Neurosensory: Stroke and Brain Tumors
Part #1 Stroke (Brain attack/CVA)
A. Pathophysiology/etiology
Normal brain physiology and stroke
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Ranks 3rd as cause death
Blood supply to one
hemisphere is typically
blocked, hence terms
right & left stroke
Functioning brain
depends on continuous
blood supply for oxygen
and glucose & remove
end products metabolism
Risk factors for stroke
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Hypertension
Heart disease
Atherosclerosis
Diabetes mellitus
Medications: birth
control pills, substance
abuse- cocaine, heroin
Sedentary life style
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Obesity
High cholesterol diet
Smoking
Stress
Age > 65 yrs
Sickle cell disease
Brain dysfunction &
length of time without blood supply
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Brain function depends on collateral circulation and
amount of cerebral edema
TIA- neuro deficits last < 24 hrs
RIND- neuro deficits last > 24 hrs but reverse not greater
than 21 days
CVA- irreversible brain damage with residual neuro
deficits
Stroke-in-evolution- progressive neuro deficits
developing over hours or days. Usual cause thrombosis
Disease process
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Ischemic stroke
 Occlusion of artery
 Generally do not
lose consciousness
 Better prognosis
than hemorrhagic
 May have TIA’s
before
 Thrombosis or
embolism
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Hemorrhagic stroke
 Bleed occurs with
activity
 Usually rapid onset
 Generally loss of
consciousness
 Poorer prognosis
 Intracranial or
subarachnoid
Ischemic stroke
Thrombosis
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Most common cause of a stroke
Cause- narrowing of artery from atherosclerotic plaques
Blood is blocked to part of brain that the artery supplies
Often occurs in older individuals who are at rest/sleeping
Tend to form in large arteries that bifurcate, internal
carotid artery common site
Can begin as TIA’s, present as stroke-in-evolution, or
have completed stroke outright
Ischemic stroke
Embolism
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Caused by: clotted blood from other arteries in
the body (heart during atrial fibrillation) fat,
bacteria (endocarditis) or air
Emboli circulate until reach an artery in brain that
is too narrow to pass through
Usually awake with rapid onset
Extent damage is less severe and recovery faster
than other strokes
Hemorrhagic stroke
Intracranial hemorrhage (ICH)
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Caused by ruptured artery in the brain
Bleeding varies in size from petechial to massive, edema
occurs around the bleed
Blood may form hematoma or be diffuse within the brain
Usually occurs rapidly with the deep arteries
Hypertension is main cause
Most common cause of death due to a stroke
Have more extensive residual deficits and slower recovery
than other causes of stroke
Hemorrhagic
Subarchnoid hemorrhage (SAH)
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Caused by bleeding into subarchnoid space from
 Extension of a intracranial hemorrhage
 Aneurysm
 AV malformation
B. Common manifestations/complicationsby body systems
By artery affected by occlusion or hemorrhage
Internal carotid
Middle cerebral artery
Middle cerebral artery
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Contralateral motor loss
in the arm and the lower
part of the face (central
facial palsy)
Contralateral sensory loss
in face and arm
Homonymous
hemianopsia
Left middlecommunication deficits
Right- spatial/perceptual
Vertebral artery
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Pain or numbness of involved side
Vertigo
Contralateral ataxia
Dysphagia, dysarthria
Cranial nerve dysfunctions
Motor deficits
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Motor nerve pathways cross in the medulla
(brainstem) Prefix hem- used to describe
Amount of motor involvement varies from
weakness (-paresis) to paralysis (-plegia).
End paralysis can be flaccid or spastic depending
on amount of damage to the motor strip
Initially flaccid and if progress spastic in 6-8
weeks.
