The Nervous System Basic concepts in the NORMAL

NEUROLOGICAL FUNCTIONING
2 major parts
1. Oxygen supply- the brain requires
• Central Nervous System
20% of the O2 in the body
• Peripheral Nervous System
2. Glucose supply- requires 65 to 70%
CNS is composed of the BRAIN and SPINAL in the body
CORD 3. Blood supply- requires 1/3 of the
cardiac output
BRAIN-cerebrum…. brain stem… cerebellum
4. Acid base balance- acidosis causes
CEREBRUM- OUTER LAYER composed of 2 cerebral vasodilation and increased
frontal lobes---2 parietal lobes--- and 2 ICP
occipitals.
Alkalosis
Cerebellum – functions are the followings
• causes cerebral vasoconstriction
1. Keep person oriented in space and and increase ICP
maintain truncal. Equilibrium • A CNS stimulant which may lead
2. Control antigravity muscles to SEIZURE
3. Check or halt volitional movement 5. Blood brain barrier- intact blood brain
barrier protects the brain. And
Physiological Changes of the NS
determine protects the brain from
AGING certain dri8gs chemicals and
1. Loss of brain cells with actual loss of microorganism
brain weight. 6. CSF volume- CSF cushions brain, it
2. GYRI of the brain surface atrophy, nourishes the brains and determine
causing widening and deepening of Ige ICP
space between gyri. Three common problems among client
3. Decrease un the blood flow > with neurologic disorders
increase reaction time and > increase
time for the decision making. 1. Increase Intracranial pressure
4. Impairment of short-term memory 2. Seizures
5. Ability of the brain to autoregulate its 3. Altered level of consciousness
blood supply >> lessens
6. Alteration of the sleep --- weak
fullness ratio. • ICP more than 15mmHg
7. Decrease ability to regulate body • Brunner- Normal ICP 10-20mmhg
temperature because of changes in
Causes
the functions of the hypothalamus.
8. Sensory and motor conduction • Head Injury
decrease in velocity of the nerve • Stroke
impulses. Sensory conduction • Inflammatory lesions
decreasing faster than motor, • Brain tumor
especially in the peripheral nerves. • Surgical complications
Cerebrospinal fluid functions Pathophysiology
1. Cushions the brain and protects it The Cranium only contains the brain
from jarring against the skull substances, the CSF and the Blood/blood
2. Nourishes the brain vessels
3. Removes metabolites from the brain
4. Regulates intracranial pressure

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MONRO-KELLIE hypothesis – an increase in • Pupillary changes- fixed, slowed
any one of the components cause a change in response
volume of the other. • Headache
• Vomiting
Any increase or alteration in these structures
will cause increased ICP. Late manifestations:
Compensatory mechanism (still in • Cushing reflex- systolic
pathophysiology)
hypertensions, bradycardia, and wide
1. Increase CSF absorption pulse pressure.
2. Blood shunting • Bradypnea
3. Decreased CSF production • Hyperthermia
• Abnormal posturing
Decompensatory mechanisms
Nursing Interventions:
1. Decreased cerebral perfusion
2. Decreased PO2 leading to brain Maintain patent airway
hypoxia
1. Elevate the head of the head of the
3. Cerebral edema
bed 15-30 degrees- to promote
4. Brain herniation
venous drainage
Decreased cerebral Blood flow 2. Assist in administering 1005 oxygen or
controlled hyperventilation- to reduce
• Vasomotor reflexes are stimulated
the CO2 blood glucose levels—
initially--- slow bounding pulses
constricts blood vessels—reduces
• Increased concentration of carbon
edema
dioxide will cause VASODILATION----
3. Administer prescribed medications-
increased flow----- increased ICP.
usually
Cerebral edema • Mannitol- to produce negative
fluid balance
• Abnormal accumulation of fluid in the • Corticosteroid- to reduce
intracellular space, extracellular edema
space or both.
• Anticonvulsants- to prevent
Herniation seizures
4. Reduce environmental stimuli
• Results from an excessive increased 5. Avoid activities that can increase ICP
in ICP when the pressure builds up like Valsalva, coughing, shivering, and
tissue and the brain presses down or vigorous suctioning.
the brain stem. 6. Keep head in neutral position – AVOID
extreme flexion, Valsalva
Cerebral response to increased ICP
7. Monitor for secondary complications
Cushing’s Response • Diabetes insipidus- output of
>200 mL/hr.
1. Vasomotor center triggers rise in BP to
• SIADH
increase ICP
2. Sympathetic response is increased Altered level of consciousness
BP but the heart rate is slow
3. Respirations become SLOW. • It is a fx and symp. of multiple
pathophysiologic phenomena.
Clinical manifestations • Causes;
Early Manifestations: o Head injury
o Toxicity
• Changes in the LOC- usually the o Metabolic derangement
earliest

