Exam 3 notes
slide - Neuroglial function alteration
slide-CNS – Brain and spinal cord – outside layer ( dura
mater(between the cerebral hemispheres and the
cerebellum is the Tentorium( protect the layer of the
brain when trauma occurs – balance the two
hemisphere)), subdural space, and arachnoid – most inner
layer Pia mater is the subarachnoid space ( CSF location) –
epidural space outer layer of the dura mater.
Reference to a tumor:
o Supratentorial – tumor above the tentorium –
monitor decorticate positioning - is seen with
interruption in the corticospinal pathway. This
finding is abnormal and is a sign that the client’s
condition has deteriorated.
o e charge
o nurse, and other health care team members should be notified immediately of this
change in status. Decerebrate
o posturing consists of external rotation and extension of the extremities.
o Hyperreflexes present as increased reflex responses.
o Infratentorial – tumor below the tentorium
 Brain division of the cerebral cortex
o cerebrum- for balance
o Frontal motor strip ot cortex( mobility)



broca’s speech center on the
dominant side – speech but
not comprehend
voluntary eye movement,
sensory perception, past
information ; experience,
affective response of the
situation
behavior regulation,
cognition, judgment,
reasoning, concertation
o
o

abstraction. Personality change.
Temporal lobe
 Auditory center for sound interpretation
 complicated memory patterns
 Wernicke area for language comprehension – pt understand but
cannot speak.
 the processing of words into
 coherent thought as well as the understanding of written or spoken
words. The temporal lobe also is
 responsible for the auditory center’s interpretation of sound and
complicated memory patterns. any complication – can cause - .
Memory loss, Difficulty with sound interpretation, Speech difficulties
 Right-sided paralysis indicates a left-brain stroke, which will lead to
difficulty with comprehension and use of language.
parietal lobe

sensory input – texture, size, shape, spatial
 three-dimensional ( Spatial) perception – singing, playing musical
instruments, and processing nonverbal visual experiences
 perception of body part and position aweraness
 taste impulses for interpretation. - Impaired taste
o occipital lobe primary for vision
Brainstem function
 Medulla
o cardiac -slowing center
o respiratory center
o cranial nerve nuclei XV glossopharyngeal, X vegus, XI ( accessory)
XII(hypoglossal), and parts of cranial nerves VII (facial) and VIII (
vestibulocochlear)- Damage to these nerves causes-impaired swallowing,
inability to shrug shoulders, and loss of the gag reflex.
 pons
o cardiac acceleration and vasoconstriction centers
o neurotoxic center the helps control raspatory ( pattern and rate )
o cranial nerve nuclei ( V trigeminal, VI (abducens) VII( facial, and VIII (
vestibulocochlear) Midbrain
o contains the cerebral aqueduct, of aqueduct of Silvius
o location of periaqueductal gray, which may abolish pain when
stimulated
o cranial nerve nuclei III ( oculomotor) and IV (trochlear)
the cercle of Willis – joint together the posterior and the anterior by small communicating arteries from
the ring base of the brain.
I -Olfactory - small
II- Optic- vision
III- Oculomotor- motor eye muscle – lateral rectus and inferior and superior rectus muscle – lip
elevation via the elevator muscle = PNS ( feed and Breed)
IV- trachea
V- trigeminal
VI- abducens
VII- facial
VIII – vestibulocochlear
IX- glossopharyngeal
X- Vagus
XI- spinal accessories
XII hypoglossal
Blood supply



Diagnosis assessment
the brain receives 750 ml/min or 15 to 20% of cardiac output
can ony used sugar for energy – ( it takes 5 min for the brain to have
irreversible brain damage) -the brain need O2 – no med goes to the brain
blood- brain barrier – molecules must be enter the brain by active transportendocytosis, exocytosis, creating highly selective barrier the guards the
neurons
CSF – analysis -colorless, clear, no blood or bacterial, white cells (0-5 – glucoses 40-80 mg protein (1645mg
 Computed tomography (CT): Uses a narrow X-ray beam to scan the body part in successive
layers
 Positron emission tomography (PET): A nuclear imaging technique that produces images of
actual organ functioning
 Single photon emission computed tomography (SPECT): Uses radionuclides and instruments to
detect single photons, and captures a moment of cerebral blood flow - Caffeine-containing
liquids and foods are central nervous system stimulants and may alter the test results. No
contrast is used; therefore, the client does not need to increase fluid intake. The client should
take cardiac medications as prescribed.
 Magnetic resonance imaging (MRI): Uses a magnetic field to obtain images of different areas of
the body- Allergies to iodine and/or shellfish need to be explored because the client may have a
similar reaction to the dye used in the procedure. In some cases, the client may need to be
medicated with antihistamines or steroids before the test is given.- Metal devices such as
internal pumps, pacemakers, and prostheses interfere with the accuracy of the image and can
become displaced by the magnetic force generated by an MRI procedure
 Cerebral angiography: An x-ray study of the cerebral circulation - it is a high risk monitor Vs
every 15 to 30 for 2 hr- 1 hr for 6 hr – 2 hr for 24
 Myelogram: An X-ray of the spinal subarachnoid space
 Noninvasive carotid flow studies: Use ultrasound to evaluate carotid and deep orbital circulation
 Electroencephalogram (EEG): Represents a record of the electrical activity generated in the
brain- Hyperventilation produces cerebral vasoconstriction and alkalosis, which increases the
likelihood of seizure activity. The client is asked to breathe deeply 20 to 30 times for 3 minutes.
◦
Avoid caffeine on day of test
◦
Wash hair, but no sprays or oils after shampoo
 accurate.
 Electromyogram (EMG): Uses needle electrodes to measure changes in the electrical potential
of the muscles and the nerves leading to them
 Lumbar puncture (spinal tap): Carried out to withdraw CSF- insertion of the needle between the
subarachnoid space between the L3 and L4 , and sometimes L4-L5 – still position



proper positioning for Lumbar puncture – fetal side-lying position to separate the
vertebrae and move the spinal nerve roots away from the area to be accessed. – local
anesthesia – slight pressure after the procedure
assess the site for CSF leak and infection - An LP should not be performed if the client
has a skin infection at or near the puncture site because of the risk
of infection




monitor VS, Headache, ------increased fluid intake – report and HA to HCP if
medication does not relieve pain. - d immediately contact the provider if the client
experiences a severe headache, nausea, vomiting, photophobia, or a change in level of
consciousness after an LP, which are all signs of increased
intracranial pressure.
rest----may position fat – bed rest and maintain flat
cheek neurological status
o complication > ICP cause by ( severe HA, nausea, vomiting, photophobia, and
change in LOC
o serious complications – brain hernation formation, infection, CSF leakage
hematoma formation
Altered cerebral function
o



