Neurologic

System
• The nervous system is the major controlling, regulatory and
communicating system in the body.
• It accounts for 3% of the total body weight, it is the most
complex organ system.
• It is the center of all mental activity, including thought,
learning and memory.
• Together with the endocrine and immune systems, the
nervous system is responsible for regulating and maintaining
homeostasis.
• Through its receptors, the nervous system keeps in touch with
the environment, both external and internal.
 NEUROLOGICAL ANATOMY AND PHYSIOLOGY

• COMPONENTS OF THE NERVOUS SYSTEM

• The central nervous system (CNS) consists of the spinal cord
and the brain and is responsible for integrating, processing
and coordinating sensory data and motor commands.
• The CNS is linked to all parts of the body by the PNS which
transmits signals to and from the CNS.
• The human PNS is composed of 43 pairs of spinal nerves that
issue in orderly sequence from the spinal cord, and 12 pairs of
cranial nerves that emerge from the base of the brain.
• The peripheral nerves carry input to the CNS via their sensory
afferent fibers and deliver output from the CNS via the
efferent fibers.
 Neurons
• Are specialized cells in the nervous system; each is comprised
of a dendrite, cell body (soma) and axon.

• The primary functional unit of the nervous system.

• Three characteristics: (1) excitability, or the ability to generate

a nerve impulse; (2) conductivity, or the ability to transmit an
impulse; and (3) influence, or the ability to influence other
neurons, muscle cells, or glandular cells by transmitting nerve
impulses to them.
• A typical neuron consists of a cell body, multiple dendrites, and an axon .
• The cell body containing the nucleus and cytoplasm is the metabolic
center of the neuron.
• Dendrites are short processes extending from the cell body that receive
• impulses from the axons of other neurons and conduct impulses toward
the cell body.
• The axon projects varying distances from the cell body, ranging from
several micrometers to more than a meter. The axon carries nerve
impulses to other neurons or to end organs. The end organs are smooth
and striated muscles and glands.
• Many axons in the CNS and PNS are covered by a myelin sheath, a white,
lipid substance that acts as an insulator for the conduction of impulses.
• Axons may be myelinated or unmyelinated. Generally, the smaller fibers
are unmyelinated.
Structural features of neurons:
dendrites, cell body, and axons.
 Glial Cells
• Glial cells (glia or neuroglia) provide support, nourishment,
and protection to neurons.
• Constitute almost half of the brain and spinal cord mass and
are 5 to 10 times more numerous than neurons.
• Glial cells are divided into microglia and macroglia.
• Microglia, specialized macrophages capable of phagocytosis,
protect the neurons. These cells are mobile within the brain
and multiply when the brain is damaged.
• Different types of macroglial cells include the astrocytes
(most abundant), oligodendrocytes, and ependymal cells.

• Astrocytes are found primarily in gray matter and provide

structural support to neurons. Their delicate processes form
the blood-brain barrier with the endothelium of the blood
vessels.
• They also play a role in synaptic transmission (conduction of
impulses between neurons).
• When the brain is injured, astrocytes act as phagocytes for
neuronal debris. They help restore the neurochemical milieu
and provide support for repair. Proliferation of astrocytes
contributes to the formation of scar tissue (gliosis) in the CNS.
• Oligodendrocytes are specialized cells that
produce the myelin sheath of nerve fibers in
the CNS and are primarily found in the white
matter of the CNS. (Schwann cells myelinat
the nerve fibers in the periphery.)
• Ependymal cells line the brain ventricles and
aid in the secretion of cerebrospinal fluid
(CSF).
• Neuroglia are mitotic and can replicate.
• In general, when neurons are destroyed, the tissue is
replaced by the proliferation of neuroglial cells.
• Most primary CNS tumors involve glial cells.
• Primary malignancies involving neurons are rare.
 Nerve Impulse
• The purpose of a neuron is to initiate, receive, and process
messages about events both within and outside the body.
• The initiation of a neuronal message (nerve impulse)
involves the generation of an action potential. Once an
action potential is initiated, a series of action potentials
travels along the axon.
• When the impulse reaches the end of the nerve fiber, it is
transmitted across the junction between nerve cells
(synapse) by a chemical interaction involving
neurotransmitters.
• This chemical interaction generates another set of action
potentials in the next neuron. These events are repeated
until the nerve impulse reaches its destination.
• Because of its insulating capacity, myelination of nerve
axons facilitates the conduction of an action potential.
Many peripheral nerve axons have nodes of Ranvier
(gaps in the myelin sheath) that allow an action
potential to travel much faster by jumping from node
to node without traversing the insulated membrane
segment. This is called saltatory (hopping) conduction.
• In an unmyelinated fiber, the wave of depolarization
travels the entire length of the axon, with each portion
of the membrane becoming depolarized in turn.
 Synapse
• A synapse is the structural and functional junction
between two neurons.
• It is the point at which the nerve impulse is
transmitted from one neuron to another. The nerve
impulse can also be transmitted from neurons to
glands or muscles.
• The essential structures of synaptic transmission are
a presynaptic terminal, a synaptic cleft, and a
receptor site on the postsynaptic cell.
• Two general classes: electrical synapses and chemical
synapses.
• Electrical synapses permit direct, passive flow of electrical
current from one neuron to another in the form of an
action potential. The current flows through gap junctions,
which are specialized membrane channels that connect the
two cells.
• Chemical synapses, in contrast, enable cell-to-cell
communication via the secretion of neurotransmitters; the
chemical agents released by the presynaptic neurons
produce secondary current flow in postsynaptic neurons by
activating specific receptor molecules.
 Neurotransmitters
• Neurotransmitters are chemicals that affect the
transmission of impulses across the synaptic cleft.
• Chemically, there are four classes of
neurotransmitters:
– 1. acetylcholine (ACh): the dominant neurotransmitter in
the peripheral nervous system, released at neuromuscular
junctions and synapses of the parasympathetic division
– 2. biogenic amines: serotonin, histamine, and the
catecholamines dopamine and noradrenaline
– 3. excitatory amino acids: glutamate and aspartate, and the
inhibitory amino acids gamma-aminobutyric acid (GABA),
glycine and taurine
– 4. neuropeptides: over 50 of which are known, amino acid
neurotransmitters being the most numerous.
 Central Nervous System

