Download - Neurology Nursing Study Guide
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Disease Brief
pathophysiology
Clinical
manifestation
/Assessment
Diagnostic
tests &
findings
Medical
management
Nursing
diagnoses
Interventions Other notes:
Altered Level
of
Consciousness
(LOC)
Not a disease
process!
3 types
-Neurologic
-Toxic
-Metabolic
Can be caused by
factors such as:
drug overdose
head injury
strokealcohol
hepatic/renal
failure
DKA
LOC is a
continuum from
A&O x3 to coma
Restlessness
Anxiety
Slow pupils
Conscious?
Decreased
verbal response
Decreased
motor response
Decreased eyeresponse
Respiratory
depression
At risk for
alterations in
any body
system!!!
Full
assessment
Neuro exam
Glasgow
coma scale
Potential labs:
Blood glucose,Electrolytes,
Liver function,
BUN, Serum
ammonia,
PT/PTT, Serum
ketone, Blood
alcohol/drug,
ABGs
Diagnostic:CT, MRI, EEG,
PET/SPECT
**Airwayis first
priority,
especially if
unconscious
-Find the cause
to find the
treatment
Ineffective Airway
clearance
Risk of injury
Deficient fluid
volume
Impaired oral
mucous
membranes
Risk for impaired
skin integrity
Impaired tissue
integrity of the
corneaIneffective
thermo-regulation
Impaired urinary
elimination
Bowel
incontinence
Disturbed sensory
perception
Interrupted family
process
Obtain/ maintain
patent airway
Protect the patient
Maintain fluid balance/
IV fluids as ordered
Tube feedings if
indicated
Mouth care
ROM
Turning/ repositioning
Keep eyes moist and
protected
Heat/cold as necessaryto maintain body
temperature
Bladder scan/ Catheter
Promote bowel
function
Provide sensory
stimulation
Care for the family
SCD hose/ DVT
prevention
Coma:
unconscious,
unrousable,
unresponsive
LockedIn
syndrome:
Inability to move
or respond except
for eye movement
(lesion of Pons)
Akinetic Mutism:
Sometimes opens
eyes but makesnot movement or
sound
Persistent
vegetative state:
devoid of
cognitive function
but has sleep-
wake cycles
Increased
Intracranial
Pressure (ICP)
Not a disease
process!
Increased ICP
occurs when one
of the three
factors
(blood,brain,CSF)
increases and the
*Earliest signs arechange in LOC,
slowed speech,
delayed response
More signs:
Restlessness
Increased
drowsiness
Confusion
**NO lumbar
punctures!!
CT, MRI, PET,
SPECT, cerebral
angiography,
transcranial
doppler,
Evoked
EMERGENCY
Intracranial
monitoring
indicated
Craniotomy,
craniectomy,
Osmotic
Ineffective airway
clearance
Ineffective
breathing pattern
Ineffective
cerebral tissue
perfusion
Deficient fluid
volume
Maintain patent
airway
Monitor respiratory
status
HOB up to 60
Avoid stimuli that
increases ICP
Hourly I/O during
acute phase
CPP: 70-100 mm
Hg
ICP in ventricles is
0-10 mm Hg, with
a max of 15 mm
Hg
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other two cannot
compensate to
maintain normal
ICP
Weakness on one
side or in one
extremity
Headache
Vomiting
Impaired gag
and/or corneal
reflexes
Progression
towards stupor
and coma
Late signs:
Coma
Fixed pupils
Decortication
Decerebration
Impaired/ absent
respirationsCushings
response:
Increased BP
Widened pulse
pressure
Cardiac slowing
Cushings triad:
Bradycardia
Hypertension
Bradypnea
potential
studies,
electrophysio-
logic
monitoring.
diuretics, fluid
restriction, CSF
drainage, fever
control,
maintaining BP
and O2 status,reducing cerebral
demands, avoid
increases r/t
increased
abdominal
pressure,
straining with
BM, high PEEP.
Risk for infection
Impaired skin/
mucous
membrane
integrity
Strict aseptic
technique with ICP
monitoring
Turn/reposition -
hygiene
Seizures Uncontrolledelectrical
discharge in the
brain.
Is either primary
or secondary to
metabolic,
systemic and
other causes.
Depends on
type of seizure
how they
present- see
note.
During a seizure
documentation:
Circumstance
before the seizureAura
Dx:
CBC, CMB, UA,
drug screen,
lumbar
puncture, CT
scan, EEG, skull
xray
Assess:
Patient Hx
Family Hx
Usually treated
with medication
though surgical
options do exist
in some cases.
