DAY 1 AM
assessment of the nervous system
NCM 216 CARE OF CLIENTS WITH
PROBLEMS IN PERCEPTION AND
COORDINATION - NEUROLOGY
Nervous System
This 5-unit course deals with understanding the
basic concepts, principles, theories and
techniques of nursing care management with
problem in perception and coordiantion. The
students are expected to showcase a
knowledge, attitude and holistic quality nursing
care in a health education setting.
COURSE OUTLINE:
1. Review of the anatomy and physiology of
the nervous system
2. Review on the neurological status
assessment
3. Discuss the different types of diagnostic
evaluation and its nursing pre and post
procedure responsibilities
4. Discuss the different types of neurologic
disorders
REVIEW ON THE ANATOMY AND
PHYSIOLOGY OF THE NERVOUS SYSTEM
CVA vs Spinal Cord injury
- CVA – Hemiphalgia paralysis
- Spinal cord injury (100% cannot move)
not Paraplegia (both hands and feet can
move); very healthy in 1 month then on
the succedding months that passed by
may complications na.
- If quadraplegic ang patient then rule out
na CVA case kasi usually ang spinal
cord injury yan.
- Pwede magkaroon ng injury sa nervous
system during hospitalization, kung ang
sakit lang sana ng patient is dizziness
then if nahulog and natamaan ang skull
area so magkaroon ng injury that could
be life threatening, healthy sa first
month then magkaproblem na after
succeeding months.
- Nurses must be skilled in the
(slurred speech – impending sign of
hemorrhagic or blood clot in brain)
Nervous system hindi madali iassess it
has process from the thought, actions
and the way he speaks like mga slurring
of speech. We can save the patient from
the complication of CVA if makita mo na
nagaslur na ang speech.
- Aneurysm – walking time bomb patients
- Major communicating and control
system within the body
- It works with the endocrine system to
control many body functions
- Neurons are the basic unit of the brain
Skull, Meninges
- Reaction (punching back your enemy) –
brought by the hormones and
communicating outputs which has an
effect to the muscles and organs they
are synchronize; every reaction may
reason
- Sensory motor = done by
neurotransmitters ; paresthesia (present
or effect in DM patients, systemic
problem; di nila ma feel na nalata ang
kanilang paa; may be amputated;
merong input pero na block na ang
pathways)
- Nervous System control all system
including Sensory, Autonomic Nervous
System (muscles you cant control;
Cardiac and Smooth Muscles – that’s
why its located in the propulsive
movement in the intestinal proportion),
Somatic (muscles = muscle that you
can control; voluntary – skeletal muscles)
- Ataxic movement - shuffling where in
nagalakad na nagasayaw
- NS reacts with all the body systems.
- Nervous System provides a rapid
response. Endocrine system provides a
slower and but often more sustained
response eto yung mga hormonal
response brought about endocrine
glands. Wherein mag produce ng
hormone then travel muna sa blood
before mag produce ng reaction
Slurring of speech is it a spinal injury or
CVA?
- If you stick out the tongue you can
determine the lesion (in CVA patients
 naga punta sa side ang tongue; if na
pull ang tongue sa left yun ang stronger
muscle – tas yan yung magturo ng
lesion, therefore nasa left ang lesion;
Nasa midbrain ang cross ang neural
pathway; if di magalaw ang right na
kamay – ang damage is sa left side ;
Midbrain = Brain stem [Amygdala and
Pons])
- The stronger muscles na hindi damage
yun ang magpull ng tongue (Ipoint ng
tongue ang lesion).
Functions of the Nervous System
1. Sensory Input: Gathering of
Information. To monitor and detect
changes occurring inside and outside of
the body. (nakita mo ang crush mo very
gwapo – wala pang reaction kasi may
hormonal reactions pa; spinal cord injury
= from spine to thalamus hindi maggawa
ang integration and it is not reversible,
even ang pag-ihi di maggawa)
2. Integration: To process and interpret
sensory input and decide if action is
needed (If maputol and integration wala
talagang reaction)
3. Motor output: A response to stimuli.
Activates muscles or glands
(If maputol ang sensory, integration and motor
talagang walang reaction ang body.)
ORGANIZATION OF THE NERVOUS
SYSTEM
- 12 Cranial Nerves
- 31 Spinal Nerves
- INTEGRATION: (Received information
will be interpreted and an appropriate
action will be initiated. Changes in
temperature have the potential to cause
damage to cells and tissue.)
- Example: an adult hyperthermia (38.5
C), Thermoreceptors in the skin (sense
organ), detects a change in a body
temperature (Stimuli)which is a
SENSORY INFORMATION
- SOMATIC MOTOR OUTPUT: Skeletal
msuscle (effector organ/ tissue) to do a
a VOLUNTARY ACTION by opening the
window and removing extra clothing.
- AUTONOMIC MOTOR OUTPUT:
Smooth muscle or a gland to do an
INVOLUNTARY ACTION. Warm blood
directed to the skin causes vasodilation
- You make use of your skeletal muscle to
answer the hyperthermia
- If ever kulang sa blood/hypovolemia /
hypovolemic shock = constricts the
peripheral area (malamig and
peripherals, kasi decreased ang blood
flow), it centralizes the blood into the
major organs
- If Hyperthermic pt = sweat glands are
present (motor function), tachycardia
(autonomic); If walang perspiration =
abnormal = disease/illness
- Motor Ouput = hindi ilang makita sa
skeletal but olsa in the major organs like
constricting and dilating the glands
Peripheral Nervous System (Sensory
division)
Sensory receptors:
Senses Internal Environment
(autonomic)
- Sight Chemoreceptors
- Hearing Baroreceptors
- Smell Osmoreceptors
- Taste (found inside the vessels, it
- Smell can constrict either dilate)
- Touch
  Relaxes bladder
 Contracts
rectum

- Medications to contrict pupils

- Tachycardic (Sympathetic)
- Sympathetic (Fight or Flight – teher is
always an increase in heart rate)
- Hypoglycemia = Stimulates glucose
Peripheral Nervous System (Motor division) release by liver (releases bile due to the
Effector organs presence of fat)
- The root of sympathetic is coming from
Somatic Autonomic (Involuntary) the cervical going to thoracic roots; wala
Voluntary sa
- Skeletal - cardiac muscle - Longer
Muscle - smooth muscle
- glands (Sympathetic and
Parasympathetic division)

- SA(Sensory Afferent)ME (Motor Efferent)

- Baroreceptors = found in the vessels
can constrict/dilate
- Osmoreceptors = found in intravascular,
a protein controlling, if may problem sa Nervous Tissues Structure and Function
osmotic pressure = edema [fluid in the (Neuron, Neuroglia)
interstitial space]
Neuron or Nerve Cell
Parasympathetic vs Sympathetic
- Transmit messages from one part of the
body to another
- The functional unit of the nervous
system
- Functional Characteristics:
o Irritablity- in reponse to a stimulus;
the ability to initiate a nervre
impulse Initiating movement; from
afferent to integration to efferent)
Parasympathetic Sympathetic o Conductivity - the ability too
 Constricts pupil  Dilates pupil conduct an impulse, to travel
 Stimulates salivation  Inhibits
 Inhibits hearts salivation Functional Classification of a Neuron
 Constricts bronchi  Accelerates 1. Sensory (Afferent) Neurons
 Stimulates digestive heart 2. Motor (Efferent) Neurons
activity  Relaxes bronchi 3. Interneurons / Assosication neurons
 Stimulates  Inhibits digestive
gallblader(if you are activity Sensory (Afferent) Neurons
eating fat)  Stimulates - Carry impulses from the SENSE ORGANS
 Contracts bladder glucose release (RECEPTORS) to the Brain and Spinal Cord
 Relaxes rectum by liver (If may - Kinds of receptors:
hypoglycemia) • Naked nerve cell – pain and temperature
 Secretion of • Meissner’ s corpuscle – touch receptor
epinephrine and • Pacinian corpuscle- deep pressure
norepinephrine • Muscle spindle (proprioceptor) – respond to
from kidney a degree of stretch or tension
Motor (Efferent = Effect) Neurons
- Cary Impulses from the Brain and Spinal
Cord to Muscles and Glands
- Muscles and Glands are Two Types of
Effectors. In response to impulses - Myelin = indicates a hormone mas
• Muscles Contract and Glands mabilis ang neurons, if walang myelin
Secrete sheath brought about by demyelinating
diseases like mawala ang myelin sheath
Interneurons = immune paresthesia
- Connect Sensory and Motor Neurons
and carry impulses between them
- They are found entirely within the
Central Nervous System

