RHONDA LUCAS

SICU
RASHID HOSPITAL
2011

NEURO
By the end of this module you will be required to:
Define Mechanism of Injury and understand its relationship to patients
clinical presentation
Describe the components of the CNS
Describe the layers of Meninges and Spaces within the skull
Discuss the anatomy and physiology of the brain
Apply the Mechanism of Injury to various regions of the brain in order
to predict expected deficits
Outline the basic functions of the 4 major areas of the brain:
Cerebrum
Diencephalon
Brainstem
Cerebellum
Outline the function of Brocas Area
Outline the function of Wernickes Area
Describe the activities at the Circle of Willis
Define the regions of the brainstem and list the functions of each
Discuss the ventricular system of the brain
Define CSF and its functions
Briefly explain the brains circulation
Relate the circulation to brain injury pathologies
Define Autoregulation
Understand the limitations of Autoregulation and relate this to brain
injuries
Describe the function of the Blood Brain Barrier
Discuss the anatomy of the spine
Identify the vertebral regions of the spine
Describe the components of the PNS
Describe the function of the ANS
Describe the function of the SNS
Discuss the basic anatomy and function of nerves
Describe Nerves Impulses and their mechanism of action
Relate the mechanism of nerve impulses to spinal injuries
Describe the medical implications of Aneurysms
Compare the etiology, presentation, diagnosis, treatment and
interventions of:
Subarachnoid Hemorrhages
Epidural Hematomas
Subdural Hematomas
AV Malformations
Tumours
Strokes
Discuss Vasospasm
Relate interventions to the prevention of Vasospasm
Understand the importance of early rehab on neuro and spinal
conditions
Understand the role of early nutrition in neuro and spinal conditions
Understand the Rashid Hospital TBI Guidelines

Define primary and secondary injuries

Define ICP
Apply the Munro-Kellie Hypothesis to the treatment of ICP
Discuss the importance of cerebral bloodflow on ICP interventions and
patient outcomes
Relate the chemical and neurological effects of the body to the
treatment of ICP
List medical and nursing interventions to treat ICP
Identify the components of an ICP waveform, and relate findings to
patient condition
Relate clinical signs of deterioration to the principles of herniation
Define Cushings Response/Cushings Triad
Develop plans of care to improve neuro patient outcomes
Familarize yourself with new innovations in neuro care
Thoroughly perform a neuro assessment
Thoroughly document a neuro assessment
Understand the importance of doing neuro checks together at shift
change
Perfrom a GCS assessment accurately
Perform cranial nerve testing and understand the implications of
findings
Understand the difference between stable vs unstable spinal fractures,
and identify nursing interventions for each
Describe spinal shock
Describe Neurogenic shock
Describe Autonomic Dysreflexia and list nursing interventions for
prevention
Discuss the nursing foci of a patient with spinal fractures
Discuss rehab measures which can be initiated in ICU
Understand the role of dermatomes testing on spinal patients,
including indications for use
Pay special attention to the objectives in this module. I have included a
great deal of extra information in this handout so that you have a full
picture of the neuro system. However, much of this is information-only,
meaning that you will not be tested on everything. You will only be tested
on the content of the objectives. I suggest you read the entire package
because it will help you apply theory to bedside practice, but when
preparing for the exam just focus on knowing what is listed above
.Abbreviations:
ICP
Intracranial Pressure
CPP Cerebral Perfusion Pressure
MAP Mean Arterial Pressure
CBF Cerebral Bloodflow
SAH Subarachnoid Hemorrhage
IVH
Intraventricular
Hemorrhage
ICH
Intracranial Hemorrhage
EDH Epidural
Hematoma/Hemorrhage

SDH Subdural
Hematoma/Hemorrhage
SCDs Sequential Compression
Devices
BP
Blood Pressure
SBP Systolic Blood Pressure
HR
Heart Rate
RR
Respiratory Rate
CNS Central Nervous System
PNS Peripheral Nervous System
SNS Somatic Nervous System

ANS Autonomic Nervous System

BBB Blood-Brain Barrier
AVM Arterio-Venous
Malformation
GCS Glascow Coma Scale
TBI
Traumatic Brain Injury

MECHANISM OF INJURY
Before starting with Neuro, I want to talk about Mechanism of
Injury. This is a trauma term that you will hear me use a lot. It tells
you a great deal about how an injury occurred and gives you an idea
of what kind of damage you can expect. For instance, looking at
spinal injuries, what kind of injury would you expect if a patient was
hit from behind in her car? What about if it was a head-on collision?
What if she were hit from the side? What if she were unbelted? Do
you see how your body responses will all be in different directions
with different impacts? We can take this a step further and discuss
gunshot wounds. What kind of bullets were used? If they were
exploding bullets what kind of damage would you expect to see vs
non-exploding bullets? What if the bullets had a high rate of
velocity or a slow rate of velocity? What if it was a shotgun instead
of a rifle/handgun?
Even though we receive the patients already diagnosed, secondary
injuries can frequently get missed in the excitement of a trauma
resuscitation. It is important that ICU nurses inquire about the
Mechanism of Injury so that when we do our assessment we can
consider what type of injuries we should be seeing and do an indepth assessment on those particular areas to ensure nothing was
missed. It is also important in many cases (especially women and
children) to be sure the injuries are consistent with what is
expected; if they are not consistent for instance, if a female says
she fell down the stairs but has very specific blunt abdominal
trauma and no other bruises, this doesnt correlate with her story.
You should consider that the story is perhaps inaccurate and this
may warrant further investigation, possibly by police.
THE NERVOUS SYSTEM
Your nervous system is divided into two sections:

The Central Nervous System (CNS). This includes

o Brain
o Spinal Cord

Peripheral Nervous System (PNS). This includes

o Cranial Nerves
o Spinal Nerves
o Autonomic Nerves

Think of the CNS being located in the central part of your body,
and the PNS as everything branching off the CNS to other parts of
your body.
We will look a little closer at these two sections now.
THE CENTRAL NERVOUS SYSTEM
Your CNS is very fragile, so the major components are surrounded by
bones to help protect things. Because of this, we should know a bit
about not only the CNS itself but also these protective coverings. So
lets look at your skull first. Your skull is made up of bones joined
together by sutures. The skull is divided into the cranium and the
facial area. Well focus on the cranium. The major bones are:

Frontal

Temporal (2)

Parietal (2)

Occipital

Aside from the bones, your brain has some other protective devices
as well there are a few linings (meninges) under your cranium
before reaching the brain. Think of cracking open an egg. There is
a slimy film covering the yoke that you can usually peel off with a
little effort. Then there is another filmy lining attached to the shell,
which you can also peel away. The inside of the cranium is similar.
These meninges lay on top of each other but are not joined; there is
a potential for space between these linings. Therefore, if a bleed
were to occur, it could separate these meninges and settle in the
space. So from skull to brain:
Skull
Epidural Space: contains small arteries and lymphatic's
Dura Mater: Flush with the bone
Subdural Space
Arachnoid: very thick; loosely encloses the brain
Subarachnoid Space: lots of spongy connective tissues. CSF
flows through here
Pia Mater: mesh-like film which lies on top of the brain along
the lumps and valleys
Brain

These linings and spaces help with shock absorption and reduce
friction by allowing fluids inside, much like your joints have synovial
fluid so the bones dont grate together.
All this protection gives you an idea of how fragile your brain is!
Also note that these layers are continuous with the spinal column as
well, as this picture illustrates:

THE BRAIN

Soft outside; hollow spaces inside called ventricles (4)

Weighs approx. 2% of your body weight

(1.4 kg in young adult male)

15-20% of cardiac output goes to brain

20% of oxygen consumed by body is to convert

Critical thinking:
the glucose which will be used directly by the brain
Why is CPR so

4 Major areas
important in

Cerebrum

an

arrest?

Diencephalon

Brainstem

Cerebellum

Lets look at these sections individually.

CEREBRUM: This is the part of your brain that looks like a brain.
The surface is made of wrinkles (gyri) and crevices (fissures). The
gray matter covering the cerebrum is called the cerebral cortex.
This is the major functional centre of the brain. It has 3 functions:
Controls Motor functions
Controls Sensory functions
Association functions
What do we mean by association functions? Things like knowing
theres a difference between colours; comparisons and contrasts;
distinguishing between dark and darker, etc. We can say, then, that
the cerebral cortex is involved in consciousness perception of
sensation, initiation of movement, and higher mental processes.

Each hemisphere controls functions on the opposite of the body.

Each side of the cerebral cortex has different functions:
Left: language, math, reasoning, logic, analysis
Right: visual, spatial, intuition, emotion, appreciation for
music, art, literature etc.

IT IS SAID THAT
YOU CAN
DEVELOP THE
OTHER SIDE
A person will usually have a dominant side of his
OF YOUR BRAIN IF
cerebrum, either right or left, which means thatYOU
they will have a skill set leaning towards those TRAIN IT AND
FOCUS ON
THOSE ASSOCIATED
more in one side than the other; however,
TASKS.
everyone uses both sides of their brainscan you
WHAT DO YOU
imagine reasoning without intuition? Of courseTHINK?
not.

Most people are dominantly left-brained. A

right-brained person will always be left-handed.
What side is your dominant side?
Over 100 different areas of the cortex have been mapped, meaning
that their specific function has been determined. Some areas have
roles in motor activity, some have roles in speech formation, etc. It
is important to note, though, that no area functions alone. The
cortex is closely associated with the thalamus (discussed below)
many pathways connect with specific parts of the thalamus to
control functions.
Underneath the gray matter is (predominantly) white matter called
the medulla. It contains neurons and glia. The gray matter that
does lie inside the brain is called the basal ganglia,
exerting an inhibitory affect on the control of fine body movements.
Damage to the basal ganglia results in increased motor tone.
The cerebrum is divided into lobes, each with specific functions:
Frontal:

High-level cognitive function

Critical

Thinking: Is a GCS

Memory storage

score applicable

to those Voluntary eye movement

with an

injury to Brocas

Influences respirations, blood pressure and

Area?

GI activity

Emotionally labile

Brocas Area: motor control of speech, language

comprehension, recognition and production (usually
located in the dominant hemisphere)

Parietal: Sensory functions there are different areas for

touch and pain, or light and deep sensations
Temporal:

Interpretive area: Visual/auditory/olfactory perception

Wernickes area (auditory association and speech

processing area). This is usually located in the dominant
hemisphere. If this area is damaged what
happens? Words are heard but they are
meaningless

Learning

Emotional affect

Detailed memories (experiences, conversations, songs,

etc.) What happens if this area is injured? Severe
intellectual impairment

Occipital: visual perception and association (knowing the

striped animal you are looking at is a tiger)
Note that the lobes have the same names as the bones of the skull,
which lie overtop of the same area, ie the parietal bone overlays the
parietal region of the cerebrum.

And what of that gray matter inside? The basal ganglia provide an
inhibitory effect on our motor control of fine body movements.
Damage to the basal ganglia results in increased motor tone.
DIENCEPHALON: The diencephalon is a relay station between
higher and lower brain areas. It contains:

Thalamus: Sensory Centre. All sensory pathways route

through here (Pain centre)

Epithalamus: Growth and Development; food-getting centre

Hypothalamus:
o Physiological needs temperature regulation, water
metabolism, endocrine function
o Physical expressions in response to emotions (blushing,
dry mouth, clammy hands)
o Sleep-wake cycle/Circadian rhythms

Subthalamus: similar functions to the basal ganglia

Pituitary Gland: Endocrine feedback mechanism command

centre. The pituitary gland is divided into anterior and
posterior lobes

Critical Thinking: Neuro patients can develop Diabetis

Insipidus. What is happening neurologically when this
happens?

BRAINSTEM: Think of the brainstem as the ice cream cone that the
brain sits on. It is composed of three areas. The higher and lower
areas of the brain communicate through these different areas, as
well as it being the relay centre for any messages between the spine
and brain. From top to bottom of the cone:

Midbrain:
o Centre for auditory and visual reflexes
o Cranial Nerves III and IV

Pons:
o Some control of respiratory function
o Cranial Nerves V VIII

Medulla:
o Motor and sensory tracts run through here
o Controls heart rate, respiratory rate,
dilation/constriction of blood vessels
o Vomiting and coughing reflexes
o Cranial Nerves IX XII
o Continuous with the spinal cord

(Well discuss Cranial Nerves later)

Critical Thinking: A patient with a severe head injury has
been having heart rate fluctuations over the last 3 hours,
ranging between 52 and 88 bpm. He has had a continuous
fever for the last 12 hours. Is the heart rate a reportable
finding? Why or why not?