Risk for injury
Fear
Ineffective
individual coping
Do not restrain
patient, pad siderails,
place on their side
Adherence to
medications is
important to prevent,
identify triggers and
avoid
***See pages 8-11
on the ch 61-62
notes packet.
Details types of
seizures, etc
**recommend re-
reading the status
epilepticus section
as well
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Head injury, CVA
are biggest causes
of new onset
seizures
What the patient
doesfirst area
affected and how,
type of
movements,
areas of body
involved, size of
pupils and if eyes
are open,
automatisms,
incontinence,
duration,
unconsciousness,
paralysis, inability
to speak,
cognitive status,
and movements
at the end ofseizure as well as
if the patient
sleeps after.
protect from
injury and do not
touch during
seizure-
Nurse then
prevents
complications andallows patient to
restbedrails up
and padded if
needed
Characteristics
of the seizures
Deficient
knowledge
Teaching about
management and
referral to counseling
Ongoing education
and encouragement.Medic alert bracelet.
Family teaching.
Headache (HA) Migraine:abnormal
metabolism of
serotoninexact
mechanism
unknown
4 phases of
migraine:
Prodrome
nondescript
symptoms
(depression,food cravings,
Detailed Hx
Medication Hx
Assessment of
head and neck
Complete
neuro exam
Abortive
medications
Prevention
techniques
(identify triggers,
etc)Analgesics
Acute pain Medication and other
nonpharmacological
measures(dark, quiet
room, cold/heat,
massage, elevate HOB
30)
Migraine in
particular can
occur with
hormonal changes
related to
menstruation
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Tension
contraction of
scalp/neck
muscles with
physical or
emotional stress
Clusterdilation
of orbital and
nearby
extracranial
arteries (theory)
feeling cold)
hours-days
before
Aura-
Not in most
patients, mayhave neuro
symptoms
Headache- 4-72
hours
Recovery
exhaustion, may
sleep for
extended
periods
Tension:
Band like pain
or like a weight
on the head.
Steady, constant
pressure
Cluster:
unilateral and
come in clusters
of 1-8 in a day.Excruciating
pain 15min-3hrs
usually in
eye/orbit region
but may radiate
Other
diagnostics not
used unless
biologic, toxic,
oncologic
causesuspected
Non-medication
therapies
(massage,
heat/cold, etc)
Deficient
knowledge
Help identify triggers
and provide teaching
on lifestyle
modifications to
prevent or reduce
occurrences. Provideteaching about
medications and to
take triptans and
ergot derivatives at
the first symptoms.
Good health Hx is
a mustas well as
good assessment
of the headache
See
questionson page
1891
Ischemic
stroke
Separated into 5
catagories based
on location/origin
but basically ablood clot or
Numbness/wea
kness of
face/arm/leg on
one side
Hx, complete
neuro and
physical exam,
-initial focus is
Thrombolytic
therapy within
less than 3 hours
unlesscontraindicated
Impaired physical
mobility
ROM, positioning,
turning q 2,
ambulation
assistance, exercises,PT consult
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plaque causes
blockage in the
brain causing
tissue death
Confusion/LOC
change
Trouble
speaking or
understanding
speechVisual
disturbances
Difficulty
walking and
dizziness
Sudden severe
headache
Hemiplegia
Sensory
loss/agnosia
airway
patency-
CT asap to
determine if
ischemic or
hemorrhagic,MRI/MRA,
ECG, carotid
ultrasound, TE
echo, and
SPECT
by INR >1.7,
anticoagulant
use, and recent
intracranial
pathology.
If not candidatefor TPA-
Heparin not
usually used but
is still an option.
Maintenance of
cerebral
hemodynamics
mannitol, PCO2
between 30-35,
preventing
increase in ICP,
and managing
complications
(UTI,
dysrhythmia, etc)
Acute pain
Self care deficit
Disturbed sensory
perception
Impaired
swallowing
Impaired urinary
elimination
Disturbed thought
processes
Impaired verbal
communication
Risk for impaired
skin integrity
Interrupted family
processes
Sexual
dysfunction
Analgesia,
amitriptyline, lamictal,
lyrica
Assistive devices,
teaching,
encouragementApproach from
unaffected side and
put objects on that
side
Special diet (thick
liquid and pureed
foods), tube feeding if
needed, swallowing
techniques
Bladder (and bowel)
training, cath if
needed
Reality orientation,
cueing,
interdisciplinary
training program
Emotional support
and understanding,
therapeutic and
facilitating
communication,speech therapy, social
contact
Patient and family
teaching and inclusion
in plan of care,
realistic approach that
progress may be slow,
emotional care
Communication,
education, counseling,medication adjust
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Hemorrhagic
stroke
Depends on
cause:
Arteriovenous
malformations,
aneurysm,
intracranialneoplasms,
subarachnoid
All cause bleeding
into the brain and
increased ICP
which can cause
brain death
The same as
intracranial
most common
complaint is
severe
headache
Key symptoms:
Vomiting
Seizures
Sudden change
in LOC
CT, MRI,
cerebral
angiography,
lumbar
puncture (only
if ICP notincreased)
Toxicology
screening
If bleeding
caused by
warfarin, Vit K or
FFP given.