Parts of a Neuron
Dendrites -portion of the neuron with a
branch-type structure with synapses for
receiving electrochemical messages that
conduct impulses toward the tell body
Cell body - the metabolic center of the neuron
and mostly located in the CNS Nuclei - cell
bodies group together in the CNS
Ganglia - cell bodies occurring in cluster;
located in the PNS
- Cluster of cell bodies with the same function
is called e.g respiratory function
Axon - portion of the neuron, a long projection
that conducts impulses away from the cell body,
delivers the impulse to another neuron or gland - From the receptor goes to the
or a muscle Spinothaalmic area = Spinal cord 
dorsal part (back/posterior)  dorsal 
Axon going to synaptic terminals who send info brain  ventral  peripheral system 
going to the dendrites other neurons kasi iangat niya ang paa (motor) kasi
intercconnected sila so ireceive ng dedndrites masakit
para may relay system.
Phases of Irritability
Nervous system has 10 million sensory
neurons that sends information. 500 thousand Polarization (Resting Inside of neurons are
motor neurons that control the muscles and State) negative charged and
glands. outside is positively
charged. Potassium is
- Synaptic = Who will send the dominant inside the
information cell and sodium is
a) Dendrites dominant outside the
b) Cell body cell
c) Axon
- 10 million sensory neurons Depolarizing Phase Stimuli excite
(action potential) neurons; Sodium
diffused intracellular
and some of the
potassium goes
 outside.
Repolarization Phase neuron is more
(propagation of action permeable to sodium.
potential)
Repolarization Phase Sodium-Potassium
Continues pump begins to
(hyperpolarization) function: sodium is
pumped out of the cell
and brings potasium
back inside the cell.
Action Potential
- Rest: Na (Out) and K (in) and vice versa
to maintain homeostasis
HOW DO NERVES WORK ?
Nerves have a much more complex job in the
They are not just the wires, but the cells that
are the sensors, detectors of the external and
internal world, the transducers that convert
information to electrical impulses, the wires
that transmit these impulses, the transistors
that gate the information and turn up or down
the volume- And finally, the activators that take
that information and cause it to have an effect
on other organs.
Consider this. Your mother gently strokes your
forearm and you react with pleasure. Or a
spider crawls on your forearm and you startle
and slap it off. Or you brush your forearm
against a hot rack while removing a cake from
the oven and you immediately recoil. Light
touch produced pleasure, fear, or pain.
Nerves are in fact bundles of cells called
neurons and each of these neurons is highly
specialized to carry nerve impulses, their form
of electricity, in response to only one kind of
stimulus, and in only one direction. The nerve
impulse starts with a receptor, a specialized
part of each nerve, where the electrical impulse
begins. One nerve's receptor might be a
thermal receptor, designed only to respond to a
rapid increase in temperature. Another
receptor type is attached to the hairs of the
forearm, detecting movement of those hairs,
such as when a spider crawls on your skin.
Yet another kind of neuron is low-threshold
mechanoreceptor, activated by light touch.
Each of these neurons then carry their specific
information: pain, warning, pleasure. And that
information is projected to specific areas of the
brain and that is the electrical impulse.
The inside of a nerve is a fluid that is very rich
in the ion potassium. It is 20 times higher than
in the fluid outside the nerve while that outside
fluid has 10 times more sodium than the inside
of a nerve. This imbalance between sodium
outside and potassium inside the cell results in
the inside of the nerve having a negative
electrical charge relative to the outside of the
nerve, about equal to -70 or -80 millivolts. This
is called the nerve's resting potential. But in
response to that stimulus the nerve is designed
to detect, pores in the cell wall near the
receptor of the cell open. These pores are
specialized protein channels that are designed
to let sodium rush into the nerve.
The sodium ions rush down their
concentration gradient, and when they do, the
inside of the nerve becomes more positively
charged- about +40 millivolts. While this
happens, initially in the nerve right around the
receptor, if the change in the nerve's electrical
charge is great enough, if it reaches what is
called threshold, the nearby sodium ion
channels open, and then the ones nearby
those,and so on, and so forth, so that the
positivity spreads along the nerve's membrane
to the nerve's cell body and then along the
nerve's long, thread-like extension, the axon.
Meanwhile, potassium ion channels open,
potassium rushes out of the nerve, and the
membrane voltage returns to normal. Actually,
overshooting it a bit. And during this overshoot,
the nerve is resistant to further depolarization-it
is refractory, which prevents the nerve
electrical impulse from traveling backwards.
Then, ion pumps pump the sodium back back - Secreted by the neuron into the
out of the nerve, and the potassium back into extracellular space at the synapse
the nerve, restoring the nerve to its normal - Some example of the neurotransmitters
resting state. The end of the nerve, the end of are:
the axon, communicates with the nerve's target. • Acetylcholine – Release in CNS, the only
neurotransmitter in our skeletal muscles
This target will be other nerves in a specialized
(only SOMATIC)
area of the spinal cord, to be processed and
• Norepinephrine – Autonomic; released in
then transmitted up to the brain. Or the nerve's
CNS
target may be another organ, such as a muscle.
• Dopamine – Autonomic and Central; wala
When the electrical impulse reaches the end of
sa somatic
the nerve, small vesicles, or packets,
Neurotransmitters
containing chemical neurotransmitters, are
- Communicate messages from one
released by the nerve and rapidly interact with
neuron to another, or from a neuron to
the nerve's target. This process is called
a specific target tissue
synaptic transmission, because the connection
- Manufactured and stored in the synaptic
between the nerve and the next object in the
vesicles
chain is called a synapse. And it is here, in this
- They enable conduction of impulses in
synapse, that the neuron's electrical
the synaptic cleft
information can be modulated, amplified,
Neurotransmitter action:
blocked altogether or translated to another
- Is to potentiate, terminate, or modulate a
informational process.
specific action and can either excite or
Neuroglia inhibit the target cell’s activity
- There are usually multiple
- Cells that provide protection and
neutrotransmitters at work in the neural
insulation to the delicate neurons
synapse
(account for more than half of the weight
NEUROTRANSM SOURCE ACTION
of the brain)
ITTER
- Within the PNS 2 types of neuroglia:
• Schwann Cells - responsible for forming ACETYLCHOLIN Many areas Usually
myelin sheath E (major of the brain; excitatory,
• Satellite Cells - function is not known transmitter of the ANS parasympat
- Within the CNS, 4 types of neuroglial parasympathetic hetic
cells: NS) effects,
(Iba ang nagaproduce ng myelin sheath sa sometimes
PNS and CNS) retrain
• Astrocytes- large quantities in neurons, (stimulation
anchors blood vessels with neurons of the heart
Blood Brain barrier – protects the brain by the vagal
from damage, too much vectors, there is a nerve)
condition that can open the blood brain
barrier Serotonin Brain stem, Restraining,
• Microglia – Protective or plice; act as a hypothalamu helps
macrophagia; if there is a microorganism it s, dorsal control
can cause phagocytosis; they act as horn of the mood and
macrophages kung may makita sila na spinal cord sleep,
foreign bodies then pwede sila magka inhibits pain
phagocytosis. pathways
• Oligodendrocytes – Closed , forma nd Dopamine Substantia Usually
maintain of the myelin sheath in CNS, nigra and restrains,
myelin sheath – hastens the process; the basal affects
one maintaining the myelin sheath in the ganglia behavior,
CNS (attention,
• Ependymal Cells - Circulate CSF emotions,)
and fine
Neurotransmitters movement
- A chemical messenger
Noerpinephrine Brain stem, Usually,
(major transmitter hypothalamu excitatory, BRAIN
of the s, affects
- the center for registering sensation,
sympathetic NS) postganglion mood and
correlating them with one another and with
ic neurons of overall
stored information, making decisions and
the activity
taking actions
sympathetic
NS - the center for the intellect emotions behavior
and memory
Gaba- Spinal cord, Excitatory
aminobutyric acid cerebellum, amino acid
(GABA) basal
ganglia,
some
cortical
areas
Enkephalin, Nerve Excitatory,
endorphin terminals in pleasurable
the spine, sensation, - Divided into 4 anatomical region
brain stem, inhibits pain 1. Cerebrum
thalamus transmissio 2. Diencephalon
and n Dequasation – crossing over @ Midbrain
hypothalamu - Most CN is root sa baba; if root is taas
s, pituitary sa taas =
glans - If right ang na damage; if same manifest
tation (Same manifestation = ipsilateral)
3. Brainstem is the smalles
- ICP = Neurologic Signs, impending
brain herniation d/t entrance from the
brainstem to the foramen magnum
(Cushings Triad = bradypnea,
bradycardia, widening of pulse pressure)
- Neurological Deficits =
Blindness,Paralysis, Slurring
- Hole in the brainstem = Foramen
Magnum
4. Cerebellum
- Low Sero – Epilepsys Layers covering the brain
- Doapmine – Parkinsons
- Nervous Tissue is easily damaged by the
2 types of Receptors pressure and therefore needs to be protected
1. Direct Receptors (Inotropic)
- The hair skin and bone offer an outer layer
- linked to ion channels and allow passage of
protection
ions when opened
- they can be excitatory or inhibitory and are
rapid acting (measured in millisecond)
2. Indirect receptors
- affect metabolic process in the cell, which can
take seconds to hours to occur

CENTRAL NERVOUS SYSTEM

1. BRAIN
- Scalp is very vascular = many blood
2. SPINAL CORD
- Dura  Arachnoid  Pia (Meninges)
Supportive and Protective Structures of the
brain
- Meninges
- Blood Brain Barrier
- Cerebral Circulation (Circle of Willis)
- CSF – Protect and Nutrition
Meninges
- Cover the delicate nervous tissue, providing
further protection on the inner layer
- also protect the blood vessels that serve
nervous tissue, and they contain CSF
- Meninges has 3 connective layers
1. Pia (Soft)Mater
2. Arachnoid Mater
3. Dura (Durable) Mater
- Cover the delicate nerve
- Attached to the braian/CNS
- Arachnodi – Skull
- Subarachnoid Space = Between
arachnoid and pia mater; sub
(below)arachnoid hemorrhage –
burrholing to evacuate the blood blot
- Dura –
- Epidural space – taas ng dura
Cerebrospinal Fluid (CSF)
- Produced by the choroid plexus in the
ventricles of the brain
- Approx. 150ml of CSF circulating
around the brain, in the ventricle, and
around the spinal cord, and replaced
every 8 hours.
- Arachnoid Villii is the site absorption of
CSF
- Functions:
1. Mechanical - shock absorbing medium
2. Chemical
3. Circulation
CEREBROSPINAL FLUID (CSF)
FORMATION
BLOOD BRAIN BARRIER
- A network of blood vessels that allows
entry of essential nutrients while
blocking other substances
- Allows: Oxygen, Glucose, essential
amino acids; antidepressant drugs,
alcohol, cocaine, bilirubin, heroin,
nicotine, coffee
- Blocks: Toxins, Bacteria, urea (if there
are problems in the kidney 
overproduction of urea)
- Not all areas of the brain have blood
brain barrier (around the area of
ventricular system)
- Cerebral artery - Endangered =
hemorrhagic stone
- Supplied by the vertebral column
(medulla and pons)
- Tehre will be a condition in the Circle of
Willis= Aneurysm (Outpouching)
Functional Anatomy of the BRAIN
A. ) CEREBRAL CORTEX - Speech, memory,
logical and emotional response, as well as
consciousness, , interpretation of sensation
and voluntary movements
LEFT HEMISPHERE RIGHT HEMISPHERE
O Control of muscles O Control of muscles
on the R side of the on the L side of the
body body
O Spoken & written O Musical & Artistic
language awareness
oNumerical & O Space & Pattern
scientific skills perception oInsight
oImagination
O Reasoning
O Generating mental
O Systematic analysis image to compare ❑Deep inside the temporal lobe: Olfactory
spatial relationship area. ❑WERNICKE’s AREA
The Structure of Human Brain 4. OCCIPITAL LOBE (If damaged there is
visual agnosia)
❑Contains the visual area.