CEREBELLUM: The cerebellum is the base or the back portion of

your brain. It is responsible for voluntary motor function control. It
processes and interprets impulses for motor function:

Coordinates movement

Maintains balance

Spatial coordination

Regulates postural reflexes

Coordinates agonist/antagonist muscle movements

Other areas of the brain:

Limbic System: Emotional responses

Reticular Formation: Maintains the cortex in an alert,

conscious state. This area has extensive connections,
therefore, with other parts of the brain

VENTRICLES: These are the hollow areas inside your brain. There
are 4 cavities:

Two lateral ventricles

One midline (3rd)

One diamond-shaped ventricle which is continuous with the

spinal cord (4th)

They hold fluid, just like the ventricles of the heart, only the brain
ventricles hold cerebrospinal fluid (CSF).

CSF:

Shock absorber for the brain and spinal cord

Contains water, O2, CO2, electrolytes, glucose, and small

amounts of protein

Most is produced in the ventricles

Direction of flow: lateral ventricles - third ventricle - fourth

ventricle - circulates around cord and brain

Small reservoir in the lumbar region around L4 (hence,

lumbar puncture)

25 ml/h produced

Most is reabsorbed...when the CSF pressure > venous

pressure the trap doors open and excess CSF heads into
sinuses

CSF is formed by three different sources:

1. Secretions are constantly secreted from the choroid plexus
(located inside the lateral ventricles). This is the primary
production source about 25 ml/hr produced here.
2. Ependymal cells lining the ventricles ad the blood vessels of
the meninges
3. Blood vessels of the brain and spinal cord (small amounts
only)
CSF flows from the choroid plexus in the lateral ventricles down into
the third and further ventricles, then into the subarachnoid space
and down along the spinal column to circulate around the brain and
spinal cord.
Now lets discuss circulation.
CIRCULATION
Like every other component of your body, the brain needs blood
flow to keep it running. Recall that the brain requires 25% of our
resting cardiac output. Cerebral bloodflow is about 750ml/min, or 3

cups. In a healthy person this actually stays pretty constant due to

regulations within the body. Blood is supplied by two internal
carotid arteries which run up the side of the neck and enter the
subarachnoid space, eventually leading to the cerebral arterial
circulation and two vertebral arteries which enter at the base of
the skull through the foramen magnum directly into cerebral
arteries. Cerebral arteries bifurcate and run throughout the brain to
ensure blood supply to all areas.
But our blood pressure fluctuates regularly. When we are asleep it goes
fairly low. How do we maintain perfusion to our vital organs? Your body
has a function called Autoregulation, the ability to constrict or dilate its
circulatory system in an effort to maintain a constant blood flow. Your
brain has this ability, thus ensuring that it is well perfused even when our
blood pressure is very low. Autoregulation in healthy people functions
within a range of MAP 70-110. If the MAP is lower, CBF will decrease; if the
MAP is higher, CBF will increase.
Cerebral arteries and veins have thinner walls than their
counterparts in other areas of the body. Additionally, in most body
systems, the arterial and venous circulation run side by side; not so
in the brain the venous return follows separate routes.
The major arteries all form join up near the centre of the cerebrum
and form a traffic circle. This is called the Circle of Willis. This is
where the major arteries for the entire cerebral circulation system
branch off. The benefit of this is that if a stroke occurs in a vessel
near here there is a good chance that blood can still pass via
collateral circulation routes. The downside is that most
subarachnoid hemorrhages tend to occur nearby so damage occurs
to the whole area, which lead to extensive ischemia to the entire
brain.

Blood-brain barrier: A filtering system that allows molecules in

the blood to be filtered through to the neurons, but it limits the
blood itself from passing through. Basically its a very tight
passageway between the blood and neurons so not much can pass
through except what is needed. The BBB guards the entrances.
Why? Many substances in the blood (ie bacteria, high concentration
of electrolytes) can be harmful to brain tissue, so the BBB prevents
these substances from crossing through.
Recall that our brain needs a high amount of glucose and oxygen,
both of which get delivered by blood. If there are blockages that
prevent this blood from getting where it needs to go, ischemia
results. Think about blocked carotid arteries for a minute. There
are only four arteries perfusing our brain and we need 25% of our
total cardiac output to be delivered to remain well oxygenated.
What happens when one of these carotids gets blocked? We can
lose up to of what we need!! Taking this a step further and
thinking about brain injuries now, do you see why it is so important
to ensure adequate bloodflow? This is why we measure CPP. Well
talk about this more later.
So thats the brain. Lets now discuss the Spine.

THE SPINE

Like the brain, the spinal cord needs protection; this comes in the
form of the Spinal Column a column of bones, ligaments, and
cartilaginous disks that encircles the spinal cord, producing a
flexible frame that protects the cord yet still allows us movement.
The spinal column is comprised of 33 bones called vertebrae
(singular = vertebra):

7 Cervical

12 Thoracic

5 Lumbar

5 Sacral (fused together)

5 Coccygeal (fused together)

Between the non-fused vertebrae lie disks. They vary in size, shape
and thickness, and contain fluid for shock absorption; when they
lose their fluid content (age, trauma), damage can occur.
THE SPINAL CORD
The spinal cord runs down through the vertebrae and is the
transmitting pathway for sensory and motor signals coming from the
brain to various parts of the body, and vice versa. Different nerve
fibres throughout the spinal cord conduct impulses at different
speeds (the thicker the myelin sheath the quicker the conduction).

Sensory impulses enter the cord from the brain via regions called
dermatomes (remember this for later). Impulses to the peripheral
regions leave via the ventral root and head out to the body. Sensory
deficits occur only when the sensory component of two or more
spinal nerves is interrupted. If only one spinal nerve is involved you
will have pain or paresthesia.
Remember how your brain has linings to protect it? Well, your
spinal cord has similar protective linings:
Dura mater: Encases spinal roots, ganglia and nerves
Arachnoid: Continuation of cerebral arachnoid
Pia Mater: Thicker and less vascular than the Cerebral Pia Mater

THE PERIPHERAL NERVOUS SYSTEM

The peripheral nervous system makes up the sensory and motor
tracts that innervate our body and keep it operational. As you
know, we control most of our functions, but there are certain
functions which are automatic and we cannot control (ie heartbeat,
breathing, etc.). These are called involuntary functions. The PNS,
therefore, is divided into the voluntary and involuntary systems.
Somatic Nervous System: This is the voluntary system. The SNS
carries messages to and from skeletal muscles, the things we
control.

12 Cranial Nerves

31 pairs of Spinal Nerves:

o 8 Cervical
o 12 Thoracic
o 5 Lumbar
o 5 Sacral
o 1 Coccygeal
Note that the nerves have the same names as the vertebrae
near where they originate.

Autonomic Nervous System: This is the involuntary system. It

regulates the activity of smooth muscles and glands; its purpose is
to maintain a stable environment for the body. Unlike skeletal
muscles, which only get activated, smooth muscles and glands need
to be regulated; they need to either speed up or slow down. The
ANS, then, is divided into two different sections to control this:

Sympathetic Nervous System: fight, fright or flight. The

neurotransmitter for this system is Noradrenaline (hence it is
considered an adrenergic system)

Parasympathetic Nervous System: conservation and

maintenance. The neurotransmitter is acetylcholine (hence,
it is a cholinergic system)

These two have an antagonistic relationship. Because it deals only

with activating involuntary functions, the ANS is made up only of
motor neurons. All sensory innervations happens via the SNS. Due
to its functions, the ANS is activated primarily in the spinal cord, the
brainstem and the hypothalamus
Critical Thinking: Think about how you would expect various
body systems to respond if acting under each system.
Would your pupils dilate or shrink if you were frightened?
Would your GI system speed up or slow down? If you think
about these responses and relate them to which system is
activated, you can also figure out how your body will
respond under the influence of adrenergic or cholinergic
medications, as well.
Weve talked about voluntary and involuntary muscle function.
What about reflexes?. Spinal reflexes are a response elicited due to
a stimulus of sufficient magnitude. There are different types of
reflexes (twitches in skeletal muscles; gagging). Also, some
reflexive activities at a young age become voluntary activities as
you age voiding and defecation, for instance.
Weve covered a lot of information up until now, and it may be a bit
confusing. To help make it easier, see the following chart.

CENTRAL NERVOUS SYSTEM

PERIPHERAL NERVOUS SYSTEM

(CNS)

(PNS)

VOLUNTARY
(SKELETAL MUSCLE)
BRAIN

INVOLUNTARY
(SMOOTH MUSCLE
SPINAL CORD

AND GLANDS)

SYMPATHETIC
PARASYMPATHETIC

NERVES
Before we get into neuro pathologies, it is important to cover the
nerves themselves, and to understand a bit about the anatomy of a
nerve, including conduction. Dont worry about memorizing this;
just have an idea in your head about how conduction occurs,
understand the neurotransmitters, and think about what happens at
this level when brain injuries occur.
There are two types of nerve cells:
A. Neuroglia cells
Provide supportive functions (structural
support, nourishment, protection) for
neurons, ie they wrap around neurons.
40% of the brain and spinal cord are made
up of neuroglia cells
(5-10 times more than neurons)
Can divide by mitosis
Major source of primary tumours
Central nervous system neuroglial cells:
1. Astroctyes: multiple processes (star-like). Responsible for
nutrition, removing debris, controlling movement of molecules
from blood to brain, regulating synaptic connectivity
2. Oligodenroctyes: have a few branching processes. Produce
the myelin sheath neurons in the CNS. An individual oligo-cell
can maintain the myelin sheaths of several axons
3. Ependyma cells: Line the ventricular system. Aid in
production of CSF; act as a barrier to foreign substances within
the ventricles
4. Microglia: scattered throughout the CNS; phagocytes for
neuron waste.
Peripheral nervous system cells:
5. Schwann cells: form myelin sheath around axons (equal to
oligo-cells but in the PNS). When they wrap around an axon
their outer layer encloses the myelin sheath. The outer layer
is called the neurolemma, and is said to be necessary for the

regeneration of axons. These non-continuous sheaths are

separated spaces called Internodes this is where ions easily
flow between the axon and the ECF.
B. Neurons
Functions:

Responding to sensory and chemical stimuli

Conducting impulses
Releasing chemical neuroregulators
Components of a neuron:
a. Cell body: includes nucleus, cell membrane and cytoplasm
b. Axon: carries impulses away from cell body. Can be very
long; branches near end of projection
c. Dendrites: direct impulses towards cell body. Extend only a
short distance from cell body and branch profusely

Neurons are classified as

a. Unipolar: one process which divides close to the cell body.
One branch (the peripheral process) carries impulses from the
periphery towards the cell body. The other branch (the central
process) conducts the impulse towards CNS
b. Bipolar: found only in specific spots; their function is related
to where they are found (ie eye)
c. Multipolar: Comprises most of the neurons in the body.
Consists of one long projection (axon) and then shorter
projections (dendrites)
Physiology of Nerve Impulses
A. Resting Membrane Potential: although a resting neuron is not
conducting an impulse it still has a charge. The potential
difference is related to the unequal distribution of potassium
and sodium on either side of the cell. Normal resting potential is
-80mV.
The cell membrane is semipermeable and selectively permeable.
Sodium and chloride are found in greater concentrations outside
the cell, caused by the sodium pump which continually pumps
sodium out of the cell. Potassium is greater inside (pumped in by
potassium pump).
B. Action Potential: the fluid and ions in the ICF create a highly
conductive solution, allowing for conduction of impulses from one
part of the cell interior to another. Various stimuli can change
the permeability of the cell membrane, resulting in changes to
the membrane potential. The stimuli must, however, be of
sufficient magnitude if it is to conduct an impulse and thus create
an action potential (the fundamental unit of nerve signals).
In unmyelinated neurons, many simultaneous discharges at the
synaptic junction must occur to create a sufficient effect on the
cell membrane. When this happens, depolarization is said to
occur and the charges reverse the intracellular surfaces now

becomes positive (20-40 mV). The change in polarity conducts

an impulse from one neuron to the next at the same amplitude
and speed. Remember how your heart conducts impulses? This
is the same thingbut different!
In myelinated neurons the action potential hops from one node of
Ranvier to the next. This is Saltatory Conduction. At the break
in the sheath the membrane is several times more permeable
than many unmyelinated nerves; impulses are conducted from
node to node rather than running along the entire axon. This is
advantageous because it increases the velocity of an impulse
and conserves energy (because only the nodes depolarize). The
velocity depends on both the thickness of the myelin and the
distance. As these two factors increase, the velocity of the
impulse increases.
C. Synapse: The junction between one neuron and the next at
which an impulse is transmitted. Three structures are necessary
for an impulse to be transmitted at a synapse:
a. Presynaptic terminals
i. Excitatory: secretes an excitatory substance into the
synaptic cleft, thereby exciting the effector neuron
ii. Inhibitory: secretes and inhibitory transmitter that
inhibits the effector neuron.
b. Synaptic Cleft: space between the presynaptic terminal
and the receptor area of the effector cell.
c. Postsynaptic Membrane: receives the signal but it gets
progressively weaker during more prolonged periods of
excitation
When an action potential spreads over the presynaptic
terminal the membrane depolarizes,emptying some of the
contents into the synaptic cleft. This released transmitter
changes the permeability of the membrane and results in
either excitation or inhibition of the neuron.
D. Neurotransmitters: Chemical substances found in the cns that
excite, inhibit or modify the responses of other cerebral cells.
Released by presynaptic terminals and affect particular
postsynaptic cells of another neuron. Over 30 neurotransmitters:

serotonin, dopa, epi, levo, amino acids, endorphins and

enkephalins.