Surgical
interventionwhen applicable
or endovascular
procedures.
Prevent/treat
rebleeding,
antiseizure meds,
DVT prevention,
Fever,
hyponatremia
and
hyperglycemia
treated, BP
stabilized
Ineffective
cerebral tissue
perfusion
Risk for bleeding
Disturbed sensory
perception
Anxiety
-others depending
on needs of the
patientsee
above
Avoid increase in ICP,
HOB 15-30, SCD, close
monitoring of VS and
status
(Rebleeding) BP
carefully maintainedand increase in ICP
avoided
r/t aneurysm
precautions, pt is on
strict bedrest with
environment keep as
calm and quiet as
possible, visitors
restricted, etc. keep
patient informed and
family when possible.
Provide reassure and
support
Head injury
(HI)
Skull fracture,
Contusion,
laceration and/or
torn blood vessels
due to impact,
acceleration-
decelerationinjuries, and
foreign object
penetration.
Increase in ICP
can cause
ischemia
Symptoms
relate to the
injury and
affected area
May have
nosebleed,
battle sign,bleeding from
pharyx or ears,
csf drainage
May have
seizures, coma,
S/S of increased
ICP
Hx, Neuro
exam, xray,
MRI, CT,
cerebral
angiography
Depends on
injury.
May have
surgical
intervention
Maintaining
cerebral
homeostasis is
key
Also depends on
type of injury and
if there is brain
damage present
and/or
neurological
symptoms anddeficits. Managing
ICP is key here so
review (again) the
second topic of
this study guide
Airway is #1
there rest are also
similar to stroke
Terms:
Concussion
Contusion
Diffuse Axonal
injury?
Epidural and
subduralhematoma
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Spinal Cord
injury (SCI)
Traumatic damage
to any level of the
spinal cord. May
have partial or
complete lesions
of either sensoryor motor or both
Dependent on
type and level of
injury.
May have
respiratory
failure, impairedsensory and/or
motor function,
dependent on
level of injury,
may be unable
to speak,
swallow
Xray, CT,
possibly MRI
Full
neurological
exam
IV corticosteroids
(methylpredniso
ne) first 24-48
hrs, respiratory
therapy
including vent ifnecessaryO2
given bc
hypoxemia
increased
secondary
damage.
Immobilization
and stability
devices. Surgical
intervention
when indicated
(compression,
fragmented or
unstable
vertebrae,
wound
penetrating cord,
bone frags in
spinal canal,
deterioration of
pt neuro status)
Long term
anticoagulation
Ineffective
breathing pattern
Ineffective airway
clearance
Impaired bed and
physical mobility
Disturbed sensory
perception
Risk for impaired
skin integrity
Impaired urinary
elimination
Constipation
Acute pain
CAUTIOUS suctioning,
close monitoring of
resp status, assisted
coughing, air
humidification
Frequent positioning
and early ambulation,
ROM
Provide prism glasses,
coping strategies,
provide emotional
support, music, touch
Turn q2, frequent
assessment, kinetic
bed, hygiene and
skin/peri care
Intermittent cath,
teach pt and family
and encourage
participation, teach to
record I/O and
monitor void status
Stool softeners, high
fiber diet, bowel
program institutionProvide comfort
measures, analgesia
Most common in
young males
MVAs, falls,
violence, sports
Respiratoryaffected T1-T11
Diaphragm
controlled by C4
Review chart 63-7
on pg 1935 &
table 63-3 on pg
1936
Autonomic
Dysreflexia
know it, know its
signs and
symptoms. Know
that can be
caused by ANY
stimulus below
level of injury
Spinal and
Neurogenic shocknot well
described in book,
google for better
idea
Also- this study
guide doesnt
cover long term
management pgs
1943-46
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Multiple
Sclerosis (MS)
Immune
mediated,
progressive
demyelinating
disease. Theory
virus triggersautoimmune
response. T cells
allow infiltrates in
that cause
demyelination.
Areas- optic
nerves chiasm and
tracts, the
cerebrum, brain
stem, cerebellum
and spinal cord.
