3.

​ Decrease in the blood flow, increased

THE NERVOUS SYSTEM
reaction time and increase time
2 MAJOR PARTS required for the decision making
4.​ Impairment in short term memory

2 MAJOR PARTS: 5.​ Ability of the brain to autoregulate its

1.​ CENTRAL NERVOUS SYSTEM blood supply = lessens

2.​ PERIPHERAL NERVOUS SYSTEM 6.​ Alteration of sleep = wakefulness ratio↑

7.​ Decrease ability to regulate body

●​ The CNS is composed of the brain and temperature because of changes in

spinal cord the function of the hypothalamus

○​ BRAIN = cerebrum, brain stem, 8.​ Sensory and motor conduction

cerebellum decreases in velocity of the nerve

impulses. Sensory conduction

CEREBRUM.. decreases faster than motor,

●​ OUTER LAYER especially in the peripheral nerves.

●​ Composed of 2 frontal lobes, 2

parietal, 2 temporal lobes, and 2 CEREBROSPINAL FLUID FUNCTIONS:

occipital 1.​ Cushions the brain and protects it from

jarring against the skull

BRAIN STEM.. 2.​ Nourishes the brain

●​ Diencephalon, midbrain, pons and 3.​ Removes metabolites from the brain

medulla oblongata 4.​ Regulates intracranial pressure

CEREBELLUM.. BASIC CONCEPTS IN NORMAL

Fx as NEUROLOGICAL FUNCTIONING
1.​ Keep person oriented in space and to
maintain truncal equilibrium 1.​ OXYGEN SUPPLY = the brain requires
2.​ Control antigravity muscles 20% of the oxygen in the body
3.​ Check or halt volitional movements 2.​ GLUCOSE SUPPLY =requires 65 to 70%
of glucose in the body
PHYSIOLOGICAL CHANGES OF THE NERVOUS 3.​ BLOOD SUPPLY = the brain requires 1/3
SYSTEM WITH AGING of the cardiac output
4.​ ACID BASE BALANCE = acidosis causes

1.​ Loss of brain cells with actual loss of cerebral vasodilation and increased

brain weight intracranial pressure

2.​ GYRI of the brain surface atrophy, ●​ Alkalosis = causes cerebral

causing widening and deepening of vasoconstriction and increased

spaces between the GYRI (Gyri: is ICP

where you can locate the neurons and ●​ A CNS stimulant which may lead

receptors). to seizure
5.​ BLOOD - BRAIN BARRIER = intact blood
brain barrier protects the brain, and
determines protects the brain from
 certain drugs, chemicals, and
microorganisms
6.​ CSF VOLUME = CSF cushions the brain, Decompensatory mechanism:
it nourishes the brain and determines 1.​ Decreased cerebral perfusion
ICP 2.​ Decreased PO2 leading to brain
hypoxia or cerebral hypoxia (caused

THREE COMMON PROBLEMS AMONG by IICP)

CLIENTS WITH NEUROLOGIC DISORDERS 3.​ Cerebral edema (could lead to icp)
abnormal accumulation of fluid in the
intracellular space, extracellular space
1.​ Increased intracranial pressure (IICP)
or both. (due to hemorrhage e.g. MVA
2.​ Seizures
and surgical operations in the brain)
3.​ Altered level of consciousness
4.​ Brain herniation (Results from the
excessive increase in ICP when the
INCREASED INTRACRANIAL PRESSURE (IICP) pressure builds up and the brain tissue
presses down on the brain stem)
●​ Intracranial pressure more than 15 ●​ Any factors that increase CSF is
mmhg obstruction of the flow of CSF which is
●​ Accdg. to Brunner = normal brain tumor = there will be
intracranial pressure 10-20 mmhg overproduction of CSF)
●​ Causes ●​ IICP = decreased O2 supply to brain
○​ Head injury
○​ Stroke (Cerebrovascular stroke) DECREASED CEREBRAL BLOOD FLOW
○​ Inflammatory lesions
○​ Brain tumor
●​ Vasomotor reflexes are stimulated
○​ Surgical complications
initially = slow bounding pulses
●​ Increased concentration of carbon
PATHOPHYSIOLOGY dioxide will cause VASODILATION =
increased flow = increased ICP
●​ The cranium only contains the brain
substance, the CSF and the CEREBRAL EDEMA
blood/blood vessels
●​ Accdg. to MONRO-KELLIE: hypothesis-
●​ Abnormal accumulation of fluid in the
“an increase in any one of the
intracellular space, extracellular space
components causes a change in the
or both (fluid or blood accumulate
volume of the other”
between spaces of brain)
●​ Any increase or alteration in these
structures will cause increased ICP
HERNIATION

Compensatory mechanisms:
1.​ Increases CF absorption ●​ Results from an excessive increase of
2.​ Blood shunting ICP when the pressure builds up and
3.​ Decreased CSF production
 the brain tissue presses down on the NURSING INTERVENTIONS
brain stem.