We frequently hear the term Diffuse Axonal Injury in brain

trauma.

What does it mean?

NEURO PATHOLOGIES AND INJURIES

STRUCTURAL ISSUES
A. Cerebral Aneurysms
Aneurysms are an outpouching or a sac of an
artery. They can be little outcroppings that happen
at bifurcations (known as berry aneurysms and
accounting for 80-90% of all aneurysms), or they can
be bulges in the arterial wall (known as fusiform
aneurysms). Ruptures of aneurysms usually result in
a subarachnoid hemorrhage (SAH).
Some facts:

Aneurysms diagnosed pre-rupture only make up about 5% of all

aneurysms!!!

Aneurysm rates are higher in women than men, although this is

reversed in childhood.

85% occur in the Circle of Willis (so what are the deficits going to
be?)

Most prevalent in 35-60 year olds

Familiar aneurysms: 6-20% of aneurysms show up in families

where 2 or more family members have them. This suggests a
genetically determined defect of the arterial wall but to date
there is no biological marker for this

Etiology: Possibly a genetic defect in wall but more likely a

degenerative problem, which is the theory that current research
favours

If these aneurysms rupture they usually result in SAH.

Infrequently they can rupture and bleed elsewhere (ventricles,
brain tissue, etc.). SAHs have poor outcomes -- 30% die within
the first two weeks and for those that survive, only 1/3 recover
without disability.

Unfortunately, most aneurysms are only detected following

rupture.

35% of patients who rupture never regain consciousness

Critical thinking: A patient with a ruptured aneurysm near

the Circle of Willis is recovering in your ICU. You are doing
neuro checks on her and you find she is emotionally labile
irritable one time and then very subdued the next. Is this an
expected finding related to her injury?
The occurrence, growth and rupture of aneurysms can be directly
related to patient hemodynamics (ie vascular injury, turbulence
through vessels, shearing forces), as well as inflammatory
mediators. Assessment of the chance of rupture is based solely
on a numbers game (based on the rupture of similar lesions), as
opposed to any pathophysiological markers. Therefore, at this time,
we continue to look at our vascular risk factors: smoking, sedentary
lifestyle, gender, race, atherosclerosis, HTN.
Aneurysms are classified by size and/or shape. They can be
traumatic, such as those that form as a result of a head injury, or
they can be a result of infection. A dissecting aneurysm is one
where the intimal layer of the artery is pulled away from the medial
layer and blood is forced into this newly created space.
What happens when they rupture? Blood enters the subarachnoid
space; the pressure of the surrounding tissue helps stop/slow the
bleeding. Fibrin, platelets and fluid form a plug that seals off the
site of bleeding. However, this leaked blood irritates the tissue,

setting up an inflammatory response that enhances cerebral edema

and increases ICP. Additionally, the clot is also taking up space,
increasing the ICP further and interfering with CSF absorption.
Signs/symptoms: As mentioned earlier, many go undiagnosed
until rupture; however, in 40% of cases there are pre-warning signs
which are undetected or ignored. It is important, then, to recognize
deficits early so that your patient can get the scans he needs to get
diagnosed. It is the nurse who is consistently at the bedside;
therefore, he or she must recognize the sometimes subtle changes
that can indicate problems. A nursing assessment can mean the
difference between life or death.
Pre-rupture:

Dilated pupil (CN III)

Eye movement deficits (CN III IV VI)

Possible ptosis (CN III)

Pain above/behind eye

Localized headache

Possible photophobia

Neck pain on flexion*

Upper back pain*

N/V*

Post-rupture:

Cardinal sign is a thunderclap headache (described as

the worst headache of my life; sudden onset at maximum
pain)

CN III, IV, VI deficits

N/V, stiff neck *

Stroke signs (hemiparesis, hemiplegia, aphasia, cognitive

deficits)

Signs of increased ICP

Pituitary dysfxn (DI, Hyponatremia)

*due to meningeal nerve irritation

As you can see, it is very important to know how to do cranial nerve
assessments and to recognize the significance of deficits. There is
a Cranial Nerve Assessment Guide at the back of this
handout.
Presentation: BP is usually elevated in the first few hours, mainly
as a compensatory response to the increased ICP. As ICP comes
down so does BP. If it remains elevated you can give Mannitol to
decrease cerebral edema. Keep SBP 120-150.
EKG changes: Prolonged QTs and T-wave inversions are seen in up
to 75% of patients, as well as the presence of a clear U-wave. The
changes reflect cardiac damage which may be a result of
catecholamine release.
Diagnosis: involves CT with contrast, or an MRI/MRA
Treatment:

Surgery

Coiling

Clipping

Medical Management

Surgical interventions is often required and outcomes are improved

with early surgical intervention (24-48 hours after
rupture).Clipping/coiling eliminates the chance of rebleeding.
Surgery also removes the clot, helping to decrease ICP.
Clipping: This ceases bloodflow to the
aneurysm, preventing further bleeding
and rupture.

Coiling: Cauterization-like procedure. A coil is

introduced into the aneurysm by a
microcatheter and electrical current is run
through the coil to cauterize the aneurysm.
Multiple coils are sometimes needed. This only
works on aneurysms that are not the result of
wall bulges. For wall-bulging types, the
neurosurgeon must use a balloon-assisted
technique to prevent the coil from slipping into
the main vessel. Many surgical interventions
are followed by the introduction of stents into
the main vessel so there is no further strain on
the wall.
Vessel occlusion: This is sometimes the only option but the
neurosurgeon must first determine if neurological function can be
maintained.
Medical management (either alone or post-op) involves:

Augmenting CBF:
o Optimize CPP
o Improving blood viscosity
o Euvolemia (no hypovolemia)
o ICP interventions

BP Control

Prevent Vasospasm

Monitor for cardiac complications

Nursing Management:
Frequent Neuro Checks, including Cranial Nerves
ICP Control (whether with ICP/EVD or not, treat as an increased
ICP patient)

 Monitor Labs (WBC, Hct, Fibrinogen and Platelets, Coagulation

profile; these are all indicators of the potential for vasospasms
(see below).
Medication Administration:

Nimodipine (see below)

Anti-seizure prophylaxis

Stool softeners

Analgesia/sedation

*The use of steroids is unclear; they may help to decrease

cerebral edema and inflammation)

Know where to expect potential vasospasms based on the

affected areas and be precise in your related neuro checks
Complications of SAH:

Rebleeding (return to surgery if feasible)

Hydrocephalus (EVD Insertion)

Cardiac complications (Limit ischemia)

Fluid and Electrolyte Imbalances

Vasospasm

VASOSPASM
Narrowing of a cerebral blood vessel causing reduced bloodflow
distally. Usually occurs 3-14 days after SAH. It is unclear why this
happens, but is thought that mediators or chemicals are released as
the clot breaks down. 1/6 of patients die from vasospasm. The site
of the original bleed can predict where a vasospasm is likely to
occur, so if you watch for deficits related to this area you can catch
things early and limit damage.
Diagnosis:

Changes in LOC; your patients behavior will mimic an

ischemic stroke.

Transcranial Dopplers

Treatment:

Triple-H therapy:
Hypervolemia (Keep CVP > 12 with fluids)
Hemodilution (Keep Hct 30-35%)
Hypertension (Norepi; titrate for CPP; during vasospasm
keep SBP>170, MAP>70)

Nimodipine: Calcium-Channel Blocker, 30mg TID (this is shown

to enhance collateral bloodflow and improve long-term
outcomes, therefore it is very important to give this med!!!
Do not hold it without checking with the doctor first! Always
try to increase your BP before administration so as to avoid
holding this med)

This keeps the blood thin, making it easier to get through the
narrower vessel to keep post-narrowing structures perfused. The
hypertension and hypervolemia help increase CBF.
Risk factors for vasospasm include electrolyte disturbances,
primarily Hyponatremia. This is a good time to discuss Sodium and
Volume Issues in Neuro patients:

DI: An inability to conserve water; the Anti-Directic Hormone is

not released/not produced. This results in polyuria. Signs of
dehydration may not be apparent due to fluid shifting related to
osmolarity gradients. BP, CVP can, therefore, be normal. Serum
Na >150. Treatment is to increase free H20 consumption and to
give Vasopressin.

SIADH (Syndrome of Inappropriate Anti-Diurectic

Hormone): Levels of ADH are elevated, resulting in decreased.
Serum Sodium will read low due to dilution (< 135), and body will
show signs of fluid overload (ie Elevated CVP). Treatment is fluid
restriction and diuretics. If sodium is dangerously low, may
replace with 3% Saline, slowly (max correction 15 mEQ in 24
hours)

Cerebral Salt-Wasting: The primary loss of sodium into the

urine without an increase in volume. This is defined as a true
hyponatremia (Na < 135). Usually caused by a transport
abnormality rather than an endocrine dysfunction. Treatment is
volume replacement as well as the sodium replacement (IV of NS
plus IV of 3% Saline.
DI

SIADH

CSW

Urine
Output
Serum Na
Urine Na
Serum

Polyuric
High
Low

Low
Low
High

Polyuric
Low
High
Normal to

Osmo
Urine

High

Low

Low
Normal to

Osmo

Low
Normal

High

Low

CVP
to Low
High
Low
Be sure to understand the chart above so that you may distinguish
which condition your patient has. Be specifically clear about the
difference between SIADH and CSW.
Case Study:

Mrs. B was brought into the ER by her family; she collapsed at home
about 20 minutes ago, right after complaining of the worst
headache shes ever had. On examination, her vitals are BP
190/120, HR 62, RR 18 and regular, Temp 37.6C, O2 saturation 94%.
You do a neuro check:
Eyes open to pain
Pupils are 4, equal and sluggish to respond
She is saying inappropriate words when aroused; otherwise
somnolent
She is moving her left arm spontaneously but is not squeezing your
hand or following commands. Her motor control is poor. Her left leg
moves laterally across the bed. There is no movement on the right
side.
A CT scan shows a ruptured aneurysm to the Right Middle Cerebral
Artery. She is taken to the OR for repair and evacuation of the clot
and then sent to you in the ICU. You look after her for 4 days in a
row.
Orders:

Routine neuro checks and vital signs

TFI 70cc/h

Keep MAP 60

Keep CVP <10

CBC, ABG, coags and lytes q 12hours x 4, then q 48h

SCDs

Keep HOB 30o; bedrest

Ranitidine 150 mg IV q8h

Jevity to start at 20cc/h and increase by 10cc/h q6h to a goal

of 50cc/h

EKG q day

CXR in a.m.

Ventilate to keep ABGs normal

Midaz/Fentanyl to keep MAAS 0-1 x 24 hours then reassess

Maintain BS 70-160 with Humulin R infusion as needed

Accucheks q 4 hours if not on infusion

Nimodipine 30 mg po TID

Normal fluid balace

1. What EKG changes might you expect to see with this patient?
2. If this patient wakes up she is likely to have difficulty with
extraocular eye movements, and possible visual impairment.
This indicates damage to which cranial nerves?