• The components of the CNS include the

cerebrum (cerebral hemispheres), brainstem,
cerebellum, and spinal cord.
• The spinal cord is continuous with the brainstem and
exits from the cranial cavity through the foramen
magnum.
• A cross section of the spinal cord reveals gray matter
that is centrally located in an H shape and is
surrounded by white matter.
• The gray matter contains the cell bodies of voluntary
motor neurons, preganglionic autonomic motor
neurons, and association neurons (interneurons).
• The white matter contains the axons of the ascending
sensory and the descending (suprasegmental) motor
fibers.
 Ascending Tracts
• The ascending tracts carry specific sensory information to higher
levels of the CNS.
• This information comes from special sensory receptors in the skin,
muscles and joints, viscera, and blood vessels and enters the
spinal cord by way of the dorsal roots of the spinal nerves.
• The fasciculus gracilis and the fasciculus cuneatus (commonly
called the dorsal or posterior columns) carry information and
transmit impulses concerned with touch, deep pressure, vibration,
position sense, and kinesthesia (appreciation of movement,
volweight, and body parts).
• The spinocerebellar tracts carry information about muscle tension
and body position to the cerebellum for coordination of
movement.
• The spinothalamic tractscarry pain and temperature sensations.
Therefore the ascending tracts are organized by sensory modality,
as well as by anatomy
 Descending Tracts
• Descending tracts carry impulses that are responsible for
muscle movement.
• Among the most important descending tracts are the
corticobulbar and corticospinal tracts, collectively termed
the pyramidal tract.
• These tracts carry volitional (voluntary) impulses from the
cerebral cortex to the cranial and peripheral nerves.
• Another group of descending motor tracts carries impulses
from the extrapyramidal system (all motor systems except
the pyramidal) concerned with voluntarymovement. It
includes pathways originating in the brainstem, basal
ganglia, and cerebellum. The motor output exits the spinal
cord by way of the ventral roots of the spinal nerves.
 Lower and Upper Motor Neurons
• Lower motor neurons (LMNs) are the final common pathway
through which descending motor tracts influence skeletal
muscle.
• The cell bodies of LMNs, which send axons to innervate the
skeletal muscles of the arms, trunk, and legs, are located in
the anterior horn of the corresponding segments of the spinal
cord (e.g., cervical segments contain LMNs for the arms).
• LMNs for skeletal muscles of the eyes, face, mouth, and
throat are located in the corresponding segments of the
brainstem.
• These cell bodies and their axons make up the somatic motor
components of the cranial nerves.
• LMN lesions generally cause weakness or paralysis,
denervation atrophy, hyporeflexia or areflexia, and
• Upper motor neurons (UMNs) originate in the cerebral cortex
and project downward.
• The corticobulbar tract ends in the brainstem, and the
corticospinal tract descends into the spinal cord. These
neurons influence skeletal muscle movement.
• UMN lesions generally cause weakness or paralysis, disuse
atrophy, hyperreflexia, and increased muscle tone
(spasticity).
 Reflex Arc
• A reflex is an involuntary response to stimuli.
• In the spinal cord, reflex arcs play an important role
in maintaining muscle tone, which is essential for
body posture.
• The components of a monosynaptic reflex arc are a
receptor organ, an afferent neuron, an effector
neuron, and an effector organ (e.g., skeletal muscle).
• The afferent neuron synapses with the efferent
neuron in the gray matter of the spinal cord.
 Brain
• The term brain usually refers to the three
major intracranial components: cerebrum,
brainstem, and cerebellum.
 Cerebrum.
• The cerebrum is composed of the right and left cerebral
hemispheres and divided into four lobes: frontal, temporal,
parietal, and occipital.
• The frontal lobe controls higher cognitive function, memory
retention, VOLuntary eye movements, voluntary motor
movement, and speech in Broca’s area.
• The temporal lobe integrates somatic, visual, and auditory
data and contains Wernicke’s speech area.
• The parietal lobe interprets spatial information and contains
the sensory cortex.
• Processing of sight takes place in the occipital lobe.
• The division of the cerebrum into lobes is useful to delineate
portions of the neocortex (gray matter), which makes up the
outer layer of the cerebral hemispheres. Neurons in specific
parts of the neocortex are essential for various highly
complex and sophisticated aspects of mental function, such as
language, memory, and appreciation of visual-spatial
relationships.
• The basal ganglia, thalamus, hypothalamus, and limbic system
are also located in the cerebrum.
• The basal ganglia are a group of structures located centrally
in the cerebrum and midbrain. The function of the basal
ganglia includes the initiation, execution, and completion of
voluntary movements, learning, emotional response, and
automatic movements associated with skeletal muscle activity
(e.g., swinging the arms while walking, swallowing saliva, and
blinking).
• The thalamus (part of the diencephalon) lies directly above
the brainstem and is the major relay center for afferent inputs
to the cerebral cortex.
• The hypothalamus is located just inferior to the thalamus and
slightly in front of the midbrain.
• It regulates the ANS and the endocrine system.
• The limbic system is located near the inner surfaces of the
cerebral hemispheres and is concerned with emotion,
aggression, feeding behavior, and sexual response.
 Brainstem
• The brainstem includes the midbrain, pons, and medulla .
• Ascending and descending fibers to and from the cerebrum and
cerebellum pass through the brainstem.
• The nuclei of cranial nerves III through XII are in the brainstem.
• The vital centers concerned with respiratory, vasomotor, and cardiac
function are located in the medulla.
• Also located in the brainstem is the reticular formation, a diffusely
arranged group of neurons and their axons that extends from the medulla
to the thalamus and hypothalamus. The functions of the reticular
formation include relaying sensory information, influencing excitatory and
inhibitory control of spinal motor neurons, and controlling vasomotor and
respiratory activity.
• The reticular activating system (RAS) is a complex system that requires
communication among the brainstem, reticular formation, and cerebral
cortex. The RAS is responsible for regulating arousal and sleep-wake
transitions. The brainstem also contains the centers for sneezing,
coughing, hiccupping, vomiting, sucking, and swallowing.
 Cerebellum
• The cerebellum is located in the posterior part of
the cranial fossa inferior to the occipital lobe.
• The cerebellum coordinates voluntary movement
and maintains trunk stability and equilibrium.
• The cerebellum receives information from the
cerebral cortex, muscles, joints, and inner ear.
• It influences motor activity through axonal
connections to the motor cortex, the brainstem
nuclei, and their descending pathways.
 Ventricles and Cerebrospinal Fluid.

• The ventricles are four interconnected

fluid-filled cavities. The lower portion of the
fourth ventricle becomes the central canal in
the lower part of the brainstem. The spinal
canal extends centrally through the full length
of the spinal cord.
 Cerebrospinal fluid (CSF)
• Circulates within the subarachnoid space that surrounds the brain, brainstem, and
spinal cord.
• This fluid provides cushioning for the brain and the spinal cord, allows fluid shifts
from the cranial cavity to the spinal cavity, and carries nutrients.
• The formation of CSF in the choroid plexus in the ventricles involves both passive
diffusion and active transport of substances. CSF resembles an ultrafiltrate of
blood.
• CSF is produced at an average rate of about 500 mL/day, many factors influence
CSF production and absorption. The ventricles and central canal are normally filled
with an average of 135 mL of CSF.
• Changes in the rate of production or absorption will result in a change in the
volume of CSF that remains in the ventricles and central canal.
• Excessive buildup of CSF results in a condition known as hydrocephalus.
• The CSF circulates throughout the ventricles and seeps into the subarachnoid
space surrounding the brain and spinal cord.
• It is absorbed primarily through the arachnoid villi (tiny projections into the
subarachnoid space), into the intradural venous sinuses, and eventually into the
venous system.
• The analysis of CSF composition provides useful diagnostic
information related to certain nervous system diseases. CSF
pressure is often measured in patients with actual or
suspected intracranial injury. Increased intracranial pressure,
indicated by increased CSF pressure, can force downward
(central) herniation of the brain and brainstem.
 Peripheral Nervous System
• The PNS includes all the neuronal structures that lie
outside the CNS. It consists of the spinal and cranial
nerves, their associated ganglia (groupings of cell
bodies), and portions of the ANS.
 Spinal Nerves
• The spinal cord can be seen as a series of spinal
segments, one on top of another.
• Each segment contains a pair of dorsal (afferent)
sensory nerve fibers or roots and ventral (efferent)
motor fibers or roots, which innervate a specific
region of the body.
• This combined motor-sensory nerve is called a spinal
nerve.
• The cell bodies of the voluntary motor system are
located in the anterior horn of the spinal cord gray
matter.
• The cell bodies of the autonomic (involuntary) motor
system are located in the anterolateral portion of the
spinal cord gray matter.
• The cell bodies of sensory fibers are located in the
dorsal root ganglia just outside the spinal cord.
• A dermatome is the area of skin innervated by the
sensory fibers of a single dorsal root of a spinal
nerve.
• The dermatomes give a general picture of somatic
sensory innervation by spinal segments.
• A myotome is a muscle group innervated by the
primary motor neurons of a single ventral root.
Dermatomes of the body
 Cranial Nerves