Most patients
have relapse
and remission
deficits may
occur and
accumulate overtime.50% of
RR progress to
secondary
progressive
course with
increase in
deficits and rare
plateaus
Primary
progressive:
Quadriparesis
Cognitive
dysfunction
Visual loss
Brain stem
syndromes
Specific
symptoms
depend on area
of brain affected
MRI,
electrophoresis
of CSF, Evoked
potential
studies,
urodynamicstudies, neuro-
psychological
testing
Sexual Hx
Pt may have:
Diplopia, pain,
fatigue,
numbness,
weakness,
blurry vision,
patchy and
total blindness,
depression,
coordination
difficulties
No Cure
Individualized
treatment based
on symptoms
Nerve blocksPossible meds:
Rebif, Betaseron,
Avonex,
Copaxone- cause
flu like
symptoms-treat
with nsaids
May take 6
months for
improvement
Baclofen, valium
for spasticity
Symmetrel,
Cylert and Prozac
for fatigue
Inderal,
Neurontin, and
Klonopin for
Ataxia
Bowel andbladder meds
Impaired bed and
physical mobility
Risk for injury
Impaired urinary
and bowel
elimination
Impaired verbal
communication
Impaired
swallowing
Disturbed thought
processes
Ineffective
individual coping
Impaired homemaintenance
management
Potential for
sexual dysfunction
Exercises, walking,
minimize spasticity
and contracture,
stretching
Gait training, assistive
devices, monitor forpressure ulcers
Void schedule,
bowel/bladder
training, self-cath
teaching, adequate
fluids and diet
including fiber
Diet modifications if
needed, speech
consult, alternate
communication
methods teaching
Pt and family
teaching, set realistic
goals, structured
environment
Support, home care,
service referrals,
assistive devices, offer
resources
Home modificationsfor independence,
assistive devices,
temperature control
Identification of the
problem, Referral to
sex counselor,
alternative methods
Onset ages 20-40
Terms:
Spasticity
Ataxia
Myasthenia
Gravis (MG)
Auto-immune
disease thattargets
Initial:
Diplopia andptosis,
Acetycholinest
erase inhibitortest.
Aimed at
improvingfunction and
Myasthenic Crisis: Education and
medication
During
Myasthenic crisisABGs,
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acetycholine and
impairs
transmission of
impulses across
the myoneural
junction.Causes weakness
of the voluntary
muscles.
80% also have
thymic
hyperplasia or
thymic tumor.
weakness of
face and throat
muscles.
Dysphonia and
generalized
weakness.
-tensilon given
IV to diagnose.
-face weakness
and ptosis
resolve for 5
minutes
MRI, EMG
targeting
antibodies
No Cure
Anticholinesteras
e mediation,
pyridostigmine,corticosteroids,
imurian, IVIG
*No Novocaine
Plasmapheresis
Thymectomy
Respiratory
Distress
Dysphagia
Dysarthria
Ptosis
DiplopiaProminent Muscle
Weakness
*Airway is priority
Nursing Diagnoses
depend on
symptoms and
course of disease.
Aimed at
preventing and
managing
complications
management
important.
Conservation of
energy.
Minimize aspiration
by timing meals at
peak effect of
anticholinesterase
medications.
Supplemental
feedings may be
needed for adequate
nutrition.
Eye care important for
prevention of corneal
damage.
Avoidance of
triggering factors and
infections.
electrolytes, i/o
and daily weight
are monitored.
NG tube if
impairedswallowing.
Sedatives and
tranquilizers
avoided.
Guillain-Barre
syndrome
Autoimmune
Attack on the
peripheral nervemyelin. The result
is acute rapid
demyelination of
peripheral nerves
and some cranial
nerves producing
ascending
weakness with
dyskinesia,
hyporeflexia andparesthesias.
Begins with
muscle
weakness anddiminished
reflexes of
lower
extremities and
may progress to
tetraplegia,
Neuromuscular
respiratory
failure, bulbar
weakness,blindness,
Patient
presents with
symmetricweakness,
diminished
reflexes and
ascending
motor
weakness.
Hx of viral
illness.
Lab tests not
useful.CSF evaluation.
** Medical
Emergencies **
Requires ICU
management.
Assessment of
muscle strength
and respiratory
function.
Intubation.
Plasmapheresis
and IVIG
continuous ECGmonitoring
Ineffective
breathing pattern
Impaired bed and
physical mobility
Imbalanced
nutrition, less
than body
requirements.
Close Monitoring and
potential mechanical
ventilation whichshould be discussed
on admission.
ROM, SCD, Position
Changes,
Anticoagulation.
IV fluids and
Parenteral nutrition,
gastrostomy
management
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Caused by
antecedent event
most often viral
infection. The
myelin damageresults from the
inability to
distinguish
between two
proteins.
inability to
swallow or clear
secretions and
autonomic
dysfunction.