Manifestation of altered cerebral function occur as a result of illness or injury
 Loc may be altered by the process that affect the arousal function of the brainstem, the
cognitive function of the cerebral hemisphere or both- Loc is a primary indicator of
Neuro PB – if lethargic – cannot answer – call HCP – request for CT scan
 Glasgow coma Scale *****
 15-13 – mild impairment
 12-9- moderate impairment
 loss of consciousness greater
than
30 minutes
 physical and cognitive
impairment with or may not
resolve
 benefit from rehabilitation
 3-8- sever impairment- candidate for
organ
doner -cannot be less than 3
 coma, unconscious state; no
meaningful response, no
voluntary activities
best response to eyes opening ****
1- no eye opening
2- eye opening to pain
3- eye opening to verbal commands
4- eyes open spontaneously
vegetative state ( less than 3)
sleep wake cycles
Arousal, but no interaction with environment – the 1 sign of anything going wrong is change LOC
damage to RAS impairs the ability to maintain wakefulness and arousal- action suppressed at
the brainstem – which proceeds edema and ischemia – may be due to tumors, hematomas or
hemorrhaged oe aneurysm

no location response to pain
Patterns of breathing are impaired as the respiratory center becomes compressed


Diencephalon: Cheyne-stokes respiration – getting worse
Midbrain- neurogenic hyperventilation uninhibited stimulation of the respiratory centers –
breathing a lot
pons- apneustic respirations, characterized by sighing on mild inspiration or prolonged inhalation and
exhalation ( excessive stimulation of the respiratory center)
medulla ---Ataxic/apna respirations (total uncoordinated and irregular probably as a result of loss of
responsiveness to CO2 – COPD- unresponsiveness to CO2 they cannot take too much O2 thay can stop
breathing
Diabetes insipidus – deficiency in production of ADH cause by organic lesion of damage to
hypothalamus – and decrease renal response the ADH – cause increase in urination > 800 ml/HR and
increased in plasma osmolarity _ > dehydration
o
Sx with DI
o
 increased in quantities of the urine with very loe specific gravity
 occurs suddenly after the heat injury, CNS infection or tumoe\r
Tx hormone of ADH or fluid replacement ( hypotonic saline is given), DDAVP-demoopressin
acetate ( po, IV, nasal spray) best for DI – hope that it will solve the PB
N/I > fluid intake and give DDAVP – accurate I/O
o
Pupillary responses – as LOC deteriorates, a predictable progression of pupillary response occurs,
o
if the lesion localized – the affects may be seeing in the same side – ipsilateral purpil)- if
generalized the p=pupils is affect equally.
 with compression of CN III the pupil may change shape or off =center -is responsible for
dilated ad constriction of the pupils – assess when shining light to the eye
 as impairment continuous it become fixed ( nonreactive) and dilated – brain damage (
poor prognostic sign, patient with his problem are sometimes referred to as having a
“Blown “pupils
 as neuro condition further deteriorates, the eye movement is lost, and the ocular
reflexes are altered
Locked -in syndrome – different from vegetable state in the client is alert and fully aware of the
environment – unable to communicated through speech or movement because of blocked efferent
pathways from the brain – motor paralysis affects all voluntary muscle. presence of restlessness and
confusion more combative
Doll’e eyes -your eye go to another direction – route through brain damage
o
o
o
cannot done on the pt with possible cervical trauma, until it rules out
the procedure is performed by holding the pt eyes open briskly and turn side by side if the reflex
is u=intake the eye will turn the opposite side from with the eye is turned
it the reflexes is absent 1- remain in the midline or move with the head – this brainstem injury
o
2- eyes move to opposite direction from one another – some degree of brain stem injury
Nystagmus – an involuntary condition in which the eyes make repetitive uncontrolled movements. to a
big deviation of the eyes – Is associated with specific lesion or chemical intoxication – don’t know affect
ICP
if both reflex lost brain function as deteriorated
Coma and brain death.
o
o
o
irreversible coma-(vegetative state)-permanent state of complete unawareness result from
death of the cerebral hemispheres- with continued function of the brainstem and cerebellum
Usually, the result of severe head injuries and anoxia
myasthenia gravis/ ALS
Brain death
o
cessation and irreversible of all brain function, including the brainstem
neurologic tests are not required to confirm brain death in some state or province
example test are – cerebral angiography, EEG, CTA, transcramial Doppler
ultrasonography
o criteria way from state to state but generally recognized criteria are:
 unresponsiveness coma – no reflex movement
 no spontaneous movement ( apnea test)
 pupils fixed and dilated -potential brain death
 absent of ocular movement and cold calories
 Flat EEG
 negative brain flow study
o nursing management – ineffective airway clearance, risk for aspiration
o loss of cough and gag reflexes
1. assess ability to clear secretion – don’t stop taking care
2. monitor breathing sound 3. period suctioning --- maintain open airway – suction – if not able to breath – put o2 on
4. turn side to side every 2 hr with HOB at 30 degree – help to grain fluid
o impaired skin integrity r/t mobility
 assess skin evry shift
 reposition every 2 hr
 prevent skin breakdown ( bathe daily. keep linens, clean and free wrinkle free, good
mouth care
 keep cornea moist- Avascular – used tape gently
o impaired physical mobility
o maintain extremities in function position by providing adequate support devices
o Use of splints. pillows, rolled wash cloths, ROM
drug therapy –
o
Mannitol, an osmotic diuretic – used to treat cerebral edema by pulling Ho2 from the brain –
more effective when given bolus – give it with Iv filter to eliminate microscopic crystals strict
o
output Avery 1 hr – serum osmolarity 310 to 320 goal every day. risk for dehydration acute
renal failure weakness, edema, and change in urine output.
furosemide – incidence from rebound from mannitol – enhance therapeutic and reduce
edema and blood volume- < sodium intake at the brain- < the production of csf from choroid
plexus.
Increased intracranial pressured ( IICP)
o
o
o
defined the rise in pressure of CSF between skull and brain ----15 mmhg ( normal 0=15 mmHg)
significant increased called intracranial hypertension
causes – neoplasms, cerebral edema, trauma, infraction, infection, abscess, hemorrhage,
hematoma, increased CSF , decreased absorption
IICP pathology ( insult to brain, tissue edema, > ICP, compression of the ventricle, compression of the
blood vessels, decreased cerebral blood flow, decreased O2, edema around the necrotic tissue,
increased in ICP with compression of brain and the respiratory center, accumulation of CO2,
vasodilation, increased in ICP resulting from increase blood volume. death.
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
o
monro-kelli hypothesis –volume of one component ( tissue, blood, CSF > voulume of another
cerebral blood flow normal 750ml/minute – brain tissue 78% blood 12%
maximum compensation -----then ICP increased - elevate BP influence ( HTN)
hypercarbia ---PaCO2 > 45 mmHg = vasodilation with increased volume => ICP
hypercarbia ---PaCO2 <25 mmHg = rebound cerebral vasodilation and loss of autoregulation (
ability to keep constant blood flow to brain)
normal cerebral perfusion pressure (CPP) 60-100mmGh --- determine CSF
CPP> 100mmHg = hyper perfusion and high> hCP
CPP< 60 mmHg = hypoperfusion / cerebral Ischemia ( irreversible/ infraction <40mmHg)
CPP -40 mmHg = brain death
compensatory mechanisms kick in with increase in ICP balance / protect brain
CSF changes via shunting into subarachnoid space to reduce pressure
decreased secretion / increased absorption of CSF.
failure to compensate mechanism = hypoxia, ischemia- herniation, brain death
when ICP nears systemic arterial [pressure CPP CBF decreased
when ICP is equal systemic arterial pressure stop --- brain death occurs
impact of elevated on circulation determined by CPP with mean arterial pressure (MAP) the
prime influence.
Manifestation of IICP
o
o
change in Loc is most reliable indication for IICP – as pressure increased, decrease in LOC rt to
impairment of circulatory blood flow
earliest sign – blurred vision ( diplopia), severe headache, papilledema/ swelling of optic disk,
and projectile vomiting – then dilated or pinpoint pupils – Cheyenne stokes raspatory,
decerebration, decorticate flaccid – late sign Cushing triad ( wide pulse pressure, bradycardia ,
irregular respiration, later tamp change)
o
change in motor ability, as contralateral ( opposite side of the mass lesion hemiparesis
hemiplegia may develop – pain stimuli 5/6 motor response withdrawal 4/6
Alteration brain activity
definitions
 seizure-uncontrolled discharge of neurons in cerebral cortex, interfere with normal function
 epilepsy-recurrent paroxysmal – cerebral function – sudden short attack – alter in consciousness
motor and sensory phenomena
 Type of seizure
 si
precipitated factors
o
o
o
o
o
o
seizure -physical exhaustion -sound odors, fever, sleep deprivation, malnutrition, stress, ETOH,
shock, drug
bacterial meningitisviral meningitis
encephalitis
brain abscess
herniated intervertebral
Stroke – brain attack or CVA
o
Type of stroke
 Hemorrhagic stroke
o
 TIA- brief interruption in the cerebral or inadequate blood flow to a part of the
brain
o
o

