CVA Flashcards
Definition of CVA
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
2 categories of CVA
- ischemic
- hypoxia or decreased oxygenation to t issue and results from poor blood supply - hemorrhagic
- abnormal bleeding from rupture of cerebral vessel
Thrombic Ischemic CVA
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
Embolic Ischemic CVA
- 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
ischemic penumbra
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
intracerebral hemorrhage
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
subarachnoid hemorrhage
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
arteriovenous malformation
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
transient ischemic attacks
“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
medical intervention
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
recovery from stroke
- 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
prevention of CVA
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
Anterior cerebral artery blood distribution
superior border of frontal and parietal lobes
anterior cerebral artery deficits
contralateral weakness and sensory loss primarily LE incontinence aphasia memory and behavioral deficits
middle cerebral artery blood distribution
surface of the cerebral hemispheres and the deep frontal and parietal lobes
middle cerebral artery deficits
contralateral sensory loss and weakness in the face and UE
less involvement of the LE
homoymous hemianopia–visual field cuts
vertebrobasilar artery blood distribution
brain stem and cerebellum
vertebrobasilar artery deficits
cranial nerve involvment
- diplopia
- dysphagia
- dysarthria
- deafness
- vertigo
- ataxia
- equilibrium disturbances
- headaches and dizziness
**locked in syndrome can occur with this
posterior cerebral artery blood distribution
occipital and temporal lobes, thalamus, and upper brain stem
posterior cerebral artery deficits
contralateral sensory loss, thalamic pain syndrome, hmonymous hemianopia, visual agnosia and cortical blindness
laclunar infarcts
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
parietal CVA
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
Thalamic Pain Syndrome
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
Pusher Syndrome
- 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
what do patients present with: Pusher Syndrome
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
flaccidity
no voluntary or reflex activity is present in the involved extremity
-initally a pt. will have flaccidity or low tone
Spasticity
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
synergy
group of muscles that work together to provide patterns of movement
7 stages of Brunnstrom
- flaccidity
- spasticity begins to develop
- spasticity increases and reaches peak
- spasticity begins to decline
- spasticity continues to decline
- spasticity essentially absent
- return to normal function
- flaccidity
no voluntary or reflex acitivity is present in involved extremity
- spasticity begins to develop
synergy patterns begin to devlop
some of the synergy patterns may appear with associated reactions
- spasticity increases and reaches its peak
movement synergies of the involved upper or lower extremity can be performed voluntarily
- spasticity begins to decrease
deviation from the movement synergies is possible
limited combinations of movement may be evident
- spasiticty continues to decrease
movement synergies are less dominant
more complex combinations of movement are possible
- spasticity essentially absent
isolated movements and combinations of movements are evident
coordination deficits may be present with rapid activities
7 return to normal function
return of fine motor skills
Brunnstrom stages of recover
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
Brunnstrom UE FLEX and EXT
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
Brunstromm synergy LE flex and ext
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
motor planning deficits
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
sensory impairments
- parietal lobe affected
- may lose tactile or proprioceptive capabilities
- partial impairments more common than total impairment
- may lose their sense of vertical
communication impairments
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
brocas aphasia
expressive disorder
wernickes aphasis
receptive disorder
global aphasia
both expressive and receptive
dysarthria
difficulty articulating words as a result of weakness and inability to control the muscles associated with speech production
emotional lability
difficulty controlling emotions
common in pts. with R. hemisphere infarcts
orofacial deficits
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
respiratory impairments
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%
visual deficits
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
reflex activity
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
bowel and bladder dysfunction
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
most common spinal reflexes seen with CVA pts
flexor withdrawl
cross extension
startle
grasp
FIM-functional independence measure
measures physical, psychological and social function
-specific items include: self-care, transfers, locomotion,communication and cognition
7pt scale:
-1 =total assist
7=independent
Fugl-Meyer Assessment
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
oral management of spasticity
baclofen, valium
- system, decrease CNS activity, promote lethargy
- dantrium is less likely to cause lethargy or cognitive changes
injections for spasticity
botulinum toxin type A-botox
injected directly into the spastic muscle, producing selective muscle weakness
can last 3-6 months
pump for spasticity
implanted into the abdominal cavity and a catheter administers the baclofen directly into the subarachnoid space and then acts directly onto muscle
Complex regional pain syndrome CRPS
result from Upper Motor Neuron injury
characterized by pain, autonomic nervous system signs and symptoms, edema, movement disorders, weakness and atrophy
Stage 1 of CRPS
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
Stage 2 of CRPS
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
Stage 3 of CRPS
begins 6-12 months after onset and may last years
S&S:
-irreversible
-atrophic changes to skin as well as contractures
treatment of CRPS
based on prevention and encouragement of active functional use of hand
-elevation, compression, loading the limb through WB and contrast baths
what causes increase risk of thrombophlebitis
decreased effciency of the calf muscle pump
acute care and PT
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
cardiopulmonary retraining
work on diaphragmatic strengthening and thoracic expansion w. inhalation
positioning a patient
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
neurodevelopmental treatment approach NDT
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
NDT treatment goals
head and trunk control midline orientation pts. ability to shift weight over BOS static and dynamic balance distal control of extremities
NDT handling
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
NDT principles of guiding or placing -8
visual observation tactile observation or feel use of key points of control open handed approach move slowly preperation give "feel" for movement communication
normal alignment of trunk and limbs SEATED
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
normal STANDING position
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
Rolling supine to prone
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
Supine to Sit
cervical spine: flexion Clavicle:retraction Scap: protraction abdominal mus: concentric contraction thoracic spine: flexion Lumbar Spine: flexion w/ posterior pelvic tilt hip: flexion
Sit to stand
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
Facilitation of lumbar exentsion
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
Facilitation of thoracic extension
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
Neck and Head control facilitation
use your back hand and arm to facilitate cervical extension
-use front hand to support patients jaw and facilitate cervical extension/retraction
dominant synergy component following CVA-UE
shoulder adduction
elbow flexion
forearm pronation
wrist and finger flexion
Dominant synergy component following CVA-LE
hip flexion and adduction
knee extension
ankle plantar flexion
raimiste’s phenomenon:
-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
souque’s Phenomenon
stim: flexion/abduction of involved UE above 90
Response: extension of the thumb or fingers
Brunnstrom stages 1-3 goals UE
- maintain ROM
- develop tension
- develop voluntary control within synergies
- -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
Brunnstrom stages 4-6 treatment UE
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
what do retinal and optic never fibers on right side of each eye see
left side and vice versa
superior retinal and optic never fibers on the ipper part of each eye see what?
lower part of the visual field and the inferior retinal and optic fibers see upper part of visual field
nasal fibers on right eye side see?
far right part of the visual field cross over to the left side of the brain
what do right temporal fibers do
see far left part of visual field but does not cross over to left side of the brain
what happens when a stroke occurs at the optic chiasm?
causes loss of the right visual field in right eye and left visual field in left eye
what happens if a stroke occurs to the right side of the brain past the optic chiasm
loss of the left visual field of each eye
what happen if a stroke occurs to the left side of the brain past the optic chaism
loss of right visual field of each eye
Brunnstrom’s UE synergy
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
Brunnstrom’s LE synergy
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