What is your primary focus during the first 24 hours:

a. Monitoring for vasospasm
b. Optimizing CPP
c. Potential for rebleeding
3. Documentation on the Kardex should include:
a. Her initial lab work
b. The length of surgery
c. Her initial deficits
4. Why should the above be included on her Kardex?
5. At 0600h you are due to give Nimodipine but your BP is only
120/60. What should you do?
a. Hold Nimodipine
b. Call the doctor
c. Give a fluid bolus to increase the BP enough to be able
to give Nimodipine
Your patient has woken up over last two nights. She was extubated
this afternoon and is currently on 4 lpm via nasal cannula. This
evening her neuro check reveals she is opening eyes spontaneously,
responding with simple words but not using full sentences, and
following simple motor commands (E4 V5 M6, total GCS 15). She is
still quite sleepy and is only arouses with direct contact. She has
had a busy day blood cultures, CT scan, full neurological exam by
neurology.
6. What is your primary focus for this shift?
a. Q hourly neuro checks
b. Quiet environment with minimal disturbances
c. Deep breathing and coughing
7. Upon reviewing the orders, which ones will you address with
the doctor during evening rounds?
a. More frequent CBC and electrolyte labwork
b. Start Clexane
c. Change Humulin R to Subcutaneous
At 0430 you go in to draw labs and your patient is slow to respond.
She eventually opens her eyes to voice and responds appropriately,
but her left arm is flaccid.

8. What is likely the cause of this?

a. Ischemic Stroke
b. This is a potentially expected finding on Day 3-5 as the clot
has lysed and chemicals interfere with normal neuro
function
c. Vasospasm
9. What treatment might the doctor order for this finding?
B. AV Malformations
These result as a failure of the embryonic vasculature to develop
normally; occurs in
1-4% of population. There are four different types of malformations,
some of which are very benign and have no clinical significance,
while others such as the AVM, involve shunting of blood back to
venous system without oxygenating tissues.
An AVM is a tangled collection of dilated vessels. They are thinwalled and lack the normal characteristics of veins or arteries. They
may be small and focused in a particular area or large, involving an
entire hemisphere. AVMs account for 9% of SAHs, and 1% of all
strokes are related to AVMs. The primary problems are the shunting
of blood and the impaired perfusion in the area of the tangled mess.
Elevated venous pressure increases ICP and impairs CPP by blocking
drainage. AVMs frequently cause headaches, seizures, neuro
deficits and hemorrhage. If they do rupture, treatment will be
surgery or embolization if the AVM can be reached.
Nursing care and interventions remain the same as with cerebral
aneurysms above, but there are no vasospasms associated with
AVMs.

HEMORRHAGES AND HEMATOMAS

Cerebral bleeds can occur either along the surface of the brain or
within the meninges. We will look at
Intraventricular Hemorrhages
Extraventricular Hemorrhages:
Epidural Bleeds
Subdural Bleeds
Subarachnoid Bleeds (covered earlier in the Aneurysm
section)
Intraventricular Hemorrhages (IVH): This is bleeding inside the
ventricles, resulting in blood in the CSF, which then circulates into
the subarachnoid space. Even though the bleed circulates into SA
space, the origin is not in the meninges.
These injuries are caused either by a stroke or from trauma, almost
always requiring a great deal of force; thus, outcomes are rarely
good. The extent of damage will depend on how well the resulting
edema and increased ICP are managed, and how much shifting and
subsequent damage occurs.
Patients present with signs of increased ICP. Treatment will depend
on the size of the bleed, possibly requiring evacuation of the clot. If
the bleed is a result of a tear to an artery, if accessible, surgery will

be undertaken. Frequently an EVD is placed to help drain the blood

from the ventricular space.
Extraventricular Hemorrhages: These are bleeds that occur outside
of the brain tissue themselves, ie in the meninges.

EXTRAVENTRICULAR HEMORRHAGE
Keep in mind all bleeds and injuries can present with a multitude of
symptoms. It is not important to know them specifically but it IS
important to be able to recognize a change in behaviour and a
change in the level of consciousness.
So, if a patient comes in after bumping his head and in a few hours
suddenly gets irritable, this is a reportable finding! REPORT ANY
CHANGES TO BEHAVIOUR OR LEVEL OF CONSCIOUSNESS!!!
Epidural Hemorrhage/Hematoma (EDH): Frequently caused by
blunt trauma, this bleed results from a tear in the meningeal artery
which runs directly below the temporal bone. This artery then
bleeds rapidly into the epidural space. Because this is an arterial
bleed, this is a serious emergency and surgery is warranted.
Presentation:

Initial confusion, decreased consciousness, or loss of

consciousness

A lucid interval then occurs in many patients a brief period

of full conciousness/restored mental status. The patient seems
back to his/her normal self.

Change in mental status again: confused, somnolent; motor

deficits

One dilated pupil

Unstable blood pressure & heart rate

If caught early, this type of injury usually results in a good

outcome; however, because the initial LOC is followed by a lucid
interval, these can go undiagnosed. Because this is a rapid
bleed, blood can accumulate quickly in this space and, if not
diagnosed early, can cause irreversible damage and death.
Treatment: Immediate surgical intervention. This is an arterial
bleed.
Nursing Management:

Frequent neuro checks

ICP Control

Monitor labs

Monitor vital signs

A. Subdural Hemorrahge/Hematoma (SDH): Most subdurals

are caused by a tearing of the veins that are located over the
brain curvatures. This is usually a result of severe blunt trauma;
however, in the elderly these bleeds can be caused by a
relatively minor bang on the head (ie a fall).
Presentation: Because these are venous in origin, these are
often slower bleeds than EDHs and progress slower. Symptoms
can take weeks to develop:

Confusion, drowsiness or lethargy

Paralysis in the arms or legs

Sensory disturbance

Nausea and vomiting

Dizziness

Difficulty with balance or coordination

Persistent headache and anxiety

If left untreated the symptoms will worsen slowly and can result
in irreversible damage and death.
SDHs are classified as acute or chronic, based on the size of the
bleed and the potential for trouble ie if we know the impact was
high-speed we will expect a more acute problem and possibly a
larger bleed. Despite being a slower bleed, acute SDHs are
the most lethal of all head injuries and have a higher
mortality rate than even EDHs.
Treatment: Depending on the size and rate of the bleed, some
can be managed medically and with time. Others may require
catheter insertion to evacuate the clot, and others still will
require surgical intervention to remove the clot and stop the
bleeding. Sadly, depending on the location and extent of a
bleed, some are inoperable and will require palliative measures.
Nursing Management: Same as above

STROKE
There are two types of strokes:
Ischemic, caused by clots, emboli, etc. Account for 85% of
strokes
Hemorrhagic, cause by an intracerebral bleed or an SAH.
These are usually caused by uncontrolled HTN, aneurysms,
AVM etc. They account for 15% of all strokes
Ischemic Strokes: This is equivalent to a heart attack in the brain. A
clot or emboli occludes the artery and causes tissue death beyond
the clot. There will be minimal blood flow to the area but maximum
vasodilation surrounding it; this is due to lactic acid formation. If
you administer a cerebral vasodilator at this time, only the healthy
areas will dilate, and this steals blood from the unhealthy area. Be
very careful with the use of antihypertensives at this time.
Goal: Reperfusion/anti-thrombolytic therapy. There is usually a 3hour window from the time of onset of symptoms to the time of antithrombolytic therapy. It is important, then, that first responders,
families and friends recognize the need to take the patient to a
stroke centre (a hospital experienced in treating strokes, that has
the systems in place to triage, assess, diagnose and treat within
those 3 hours. Much like reperfusion treatment post-MI, the
outcomes are quite favourable.

In a hemorrhagic stroke, the sites of these strokes are usually small.

Nonetheless, there is an immediate rise in ICP followed by cerebral
edema. CPP becomes compromised. The timing can be a few hours
to a few weeks after the arterial occlusion. Keep an eye on rapid
rises in blood pressure; this is a good clue to a pending hemorrhagic
stroke.
Treatment: the same as other hemorrhages
The main sites of strokes and there corresponding deficits are:

Inferior Communicating Artery: sensory and motor deficits of

opposite face, arm, leg; aphasia if the dominant hemisphere is
involved in stroke

Middle Communicating Artery: hemiplegia of face and arm on

opposite side. Leg has less deficits; Aphasia if dominant side
involved

Anterior Communicating Artery: sensory loss/paralysis of

opposite foot and leg; impaired gait; slow to respond or
perform; flat affect, urinary incontinence; cognitive
impairment

TIAs: Transient Ischemic Attacks. This is angina for the brain!

These are mini ischemic strokes. The signs/symptoms last less than

24 hours, but they are a forewarning of a full-on stroke. Get the

patient to a hospital for an immediate workup (CT, carotid dopplers,
etc.). The focus is on prevention of a full-on stroke. The patient will
likely be started on anticoagulants/antiplatelets.
SEIZURES
Seizures are transient episodes of abrupt and temporary alteration
in cerebral function. The pathophysiology behind seizures is
thought to be related to sodium/potassium channels and/or
neurotransmitter channels, but basically there is an imbalance
between excitation/inhibition.
Seizures can be a result of injury, swelling of the brain, tumours, or
epilepsy a condition associated with abnormal electrical activity in
the brain.

Terminology:
Epileptic seizures: recurrent seizures. Usually associated with
a specific focal point
Aura: pre-monitory warning; remembered. Can be visual,
auditory, olfactory, etc.
Automatisms: coordinated but involuntary motor activities
that occur during a state of impaired consciousness (lip
smacking, fidgeting). Often assocd with temporal lobe
seizures
Clonus: spasms; a continuous pattern of rigidity and
relaxation repeated. 2nd phase of a seizure
Ictus: actual seizure
Postictal
Tonus: degree of tone or contraction present in muscles when
it is not undergoing shortening.
Todds paralysis: temporary focal weakness following a
seizure; can last up to 24 hours. neuronal exhaustion.
During Todds paralysis, depending on whats not working, you
can determine the focal site of the seizure.
Status Epilepticus: continuous seizures lasting at least 5
minutes, or two or more distinct seizures between which there
is incomplete recovery.
Classifications:
1. Partial (aka Focal): 3 types - simple, complex and evolving (into
generalized). If consciousness is not impaired we call it a simple
partial; if consciousness is impaired we call it a complex partial. .
2. Generalized: 6 types
a. Absence (aka Petit-Mal): Absences seizures are brief, usually
less that 20 seconds. They have a sudden onset and

termination. They involve a loss of consciousness and dont

usually have muscle involvement.
b. Myoclonic: Cause abnormal muscle movements on both sides
of the body at the same time. Frequently seen in children.
c. Tonic-clonic (aka Grand-Mal): Starts with prodromal phase,
which is a period of irritability and tension and can precede
the seizure by hours or days. Some people have an aura;
others do not.
The seizure usually starts with a sudden loss of consciousness.
There are major tonic contraction (body stiffens); the jaw
snaps shut; pupils dilate. Apnea occurs but usually only for a
few seconds. This phase usually lasts less than a minute.
It is followed by a clonic phase which is evidenced by violent
rhythmic muscular contractions accompanied by
hyperventilation. Eyes roll; salivation.
The postictal phases results in a gradual subsiding of this
activity, in frequency an amplitude. Everything goes limp.
d. Clonic: Patient has violent rhythmic muscular contractions but
none of the tonic/rigid components
e. Tonic: Body stiffening not accompanied by rhythmic muscular
contractions.
f. Atonic (aka Drop): These consist of a brief lapse in muscle
tone, which frequently result in the patient falling. The
seizures are brief - usually less than fifteen seconds. They
begin in childhood and may persist into adulthood

Managing a Seizure:
Lie the patient somewhere at no risk for falls (ie bedrails up)
or injury (away from sharp edges or hard surfaces they can
bang into, such as the base of the toilet or bathtub)
Remove eyeglasses and restrictive clothing

 Do not try to force anything into the mouth

Aim to prevent injury; do not restrain
Dont interfere during a seizure unless they are losing their
airway or have extended periods of apnea
Post-Seizure: Immediately post-seizure, place patient in the
recovery position to facilitate secretion drainage. Provide high-flow
oxygenation (remember that the brain has been hypoxic for
awhile!). Transfer to a monitored bed. Allow patient to sleep.
Reorient after he wakes up. **As soon as patient awakes do a
complete neuro check to determine the deficits. This
information will help the neurologist locate the area of
seizure initiation.
Documentation: What to include in seizure documentation?
Witnessed or nonwitnessed?
Any pre-warning signs (aura?)
Where did it beginhow did it proceed (head to toe? Toe to
head? Fine motor movement to gross?)
Pupil changes
Conscious or unconscious prior to/during/after the seizure?
Any changes in behavior/neurological function after the
seizure
Any weakness or paralysis afterwards (ie where is Todds
paralysis)
How long did the patient sleep post-seizure
Treatment:

Treat underlying cause (excise the tumour, decrease ICP, correct

electrolytes)

Avoid precipitating factors, if known

Medications: Should be seen by neurologist for most effective

regimen prescription, based on seizure characteristics

Vagal Nerve Stimulation (for those refractory to meds).