MAINTAIN PATENT AIRWAY

CEREBRAL RESPONSE TO INCREASED ICP 1.​ Elevate the head of the bed 15-30
degrees- to promote venous drainage
1.​ CUSHING’S SYNDROME (Elevate the head of the bed to semi-
-​ Vasomotor center triggers rise in BP to fowlers lateral position
increase ICP (15-30-45:maximum degrees angle) to
-​ Sympathetic response is increased BP promote CSF)
but the heart rate is SLOW 2.​ assists in administering 100% oxygen or
-​ Respiration becomes SLOW controlled hyperventilation- to reduce
the CO2 blood levels = constricts blood

CLINICAL MANIFESTATIONS vessels = reduces edema

3.​ Administer prescribed medications-
usually
EARLY MANIFESTATIONS
●​ Mannitol (osmotic diuretic) -
●​ Changes in the LOC- usually the
to produce negative fluid
earliest
balance
●​ Pupillary changes- fixed, slowed
●​ Corticosteroid - to reduce
response
edema (!! The ONLY drug that
●​ Headache
could pass through BBB
●​ Vomiting
because it is a lipid soluble med
>> Taken with antacids orH2
LATE MANIFESTATIONS:
receptor blockers (Ranitidine)
●​ Cushing reflex - systolic hypertension,
(Rationale: neutralize stomach
bradycardia and wide pulse pressure
acid because corticosteroids
(The heart needs a longer time to relax
increases GI irritation)
therefore the diastolic is either
●​ Anticonvulsants - to prevent
decreasing or as is.)
seizures (e.g. diazepam)
●​ Hyperthermia
●​ Anticoagulants - to prevent
●​ Bradypnea
thromboembolism
●​ Abnormal posturing
4.​ Reduce environmental stimuli
5.​ Turn the patient q 2 hrs. to prevent
Anisocoria : a condition where the pupils of
decubitus ulcers
the eyes are of unequal sizes due to the
6.​ Avoid activities that can increase ICP
compression of CN III (oculomotor nerve)
like valsalva, coughing, shivering, and
vigorous suctioning
Brainstem is affected: there could be “doll’s
7.​ Keep your head in a neutral position.
eye” (the movement of the eye follows the
AVOID - extreme flexion, valsalva
movement or direction of the head. There’s
8.​ monitor for secondary complications
decortication of limbs.
●​ Diabetes insipidus- output of
>200 mL/hr
●​ SIADH
 ●​ COMA= clinical state of
●​ drainage from the subarachnoid unconsciousness where patient is NOT
spaces of the spinal cord and also aware of self and environment
promote high expansion.
●​ DON’T elevate the head in 90 degrees ASSESSMENT
angle because it could cause brain
herniation
●​ Orientation to time, place and person
●​ Motor function
Reminders to avoid ↑ ICP: ●​ Decorticate
●​ AVOID Too much straining
●​ Decerebrate
●​ AVOID Nausea and vomiting
●​ Sensory function
●​ AVOID Suctioning EXCESSIVELY
●​ AVOID Rectal examination ★​ Behavioral changes initially
●​ AVOID Giving Enema ★​ Pupils are slowly reactive
●​ AVOID Bending and stooping ★​ Then , patient becomes unresponsive
●​ Coughing and sneezing (advice to and pupils become fixed dilated
open the mouth during this time) ★​ Glasgow Coma Scale is utilized
●​ Control hypertension to reduce
cerebral tissue perfusion
●​ Restrict fluid intake: from 1,200 to 1,500 ETIOLOGIC FACTORS
mL/day

1.​ Head injury

ADDITIONAL NOTES:
●​ Foot Drop: a condition where the front 2.​ Stroke
part of the foot cannot be lifted, 3.​ Drug overdose
causing the toes to drag while walking. 4.​ Alcoholic intoxication
It is typically caused by weakness or 5.​ Diabetic ketoacidosis
paralysis of the muscles responsible for 6.​ Hepatic failure
lifting the foot.
●​ Use artificial tear drop (eye drop): use
for patients with coma who tend to NURSING INTERVENTIONS
have eye dryness.
●​ Stool softener: laxatives (SE: diarrhea)
1.​ Maintain patent airway
●​ Elevate the head of the bed to
2. ALTERED LEVEL OF CONSCIOUSNESS 30 degrees
●​ It is a function and symptom of ●​ Suctioning
multiple pathophysiological 2.​ Protect the patient
phenomena ●​ Pad side rails
●​ Causes: head injury, toxicity and ●​ Prevent injury from equipments,
metabolic derangement restraints.
●​ Disruption in the neuronal transmission 3.​ Maintain fluid and nutritional balance
results to improper function ●​ Input and output monitoring
●​ Patient is not oriented ●​ IVF therapy
●​ Patient does not follow command ●​ Feeding through NGT
●​ Patient needs persistent stimuli to be 4.​ Provide mouth care
awake ●​ Cleansing and rinsing of mouth
 ●​ Petrolatum on the lips 4. MIGRAINE
5.​ Maintain skin integrity ●​ Pain: throbbing pulsating
●​ Regular turning every 2 hours ●​ Stimulants: coffee, chocos, citrus fruits
●​ 30 degrees bed elevation a.​ Aura phase – bright spots or flashing
●​ Maintain correct body light
alignment by using trochanter -​ Lasts from 5-60 minutes
rolls, foot board -​ Initial stage of vasoconstriction
6.​ Preserve corneal integrity b.​ Headache
●​ Use of artificial tears every 2 -​ Cerebral vasodilation
hours -​ Decrease serotonin levels
7.​ Achieve thermoregulation -​ Headache both sides, NV
●​ Minimum amount of beddings c.​ Recovery phase – HA area is sensitive
●​ Rectal or tympanic temperature to touch
●​ Administer acetaminophen as -​ Feeling of exhaustion
prescribed
8.​ Prevent urinary retention NURSING INTERVENTIONS
●​ Use of intermittent
catheterization
1.​ Avoid precipitating factors
9.​ Promote bowel function
2.​ Modify lifestyle
●​ High fiber diet
3.​ Relieve pain by pharmacologic
●​ Stool softeners and suppository
measures
10.​Provide sensory stimulation
●​ Beta-blockers
●​ Touch and communication
●​ Serotonin antagonists- “triptan"
●​ Frequent reorientation
Example: Imitrex
-​ Taken with a full glass of water >
3. HEADACHE
-​ CONTRAINDICATIONS: hypertensive,
●​ Cephalgia
renal and hepatic impairment
●​ Primary headache- no organic cause
●​ Secondary headache- with organic
cause DEMYELINATING DISEASES