Motor deficits
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Characteristic body
posture
Motor deficits
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Facial palsy(central/UMN) where
lower part face
affected
Bells palsy (LMN- 7th
CN) where the whole
side of face affected
Elimination Deficits
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Partial loss of sensation (hemi) can affect
perception of need to eliminate bowel/bladder
Cognitive problems may affect the social aspect
of elimination
Level of consciousness, immobility, dehydration,
diet changes
Sensory-perceptual deficits
Lack of sensation/propriocetion
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Lack of sensation (hemi)- inability to
perceive/interpret pain, touch, pressure( post
central gyrus)
Lack of/decrease in proprioception or the
inability to know where body part is without
having to look at it; body’s ‘position sense’
Sensory-perceptual deficits
Visual field deficits
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Disruption anywhere
along the pathway
Homonymous
hemianopsia- most
common. Loss of half
of visual field in each
eye. Can’t see toward
the same side as the
paralysis
Sensory-perceptual deficits:
Agnosia
Apraxia
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Inability of the senses
to perceive stimuli
that were previously
familiar.
May be any of the
senses and varying
degrees
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Inability to carry out
purposeful task in the
absence of paralysis
or the individual
carries out task
inappropriately
Sensory-perceptual deficits
Neglect syndrome (unilateral neglect)
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Attention disorder in which individual ignores
affected part of the body,
Cannot integrate or use perceptions from affected
side
More common in right CVA’s
Communication Deficits
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Motor, speech, language, memory, reasoning,
emotions can be affected
Dominant hemisphere for the brain centers is left
in most individuals
Global (mixed) aphasia- both expressive and
receptive aphasia
Dysarthria- difficulty with articulation or
muscular control for speech. Sound like have
mashed potatoes in their mouth
Communication Deficits
Broca’s and Wernicke’s aphasia
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Broca’s, expressive or
nonfluent aphasia
where unable to
express- understands
Wernicke’s, receptive,
fluent aphasia where
unable to understand
Broca speech area
Wernicke speech area
Communication Deficits
Normal process recovery
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Begin with one word speech- swearing,
‘ouch’
Progress to sayings – days of week, social
speech, singing
Volitional- normal speech
Recovery may stop at any point
Cognitive and behavioral deficits
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Change level consciousness- confusion to coma
Emotional liability
Loss of self control, decrease tolerance for stress
Intellectual changes resulting in memory loss,
decreased attention span, poor judgment, inability
to think abstractly
C. Therapeutic interventions
Diagnostic tests
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CT/MRI- bleeding, edema, tissue necrosis,
shifting intracranial contents
Arteriogram- abnormal structures; vasospasm,
stemosis
PET- cerebral blood flow and metabolic activity
Transcranial ultrasound doppler velocity of blood
flow, degree of occlusion
Lumbar puncture- obtain CSF, bleeding
Therapeutic interventions
Rehabilitation
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Outpatient or in-house
Physical therapy
Occupational therapy
Speech therapy
Cognitive therapy
Therapeutic interventions
Thrombolitic stroke
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Medication
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Thrombolitic agents to dissolve clot- 3 hrs!!!
Anticoagulants to prevent further extension
Antithrombolitic inhibit platelet phase of clot
formation
Anticonvulsants
Surgical
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Endarterectomy
Angioplasty, carotid artery stenting
Bypass superficial temporal to middle cerebral
Therapeutic interventions
Embolic/intracranial stroke
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Embolic stroke
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Medications: If blood clot- anticoagulants,
thrombolitic agents, antiarrhythmics; If bacterialantibiotics
Intracranial hemorrhage (ICH) stroke
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Bedrest
Medication- antihypertensives to normal BP
Surgery- remove hematoma if possible
D. Nursing assessment specific to stroke
Health history & physical exam
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Health history
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Risk factors; when symptoms began; describe
symptoms; current medications (legal/illegal); other
health problems
Physical exam
Vital signs; neuro vital signs (LOC, pupils, motor,
sensory); continued next slides
Nsg assess- neuro deficits common in stroke
Motor
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Movement, strength (with & without resistance),
symmetry of all extremities
Pronator drift- detects weakness of upper
extremity. Hold arms, palms up in front with eyes
closed- should be able to hold for 30 seconds.