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 • Disruption in the neuronal • Regular turning every 2 hours
transmission • 30 degrees bed elevation
• Results to improper function • Maintain corrects body
• Orientation to time alignment by using trochanter
• Motor function roils, foot board
• Decorticate 6. Preserve corneal integrity
• Sensory function • Used artificial tears every 2
hours
7. Achieve thermoregulation
• Minimum amount of beddings
• Rectal or tympanic
temperature
• administer acetaminophen as
prescribed
8. Prevent urinary retention
• Use of intermittent
Etiologic Factors catheterization
1. Head injury 9. Promote bowel function
2. Stroke • High fiber diet
3. Drug overdose • Stool softeners and
4. DKA suppository
5. Hepatic failure 10. Provide sensory stimulation
• Touch and communication
Assessment
• Frequent reorientation
1. Behavioral changes
2. Pupils are slowly reactive
3. The, patient becomes unresponsive • Cephalgia
and pupils become fixed dilated • Primary headache- no organic cause
• Glasgow coma Scale is • Secondary headache- with organic
utilized
Cause
Nursing interventions
• Migraine headache- periodic attacks
1. Maintain patent airway of headache due to vascular
• Elevate the head of the bed to disturbance
40 degrees
• Suctioning
2. Protect the patient 1.Aura phase – bright spots or flashing light
• Pad side rails • Lasts from 5-60 minutes
• Prevent injury from • Initial stage of vasoconstriction
equipment, restraints
3. Maintain fluids and nutritional 2.Headache
balance
• Cerebral vasodilation
• Input and output monitoring
• Decrease serotonin levels
• IVF therapy
• Headache both sides, NV
• Feeding through NGT
4. Provide mouth care 3.Recovery phase – HA area is sensi to touch
• Cleansing and rinsing of
• Feeling of exhaustion
mouth
• Petrolatum on the lips
5. Maintain skin integrity

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 Nursing Interventions

1. Avoid precipitating factors

2. modify lifestyle

3. relieve pain by pharmacologic measures

• Beta-blockers
• Serotonin antagonists- “triptan"

DEMYELINATING DISEASES

• Clinically isolated syndrome (CIS):

This is a single, first episode. with
symptoms lasting at least 24 hours
• CAUSE- unknown • Primary progressive MS (PMS):
• Multiple factors- viral infection, genetic Symptoms worsen progressively,
predisposition without early relapses or remissions.
• Common in WOMEN ages 20-40 Some people may experience times
of stability and periods when
symptoms worsen and then get
• Autoimmune better.
• Demyelination of CNS
• Relapse-remitting MS (RRMS): This
(myelin&oligodendrocytes)
episodes of new or increasing
symptoms, followed by periods of
1. MRI- primary diagnostic study remission, during which symptoms go
away partially or totally.
2. CSF Immunoglobulin G • Secondary Progressive MS (SPMS): At
first, people will experience episodes
MS results from progressive demyelination of
of relapse and remission, but then the
the white matter of the brain and spinal cord,
leading to widespread neurologic dysfunction disease will start to progress steadily.