Thrombotic
Embolic
Risk factor of stroke
o hypertension
o metabolic syndrome
o Heart disease
o heavy alcohol consumption
o poor diet- diabetes
o drug abuse
o
o
o
o
sleep apnea
obesity
physical inactivity
smoking
blood supplies to the brain

Internal carotid arteries
o frontal lobe
o Parietal lobe
o temporal lobe
CNS neoplasms
brain tumor
 primary originated in the brain
 secondary – original in other place then the brain due to metastatic
 65 % id gliomas -originates in the astrocytes- the most common glioblastoma
multiforme – very malignant and invasive
 Sx/S headache- more in the norming
 nausea vomiting –
 cognitive pb- memory -sign of brain- frontal lobe– personality change and judgment
seizure
 seizure
 mood and personality change
 sensory loss. increased ICP
specific SX –





frontal ( seizure) cognitive pb- memory personality change and judgment
parietal speech disruption writing struggle spatial disorder
occipital seizure blindness
temporal - dysphagia seizure
cerebellar- headache, papilledema, > ICP, ataxic, gait, vertigo, tinnitus, deafness
Tumor in the pituitary
 transsphenoidal ( hypophysectomy)
-upper lip and gingiva are cut and access is obtained through the floor of the nose and sphenoid
sinuses
nursing care- neuro check per order – check nasal for sign of CSF halo in the white gauze.
instruct the pt do not blow the nose ot brush the teeth.
Tx hormone replacement – vasopressin dacaton) ti < icp- dilantin antiemertic
dx histologic study and endocrine study. will be indicated
Spinal cord tumors

most common cause Motor vehicle collisions (MVC) 42%, fall, violence, sport injury. and
miscellaneous 8 %
o falling object, diving, sking,boating, football, penetrating trauma ( gunshot, stabling)
o