• The cranial nerves (CNs) are the 12 paired nerves composed

of cell bodies with fibers that exit from the cranial cavity.
• Just as the cell bodies of the spinal nerves are located in
specific segments of the spinal cord, so are the cell bodies
(nuclei) of the CNs located in specific segments of the brain.
• Exceptions are the nuclei of the olfactory and optic nerves.
The primary cell bodies of the olfactory nerve are located in
the nasal epithelium, and those of the optic nerve are in the
retina.
 Autonomic Nervous System.
• The autonomic nervous system (ANS) is divided into the
sympathetic and parasympathetic systems.
• The ANS governs involuntary functions of cardiac muscle,
smooth muscle, and glands through both efferent and
afferent pathways.
• The preganglionic cell bodies of the sympathetic nervous
system (SNS) are located in spinal segments T1 through L2.
The major neurotransmitter released by the postganglionic
fibers of the SNS is norepinephrine, and the neurotransmitter
released by the preganglionic fibers is acetylcholine.
• The preganglionic cell bodies of the parasympathetic nervous
system (PSNS) are located in the brainstem and the sacral
spinal segments (S2 through S4). Acetylcholine is the
neurotransmitter released at both preganglionic and
postganglionic nerve endings.
• SNS stimulation activates the mechanisms required for the
“fight-or-flight” response that occurs throughout the body.
• The PSNS is geared to act in localized and discrete regions
 Cerebral Circulation
• The brain’s blood supply arises from the internal
carotid arteries (anterior circulation) and the
vertebral arteries (posterior circulation).
• The internal carotid arteries provide blood flow to the
anterior and middle portions of the cerebrum.
• The vertebral arteries join to form the basilar artery and
provide blood flow to the brainstem, cerebellum, and
posterior cerebrum.
• The circle of Willis is formed by communicating arteries that
join the basilar and internal carotid arteries.
• The circle of Willis is a safety valve for regulating cerebral
blood flow when differential pressures or vascular occlusions
are present.
• Superior to the circle of Willis, three pairs of arteries
supply blood to the left and right hemispheres.
• The anterior cerebra artery feeds the medial and
anterior portions of the frontal lobes.
• The middle cerebral artery feeds the outer portions of
the frontal, parietal, and superior temporal lobes.
• The posterio cerebral artery feeds the medial portions
of the occipital an inferior temporal lobes.
• Venous blood drains from the brain through the dural
sinuses, which form channels that drain int the two
jugular veins.
• The blood-brain barrier is a physiologic barrier between
blood capillaries and brain tissue.
• This barrier protects the brain from harmful agents, while
allowing nutrients and gases to enter.
• Lipid-soluble compounds enter the brain easily, whereas
water-soluble and ionized drugs enter the brain and the spinal
cord slowly.
• Thus the blood-brain barrier affects the penetration of drugs.
 Protective Structures
• The meninges consist of three protective membranes that
surround the brain and spinal cord: dura mater, arachnoid,
and pia mater .
• The thick dura mater forms the outermost layer.
• The falx cerebri is a fold of the dura that separates the two
cerebral hemispheres and slows expansion of brain tissue in
conditions such as a rapidly growing tumor or acute
hemorrhage.
• The tentorium cerebelli is a fold of dura that separates the
cerebral hemispheres from the posterior fossa (which
contains the brainstem and cerebellum).
• Expansion of mass lesions in the cerebrum forces the brain to
herniate through the opening created by the brainstem. This
is termed infratentorial herniation.
• The arachnoid layer is a delicate membrane that lies between
the dura mater and the pia mater (the delicate innermost
layer of the meninges).
• The area between the arachnoid layer and the pia mater is
the subarachnoid space and is filled with CSF.
• Structures such as arteries, veins, and cranial nerves passing
to and from the brain and the skull must pass through the
subarachnoid space.
• A larger subarachnoid space in the region of the third and
fourth lumbar vertebrae is the area used to obtain CS during a
lumbar puncture.
• Skull. The skull protects the brain from
external trauma. It is composed of eight
cranial bones and 14 facial bones.
• Vertebral Column. The vertebral column
protects the spinal cord, supports the head,
and provides flexibility. The vertebral column
is made up of 33 individual vertebrae: 7
cervical, 12 thoracic, 5 lumbar, 5 sacral (fused
into one), and 4 coccygeal
• ASSESSMENT OF NERVOUS SYSTEM
 Subjective Data
• Important Health Information
• Past Health History. Consider three points when taking a
history of a patient with neurologic problems.
• First, avoid suggesting symptoms or asking leading questions.
• Second, the mode of onset and the course of the illness are
especially important aspects of the history. Obtain all
pertinent data in the history of the present illness, especially
data related to the characteristics and progression of the
symptoms.
• Third, if the patient is not considered a reliable historian,
confirm or obtain the history from someone with firsthand
knowledge of the patient.
• Medications. Obtain a careful medication history, especially
the use of sedatives, opioids, tranquilizers, and mood
elevating drugs. Many other drugs can also cause
neurologic side effects.
• Surgery or Other Treatments.
• Inquire about any surgery involving any part of the nervous
system, such as head, spine, or sensory organs. If a patient
had surgery, determine the date, cause, procedure,
recovery, and current status.
• Growth and developmental history can be important in
ascertaining whether nervous system dysfunction was
present at an early age. Specifically inquire about major
developmental tasks such as walking and talking.
• Functional Health Patterns. Key questions to
ask a patient with a neurologic problem are
presented in Table 56-5.
 Objective Data
• Physical Examination. The standard neurologic examination
helps determine the presence, location, and nature of disease
of the nervous system.
• The examination assesses six categories of functions: mental
status, cranial nerve function, motor function, sensory
function, cerebellar function, and reflexes..
• Mental Status. Assessment of mental status
(cerebral function) gives a general impression of how
the patient is functioning.
• It involves determining complex and high-level
cerebral functions that are governed by many areas
of the cerebral cortex.
• .
 The components of the mental status examination include:

• • General appearance and behavior: This component includes level of

consciousness (awake, asleep, comatose), motor activity, body posture,
dress and hygiene, facial expression, and speech pattern.
• • Cognition: Note orientation to time, place, person, and situation, as well
as memory, general knowledge, insight, judgment, problem solving, and
calculation. Common questions are “Who were the last three presidents?”
“Does a rock float on water?” “How much money is a quarter, two dimes,
and a nickel?” Consider whether the patient’s plans and goals match the
physical and mental capabilities. Note the presence of factors affecting
intellectual capacity such as cognitive impairment, hallucinations,
delusions, and dementia.
• • Mood and affect: Note any agitation, anger, depression, or euphoria and
the appropriateness of these states. Use suitable questions to bring out
the patient’s feelings.
• Conscious State
• Arousal and awareness are the fundamental constituents of
consciousness and should be evaluated and documented
repeatedly for trend analysis. Changes in the conscious state are
the first to change in deterioration.
• Arousal assessment
• The evaluation of arousal focuses on the ability to be able to
respond to a variety of stimuli and can be described using the
AVPU scale or disorientated, lethargic, or obtunded.
• The advanced trauma life support course recommends an initial
assessment during initial resuscitation based on the response to
stimulation: Awake, Verbal, Pain, Unresponsive (AVPU).
• Observe the patient’s response (verbal or motor). If there is no
response to voice or light touch, painful stimulus is needed to
assess neurological status.
• Assessment of awareness
• If arousable, progress to assessment of awareness using the
Glasgow Coma Scale (GCS).
• Teasdale and Jennett designed the GCS to establish an
objective, quantifiable measure to describe the prognosis of a
patient with a brain injury and include scoring of separate
subscales related to eye opening, verbal response and motor
response.
• Eye and pupil assessment
• Pupillary responses, including pupil size and reaction to light,
are important neurological observations and localize cerebral
disease to a specific area of the brain.
• The immediate constriction of the pupil when light is shone
into the eye is referred to as the direct light reflex.
• Withdrawal of the light should produce an immediate and
brisk dilation of the pupil.
• Introduction of the light into one eye should cause a similar
constriction to occur in the other pupil (consensual light
reaction).
 Other points to consider when conducting pupillary
observations include the following
• pinpoint non-reactive pupils are associated with opiate
overdose
• non-reactive pupils may also be caused by local damage
• atropine will cause dilated pupils
• one dilated or fixed pupil may be indicative of an expanding
or developing intracranial lesion, compressing the
oculomotor nerve on the same side of the brain as the
affected pupil
• A sluggish pupil may be difficult to distinguish from a fixed
pupil and may be an early focal sign of an expanding
intracranial lesion and raised intracranialpressure. A
sluggish response to light in a previously reacting pupil must
be reported immediately.
• Assessment of pupillary function focuses on three
areas:
• (1) estimation of pupil size and shape;
• (2) evaluation of pupillary reaction to light;
• (3) assessment of eye movements.
• Eye and eyelid movements
• Patients who are comatose will exhibit no eye opening.
• In patients with bilateral thalamic damage, there may be normal
consciousness, but an eye opening apraxia may mimic coma. If the
patient’s eyes are closed, the clinician should gently raise and release the
eyelids. Brisk opening and closing of the eyes indicates that the pons is
grossly intact.
• If the pons is impaired, one or both eyelids may close slowly or not at all.
• In the patient with intact frontal lobe and brainstem functioning, the eyes,
when opened, should be pointed straight ahead and at equal height. If
there is awareness, the patient should look towards stimuli after eye
opening.
• Eye deviation indicates either a unilateral cerebral or brainstem lesion. If
the eyes deviate laterally, gently turn the head to see if the eyes will cross
the midline to the other side. A pattern of spontaneous, slow and random
movements (usually laterally) is termed roving-eye movements. This
indicates that the brainstem oculomotor control is intact but awareness is
significantly impaired.
• Limb movement
• Assessment of extremities and body movement (or motor
response) provides valuable information about the patient
with a decreased level of
• Decorticate (flexor) posturing is seen when there is
involvement of a cerebral hemisphere and the brain stem.
• It is characterised by adduction of the shoulder and arm,
elbow flexion, and pronation and flexion of the wrist while
the legs extend. In terms of the GCS motor score, the
withdrawal flexor scores a higher (4/6) than a spastic flexor
movement (3/6).
• Decerebrate (extensor) posturing is seen with severe
metabolic disturbances or upper brainstem lesions. It is
characterised by extension and pronation of the arm(s) and
extension of the legs. Patients may have an asymmetrical
response and may posture spontaneously or to stimuli.
• Motor tone is first assessed by flexing the limbs and noting
increased or absent tone. If no tone is present, the hand is
lifted approximately 30 cm above the bed and carefully
dropped while protecting the limb from injury. The test is
repeated with all extremities. Typically, the lower the level of
consciousness, the closer to flaccid the limb(s) will be. An
asymmetrical examination may indicate a lesion in the
contralateral hemisphere or brainstem.
• Facial symmetry
• Facial symmetry is often difficult to appreciate in, for
example, severely ill patients due to oedema, endotracheal
tube tape and nasogastric tubes. An asymmetric response is
indicative of a lesion of CN VII. Complete hemi-facial
involvement is typically seen in peripheral dysfunction (Bell’s
palsy), whereas superior division (forehead) sparing weakness
indicates a pontine/medullary (central) involvement.
• Corneal reflexes
• The corneal reflex is assessed by holding the patient’s eye
open and lightly stimulating the cornea. The stimuli should
result in a reflexive blink, best seen in the lower eyelid. The
traditional assessment technique involves using a wisp of
cotton, lightly brushed along the lower aspect of the cornea.
An alternative, and less potentially traumatic, method is to
gently instil isotonic eye drops or saline irrigation ampoules
onto the cornea. This reflex is dependent upon CN V for its
sensation and CN VII for its motor response. Loss of this reflex
is indicative of lower brainstem damage, but may be absent
due to trauma, surgery, or long-term contact lens usage.
• Oropharyngeal reflexes
• The oropharyngeal reflexes are controlled by CN IX and CN X.
The gag reflex is elicited by lightly stimulating the soft palate
with a suction catheter or tongue blade. Clinicians should
always avoid stimulating a gag reflex by wiggling the
endotracheal tube because doing so may result in an
inadvertent extubation. A gag reflex is a forceful, symmetrical
lowering of the soft palate. The cough reflex is usually
assessed only in patients with an endotracheal tube. This
reflex is elicited by gently passing a suction catheter through
the tube and stimulating a cough. Loss of these reflexes is
indicative of lower brainstem damage.
• Cranial Nerves. Testing each CN is an essential
part of the
• neurologic examination
• Motor System. The motor system examination
includes assessment of strength, tone, coordination,
and symmetry of the major muscle groups.

• Test muscle strength by asking the patient to push

and pull against the resistance of your arm as it
opposes flexion and extension of the patient’s
muscle. Ask the patient to offer resistance at the
shoulders, elbows, wrists, hips, knees, and ankles.
• Test muscle tone by passively moving the limbs through their
range of motion. There should be a slight resistance to these
movements.
• Abnormal tone is described as hypotonia (flaccidity) or
hypertonia (spasticity). Note any involuntary movements such
as tics, tremor, myoclonus (spasm of muscles), athetosis
(slow, writhing, involuntary movements of extremities),
chorea (involuntary, purposeless, rapid motions), and
dystonia (impairment of muscle tone).
• Test cerebellar function by assessing balance and
coordination.
• A good screening test for both balance and muscle strength is
to observe the patient’s stature (posture while standing) and
gait. Note the pace and rhythm of the gait and observe for
normal symmetric and oppositional arm swing.
• The patient’s ability to ambulate helps to determine the level
of nursing care required and the risk of falling.
• The finger-to-nose test (having the patient alternately touch
the nose, then touch the examiner’s finger) and the
heel-to-shin test (having the patient stroke the heel of one
foot up and down the shin of the opposite leg) test
coordination and cerebellar function.
• Other tests include asking the patient to pronate and supinate
both hands rapidly and to do a shallow knee bend, first on
one leg and then on the other. Note dysarthria or slurred
speech because it is a sign of incoordination of the speech
muscles.
• Sensory System. Several modalities are tested in the somatic
sensory examination. Each modality is carried by a specific
ascending pathway in the spinal cord before it reaches the
sensory cortex.
• As a rule, perform the examination with the patient’s eyes
closed and avoid providing the patient with clues. Ask “How
does this feel?” rather than “Is this sharp?”
• Touch, Pain, and Temperature.
• Light touch is usually tested first using a cotton wisp or light pin prick.
• Gently touch each of the four extremities and ask the patient to indicate
when he or she feels the stimulus.
• Test pain by alternately touching the skin with the sharp and dull end of a
pin. Tell the patient to respond “sharp” or “dull.” Evaluate each limb
separately.
• Extinction is assessed by simultaneously touching both sides of the body
symmetrically. Normally, the simultaneous stimuli are both perceived
(sensed). An abnormal response occurs when the patient perceives the
stimulus on only one side. The other stimulus is “extinguished.”
• The sensation of temperature (only to be tested when the response to
deep pain is abnormal) can be tested by applying tubes of warm and cold
water to the skin and asking the patient to identify the stimuli with the
eyes closed. If pain sensation is intact, assessment of temperature
sensation may be omitted because both sensations are carried by the
same ascending pathways.
• Vibration Sense. Assess vibration sense by applying a vibrating
tuning fork to the fingernails and the bony prominences of the
hands, legs, and feet. Ask the patient if the vibration or “buzz” is
felt. Then ask the patient to indicate when the vibration ceases.
• Position Sense. Assess position sense (proprioception) by placing
your thumb and forefinger on either side of the patient’s
forefinger or great toe and gently moving his or her digit up or
down. Ask the patient to indicate the direction in which the digit is
moved.
• Another test of proprioception is the Romberg test. Ask the
patient to stand with feet together and then close his or her eyes.
If the patient is able to maintain balance with the eyes open but
sways or falls with the eyes closed (i.e., a positive Romberg test),
vestibulocochlear dysfunction or disease in the posterior columns
of the spinal cord may be indicated. Be aware of patient safety
during this test.
• Cortical Sensory Functions. Several tests evaluate cortical
integration of sensory perceptions (which occurs in the parietal
lobes).
• Assess two-point discrimination by placing the two points of a
calibrated compass on the tips of the fingers and toes. The
minimum recognizable separation is 4 to 5 mm in the fingertips
and a greater degree of separation elsewhere. This test is
important in diagnosing diseases of the sensory cortex and PNS.
• Graphesthesia (ability to feel writing on skin) is tested by having
the patient identify numbers traced on the palm of the hands.
• Stereognosis (ability to perceive the form and nature of objects) is
tested by having the patient close the eyes and identify the size
and shape of easily recognized objects (e.g., coins, keys, safety
pin) placed in the hands.
• Reflexes. Tendons have receptors that are sensitive to
stretch.
• A reflex contraction of the skeletal muscle occurs when the
tendon is stretched. In general, the biceps, triceps,
brachioradialis, and patellar and Achilles tendon reflexes are
tested.
• Initiate a simple muscle stretch reflex by briskly tapping the
tendon of a stretched muscle, usually with a reflex hammer.
• The response (muscle contraction of the corresponding
muscle) is measured as follows:
– 0/5 = absent,
– 1/5 = weak response
– 2/5 = normal response
– 3/5 = exaggerated response,
– 4/5 = hyperreflexia with clonus.
• Clonus, an abnormal response, is a continued rhythmic
contraction of the muscle with continuous application of the
stimulus.
• ASSESSMENT OF THE INJURED BRAIN
• The primary aim of managing patients with acute brain injury
in the critical care unit is to maintain cerebral perfusion and
oxygenation.
• Continuous monitoring of the central nervous system in the
ICU serves three functions:
• 1. determine the extent of the primary injury
• 2. early detection of secondary cerebral insults so that
appropriate interventions can be instituted
• 3. monitoring of therapeutic interventions to provide
feedback.
 Brain Imaging Techniques