The structures usually involved are the optic

and oculomotor nerves and the spinal nerve
tracts. The disorder does not affect the PNS

The most common areas affected are:

• Optic nerves and chiasm

• Cerebellum
• Cerebrum
• Spinal cord

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 • Exercise
• Wheelchair
• Aspiration precaution
• Eye patch
• Warm packs
• Stress mgt.
• Speech therapist

• Guillain- Barre syndrome is an acute

autoimmune disease marked by
inflammation of the peripheral
nerves, affecting arms and legs and
involves destruction of the myelin
sheath surrounding largest, most
myelinated sensory and motor fibers,
resulting in disrupted proprioception
and weakness.
• GBS is a rare disorder in which body’s
immune system attacks nerves and
causes damage to the peripheral
nerves.
• The nerve injury often causes muscle
weakness, cause paralysis and
sensitivity problems, including pain,
tingling or numbed

CAUSE: unknown origin commonly follows

viral infection

• Demyelination of PNS (myelin only,

intact Schwann cells thus allowing
recovery)
• Ascending weakness and paralysis
• diminished reflexes of the lower
extremities
• Paresthesia

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• potential respiratory failure

• GBS is a result of a cell-mediated

• Initially pain in muscles
immune attack on peripheral nerve
• Weakness of muscle
myelin proteins.
• The onset is gradual and progresses
• The immune system cannot
over days or weeks
distinguish between the two proteins
• Usually begins in the lower
and attacks and destroys peripheral
nerve myelin extremities and progressively involves
the trunk, the upper limbs, and finally
• With the autoimmune attack there is
the bulbar muscles
an influx of macrophages and other
• This pattern is known as Landry
immune mediated agents that attack
myelin, cause inflammation and ascending paralysis
destruction, and leave the axon • Respiratory insufficiency due to
unable to support nerve conduction intercostal and diaphragmatic muscle
• Infectious organism contains an paralysis dysphagia and facial
amino acid that mimics the peripheral weakness
nerve myelin protein. • Papilledema
• The ganglioside GM1b, is the most • Oculomotor and other cranial
likely target of the immune attack. neuropathies

• CPT
• Prevent complications of immobility
• Improve communication

• ICU admission
• Mechanical Ventilation
• PLASMAPHERESIS
• TPN and IVF
• IV IMMUNOGLOBULIN

• Chronic, progressive & degenerative

brain disorder

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 • Profound effects on memory,
cognition & ability for self-care
• Due to destruction of neurons by the
Beta Amyloid plaques

CAUSES:

• Unknown
• Potential factors- Amyloid plaques in
the brain

• it is a degenerative brain disorder of

unknown etiology which is the most
• Alzheimer’s disease attacks nerves
common form of dementia., that
and brain cells as well as
usually starts in late middle age or in
neurotransmitters.
old age, results in progressive
• The destruction of these parts causes
memory loss, impaired thinking,
clumps of protein to form around the
disorientation, changes in personality
brain’s cells. These clumps are known
and mood. There is degeneration of
as “plaques” and b’Bundles”.
brain neurons especially in the
• The presences of the plaques and
cerebral cortes and presence of
bundles starts to destroy more
neurofibrillary tangles and plaques
connections between the brain cells,
containing beta-amyloid cells.
which makes the condition worse.
• It is a chronic, irreversible disease
that affects the cells of the brain and
causes impairment of intellectual
functioning.
• It gradually destroys the ability to
reason, remember, imagine, and
learn.

• memory loss

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 • difficulty to perform familiar tasks
• problems with language
• It is one among the disease affecting
• disorientation to time and place
the basal ganglia and the brain stem.
• Poor or decrease judgment
There is degeneration of
• Problems with abstract thinking
dopaminergic neuron.
• Misplacing things
• There is either reduction of voluntary
• Changes in mood or behavior
movement or abundance of
• Changes in personality involuntary movement
• Loss of initiative • It is the 2nd most common disorder
LATE CLINICAL MANIFESTATIONS next to AD

• Difficulty in abstract thinking

• Difficulty communicating • Destruction of substantia nigra
• Severe deterioration in memory, • Decreased dopamine
language and motor function • Imbalance of Dopamine &
• personality changes Acetylcholine in the corpus striatum
thus impaired in controlling complex
& fine body movements
• No definitive examination
• Brain scan could help CAUSATIVE FACTORS:
• Confirmatory test? • unknown
• Autopsy results • Genetics
• Atherosclerosis

Acetylcholinesterase inhibitors- prevent the

breakdown of acetylcholine, a chemical
messenger important for learning and
memory

• eg. Donepezil (Aricept)