LMN – lower motor neurons- skeletal muscle of the eyes, mouth, throat – segment of
the brain – any lesion – weekends paralysis, denervation , atrophy hyporeflexia, or
areflexia – decrease muscle tone ( flaccidity )0,1
o UMNs (upper motor neurons) – from the cerebral cortex downward – increased muscle
tone( spasticity) – irritation restlessness, agitation, tachypnea, bradycardia, oliguria,
diarrhea, borborygmi. reflexes 3, 4
o Basal ganglia – both cerebral – control and vacillated learned of automatic movement
risk factors – age gender, and alcohol or drug use ( young male ( 18-30) most common is
cervical, least thoracic.
paraplegia – lower extremities ( T1-S5)
tetraplegia – paralysis in arms, legs trunk, pelvis- injury of the C-spine- total sensory loss C7
Spinal shock
o decrease reflexes-0,1
o sensory loss
o flaccid below the injury site
o bowel and bladder dysfunction
o loss of sensation of pain, touch temperature, below the level of the injury.
o begin immediately after the complete transection of the cord – connection between the
brain and the cord in interrupted.
o last day and month – then reflex activity returns.
Neurogenic shock – c-spine from C7 higher plan on ventilation support – BP<80 HR<40 everythings slow
down. more cervical assess for respiration statute
o
o
o
Shock cause by > PNS or parasympathetic stimulation or inhibit SNS or sympathetic stimulation
of muscle of the blood vessels.
loss of vasomotor tone
vasodilation, hypotension, bradycardia, warm and dry extremities, < CO
Autonomic dysreflexia – occurs in T6 and higher injury – seen after the spinal shock when the stimulus
cannot ascend the spinal cord.
o
o
o
o
is an exaggeration sympathetic response
when this happened – massive vasoconstriction above the injury and vasodilation below the
injury
fecal impaction – constipation – stool softener all the time
symptoms – early-sx SCI- back pain that worsen with activity.
 bounding headache- check BP
 bradycardia
 hypertension
 flushed warm skin with perfusion sweating above the lesion and pale cold dry skin
below ( skin Flushed, worm and wait above the injury and cold and dry below the
injury). Dilation above the eight - sitting for the blood to go dependent.
complication SCI

stress ulcer






paralytic ileus ( constipation)
decubitus – stage
stool impaction
decreased venous return
fracture r/t bone demyelination
joint contracture – PT, OT
Nursing care






















c-spine C7 – ABC Brown-Sequard syndrome – complete motor and sensory loss below C7 (
ipsilateral and contralateral)
monitor LOC – maintain the head in the neutral position – sbrserve spontaneous movement
compare data – more breathing
assess foe sexual activity – women can still have sex
suction carefully to avoid vagus nerve stimulation – bradycardia cardiac arrest.
percussion and chest PT for weak cough
breathing exercise
hydrate/ humidity to thin secretion
fecal impaction ( autonomic dysreflexia)
rise HOB / removed compression hose to decrease venous return and BP
report any deterioration ASP
neuro monitoring – 1 hour
ROM – 2hr UAP PT,
monitor BP, cv for dysrhythmia
assess DVT, emboli
maintain skin integrity- massage. barriers cream
promote urinary elimination with inter-mitten catherization ( to keep the bladder empty) used
the indwelling catheter for acute phase
pour arm water in the perineal area, follows all this with catheterization if need it ---<80 residual
is acceptable. – no foley catheter
promote bowel function with feel tube followed bt residual check
offer high calory diet, > protein. > fiber
used bowel retrain process – stool softener, rectal suppository, digital stimulation after meals.
halo brace care – infection prevention by shaving hair. around pins – clean with ½ H2O2 and
1/2NaCL. topical ABOs,
Diagnostic test




spine Xrays
myelogram
CT scan
CBC, lytes, ABCs, glucose H&h, UA,EMG
MEDs –


stool softener, H2 antagonist - or antacids.
low dose anticoagulant, corticosteroid NSAID

antispasmodics, antidepressant, topical ABOs prn
Seizure- resulting from metabolic disturbances
-
clinical manifestation
Simple partial seizure – consciousness – motor sx, one part of the body- sensory
symptoms tingling numbness, visual, auditory, hearing, taste =- vertigo spells
Complex partial seizure – repetitive movement like lips smacking antisocialist/
aggressive behavior
-
-
-
-
characteristic
 psychomotor seizure with repetition beaver and lips smacking
 altered memory, sexual sensations and disorder of visual or
auditory sensations
 often involves behavioral, emotional and cognitive behavior that
altered LOC
Absent seizure( petite mal) – short period – 5-30 secs up tp 100days -eye fluttering,
lips smacking – more in children ( typical absence seizure staring spell, daydreaming
that last a few minutes and unnoticed ) if untreated it can go 100 time a day.atypical – staring spell accompanied by the s/sx brief warnings, peculiar behavior
during seizures and confusion after seizure more longer.
Generalizes seizure – or grand- mal seizure is a bilateral synchronous epileptic
discharge affecting the whole brain at the onset seizure – tonic-clonic, tonic,
absence, myoclonic(single jark just for a second) cause by sudden abnormal bursts
of electrical brain activity
tonic-clonic – grand mal – most common type ( stiffness-jerking( eye roll ) –
postictal phase ( unconscious and unresponsive to stimuli)- relaxed- rapid breathing
– sleeping ( let them sleep)***- fatigue – often accompanied by incontinence and
tongue biting – breathing ceases 15 s to 1 min during the tonic phase- may be
hyperventilated eyes rolling on the colonic phase- cyanosis exercise salivation
- atonic seizure (drop attack)– paroxysmal loss of muscle tone and sudden
falling on the ground and return of consciousness, - risk of heard injury –
often were protective helmets,
- Tonic sudden unset of maintained increased tone in the extensor muscles
and fall result.
- clonic begins with loss LOC and sudden loss of muscle tone. and jerking
movement.
status epilepticus – ER – continues tonic-clonic cycle- interference with respiration (
hypoxia, hyperthermia, hypoglycemia, exhaustion ( if not stop in 30 minutes can
cause brain damage)- tx give adtivant( larasepam)**** or Dilantin ( bolus) and
prepare for intubation – more prone to death. they don’t stop seizing – no breathing
– give adtivant – O2, be ready to intubate – anesthesia
- epileptic – gliosis is a scar tissue around the area of the brain epilepsy occurs –
interfere with normal brain neuron function.
- the astrocytes may be a key role in recurring of the seizure
Nursing intervention for seizure
 record all the aspect of the seizure
 note the time in wish the seizure occurs and the duration
 the event proceeds the seizure
 the priority intervention is to maintain airway during seizure
- promote drainage secretion without aspiration; suction, O2 no oral object in the
mouth. no restrain during injury, place padding under the head.
- take the pt out of bed, NPO nothing in the mouth, time it, what type of seizure
tonic-clonic, medication, notified the hcp
 protect the pt head for injury and turn the pt on the side, loosen constructive close ease
pt on the floor
 do not restrain the patient
 do not place any object in the pt mouth.
 after seizure, reposition the pt and maintain airways suctioning, and oxygen.
Focus assessment