Programmable signal generator planted in chest

Surgery (lobectomy, partial lobectomy)

Patient and Family Education (PFE):

How to manage a family member who is having a seizure

Do not stop your meds

Get medication levels regularly checked to ensure theyre within

therapeutic range

Keep track of seizure activity; try to find the precipitating factors

and identify Todds Paralysis

Learn to recognize auras

BRAIN TUMORS
Tumours arise in association with multiple specific
structural/molecular alterations within cells, and can cause the cell
to proliferate abnormally and/or to invade surrounding tissues.
Tumours can be caused by a cessation of cellular activities or an
increase in them. These space-occupying lesions compress healthy
brain tissue, causing an increased ICP. Patients will present with a
variety of symptoms, depending on location of tumour and how
much it is compressing healthy tissue headaches, altered LOC,
seizures, motor or sensory deficits, etc. Tumours are named for the
structure they invade:
Astrocytoma
Glioblastoma
Ependymoma
Oligodendroglioma
Meningioma
Neuroma
Adenoma

Some are fast-growing while others can take years to progress to

dangerous sizes. Treatment is either surgical or medical in nature.
Nursing Interventions are the same as other neuro conditions:

Control ICP

Prevent Infection

Neuro Checks

Be familiar with the expected deficits, based on region

Patient/Family Education

Possible palliative measures

NEURO REHAB

In all neuro and injuries the focus is turning towards early

rehab...much like we now start to do discharge planning upon
admission, we should also consider physio and rehab as soon as we
are able to do so. In ICU this means early physio even if sedated (as
long as ICP permits). Awake patients should be sitting
up/dangling/getting out of bed. An ETT is not a contraindication for
being up in the chair. Extubated patient should receive ambulation
as soon as possible. ADLs are returned to the patient they brush
their own teeth, shave, do their own bath these all constitute
physiotherapy! Provide early stimulation (encourage portable dvd
players, newspapers) once awake. Encourage cognitive stimulation:
word puzzles, get them talking on a subject that requires lots of
talking and descriptives (ie their family; travels). Get
Physio/Occupational Therapy involved early.

TRAUMATIC BRAIN INJURY (TBI)

Please read the Rashid Hospital TBI Guidelines and
familiarize yourself with them, especially the TBI Protocol.
You should know these by heart. These can be found on
Filenet. Think of the interventions as a bundle outcomes
are much improved if everything is addressed altogether.
When we talk of TBI, we think in terms of primary and secondary
injuries. The primary injury is the actual incident this the the
accel-decel injury, the rotational injury, etc. We cant help that (its
already happened). It is the secondary injuries that we focus on in
an attempt to limit further damage.
Secondary injuries are classified as systemic (hypotension,
hyperthermia, hypoxia, anemia) or intracranial (seizures, shifting,
edema). The degree and type of secondary injuries have an effect
on patient outcomes, so our goal is to prevent these. Secondary
injuries result in either ischemia (reversible alteration in cell
function) or infarction (irreversible damage). At all costs, therefore,
we need to avoid hypotension and hypoxia, both of which effect
cerebral bloodflow and can result in permanent damage.
INTRACRANIAL PRESSURE (ICP)
What happens when you bang into a wall and get a bruise on your
arm? It swells and the area gets hard, doesnt it? Luckily, your arm
tissues are soft, allowing the bruise to spread out in an effort to
keep the pressure around the bruise a bit lower. Not so with your
brain. If you get a bump on the brain and it needs to swell, your
hard skull impedes this process! When this happens, pressure
builds up inside the brain. With nowhere to expand, damage starts
to occur.

Intracranial pressure is the pressure inside your skull. The normal is

0-10, but this is a fluctuating number. If we were to measure ICP in a
normal adult going about their daily lives, the reading would change
constantly. That nice static number we see on the monitor is solely
because weve sedated the person and theyre activities are nil.
Likewise, when you cough or sneeze, ICP goes up higher than
normal but quickly returns to baseline. No damage occurs. The
problem is when the pressure in the brain is consistently high.
ICP varies from compartment to compartment. The pressure near
the injury can be much higher than the pressure in a neighboring
compartment or even in the ventricles.
Munro-Kellie Hypothesis: Do you remember this from nursing
school? The M-K Hypothesis states that the space inside your skull
is finite and can only hold so much. If any content increases, the
others must decrease in order for everything to still fit and for
pressure to remain normal and constant.
What is inside your skull? Brain (80%), Blood (10%) and CSF (10%).
So if you have cerebral edema and your brain gains an extra 10%
volume, the volume of the blood and/or the CSF must decrease by
the same amount. This is the problem we face with neuro injuries.
As we know, any soft tissue injury results in swelling and edema, so
if we have a head injury we can expect swelling. We must figure out
a way to juggle the components in order to allow for swelling inside
the closed confines of ones skull, while at the same time not
compromising perfusion.
What causes increased ICP? Any brain injury! A bleed in the
subdural space will develop a space-occupying clot which will push
the brain tissue out of the way. A head injury will develop cerebral
edema and the brain will swell, constricting blood vessels and
ventricles. A tumor will take up space and push the brain tissues

away or constrict the arteries/veins. In short, anything that will

increase the volume of brain/blood/CSF will cause increased ICP.
It is important to speak here of cerebral compliance, which refers to
the adaptive capacity of the brain to respond to challenges. It is
sometimes described as a measurement of brain stiffness. In a
healthy person with normal compliance, a sneeze and the
accompanying spike in ICP doesnt cause damage and things revert
quickly to normal. In a compromised brain, however, these spikes
are not as well-tolerated; the ICP may be slow to return to normal or
it may not return at all damage can occur. This will lead to a
disproportionate response to further stimulation; for instance, a
healthy patient will tolerate a turn and ICP will return to baseline
afterwards, but a patient with reduced compliance will over-respond
with an increased ICP.
Factors affecting compliance:
The degree of volume increase
The duration of time over which this increase takes place
(think of a flood zone; if the rains come gradually then the
rivers can accommodate this, but if there is a deluge, the river
floods its banks)
Frequently in patients suspected of having a high ICP we will
monitor them. But if we dont have a means in place to measure it
do we pretend its not an issue? If we have the patient hooked to an
ICP measuring device we can read the number; if the patient has an
EVD we can assume we are treating for high ICP. But what about
the patient with a subdural hemorrhage who has a GCS of 12? What
about a stroke patient? Neither of the latter two patients will
necessarily be on ICP protocols, but we still have to assume that
there is increased pressure in the skull and the potential for
deterioration is there if anything goes wrong. Treat a neuro patient
like he has a risk of high ICP even if that risk is small.

Broadly speaking, how do we treat increased ICP? The object is to

decrease the volume of one of the components. If the brain is
swollen we can try Mannitol, which will pull the excess fluid out of
the brain in an attempt to return it to normal size. If there is a bleed
we can stop the bleeding and evacuate the clot. If a patient has
hydrocephalus and is producing excess CSF we can install a shunt to
help drain the excess.
This sounds easy enough; the question is whether we can make
enough of an adjustment to keep volumes within limitsand thats
where the challenge lies. We stated earlier that normal ICP is 0-10;
an acceptable norm is usually stretched up to 0-15. Anything above
15 and we start interventions to bring it down. An ICP sustained
above 20 is considered dangerous and should be treated
aggressively. The number, however, is not as important as the
trend. If, for instance, an ICP starts at 11, 13, and then heads up to
15, this is a problem this is just as much of a problem as the person
is sustaining an ICP of 18. It tells you the pressure is trending
upwards; we dont wait for it to hit 20; we report these findings right
away so that we can act now and prevent damage.
Additionally, keep in mind that when we measure ICP on the monitor
it is the mean ICP which is displayed, and the actual ICP will range
from a bit higher to a bit lower, much like the CVP reading (it is the
middle portion of the waveform that is being read, but the top will
be 1-2 units higher and the bottom will be 1-2 units lower). So even
though your ICP may show 16 on the monitor, the peak of the
pressure may actually be 18.
So, controlling the ICP is very important. But what about oxygen
delivery to the brain? This is even more important. Some years ago
the focus was primarily on keeping the ICP down by stealing space
from the volume dedicated to blood or CSF. We would hyperventilate
a patient and to bring down the PCO2 and constrict the cerebral
arteries. However, we soon realized that if we limit cerebral

bloodflow too much we risk poor oxygenation, so now before we rob

Peter to pay Paul we look at having the vascular system contribute
as little as possible to cerebral pressure while still maintaining
adequate oxygen delivery. We call this Cerebral Perfusion
Pressure, or CPP.
CPP in a healthy individual is considered 65, so for an individual
who may have greater oxygen and glucose requirements in order to
heal, the usual aim is 70. Studies have shown that if CPP is
maintained at 80, mortality is about 35-40%, and drops by 20% for
each 10-point drop in CPP. Once below 60, mortality is about 95%.
So how do we know when were achieving 70? We can measure it
indirectly. CPP is essentially the pressure required to push the blood
into the cranium against the pressure inside.
CPP = MAP ICP
CPP, therefore, can be measured indirectly if we know the MAP and
the ICP. CPP; mortality at cpp80 = 35-40%; and drops by 20% for
each cpp drop of 10. Once below 60, mortality is about 95%
Essentially then, treatment can be summed up this way:
If we want to increase our CPP then we must either increase
our MAP or decrease our ICP.
Lets look at an example to see how this is done.
A patient has an ICP of 25; we want the CPP 70. His BP is 148/66
and his MAP is 84. First of all, what does our MAP have to be? It will
have to be at least 95, correct? So what to do?
1. Increase our MAP. Wow, a MAP of 95how can a patient do
this? First of all, your body will try Autoregulation to meet these
requirements (recall that we discussed this earlier), but it may
not be enough. Autoregulation is impaired when ICP is sustained

above 20. So we may need to augment the bodys efforts. We

will have to constrict our arteries in order to get our MAP that
highhow do we do that?
a. Volume: Aim only for euvolemia never more because this
will increase circulating volume and increase CBF. If euvolemia
is not enough,
b. Vasoconstrictors: Most of the time we choose to use
Norepinephrine. We titrate this drug to achieve arterial
constriction, but the ultimate goal is to keep our CPP at target.
The doctors orders will usually be written something like
Norepinephrine to keep CPP >70. This means that as our
ICP fluctuates we will need to adjust our drug accordingly.

2. Decrease our ICP. How do we do that? Lets look at our 3

components again and address it from that perspective.
a. Blood: Weve already discussed the importance of keeping
CBF no higher than it needs to be, but what about outflow? It
is important to also optimize venous drainage. By keeping the
veins clear of obstruction and limiting intrathoracic pressure
for venous blood to push against, we can ensure that drainage
is optimal. How to do this?

HOB 30o

Head in alignment

Keep an eye on tightness of ETT ties and Hard Collars

No flexion of knees; no excessive flexion of hips

And what about those pesky clots? Sometimes, clots are small
enough that they are not impeding ICP substantially, or they
are in an area where surgeons cannot reach. In these cases,
you must wait several days for the clots to lyse by themselves
and get reabsorbed. If the clots are large enough, though,
immediate evacuation is warranted in order to prevent
damage.
b. Brain: What about limiting ICP from a brain tissue standpoint?
We can only consider shrinking the edema, really. Hence, we
give Mannitol. If the brain continues to swell, however, we
can think about giving it more space.via a Bone Flap. If we
remove a piece of skull bone then suddenly theres more room
to shift/to swell, etc.
c. CSF: Normally the appropriate amounts of CSF will slip down
into your spinal column, or get reabsorbed via the venous
circulation. But if our brain is swollen perhaps these avenues
arent working optimally. What we want to do is provide
another route for CSF to exit. Hence, the EVD. By decreasing

the amount of CSF in the ventricles, they will shrink and allow
the brain to swell a bit more. We will discuss EVD
management later.
This is how you approach ICP management. But there are a few
more things we can do to help control ICP, and it goes back to
optimizing bloodflow. What are some other influences on dilation
and constriction?
Natural neurogenic regulators will help regulate CBF: The
release of norephinephrine will constrict (sympathetic response)
while acetylcholine will dilate (parasympathetic response).
CO2: This is the major influence on blood vessel dilation. When
the PCO2 is high, dilation occurs, which increases cerebral bloodflow
(which means it takes up >10% of the space in your skull, leaving
less room for the brain to swell). When the PCO2 is low CBF
decreases, allowing brain swelling to take up more space without
compromising ICP.
If our goal is to limit bloodflow while not compromising perfusion, we
should aim, then, for a CO2 on the lower side of normal (ie 35-38).
So if you have a patient with a risk of increased ICP you should
monitor your ABGs frequently to ensure you keep things where they
need to be.
pH: pH affects CBF as well Acidosis will cause vasodilation,
whereas alkalosis will produce vasoconstriction.