DIENCEPHALONS
1. THALAMUS - The relay station for sensory
impulses passing upward the sensory cortex.
2. HYPOTHALAMUS
• Regulation of Body temperature
• Water balance
• Metabolism
• Center for emotions
• Regulates pituitary gland
3. EPITHALAMUS
• Pineal body
REGIONS OF THE BRAIN
• Probable role in growth & development.
1. FRONTAL LOBE
• Regulate the food getting reflex
❑Controls voluntary motor activity.
❑Reasoning, concentration, abstraction
BRAIN STEM
❑Contains the BROCA’S AREA
1. MIDBRAIN
❑Voluntary eye movement
❑Responsible for motor coordination
❑Access to current and past information
experiences ❑Visual reflex and auditory relay centers.

❑Judgment 2. PONS

❑Regulates behavior based on judgment & ❑Contains respiratory center

foresight
2. PARIETAL LOBE
❑ Contains Somatic Sensory Areas
(Sensation, texture, size, shape & spatial
relationship
❑Pain, coldness, light touch.
❑Taste impulses for interpretation
❑Regulates breathing
❑PNEUMOTAXIC- limits duration of
inspiration ❑APNEUSTIC-prolong inspiration.
3. MEDULLA OBLONGATA
❑It contains centers that control: Heart rate,
Blood pressure, Breathing, Swallowing,
Vomiting

❑ Perception of body parts and body position ❑Cardiac Slowing

awareness
❑Important for singing, playing musical RETICULAR FORMATION - Are involved in
instrument, and processing nonverbal motor control of visceral organs
experiences
RETICULAR ACTIVATING SYSTEM - Plays a
3. TEMPORAL LOBE (If damaged there is role in consciousness and the awake/sleep
dyxlexia) cycles.
❑Auditory area
CEREBELLUM  Psychiatric practice; history and
examination
- Controls balance and equilibrium
 A structured way of observing and
- If damaged: cerebellar ataxia
describing a patient’s current state of mind
under the domains
Limbic System  Orientation: knowing where he is, the
time and date
- Function: Emotions
 Attention: concentrate on a mental task
- The limbic system (or the limbic areas) is a (simple substractions)
group of structures that includes the amygdala,
the hippocampus, mammillary bodies and  Registration: listen and repeat backs a
cingulate gyrus. These areas are important for few word
controlling the emotional response to a given
 Recall: remembers words a few
situation. The hippocampus is also important
minutes later
for memory.
 Constructional or visuospatial: copy or
draw an object or diagram
Spinal Cord
 Abstract thinking: explain a meaning of
 17 inches long a proverb or to explain a difference in
two objectsy
 MAJOR
REFLEX
CENTER
 Has 31 pairs
of spinal
nerves
 C1-C8, T1-
T12, L1-L5,
S1-S5,
SPINAL CORD
 Cervical nerves (nerves in the neck) –
supply movement and feeling to the arms,
neck and upper trunk. • Thoracic nerves EYE OPENING: 4 highest
(nerves in the upper back) – – supply the  SPONTANEOUS: if patient talks, converse
trunk and abdomen • Lumbar and sacral with u spontaneous. Pero pag gising ng
nerves (from the lower back) – supply the patient tas nag sleep again then it is not
legs, the bladder, bowel and sexual organs. spontaneous so to speech lang yan. To
• CAUDA EQUINA- collection Spinal N. at speech: drowsy lang masyado. Do pain
inferior end of spinal canal method kung wla talga opening by using
pen.
BEST VERBAL RESPONSE: 5 highest

ASSESSMENT AND DIAGNOSTIC EXAM  ORIENTED TO TIME PLACE AND

PERSON: what have u eaten before, what
have u done before, where u now. But
when the pt answers back na I don’t know
her. Confused if kumain ng manga pero
kumain ng papaya talaga. Inappropriate if
hindi in line sa question. Incomprehensible
like di mo maunderstand ang sinasabi like
slurred masyado
MENTAL STATUS EXAM: usually
 If intubated write I or NT sa table
BEST MOTOR REPSONSE
 OBEYS COMMAND: if nag follow ng SPECIAL NEURO ASSESSMENT
command. If wala apply pain by trapezius
squeeze, supraorbital notch and last sa
breastbone kasi masakit. Localized alam
nya where. Withdrawal nagmove sya pero
wala nag decorticate. Pero if
nagdecorticate ang arms where mag move
towards the body.
Video how to do motor examination
1. BRUDZINSKI’S SIGN (Indicates irritable
meninges)
Motor Assessment:
2. KERNIG’S SIGN (Indicates harmstring
Muscle Size
problem because meningeal irritaiton)
 Severe atrophy suggest denervation of a
3. LHERMITTE SIGN or Barber’s Sign (kay
muslce (Low Motor Neuron damage)
ginapaduko sa barber)
Muscle Tone:
 An electrical sensation that runs down the
 Rigidity - Parkinson’s disease back and into the libs
 Spasticity - upper motor neuron damage 4. UHTOFF’S PHENOMENON
Strength:  A visual problem
ROMBERGS TEST
 Ask the subject to stand erect with feet
together and eyes closed
TYPES OF DIAGNOSTIC EXAMINATION
 Positive Romberg test suggest that
NON-INVASIVE INVASIVE
ATAXIA is SENSORY IN NATURE. A
negative Romber test suggests that  SKULL AND  LUMBAR
ATAXIA is cerebellar (motor) in nature SPINAL PUNCTURE
REFLEXES RADIOGRAPHY
 MYELOGRAM
 COMPUTE
1. BABINSKI:  CEREBRAL
TOMOGRAPHY
ANGIOGRAPHY
 Dorsiflexion of the ankle and great toe with (CT) SCAN
fanning of the other toes may --  ELECTROMYO
 MAGNETIC
spinothalamic problem GRAPHY
RESONANCE
 Indicates an aupper motor neuron damage IMAGING (MRI)
2. CORNEAL  ELECTROENCEP
HALOGRAPHY
 Loss of blink reflex; Cranial Nerve V
dysfunction  POSITRON
EMISSION
3. GAG
TOMOGRAPHY
 Loss of gag reflex, Cranial Nerve IX (PET)
 CAROTID /
TRANSCRANCIAL
DOPPLER

NON-INVASIVE TESTS:
1. SKULL and SPINAL RADIOGRAPHY
 SKULL: Reveal the size and the shape of
the skull bones, suture separation in infants,
fractures or bony defects or calcifications
 SPINAL: identify fractures, dislocation,
compression, curvature, erosion, narrowed
spinal cord and degenerative processes
PRE-PROCEDURE
 Maintain immobilization of the neck if spinal
fracture is suspected
 Remove metal items from body parts
 Document if the patient has thick and
heavy hair because it may affect the
interpretation of the XRAY film
POST-PROCEDURE
 Maintain immobilization until the results are
known
2. COMPUTED TOMOGRAPHY SCAN
 A type of brain scanning that may or may
not require an injection of a dye
 Detect intracranial bleeding, lesions,
edema, infarctions, hydrocephalus and
cerebral atrophy
PRE-PROCEDURE
 Informed consent if with dye
 (+) hot, flushed and metallic taste in the
mouth
 Contraindicated to patients with
pacemakers, implanated defibrillators,
metal implants
 Assess for claustrophobia
 Determine if contrast agent will be given
 Instruct to remain still during the procedure
POST-PROCEDURE
 Normal activities; diuresis if with contrast
agent
4. ELECTROENCEPHALOGRAPHY
 A graphic recording of electrical activity of
the superficial layers of the cerebral cortex
PRE-PROCEDURE
 Wash hair
 Inform that electrodes are attached, and
that electricity DOES NOT enter
 Withhold stimulants, antidepressants,
tranquilizers, anticonvulsants for 24-48
hours before the test
 Premedicate as prescribed
POST-PROCEDURE
 Wash hair
 Maintain safety if patient was sedated
5. POSITRON EMISSION TOMOGRAPHY

 Assess for allergies and claustrophobia
 Instruct to lie still and flat during the test
 Remove objects from the head
 Inform of the possible mechanical noises
POST-PROCEDURE
 Replacement fluids for diuresis
 Allergic reactions to dye
 Assess dye injection site for bleeding,
hematoma, extremity color and pulses
 a test that uses a special type of camera
and a tracer (radioactive chemical) to look
at organs in the body
 Do not smoke or drink caffeine or alcohol
for 24 hours before this test.
 Do not eat or drink for 8 hours before this
test
 The tracer may make you feel warm and
flushed
6. CAROTID/ TRANSCRANIAL DOPPLER