monitor pupils size reaction, cyanosis, sweating, salivation, LOC, incontinence during
surgery
monitor time of the seizure and duration activity, movement thrigger Aura
monitor poetical period (30-90 min) for confusion sleepiness, arousal issues, muscle
aches, headache, weakness, aphasia, partial paralysis.
inpesct foe injury especially the tongue – anything in the mouth.
turn to the side to maintain airway
meds. dilantin, Depakote, Tegretol, neurotin, klonopin, Lamictal, also valium or
phenobarbital status epilepticus.
teach ID alert , trigger and support.
headaches – intracranial source origin.
- type of HA
primary cause by disease ( tension, migraine, cluster)
- secondary cause by condition or disorder( sinus disorder, neck, injury, stroke
hemorrhagic ).
 Cluster- it is a most sever and repeated HA that occurs for months a
at time following the period of remission. – abrupt onset usually, 2-3
hours after falling as sleep in spring or fall-cause by trigeminal(tic
douloureux) (CNV) that conduct pain – the imagery shows
hypothalamic at the onset of the cluster HA, alcohol the only trigger
- it is shaped and stabbing – pain is in around the eye and radiated to

the forehead cheek, nose, or gums and swelling around the eyes.
may be accompanied by unilateral ptosis or lacrimation.
 dx – keep a headache diary can be useful. CT and
MRI may rule out aneurysm
 Migraine- unknown cause -recurring and unilateral- steady
throbbing pain with synchronous pulse- autonomic more femalerisk factors – education family hx- type common(without aura and
classic( aura such as headache for hours or days prodrome (
photophobia, psychologic, hyperactivity, irritability, and food craving
)- subjective hyperexcitability. associated with seizure, ischemic
stroke, Asthma, depression, anxiety, myocardial infraction Raynaud’s
syndrome and irritable bowel syndrome. may last 72 hours. hibernate to color, light, odors, and the presence of people)
 Aura is neurologic neuro symptoms ( bright light,
scotomas( patchy blindness) visual distortion ( zigzag
line) weakness, paralysis, feeling of limbs are moving)
precedes HA 10 to 30 minutes.
 diagnosis – pt history CT, MRI
 drug triptan (sumatriptan) is a specific serotonin
agonist that cause vasoconstriction _ pt with heart
disease and stroke should avoid it – used for cluster HA
 Frontal-type(migraine and tension) -the Dx is trough thorough family
hx
 Tension type - Stress HA- bilateral location, pressing and tightening
quality(last day and night). episode and chromic – constant dull
pressing or bandlike headache associated with neck pain and
increased in tone in the cervical and neck muscle. involve in the light
and sound photophobia – activity does not aggravated symptoms.
dx history assessment most important and electromyogram
(EMG)
Restless leg syndrome (Willis-Ekbom diseases) – unpleasant sensory ( paresthesia) and
motor abnormally on one or both leg –
 primary (idiopathic)– abnormal iron metabolism
 secondary- metabolic abnormality r/t iron deficiency, renal failure,
polyneuropathy associated with DM, RA, pregnancy. amenia
 is related to dysfunction in the brain ganglia circuits that used neurotransmitter
dopamine, which controls movement.- cause the urge to move the legs
 clinical manifestations
 paresthesia, numbness, tingling,subjective- sensation of bugs creeping or
crawling on the legs , pain localizes on the cap muscles sleep disturbance- pins
and needle sensation to severe pain
 motor abnormalities voluntary restlessness
 periodic involuntary movement




DX – CBC serum ferritin and renal function test – hx od DM pt,
polysomnography studies (apnea)
encourage -non drug encourage sleep and exercise
more then one drug therapy – Sinemet( cardopa/levodopa), permax, ,
Neurontin, Depakote, clonidine. dopamine agonist ( ropinirole (requip),
Mirapex(pramipexole) benzodiazepine, low dose oxycodone
eliminated – aggravating factors – such caffeine, alcohol, certain drugs, (
neuroleptics, lithium, antihistamines, antidepressant)

Alzheimers diseases- over production of B amyloid protein
o stage 1- healthy and alert, restlessness, forgetful uncoordinated
o stage 2 –memory deficits become more apparent, language deficit (wrong word
and repetition of words or phrases), lose ability to complete simple tacks. sleep
disturbances. depression, sundowning reaction is agitation, disorientation and
wandering behaviors in late evening or night.
o Stage 3 - increased dependence, inability to communicate, loss of continence
and progressive loss of cognitive abilities
o 7 years od life expectancy.
o dx EEG, MRI, PET, psychometric evaluation ( Folstein mini mental exam)
o meds – cholinesterase inhibitor ( mild to moderate) Aricept(donepezil),
Exelon(rivastigmine) , razadyne ) > ADL, decreased agitation, and hallucinations
o Namenda SR(Mentatine (NMDA) ) – protect brain cells from people that
experience decrease in cognitive.
o depression med lorazepam (Ativan), risperidone (risperidone), and sertraline
(Zoloft)
o nursing care – lifeline program. reminder ( alarm clock, pocket computer, simple
yes or no question in the early stage 1
o constant reorientation- stage 1
o sundowning is a disruption in circadian rhythms – daylight will help to restablish
a more normal circadian pattern