O2: Oxygen has the opposite effect on vessels they dilate when
oxygen is low and constrict when oxygen is high (this makes sense;
if your body feels there is an oxygen deficit to the tissues it is going
to send more blood there). Usually we try to reduce FiO2 to the
lowest possible levels as long as PaOs is 80-100, but in the case of
ICP patients, as long as you are not in the toxic range of FiO2
(>50%), you neednt rush to keep your PaO2 within normal limits.
Temperature: As you know, patients suffer vasodilation when they
are febrile. You now know that we need to limit vasodilation in an
effort to control CBF; therefore, we keep the patient cool, aiming for
35-37oC. For every 1 rise in temp, cerebral metabolic rate s by 5-7
% and oxygenation requirements by ~ 18%.
Another reason to keep a patient afebrile is their metabolic rate,
which increases with fever. We know that the brain is already a
major user of oxygen and glucose. With a fever we need even more
in order to combat it; if we can limit that then these nutrients can go
towards healing. The cerebral metabolic rate of oxygen extraction is
d 50-75 % for every 1 drop in Temp.
It is important to catch rises in temperature early so that we can act
before problems get too bad. It is important, therefore, to keep a
close eye on your patients temperature; you should be doing temps
every hour at minimum. Better yet, your patient should have a
continuous temperature probe.
One more influence on cerebral bloodflow is blood viscosity. A low
hemoglobin could increase bloodflow by 30%. It is important,
therefore, to monitor a CBC and transfuse to keep hemoglobin
elevated.
MEDICAL AND NURSING INTERVENTIONS

Weve outlined the basic goals of increasing MAP and decreasing

ICP; lets look now at specifics. Im lumping the medical and nursedriven interventions together because as patient advocates we need
to be thinking about the medically-driven interventions as well.
Interventions:

Mannitol: This is a diuretic which helps to reduce cerebral

edema by removing water from the brain and dumping it into
the venous system. If you give Mannitol, make extra sure
your head is in alignment or the excess fluid cannot drain.
Effects last 1-3 hours; do not give if serum osmo > 320.

Norepinephrine: Helps keep MAP elevated to optimize CPP

Narcotics/Sedation

Barbiturate Coma (Thiopental): provides a rapid decrease in

cerebral meteabolism (Thiopental is stored in fat and
interferes with braindeath studies; therefore, levels must be
drawn to ensure its out of the system before braindeath
testing is done)

Neuromuscular Blockades/Chemical Paralytics: to prevent

posturing or ventilator dysychrony, both of which can increase
ICP

Avoid hypotension (defined as a single episode observation of

SBP < 90; this must be avoided or rapidly corrected

No single incident of hypoxia (defined as a PaO2 < 60)

Maintain PaCO2 30-35 (dont wait for the doctor to approach

you; if you feel an ABG is warranted you must seek him out or
order the ABG yourself)
(Contd)

Temperature Control (possibly reduces mortality if cooling is

maintained > 48 hrs)

Optimize venous drainage/limit intrathoracic pressure (see

above)

Avoid hyperventilation during the first 24 hours (CBF during

the first day after injury is approximately of normal)

Avoid constipation

Advocate for early nutrition

Electrolyte Balance

Monitor Blood Sugar

Quiet environment

Reduce Stimulation

Turn patients GENTLY!!! (how would you like to be awakened

roughly???)

Plan your activities so that there are not constant miniinterruptions

Finally, spread out your major patient interventions

Why is this last one so important?

Remember earlier we said that decreased compliance means that

the brain doesnt return to pre-activity ICP levels as quickly as a
healthy brain? As a matter of fact, it frequently takes 15 minutes or
more for neuro patients to return to baseline. This means that if you
turn a patient and his ICP shoots up, dont instantly assume that you
need to put him back where he was. Give him 15 minutes to

recover. If hes still not returning to baseline, give him a bolus of

sedation. If ICP continues to remain elevated in the danger zones
then you will have to return the patient to where he was, but
remember to put all your interventions to good use before doing so.
Patients need to be turned. A bedsore is painful and this will only
serve to increase your ICP anyway.
Additionally, if a patients ICP is 12 and a turn takes it up to 16, this
is an acceptable increase. If a turn takes the patient up to a
sustained ICP >20, further intervention is warranted.
When you cannot turn a patient it doesnt mean you stop trying.
Attempts to turn should be reassessed every shift.
ICP WAVEFORMS
There are 3 components to an ICP waveform:
1. P1: The percussion wave:

Arterial in origin
Transmission is from the intracerebral blood vessels
to the brain parenchyma and CSF, and/or from the
choroid plexus to the CSF and parenchyma

Sharply peaked and fairly consistent in amplitude

2. P2: The tidal wave:

Primarily arterial in origin

Is more variable and ends on the dicrotic notch

A reflection of cerebral compliance: a rise is ICP is

reflected as a progressive rise in P2

Associated with sustained increases in ICP. However, note

that sustained increases in ICP can occur without P2
elevation

3. P3: The Dicrotic wave

Immediately follows the dicrotic notch

Venous in origin

Why are these important to know? With raised ICP, cerebral

compliance is progressively reduced and a rise is seen in P2. The
height of P2 and P3 finally exceed that of P1 with P1 and P3 rising to a
lesser degree giving the overall waveform a rounded appearance.
When you see changes occurring you can immediately notify the
doctor that cerebral compliance is being reduced, and immediate
interventions can be done.

In addition to the previous waves, there are some other abnormal

findings you should be aware of:

A-waves (plateau waves):

o Rapid onset and resolution, often beginning from an
already elevated ICP (ie 50-100).
o Last about 20 minutes
o A serious sign suggesting impending herniation

B-waves:
o Sharp spikes every 30 seconds or so, occurring with
normal or elevated ICP.
o Results in ICP peaks up to 50, but not sustained
o Related to fluctuations in CBF and are usually due to
increased compliance

C-waves:
o 4-8 times/minute, occurring with normal changes in
systemic BP
o Can create nonsustained peaks up to 20
o Not clinically significant

HERNIATION
Herniation is a shifting of the brain from an area of high pressure to
an area of lower pressure. As pressure is exerted on the brain

tissue, it gets pushed out of the way. There are a few types of
herniations, some of which result in lateral movement and others
which result in vertical movement. The important thing to think
about is that if herniation is occurring it is because swelling inside
the head is still going on and theres just nowhere else to go. The
situation is worsening.
Central (Transtentorial Herniation): This is also known as Coning.
A downward displacement of the cerebral hemispheres occurs,
putting pressure onto the brainstem. This is almost always fatal.
Signs of Deterioration

Transient Signs: You may see various transient signs

hypoxia, periods of increased ICP, fluctuations in BP or HR,
altered LOC for short intervals, motor and sensory deficits,
etc.

Cushings Response: This is a compensatory response that

attempts to provide adequate CPP in the presence of a
rising ICP:
Rising systolic pressure Widening pulse pressure (the
difference between systolic and diastolic)
Bradycardia (and then later irregular tachycardia
when the system can no longer compensate and
when the pressure on the brainstem causes
irregularities)
This later leads to Cushings Triad:
Marked systolic Hypertension/Continued widening
pulse pressure
Bradycardia(and then later irregular tachycardia)
Abnormal respiratory patterns

Critical Thinking: A TBI patient has a widening pulse

pressure, his heart rate and breathing are irregular, and his
pupils are 6 and fixed. Why are his vital signs fluctuating?

Frequently our neuro patients develop hypertension; when this

begins, always do a neuro check, especially pupils. Too many times
it coincides with sedation weaning and we consider the
hypertension as signs of waking up. In fact, it could also be that the
added stress of consciousness has caused the ICP to increase,
resulting in the early stages of herniation.
Cerebral Storming (CS): Much like a spinal injury patient may go
through spinal shock, a head injury patient may go through Cerebral
Storming. This is an exaggerated stress response and it can happen
at two distinct times: during the first 24 hours after injury, or weeks
down the road. This makes it a bit difficult to diagnose! As well,
symptoms can be indicative of other problems, so CS frequently
gets overlooked. Frequently CS will develop immediately after
stimulation such as suctioning or turning, and can last for hours or
end abruptly. The behaviours are often attributed to withdrawal of
sedation/narcotics. Symptoms:
Posturing/Dystonia
Hypertension, Tachycardia, Tachypnea
Pupil dilation
Diaphoresis, Fever

It is most commonly seen in patients with diffuse axonal injury. The

concern is that these secondary issues will cause further damage. If
patient remains ventilated, re-sedate him to preserve brain function.
NEW INNOVATIONS IN NEURO MONITORING

A thorough discussion about the neuro system would not be

complete without discussing the latest trends in treatment.
COMING SOON, TO AN ICU NEAR YOU.
1. Cerebral Microdialysis: An end-user technique used to
measure glucose, lactate, pyruvate and glycerol levels in the
brain. Cerebral ischemia may be detected on the basis of
brain metabolism byproducts. The levels of these metabolites
increase in the presence of anaerobic metabolism.
2. Secondary to the above, avoiding low levels of brain glucose is
important; therefore, allowing for a higher blood glucose
range, and initiating earlier-than-usual nutrition, is in favour
now.
3. Pupillometers: These are computerized pupil-checkers.
Instead of pupil checking being subjective, it now becomes
objective, measuring the differences from hour to hour, and
the speed of reaction a speed below threshold levels
indicates an elevated ICP.
4. Cerebal Bloodflow Monitoring Systems: Many of the ICP
monitors now have CBF measurement capabilities to measure
tissue perfusion levels within the brain.
5. Transcranial Doppler: Can help measure velocity and direction
of CBF
6. Brain Tissue Oxygenation Monitors: A few of the ICP monitors
now include this as an additional measurement device. Placed
in or near the injured tissue, it will tell you about oxygenation
to the area. Depending on the findings, you can interpret the
cause of low oxygenation, as well either decreased delivery
or increased use.

NEURO ASSESSMENTS
ITS NOT JUST A GCS!!!!!!!!!!!

A good neuro assessment includes so much more information than

your basic GCS. Think about it for a minute: A GCS records the best
score. So you do an assessment on a patient and he withdraws
equally with both upper limbs (M5). The next hour you do your GCS
and he still withdraws with both limbs but he is now much weaker
on the left. He still gets an M5 doesnt he? But is this an important
finding? Of course it is, and it requires further investigation and
information.
I think of GCS as a measure of the patients cognitive ability to
perform tasks. If a patient can follow a command, or try to withdraw
a painful stimuli, or say the right words in the right context these
are all measures of the level of cognitive ability a patient has. But
while it gives us a picture of a patients best ability, it doesnt tell us
what hes actually doing at this moment. For that we need a more
thorough neuro assessment. This section will cover a
comprehensive nursing neuro assessment.
A baseline assessment is made immediately upon admission to the
unit, and documented. All subsequent neuro checks are made
relative to this. This will help detect trends and deviations during the
course of illness. Keep in mind that change can happen slowly or
rapidly. The longer the duration of deficits and the more severe the
dysfunction, the less likely there is of complete recovery.
Neuro checks should be done at minimum of every 4 hours;
however, if your patient is having fluctuations, then it must be done
at more frequently. For neuro patients it is not acceptable to go
more than two hours between checks unless the patient is chronic
and/or it has been decided there will be no escalation of care. Just
because it has not been specified to do the GCS more frequently,
the nurse must use clinical judgement and perform checks
according to patient condition Doctors orders only cover the
minimum requirements it is negligence if a nurse does not do

a neuro check when there are indications for it, regardless

of the doctors orders.
GCS: This should always be recorded and reported as both a whole
number and a breakdown by components E-M-V. The whole number,
on its own, is not enough to tell us what we need to know about
deficits. Suppose for instance the doc comes in at 0830 and asks for
the patients GCS and you report GCS is 9. (He is opening his eyes
to speech, hes intubated, and hes withdrawing to pain.) In the
afternoon you extubate your patient. On your next neuro check he
now opens his eyes to pain, hes confused and hes now got
abnormal flexion. The doc asks and you say GCS is 9. But how
different these two situations are!!! The second scenario requires
immediate intervention, yet the GCS is the same. If you present
these cases as E3 V1T M5, and E2 V4 M3 then its clear that
even though hes should be scoring higher now that hes extubated,
his score is the same. Always break your GCS scores down so that
you have a clear picture of whats going on. Your GCS should also
be graphed in order to give you a quick visual reference.