3. MAGNETIC RESONANCE IMAGING

 Identifies types of tissues, tumors and
vascular abnormalities
 Similar to CT scan but provides more
detailed pictures
PRE-PROCEDURE
 Remove all metal objects
 Uses sound frequency to produce images
of the carotid arteries in the neck in viewing
screen
 A computer converts the Doppler sounds
into colors that are overlaid on the image of
the blood vessel
 Gel is applied to the neck area to provide
good contact for the handheld transducer
INVASIVE TESTS:
1. LUMBAR PUNCTURE
 Insertion of a spinal needle through the L3-
L4 interspace into the lumbar subarachnoid
space to obtain CSF, measure CSF
pressure or instill dye or medications
 CSF drawn drawn from between two
vertebraes
CONTRAINDICATED: increase ICP d/t rapid
decrease of CSF around the spinal cord =
brain herniation
PRE-PROCEDURE
 Informed consent
 Empty bladder
DURING THE PROCEDURE
 Lateral recumbent with knees drawn up to
the abdomen and chin onto the chest
 Maintain strict asepsis
POST-PROCEDURE
 Monitor VS and NVS
 Position flat as prescribed
 Monitor I/O, force fluids
2. MYELOGRAM
 Injection of dye or air into the subarachnoid
space to detect abnormalities of the spinal
cord and vertebrae
PRE-PROCEDURE
 Obtain informed consent
 Assess for allergies of iodine
 Premedicate for sedation if prescribed
POST-PROCEDURE
 Asses VS and NVS
 Dye:
 Water based
 elevate head 15-300; 6-8 hrs
 Oil based
 flat for 6-8 hrs
 Air
 Keep head lower than trunk 48hrs
 Monitor I/O, bladder distention and
vomiting
3. CEREBRAL ANGIOGRAPHY
 Injection of a contrast through the femoral
artery into the carotid arteries to visualize
the cerebral arteries and assess for lesions
PRE-PROCEDURE
 Informed consent
 Assess for allergies
 NPO status 4-6 hours prior
 Obtain baseline neurological assessment
 Mark peripheral pulses
POST-PROCEDURE
 Monitor VS, NVS
 Assess for allergic reaction- swelling of
neck or difficulty breathing
 Elevate head of bed 15-30 degrees only if
prescribed
 Keep bed flat if femoral artery is used
 Assess peripheral pulses
 Apply sandbags and pressure dressing; ice
on puncture site
4. ELECTROMYOGRAPHY
 test that checks the health of the muscles
and the nerves that control the muscles;
shows impaired muscle strength
 a very thin needle electrode will be inserted
through the skin into the muscle and picks
up the electrical activity which will be
displayed on an oscilloscope
 NEUROLOGICAL DISORDERS
1. HEADACHE aka CEPHALGIA
Classification of Headache:
A. PRIMARY
- is one for which no organic cause can be
identified.
B. SECONDARY
- Is a symptom associated with an organic
cause, such as in brain tumor or an aneurysm.
QUESTIONS SPECIFIC FOR HEADACHE
 Where was the headache hurt, and what
were you doing when the headache started?
 How long do they usually last, and do the
headache recur? Gaano ba katagal like
very painful, naga recur ba in a certain time
 Do you have trouble with your vision before?
Sometimes because squinting
 Do you take any OTC meds? NSAIDs,
Paracetamol,
positioning pinakalit na lingi, kasi and
strutures maraming nerves)
 Structures: trigeminal, facial,
glossopharyngeal, vagus and cervical
nerves.
 Chronic or Episodic
Classification & Etiology: results from muscle
contraction
 describe as a tight band-like discomfort
that is unrelenting; with few h/a free
intervals not associated with nausea or
vomiting or worsened by activity.
 Due to fatigue/stress
Moderate pain that could be constant, parang
nanjan lang palagi and ginapressure ang brain
known also as headband headache kasi frontal
area.
Trigeminal CN V (Sensation: upper scalp,
upper eyelid, nose, nasal cavity, cornea and
lacrimal, upper teeth, cheek, sensation of
tongue)

 Have you been depressed? Isa din ito sa CN VII Facial (face, facial expression, eyelid
cause like overthinking sometime parang na paralyze ang
manifestation ptosis)
 Do you have any family member with
history of headache? It could be familial CN IX Vagus (swallowing, regulation of cardiac
rate) Vagus Nerve has a very important role in
cardiac rate because sometimes pag mag NGT
TYPES OF PRIMARY HEADACHE nagkakaroon ng cardiac rate increase na
magka MI. If you are doing something or
CLUSTER TENSION MIGRAINE nagawork ka it could worsen.
HEADACHE HEADACHE
- Pain,
- Pain is in - Pain is like a nausea and
and aorund in band visual 2. CLUSTER HEADACHE
one eye squeezing the changes are  have cyclical pattern of 1-3 short-lived
head typical classic attacks of periorbital pain. “alarm clock
form headache”
Both side
One side but
One side  Ipsilateral pain
in one specific
eye  Occurs more often in men
 TRIGGERED BY ALCOHOL ROH
Recurrence is very important because it is the CONSUMPTION (Alcohol vasodilates the
start of the investigation why is is recurring vessel)
what is the time of the day and what are you  Pain described as deep, boring, intense
doing that time pain of such severity that the client has
Primary has no organic cause! difficulty remaining still (Cluster headache
tearing parang nagaluha luha sa pain yung
boring may pinakalit na stab-like pain)
1. Tension headache 3. MIGRAINE HEADACHE
 Caused by irritation of pain-sensitive
structures of the brain. (yung mga
 Considered as “vascular headache”,
vasospasm & ischemia of intracranial
vessel being the cause of pain.
 Headache is most often unilateral, but pain
may occur on alternate sides with different
attack
 No stab-like pain
Vasospasms means there is vasoconstriction
There is a sudden constriction of the artery
leading to the decrease inits diameter in the
amount of blood that would deliver to the area
of the brain which causes headache. So less
blood or may ischemia
If there is vasoconstriction then decrease blood
flow of the area. After constriction it will dilate
again so may pooling again of blood
CATEGORIES OF MIGRAINE HEADACHE
WITH AURA WITHOUT AURA
– Headache lasts 1-2 – Aura develops 5-20
days aggravated by mins before headache
physical activity
– With nausea and
vomiting
– Photophobia
– phonophobia as well
as yung pandinig
Etiology of Migraine Headache: Idiopathic
Risk Factors: ❑Menstrual Cycle ❑Stress
❑Depression ❑Sleep Deprivation ❑Fatigue
❑Overuse of Meds ❑Tyramine-rich foods
(Blue cheese, Parmesan, Aged Cheese)
Pathophysiology of Migraine
IV. Recovery Phase
Prodrome Phase (24-48 hours prior attack)
• Fatigue • Frequent yawning • Fluid retention •
Increased urinat ion • Muscle stiffness,
especially in the neck, back and face •
Constipation or diarrhea • Food cravings •
Depression or irritability • Difficulty conce
ntrating • Feeling cold
Aura
• Blurred vision • Appearance of floaters (tiny
specks that float before the eyes) • Flashes of
light or color, or blurry vision • A blind spot or
even complete blindness in one eye •
Numbness or tingling of the hands, feet, and/or
face (particularly around the mouth) • Stiff neck
• Weakness • Vertigo or Dizziness • Loss of
balance • Ringing in the ears • Double vision •
Difficulty talking • Slow thinking or confusion •
Problems with concentration • Changes in
mood and activity level
Headache 4-72 hours
• Extreme sensitivity to light and sound and
smell • Nausea • Vomiting • Increased pain
with physical activity (such as walking or going
up or down stairs) • Status migrainosus
(does not respond to medication / di
marelieve) • A debilitating Migraine attack
lasting for more than 72 hours. • Risk for stroke
Recovery
• Fatigue • Weakness • Irritability • Anxiety •
Depression • Difficulty concentrating • Scalp
tenderness
TYPES OF SECONDARY HEADACHE
LUMBAR PUNCTURE POST
HEADACHE CONCUSSION
HEADACHE
❑ loss of CSF volume
with LP decreases the ❑ after seemingly
brain supportive trivial head injuries &
cushion particularly after rear-
end motor Vehicle
collisions

Kunan ang CSF kaya

4 Phases of Migraine: Though walang injury
mangyari kay may
and na jarr lang ang
I. Prodrome headache kasi
nahead wala
decrease ang brain
concussion parang
II. Aura supportive cushion
nauyog lang ang ulo
III. Headache phase
Diagnostic Tests for Headache: blood (hemorrhage), brain tissue (tumor
preliforate) and CSF)
• Detailed History Taking
 (CSF) 7–15 mmHg
• Complete Physical & Neurological
Examination CEREBROSPINAL FLUID PRESSURE
• CT-Scan  intrathoracic pressure during coughing
(intraabdominal pressure)
• MRI
 valsalva maneuver
• Cerebral Angiography
 venous and arterial systems
INCREASED INTRACRANIAL PRESSURE
Medical Management:
 Intracranial hypertension associated with
 Approaches:
altered states of consciousness.
 Abortive (symptomatic) - for less
 Monro - Kellie Hypothesis: The pressure-
frequent attacks-limiting headache at
volume relationship between ICP, volume
the onset or progress
of CSF, blood, and brain tissue, and
 Preventive - for more frequent attacks cerebral perfusion pressure (CPP)
 Medications - Monro-kellie hypothesis any increased of the
3 components then it causes ICP; do not let
1. Serotonin receptor antagonist them cough, sneezing and lifting object are
✓ Sumatriptan(Imitrex) valsva manuevers so we should prevent it from
2. Ergotamines patient who had post op surgery esp brain
✓ Ergotamine tartrate surgery.