Evoked
potential
studies.
Hypotension
managed with
fluid.
Impaired verbal
communication
Fear and anxiety.
Picture Cards, Eye
blink system, speech
consult.
Encourage family
participation in care,
increase patient senseof control, provide
information about the
condition, teach
relaxation and
distraction,
diversional activities,
encourage visitors,
listening to music,
reading, TV.
Bells PalsyParalysis of the
face caused by
unilateral
inflammation of
cranial nerve VII.
Exact cause
unknown,
theories include
vascular ischemia,
viral disease,
autoimmune
disease or acombination.
May be a type of
pressure paralysis.
Increased
lacrimation,
painful
sensation in the
face behind the
ear and in the
eye, speech
difficulties,
unable to eat on
affected side.
No Diagnostics Treatment aimed
at maintaining
muscle tone and
preventing or
minimizing
denervation.
Corticosteroids,
analgesics,
surgical
exploration if
tumor suspected
or to decompressnerve if doesnt
resolve.
Acute pain
Risk for Corneal
injury
Analgesic and facial
massage when
tolerated.
Eye patch, eye
ointment,
moisturizing drops,
eye shield and use of
wrap around glasses
during the day to
minimize moisture
loss.
Most patients are
younger than 45.
Meningitis Septic=bacterialinfection.
Aseptic=viral
infection.
Can be blood
stream or direct
Nuchal
rigidity=early
sign. +kernigs
sign.
+brudzinskis
sign.
photophobia
CT, MRI, CSF
studies may
demonstrate
low
glucose/high
WBC/high
protein.
Antibiotics for
bacterial (vanco,
cephalosporins).
Decadron,
dexamethasone,
dehydration and
shock are treated
Hypovolemia.
Actual infection.
Risk for injury r/t
seizures.
Impaired gas
exchange.
ABGs and PO2 to
identify need for
support if increasing
ICP compromises
brain stem. Possible
trach. Possible
mechanical
Protect patient
from further
injury and
infection.
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introduction
through trauma.
with fluids.
Phenytoin for
seizures.
ventilations. Monitor
BP. Rapid fluid
replacement but take
care to prevent
overload. Fever
reduction.Creutzfeldt-
Jakob disease
Caused by a prion.
It causes
spongiform
changes in the
brain
(degeneration of
brain tissue).
Muscle spasms,
rigidity,
dysarthria,
incoordination,
cognitive
impairment.
Mental
deterioration,
memory loss,
paralysis.
MRI, EEG, CSF,
brain biopsy
No effective
treatment. Death
is inevitable.
Palliative care
Ineffective coping
Grief
Offer support to the
patient and family.
Palliative care. Offer
emotional support.
Progression of the
disease occurs
quickly after the
onset of specific
neurologic
symptoms.
Survival is an
average of
22months.
Trigeminal
Neuralgia
As the brain ages
a loop of cerebral
artery or vein may
compress the
nerve root entry
point.
Pain ends as
abruptly as it
starts and is
usually
unilateral and
described as
shooting or
stabbing.
MRI, assessing
trigger points
Pharm:
antizeisure
agents,
gabapentic,
baclofen
Surg:
decompression
of the nerve,
radiofrequency
thermal
coagulation,percutaneous
balloon
microcompressio
ns.
Acute pain.
Risk for injury.
Educating on
preventative
strategies such as
avoiding too hot or
too cold foods, drinks,
water. The nurse
needs to assist with
the care of the
anxiety, depression,
and insomnia that
often accompaniesthe chronic pain.
Occurs most often
before the age of
35 and is more
common in
women and
people with MS
compared to the
general
population.
Peripheral
neuropathy
Most commonly
caused by
diabetes and poor
glycemic control.
Loss of
sensation and
muscle atrophy
and weakness.
Diminished
reflexes.
Physical
assessment
and findings.
Pain and
sensation
Gabapentin,
lyrica,
Chronic pain.
Risk for injury/fall
Diabetes education
and management.
Depression and
anxiety are common
side effects and
It is important
that it is
prevented b/c
there is no cure.
Educating
diabetics on the
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Parasthesia and
pain.
testing of
extremities.
support for these are
important.
importance of
blood sugar
management is
key.
Huntingtons
Disease
Premature death
of cells in thestriatum of the
basal ganglia. Cells
are also lost in the
cortex (the region
associated with
thinking, memory,
perception,
judgment) and in
the cerebellum
(the region
responsible for
coordinated
voluntary muscle
movement)
Abnormalinvoluntary
movement
(chorea),
intellectual
decline,
emotional
disturbance,
constant
writhing,
motions are
devoid of
rhythm or
purpose.
Positive family
history.Presence of
genetic
markers.