If there are changes in the GCS you should also report how long it
has been since the last check (ie 4 hours, 1 hour) so clinicians have
an idea of how quickly things are changing.

EYE OPENING:
4

Opens Eyes Spontaneously

Opens Eyes to Verbal Command

Opens Eyes to Pain

No Response

Best Verbal Response:

5

Alert and Oriented

Confused

Inappropriate Words

Incomprehensible Sounds

No Response

Best Motor Response:

6

Obeys Simple Commands

Localizes to Painful Stimuli

Withdrawal

Spastic (abnormal) Flexion

Extension

No Response

Now that weve done our GCS we must do a more thorough investigation for all the components:
Pupil Size: After changes start to occur braindeath is already in progress and deterioration can occur rapidly
Interaction with environment: Stating that the patient is opening his eyes spontaneously does not tell us about his level of
consciousness, does it? Think about it: What about the patient who has his eyes open but is staring straight ahead, not
focusing, barely blinking...hes scoring well on his GCS but hes still not in a good way, is he? Hence we need to assess how
the patient is interacting with his environment:
o Is he focusing on objects?
o Is he tracking your movement as you walk around the room?
o

Is he interacting with his environment or just laying there passively?

(contd)

 Motor tone and strength: Remember that the GCS is the best score. A persons ability to recognize a painful stimulus and try
to remove it tells us that that particular part of his brain is still able to interpret signals, but it doesnt tell us much about his
actual motor function.
o Is the movement spontaneous or just to command?
o Is it purposeful? For example, is he actually straightening his bedsheets or is he just playing with them in his fingers?
o Hand grasps are they equal in strength
o Movement of all extremities are these equal?
o Define the maximum ability:

Against resistance

Against gravity

Laterally Only

Gross vs fine motor movement:

o Where does the patient have movement his shoulder? His elbow? His fingers?
o Can he hold the callbell or a vial of saline? Do his fingers clasp around objects or does he try to grip by squeezing his
palm?
Questions and Answers:
o Does the patient remember his wifes name or the city he lives in?
o Can he give names to objects? (pen, clock)
o Can he count to 10? Can he identify how many?

DO YOU SEE WHY ITS SO IMPORTANT TO DO YOUR NEURO CHECKS TOGETHER AT SHIFT CHANGE??

Your assessment, and subsequent actions, should be guided by the following questions:
1.
2.
3.
4.

What do I see?
What does it mean?
How does it relate to previous assessments? (Is there a deterioration going on?)
What do I need to do?

Also, keep in mind that auditory, tactile, and peripheral painful stimuli could result in reflexive movements. Its better to use a
central stimulus when doing neuro checks.
We will cover GCS and motor checks more in-depthly in class.

Other neuro checks:

1. Presence of cough/gag: Muscular responses to sensory receptors lining the respiratory tract
2. Presence of corneal reflexes: Use the corner of a gauze or, better yet, a few drops of Saline (does not cause corneal
abrasions). If the patient blinks, corneal reflexes are intact.
3. Presence of Dolls Eyes: Open the eyelids and rapidly shake the head from side to side. If the eyes dont follow the head,
brainstem function is intact. If the eyes follow the head, brainstem function is impaired. This is a precursor test to caloric
reflex testing.
4. Babinskis Sign: Babinskis reflex occurs when the big toe moves toward the top of the foot and the other toes fan out after
the sole of the foot is firmly stroked. This reflex is abnormal after the age of two. A positive Babinskis is a sign of damage
to the nerves connecting the brain and the spinal cord. It can occur on either side or on both sides.

What cranial nerves are involved in the corneal reflex? What about Dolls Eyes?

Documentation: All of the above findings need to be documented; as well, you should also be very specific as to the type of
stimulus you applied (did you pinch a trapezius or did you perform nailbed pressure? Did you get a better response talking into
the patients left ear than you did his right ear?). You can never document too much in a neuro assessment.
CRANIAL NERVES

On Old Olympus Towering Top, A Fin And German Viewed Some Hops
Do you remember what mnemonic you used to remember the cranial nerves?
Before we discuss the cranial nerves, lets think about why we, as nurses, should know these and how to test for them.
I

OLFACTORY

SMELL

II

OPTIC

VISION, RESPONSE TO LIGHT

III

OCULOMOTOR

PUPIL S (SIZE, SHAPE, SYMMETRY,

RESPONSE TO LIGHT); EYELID
ELEVATION; EYE MOVEMENT

IV

TROCHLEAR

EYE MOVEMENT

TRIGEMINAL

CORNEAL REFLEXES; CHEWING;

FACIAL SENSATION

VI

ABDUCENS

EYE MOVEMENT

VII

FACIAL

TASTE, EXPRESSION

VIII

ACOUSTIC

IX

GLOSSOPHARYNGEAL

TASTE; GAG; SWALLOW

VAGUS

SPEECH; GAG; SWALLOW

XI

SPINAL ACCESSORY

HEAD ROTATION; SHOULDER SHRUG

XII

HYPOGLOSSAL

TONGUE, SPEECH ARTICULATION

HEARING; BALANCE; CORNEALS

NOTES:
I IV ORIGINATE IN MIDBRAIN
V-VIII ORIGINATE IN PONS
IX XII

ORIGINATE IN MEDULLA

Check III, IV, VI together by having patient trace your finger movement (up down, sideways, diagonal and in an H-pattern)
Check IX, X together with a gag check
SPINAL CORD INJURIES

In spinal injuries it is important to consider the mechanism of injury so that we can have an idea of where to look for damage.
Vertebrae are small and tiny fractures can be easily missed. If we know we are looking for a side-to-side injury then perhaps we
wont overlook that small crack in the bone.
Anatomy and Physiology

There are two main parts to a vertebra: the body and the arch. Vertebral bodies are separated by discs (shock absorbers). The
arch is created by a series of irregularly shaped projections. Down the middle of it all runs the spinal cord. Because everything is
jammed into a small space, the possibility of injury is high and the possibility of one injury affecting another is higher yet.

The Cervical Spine supports the head and has an 80 degree arc of movement front to back. Side to side neck rotation is possible
due to the shapes of the C-spine vertebra. The rest of the spine moves much less. Because the C-spine is not fixed like the other
parts, it is more susceptible to injuries.
INJURIES
Acceleration-Deceleration injuries are the most frequent, with deceleration being the major contributor to the injury. These are
caused by rear-end and head-on injuries (RTAs, sports injuries).
Body responses:
Hyperflexion produces compression of the v bodies
Hyperextension causes fractures of the posterior elements of the spinal column
Deformation happens to soft tissues and bones as a result of trying to accommodate the abnormal movements
Axial loading also known as vertical compression (up-down injuries, ie diving, falls)
Excessive rotation: Caused by side impacts. Results in fractures or tearing, fractured articular processes
The spinal cord can be involved in a variety of ways, either directly when the accel-decel forces throw your head back and sever
your cord, or from an axial loading/rotation situation where bones break and the resultant pieces sever the cord

Stable vs Unstable fractures: These diagnoses are often based on the posterior ligaments. If theyre intact, the injury is
considered stable. If ligaments are torn, the injury is unstable. Or, if more than one area of the vertebra is broken the fracture is
frequently labeled as unstable. Basically, a stable fracture is not likely to displace more than it was at the time of injury, but
unstable fractures have the potential to displace further and damage the cord.

Many spinal cord injuries can be temporary as a result of compression or edema. The resultant deficits can vary, depending on
the location of the compression (ie the anterior part of the cord, vs a lateral side). Complete cord transaction is rare. However,
partial transections can present as complete transections due to edema or compression. It is important to get good diagnostics
and to logroll a person if a complete transection cannot be radiographically visualized.
If you dont know for sure, assume neck pain.
This is the cardinal rule for spinal safety. If the patient is unable to tell you if they have neck pain, then treat them like a spinal
cord injury until cleared radiographically.
Stable vs Unstable status is important to know, in order to ensure you are providing the safest care for your patient. Even if the
doctor has ordered the removal of a collar or has said the patient can be AAT (activity as tolerated), misinformation can be costly
to the patient. If you are familiar with what constitutes a stable or unstable fracture, you can read the notes and determine for
yourself
whether the orders are safe. If there is conflict, reconfirm it with the doc read the notes back to him if need be.
Clearance of Spines must be done by the trauma team and must be written as an order. It is not sufficient to write it in the
progress notes. This is in our Standards of Care. If it is not written as an order you cannot d/c the precautions. If they refuse to
write it as an order, inform the ICU doctors.

Presentation: Cord injuries are primary (caused by the actual injury) or secondary, in which chemical and vascular changes
occur following an injury; these cause the spinal cord to initiate an intrinsic process of self-destruction. For example: edema,
altered blood flow, release of cytotoxic mediators, membrane injury, electrolyte abnormalities, enzyme release. This results in
necrosis of blood vessels and neurons. Ischemia to CNS cells can happen within 30 minutes and can lead to irreversible damage.
Because edema can ascend the cord quickly, you need to be prepared for ventilation in all patients. The good news is that some
deficits that are presenting above the injury will return once edema subsides.
The higher the injury the greater the deficits. To determine the extent of paralysis, it is easiest to think that everything below the
level of injury will be affected. Anything C-4 and above will be ventilator-dependent for life, as the diaphragm is innervated at
this level. C-5 and C-6 may be non-ventilator dependent or partially-ventilator dependent. Although rare, some C-6 patients have
full function of their upper body and are classifieds as paraplegics only; they can drive, etc.
Immediate signs/symptoms of a spinal cord injury:

Spinal shock at sight of transaction (see below)

Flaccid paralysis below injury

Loss of sensation below injury

Pain can be felt at sight of injury

Loss of ability to perspire below injury

Bowel/bladder dysfunction

Spinal shock: Loss of all neuro function below the injury during the acute phase. Patients temperature goes lower than normal
because of the break between the hypothalamus and the SNS. Recovery takes 4-6 weeks. The flaccidity is replaced by spastic
hyperreflexia and bilateral Babinski reflexes. Recovery is gradual as spinal neurons slowly regain their excitability. The return of
anal reflexes signal the end of spinal shock.
Neurogenic shock: The temporary loss of autonomic function as a result of the loss of SNS input to the systemic vasculature of
the heart; this leads to a subsequent decreased peripheral vascular resistance which causes hypotension. It can occur in severe
cervical and upper thoracic spinal cord injuries (SCIs). Symptoms are hypotension and bradycardia. Neurogenic shock is shortlived, about 24-48hours, so avoid fluid overloading; accept a slightly lower blood pressure if not otherwise contraindicated (ie
head injury) the system will right itself soon enough.
Treatment: The primary goal is to optimize outcomes. This involves neural decompression, realignment and stabilization of the
vertebra and surrounding tissues. If there is cord involvement then additional goals become early rehab and prevention of
complications.
Nursing Foci:

Potential for Respiratory complications

Altered Temperature regulation

Cardiac Dysrhythmias

Pain

Sensory impairment

Muscle Wasting

Sexual Dysfunction

Loss of Independence/Control

Financial complications

Self-care deficits

Bowel and bladder function deficits

Risk for pressure ulcers

Risk for infection

Risk for DVTs

Emotional/Grieving/Depression/Hopelessness

Nutrition: As with all trauma patients, it is important to feed Spinal Cord Injury (SCI) patients early. They are frequently in a
hypermetabolic state and require hi-caloric intakes.
Psychological Issues: People have a hard time believing they cannot get their body to move on command. It is difficult for
anyone to accept that they will never walk again, or have the use of their arms, never hold their child, lose their independence,
not be able to drive or play football or go to the coffee shop with friends, not be able to toilet independently, be ventilatordependent for life

Do you remember Kubler-Ross 5 Stages of Grieving?