●​ Migraine headache- periodic attacks

MULTIPLE SCLEROSIS
of headache due to vascular \

disturbance ●​ CAUSE - unknown

●​ Cluster headache- short extremely ●​ Multiple factors- viral infection, genetic
painful typeof headache that occurs in predisposition
cyclical patterns or "clusters” (multiple ●​ Common in WOMEN ages 20-40
times a day/wks/mos. At the same ●​ MS results from progressive
time each day) There’s an intense, demyelination of the white matter of
deep throbbing, unilateral (one-sided) the brain and spinal cord, leading to
pain starting from around the eye or widespread neurologic dysfunction
temple→head→neck >>Precipitated by ●​ The structures usually involved are the
alcohol optic and oculomotor nerves and the
 spinal nerve tracts. The disorder does PATHOPHYSIOLOGY:
not affect the PNS The most common areas affected are:
●​ Optic nerves and chiasm
What went wrong? ●​ Cerebellum
●​ Autoimmune ●​ Cerebrum
●​ Demyelination of CNS ●​ Spinal cord
●​ (myelin & oligodendrocytes)

DIAGNOSTIC TESTS
1.​ MRI- primary diagnostic study
2.​ CSF Immunoglobulin G

TYPES:
●​ Clinically isolated syndrome (CIS):
This is a single, first episode. with
symptoms lasting at least 24 hours
●​ Primary progressive MS (PMS):
Symptoms worsen progressively,
without early relapses or remissions.
Some people may experience times of
stability and periods when symptoms
worsen and then get better.
●​ Relapse-remitting MS (RRMS): These
episodes of new or increasing
symptoms, followed by periods of
remission, during which symptoms go
away partially or totally.
●​ Secondary Progressive MS (SPMS): At
first, people will experience episodes of
relapse and remission, but then the
disease will start to progress steadily. CLINICAL MANIFESTATIONS:
●​ Muscle weakness: lack of use or
stimulation and nerve damage.
●​ Numbness and tingling: A pins and
needles-type sensation in the face,
body, or arms and legs.
●​ Lhermitte's sign: an electric shock like
sensation when they move their neck,
●​ Bladder problems: difficulty in
emptying their bladder or need to
urinate frequently or suddenly. Loss of
bladder control.
●​ Bowel problems: Constipation can MEDICAL MANAGEMENT:
cause fecal impaction, which can lead 1.​ Corticosteroids
to bowel incontinence. ●​ To reduce edema and
●​ Fatigue inflammation of myelin sheath
●​ Dizziness and vertigo ●​ Eg. Corticotropin, Prednisone,
●​ Sexual dysfunction: Both males and Dexamethasone
females may lose interest in sex. 2.​ Interferon beta-1a or interferon
●​ Spasticity and muscle spasms: beta-1b
Damaged nerve fibers in the spinal ●​ to decrease the frequency of
cord and brain can cause painful relapses.
muscle spasms, particularly in the legs. 3.​ Chlordiazepoxide
●​ Tremor: involuntary quivering ●​ to mitigate mood swings,
movements. 4.​ Baclofen or dantrolene
●​ Vision problems: double or blurred ●​ to relieve spasticity, and
vision, a partial or total loss of vision, or 5.​ Bethanechol or oxybutynin
red- green color distortion. ●​ to relieve urine retention and
●​ Gait and mobility changes: MS can minimize urinary frequency and
change the way people walk, because urgency.
of weakness and muscle problems
with balance, dizziness, and fatigue. NURSING INTERVENTIONS:
●​ Emotional changes and depression: ●​ Exercise
Demyelination and nerve-fiber ●​ Wheelchair
damage in the brain can trigger ●​ Aspiration precaution
emotional changes. ●​ Eye patch
●​ Learning and memory problems: These ●​ Warm packs
can make it difficult to concentrate, ●​ Stress mgt.
plan, learn, prioritize, and multitask. ●​ Speech therapist
●​ Pain: Neuropathic pain is directly due
to MS. Other types of pain occur GUILLAIN - BARRE SYNDROME (GBS)
because of weakness or stiffness of
muscles.
●​ Guillain- Barre syndrome is an acute
●​ Less common symptoms include:
autoimmune disease marked by
○​ Headache
inflammation of the peripheral nerves,
○​ Hearing loss
affecting arms and legs and involves
○​ Itching
destruction of the myelin sheath
○​ Respiratory or breathing
surrounding largest, most myelinated
problems
sensory and motor fibers, resulting in
○​ Seizures
disrupted proprioception and
○​ Speech disorders
weakness.
○​ Swallowing problems
●​ GBS is a rare disorder in which the
body's immune system attacks nerves
and causes damage to the peripheral
nerves.
 ●​ The nerve injury often causes muscle CLINICAL MANIFESTATIONS:
weakness, cause paralysis and ●​ Initially pain in muscles
sensitivity problems, including pain, ●​ Weakness of muscle
tingling or numb ●​ The onset is gradual and progresses