Weakness pronates and drifts downward
Use similar techniques used to assess motor SCImotor pathways affected begin motor strip brain
Test facial movement- smile/frown test for Bell’s
(7th CN) and central facial (motor strip)
Nursing assess- neuro deficits common stroke
Motor
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EOM’s- head still, follow
your finger in all
quadrants. Eyes should
move together (conjugate
gauze) Abnormal:
dysconjugate gauze;
nystagmus; 3rd nerve
palsy (occulomotor); 6th
nerve palsy (abducens)
Nursing assess neuro deficits: Motor
3rd nerve palsy
6th nerve palsy
Nursing assess- neuro deficits common stroke
Motor
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Assess ability to void and
move bowels
Assess communication
ability
Assess cognitive and
behavioral aspects
Nursing assess-neuro deficits common stroke
Sensory deficits
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Superficial sensation
With paperclip and
eyes closed alternate
sharp and dull ends
Reference is the
sensory strip on the
parietal side
Nursing assess- neuro deficits common stroke
Sensory- visual field loss
common- homonymous hemianopia
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Patients’ head in still
position & cover one
eye- test one at time
Move your wiggling
finger into the
patients field of
vision- in all 6
quadrants
State when 1st sees
Nursing assess- neuro deficits common stroke
Sensory
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Proprioceptionposition sense
With eyes closed and
hoding the toe on the
sides, move toe up &
down (not touching
the other toes), stopthen ask is toe up or
down
Nursing assess- neuro deficits common stroke
Sensory-perceptual
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Visual agnosia: individual becomes lost on unit;
cannot read sign/symbols; difficulty estimating
distance (spills food); cannot find objects; does
not recognize faces on photo or own image
Auditory agnosia: ind appears bewildered by
sounds; and does not respond approp- phone
ringing; can’t identify sound as running water
Tactile agnosia- with eyes closed can’t recognize
familiar objects- comb, pencil; unaware location;
diff positioning self- slouches to one side
Nsg assess- neuro deficits common stroke
Sensory-perceptual
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Apraxia- stares at food tray unaware of how to
get food to mouth; combs hair with toothbrush;
puts shirt on legs
Unilateral neglect; ignores paralyzed arm or leg;
may claim it is not theirs; bumps into wall as
going down hall; unaware of objects place on
paralyzed side
Nursing assessment specific to stroke
National institute health (NIH) stroke scale
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An assessment scale to reflect the degree of
neurologic dysfunction specifically for stroke
A high score correlates with a large stroke
Based on level of consciousness, gaze, visual,
facial palsy, motor, ataxia, sensory, language,
dysarthria, and extinction and inattention
(neglect)
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http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf
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E. Nursing problems/interventions
1. Ineffective tissue perfusion (cerebral)
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Monitor resp status; provide O2; suction needed
Monitor neuro, specifically increasing neuro
deficits, seizures, and ICP; HOB 30 degrees
Monitor cardiac status, esp dysrhythmias
If individual unconscious- coma care
Nursing problems/interventions
2. Impaired physical mobility
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Encourage active (when possible)& passive ROM
Change position every 2 hrs, esp if comatose
Monitor/prevent thrombophlebitis
Work with Rehab team
Arm sling- used to prevent subluxation of the
shoulder from a paralyzed arm when OOB
Splints- hand/foot to prevent contractures; set up
schedule- on 2 hrs off 2 hrs- use ROM
Nursing problems/interventions
3. Self-care deficit
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Eourage use of paralyzed extremity
Teach dsg tech- affected arm in clothing first
Work with rehab team regarding ADL’s, use of
assistive devices, plans for progress, home care
Allow time and encouragement ADL’s
Assess both physical cognitive ability ADL
With agnosia encourage pt use other senses
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With apraxia- break complex tasks down into
simple steps; have a single item out at one time;
use colored labels on clothes or velcro on one
sleeve; allow time; encourage independence
Perseveration- may have to tell person to stop
action that they are perseverating about or may
have to physically stop them
Nursing problems/interventions
4. Impaired verbal communication
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Assess speaking, writing, gestures, understanding
Support speech therapist plan
Support guidelines as LeMone p. 1317
Swearing may be first sign of return of speech,
not directed at you or family
Nursing problems/interventions
5.Impaired urinary elimination/riskcontipation
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Set up schedule to void
Support guidelines LeMone 1317
Nursing problems/interventions
6. Impaired swallowing
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Dysphagia- difficulty swallowing LeMone 1317
Provide safety when eating
Occupation therapy and /or speech therapy can
evaluate the individuals ability to get food to
mouth and to swallow
Swallow studies
Nursing problems/interventions
7. Home care
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May return home, go to a rehabilitation center
(in-house or outpatient) or may be placed in a
nursing home
Home evaluation by rehabilitation team
Encourage self-care as much as possible with
family involvement
Community resources should e evaluated for each
ind with stroke, including family support
Subarachnoid hemorrhage
A. Pathophysiology/etiology
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Subarachnoid hemorrhage- aneurysm or A-V
malformation
Usually occur in younger adults 30-60 than other
strokes
SAH- Pathophysiology/etiology
Aneurysm
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Occur at bifurcations,
braches of carotids &
vertebrobascular
arteries
85% base brain in
anterior circulation
Caused by trauma,
congential,
arteriosclerosis
SAH Pathophysiology/etiology
A-V malformation
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Congential abnormal
joining of arteries to
veins in the brain.