• Computed tomography
• CT is the primary neuroimaging technique in the
initial evaluation of the acute brain injury patient and
uses a computer to digitally construct an image
based upon the measurement of the absorption of
X-rays through the brain.
• The advantages of CT are: (1) it is rapidly done, which is
especially important in neurological emergencies; (2) it clearly
shows acute and sub-acute hemorrhages into the meningeal
spaces and brain; and (3) it is less expensive than a MRI.
• Disadvantages include: (1) it does not clearly show acute or
sub-acute infarcts or ischemia, or brain edema, only
established injury; (2) it does not clearly differentiate white
from grey matter as clearly as an MRI; and (3) it exposes the
patient to ionizing radiation. Despite these limitations it is still
the most prevalent form of neurological imaging.
• Magnetic resonance imaging
• The tissues of the body contain proportionately large
amounts of protons in the form of hydrogen and function like
tiny spinning magnets. Normally, these atoms are arranged
randomly in relation to each other due to the constantly
changing magnetic field produced by the associated
electrons. Magnetic Resonance Imaging (MRI) uses this
characteristic of protons to generate images of the brain and
body.
• The advantages of MRI are: (1) it can be manipulated to
visualize a wide variety of abnormalities within the brain; and
(2) it can show a great deal of detail of the brain in normal
and abnormal states.
• The disadvantages of MRI are: (1) it does not show acute or
sub-acute hemorrhage into the brain in any detail; (2) the
time frame and enclosed space required to perform and
prepare a patient for the procedure is not advantageous for
neurological emergencies; (3) relatively more expensive
compared to CT; (4) the loud noise of the procedure needs to
be considered in the patient management; and (5) equipment
for life support and monitoring needs to be non-magnetic due
to the magnetic nature of the procedure
• Cerebral angiography
• Cerebral angiography involves cannulation of cerebral vessels
and the administration of intraarterial contrast agents and
medications for conditions involving the arterial circulation of
the brain. This procedure also has the benefit of using
non-invasive CT or MRI with or without contrast to guide the
accuracy of the procedure. For example, intracranial
aneurysms and arteriovenous malformations can be
accurately diagnosed and repaired without surgical
intervention.
• Cerebral perfusion imaging techniques
• The main imaging techniques dedicated to brain
hemodynamics are positron emission tomography (PET),
single photon emission computed tomography (SPECT),
xenon-enhanced computed tomography (XeCT), dynamic
perfusion computed tomography (PCT), MRI dynamic
susceptibility contrast (DSC) and arterial spin labelling (ASL).
All these techniques give similar information about brain
hemodynamics in the form of parameters such as CBF or CBV.
• Intracranial Pressure Monitoring
• Invasive measures for monitoring intracranial pressure (ICP)
are commonly used in patients with a severe head injury or
after neurological surgery.
• The normal ICP is 7–15 mmHg in a supine adult, 3–7 mmHg in
children, and 1.5–6 mmHg in term infants. The definition of
intracranial hypertension depends on the specific pathology
and age, although ICP >15 mmHg is generally considered to
be abnormal.
• Pulse waveforms
• Interpretation of waveforms that are generated by the
cerebral monitoring devices is important in the clinical
assessment of intracranial adaptive capacity (the ability of the
brain to compensate for rises in intracranial volume without
raising the ICP).
• Brain tissue pressure and ICP increase with each cardiac cycle
and, thus, the ICP waveform is a modified arterial pressure
wave.
• The cardiac waves reach the cranial circulation via the choroid
plexus and resemble the waveforms transmitted by arterial
catheters, although the amplitude is lower.
• There are three distinct peaks seen in the ICP waveform:61
• P1: the percussion wave, which is sharp and reflects the
cardiac pulse as the pressure is transmitted from the choroid
plexus to the ventricle;
• P2: the tidal wave, which is more variable in nature and
reflects cerebral compliance and increases in amplitude as
compliance decreases;
• P3: which is due to the closure of the aortic valve and is
known as the dicrotic notch. Of recent importance is that the
elevation of the P3 may indicate low global cerebral
perfusion.
• Assessment of Cerebral Perfusion
• Cerebral perfusion pressure is calculated as the
mean arterial pressure minus the intracranial
pressure (ICP) and represents the pressure
gradient across the vessel that drives cerebral
blood flow (CBF):
• CPP=MAP−ICP
• CPP is a pressure-based indicator of oxygen and
metabolite delivery. There is no evidence for the
optimum level of CPP, but 70–80 mmHg is
probably the critical
• ASSESSMENT OF CEREBRAL OXYGENATION
• Jugular Venous Oximetry
• Jugular venous catheterization is used for deriving oxygen
based variables.
• It facilitates the assessment of jugular venous oxygenation
(SjvO2), cerebral oxygen extraction (CEO2), and arteriovenous
difference in oxygen (AVDO2).
• All of these variables indicate changes in cerebral metabolism
and blood flow, and therefore the catheter generates
continuous data that reflect the balance between supply and
demand of cerebral oxygen.
• Microdialysis
• Cerebral microdialysis (using a catheter ideally placed in the
frontal lobe) is a tool for investigating the metabolic status of
the injured brain and is part of multimodal monitoring.
• The microdialysis probe is inserted into the cerebral tissue
where substances in the extracellular fluid surround the
semipermeable membrane at the tip of the catheter.
• Following equilibration of the tissue metabolites with the
perfusion fluid, the dialysate can be analyzed for
concentrations of products of energy metabolism (glucose,
lactate, pyruvate) as indicators of hypoxia and ischemia.
• Continuous Electroencephalography
• Electroencephalography (EEG) is the recording of electrical
activity by sensors along the scalp produced by the firing of
neurons within the brain.
• Continuous EEG (cEEG) has the advantage of being
continuous, noninvasive and carrying the potential to detect
alterations in brain physiology at a reversible stage, which
may trigger treatment before permanent brain injury occurs.
• Near-Infrared Spectroscopy
• Near-infrared spectroscopy (NIRS) is a non-invasive method of
monitoring continuous trends of cerebral oxygenated and
deoxygenated haemoglobin by utilising an infrared light beam
transmitted through the skull. Oxygenated and deoxygenated
haemoglobin have different absorption spectra and cerebral
oxygenation and hemodynamic status can be determined by
their relative absorption of near-infrared light. NIRS allows
interrogation of the cerebral cortex using reflectance
spectroscopy via optodes, light transmitting and detecting
devices, placed on the scalp. Normal saturation is 70%.
Neurological Alterations and
Management
• ALTERATIONS IN CONSCIOUSNESS
• In critical illness, impaired consciousness is often the first sign
of a severe pathological process. Consciousness is defined as
recognition of self and the environment, which requires both
arousal and awareness. There are different types of
depressed consciousness through to coma, the most severe
form of absolute unconsciousness.
• Altered Cognition and Coma
• Coma is a state of unresponsiveness from which the patient,
who appears to be asleep, cannot be aroused by verbal and
physical stimuli to produce any meaningful response;
therefore, the diagnosis of coma implies the absence of both
arousal and content of consciousness.1 Coma must be
considered a symptom with numerous causes, different
natural modes, and several management modes.
• Stupor is a state of unconsciousness from which the patient
can be awakened to produce inadequate responses to verbal
and physical stimuli.
• Somnolence is a state of unconsciousness from which the
patient can be fully awakened.
• Etiology of altered cognition
• Recently gained confusion, severe apathy, stupor or coma implies
dysfunction of the cerebral hemispheres, the diencephalon and/or the
upper brainstem.
• Focal lesions in supratentorial structures may damage both hemispheres,
or may produce swelling that compresses the diencephalic activating
system and midbrain, causing transtentorial herniation and brainstem
damage.
• Primary subtentorial (brainstem or cerebellar) lesions may compress or
directly damage the reticular formation anywhere between the level of
the midpons and, (by upward pressure), the diencephalon.
• Metabolic or infectious diseases may depress brain functions by a change
in blood composition or the presence of a direct toxin. Impaired
consciousness may also be due to reduced blood flow (as in syncope or
severe heart failure) or a change in the brain’s electrical activity (as in
epilepsy).
• Concussion, anxiolytic drugs and anesthetics impair consciousness without
producing detectable structural changes in the brain.
• Seizures
• A seizure is an uninhibited, abrupt discharge of ions from a
group of neurons resulting in epileptic activity.
• Seizures are classified depending on how they start as (a)
partial or focal seizures, (b) generalized or full body seizures
involving both cerebral hemispheres, or (c) partial seizures
with secondary generalization.
Etiology of seizures
• Seizures can be due to vascular, infectious, neoplastic,
traumatic, degenerative, metabolic, toxic or idiopathic causes.
• Factors influencing the development of posttraumatic
epilepsy include an early posttraumatic seizure, depressed
skull fracture, intracranial hematoma, dural penetration, focal
neurological deficit and posttraumatic amnesia (PTA) over 24
hours with the presence of a skull fracture or hematoma.
• Seizures in critically ill patients are most commonly due to
drug effects; metabolic, infectious or toxic disorders; and
intracranial mass lesions although they may be due to trauma
or neoplasm
• ALTERATIONS IN MOTOR AND SENSORY FUNCTION
• Alterations of motor and sensory function include skeletal
muscle weakness and paralysis. They result from lesions in
the voluntary motor and sensory pathways, including the
upper motor and sensory neurons of the corticospinal and
corticobulbar tracts, or the lower motor and sensory neurons
that leave the CNS and travel by way of the peripheral nerve
to the muscle and sensory receptors.
• Upper motor neuron lesions produce spastic
paralysis, and lower motor neuron lesions produce
flaccid paralysis. Damage to the upper motor and
sensory neurons of the corticospinal, corticobulbar
and spinothalamic tracts is a common component of
stroke.
• Lesions of the corticospinal and corticobulbar tracts: result in
weakness or total paralysis of predominantly distal voluntary
movement, Babinski’s sign (i.e. dorsiflexion of the big toe and
fanning of the other toes in response to stroking the outer
border of the foot from heel to toe), and often spasticity
(increased muscle tone and exaggerated deep tendon
reflexes).
• Disorders of the basal ganglia: (extrapyramidal disorders) do
not cause weakness or reflex changes.
• Their hallmark is involuntary movement (dyskinesia), causing
increased movement (hyperkinesias) or decreased movement
(hypokinesia) and changes in muscle tone and posture.
• Cerebellar disorders: cause abnormalities in the range, rate
and force of movement. Strength is minimally affected.
• Autonomic Nerve Dysfunction
• Dysfunctions of the autonomic nervous system (ANS) or
autonomic dysreflexia are recognised by the symptoms that
result from failure or imbalance of the sympathetic or
parasympathetic components of the ANS such as (i) increased