●​ GBS is a result of a cell-mediated over days or weeks
immune attack on peripheral nerve ●​ Usually begins in the lower extremities
myelin proteins. and progressively involves the trunk,
●​ Infectious organisms contain an amino the upper limbs, and finally the bulbar
acid that mimics the peripheral nerve muscles
myelin protein. ●​ This pattern is known as Landry's
●​ The immune system cannot ascending paralysis
distinguish between the two proteins ●​ Respiratory insufficiency due to
and attacks and destroys peripheral intercostal and diaphragmatic muscle
nerve myelin paralysis
●​ The ganglioside GM1b, is the most likely ●​ dysphagia and facial weakness
target of the immune attack. ●​ Papilledema
●​ With the autoimmune attack there is ●​ Oculomotor and other cranial
an influx of macrophages and other neuropathies
immune mediated agents that
●​ attack myelin, cause inflammation and NURSING MANAGEMENT:
destruction, and leave the axon unable ●​ CPT
to support nerve conduction ●​ Prevent complications of immobility
●​ CAUSE: unknown origin commonly ●​ Improve communication
follows viral infection
MEDICAL MANAGEMENT:
What went wrong? ●​ ICU admission
●​ Demyelination of PNS (myelin only, ●​ Mechanical Ventilation
intact Schwann cells thus allowing ●​ PLASMAPHERESIS
recovery) ●​ TPN and IVF IV
●​ Ascending weakness and paralysis ●​ IMMUNOGLOBULIN
●​ Diminished reflexes of the lower
extremities ALZHEIMER’S DISEASE
●​ Paresthesia
●​ Potential respiratory failure
●​ It is a degenerative brain disorder of
unknown etiology which is the most
PATHOPHYSIOLOGY:
common form of dementia., that
usually starts in late middle age or in
old age, results in progressive memory
loss, impaired thinking, disorientation,
changes in personality and mood.
There is degeneration of brain neurons
especially in the cerebral cortex and
 presence of neurofibrillary tangles and 10 WARNING SIGNS OF ALZHEIMER’S DISEASE:
plaques containing beta-amyloid cells. 1.​ Memory loss
●​ It is a chronic, irreversible disease that 2.​ Difficulty to perform familiar tasks
affects the cells of the brain and 3.​ Problems with language
causes impairment of intellectual 4.​ Disorientation to time and place
functioning. 5.​ Poor or decrease judgment
●​ It gradually destroys the ability to 6.​ Problems with abstract thinking
reason, remember, imagine, and learn. 7.​ Misplacing things
8.​ Changes in mood or behavior
WHAT WENT WRONG? 9.​ Changes in personality
●​ Chronic, progressive & degenerative 10.​ Loss of initiative
brain disorder
●​ Profound effects on memory, cognition CLINICAL MANIFESTATIONS:
& ability for self care ●​ Amnesia – loss of memory
●​ Due to destruction of neurons by the ●​ Apraxia – unable to determine
Beta Amyloid plaques function & purpose of object
●​ Agnosia – unable to recognize familiar
CAUSES: object
●​ Unknown ●​ Aphasia - language disorder that
●​ Potential factors- Amyloid plaques in affects communication
the brain
LATE CLINICAL MANIFESTATIONS:
PATHOPHYSIOLOGY: ●​ Difficulty in abstract thinking
●​ Alzheimer's disease attacks nerves and ●​ Difficulty communicating
brain cells as well as ●​ Severe deterioration in memory,
neurotransmitters. language and motor function
●​ The destruction of these parts causes ●​ Personality changes
clumps of protein to form around the
brain’s cells. These clumps are known DIAGNOSTIC TEST:
as “plaques” and b’Bundles”. The ●​ No definitive examination
presences of the plaques and bundles ○​ Brain scan could help
starts to destroy more connections ●​ Confirmatory test?
between the brain cells, which makes ○​ Autopsy results
the condition worse
DRUG THERAPY:
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)
 ●​ Stiffness of the limbs and trunk
Anti-amyloid therapy ●​ Slowness of movement
●​ it is a compound that binds to soluble ●​ Impaired balance and coordination,
amyloid-beta peptide and inhibits the sometimes leading to falls
formation of neurotoxic aggregates
that leads to amyloid plaque 4 CARDINAL SIGNS:
deposition in the brain ●​ Tremor
-​ Eg. tramiprosate (Alzhemed) ●​ Bradykinesia
●​ Rigor
NURSING INTERVENTIONS: ●​ Postural instability
●​ Use short simple sentences, words and
gestures NURSING MANAGEMENT:
●​ Maintain a calm and consistent ●​ Assess neurological status
approach ●​ Assess ability to swallow and chew
●​ Keep bed in low position ●​ Provide high calorie, high protein, high
●​ Provide adequate lightning fiber diet with small frequent meals
●​ Increase fluid intake to 2LPD if not