No cure just treat
the symptoms.Dopamine
receptor
blockers.
Antiparkinsons
medications for
rigidity.
Risk for injury.
Focus on thepalliative and
coping
Look beyond the
disease and focus onthe patients needs
and capabilities. End
of life care will be a
priority. Teach
strategies to manage
symptoms. Increased
risk for aspiration
pneumonia.
If there is a family
history, peoplecan be tested for
the genetic
marker before
symptoms occur.
Degenerative
Disc Disease
Herniation of the
intervertebral disc
with subsequent
compression it is
preceded by
degenerative
changes thatoccur with aging.
C/M depends on
the location in
the spine.
Health HX.
Physical exam.
MRI, CT
Neurologic
exam.
Bedrest and pain
medications for
cervical and
lumbar disks.
Surgical excision
of the herniated
disc.,laminectomy,
fusion.
Pain.
Infection risk if
surgery is
undertaken.
Pain management and
support.
Often prescribed
many pain
medications and
can have chronic
narcotic use
resulting in
increased need forpain medications.
Cervical
Herniation
The same at DDD
but with the risk
of lesions forming
on the spinal cord.
Typically occurs
at the C5-C7
interspaces.
Pain and
stiffness of the
neck.
Parasthesia.
MRI of the C-
spine.
Pain medications
and rest of the
surgical spine to
allow the C spine
to heal and
reduce
inflammation.
Surgical excision
Pain. Infection risk
if surgery.
Skin integrity is at
risk d/t bedrest.
May be flat bedrest
after surgery. Watch
for excruciating pain
after surgery. Could
mean a need for
further surgery. Neck
should be kept
Hospital stay is
likely to be short.
Self care must be
promoted and
taught.
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of the herniated
disk may be
necessary.
midline and in a
neutral position.
Brain Abscess Collection ofinfectious
material withinthe tissue of the
brain.
Can be caused by:
-intracranial
surgery,
penetrating head
injury, of tongue
piercing.
-Headache,
usually worse in
the morning-fever
-vomiting
-focal
neurologic
deficits
-Decrease LOC
-seizure
-MRI or CT scan
-blood cultures
-Chest x-ray-EKG
-Control ICP
-drain abscess
-Antimicrobialtherapy
-high dose
antibiotics
-Corticosteroids
-Antiseizure
meds
-Acute confusion
-fear
-Grieving-Decreased
intracranial
adaptive capacity
-Acute pain
-Vision loss
-Risk for injury
-Vision loss
-Prevention such as
promptly treating
otitis media,mastoiditis,
rhinosinusitis, dental
infections, and
systemic infections.
-monitor neuro status
-admin meds
-assess response to
treatment
-supportive care
-monitoring safety
-educate patient and
family
-Seizures are
common.
Alzheimers A chronic,
progressive, and
degenerative
brain disorder
that is
accompanied by
profound effects
on memory,
cognition, andability for self-care
-loss of memory
and cognition
that disturbs
daily life
-Trouble
understanding
visual images
and spatial
relationships-Problems with
words or
speaking
-Misplacing
things and
losing the ability
to retrace steps
-Poor judgment
-withdrawn
from activities
-Medical
history
including
family history
-Mental status
testing
-physical and
neurological
exam-Blood test to
rule out other
causes
-MRI & CT
usually used to
rule out other
causes
-goal is to
manage
symptoms
-assessing for
underlying
depression
-pharm to treat
symptoms but
does not stop theprogression.
-behavioral and
psychosocial
therapies
-Wandering
-impaired memory
-impaired physical
mobility
-self-neglect
-risk of loneness
-caregiver role
strain
-chronic confusion-hopelessness
-powerlessness
-Promoting patient
function and
independence.
-promoting safety
-reducing anxiety and
agitation
-providing
socialization
-adequate nutrition-supporting and
education patient and
family
-definitive
diagnosis can be
made only at
autopsy
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-Change in
mood or
personality
Parkinsons -Slowly
progressingneurologic
movement
disorder that
eventually leads
to disability.
-decresed level of
dopamine
resulting from
destruction of
pigmented
neuronal cells in
the substatia nigra
in the basal
ganglia region of
the brain. The loss
of dopamine
results in more
excitatory
neurotrasmitters
than inhibitory
neurotransmitters, leading to an
imbalance that
affects voluntary
movement.
Gradual onset
and symptomsprogress slowly.
