bed positioning to favor the weaker synergy
    self PROM, AAROM
    -use reflexes and associated reactions along with manual resistance to facilitate muslce tone

2&3:

  • muscle contraction progression
  • focus on flexion synergy or extension synergy
85
Q

Brunnstrom stages 4-6 treatment UE

A

goal: voluntary movement outside of flexion synergy
D/C use of reflexes and reactions as facilitation techniques
begin use of proprioceptive facilitation of whole movement patterns
vary positions
coordination of smooth and increase muscle tension
increase speed and reciprocal motion to break up synergy

86
Q

what do retinal and optic never fibers on right side of each eye see

A

left side and vice versa

87
Q

superior retinal and optic never fibers on the ipper part of each eye see what?

A

lower part of the visual field and the inferior retinal and optic fibers see upper part of visual field

88
Q

nasal fibers on right eye side see?

A

far right part of the visual field cross over to the left side of the brain

89
Q

what do right temporal fibers do

A

see far left part of visual field but does not cross over to left side of the brain

90
Q

what happens when a stroke occurs at the optic chiasm?

A

causes loss of the right visual field in right eye and left visual field in left eye

91
Q

what happens if a stroke occurs to the right side of the brain past the optic chiasm

A

loss of the left visual field of each eye

92
Q

what happen if a stroke occurs to the left side of the brain past the optic chaism

A

loss of right visual field of each eye

93
Q

Brunnstrom’s UE synergy

A 
Flex:
scap elevation or retraction
shoulder abduction or ER
elbow flexion
forearm supination
wrist and finger flexion
Ext:
scap protraction
shoulder adduction or IR
forearm pronation
wrist finger flexion
94
Q

Brunnstrom’s LE synergy

A 
Flex:
hip flexion. abduction and ER
knee flexion
DF and inversion
toe ext

EXT:

Hip ext adduction and IR
knee extension
PF and inversion
toe flexion

Neuro (11 decks)

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