• tacrine HCl (Cognex)
• Rivastigmine (Exelon)
• Galantamine (Razadyne)

Anti-amyloid therapy- it is a compound that

binds to soluble amyloid-beta peptide and
inhibits the formation of neurotoxic
aggregates that leads to amyloid plaque • Tremor in hands, arms, legs, jaw or
deposition in the brain head
• Stiffness of the limbs and trunk
• Eg. tramiprosate (Alzhemed)
• Slowness of movement
• Impaired balance and coordination,
sometimes leading to falls
• Use short simple sentences, words
and gestures
• Maintain a calm and consistent
• Tremor
approach
• Bradykinesia
• Keep bed in low position
• Rigor
• Provide adequate lightning
• Postural instability

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 • Myasthenia gravis has an
unpredictable course that includes
periods of exacerbation and
remission.
• There’s no known cure.
• Drug treatment has improved the
prognosis and allows patients to lead
relatively normal lives, except during
exacerbations.
• if the disease involves the respiratory
• Assess neurological status
system, it can be life-threatening.
• Assess ability to swallow and chew
• Myasthenia gravis affects 2 to 20
• Provide high calorie, high protein, high
people per 100,000.
fiber diet with small frequent meals
• It’s most common in women between
• Increase fluid intake to 2LPD if not
ages 18 and 25 and men between
contraindicated
ages 50 and 60
• Monitor for constipation
• Promote independence along with
safety measures
• The cause of myasthenia gravis isn’t
known it commonly accompanies
autoimmune and thyroid disorders.
1. Anti-parkinsonian drugs- Levodopa,
• 15% of all patients with myasthenia
Carbidopa
gravis have thymomas.
2. Anti-cholinergic therapy -Trihexyphenidyl,
benztropine, orphenadrine, biperiden
• antibodies directed at the
3. Antiviral therapy- Amantadine
Acetylcholine receptor sites
4. Dopamine Agonists- bromocriptine and myoneural junction, thus impaired
Pergolide transmission of impulses

5. Anti-depressants- Sertraline, fluoxetine,

citalopram, amitriptyline
• Autoimmune disease
• Common to women

• It is a chronic autoimmune disorder

affecting the neuromuscular
transmission of impulse in the
voluntary muscle of the body (skeletal
muscle)
• produces sporadic but progressive
weakness and abnormal fatigue in
striated (skeletal) muscles.
• This weakness and fatigue are
exacerbated by exercise and repeated
movement but improved by
anticholinesterase drugs.
• Usually, myasthenia gravis affects
muscles innervated by the cranial
nerves (face, lips, tongue, neck, and
throat), but it can affect any muscle
group.

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 transmission of nerve impulses at the
neuromuscular junction.
1.Ocular form – only eye muscles are involved
• During normal neuromuscular
• Diplopia transmission, a motor nerve impulse
• Ptosis – drooping of eyelids travels to a motor nerve terminal,
stimulating the release of a chemical
2. Generalized form – weakness of the
neurotransmitter called acetylcholine
muscles of the face and throat (bulbar
(ACh). When ACh diffuses across the
symptoms), limb and respiratory weakness
synapse, receptor sites in the motor
• Facial muscle weakness – end plate react and depolarize the
bland/masklike facial expression muscle fiber. The depolarization
• Laryngeal involvement – dysphonia spreads through the muscle fiber,
(voice impairment) causing muscle contraction.
• Dysphagia (difficulty swallowing) – • In myasthenia gravis, antibodies
increases the risk of choking and attach to the ACh receptor sites. They
aspiration (pharyngeal involvement) block, destroy, and weaken these
• Generalized weakness of the sites, leaving them insensitive to ACh,
extremities, and intercostal muscles thereby blocking neuromuscular
decreased vital capacity, and transmission
respiratory failure => MYASTHENIC
CRISIS

• The patient’s blood cells and thymus

gland produce antibodies that block,
destroy, or weaken the
neuroreceptors that transmit nerve
impulses, causing a failure in the