-Cardinal
manifestations:
-Tremors
-Rigidity
-Bradykinesia
-Postural
instability
-PET & SPECT
scans-diagnosed
clinically from
the patients
history and the
presence of
two of the four
cardinal
manifestations
Focuses on
controllingsymptoms and
maintaining
functional
independence
-Pharm therapy:
antiparkinsonian
meds (ex.
levodopa)
-stereotactic
procedures
-neural
transplantation
-Deep brain
stimulation
-Impaired physical
mobility-Self-care deficits
-Constipation
related to
medication and
reduced activity
-imbalanced
nutrition
-impaired verbal
communication
ineffective coping
-Improving mobility
-Enhancing self-careactivities
-Improving bowel
elimination
-Improved nutrition
-enhancing swallowing
-encouraging the use
of assistive devices
-Improving
communication
-supporting coping
abilities
-promoting home and
community-based
care
Cerebral
metastases
-cancer that has
metastasized
(spread) to the
brain from
another location
in the body
-neurologic
exam
-Headache
-gait
disturbances
-MRI along
with S/S
-palliative and
involves
eliminating of
reducing serious
symptoms.
-Self-care deficit
-Imbalanced
nutrition
-Anxiety
-Interrupted
family processes
-Pain management
-improve nutrition
-compensation for
self-care deficits
-relieving anxiety
-survival time:
*no treatment for
brain metastases:
1 month
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-visual
impairment
-personality
changes
-altered
mentation(memory loss
and confusion)
-focal weakness
-paralysis
-aphasia
-seizures
-Radiation
therapy
-surgery
-Chemotherapy
-Corticosteriods
-Osmoticdiuretics
-Antiseizure
agents
-enhancing family
processes
-promoting home and
community-based
care.
*corticosteroid
treatment alone:
2 months
*Radiation
therapy: 3-6
months.
Spinal tumors Tumor within thespine. Classified
by anatomic
relation to the
spinal cord.
-intramedullary
lesions: within the
spinal cord
-extramedullary-
intradural lesions:
within or under
the spinal dura
-extramedullary-
extradural lesions:outside the dural
membrane
-localized or
shooting pains
and weakness
and loss of
reflexes above
the tumor level
-neurologic
examiniation:
assess pain, loss
of refexes, loss
of sensation or
motor function,
and the
presence of
weakness andparalysis
-pain longer
than 1 month
-MRI scans:
most common
used.
-x-ray
-radionuclide
bone scan
-CT scans
-biopsy
-Surgical
interventions:
primary
treatment
-partial removal
of the tumor
-decompression
of the spinal cord
-chemotherapy
-radiation
therapy
-Provide per and post-
operative care
-Managing pain
-monitoring for
complications
-Patient and family
teaching.
-compensation for
self-care deficits
ALS Unknown cause,there is a loss of
motor neurons in
the anterior horns
of the spinal cord
and the lower
-depends on
location of the
affected motor
neuron
-fatigue
Diagnosed on
the basis of the
signs and
symptoms, no
clinical or
laboratory test
NO specific
therapy exists for
ALS. The main
focus of medical
and nursing
management is
on interventions
-ineffective
breathing pattern
-impaired verbal
communication
-decisional conflict
-Chronic sorrow
-Monitor for
aspiration may in
enteral feeds
-maintain or improve
function, well-being,
and quality of life
-The average
survival time is 3-5
years with death
due, most
commonly to
respiratory
insufficiency.
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nuclei of the
lower brain stem.
-progressive
muscle
weakness,
-cramps,
-facial twitching
-loss ofcoordination
are specific for
this disease.
-Electro-
myography and
muscle biopsy
may be done-MRI
-Neuro-
psychological
testing
to maintain or
improve
function, well-
being, and
quality of life.
-riluzole (Rilutek),a glutamate
antagonist, is the
only med
approved for the
treatment of ALS.
-Impaired
swallowing
-Risk for
aspiration
-anxiety
Muscular
Dystrophies
Incurable muscle
disorders
characterized by
progressive
weakening and
wasting of the
skeletal or
voluntary
muscles.
-Muscle wasting
and weakness
-abnormal
elevation in
serum levels of
muscle
enzymes.
-elevated
muscle
enzymes.
-focuses on
supportive care
and prevention
of complications
-individualized
therapeutic
exercise program
-spinal fusion
-intense therapy to
keep the muscles
active and functioning
normally
-night splints
-teaching patient self-
care
-Most of these
disorders are
inherited.
-spinal deformity
is a severe
problem.