PARKINSON’S DISEASE contraindicated

●​ Monitor for constipation
●​ Promote independence along with
●​ It is one among the diseases affecting
safety measures
the basal ganglia and the brain stem.
●​ There is degeneration of dopaminergic
MEDICAL MANAGEMENT:
neurons. There is either reduction of
1.​ Anti-parkinsonian drugs
voluntary movement or abundance of
-​ Levodopa, Carbidopa
involuntary movement
2.​ Anticholinergic therapy
●​ It is the 2nd most common disorder
-​ Trihexyphenidyl, benztropine,
next to AD
orphenadrine, biperiden
3.​ Antiviral therapy
WHAT WENT WRONG?
-​ Amantadine
●​ Destruction of substantia nigra
4.​ Dopamine Agonists
●​ Decreased dopamine
-​ Bromocriptine and Pergolide
●​ Imbalance of Dopamine &
5.​ Antidepressants
Acetylcholine in the corpus striatum
-​ Sertraline, fluoxetine, citalopram,
thus impaired in controlling complex &
amitriptyline
fine body movements

CAUSATIVE FACTORS: UNKNOWN MYASTHENIA GRAVIS

●​ Genetics
●​ Atherosclerosis ●​ It is a chronic autoimmune disorder
affecting the neuromuscular
SYMPTOMS: transmission of impulse in the
●​ Tremor in hands, arms, legs, jaw or voluntary muscle of the body (skeletal
head muscle)
 ●​ Produces sporadic but progressive MANIFESTATION:
weakness and abnormal fatigue in ●​ Drooping
striated (skeletal) muscles. ●​ Diplopia
●​ This weakness and fatigue are ●​ Dysphonia
exacerbated by exercise and repeated ●​ Dysphagia
movement but improved by ●​ Dyspnea
anticholinesterase drugs. §Usually, ●​ Distress
myasthenia gravis affects muscles ●​ Weakness
innervated by the cranial nerves (face,
lips, tongue, neck, and throat), but it WHAT TO LOOK FOR:
can affect 1.​ Ocular form – only eye muscles are
●​ Myasthenia gravis has an involved
unpredictable course that includes ●​ Diplopia
periods of exacerbation and remission. ●​ Ptosis – drooping of eyelids
●​ There’s no known cure. 2.​ Generalized form – weakness of the
●​ Drug treatment has improved the muscles of the face and throat (bulbar
prognosis and allows patients to lead symptoms), limb and respiratory
relatively normal lives, except during weakness
exacerbations. ●​ Facial muscle weakness –
●​ If the disease involves the respiratory bland/mask like facial
system, it can be life-threatening. expression
●​ Myasthenia gravis affects 2 to 20 ●​ Laryngeal involvement –
people per 100,000. dysphonia (voice impairment)
●​ it’s most common in women between ●​ Dysphagia (difficulty
ages 18 and 25 and men between ages swallowing) – increases the risk
50 and 60 of choking and aspiration
(pharyngeal involvement)
WHAT CAUSES IT? ●​ Generalized weakness of the
●​ The cause of myasthenia gravis isn’t extremities, and intercostal
known musclesà decreased vital
●​ it commonly accompanies capacity, and respiratory failure
autoimmune and thyroid => MYASTHENIC CRISIS

WHAT WENT WRONG? PATHOPHYSIOLOGY:

●​ Antibodies directed at the
Acetylcholine receptor sites myoneural
junction, thus impaired transmission of
impulses
●​ ETIOLOGY
●​ Autoimmune disease
●​ Common to women
WHAT HAPPENS IN MYASTHENIA GRAVIS? Weakness that occurs during this test
●​ The patient’s blood cells and thymus is called FATIGABILITY.
gland produce antibodies that block, ●​ Chest X-ray and CT scan
destroy, or weaken the neuroreceptors ●​ May be performed to detect enlarged
that transmit nerve impulses, causing thymus (thymoma, which is common
a failure in the transmission of nerve in MG
impulses at the neuromuscular ●​ The Tensilon test confirms the
junction. diagnosis by temporarily improving
●​ During normal neuromuscular muscle function after an I.V. injection of
transmission, a motor nerve impulse edrophonium or neostigmine.
travels to a motor nerve terminal, ●​ Long-standing ocular muscle
stimulating the release of a chemical dysfunction, however, may not
neurotransmitter called acetylcholine respond. This test also differentiates a
(ACh). When ACh diffuses across the myasthenic crisis from a cholinergic
synapse, receptor sites in the motor crisis.
end plate react and depolarize the ●​ Edrophonium Chloride IV – 30 seconds
muscle fiber. The depolarization after injection, facial muscle weakness
spreads through the muscle fiber, and ptosis should resolve for about 5
causing muscle contraction. minutes
●​ In myasthenia gravis, antibodies ●​ Immediate improvement in muscle
attach to the ACh receptor sites. They strength -> (+) test – confirms the
block, destroy, and weaken these sites, diagnosis
leaving them insensitive to ACh, ●​ ATROPINE SULFATE – used to control
thereby blocking neuromuscular potential side effects of edrophonium
transmission chloride => bradycardia, systole,
bronchoconstriction, sweating,
DIAGNOSTIC EVALUATION: cramping
●​ Blood test
●​ it is performed to determine serum MEDICAL THERAPY:
levels of certain antibodies ●​ Anticholinesterase drugs - 1st line;
(AChR-binding antibodies, enhances neuromuscular
AChR-modulating antibodies, anti transmission; provides symptomatic
striational antibodies), High levels of relief by inhibiting breakdown of Ach
these antibodies may indicate MG and increasing concentration of
●​ Neurologic Examination available Ach at the neuromuscular
●​ It involves testing muscles and reflexes. junction
MG may cause abnormal eye ●​ Pyridostigmine - counteract fatigue
movements, inability to move the eyes and muscle weakness and enable
normally, and drooping eyelids. To test about 80% of normal muscle function
arm and leg muscles, the patient may ●​ Neostigmine- given IV in myasthenic
be instructed to maintain a position crisis
against resistance for a period of time.
Adverse effects: respiratory failure related to
●​ Diarrhea myasthenic or cholinergic crisis
●​ Abdominal cramps 2.​ Be alert for signs of impending crisis:
●​ Excessive saliva (Myasthenic Crisis)
●​ Corticosteroids (Prednisone) - when ●​ Sudden respiratory distress
weakness is not controlled by ●​ Signs of dysphagia, dysarthria,
anticholinergics to suppress the ptosis, diplopia
immune response ●​ Tachycardia, anxiety
●​ Initial dose given daily and maintained ●​ Rapidly increasing weakness of
for 1 – 2 months extremities and trunk
●​ IVIG – to treat exacerbations; could be 3.​ Monitor the patient’s response to drug
used as a long-term adjunct
medication SUPPORTIVE CARE:
1.​ Administer medications so their peak
Adverse effects: effect coincides with meals
●​ HA 2.​ Help the patient develop a realistic
●​ Migraine exacerbation activity schedule
●​ Aseptic meningitis 3.​ Allow for rest periods throughout the
●​ Flu Like sx day to minimize fatigue
●​ PROCAINE – contraindicated for 4.​ If the patient has diplopia, provide an
patients with MG eye patch to use on the alternate eye
●​ ATROPINE – give IV in cholinergic crisis to minimize the risk of tripping and
to reduce the effects of Ach; falling
anticholinesterase overdose or toxicity. 5.​ Avoid aspiration
●​ Plasmapheresis- px’s plasma and ●​ teach the px to position the
plasma components are removed head in a slightly flexed position
●​ Blood cells and antibody - containing to protect the airway during
plasma are separated, then the cells eating
and a plasma substitute are reinfused ●​ Have suction available that the
px can operate
THYMECTOMY: ●​ If px is in crisis or has impaired
●​ Surgical removal of the thymus gland swallowing, administer IV fluids
●​ Can produce Ag-specific and foods through NG tube;
immunosuppression elevate the head of the bed
●​ Elective surgery; done when the clinical after feeding
course of the disease is stable ●​ Plan periods of exercise, meals,
●​ Post-op: monitor respiratory function patient care, and daily activities
to take advantage of peaks in
NURSING INTERVENTION: the patient’s energy level.
1.​ Monitor the patient’s respiratory rate, ●​ Provide soft, solid foods instead
use of accessory muscles, and oxygen of liquids to reduce the risk of
saturation to watch for possible choking.
●​ Always sit the patient up to eat.
 ●​ Encourage the patient to take NURSING INTERVENTIONS:
an active role in deciding about 1.​ Administer prescribed medication as
his care. scheduled
●​ Evaluate the patient. Look for 2.​ Aspiration precaution
normal vital signs, evidence of 3.​ Promote respiratory function
adequate hydration and normal 4.​ Prepare for complications like
elimination, skin that’s free from myasthenic crisis and cholinergic crisis
sores or problems, and an
optimal capacity for activity. MENINGITIS
●​ Encourage the patient and his
family to discuss their feelings,
●​ It is an inflammation of the arachnoid
especially feelings of frustration,
and pia mater of the brain and spinal
grief, or loss. Listen and provide
cord
emotional support.
●​ The inflammation may be caused by
●​ Teach the patient how to
infection (virus, bacteria, or other
recognize adverse effects and
microorganism) and less commonly
signs of toxicity of
by certain drugs.
anticholinesterase and steroids
●​ It can be life threatening because of
●​ headache
the inflammation’s proximity to the
●​ weakness, sweating,
brain and spinal cord; therefore the
●​ abdominal cramps nausea,
condition is classified as a medical
●​ vomiting, diarrhea,
emergency
●​ excessive salivation,
bronchospasm
SIGNS AND SYMPTOMS:
●​ Warn him to avoid strenuous
●​ The most common symptoms of
exercise, stress, infection, and
meningitis are headache and neck
unnecessary
stiffness associated with fever,
●​ exposure to the sun or cold
confusion or altered consciousness,
weather.
vomiting and an inability to tolerate
light (photophobia) or loud noises
COLLABORATIVE MGT:
(phonophobia)
1.​ Myasthenic or cholinergic crisis –
●​ Personality and behavior changes
airway maintenance, oxygen, and
●​ A rash can be a striking feature of N.
mechanical ventilation is indicated
Meningitidis
2.​ Plasmapheresis - to temporarily
remove circulating Ach antibodies
MANIFESTATIONS: (KNOB)
from the blood in crisis; to treat
●​ Kernig's sign (knee flexion)
exacerbations
●​ Nuchal rigidity (neck stiffness)
3.​ Thymectomy – when thymoma or
●​ Opisthotonus (over bending or
hyperplasia exists; may provide
arching of the back)
remission in some patients
●​ Brudzinski’s sign (batok, balakang)
DIAGNOSIS: (neurogenic shock) -> decrease BP, decrease
●​ LUMBAR PUNCTURE - used to diagnose HR, flaccid paralysis
or exclude meningitis RISK FACTORS: (SPINAL)
●​ This involves inserting a needle into the ●​ S - sports
spinal canal to extract a sample of CSF ●​ P - pounding
●​ I - industrial
TREATMENT: ●​ N - number of case/year
●​ The usual treatment for meningitis is ●​ A - accidents (VAr/t alcohol)
prompt application of antibiotics and ●​ L - lalaki (male)
sometimes antiviral drugs
●​ In some situations, corticosteroids can SPINAL CORD:
also be used to prevent complication ●​ 8 cervical
from overactive inflammation ●​ 12 thoracic
●​ 5 lumbar
NURSING INTERVENTIONS: ●​ 5 sacral
●​ Assess the patient's mental status and ●​ 1 coccygeal
provide psychological support if the = 31 pairs of spinal nerves
patient is conscious.
●​ Elevate the head of the bed to 30
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.