3. Anti-epileptics - If you cough sneeze lift heavy object it could

✓ Topiramate ✓ Gabapentin
Nursing Interventions for Headache
H-eat application or massage
E-ducate on prevention
A-nti-emetic medications
D-im or dark environment
A-dminister analgesics
C-oach on habit and lifestyle changes
H-ead elevation (to decrease blood flow sa
brain area kasi if more pressure then there will
ICP)
E-xercise programs
INTRACRANIAL PRESSURE
 is the pressure inside the skull and thus in
the brain tissue and cerebrospinal fluid
(skull is enclosed area walang margin of
increased pressure so kung mataas then
definitely may headache; any increased of
increase the ICP
Causes of Increased ICP
 Cerebral edema (third spacing / third space
fluid)
 Brain surgery (Can also cause cerebral
edema because there is inflammation)
 Mass lesions in the brain (Even if its
benign, since enclosed ang area talagang
magkaproblem kasi increased ang tissue)
 obstruction to CSF flow and/or absorption
(If blocked ang flow then it could cause
accumulation of CSF inside the which
cause increased ICP
 NON-COMMUNICATING
HYDROCEPHALUS: Occurs when
there is a blockage of CSF Flow
 COMMUNICATING
HYDROCEPHALUS: Occurs because
there is a problem is with the arachnoid
villi which causes not to absorb the
CSF; usually in adult kasi enclosed na
ang skull.
 Increased venous pressure
 • Hypercapnea = vasodilatation ‐ Increased
CBF
• Hypocapnea = vasoconstriction ‐Decreased
CBF
• PaO2 (hypoxia) <40‐45mmHg =
vasodilatation
If there is cranial insult or injury, usually pH
magkaka edema or inflammation yan causing
vasodilation and eventually tissue edema • Acidosis = vasodilatation & Increased CBF
which caues increase ICP then there is • Alkalosis = vasoconstriction & Decreased
compression of blood vessels and decreased CBF
blood flow leading to decreased oxygen with
the death of brain cells in a matter of minutes
so the Increase ICp with compression of Cerebral perfusion pressure (CPP) (very
brainstem and respiratory center can cause crucial it tells you the perfusion is good)
Accumulation of CO2 and can lead to
Vasodilation. (Pag may brain herniation  the pressure of blood flowing to the brain.
magpasok sa foramen magnum so maipit then
 Normal: 70-100 mm Hg
magkaroon ng problem sa breathing usually
bradycardia, bradypnea and wide pulse  CPP = MAP − ICP
pressure aka CUSHING’S TRIAD) (Pag may
 MAP = [(2 x diastolic)+systolic] / 3]
Vasodilate na ang cerebral vessel na it can
cause a sudden gush of blood sa area ng brain  N: 70-110 mm Hg
kaya mas lalo mag result to injury) (Sa
accumulation ng CO2, we should normalize it  Decrease CPP (>40 mmhg) causes:
or level sa mere normal kasi magcause ng  raise systemic blood pressure and
vasodilation. So once mag insert ng Intubation dilate cerebral blood vessels =
even if you are not instructed by the Doctor ischemia, brain infarction (no blood),
Perform hyperventilation to expel the intracranial hemorrhages and
carbon dioxide) increasing ICP
We are breathing because of our CO2 How measure ICP: lumbar puncture; Elevate
the Head para decrease ang blood flow.

Compensation for increases in ICP

• CSF regulation
• Autoregulation of blood flow (dapat di Clinical manifestation of increased ICP
magdilate kasi more problems)  Changes in LOC
• Metabolic regulation to blood flow (Metabolic  Cushing’s Triad
mechanism should answer kasi may
respiratory. Brain tissues have limited space  Hyperthermia
because close masaydo so compensation  Cushing’s ulcer (type of ulcer na
typically occurs by displacing the CSF mag associated sa brain)
increased absorption and decreased blood flow
so wag idilate para magkaroon ng  Seizure
normalization; without such changes it could  Papilledema (use opthalmoscope)
cause death of the tissue )
 Projectile vomiting: magsuka ang patient
tas nanjan ka sa harap then papunta sayo
Chemical‐Metabolic Regulation of Cerebral kasi normal pababa lang suka
Blood Flow (CBF) CUSHING’S TRIAD
PaCO2  Compensatory mechanism that tries to
raise CPP even though ICP is increasing
 due to pressure on the brain stem elevate systolic BP
 Widening of pulse pressure • Neuronal oxygenation
compromised
 Bradycardia
Stage 3 • Compensatory mechanisms
 Decreased respiratory rate
are exhausted (compensate and
 A grave sign: impending brain herniation metabolic and respiratory)
• Dramatic increase in ICP
Early of Increase ICP • Changes are occuring rapidly
 Restless, agitated Stage 4 • Brain herniation
 Sluggish pupil • ischemia and hypoxia in
herniated tissue
 Pronator drift (pic)
• displaced brain tissue.
 Slow, slurred speech
Effects of Stage 4
• Hemorrhages
Late Symptoms of ICP
• obstructive hydrocephalus
 Rapid deterioration of condition
(from infants to elderly a non
 New onset of seizures communicating hydrocephalus,
no blockage but may problem sa
 Decorticate (brain stem) or decerebrate
CSF absorption)
posture
• Respiratory and or cardiac
 Glascow Coma Scale of < 8 arrest due to brain stem
 Hypotension right before death herniation

