Neurological Disorder 1.

Acetylcholine *BOTH*
ANATOMY AND PHYSIOLOGY (Excitatory and inhibitory)
● (major transmitter of PNS)
1. Central Nervous System (CNS) ● Usually excitatory;
• Brain - parasympathetic effect
•Spinal cord sometimes inhibitory
2. Peripheral Nervous System (stimulation of heart by vagal
(PNS) nerve)
• Cranial nerves ● Excitatory // Inhibitory
•Spinal nerves ● Controls sleep and wakefulness
• Autonomic nervous system cycle
Neuron ● Signals muscles to become alert
• Basic functional unit of the brain
2. Serotonin (*INHIBITORY*)
• Dendrites – receives electrochemical
● Inhibitory
messages
● Controls fluid intake, sleep and
- Extensions that carry impulses
wakefulness temperature
toward the cell body.
regulation pain control, sexual
• Axon – carries electrical impulses
behaviours regulation of
away from the cell
emotions
• Myelin sheath – increases speed of
● Mood control and sleep
conduction
● Inhibits pain pathways
- oligo - gumagawa ng myelin
3. Dopamine (*EXCITATORY*)
TYPES OF NEURONS
● excitatory
Sensory Neurons
● Usually inhibitory??
- Also knowns as afferent neurons
● Affects behaviour (attention and
- Transmit impulses from
emotion) fine movements
receptors to the cns
● Controls complex movements,
Motor Neurons
motivation, cognition.
- Also termed as Efferent Neurons
● Regulates emotional response
- Transmits impulses from the
central nervous system to the
4. Norepinephrine
effectors (Muscle, Glands)
(*EXCITATORY*)
Interneurons
● (major transmitter of SNS)
- Found entirely within the
● Usually excitatory
central nervous system
● Affects mood and overall action
- Specialized to transmit sensory
● Causes changes in attention,
motor impulses.
learning and memory sleep and
Neurotransmitters
wakefulness. mood.
● Communicate messages from
one neuron to another or from a
5. Gamma-aminobutyric acid
neuron to specific target tissue.
(GABA) (*INHIBITORY*)
● Potentiate or modulate a
● Inhibitory - Patulugin
specific action and can either
● Modulates other
excite or inhibit the target cell's
neurotransmitters.
activity.
6. Enkephalin, Endorphins
● Manufactured and stored in
(*BOTH*)
synaptic vesicles
● Excitatory
● Diffuses/transported across the
● Pleasurable sensations
synapse, binding to receptors in
● Inhibits transmission
the postsynaptic cell membrane
● Controls fight to fight response.
Action:
7. GLUTAMINE (*EXCITATORY*)
• Potentiates
● Excitatory
• Terminates
● Results in neurotoxicity are too
• Modulates
high.
• Excite
• inhibit
Potentiates - nagpapabilis
Terminates -
Modulates
Excite -
Inhibit
Serotonin - Mood control
Dopamine
- Decrease (Parkinson, due to lack
of dopamine.
Norepinephrine
- Decrease or increase ( Anxiety)
Gaba
- Inhibitory
- At evening
Enkephalin
- Excitement
CENTRAL NERVOUS SYSTEM
1. CEREBRUM
Frontal Lobe
- Largest Lobe
- Major Function concentration
abstract thought information
storage and memory function.
- Contains Broca’s Area (Motor
Control of speech.)
- Generates the impulses that
bring about voluntary
movement.
Parietal Lobes
- sensory functions
- Touch. Taste, temperature
- This sensation is felt.
Temporal lobe
● Located on the side of the head
(temporal means “near the
temples”), and is associated
with hearing, memory, emotion,
and some aspects of
understanding Language and
music.
● Hearing and olfaction
3. MEDULLA
- Contains Cardiac centers,
respiratory centers, vasomotor
centers and reflex centers
(Coughing sneezing, swallowing
and vomiting)
4. PONS
- Anterior to the cerebellum and
superior to the medulla
- Contains two respiratory centers
(apneustic & pneumotaxic)
responsible to produce normal
breathing rhythm.