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 • symptomatic relief by inhibiting
breakdown of Ach and increasing
• Blood test
concentration of
• it is performed to determine serum
• available Ach at the neuromuscular
levels of certain antibodies (AChR-
junction
binding antibodies,
• AChR-modulating antibodies,
antirational antibodies), High levels of
• pyridostigmine- counteract fatigue
these antibodies may indicate MG
and muscle weakness and enable
• Neurologic Examination
about 80% of normal
• It involves testing muscles and
• muscle function
reflexes. MG may cause abnormal eye
movements, inability to move the
eyes normally, and drooping eyelids.
• neostigmine- given IV in myasthenic
To test arm and leg muscles, the
crisis
patient may be instructed to maintain
a position against resistance for a • Adverse effects:
period of time. Weakness that occurs • Diarrhea
during this test is called FATIGABILITY. • Abdominal cramps
• Chest X-ray and CT scan • Excessive saliva
• May be performed to detect enlarged • Corticosteroids (Prednisone)- when
thymus (thymoma, which is common weakness is not controlled by
in MG anticholinergics to suppress the
• Tensilon test often use to diagnose immune response
MG. • Initial dose given daily and maintained
• The Tensilon test confirms the for 1 – 2 months
diagnosis by temporarily improving • IVIG – to treat exacerbations; could be
muscle function after an I.V. injection used as a long-term adjunct
of edrophonium or neostigmine. medication
• Long-standing ocular muscle • Adverse effects:
dysfunction, however, may not • HA
respond. This test also differentiates a • Migraine exacerbation
myasthenic crisis from a cholinergic • Aseptic meningitis
crisis. • Flulike sx
• Edrophonium Chloride IV – 30 • PROCAINE – contraindicated for
seconds after injection, facial muscle patients with MG
weakness and ptosis should resolve • ATROPINE – give IV in cholinergic
for about 5 minutes crisis to reduce the effects of Ach;
• Immediate improvement in muscle anticholinesterase overdose or
strength -> (+)test – confirms the toxicity.
diagnosis • Plasmapheresis- px’s plasma and
• ATROPINE SULFATE – used to control plasma components are removed
potential side effects of edrophonium • Blood cells and antibody-containing
chloride => bradycardia, systole, plasma are separated, then the cells
bronchoconstriction, sweating, and a plasma substitute are reinfused
cramping • Thymectomy

• Anticholinesterase drugs-1st line; • Surgical removal of the thymus gland

enhances neuromuscular
transmission; provides

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 • Can produce Ag-specific take advantage of peaks in the
immunosuppression patient’s energy level.
• Elective surgery; done when the • Provide soft, solid foods instead of
clinical course of the disease is stable liquids to reduce the risk of choking.
• Post-op: monitor respiratory function • Always sit the patient up to eat.
• Encourage the patient to take an
active role in deciding about his care.
1.Monitor the patient’s respiratory rate, use of • Evaluate the patient. Look for normal
vital signs, evidence of adequate
accessory muscles, and oxygen saturation to
hydration and normal elimination,
watch for possible respiratory failure related skin that’s free from sores or
to myasthenic or cholinergic crisis problems, and an optimal capacity for
activity.
2.Be alert for signs of impending crisis:
• Encourage the patient and his family
(Myasthenic Crisis)
to discuss their feelings, especially
• Sudden respiratory distress feelings of frustration, grief, or loss.
• Signs of dysphagia, dysarthria, ptosis, Listen and provide emotional support.
• diplopia • Teach the patient how to recognize
• Tachycardia, anxiety adverse effects and signs of toxicity of
• rapidly increasing weakness of anticholinesterase and steroids
extremities and trunk • headache
• weakness, sweating,
3. Monitor the patient’s response to drug
• abdominal cramps nausea,
therapy
• vomiting, diarrhea,
• excessive salivation, bronchospasm
1.Administer medications so their peak effect • Warn him to avoid strenuous exercise,
coincides with meals stress, infection, and unnecessary
• exposure to the sun or cold weather.
2.Help the patient develop a realistic activity
schedule