(>120/min) or decreased (<50/min) heart rate, (ii) increased
respiratory rate (>24/min), (iii) raised temperature (>38.5°C),
(iv) increased (>160 mmHg) or decreased (<85 mmHg) systolic
blood pressure, (v) increased muscle tone, (vi) decerebrate
(extensor) or decorticate (flexor) posturing, and (vii) profuse
sweating.
• ALTERATIONS IN CEREBRAL METABOLISM aND PERFUSION
• Impairment of cerebral metabolism has been attributed to
impaired oxygen delivery, mediated by reduced cerebral
perfusion in the swollen cerebral parenchyma.
• Cerebral Ischemia
• Ischemia is the inadequate delivery of oxygen, the inadequate
removal of carbon dioxide from the cell, and an increase in
the production of intracellular lactic acid.
• Ischemia can be caused by an increase in nutrient utilization
by the brain in a hyperactive state, a decrease in delivery
related to either cerebral or systemic complications, and/or a
mismatch between delivery and demand.
• Cerebral Edema
• Cerebral edema is defined as increased brain water content.
The brain is particularly susceptible to injury from edema,
because it is located within a confined space and cannot
expand, and because there are no lymphatic pathways within
the CNS to carry away the fluid that accumulates.
• The white matter is usually much more involved, as
myelinated fibres have a loose extracellular space, while the
grey matter has a much higher cell density with many
connections and much less loose extracellular space.
• The two main subdivisions of cerebral edema are extracellular
and intracellular.
• Intracellular (cytotoxic) oedema
• Cellular swelling, usually of astrocytes in the grey matter, is
generally seen after cerebral ischemia caused by cardiac
arrest or minor head injury. The blood–brain barrier (BBB) is
intact and capillary permeability is not impaired. The cause of
intracellular edema is anoxia and ischemia; it is usually not
clinically significant, and is reversible in its early phases.
• Extracellular (vasogenic) edema
• Extracellular edema involves increased capillary permeability,
and had been termed ‘BBB breakdown’.20 Rises in brain
water content with extracellular edema are often quite
dramatic, because the fluid that results from increased
capillary permeability is usually rich in proteins, resulting in
the spread of edema and brain ischemia. This can lead to
cytotoxic edema, and to the progressive breakdown of both
astrocytes and neurons. Ultimately, these changes can lead to
raised intracranial pressure and herniation.
• Hydrocephalus
• Hydrocephalus is the result of an imbalance between the
formation and drainage of cerebrospinal fluid (CSF). Reduced
absorption most often occurs when one or more passages
connecting the ventricles become blocked, preventing
movement of CSF to its drainage sites in the subarachnoid
space just inside the skull. This type of hydrocephalus is called
‘non-communicating’. Reduction in absorption rate, called
‘communicating hydrocephalus’ can be caused by damage to
the absorptive tissue.
• Hydrocephalus may be caused by: congenital brain defects;
hemorrhage, in either the ventricles or the subarachnoid
space; CNS infection (syphilis, herpes, meningitis, encephalitis
or mumps); and tumors.
• Irritability is the commonest sign of hydrocephalus in infants
and, if untreated, may lead to lethargy. Bulging of the
fontanel, the soft spot between the skull bones, may also be
an early sign. Hydrocephalus in infants prevents fusion of the
skull bones, and causes expansion of the skull.
• Symptoms of normal pressure hydrocephalus include
dementia, gait abnormalities and incontinence.
• Treatment includes ventriculostomy drainage of CSF in the
short term, or a surgical shunt for those with chronic
conditions. Either is predisposed to blockage and infection.
• Intracranial Hypertension
• Intracranial pressure is the pressure exerted by the contents
of the brain within the confines of the skull and the BBB. The
Munro–Kelly hypothesis states that the contents of the
cranium (60% water, 40% solid) are not compressible and
thus an increase in volume causes a rapid rise in pressure and
changes to the comensatory reserve and pulse amplitude.
• Normal ICP is 0–10 mmHg, and a sustained pressure of >15
mmHg is termed intracranial hypertension, with implications
for CBF. Areas of focal ischemia appear when ICP is >20
mmHg and global ischemia occurs at >50 mmHg.
 NEUROLOGICAL THERAPEUTIC
MANAGEMENT
• OPTIMISING CEREBRAL PERFUSION AND OXYGENATION
• Intracranial hypertension and cerebral ischemia are the two
most important secondary injury processes that can be
anticipated, monitored and treated in the ICU.
• Management of Intracranial Hypertension
• Raised ICP is treated by removing mass lesions and/or
increasing the volume available for expansion of injured
tissue. This may be achieved by reducing one of the other
available intracranial fluid volumes:
• 1. CSF by ventricular drainage (as discussed previously)
• 2. cerebral blood volume by hyperventilation, osmotic
diuretic therapy or hypothermia
• 3. brain tissue water content by osmotic diuretic therapy
• 4. removing swollen and irreversibly injured brain
• 5. increasing cranial volume by craniotomy decompression.
• Hyperventilation
• Hyperventilation reduces PaCO2 and will reduce ICP by
vasoconstriction induced by alkalosis but it also decreases
cerebral blood flow. The fall in ICP parallels the fall in CBV.
Hyperventilation decreases regional blood flow to
hypoperfused areas of the brain. Thus, generally PaCO2
should be maintained in the low normal range of about 35
mmHg. Hyperventilation should be utilised only when ICP
elevations are refractory to other methods and when brain
tissue oxygenation is in the normal range. The BTF Guidelines
recommend hyperventilation therapy only for brief periods
when there is no neurological deterioration or for longer
periods when ICP is refractory to other therapies
• Osmotherapy
• Acute administration of an osmotic such as mannitol or
hypertonic saline produces a potent antioedema action,
primarily on undamaged brain regions with an intact BBB. This
treatment causes the movement of water from the interstitial
and extracellular space into the intravascular compartment,
thereby improving intracranial compliance or elastance. In
addition to causing ‘dehydration’ of the brain, osmotic agents
have been shown to exert beneficial non-osmotic cerebral
effects, such as augmentation of cerebral blood flow (by
reducing blood viscosity, resulting in enhanced oxygen
delivery), free radical scavenging, and diminishing CSF
formation and enhancing CSF reabsorption
• Normothermia
• Hyperthermia occurs in up to 40% of patients with ischemic stroke and
intracerebral hemorrhage and in 40–70% of patients with severe TBI or
aneurysmal subarachnoid haemorrhage.
• Hyperthermia is independently associated with increased morbidity and
mortality after ischemic and hemorrhagic stroke, and in subarachnoid
hemorrhage and TBI patients temperature elevation has been linked to
raised intracranial pressure. Temperature elevations as small as 1–2°C
above normal can aggravate ischemic neuronal injury and exacerbate
brain edema.
• Mild hypothermia protects numerous tissues from damage during
ischemic insult. The use of paracetamol, cooling blankets, ice packs,
evaporative cooling and new cooling technologies may be useful in
maintaining normothermia.
• Hyperemia (increased blood flow) may occur during rewarming, resulting
in acute brain swelling and rebound intracranial hypertension.
• Maintenance of body temperature at 35°C may be optimal.
• Corticosteroids
• Excessive inflammation has been implicated in the
progressive neurodegeneration that occurs in multiple
neurological diseases, including cerebral ischemia.
• The efficacy of glucocorticoids is well established in
ameliorating edema associated with brain tumors and in
improving the outcome in subsets of patients with bacterial
meningitis.
• Barbiturates and sedatives
• The BTF Guidelines state that high-dose barbiturate therapy
may be considered in haemodynamically salvageable severe
TBI patients with intracranial hypertension refractory to
maximal medical and surgical interventions.
• The utilization of barbiturates for the prophylactic treatment
of ICP has not been indicated.
• Barbiturates exert cerebral protective and ICP-lowering
effects through alteration in vascular tone, suppression of
metabolism and inhibition of free radical-mediated lipid
peroxidation.
• Barbiturates may effectively lower cerebral blood flow and
regional metabolic demands.
• The lower metabolic requirements decrease cerebral blood
flow and cerebral volume.
• Surgical interventions
• The European TBI Guidelines suggest that operative
management
• be considered for large intracerebral lesions
• within the first four hours of injury. The use of unilateral
• craniectomy after the evacuation of a mass lesion, such
• as an acute subdural haematoma or traumatic intracerebral
• haematoma, is accepted practice. Surgery is also
• recommended for open compound depressed skull
fractures
• that cause a mass effect
• CENTRAL NERVOUS SYSTEM DISORDERS
• CNS disorders include brain and/or spinal
injury from trauma, infection or immune
conditions.
• TRAUMATIC BRAIN INJURY
• Head injury is a broad classification that includes injury to the
scalp, skull or brain.
• Traumatic brain injury (TBI) is the most serious form of head
injury. The range of severity of TBI is broad, from concussion
through to post coma unresponsiveness
• Etiology
• Motor vehicle-related trauma accounts for about
two-thirds of moderate and severe TBI, with falls and
assaults being the next most common causes.
 Pathophysiology of TBI
• The mechanisms of injury forces inflicted on
the head in TBI produce a complex mixture of
diffuse and focal lesions within the brain
• Damage resulting from an injury can be
immediate (primary) or secondary in nature.
• Secondary injury results from disordered auto
regulation and other pathophysiological
changes within the brain in the days
immediately after injury.
• Focal injury
• Because of the shape of the inner surface of
the skull, focal injuries are most commonly
seen in the frontal and temporal lobes, but
they can occur anywhere.
• Diffuse injury
• Diffuse (axonal) injury (DAI) refers to the shearing of axons and
supporting neuroglia; it may also traumatise blood vessels and can
cause petechial haemorrhages, deep intracerebral haematomas
and brain swelling.
• DAI results from the shaking, shearing and inertial effects of a
traumatic impact. Mechanical damage to small venules as part of
the BBB can also trigger the formation of haemorrhagic
contusions. This vascular damage may increase neuronal
vulnerability, causing post-traumatising perfusion deficits and the
extravasation of potentially neurotoxic blood-borne substances.
• The most consistent effect of diffuse brain damage, even when
mild, is the presence of altered consciousness
• Skull fractures
• Skull fractures are present on CT scans in about twothirds of
patients after TBI. Skull fractures can be linear, depressed or
diastatic, and may involve the cranial vault or skull base. In
depressed skull fractures the bone fragment may cause a
laceration of the dura mater, resulting in a cerebrospinal fluid
leak.
• Basal skull fractures include fractures of the cribriform plate,
frontal bones, sphenoid bones, temporal bone and occipital
bones.
• The clinical signs of a basal skull fracture may include: CSF
otorrhoea or rhinorrhoea, haemotympanum, postauricular
ecchymoses, periorbital ecchymoses, and injury to the cranial
nerves: VII (weakness of the face), VIII (loss of hearing), olfactory
(loss of smell), optic (vision loss) and VI (double vision).
• Nursing Practice
• The surveillance and prevention of secondary
injury is the key to improving morbidity and
mortality outcomes.
 SPINAL CORD TRAUMA