 Respiratory changes
STAGES OF INCREASE IN ICP
Stage 1 • changes in LOC
• trouble remembering
• personality changes
• Drowsiness
• Headache esp in AM or
morning
Stage 2 • present consistent s/s
• systemic vasoconstriction to
Brain Herniation
 Displacement of
brain tissue under
the falx cerebri
 Falx
cerebriseptum that divides two hemisphere
Brain Herniation refers to the shifting of the
brain tissue from the area of high pressure. If
may impeding brain herniation pwede ang
brain stem magpasok sa foramen magnum but
if the bleeding is on the other like the Pic
Above, then ang compression mag Mid Line
shift so magpasok sya sa area na wala.
MIDLINE SHIFT
 a dangerous sequela in which the brain
moves toward one side as the result of
massive swelling in a cerebral hemisphere
 Caused by a raised ICP due to a unilateral
space-occupying lesion (e.g. a hematoma)
NEUROLOGIC CHANGES
 due to hypoxia and hypercapnea
 decreased level of consciousness (LOC),
 Cheyne-stokes respiration- deeper &
faster breathing followed by apnea
(cheynes-strokes respiration problem
sa neurologic function parang gasping
and may moment na no breathing at all. )
 hyperventilation
 sluggish dilated pupils
 widened pulse pressure.
Changes in Vital Signs as ICP rises
 Systolic BP increases (WIDENED PULSE
PRESSURE)
 Pulse decreases
 Temperature increases
 Respirations abnormal
 VS as client approaches brain death
 Hypotension
 cardiac and ventilation collapse
occur (because of the brain
herniation esp pag maipit na ang )
Diagnostic Tests:
1. CSF Analysis with manometer – A
manometer equipped with a 3 way stop cock
can be attached to the hub of the LP needle
after the needle is corrected inserted
Manometer: measures the ICP
PERFORM LUMBAR PUNCTURE FIRST
THEN ATTACHED MANOMETER.
HOWEVER,LUMBAR PUNCTURE CAN
CAUSE BRAIN HERNIATION KASI PARANG
BALLOON PAGITUSOK KASI ENCLOSED
AND CONTINUOUS ANG BRAIN AND
SPINAL CORD SO PAGITUSOK NA
MARELEASE ANG PRESSURE SO SUDDEN
DECREASE OF PRESSURE CAN CAUSE
BRAIN HERNIATION SO WAG BASTA BASTA
MAG LUMBAR PUNCTURE KUNG DI BABA
ANG ICP.
THERE ARE MEDICATIONS BEFORE DOING
THE LUMBAR PUNCTURE TO LOWER THE
ICP
2. ICP Monitoring
Device – a device
placed inside the
head, which senses
the pressure inside
the skull and sends
its measurements to
a recording device.
May transducer that will be placed on the
subarachnoid; pwede rin mag burrholes
MEDICAL MANAGEMENT:
 Mannitol mechanism
 Decrease blood viscosity
 Reflex vasoconstriction (decrease CBF)
 Increase intravascular volume (increase
CPP) side effect
 Volume depletion, hypotension
 Rebound phenomenon
Furosemide
 no reflex vasoconstriction effect
 synergist with mannitol
 not effective in dysautoregulation brain
edema. Calcium channel blockers
 To decrease MAP
Analgesia and sedation
 used to reduce agitation and metabolic
needs of the brain
 Propofol (sedative-hypnotic)
Surgical Management
1. Craniotomies - are holes drilled in the skull
to remove intracranial hematomas or relieve
pressure from parts of the brain
2. Decompressive craniectomy - a part of
the skull is removed and the dura mater is
expanded to allow the brain to swell without
crushing it or causing herniation
3. Cranioplasty  EPILEPSY- is a chronic disorder of
recurrent seizure
 Seizure and its Etiology:
REDUCING CSF AND INTRACRANIAL
BLOOD VOLUME  Mainly Idiopathic
 Ventriculostomy drain - CSF Drainage =  Pathologically acquired epilepsy
reduced ICP and restore CPP
 Biochemical Epilepsy
 Excessive drainage may result collapse
 Posttraumatic
of the ventricles
 Trauma / damage
 Hyperventilation = results in
vasoconstriction; Maintain PaCO2 at 30-35  Abnormality in the brain
mmHg
 Infectious diseases
NURSING INTERVENTIONS
IF ONCE LANG NANGYARI THEN IT IS NOT
R- educing CSF & Intracranial Blood volume EPILIPESY. IT COULD BE CONVULSION OR
SEIZURE LANG
E- dema decrement
INTERNATIONAL CLASSIFICATION OF
D- ecrease of metabolic demand
SEIZURES
U- pright position
1. PARTIAL SEIZURES
C-ontrolling fever E-nsure oxygenation
a) SIMPLE PARTIAL SEIZURES
D-rug administration
b) COMPLEX PARTIAL SEIZURES
2. GENERALIZED SEIZURES
a) TONIC-CLONIC SEIZURES (Grand mal)
b) ABSENCE SEIZURES (Petit mal)
c) MYOCLONIC SEIZURES
d) ATONIC SEIZURES
Increased ICP and Interventions
Clinical Findings: TYPES OF SEIZURE
I. PARTIAL SEIZURE
a) SIMPLE-PARTIAL
- Originate in the motor cortex of the
frontal lobe.
- Not accopmanied by loss of
consciousness
- Characterized by JACKSONIAN MARCH
(because of tingling or twitching in the area
and then marches into the larger area. Like
from small digits of the hands magtravel
seizure eventually to the forearm)
b) COMPLEX-PARTIAL
SEIZURE DISORDER - Originate in the temporal lobe and limbic
 Is a sudden, abnormal electrical discharge system
from the brain that results in changes in - Characterized by AUTOMATISM.
sensation, behavior, movements, (Automatism: di nya mapigilan like
perception and consciousness (Abnormal automatic na mag lip smacking and kagat)
firing)
SIMPLE-PARTIAL SEIZURE
1. With motor signs – JACKSONIAN MARCH
2. With sensory symptoms – Tingling
sensation, visual, auditory, gustatory or
olfactory (Phantosmia) phenomena
3. With autonomic symptoms or signs – c) ❖ Ictal Phase (2 phases):
Tachycardia, diaphoresis, hypotension /
hypertension
4. Psychic symptoms
a) Detachment, depersonalization
b) Dreamy state
c) Time Distortion
d) Memory distortion:
 deja vu (feeling that one has seen
something before),
 deja entendu (feeling that one has
heard something before)
 jamais vu (feeling that one has
never seen something that is
familiar),
 jamais entendu (feeling that one
has never heard something that is
familiar),
 panoramic vision (rapid recall of
past events)
COMPLEX-PARTIAL SEIZURE
 Involves impairment of consciousness
 "vacant" or "frightened" look
 Five types of automatisms:
 Alimentary: chewing, increased
salivation, borborygmi
 Mimetic: facial expressions of fear,
bewilderment, discomfort, tranquility,
laughter, crying
 Gestural: repetitive movements of the
hands, fingers, sexual gestures
 Ambulatory: wandering, running
 Verbal: repeated short phrases or
swearing
II. Generalized Seizure (nonspecific and
affects the entire brain simultaeneously while
Partial seizures are focal in origin )
1. GRANDMAL SEIZURE (tonic-clonic)
a) ❖ Pre-ictal (before the seizure
happened makakita ng flashes of light
or very warm or cold air)
b) ❖ Aura
 TONIC - muscular rigidity/ extension of
extremities; 10-20 secs
 CLONIC- muscular jerking (muscle
fatigue); 2 minutes
 Post-ictal Phase: Sleep
2. PETIT-MAL (aka absence seizure)
 Occurs to children ages 4- puberty
 The victim appears to be daydreaming.
 30 seconds
 (naga day dream lang di sumasagot and di
gumagalaw; hard to diagnose )
3. MYOCLONIC
 Involve a sudden uncontrollable jerking
movements of either a single muscle group.
 (pagmaglakad kalit magsipa)
4. ATONIC
 Associated with total loss of muscle tone.
 Known as drop attacks
 (natumba agad ang patient)
5. Febrile Seizures
Complication:
STATUS EPILEPTICUS - continuous seizure
lasting for more than 30 minutes without full
recovery in between. (Muscles are rigid,
magkakaroon ng breathing kasi magbalik ng
balik)
Diagnostic Tests for Seizure Disorders:
1. EEG
2. MRI
3. PET Scan
Medications for Seizure Disorders:
 Phenytoin (Dilantin) - seizure
 Phenobarbital (Luminal) - epilepsy
 Carbamazepine (Tegretol) - anticonvulsant
 Ethosuximide (Zarontin) - absence seizure
 Valproic Acid (Valproate) - epilepsy
 Diazepam
Surgical Management for Seizure Disorders:
1. Cortical Resection/ Corpus Callosotomy -
surgical procedure that disconnects the
cerebral hemispheres, resulting in a condition
called splitbrain. (To stop the over firing; split
brain surgery wala na continued electrical
activity)
2. Temporal Lobectomy – removal of a lobe
3. Hemispherectomy – very rare surgical
procedure where one cerebral hemisphere
(half of the brain) is removed or disabled
4. Vagal nerve Stimulator Implants
NURSING MANAGEMENT FOR SEIZURE
DISORDERS:
SEIZURE PRECAUTIONS
1. Monitor temperature & Respirations
2. Note level of consciousness
3. Provide a quiet, dimly lighted rooms.
4. Prepare plastic airways and suction machine
Safety
 Side-rails up
 Ease the patient to the floor (if sitting on a
chair)
 Remove pillow (if in bed)
 Loosen constrictive clothing
 Position patient on one side if possible
 Do not restraint
Airway
 Suctioning
 oxygen
NEUROLOGICAL TRAUMA
HEAD INJURY
 The National Head Injury Foundation
defines TBI as a traumatic insult to the
brain capable of causing physical,
intellectual, emotional, social, and
vocational changes.
1. HEAD INJURIES
 Injury to the scalp, skull or brain
 Traumatic Brain Injury (TBI) is the most
serious form of head injury
 PRIMARY INJURIES - CONTUSSION,
CONCUSSION
 SECONDARY INJURIES - HOURS
AFTER OR THE DAY AFTER
TRAUMATIC BRAIN INJURY (TBI)
 The damage to the brain from an external
mechanical force and not caused by
neurodegenerative or congenital conditions
 TBI can lead to temporary and permanent
impairment of cognitive, physical and
psychosocial functions
TYPES OF HEAD INJURY
A. SCALP INJURY
B. SKULL FRACTURE - A skull fracture is a
break in the continuity of the skull caused by
forceful trauma
OPEN HEAD INJURY
 Linear Fracture
 Depressed Fracture
 Open Fracture
 Comminuted Fracture
 Basilar Skull Fracture (Has racoon eyes or
Battle’s Signs)

CLOSED HEAD INJURY

 Concussion
 Cerebral Contusion
 Diffuse Axonal Injury
 Intracranial Hemorrhage
  Epidural
 Subdural
 Subarachnoid
 Intracerebral (severe because hard to
operate)

SKULL FRACTURE MANIFESTATION Mechanism of Brain Injury:

 Battle’s sign A. Acceleration
 Racoon’s eye B. Deformation
 Subconjunctival hemorrhage C. Deceleration
 Rhinorrhea
 Otorrhea RISK FACTORS:
 HALO SIGN (has leaking of CSF; parang  Blunt Trauma: pwede gihit or gibunalan
sipon na halong dugo CSF na pala)
 Penetrating Trauma: MALAKAS TALAGA
ANG FORCE KAYA NAGPASOK SA
SKULL AREA
 Coup & Countercoup: OCCURS DURING
THE INJURY; WHEN U ARE RIDING A
CAR TAPOS MAY SUDDEN BRAKE SO
BOTH SIDE NG BRAIN MAY INJURY SA
KALAKAS NG FORCE; BOTH SIDE OF
THE BRAIN HAS INJURY FRONTAL AND
OCCIPTAL; FAST FORWARDS
MOMENTUM THEN SUDDENLY STOPS

PATHOPHYSIOLOGY OF BRAIN INJURY

1. CONCUSION - A jarring of the brain within ❑Supportive Measures:
the skull with temporary loss of consciouness
❖Mechanical ventilation
2. CONTUSION - A bruising type of injury to
❖Seizure Prevention
the brain.
❖F & E Maintenance
3. DIFFUSE AXONAL INJURY - Diffuse
Axonal injury involves widespread damage to ❖Nutritional support ❖Pain
axons in the cerebral hemispheres, corpus Management
callosum, and brainstem (severe)
4. INTRACRANIAL HEMMORHAGE (most
severe) Surgical Management

 EPIDURAL HEMATOMA - Meningeal Goal: Decompression

artery affectation. 1. CRANIECTOMY - excission of the cranial
 SUBDURAL HEMATOMA - Is a bone without replacing it
hemorrhage from small vessel between 2. BURR HOLE - decompressio n, evacuation
the dura and arachnoid. of clot & abscess.
 SUBARACHNOID HEMORRHAGE - 3. CRANIOTOMY Opening to the cranium
Results from blunt trauma ; S/SX:
nuchal rigidity, (+) Kernig’s, (+) Surgical Approach:
Brudzinski ; Deterioration of LOC, 1. SUPRATENTORIAL
hemiparesis.
• Provide access to the frontal, temporal,
 INTRACEREBRAL HEMATOMA - occipital and parietal lobe.
Bleeding into brain tissue from
contusion or laceration Post-operative: • Position: Head
Elevated
2. INFRATENTORIAL
Assessment:
• Provide access to the lesion in brainstem.
 Headache
• Post-Operative: Position: Flat on bed
 Confusion
 Altered LOC
NURSING MANAGEMENT
 Absent corneal reflex
❑Maintain Patent Airway
 Pupillary abnormalities
❑Neurological assessment
 Vision & hearing impairment
❑Treatment of ICP
 Sudden Onset of neurological deficits
❑Supportive measures
 Seizures
❑Electrolyte & Fluid Balance
 S/sx of Increased ICP
❑Adequate Nutrition
❑Prevention of Injury
DIAGNOSTIC TESTS:
❑Maintaining Skin integrity
1. Skull X-ray
2. 2.CT-Scan
SPINAL CORD INJURY
3. 3.MRI
❑Is generally the result of trauma to the
4. Cerebral Angiography vertebra column.
Spinal Cord Injury Categories
MEDICAL MANAGEMENT: 1. PRIMARY
❑Treatment of Increased ICP
- result of the initial insult or trauma, usually
permanent
2. SECONDARY
- result of a contusion or injury in which the
fibers begin to swell and disintegrate (break up
/ deteriorate)
- a secondary chain of events produces edema,
hyposxia, ischemia and hemorrhagic lesions,
which in turn result in destruction of myelin and
axons
2. COMPLETE SPINAL CORD LESION - can
result in:
a) Paraplegia - paralysis of the lower
body
b) Quadriplegia - paralysis of all four
extremities
 Neurologic Level - refers to the lowest level
at which sensory and motor functions are
normal