5. MIDBRAIN
- Regulates Visual reflexes,
Auditory reflexes and righting
reflexes.
6. HYPOTHALAMUS
FUNCTIONS
- Productions of hormones
- Regulation of body temperature
- Regulation of food and fluid
intake
- Integration of the functioning to
the autonomic nervous system.
7. THALAMUS
- Functions are primarily
concerned with sensation
- Capable of suppressing minor
sensations.

Occipital lobe
● Located at the very back of the
brain, and contains the primary
visual cortex, which is
responsible for interpreting
incoming visual information.

2. CEREBELLUM
- Controls movement, balance
and position or
preprioconception.
AUTOIMMUNE DISORDERS OF ❖ CHARCOTTS TRIAD
THE NERVOUS SYSTEM *Scanning speech
- Pababain *Intentional Tremors
- Anti inflammatory *Nystagmus
- atelectasis do breath deep
breathing ❖ VISUAL DISTURBANCES
Optic nerve lesions or their
1. MULTIPLE SCLEROSIS
connection:
● Immune-mediated, progressive,
❑Blurring of vision
DEMYELINATING disease of the
❑Diplopia (double vision)
CNS resulting to impaired
❑Scotoma (patchy blindness)
transmission of nerve impulses
❑Total blindness
● *demyelination – destruction of
the myelin sheath’
❖ SENSORY NERVE
● Affects WOMEN than MEN
DISTURBANCES
● Degenerative disease
-Paresthesia
● Remission and exacerbation
- Proprioception Loss
- Pain
PATHOPHYSIOLOGY
❖ COGNITIVE DISTURBANCES
-Memory Loss
-Decreased Concentration
-Dementia
-Poor Abstract Reasoning
❖ CEREBELLUM / BASAL
INVOLVEMENT
-Ataxia
-Tremors
-Weakness of muscle in throat and
face

❖ OTHERS
-Bowel and Bladder dysfunction
- Impotence
-Muscle Hypertonically
CAUSES:
- Unknown
Spasticity (muscle hypertonicity)
- Post Viral Infection
❑Involvement of motor pathways

CLINICAL MANIFESTATION
Frontal and Parietal lobe
● Relapsing-Remitting Course
involvement
- S/sx depends on the location of
❑Cognitive and psychosocial
lesion (plaque)
involvement

PRIMARY symptoms:
DIAGNOSTIC FINDINGS
❑Fatigue
❑MRI
❑Depression
- Multiple plaques in CNS
❑Weakness
❑CSF electrophoresis
❑Numbness difficulty in coordination
- Presence of oligoclonal bonding
❑Ataxia (cerebellar and basal ganglia
(bands of IgG)
involvement)
❑Pain (lesion on sensory pathways)
MEDICAL MANAGEMENT
❑IV methylprednisolone
❑Key agent for acute relapse
❑Anti-inflammatory effect
❑Mitoxantrone (Novantrone)
❑Check for cardiac toxicity
Symptom Mng:
❑Baclofen (Lioresal) – GABA agonist
Medication of choice for SPASTICITY
❑Amantadine (symmetrel)
- Treatment of fatigue
❑Beta-blockers, antiseizure agents,
benzodiazepines
- Ataxia
❑UTI
- Vitamin C (increases the acidity
of urine)
NURSING MANAGEMENT
❑Promote physical mobility
- Walking (improves gait and
loss of position sense)
- Daily exercise
❑Minimize spasticity
- Warm packs
- NOT Hot baths (avoided:
risk of burn injury secondary
to sensory loss)
❑Minimize effects of immobility
- Coughing and deep
breathing exercises
❑Prevent injury
- Walking with feet apart
(widens the base)
❑Enhance bowel and bladder
function
- Encouraged scheduled
toileting rounds
❑Enhance communication and
manage swallowing difficulties
- Suctioning
- Careful feeding
- Proper position for eating
❑Vision problems (Diplopia)
- Patch one eye
❑ Swimming and stationary
Bicycling are useful in treating muscle
spasticity.