SPINAL CORD INJURY

●​ Insult to the spinal cord resulting in a

change in the normal motor, sensory
or autonomic function. This change is
SCI:
either temporary or permanent.
●​ Injury from C1 – C8 = quadriplegia
●​ Injury from C1 – C4 = resp. failure
Mechanism:
●​ Injury from T1 – T12 = paraplegia
●​ Direct trauma
●​ Injury from T6 = autonomic dysreflexia
●​ Compression by bone fragments
-> distended bladder -> catheter
/haematoma/ disc material
●​ Ischemia from damage / impingement
●​ The most frequent vertebrae – C5-C7,
on the spinal arteries
T12 and L1
●​ Concussion
SCI -> paralysis below the level of injury ->
●​ Contusion
decrease autonomic function -> spinal shock
●​ Compression
 ●​ Transection DIAGNOSTIC TEST:
●​ Spinal x-ray
SPINAL CORD INJURY CLASSIFICATION: ●​ CT scan
1.​ Quadriplegia: injury in cervical region ●​ MRI
4 extremities affected
2.​ Paraplegia: injury in thoracic, lumbar EMERGENCY MANAGEMENT:
or sacral segments; 2 extremities ●​ A-B-C (Airway, Breathing, and
affected Circulation)
●​ Immobilization
INJURY EITHER: ●​ Immediate transfer to tertiary facility
1.​ COMPLETE
●​ Loss of voluntary movement of NURSING INTERVENTIONS:
parts innervated by 1.​ 1. Promote adequate breathing and
segment,this is irreversible airway clearance
●​ Loss of sensation 2.​ Improve mobility and proper body
●​ Spinal shock alignment
3.​ Promote adaptation to sensory and
2.​ INCOMPLETE perceptual alterations
●​ Some function is present below 4.​ Maintain skin integrity
site of injury 5.​ Maintain urinary elimination
●​ More favourable prognosis 6.​ Improve bowel function
overall 7.​ Provide Comfort measures
●​ Are recognisable patterns of 8.​ Monitor and manage complications
injury, although they are rarely ●​ Thrombophlebitis
pure and variations occur. ●​ Orthostatic hypotension
●​ Spinal shock
CLINICAL MANIFESTATIONS:
●​ Paraplegia TREATING SCI:
●​ Quadriplegia ●​ Position: flat, neck immobilized
●​ Spinal shock ●​ Assess neurologic & respiratory status
●​ VS, IO, pulse oximetry

SPINAL SHOCK ●​ Reposition Q2 hrs

●​ Check for autonomic dysreflexia
●​ Provide skin care
●​ Transient reflex depression of cord
●​ Glucocorticoids
function below level of injury
●​ Cervical collar
●​ Initially hypertension due to release of
●​ Maintenance of vertebral alignment:
catecholamines
○​ Crutchfield tongs, Halo brace
●​ Followed by hypotension
●​ Flaccid paralysis
●​ Bowel and bladder involved
●​ Sometimes priapism develops
●​ Symptoms last several hours to days
 SEIZURE PARTIAL SEIZURE

●​ Episodes of abnormal motor, sensory, ●​ Most common form in adults with

autonomic activity resulting from Epilepsy
sudden excessive discharge from
cerebral neurons TYPES:
●​ A part or all of the brain may be 1.​ Simple partial – no alterations in
involved consciousness
●​ Layman's term: convulsion ●​ One cerebral hemisphere

PHASES: 2.​ Simple motor – frontal lobe

●​ Pre-ictal (aura): the period before the ●​ Seizures begins from hands &
seizure face
●​ Ictal: the period during the seizure ●​ Stiffening or jerking of hands &
●​ Inter-ictal: the period between face
occurrences of seizure activity ●​ Butterflies in the stomach
●​ Post-ictal: the period immediately (sensory signs)
after the seizure

GENERALIZED SEIZURE
PATHOPHYSIOLOGY:
●​ An electrical disturbance in the nerve
●​ Both hemispheres of the brain as well
cells in one brain section----> EMITS
as deeper structures such as
ELECTRICAL IMPULSES excessively
thalamus, basal ganglia & upper brain
stem
●​ Consciousness is always impaired
●​ Immediate without any warning