3.Allow for rest periods throughout the day to 1.Myasthenic or cholinergic crisis – airway
minimize fatigue maintenance, oxygen, and mechanical
ventilation is indicated
4.If the patient has diplopia, provide an eye
patch to use on the alternate eye to minimize 2.Plasmapheresis - to temporarily remove
the risk of tripping and falling circulating Ach antibodies from the blood in
crisis; to treat exacerbations
5.Avoid aspiration
3.Thymectomy – when thymoma or
• teach the px to position the head in a hyperplasia exists; may provide remission in
slightly flexed position some pxs
• to protect the airway during eating
• Have suction available that the px can
operate 1. Administer prescribed medication as
• If px is in crisis or has impaired scheduled
swallowing, administer IV fluids and
2. Aspiration precaution
foods through NG tube; elevate the
head of the bed after feeding 3. Promote respiratory function
• Plan periods of exercise, meals,
patient care, and daily activities to

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4. Prepare for complications like
myasthenic crisis and cholinergic
crisis

• LUMBAR PUNCTURE- used to

diagnose or exclude meningitis
• This involves inserting a needle into
the spinal canal to extract a sample of
CSF

• The usual treatment for meningitis is

prompt application of antibiotics and
sometimes antiviral drugs
• In some situations, corticosteroids
• The most common symptoms of can also be used to prevent
meningitis are headache and neck complication from overactive
stiffness associated with fever, inflammation
confusion pra;tered consciousness,
vomiting and an inability to tolerate
light (photophobia) or loud noises • Assess the patient's mental status
(phonophobia) and provide psychological support if
• Personality and behavior changes the patient is conscious.
• rash can be a striking feature of N. • Elevate the head of the bed to 30
Meningitidis degrees with a straight neck for
venous drainage from the brain.
• Ensure the patient has an IV line for
fluids and medications.
• Administer antibiotics/antivirus as
prescribed.

SCI -> paralysis below the level of injury ->

decrease autonomic function -> spinal shock
(neurogenic shock) -> decrease BP, decrease
HR, flaccid paralysis

• S-sports
• P-pounding
• industrial
• N- number of case/year
• A-accidents (VAr/t alcohol)
• L-lalaki (male)

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 Paraplegia: injury in thoracic, lumbar or
sacral segments; 2 extremities affected

Complete

• Loss of voluntary movement of parts

• innervated by segment,this is
• irreversible
• Loss of sensation
• Injury from C1 – C8 = quadriplegia • Spinal shock
• Injury from Incomplete
• C1 – C4 = resp. failure
• Injury from T1 – T12 = paraplegia • Some function is present below site
• Injury from T6 = autonomic dysreflexia of injury
-> distended bladder -> catheter • More favorable prognosis overall
• Are recognizable patterns of injury,
The most frequent vertebrae – C5-C7, T12 although they are rarely pure and
and L1 variations occur.
Concussion

Contusion

Compression

Transection

1. Paraplegia

2. quadriplegia

3. spinal shock

Quadriplegia: injury in cervical regional 4

extremities affected

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 • Reposition Q2hours
• Check for autonomic dysreflexia
• Transient reflex depression of cord
• Provide skin care
function below level of injury
• Glucocorticoids
• Initially hypertension due to release of
• Cervical collar
catecholamines
• Maintenance of vertebral alignment:
• Followed by hypotension
o Crutchfield tongs, Halo brace
• Flaccid paralysis
• Bowel and bladder involved
• Sometimes priapism develops
Episodes of abnormal motor, sensory,
• Symptoms last several hours to days
autonomic activity resulting from sudden
excessive discharge from cerebral neurons

• CT scan A part or all of the brain may be involved

• MRI

• Pre-ictal: the period before the

• A-B-C seizure (aura)
• Immobilization • Ictal: the period during the seizure
• Immediate transfer to tertiary facility • Inter-ictal: the period between
occurrences of seizure activity
• Post-ictal: the period immediately
1. Promote adequate breathing and airway after the seizure
clearance

2. Improve mobility and proper body

• An electrical disturbance in the nerve
alignment
cells in one brain section----> EMITS
3. Promote adaptation to sensory and ELECTRICAL IMPULSES excessively
perceptual alterations

4. Maintain skin integrity

5. Maintain urinary elimination

6. Improve bowel function

7. Provide Comfort measures

8. Monitor and manage complications

• Thrombophlebitis
• Orthostatic hypotension Most common form in adults with Epilepsy
• Spinal shock