• SCI occurs three times more often in men, and the incidence
among those aged 15–34 years is roughly double the rate in
those 35 years and over. More than half of the SCIs are due
to vehicular trauma and a quarter due to motorcycle crashes.
Falls account for nearly a third of the injuries, with nearly half
occurring in older people.
• Recreational and sporting injuries account for 15% of SCI, and
19% are work-related. Of all SCI cases, 51% resulted in
complete tetraplegia (loss of function in the arms, legs, trunk
and pelvic organs). The predominant risk factors for SCI
include age, gender, and alcohol and drug use.
• The vertebrae most often involved in SCI are the 5th, 6th and
7th cervical (neck), the 12th thoracic, and the 1st lumbar.
These vertebrae are the most susceptible because there is a
greater range of mobility in the vertebral column in these
areas.
• Damage to the spinal cord ranges from transient concussion
or stunning (from which the patient fully recovers) to
contusion, laceration and compression of the cord substance
(either alone or in combination), to complete transection of
the cord (which renders the patient paralysed below the level
of the injury).
• Mechanisms of Injury
• Cervical injury can occur from both blunt and
penetrating trauma but in reality is a
combination of different mechanisms of
acceleration and deceleration with and
without rotational forces and axial loading
 Cervical trauma is produced by a combination of these
mechanisms as listed below