Parkison’s disease
o basal ganglia – down in initiated and execute movement
- > muscle tone, tremor, at rest , impaired pasture reflexes
o show degeneration of dopamine – product by substantia nigra the mid brain.
Sign start after 80% of the neuro is lost – before you start getting the symptoms
o sign - ESP + tremors at rest
- onset is gradual and insidious
- than mild tremor, a slight limb, decrease arm swing
- later sever – short shuffering gait , propulsive gait with arm flex and
lost of posture reflexes. rigidity is typical by jerky motion and slowness
of movement
-
o
o
o
o
o
o
o
Bradykinesia – loss od autonomic movement such as blinking,
swallowing, of salivation, self-expression with facial and hand
movement.
- stooped posture = blank mask like facial expression, drooling of saliva,
and suffering gait- care full when the eat – risk for aspiration.
Complication
progressive deterioration with the loss of spontaneity movement
swallowing difficulty
severe debilitation leads to pneumonia
UTI and skin breakdown
decreased mobility
- gait is slow and shuffling
- head and trunk and bent forward and legs are constantly flexed
Diagnosis is base on solely on hx and clinical features
- two/three of tremor, rigidity, bradykinesia ( slowed movement)
- positive to response to antiparkinson’s med – is the ultimate
confirmation of the disease
- dementia 40 %
o
o
o
o
o
o

Meds is to correct the imbalance neurotransmitter with the CNS
to > dopamine and < cholinergic to brain
levodopa – cross the brain- barrier and convert to DA in the basal ganglia
levodopa cabidopa ( Sinemet) is the drug od choice) – inhibit enzyme od
dopamine in the prereferral and help to enter the brain.
o MAO inhibitor selegeline – to control rigidity and bradykinesia movement.
o surgery is to provide an arm relive
o Ablation surgery tx PD and it replace by deep brain stimulation (DBS)
- placing electrode In the thalamus, globus pallidus, or subthalamic
connect the generator with upper chest deliver specific electricity to
the brain
- transplantation of fetal neural tissue into the basal ganglia provides
DA in the brain still on experimentation.
NI- cut into small size – several small meals provid time to eat
levodopa impaired protein _ decreased intake in protein- decreased the abruption of
dopamine in the brain.
Multiple sclerosis – SNS – everything go Up
o chronic -muelin and nerve axon in brain/spinal cord destroyed lead to
interruption of the nerve impulse.
o plaque formation of the write matter after C,T,L spinal cord cause inflammation
and scaring lead to disability.
o benign relapse collapse remission – progressive primary and secondary
o exacerbated y stress fever, fatigue, pregnancy
o
o
o
o
o
o

unknown cause -auto/ genetic. viral
manifestation- visual disturbance
- sudden progressive weakness- early weakness in the leg start first
- spasticity Spasm, tremors, gait inability,
- bladder/bowel dysfunction incontinence
- depression
Diagnosis
- lumbar puncture for CSF – clonal IgG bands - > protein > WBC
- MRI , CT, Muscle testing hx physical
meds
- corticosteroids- ACTH, prednisone
- immunomodulators glatiramer acetate copaxone, avonex- teach how to
draw-up and administer med
- immunosuppressant novantrone
- prostigmine, Urecholine- cholinergic
- Ditropan, damtrium, lioresol- anticholinergic
- antibitotics ( UTI)
- check the creatine before give fampridine (Ampyra)
N/I rest period, prevent fatigue, fluid intake 2000ml /day minimum, promote
independence
teach the pt for crede method for flaccid bladder. to improve bladder emptying
Myasthenia gravis
- autoimmune anti body destroyer the cholinergic receptor at the neuromuscular
junction
- chronic progression of PNS ( everything will go down) r/t to nerve transmission
to voluntary muscle = fluctuating weakness, fatigue on exertion and relive with
rest.
- unknown cause – autoimmune disorder thyroid ( lack of tyrosine kinase- tymus
tissue )
- autoantibodies , between receptors =wider gap between axon ending and
muscle in neuromuscular junction.
- Muscle contraction hindered; receptors dis
- the onset is slow; precipitated by stress, hormonal change r/t pregnancy,
menses, thyroid disorder, infection, vaccination trauma, surgery, extreme
temperature excess, in exercise, meds that bock the neurotransmitter, opioid,
sedative, bars, ETOH,
- diagnosis test ABCs, PFT EMG,
- Tensilon test= IV administration with promote voluntary muscle contraction by
allowing acetylcholine to bind with receptors to improve symptoms , weakness,
returns after tension effects gone.



after injection tension if there is an improve in muscle contraction ( pt
has MG) -if the worsening of the Sx the cholinergic crisis and should
have atropine ready when testing.
- positive test finding confirms diagnosis MG
- Manifestations
 mild diplopia; unilateral ptosis, constricted pupils.
 muscle weakness of the face, jaw, neck, hip
 muscle related to chewing, swallowing, respirations serious -are the
most serious
 bowel and bladder incontinence
 paresthesia pain
 myasthenic crisis( under medicated) sudden motor weakness, risk for
respiratory failure and aspiration. – positive Tensilon test
 cholinergic crisis (over medicated) sevre mucle weaknes with cramps,
diarrhea, bradycardia, bronchial spasm.
- nursing care focus
 maintain airway/effective respiration assess for respiratory infection.
 monitor meal time bent forward slightly to avoid meal aspiration
 provide adequate nutrition small frequent meals
 30 to 45 mins per meals for peak muscle strength at meals ; IV flds, NG
 promote mobility = PT, OT ,
 eye care = artificial tears. patch, sunglasses
 meds=pyridostigmine, Mestinon, steroids, Imuran, Cytoxan,
 teach to take the med 30 minute prior to meals.
 educate about rest energy conservation, activity with peak med effects.
 avoid extremes hot/cold exposure to infection; stress’ meds, that
precipitate exacerbation like ETOH, sedative, local anesthetics
 signs of crisis; med alert ID
 communication options =flash cards/boards.
Amyotrophic lateral sclerosis (ALS)(lou Gehrig’s disease)
quinidine/anesthetics and thymus disorders.
- destruction of the motor neuron in the brainstem and spinal cord gradually
degenerated – motor neurons last with axon degeneration that causes
demyelination. lack in transfer signal to the brain.
- affected the cranial nerve III, IV, VI
- lead to death with 3 to 5 years
- cause is unknow – viral, metabolic, trauma, familial.
- UMN= spasticity weakness muscle > in reflexes
- LMN- muscle atrophy, flaccid paralysis,
- loss muscle innervation=muscle atrophy=disease muscle mass= increased
fatigue
- typical symptoms – limb weakness, dysarthria, and dysphagia
-
-
others sleep disturbance, pain, spasticity, drooling, emotional lability,
depression, constipation, and esophageal.
- death result from respiratory infection r/t compromise on respiratory function.
- no cure riluzole slow the prohression by decreasing the glutamate( excitatory
neurotransmitter) in the brain
- meds – steroids, ABO’s anticholinesterase (neostigmine), muscle relaxants.
- discuss the artificial method of ventilation and advance director. go to be on
ventilation
- Diagnosis test
 > CRP and protein in CSF- show muscle damage
 CT scan
 Myelography
 muscle biopsy
 EMG – for muscle recirculation.
nursing focus – airways-O2, suction. vent support PRN, cardiac status VS,
 Guillain-barre syndrome (GBS)
-CN(III, V, VI, VII, X, XII)
full recovery is expected
paralysis of the ascending to the nerves that stimulated the thoracic area
 Huntington disease
 hereditary disorder – autosomal dominant trait at the time of conception –
(congenital )- form both men and women. – offspring have 50 % of chance to
have
 movement disorder characterized by both neurologic and behavioral symptoms.
- the pathogen of HD is involved in the basal ganglia and extrapyramidal
motor system cause deficiency in DA the neurotransmitter Ach and yaminobutyric ( GABA) and in DA ( dopamine) that lead to symptoms
opposite with is excess in DA parison’s diseases
- tx tetrabenazine (xenazine) to tx chorea and decreased DA at the
synapses of the brain. more palliative care
- used antibiotic to tx infections and guardianship
 gradually clinical onset of mental status change, leading to dementia and
choreiform (chorea) excursive writhing and twitching movement of the limbs,
trunk, and facial muscles( chewing and swallowing -lead to aspiration and
malnutrition) gaits and ambulation become impossible due to chorea calory
requirement is elevated 4000 to 5000 calories /day to maintain body weightdifficulty to hold the head still as a disease progressed presence of swallowing
difficulty.
 three stage the last 5 years for the total of 15 years. death is possible ( 10 to 20
years of the onset of the problem) due to pneumonia followed by suicide.
 management no know cause – genetic counseling antipsychotic med such as
med for anxiety, depression, Obsessive compulsive behavior
 monoamine-depleting agents to management the movement abnormalities and
disabling or interfere with ADLs. and safety