9. Assists with surgical reduction and

• Simple partial – no alterations in
stabilization of cervical vertebral column
consciousness
• One cerebral hemisphere
• Position: flat, neck immobilized Simple motor – frontal lobe
• Assess neurologic & respiratory
status • Seizures begin from hands & face
• VS, IO, pulse oximetry • Stiffening or jerking of hands & face
• Butterflies in the stomach (sensory
• signs)

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 2.Fever

Both hemispheres of the brain as well as 4.CNS infection

deeper structures such as thalamus, basal
3.Head injury
ganglia & upper brain stem
5.Metabolic and toxic conditions
Consciousness is always impaired

Immediate without any warning

During seizure
Forms
1. remove harmful objects from the patient’s
Grand mal – generalized tonic clonic
surrounding
• Proceeds as sudden LOC ->tonic-
2. ease the client to the floor
>clonic
3. protect the head with pillows when she
Absence or Petit Mal – begins during
happens to be standing
childhood
4. Observe and note for the duration, parts of
• Sudden brief cessation of all motor
body affected, behaviors before and after the
activity accompanied by blank stare &
seizure
unresponsiveness lasting for 5-30
secs 5. loosen constrictive clothing especially
around the neck

6. DO NOT restrain, or attempt to place

A complication of epilepsy that is considered tongue blade or insert oral airway
as medical emergency wherein seizure
activity becomes continuous POST seizure

1. Promote a potent airway. place patient to

the side to drain secretions and prevent
1. Patent airway
aspiration
2. Drug therapy
o Anticonvulsant & sedative 2. help re-orient the patient if confused
o Phenobarbitals, Diazepam
3. provide care if patient became incontinent
3. Close monitoring
during the seizure attack

4. stress importance of medication regimen

= occurs in rapid sucession and
consciousness is not regained between
seizure Anticonvulsants are classified as central
nervous system depressant = it suppresses
= BrAin damage may occur due to prolonged
abnormal electrical impulses from the
hypoxia and exhaustion
seizure focus to other cortical areas.
= client is often in coma for 12 to 24 hours.
HYDANTOINS = Phenytoin / Mephenytoin /
And recurring seizres may occur during this
Ethotoin
time.
• these anticonvulsant drugs have the
= the attack is usually related to failure to take
least toxic effect, small effect on
anticonvulsant drugs.
general sedation and is non addicting.
• Therapeutic level of phenytoin is 10 to
20 mcg / ml
1.Idiopathic
• Intravenous infusion of phenytoin
should be administered to a large
vein.

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 • It should be diluted with normal anomalies such as cardiac defects,
saline solution. cleft lip and cleft palate.
• Dextrose solution should not be use
Phenytoin causes pinkish or reddish urine
because it will precipitate
to brown discoloration. This harmless
• Intramuscular injection of phenytoin
effect
irritates tissues and may damage, that
is why it is discourage. Withdraw drug gradually to prevent status
• Continuous IV infusion of epilypticus
PHENYTOIN should not be used
because it can cause hypotension
and cardiac dysrhythmias.
• Mephenytoin is more toxic than
phenytoin. Used for severe grand mal
and psychomotor seizures that does
responds to phenytoin and other
anticonvulsant.
• Ethotoin - produces similar
responses to phenytoin. But has a
short half-life of 3 – 6, therefore, the
chance of. cumulative drug effect
decreases.

Phenytoin ( Dilantin )

Nursing intervention

• Monitor serum drug level to prevent

toxicity
• Ensure adequate nutrition, because it
causes anorexia, nausea and
vomiting
• Avoid driving and operating
machineries and hazardous activities
because drowsiness is apt to occur.
• Avoid alcohol and CNS depressants,
these lowers seizures threshold
• Prevent gum hyperplasia by having
good oral hygiene, massage the gums,
soft bristle toothbrush
• Monitor blood glucose level in
diabetic patient, because phenytoin
inhibits Insulin release causing
hyperglycemia
• Monitor CBC because phenytoin may
cause bone marrow depression and
aplastic anemia
• Take the drug at same time every day
with food or milk to prevent gastric
irritation
• Phenytoin is contraindicated in
pregnancy. Can lead to fetal

S.M.L