As pressures changes
occur becomes
tangled collection of
dilated vessels.
B. SAH- Common manifestation/complication
Aneurysm
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Aneurysms are graded 0-V on the Hunt/Hess
scale; higher the number, poorer chance survival.
Based on LOC & quality of cerebral function
Aneurysm are usually asymptomatic until rupture
Ruptured- sudden explosive headache; loss of
consciousness; N & V; nuchal rigidity (stiff neck)
and photophobia from meningeal irritation;
cranial nerve deficits
SAH- Common manifestation/complications
A-V malformation
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Ischemia symptoms-seizures and interference
with normal function of those brain cells
As pressures changes occur the malformation
ruptures and get bleed symptoms (SAH)
SAH- Common manifestation/complications
Major complications
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Rebleed due to
reabsorption of the clot
that is stopping the bleed
Vasospasms due to
irritation of the blood
vessels
Hydrocephalus from
blockage of normal
absorption of CSF
C. Therapeutic interventions SAH
Diagnostic tests
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CT/MRI
Angiogram- outline the
blood vessels
Lumbar puncture- blood
in CSF
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Risk of bleeding
Herniation with LP
Therapeutic interventions SAH
Treatments
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Aneurysm precautions- decrease external/internal stimuli
Medications
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Aide with aneurysm precautions- stool softners, antinausea,etc
To prevent rebleed/lysis of clot- Ammicar
To prevent vasospasms- Nimodipine
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Before OR- Ca channel blocker- Nimodipine
After OR-triple H- vasodilators (Isuprel); induced arterial
hypertension (Dopamine); hypervolemic hemodilution (Albumin)
Prophylactic antiepileptic- Cerebex/Dilantin
Therapeutic interventions SAH
Treatments
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Surgical intervention
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Aneurysm-clip
aneurysm, wrap with
muslin or muscle, insert
endovascular coils. If
unstable may delay OR
A-V mal- embolization;
ligation of feeders, laser
surgery to remove
malformation
Therapeutic intervention SAH
Treatments
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Gamma Knife- radiation
to reduce size of A-V
malformation> over
Cyberknife below
LeMone Blackboard site Care Plan:
Elizabeth with a Subarachnoid Hemorrhage
http://wps.prenhall.com/chet_lemone_medi
calsurg_3/0,7859,757263-,00.html
Nursing Care Plan: A Client with a Stroke
LeMone p. 1319
http://wps.prenhall.com/wps/media/objects/
737/755395/stroke.pdf
Added Critical thinking questions: Nursing
Care Plan: A Client with a Stroke p. 1319
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1.What could be the possible cause of Orville’s ‘spells’
the week before his stroke?
2. Are Orville’s symptoms consistent with right middle
cerebral artery thrombolitic stroke? Describe.
3. Had Orville gotten to the ER in 3 hrs, what could they
have done that may have completely reversed the stroke?
4. Is the fact that Orville is left handed significant?
5. Which side will Orville not be able to see toward due to
his homonymous hemianopia? How do you test?
6. Does he have neglect syndrome?
7. What type of aphasia does Orville have?