LEVEL FUNCTION
MECHANISM OF INJURY
C1-C6: NECK FLEXORS
A. Distraction: the pulling apart of the spine
C1-T1: NECK EXTENSORS
 Ex: suicide by hanging, Gunshot wounds to
the C3, C4, C5: SUPPLY DIAPHRAGM

chest, back, and abdomen C5-C6: Shoulder movement, raise arm

(deltoid);flexion of elbow
B. Lateral Bending:the head and neck are (biceps); C6 externally rotates
bent to one side, beyond the arm (supinates)
normal limits. C6-C7: Extends elbow and wrist (triceps
C.Hyperflexion: the act of bending or the and wrist extensors); pronates
condition of being bent (paharap) wrist

D. Hyperextension: movement by which the C7-T1: SUPPLY SMALL MUSCLES OF

two elements of any jointed part are drawn THE HANDS
away from each other(patalikod) T1-T6: INTERCOSTALS AND TRUNK
E. Axial Loading: a sudden, excessive ABOVE THE WAIST
compression which drives the weight of the T7-L1: ABDOMINAL MUSCLES
body against the head
L1-L4: THIGH FLEXION
 Ex: downward blow to the head, upward
force to the feet L2-L4: THIGH ADDUCTION

F. Excessive Rotation: movement of the body L4,L5,S1: THIGH ABDUCTION

about the body's axis
L5, S1, S2 EXTENSION OF LEG AT THE
HIP (GLUTEUS MAXIMUS)
CAUSES OF SPINAL COR INJURY: L2-L4 EXTENSION OF LEG AT THE
KNEE (QUADRICEPS
 MVA
FEMORIS)
 FALLS
L4,L5,S1,S2 FLEXION OF LEG AT THE
 VIOLENCE KNEE (HAMSTRINGS)
 SPORT-RELATED L4, L5, S1 DORSIFLEXION OF FOOT
(TIBIALIS ANTERIOR)
EXTENSION OF TOES
TYPE AND LEVEL OF SPINAL CORD
L5, S1, S2 PLANTAR FLEXION OF FOOT
INJURY
FLEXION OF TOES
1. INCOMPLETE SPINAL CORD LESION -
classified according to the area of spinal cord
damage: Central, lateral, anterior or peripheral
DEGREE OF INJURY
I. Complete Cord Involvement - no
functioning nerves remain below the level of
injury.
II. Incomplete Cord - Involvement of some
function remains below the level of injury; has
4 types
 Anterior cord syndrome
 Central cord syndrome
 Posterior cord syndrome
 Brown-sequard syndrome
1. Anterior Cord Syndrome
 Characteristics: Loss of pain, temperature,
and motor function is noted below the level
of the lesion; light touch; position, and
vibration sensation remain intact
 Cause: The syndrome may be caused by
acute disk herniation or hyperflexion
injuries associated with fracture-dislocation
of verterbra
 It also may occur as a result of injury to the
anterior spinal artery, which supplies the
anterior two thirds of the spinal cord.
 when the damage is towards the front of
the spinal cord.
 loss or impaired ability to sense pain,
temperature and touch sensations below
their level of injury
2. Central Cord Syndrome
 when the damage is in the centre of the
spinal cord
 loss of function in the arms
3. Posterior Cord Syndrome
 when the damage is towards the back of
the spinal cord
 difficulty in coordinating movement of their
imbs and epicritic sensation
4. Brown-sequard Syndrome or Lateral
Cord Syndrome:
 When damage is towards one side of the
spinal cord
 loss of movement to the injured side
 Pain and temperature impairement
 Characteristics: Ipsilateral paralysis or
paresis noted, together with ipsilateral loss
of touch, pressure, and vibration and
contralateral loss of pain and temperature
 Cause: The lesions is caused by a
transverse hemisection of the cord (half of
the cord is transected from North to South),
usually as a result of a knife or missile
injury, fracture dislocation of a unilateral
articular process, or possibly an acute
rupture risk
 (NO CONTRALATERAL MANIFESTATION
IN SCI ONLY IN CVA)
CERVICAL INJURY
LEVEL AFFECTED FUNCTION
C1-C2: LOSS OF BREATHING
C3 ABOVE RESULTS IN LOSS
OF DIAPHRAGM FUNCTION
C4 LOSS OF FUNCTION AT THE
BICEPS AND SHOULDERS
C5 LOSS OF FUNCTION AT THE
SHOULDERS AND BICEPS,
AND COMPLETE LOSS OF ASSESSMENT:
FUNCTION AT THE WRISTS General:
AND HANDS.
❑ Poikilothermia
C6 LIMITED WRIST CONTROL,
AND COMPLETE LOSS OF Integumentary:
HAND FUNCTION ❑ Warm, dry skin below level of injury
C7 AND T1 LACK OF DEXTERITY IN THE Respiratory:
HANDS AND FINGERS, BUT
ALLOWS FOR LIMITED USE ❑ Lesions at C1-C3: apnea, Inability to cough
OF ARMS
❑ Lesions at C4: poor cough, diaphragmatic
breathing, hypoventilation
THORACIC INJURY ❑ Lesions at C5-T6: decreased respiratory
LEVEL AFFECTED FUNCTION reserve

T1-T8 INABILITY TO CONTROL Cardiovascular

THE ABDOMINAL MUSCLES ❑ Lesions above T5: bradycardia, hypotension,
T9-T12 PARTIAL LOSS OF TRUNK postural
AND ABDOMINAL MUSCLE hypotension,
CONTROL
absence of vasomotor tone
(Postural hypotension where in galing ka sa
LUMBOSACRAL INJURY bed then nagrun ka papunta cr tapos nalipong
 Dysfunction of bowel, bladder and sexual nakuyapan ka)
function Gastrointestinal
❑ Decrease or absent bowel sound (paralytic
ileus in
lesions above T5)  S/SX: LOW BLOOD PRESSURE, LOW
HEART RATE
❑ Abdominal distention
❑ Constipation
3. AUTONOMIC DYSREFLEXIA
❑ Fecal incontinence
❑Is a complication with a lesion T4-T6.
❑ Fecal impaction
❑A hypertensive medical emergency.
Urinary
❑Caused by:
❑ Retention for lesions between T1 and L2
✓Overdistended bladder
❑ Flaccid bladder (acute stage). Loss of nerve
✓Rectal stimulation
innervations causes atony of the bladder which
✓Impaction
causes urine retention.
S/Sx:
❑ Spasticity with reflex bladder emptying (later
stage) ❑Piloerection (goosebumps)
Reproductive ❑Severe HPN
❑ Priapism (prolonged penile erection) ❑Headache
❑ Loss of sexual function ❑Diaphoresis
Musculoskeletal ❑Nasal congestion
❑ Muscle atony (in flaccid state)
❑ Contractures (in spastic state) MANAGEMENT:
Neurologic 1. Elevate head of the bed
I. Complete 2. Check the patency of catheter
❑ Flaccid paralysis & anesthesia below level 3. Administer Hydralazine (Apresoline)
of injury
❑Quadriplegia / Tetraplegia
DIAGNOSTIC TESTS
❑ Paraplegia
❑Spinal RADIOGRAPHY
II. Incomplete - Weakness in the body below
❑CT/MRI
the site of the injury.
❑ECG

COMPLICATIONS
EMERGENCY MANAGEMENT
1. SPINAL SHOCK
1.Immobilize on a spinal back board (WAG
❑S/SX: no reflexes, no sensation, no somatic
MAGPAHERO HERO)
and visceral distention.
2.Avoid flexion, rotation and extension of
❑Indication of Recovery:
patient’s neck and head
- Reappearance of reflex activity,
3.Transport the patient to spinal injury or
hyperreflexia, spasticity, reflex emptying of the
trauma centers (WITH THE USE OF LIFTING
bladder
BOARD)

2. NEUROGENIC SHOCK
 Pharmacologic Therapy
 develops due to the loss of autonomic
 Respiratory Therapy
nervous system function below the level of
the lesion.  Skeletal Fracture Reduction & Traction
 ❑Alcohol abuse
SURGICAL MANAGEMENT: ❑Stimulant drug abuse
1. LAMINECTOMY - To remove the lamina aka ❑Aging process
DECOMPRESSION SURGERY

ANEURYSM CLINICAL MANIFESTATIONS:

NURSING MANAGEMENT
I. Promoting adequate breathing & airway
II. Improve Mobility
III.Promoting adaptation top sensory &
Perceptual alterations
IV.Maintaining skin integrity
V. Maintaining urinary elimination
VI.Improving bowel function
VII.Providing comfort measures
VIII.Prevention of thrombophlebitis
(log roll the patient; turning to side to prevent
pressure ulcers)
Spinal stenosis
AUTOIMMUNE PROCESS
1. ANEURYSM
 An intracranial aneurysm is the weakness
in the tunica media, the middle layer of the
blood vessels.
 The most common type is saccular or berry
aneurysm.
 Are found more often in the anterior
cerebral circulation
 ASYMPTOMATIC
 RUPTURED ANEURYSM
 Sudden onset of headache “Worst
headache of my life”
 Vomiting • Generalized seizure •
 Decrease LOC: confused, lethargic,
coma
 S/sx of Menigeal Irritation( Nuchal
rigidity, photophobia)
 Focal motor & Sensory Deficits
Hunt-Hess Clinical Grading Scale (Used for
clients with Aneurysmal SAH)
I. Alert, minimal headache
II. Alert, moderate to severe headache (cranial
nerve palsy allowed)
III. Lethargic or confused, mild or focal deficit
IV. Stuporous, moderate to severe hemiparesis,
possible early decerebrate rigidity
V. Deep coma, decerebrate rigidity, moribund
appearance.
ANEURYSM DIAGNOSTIC TESTS:
 History Taking
 Physical Assessment
 CT Scan
 MRI
 Transcranial Doppler

Medical Management
1. Neurologic Assessment
2. Maintain a patent Airway

RISK FACTORS: 3. Continuous hemodynamic monitoring

❑Smoking 4. Nimodipine administration

❑Hypertension 5. Morphine administration

❑Atherosclerosis 6. I & O monitoring

Surgical Management
1. ANEURYSM CLIPPING
❑Surgical obliteration of the aneurysm with a
metal clip to eliminate the risk of rebleeding.
2. ENDOVASCULAR THERAPY &
EMBOLIZATION
❑Involves obliteration of the aneurysm by
means of platinum coils.