❑ Strenuous exercise should be
avoided because it may exacerbate
symptoms
❑Bowel and bladder program
❑ Instruct patient to avoid cuts and
burns
❑Respiratory distress precaution
2. MYASTHENIA GRAVIS
❑Autoimmune disease affecting the
MYONEURAL junction that causes
weakness of voluntary muscles
❑Women are more affected than men
● Myasthenia gravis (MG) is a
chronic autoimmune
neuromuscular disease
characterized by varying
degrees of weakness of the
skeletal muscles of the body.
● Purely motor disorder (no effect
on sensation and coordination)
Cause: unknown but abnormal
thymus gland
Pathophysiology: Destruction of
acetylcholine receptors at
neuromuscular junction.
MANIFESTATION!!
Muscle weakness
Double vision (diplopia)
weak eyelids (unilateral ptosis)
Difficulty speaking or smiling
Difficulty chewing and swallowing
DIAGNOSTIC FINDING
❑Acetylcholinesterase inhibitor test
❑a.k.a TENSILON TEST
- Tensilon test- in Myasthenia
gravis reveal improved muscle
contractility after edrophonium
chloride (tensilon)
❑Stops acetylcholine breakdown
making it available for binding in
myoneural junction
Edrophonium Chloride (Tensilon)
❑Fast acting anticholinesterase is
administered IV
❑30 secs after injection:
❑Resolution of symptoms (facial
muscle weakness and ptosis) after 5
mins CONFIRMS the diagnosis.
❑*ATROPINE (anticholinergic)
antidote for side effects
Assessment of Labs/Diagnostics
- Arterial Blood Gas & Pulmonary
function tests For respiratory
compromise
- Electromyography (EMG)
Decreased amplitude when
motor neurons are stimulated
- Confirming diagnosis
- IV administration of edrophonium
chloride (Tensilon)
- Allows acetylcholine to bind with
its receptors and temporarily
improves symptoms
- Weakness returns after effects of
Tensilon are discontinued
MEDICAL MANAGEMENT
❑Anticholinesterase medications
❑Pyridostigmine Bromide (first line of
therapy)
❑Increases acetylcholine availability
❑Gradually adjusted
❑Myasthenic crisis (Underdosage)
❑Cholinergic crisis (Overdosage)
Differentiate:
❑Tensilon test
❑Relief of symptom: MYASTHENIC
CRISIS
❑Pyridostigmine bromide
(Neostigmine)
❑Exacerbation of symptom:
CHOLINERGIC CRISIS
❑Atropine (anticholinergic)
IMMUNOSUPPRESSIVE THERAPY
❑Corticosteroid
❑Suppresses immune response
❑Decreasing amount of antibodies
❑IV immunoglobulin (IVIG)
❑Azathioprine
❑Inhibits T lymphocytes and reduces
antibody level
❑Procaine is avoided
❑Dentist is informed of diagnosis
PLASMAPHERESIS (plasma
exchange)
❑Patient’s plasma and plasma
components are removed through a
centrally-placed large-bore
double-lumen catheter
❑Blood cells and antibody is
separated then plasma substitute are
reinfused
❑Produces TEMPORARY reduction in
circulating antibodies
THYMECTOMY
❑Antigen-specific
immunosuppression
NURSING MANAGEMENT
❑Teaching strategies to conserve
energy
❑Minimize risk of aspiration
❑Mealtime coincides the PEAK effect
of medication
❑Rest before meals
❑Sit upright when eating
❑Soft diet
❑Eye problems
❑Tape the eyes
❑Artificial tears
- Maintain effective breathing
pattern and airway clearance
Assess for respiratory distress
- Monitor meals and teach client
to bend head slightly forward
while eating and drinking to
improve swallowing
- Teach client to avoid exposure to
infections
- Teach client to effectively
coughing, use chest
physiotherapy and incentive
spirometry
- Provide adequate nutrition
Schedule meds minutes before
eating for peak muscle strength
- Offer food frequently in small
amounts that are easy to chew
and swallow (soft or semisolid)
- Promote improved physical
mobility with referrals to
physical therapy and/or
occupational therapy
- Provide eye care: instill artificial
tears; use a patch over one eye
for double vision; wear
 sunglasses to protect eyes from
bright lights
3. GUILLAIN-BARRE
SYNDROME
- Galing baba syndrome
- Lower to upper extremity
- Ground brain
❑Autoimmune neurologic condition
demyelinating disease of the PNS
- Attacking nerve in PNS
Nervous system and Cranial
Nerves
❑Resulting to acute, rapid segmental
demyelination of peripheral nerves
and some cranial nerves producing
ASCENDING WEAKNESS
❑Viral infection: common antecedent
effect
- Does not occur in Central
nervous system
MUST KNOW!!