Post-Polio Unknownpriorpolio infection
Post-Polio
symptoms:
-Progressive
muscle and joint
weakness and
pain-General fatigue
and exhaustion
with minimal
activity
-Muscle atrophy
-Breathing or
swallowing
problems
-Sleep-related
breathing
NO diagnostic
test for this**
Hx, physical
exam and
exclusion of
other medicalconditions
No specific
treatment
focus on
symptoms
Activity
intolerance
Chronic pain
Risk for ineffectivebreathing pattern
Imbalanced
nutrition: more
than
requirements
Disturbed sleep
pattern
Risk for injury/falls
Plan activities to
conserve energy,
schedule rest periods,
use assistive devices
Heat/Cold, cautious
use of medications
Pulmonary hygiene,adequate fluid intake,
CPAP if applicable
Provide teaching and
resources for diet and
safe exercise
Limit caffeine, assess
for nocturia
Use of assistive
devices, fall
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disorders (as
sleep apnea)
-Decreased
tolerance of
cold temps
prevention, and
osteoporosis
(common with post-
polio) management
Primary Braintumors
Note: I
recommend
re-reading this
section: brief
synopsis only
included here
+ the following
sections on
pre/post
surgical care
Glioma:most common
type, with the
most common
type of glioma
being an
astrocytoma
which is also
graded
Meningioma:Common,
benign and slow
growing.
Manifestations
are result of
pressure.
Surgery is
preferred
treatment
Acousticneuroma:
8th cranial
nerve tumor-
tinnitus,
hearing loss,
vertigo,
stagger- most
benign and
managed
conservatively
Pituitaryadenoma:
Either cause
pressure effects
or hormonal-
usually prolactin,
growth hormone
and ATCH- also
rarely TSH, FSH
and LH.
Angioma:Abnormal clusters
of blood vessels
cause
hemorrhagic
stroke in
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Burr holes: either
to facilitate a
craniotomy OR as
a means of
pressure relief
(also usually forpressure relief,
but can be used
for access of
specific site)
Likely ET tube.
Assess:
Respiration
and
oxygenation
status, VS, LOC,bleeding/CSF
leakage,
seizure, I/O
ICP monitoring
ABGs
CBC/CMB
BUN/
Creatinine,
blood glucose,
phenytoin
levels (10-20
mcg/mL)
Ineffective
cerebral tissue
perfusion
Risk of
imbalanced body
temperature
Potential for
impaired gas
exchange
Disturbed sensory
perception
Body image
disturbance
Impaired
communication
Risk for impairedskin integrity
Risk for infection
Risk for fluid and
electrolyte
imbalance
Q15-60min VS/Neuro
assessment, HOB flat
or 30 degrees, control
cerebral edema and
ICPCover pt
appropriately, treat
hyperthermia
aggressively
Deep breathing/
Incentive spirometer,
Cautiously suction/
help pt cough,
humidify air
Announce presence,
cool compresses and
HOB elevation (30) to
decrease periorbital
edema
Verbalization,
interaction, grooming,
cover head with
turban (later, a wig)
Use of communication
boards, signals
Turning q 2 hours,hygiene care
Aseptic technique
with ICP monitoring
Monitor I/O,
electrolyes, and urine
specific gravity, fluid
restriction, IV
fluids/diuretics as
ordered
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Trans-
sphenoidal
surgery
Description:
Access to the
brain (usually the
pituitary gland)
through the
mouth andsinuses
Also used for
ablation of the
pituitary with
disseminated
breast or prostate
cancer
Pre-Op:
Depends on
reason for
surgery. May
have increased
ICP and alteredLOC
Post-Op:
Swollen/
bruised face
Nasal packing
cannot remove
blood around
until packing
removed!
Pre-Op:
Endocrine
workup
Rhinologic
evaluation
Nasopharyngeal culture
(surgery
contraindicate
d with sinus
infection)
Visual
evaluation
Neuro-
radiologic
studies
Post-Op:
Urine specific
gravity after
EACH urination
to monitor for
diabetes
insipidus and
SIADH
ICP monitoring
CMBCBC
Pre-Op:
May have
corticosteroids,
phenytoin,
and/or
prophylacticantibiotics
prescribed
before surgery
Post-Op:
Antibiotics
Corticosteroids
Analgesics
-medication for
diabetes
insipidus if
indicated
(Desmopressin)
Pre-Op: Same as
above
Post-Op: Same as
above
Impaired oral and
nasal mucous
membranes
**Disturbed
sensory
perception r/t
proximity to optic
chiasm
Pre-Op: Same as
above
Post-Op: Same as
above
Mouth rinses every 4
hoursno brushing
until incision heals
Petrolatum for lips
Use of air humidifier
Monitor visual fields
and acuity frequently
-decreasing acuity
suggests expanding
hematoma
***Deficient
knowledge of
Post-Op
expectations/care
needs to be
addressed BEFOREsurgery
HOB at 60 for at
least 2 weeks to
promote venous
drainage from site
Teaching:
Post Op
expectations,
potential
complications,
cares, Deep
breathing,
avoidance of
increasing ICP
(coughing,
sneezing etc)