bell’s -CN(VII)- or facial paralysis
 unilateral paralysis of the facial muscle -Affects the motor branches of the facial
nerve. for expression foe one side of the face.
 the sensory portion innervates the anterior two-thirds of one side of the
tongue. unknown cause
 the onset is sudden is almost involve one side of the face. pain behing the ear
and jaw may precede the paralysis. – some cannot blink---may need artificial
tears uncreased tearing on the affected side – no lb study or meds ( steroid)
 Manifestation- numbness ant stiffness on one side of the face
 facial paralysis causes the entire face to droop- private place when eating
 pt believe they have stroke because they cannot wrinkle forehead, close the eye
or pucker lips on the affected side.
 precipitation factors herpes simplex virus
 complete recovery few weeks or months – but permanent paralysis can occurs
with older and diabetes pt
 treatment – corticosteroid, moist heat, gentle massage, electrical stimulation of
the nerve – exercise
 inability to close the eyelid, with an upward movement of the eyeball, when
closure is attempted
 protect eye with sunglass, artificial tearing, tape the eyelid close at night, oral
hygiene

Trigeminal - CN (V) tic douloureaux- chronic disease that affect more women than men
with unknow cause
 characterized by brief repetition of severe facial pain- over the surface of the
skin that often begins near one side of the mouth and continuous ear, eye or
nutrition the same side of the face. and subjective as stabbing pain. decrease in
pain is the higher priority
 pain is initiated by many factors -light touch, eating, swallowing, talking,
sneezing, shaving, chewing gum, brushing, teeth or washing the face.
 change in temperature cold and wind can cause pain. more pain in winter
 Treatment – anticonvulsant –Tegretol, Dilantin (level 10- 20), Neurontin may be
used.to decrease paroxysmal afferent impulse and stop pain – SE- dizziness,
drowsiness, bone marrow function. monitor the drug
 surgery intervention- rhizotomy – surgical reserving of the nerve route
o glycerol rhizotomy -less danger, less sensory aberration ( pain)
o Gamma knife radiosurgery -radiation to reduce pain
o microvascular decompression- greater relieve of pain
o percutaneous radiofrequency rhizotomy- greater relieve of pain
- post-surgery numbness but no residual paralysis – will have loss of
facial sensation to temperature and touch
 nursing care pain management Tegretol
o
o





improving nutrition – refused to eat during period of the attacks.
teach to prevent injury and disease process.
Tetanus or lockjaw – (SNS)
provide by wound contamination tonic spasm or seizure can be prevent by vaccination
 disorder of the nerve system characterized by neurotoxin clostridium tetani.
 when the spore of the neurotoxin inters the open wound, they germinated and
produce toxin incubation 8-12 days or longer
 toxin- peripheral nerve- spinal cord- uncontrolled muscle spasm.- make sure
the vaccine is up to date ( 10 years) ICU on ventilator
 Manifestation
o Pain at the side ( lockjaw)
o stiffness of the jaw and neck’
o dysphagia
o profuse perspiration and drooling
o hyperreflexia
o rigidity and spams on the abdomen neck and back muscle.
o general seizure – typical opisthotonos position- head retracted, back
arched and feet are extended.
o unable to breathe intubation/ ventilator
o urinary retention
o nursing intervention -promote safety, nutrition, cv pulmonary
- place the pt in the dark and quiet to decrease stimulation
- maintain oxygenation trough mechanical ventilation.
- clean the wound with soap and water only- and keel all bacterial
o nursing management
- maintain IV access
- administrate adequate antibiotics
- monitor fluid electrolyte status / UO
- teach for immunization – wound care – wash thoroughly with
soap and water
Botulism
food poisoning cause by indigestion of food contaminated with toxin of bacillus
clostridium botulinum. – anaerobic and does not need o2 found in the soil
can have it by eating uncooked foods- especially home – canned vegetables and fruitd
smoked meats, and vacuum-packed fish.
manifestation – GI tract bound to nerve tissue blocked the relieve of acetylcholine from
nerve endings and cause respiratory paralysis due to the paralyses of skeletal muscle –
after 12-6 hours of indigestion.
o visual disturbance – diplopia, loss of accommodation and fixed, dilation
pupils ( CNIII, VI,IV)
o ptosis
o Gi N/V/D and dry mouth – cathartics enemas gastric lavage
o
o
o
o
o
paralysis of all muscle of the body
respiratory paralysis cause death if not placed on mechanical
ventilation
no effect on mental statute. alert and oriented
CDC notification – located and observe all people
nursing management
- ICU- ventilator tracheostomy / suctioning , rehydration, NPO,
I/O, education ( if the ventilation id maintain the pt can recover
without deficits)
Infection of the brain
o
o
Meningitis – inflammation cause by pathogen – IICP ( brain damage – death)- decrease cerebral
perfusion
main cause is infection.
 inflammation of
 pia-matter
 arachnoid
 subarachnoid place