● GBS IS IDIOPATHIC
(UNKNOWN)
● Preceded by Viral infection
(respiratory and gastro)
● Also known as (Infectious
Polyneuritis)
● It is not contagious or
communicable disease
● ASCENDING PARALYSIS
- Galing baba syndrome
- Lower - upper extremities
Duration of GBS??
● ONSET: Hours or days (ACUTE)
or four weeks
● At 3rd week of the illness 90%
all of patient is at their
(WEAKEST)
RISK FACTORS:
Viral Illness (CMV) (Cytomegaly)
Influenza vaccinations (flu shots)
Respiratory or Gi Infections (C. Jejuni)
Age: ANy age (> 50 has the greatest
risk)
Lalake is the most common esp.
Middle ages:
- Common Illness in GBS (CMV)
MUST KNOWS
- Common type of Gbs is Acute
Inflammatory demyelinating
polyneuropathy (AIDP)
- Common Illness: Viral infection
Cytomegalovirus
Common Bacterial Cause:
Campylobacteriosis Jejuni
gastroenteritis
Main features of GBS Include:
- Acute
- Ascending
- Symmetrical weakness of the
limbs
First Symptoms of weakness in GBS
● Paresthesia - tingling and
numbness
● Hypotonia
GBS Signs and Symptoms will
most Likely to start in the
LOWER EXTREMITIES (ex. feet)
- Symmetrical (sabay) and will
gradually spread upward
(ASCENDING) to the head and
Ataxia
- Ascending motor weakness -
acute stage
Motor Manifestation:
- Ascending motor and muscle
weakness or paralysis without
muscle atrophy
1. FLACCID - Type of Paralysis
2. Ataxia - Difficulty of walking /
gait is affected
3. Respiratory Failure
4. Loss of bowel and Bladder
control
Initial: Paresthesia and symmetrical
muscle weakness
*Distal to proximal Paralysis
experiences muscle weakness FIRST*
TAKE NOTE!!
- Ascending Motor weakness is
common verbalization of the
patient with GBS regarding the
EARLY Onset of symptoms
- GBS results in motor weakness
in a distal to proximal
progression.

CRANIAL NERVE INVOLVEMENT
(5 D’s)
● Drooping face (Facial
weakness)
● Difficulty in speaking
● Difficulty in Chewing
● Difficulty in Swallowing
(Dysphagia)
● Diplopia and blindness
(Opthalmoplegia)
An indicator of Cranial Nerve
Involvement:
- Difficulty of speaking and
Chewing
Cranial Nerve 7 - Affects patient ability
to smile, frown, whistle , and drink
from straw
Cranial Nerve 9 and Cranial 10
- Glosso and vagus
- Ability to cough, gag and
swallow
What is Not affected in Gbs?
- Cognition and LOC (Level of
consciousness?)
What are the most commonly
affected?
- Muscles
- Sensory Nerves
- Cranial Nerves
Which of the following clinical
manifestations would the nurse
expect to find when performing
admission assessment?
- Ascending Paralysis with
ATAXIA
❑Dyskinesia (inability to execute
voluntary movements)
❑Hyporeflexia
❑Paresthesias (numbness)
❑Weakness beginning from LEGS and
progresses UPWARD
❑Does not affect cognitive function
Priority Nursing DIAGNOSIS IN GBS?