Denial

Anger

Bargaining

Depression

Acceptance

It is important to keep in mind that in the acute stages of illness, such as we see in ICU, we are likely going to be exposed to only
the first three stages. To help the patient pass through these stages we need to get them involved early in their own care so they
move out of denial as soon as possible.
Anger guess who is on the frontlines for this? Yes, nurses. While we can absorb some of this anger and accept that it is not
really directed at us, we still must not condone nurse abuse. Behavioral conditioning!!! If we allow poor behavior to be accepted
this provides positive reinforcement and they will continue to behave this way to the future rehab nurses and their families. We
need to be firm for their own sake.
Revisit all those psych rotation interventions from nursing school: setting firm guidelines, making contracts and discouraging
manipulation while allowing for the patient to retake some semblance of control. Let them decide what time their bath will be,
but dont let them decide that they wont have one! Repositioning: After this is done, to avoid being called in every few minutes
for adjustments, ask if everything is OK and offer to make changes at that time. If all is well, reiterate to the patient that you will
return at x time to make minor adjustments but that they must stay on this

side for two full hours. And you must hold up your end of the bargain make sure you return when you say you will and make
minor adjustments.
Finally, human touch is a very social behavior (think of monkeys grooming each other!). The fact that these patients have
sensory deficits can be very isolating. Be sure to provide touch to the patient in an area they still have sensation, preferably
within their line of vision.
Physiotherapy/Activity/Positioning: This includes passive isometric exercises to maintain muscle mass and avoid
contractures. Get your patients involved in this early. They should be working out their upper body but they should also be
performing leg exercises by themselves. Ossification of joints, especially at the hips, can occur at 12 weeks.
A very important part of patient safety is having them be conscientious about positioning. This is an area they need to really be
involved in. When paraplegics are repositioned they should be visually inspecting their position to ensure they are not sitting on
anything, their linens are wrinkle-free and their bony structures are not rubbing together. They should frequently reposition
themselves are get assistance to do so.
This is an area we can start working on with quadriplegics as well. After repositioning a quad, encourage them to ask, Am I
lying/sitting on anything? Are my linens without wrinkles? Are my knees/ankles not rubbing together? Do I have any red
spots? This gives them responsibility for their own safety.

Aside from avoiding pressure sores, why is this so important? Do you remember the term Autonomic Dysreflexia? This is a
condition involving strong muscle spasms presented by stimuli (which, of course, the patient cannot feel). With altered
sensation, they may not know theyre sitting on their scrotum, or have a distended bladder. Signs will be extreme HTN and
tachycardia, SOB, a major headache, dysrhythmias, and sweating. The treatment is to fix the cause, but more importantly, to
avoid the cause. Always be vigilant when positioning spinal cord injured patients. Another preventative measure is to use
anesthetics on pressure ulcers. Avoid ingrown toenails; check to ensure shoes are not too tight. For men, make sure theyre not
sitting on their scrotum. Even though the patient is unaware of the pain, it may cause AD. Likewise, it is important to prevent
joint ossification, which can also cause AD.
Rehab: When does rehab begin? It begins with diagnosis. We have to instantly begin to consider patient preservation. While
quadriplegics will generally need full care with their ADLs, paraplegics will eventually perform many ADLs independently:
Bladder Training: Many paraplegics learn to catheterize themselves at intervals throughout the day. We dont usually get
involved in this at this stage but if you are changing a paraplegics catheter you can begin education by telling him he will soon
learn to do this on his own encouraging the patient to regaining some control over his care.
Bowel Training: Paraplegics learn to recognize their bowel rhythms and by doing so can avoid accidents. Recall that the major
mass movements of peristalsis in the colon happen about four times per day only. A patient will soon recognize his times and
can work his schedule around this. Also, note that constipation is a frequent problem with paraplegics due to their lower activity
level, and they frequently need laxatives/suppositories for assistance.

A patient can help the process along by placing warm towels on their abdomen or by pushing in rhythmic motions over his
abdomen and diaphragm, stimulating movement.
This is something we can start early while patients are still in the ICU.

DERMATOMES
A dermatome is an area of skin that is mainly supplied by a single sensory spinal nerve which provides sensation to a specific
area of skin. Dermatomes are useful, therefore, for finding the site of damage to the spine.

Neuro injuries are classified as complete (no functional motor or sensory preservation)or incomplete (some sensory or motor
preservation). As mentioned earlier, complete cord transection is rare, but partial transections can present with total injury.
However, because of edema and spinal shock, it is often difficult to tell whether complete injury is present. For this reason we
test dermatomes.
The dermatomes chart on the next page, from the American Spinal Injury Association, is a standard for dermatomes testing, and
covers all the areas of the body. Some experts argue the need to include anal sphincter tests as well but to date there is no
consensus.
How to Test: As noted on the chart, testing is done with light touch (many ICUs use a cotton ball), and with a gentle pinprick.
There is evidence to show that pinprick testing is less reliable than cold sensation testing using ice cubes; however, your
institution will have developed their own policy and testing will be done accordingly.
Testing is usually done once per shift but if there are signs that spinal shock is waning or that sensation is returning, they will
frequently be done more often.
If you are interested, the following website offers dermatomes learning and testing quiz online:
http://quizlet.com/2481001/testing-dermatomes-flash-cards/

ANSWERS TO ACTIVITIES
1. Why is CPR so important in an arrest?

15-20% of cardiac output goes to brain

20% of oxygen consumed by body is to convert the

glucose which will be used directly by the brain

2. It is said that you can develop the other side of your brain if
you train it and focus on those associated tasks. What do you
think?
Studies show that yes, you can train your nondominant side to be more active. I have my doubts
youve all seen my drawings!
3. Is the GCS score applicable to someone with an injury to
Brocas Area?
Yes, GCS is still applicable. You would score it the
same way even though your verbal score will obviously
be affected. You can write in your notes that the injury
is in Brocas area, but the scoring is done the same
way think of how we score a patient whos had a
stroke and has motor deficits. Its the same thing.
4. Neuro patients can develop Diabetes Insipidus. What is
happening neurologically when this happens?
There is injury to the pituitary gland, making the ADH
feedback mechanism is not working properly.
5. A patient with a severe head injury has been having heart rate
fluctuations over the last 3 hours, ranging between 52 and 88
bpm. He has had a continuous fever for the last 12 hours. Is
the heart rate a reportable finding? Why or why not?
This is a reportable finding which has nothing to do
with the fever. This could be a sign of brainstem
involvement (the medulla is the heartrate regulation
centre).
6. Think about how you would expect various body systems to
respond if acting under each system. Would your pupils dilate
or shrink if you were frightened? Would your GI system speed
up or slow down? If you think about these responses and
relate them to which system is activated, you can also figure

out how your body will respond under the influence of

adrenergic or cholinergic medications, as well.
When your sympathetic nervous system kicks in, all the
non-vital functions slow down and the vital functions
become hyperactive.
Respiratory: increased rate of breathing to supply
increased oxygen to tissues; dilation of respiratory
tract
Cardiac: increased HR to increase Cardiac Output
Pupils: Dilate to let in more information about the
situation
Muscles: Increased tension (to act like springs!)
GI: Motility decreases this is no time to be distracted
by food
GU: Sphincter closes; decreased urine production
The parasympathetic nervous system acts in the
opposite way
7. We frequently hear the term Diffuse Axonal Injury in brain

trauma. What does it mean?

Damage occurs over a widespread area; there are
extensive lesions in the white matter, leading to a
persistent vegetative state.
8. A patient with a ruptured aneurysm near the Circle of Willis is
recovering in your ICU. You are doing neuro checks on her and
you find she is emotionally labile irritable one time and then
very subdued the next. Is this an expected finding related to
her injury?
This is an expected finding because the Circle of Willis
has extensive tracts to all parts of the brain, and if
there is a bleed in this area many areas could be
affected.
9. A TBI patient has a widening pulse pressure, his heart rate and
breathing are irregular, and his pupils are 6 and fixed. Why
are his vital signs fluctuating?
This is Cushings Response, signalling that there is
vertical herniation occurring, putting pressure on the
brainstem and affecting the medulla.

10.

What cranial nerves are involved in the corneal reflex?

What about Dolls Eyes?

Corneal Reflex is CN V and VII. Dolls Eyes is CN III

Case Study 1:
Mrs. B was brought into the ER by her family; she collapsed at home
about 20 minutes ago, right after complaining of the worst
headache shes ever had. On examination, her vitals are BP
190/120, HR 62, RR 18 and regular, Temp 37.6C, O2 saturation 94%.
You do a neuro check:
Eyes open to pain
Pupils are 4, equal and sluggish to respond
She is saying inappropriate words when aroused; otherwise
somnolent
She is moving her left arm spontaneously but is not squeezing your
hand or following commands. Her motor control is poor. Her left leg
moves laterally across the bed. There is no movement on the right
side.
A CT scan shows a ruptured aneurysm to the Right Middle Cerebral
Artery. She is taken to the OR for repair and evacuation of the clot
and then sent to you in the ICU. You look after her for 4 days in a
row.
Orders:

Routine neuro checks and vital signs

TFI 70cc/h

Keep MAP 60

Keep CVP <10

CBC, ABG, coags and lytes q 12hours x 4, then q 48h

SCDs

Keep HOB 30o; bedrest

Ranitidine 150 mg IV q8h

Jevity to start at 20cc/h and increase by 10cc/h q6h to a goal

of 50cc/h

EKG q day

CXR in a.m.

Ventilate to keep ABGs normal

Midaz/Fentanyl to keep MAAS 0-1 x 24 hours then reassess

Maintain BS 70-160 with Humulin R infusion as needed

Accucheks q 4 hours if not on infusion

Nimodipine 30 mg po TID

Normal fluid balace

10. What EKG changes might you expect to see with this patient?
Prolonged QT interval, T-wave inversion, presence of a
U-wave
11.

If this patient wakes up she is likely to have difficulty

with extraocular eye movements, and possible visual

impairment. This indicates damage to which cranial nerves?
CN II and III

12.

What is your primary focus during the first 24 hours:

d. Monitoring for vasospasm

e. Optimizing CPP this is your focus for the first 24 hours.
It is important to optimize cerebral bloodflow so the tissues
remain well perfused. Vasospasm is not expected until at
least day 3; rebleeding doesnt usually happen until later.
f. Potential for rebleeding
13.

Documentation on the Kardex should include:

a. Her initial labwork
b. The length of surgery
c. Her initial deficits it is important to document her
initial deficits and related them to where her injury is so
you can watch for these deficits to reappear and
potentially alert you to possible vasospasms

14.

Why should the above be included on her Kardex?

See above
15.

At 0600h you are due to give Nimodipine but your BP is

only 120/60. What should you do?

a. Hold Nimodipine
b. Call the doctor Never hold your Nimodipine without
getting a doctors order to do so. You dont want to give
fluid at this stage because we are trying to optimize
cerebral bloodflow while limiting potential increases in
ICP. Additionally, your patients BP should never be this
low with a SAH. Vasospasm is caused by narrowing of
the arteries; we want to keep them expanded. Lastly,
this BP is too low to maintain adequate CBF.
c. Give a fluid bolus to increase the BP enough to be able
to give Nimodipine
Your patient has woken up over last two nights. She was extubated
this afternoon and is currently on 4 lpm via nasal cannula. This
evening her neuro check reveals she is opening eyes spontaneously,
responding with simple words but not using full sentences, and
following simple motor commands (E4 V5 M6, total GCS 15). She is

still quite sleepy and is only aroused with direct contact. She has
had a busy day blood cultures, CT scan, full neurological exam by
neurology.
16.

What is your primary focus for this shift?

d. Q hourly neuro checks despite having a GCS of 15, this

lady is at high risk by Day 3 for vasospasms. Hourly neuro
checks are warranted, despite what the doctor orders. If
the doctor tells you to let her rest, have him write this as
an order.
e. Quiet environment with minimal disturbances
f. Deep breathing and coughing
17.

Upon reviewing the orders, which ones will you address

with the doctor during evening rounds?

d. More frequent CBC and electrolyte labwork you
know that Hyponatremia and other electrolyte disturbances
are a risk factor for vasospasms, as is viscous blood. It is
important to keep a close eye on labwork at this stage of
recovery to prevent further injury, especially Sodium levels.
e. Start Clexane
f. Change Humulin R to Subcutaneous

At 0430 you go in to draw labs and your patient is slow to respond.

She eventually opens her eyes to voice and responds appropriately,
but her left arm is flaccid.
18.

What is likely the cause of this?

d. Ischemic Stroke
e. This is a potentially expected finding on Day 3-5 as the clot
has lysed and chemicals interfere with normal neuro
function
f. Vasospasm
19.

What treatment might the doctor order for this finding?

Hopefully the patient has been receiving Nimodipine

already! We will now add Triple-H therapy:
Hemodilution (keep Hct 30-35%); Hypervolemia we
can give IVF at this time in order to achieve this.
Hypertension (keep SBP >170). This is all in an effort
to keep the artery dilated while avoiding turbulent
bloodflow.