Meningitis Bacterial most common
- bacterial - Neisseria meningitis, meningococcal, streptococcus,
pneumoniae( mild ear infection), haemophilus influenzae and
E-coli.
- Manifestation – Up –
- early -restlessness, agitation, and irrigation( nuchal rigidity (
stiff neck)
- severe HA
- chills and high fever
- confusion and alteration in LOC
- photophobia
- sign late –
seizures
- of increased IICP( Cushing trail)- widened pulse pressure
,bradycardia , irregular respiration, decreased in loc HA and
vomiting projectile.
- petechial rash ( meningococcal) isolation for droplet( N95) until
lab comes back – increased risk of contagious – other type need
standard precautions (mask, glove, gown)
- Dx lumbar puncture
o complication- arthritis, CNS damage , CNIII- hearing loss , DVT ( infraction
cerebral blood vessel)
o
prevention – vaccination – 11-12 repeated 16 yo – if unvaccinated 13-18one dose if first dose 16yo
- bexsero
- trumba

o
o

Meningitis Virus – or aseptic meningitis - may be cured
- cause by viruses – herpes simplex, zoater, Epstein-barr-viruss or
cytomegalovirus ( CMV)
- manifestation – mild HA- with malaise, V?N and lethargy = mild flu like illnss
prior to the onset of meningitis - > protein and < glucose >WBC
Encephalitis
 acute inflammation of the parenchyma of the brain
 always cause by virus ma may bacteria, fungi ( antifungal med ( amphotericin B or
difuran) or other organism
 may be progressive to coma
Brain Abscess
 purulent material in the brain ( cerebrum and cerebellar)
 cause open wound, infection of the mastoid and the middle ear, nasal cavity or nasal
sinuses
 secondary in infection from cancer / metastatic spread from the lung and heard
 result microorganism of the brain tissues
 Sx of infection: fever, chills, malaise, anorexia
 late seizure and alteration on LOC-sing of < LOC – comatose
 Treatment
 broad spectrum antibiotics for unknow organism ( bacterial_rifampin, or vancomycin,
claforan, give foe7-21 days + steroids to suppressed infalmation.
 interventional method (Ommoya reservoir) – implanted in the lateral part of the brain.
 diagnostic test.
- bacterial -lumbar puncture turbid fluid ( cloudy) and < glucose - gram- stain for bacterial infection
- CT – increased in contraction surrounding show low density care with brain
abscess.
- MRI-hemorrhage
N/I
- monitor LOC
- assess foe seizure precaution
- ABC
- cranial nerve assessment
- IICP symptoms.
herniated intervertebral disk or rupture disk

is the rupture of the protrusion of the nucleus pulposus that surrounding the cartilage between
the inner and outer collar of the intervertebral disk? more in the lower back pain(L4-5 or S1) and
in men more often( 30 to 50 yo)



surgery if the conservation measure if not working
bone graft done if pt has spinal fusion ‘laminectomy an artificial disk replacement
order morphine for decreased in pain.
N/I up right the way












monitor DVT
monitor CSF halo
turn cough and deep breath to prevent otosclerosis or pneumonia
Discharge after surgery
limited stair climbing
limit driving
no lighting object more than 5 lb
restrict pushing and pulling activity
avoid bending or twisting at waist
take a daily work.
head trauma
Review – caring with pati with seizure – safety – O2 whan cane of seizure how long if last,
incotinant – call the doctor – no restrain, any thing on the mouthe
med – takedon – steroid ( < swelling)
mannitol – asmolatiti < fluid > UO
ASA- TIA – keep the platelet from tiking together baby asa 81 mg – going TIA ( iskemic stroke –
go away in the coup a day
spinal injury shock (Spasticity and hyperactive reflexes, Lack of movement and sensation below
the level of injury) neurogenic shock ( hypotension, bradycardia, warm extremities) , Autonomic
dysreflexia ( T6 -bowel assessment, hypertension, bradycardia, throbbing headache, and
diaphoresis. ) ( they can feel) _ > HTN – transition that noting can ascent – know the difference
IICP – sx _ <LOC, restleness , and confusion – awake, and 2 hrs later very lathegic – cuching triad
( widen pulse peruse ) shyn staoc long period of apnea
epidural hematomas – is arterial – is ER – uncouscouis then wake up – don’t see immmediated
medical tx –
subdural is veonus – slow – need a let of timw
older people – the brain shweng – no sx for 2 or 3 days and lathalgy – bc the have more room
CN III< IV< VI
delegated qieustion LPN – can not do primary assess no IV push, they can give grug
CAN= set the room for isolation
eyes disordie glucama detached reine
muscular disorder –
no > temperature in stroke pt - > metabolic demanded -> ICP
put the catheter into the ventricle – sterile technique
Aneurysm sx
meningitis bacterial – isolation droplet – cloudy, <glocuse > protein
test the ring around gauze blood Halo –for sugar
maysimax – graives tenseltong - too much monotir respiration status
retrain – midtens – reatelness put the IV
ICU propofol – short minute , brain injury- < propofal make the pt wake
weakness in the leg.
status epilatus – make the seizure stop - > HR, death O2 intubation ( drugs larazepain (adtivent )
broca’s /winkes ( they can speak but they can understand speck
85 questions