- Ineffective Breathing Pattern
Appropriate Diagnosis in GBS?
- Alteration in nutritional status
related to possible choking.
Priority of care in GBS?
- Maintenance of Respiratory
Function
Important Nursing Interventions in
GBS?
- Assess patient for any
respiratory distress (Dyspnea,
shortness of breath weak
cough)
DIAGNOSTIC TEST:
1. Lumbar Puncture
Pre Procedure: Assist patient to void to
prevent accidents puncturing of
bladder (empty bladder)
Post Procedure
- Flat in bed and increase fluid
intake to prevent post
procedural headache
RESULT IN GBS: HIGH PROTEIN with
normal wbc
2. Electromyography - reflects
peripheral nerve functions
3. Nerve conduction studies
TAKE NOTE:
Assessment and interventions
for the following diagnosis of
GBS is to “ASSESS DEEP
TENDON REFLEX”
DIAGNOSTIC FINDINGS
❑History of viral illness in the previous
week suggest the diagnosis
❑Elevated protein in CSF
❑Other serum labs are not
MEDICAL MANAGEMENT
Considered a MEDICAL EMERGENCY!
❑Mechanical ventilation : respiratory
failure
❑Prevent immobility complications:
❑Anticoagulants
❑Antiembolic stockings
❑Plasmapheresis
❑IVIG (therapy of choice: fewer side
effects)

NURSING MANAGEMENT
❑Enhancing physical mobility
❑AROMEs in paralyzed extremities
twice a day
❑Position changes
❑Anticoagulation administration
❑Antiembolic stockings
❑Padding bony prominences
❑Nutrition
❑Improve communication
❑Picture cards/ eye-blink system
❑Decrease fear and anxiety
❑Diversional activity
PROGRESSION OF GBS
1. ACUTE STAGE
- Ascending Paralysis: 1-3 weeks
- Ventilatory Support: is critical
during the acute phase
Most essential in patient room:
(Electrodes & intubation tray
Electrodes because of dysthymia
Assessment is the most important
aspect of nursing care during phase
of GBS
● Asses for respiratory and cardiac
Function
● Monitor Abg’s and Vital Capacity
- High Fowler// SEMI FOWLER (45
degree angle) to increase lUng
expansion especially in
dysthymias.
2. PLATEAU STAGE // STABILIZING
PHASE
● No New symptoms occure
● No changes in status
● No improvement 1-3 weeks.
3. RECOVERY PHASE
● Improvement with
remyelination of peripheral
nerve and axonal regenerations
● Most changes in 6 months but.
Improvement is up to 2 years.
● Rehabilitations prior to
discharge are BEST described
as Long and One requiring
involvement of significant
others.
NEUROLOGICAL FUNCTION
RETURNS:
- Proximal to distal Pattern
- In the recovery phase
remyelination occurs slowly
If the patient is unable to talk, The
nurse best communicate to the
patient by: Enunciating the words
slowly and well
Best Way for a ventilated client to
communicate is to instruct:
- Blink eyes for “NO”
- Blink Twice for “YES”
APPROPRIATE LONG TERM GOAL:
- Prevent Muscle atrophy
INTERVENTIONS USE IN GBS
1. PLASMAPHERESIS
- Removes antibody -
antigen complexes from
circulation
- It is use 5 times either
daily or every other day in
2 weeks
PREPROCEDURE:
- Nurse use determines patency
of clients arteriovenous shunt
by “presence of bruits”
because it determines if the
arteriovenous shunt is patent.
- Check bruits every 2-4 hours
DURING PROCEDURE:
- Monitor Hypovolemia (Cold
clammy skin)
- Monitor fluid status, V/S and
replaced IVF
- Hypocalcemia (tingling,
numbness during procedure)
COMPLICATION IN PLASMAPHERESIS
- Low platelets
- Hypocalcemia
- Clotting
- Anemia