STROKE RISK FACTORS

NON-MODIFIABLE MODIFIABLE
 Age  Hypertension
 Gender  Heart Disease
 Race  DM
 Family History  Sleep apnea
 Blood Cholesterol
level
 Smoking
 Sickle Cell
Disease
Nursing Management  Substance abuse
A-ssess neurologic status  Intracranial
haemorrhage
E-levate heat at 30 degrees
 Obesity
U- rine output monitoring
R-espi and cardio monitoring
Y-ou keep patient & family members in a quite
and comfortable environment
S-urgery preparation M-edication
administration

2. STROKE
BRAIN ATTACK - Is a syndrome of a group of
sudden focal neurological deficit resulting from
interruption of cerebral blood flow.
Classification of Brain Attacks:
❑Ischemic (emboli, Thrombus)
❑Hemorrhagic
  Cognitive Deficits
 Sensory & Perceptual deficits
 Motor deficits
 Sensory Deficits

Cognitive Deficits
❑ Changes in LOC
❑ Spatial and proprioceptive dysfunction
❑ Impairment in memory, judgment, or
problem-solving and decision-making process
❑ Decreased ability to concentrate and attend
to task
STROKE INITIAL MANIFESTATIONS
❑ Aphasia
S- evere & sudden headache
❑ Alexia
T- T-trouble in speaking
❑ Agraphia
R-ight or left hemiparesis
❑ Acalcula
O-cular disturbances
K-onfusion
Sensory & Perceptual deficits
F-mpairement in coordination
❑Homonymous hemianopia
❑Agnosia
Left hemisphere vs Right Hemisphere
❑Apraxia
Affected
Left Hemisphere Right Hemisphere
Motor deficits
 Aphasia  Spatial-perceptual
deficits ❑Hemiplegia
 Agraphia
 Lack of inhibitions ❑Hemiparesis
 Alexia
 Inappropriate ❑Ataxia
 Acalculia
social behavior
❑Dysarthria
 Dysarthria
 Short attention
❑Dysphagia
 Hemiplegia span
❑Flaccidity of the muscles associated with
 Homonymous  Poor judgment
paralysis on the motor neurons.
hemianopsia
 Hemiplegia
❑Spasticity
 Short-term
 Hemiparesis
memory
 Anosognosia
 Depression Sensory Deficits
(Denial of affected
 frustration Side) ❑Ptosis
 Apraxia (Inability ❑Unilateral neglect syndrome
to use objects or
words) ❑Amaurosis fugax

STROKE DIAGNOSTIC TESTS:

ASSESSMENT
❖CT Scan
❖MRI
❖Cerebral Angiography
❖Doppler Flow studies

MEDICAL MANAGEMENT:
❑Maintenance of a patent airway and optimal
oxygenation
❑Control cerebral edema
❑Control of fluid and electrolyte balance
❑Maintenance of adequate cerebral blood flow
and cerebral perfusion pressure
Medications:
• Antihypertensive.
• Platelet Aggregant
• Aspirin • Ticlodipine
• Anticoagulant
• Heparin • Warfarin
• Thrombolytics
• t-PA • urokinase-. • streptokinase
• Calcium channel blockers
• Mannitol
• Dexamethasone

SURGICAL MANAGEMENT
❑Carotid Endarterectomy
❑Transluminal Angioplasty
❑Stenting
❑Extra-Intracranial (ECIC) Bypass
NURSING MANAGEMENT: C. GENERALIZED FORM: Involves the
proximal muscles of the limbs and neck,
❑ Optimizing cerebral tissue perfusion
usually with both ocular and bulbar
❑ Improving Mobility and Preventing Joint manifestations
Deformity
STAGES OF GENERALIZED FORM
❑ Enhancing Self-Care
a) Mild
❑ Managing Sensory-Perceptual Difficulties
b) Moderate
❑ Assisting with Nutrition
c) Acute Fulminating
❑ Attaining Bowel and Bladder Control
d) Late Severe
❑ Improving Communication
Diagnostic Tests:
❑ Maintaining Skin Integrity
❑Endrophonium/T ensilon Testing
❑EMG
3. MYASTHENIA GRAVIS
❑Serum Radioimmunoflu orescencea
 Is an autoimmune neuromascular disorder
in which there is chronic, progressive
decreased amplitude of the nerve impulse MEDICAL MANAGEMENT:
at the myoneural junction. (somatic
1. Drug Therapy
muscles)
❑Anticholinesterase drugs
 an autoimmune disorder, in which
weakness is caused by circulating ❑Pyridostigmine (Mestinon)
antibodies that block acetylcholine
receptors at the postsynaptic ❑Neostigmine (Prostigmin)
neuromuscular junction, inhibiting the ❑Corticosteroids
excitatory effects of the neurotransmitter
acetylcholine at nicotinic acetylcholine ❑Prednisone
receptors ❑Cyclosporine
MYASTHENIA GRAVIS RISK FACTORS ❑Cytotoxic and Immunosuppressive drugs
 GENDER: FEMALE ❑Azathioprine

 AGE: 20-40 YEARS OLD 2. Plasmapheresis

 THYMIC TUMOR MYASTHENIA GRAVIS COMPLICATIONS

MYASTHENIA GRAVIS CLINICAL 1. ) MYASTHENIC CRISIS

FEATURES • Cause: undermedication, stress, infection
 FATIGABILITY • Any infection may precipitate the condition.
 PTOSIS 2. ) CHOLINERGIC CRISIS
 DIPLOPIA • Cause: overmedication with
 DYSPHAGIA anticholinesterase

 RESPIRATORY MUSCLE WEAKNESS • S/SX: nausea, vomiting, diarrhea, pallor,

cramps, sweating, salivation, bradycardia
 SKELETAL MUSCLE WEAKNESS
• Antidote: Atropine S04
MYASTHENIA GRAVIS CLASSIFICATIONS
SURGICAL MANAGEMENT
A. OCULAR FORM: a form of myasthenia
gravis (MG) in which the muscles that move  THYMECTOMY
the eyes and control the eyelids are easily
fatigued and weakened.
B. BULBAR FORM: involves breathing,
swallowing, and speech.
NURSING MANAGEMENT:  (ANTIBIOTICS, ANALGESIC,
ANTICOAGULANTS, AZATHRIPINE &
1. Promote Effective breathing pattern
CYCLOPHOSPHAMIDE)
2. Improved Airway clearance
NURSING MANAGEMENT:
3. Ensure adequate nutrition
1. Maintaining Respiratory Function
4. Increase activity tolerance
2. Enhancing physical mobility
5.Provision of optimum vision
3. Providing adequate nutrition
4. GUILLANE-BARRE SYNDROME
4. Improving communication
 Landrys paralysis, Landry-GBS-Strohl
5. Decreasing fear and anxiety
 Is an autoimmune attack of the peripheral
5. MULTIPLE SCLEROSIS
nerve myelin.
 Progressive, degenerative disease of the
GUILLANE-BARRE SYNDROME RISK
CNS
FACTORS:
 Etiology: UNKNOWN
❑ Viral infection- history of upper respiratory
and GI infection  Abnormalities in T-helper cells,
Tsuppresor, B-lymphocytes
❑ CMV
 Viral: mumps, measles, rubella
❑ EBV
 Stress
❑ Hepatitis
 Trauma
❑ HIV
 Pregnancy
❑ Rubella & rubeola
 Age: 20-45 year old
❑ Varicella
 Female
Clinical Manifestations
 Bilateral weaknes in the legs
 Respiratory dysfunction
 Dysphagia
 CN VII (facial)
 Horner’s Syndrome
 Ipsilateral ptosis
MULTIPLE SCLEROSIS CLINICAL
 Enophthalmos
FEATURES:
 Anhidrosis
Common initial symptoms:
DIAGNOSTIC TESTS:
 Tingling sensation
 CSF analysis
 Numbness
 EMG
 Sensory symptoms:
 Lhermitte’s sign
MEDICAL MANAGEMENT:
 Motor Symptoms:
 Plasmapheresis
 Uhthoff’s phenomenon
 Steroids
 Charcot’s Triad
 Immunoglobulin infusion
 Scanning of speech
 Ace inhibitors
 Nystagmus
 Medications:4A’S
  Tremors
DIAGNOSTIC TEST:
❑CT-Scan
❑CSF Analysis
❑MRI

MEDICAL MANAGEMENT:
1. PHARMACOLOGIC THERAPY
❑ Disease –modifying therapies
❑ Symptoms management
❑ Baclofen
❑ Valium
❑ Symmetrel
❑ Propranolol
❑ Anticholinergics, antispasmodics,
ACE inhibitors

NURSING MANAGEMENT:
1. Promoting physical mobility
2. Prevent Injury
3. Enhancing bladder and bowel control
4. Enhancing communication
5. Manage feeding difficulties
6.Improve sensory & cognitive function