FORMS:
1.​ Grand mal (common type) –
generalized tonic clonic
●​ Proceeds as sudden LOC
->tonic->clonic
●​ Characterized by aura (it is the
visual wherein there is flashing
lights sensations have smells,
and spotting and dizziness)
●​ Tonic clonic phase -
accompanied by dyspnea and
running of saliva and
sometimes there is urinary
incontinence
 ●​ Post ictal - it is characterized by ●​ Mostly there is mental
exhaustion, headache cloudening, pt is out of touch, pt
drowsiness, and usually pts appears intoxicated and during
have deep sleep of 1-2 hrs and LOC there are ongoing physical
when they wake up they are activity
disoriented ●​ Usually manifested by
confusion, amnesia, and need
2.​ Absence or Petit Mal – begins during for sleep
childhood ●​ During this time, the client may
●​ Sudden brief cessation of all commit violent actions like they
motor activity accompanied by become antisocial even after
blank stare & unresponsiveness regaining consciousness they
lasting for 5-30 secs are still violent running amok
●​ Absent seizure or little sickness
●​ There is no aura 5.​ Febrile seizure
●​ No tonic clonic movements ●​ Common in children under 5
●​ Only sudden sensation of years old
ongoing physical activity like ●​ Cause is the rising of body
staring blankly, eyeball rolling temperature
upwards, lip chewing, and
there's cheek smocking STATUS EPILEPTICUS
●​ Regain consciousness as rapid
as it was lost
●​ A complication of epilepsy that is
●​ Lasts about 10-20 seconds
considered as medical emergency
●​ Very common during childhood
wherein seizure activity becomes
to adolescence
continuous
●​ occurs in rapid succession and
3.​ Jacksonian seizure
consciousness is not regained
●​ Is common among clients with
between seizure (no full
organic brain lesions
consciousness)
○​ Frontal lobe tumors
●​ Brain damage may occur due to
●​ There is tonic clonic movements
prolonged hypoxia and exhaustion
wherein muscles of the hands
●​ Clients are often in a coma for 12 to 24
are twitching which would lead
hours or longer. And recurring seizures
to grand mal
may occur during
●​ Has aura
●​ The attack is usually related to failure
●​ Could lead to grand mal
to take anticonvulsant drugs.

4.​ Psychomotor seizure

TREATMENT:
●​ It has psychiatric components
1.​ Patent airway
●​ Has aura
2.​ Drug therapy
●​ There is hallucination and
●​ Anticonvulsant & sedative
notions
●​ Phenobarbitals , Diazepam
 3.​ Close monitoring
POST SEIZURE
ETIOLOGIC FACTORS: 1.​ Promote a potent airway. place patient
1.​ Idiopathic to the side to drain secretions and
2.​ Fever prevent aspiration
3.​ CNS infection 2.​ help re-orient the patient if confused
4.​ Head injury 3.​ provide care if a patient became
5.​ Metabolic and toxic conditions incontinent during the seizure attack
4.​ stress importance of medication
MANAGEMENT: regimen
1.​ Nurses should stay with the client
during seizure, observe the start and PHARMACOTHERAPY:
end of seizure Anticonvulsants are classified as central
2.​ Protect client from injury nervous system depressants as well as
3.​ Put up side rails and must be padded antidepressants = it suppresses abnormal
4.​ If the client is sitting or standing, help electrical impulses from the seizure focus to
the client to sit on the floor. Make sure other cortical areas thus preventing seizures
there is a pillow to protect the head but on eliminating the cause.
5.​ Do not apply restraints as it could lead Ex. hydantoins, barbiturates, oxinates,
to fractures benzodiazepines, valproic
6.​ Do not insert thumb plate during tonic
clonic movements HYDANTOINS = Phenytoin / Mephenytoin /
7.​ Promote a patent airway by turning Ethotoin
client to the side, just in case there is ●​ These anticonvulsant drugs have the
drooling to prevent aspiration least toxic effect, small effect on
8.​ Loosen clothing of client especially on general sedation and are non
the neck addicting.
9.​ Make an observation and document ●​ If giving phenytoin, monitor serum level
●​ Therapeutic level of phenytoin is 10 to
NURSING INTERVENTIONS: 20 mcg / ml
DURING SEIZURE ●​ Intravenous infusion of phenytoin
1.​ remove harmful objects from the should be administered to a large vein.
patient’s surroundings It should be diluted with normal saline
2.​ ease the client to the floor solution.
3.​ protect the head with pillows when she ●​ Dextrose solution should not be use
happens to be standing because it will precipitate
4.​ Observe and note for the duration, ●​ Intramuscular injection of phenytoin
parts of body affected, behaviors irritates tissues and may damage, that
before and after the seizure is why it is discourage
5.​ loosen constrictive clothing especially ●​ Continuous IV infusion of PHENYTOIN
around the neck should not be used because it can
6.​ DO NOT restrain, or attempt to place cause hypotension and cardiac
tongue blade or insert oral airway dysrhythmias.
 ●​ Mephenytoin is more toxic than
phenytoin. Used for severe grand mal
and psychomotor seizures that do
respond to phenytoin and other
anticonvulsants.
●​ 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 interventions:
●​ 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 inhibit
Insulin release causing hyperglycemia
●​ Monitor CBC because phenytoin may
cause bone marrow depression and
aplastic anemia
●​ Take the drug at same time everyday
with food or milk to prevent gastric
irritation
●​ Phenytoin is contraindicated in
pregnancy. Can lead to fetal
anomalies such as cardiac defects,
cleft lip and cleft palate.

Phenytoin causes pinkish or reddish urine to

brown discoloration. This harmless effect

Withdraw drug gradually to prevent status

epilepticus