• l Hyperflexion: These injuries usually result from forceful decelerations

and are often seen in patients who have sustained trauma from a head-on
motor vehicle collision (MVC) or diving accident. The cervical region is
most often involved, especially at the C5–C6 level.
• l Vertical compression or axial loading: This typically occurs when a person
lands on the feet or buttocks after falling or jumping from a height. The
vertebral column is compressed, causing a fracture that result in damage
to the spinal cord.
• l Hyperextension: This is the most common type of injury. Hyperextension
injuries can be caused by a fall, a rear-end MVC, or hit on the head (e.g.
during a boxing match). Hyperextension of the head and neck may cause
contusion and ischaemia of the spinal cord without vertebral column
damage. Whiplash injuries are the result of hyperextension. Violent
hyperextension with fracture of the pedicles of C2 and forward movement
of C2 on C3 produces the ‘Hangman’s fracture’.
• Extension–rotation: Rotational injuries result from forces that
cause extreme twisting or lateral flexion of the head and
neck. Fracture or dislocation of vertebrae may also occur. The
spinal canal is narrower in the thoracic segment relative to
the width of the cord, so when vertebral displacement occurs
it is more likely to damage the cord. Until the age of , the
spine has increased physiological mobility due to lax
ligaments, which affords some protection against acute SCI.
Elderly patients are at a higher risk due to osteophytes and
narrowing of the spinal canal.
• Classification of Spinal Cord Injuries
• SCIs can be broadly classified as complete or incomplete.
• The diagnosis of complete SCI cannot be made until spinal
cord shock resolves. If the bulbocavernosus reflex (BCR) is
present (involuntary contraction of the rectal sphincter after
squeezing the glans penis or clitoris or tugging on an
indwelling urinary catheter) it indicates a complete injury.
• If, after the return of the BCR, the patient has some sensation
below the level of injury, he/she is considered to be
sensory-incomplete.
• If the BCR has returned and the patient has some motor
function and sensation below the level of injury, he/she is
considered to be sensory- and motor-incomplete.
 There are four incomplete SCI syndromes as follows:
• Anterior cord syndrome: Injury to the motor and sensory
pathways in the anterior parts of the spine; thus patients are
able to feel crude sensation, but movement and detailed
sensation are lost in the posterior part of the spinal cord.
Clinically, the patient usually has complete motor paralysis
below the level of injury (corticospinal tracts) and loss of
pain, temperature, and touch sensation (spinothalamic
tracts), with preservation of light touch, proprioception and
position sense. The prognosis for anterior cord syndrome is
the worst of all the incomplete syndrome prognoses.
• Posterior cord syndrome: This is usually the result of a
hyperextension injury at the cervical level and is not
commonly seen. Position sense, light touch and vibratory
sense are lost below the level of the injury.
• Central cord syndrome: Injury to the center of the cervical spinal
cord, producing weakness, paralysis and sensory deficits in the
arms but not the legs. Hyperextension of the cervical spine is
often the mechanism of injury, and the damage is greatest to the
cervical tracts supplying the arms. Clinically, the patient may
present with paralyzed arms but with no deficit in the legs or
bladder.
• Brown-Séquard syndrome: This involves injury to the left or right
side of the spinal cord. Movements are lost below the level of
injury on the injured side, but pain and temperature sensation are
lost on the opposite side of injury. The clinical presentation is one
in which the patient has either increased or decreased cutaneous
sensation of pain, temperature and touch on the same side of the
spinal cord at the level of the lesion. Below the level of the lesion
on the same side, there is complete motor paralysis. On the
patient’s opposite side, below the level of the lesion, there is loss
of pain, temperature and touch, because the spinothalamic
tracts cross soon after entering the cord.
 Pathophysiology
• SCIs can be separated into two categories: primary injuries
and secondary injuries.
• Primary injuries are the result of the initial insult or trauma,
and are usually permanent. The force of the primary insult
produces its initial damage in the central grey matter of the
cord.
• Secondary injuries are usually the result of a contusion or
tear injury, in which the nerve fibers begin to swell and
disintegrate. Secondary neural injury mechanisms include
ischemia, hypoxia and edema
• Ischemia, the most prominent post-SCI event, may occur up to 2
hours post-injury and is intensified by the loss of auto regulation
of the spinal cord microcirculation This will decrease blood flow,
which is then dependent on the systemic arterial pressure in the
presence of hypotension or vasogenic spinal shock.
• Edema develops at the injured site and spreads into adjacent
areas.
• Hypoxia may occur as a result of inadequate airway maintenance
and ventilation. Immune cells, which normally do not enter the
spinal cord, engulf the area after a spinal cord injury and release
regulatory chemicals, some of which are harmful to the spinal
cord. Highly reactive oxidizing agents (free radicals) are produced,
which damage the cell membrane and disrupt the
sodium–potassium pump. Free-radical production and lipid
peroxidation lead to vasoconstriction, increased endothelial
permeability and increased platelet activation.
• Spinal shock occurs with physiological or anatomical
transection or near-transection of the spinal cord; it occurs
immediately or within several hours of a spinal cord injury
and is caused by the sudden cessation of impulses from the
higher brain centers.
• It is characterized by the loss of motor, sensory, reflex and
autonomic function below the level of the injury, with
resultant flaccid paralysis.
• Loss of bowel and bladder function also occurs
• The body’s ability to control temperature (poikilothermia) is
lost and the patient’s temperature tends to equilibrate with
that of the external environment.
• Neurogenic spinal shock occurs as a result of mid-
tupper-level cervical injuries and is the result of sympathetic
vascular denervation and peripheral vasodilation.
• The loss of spinal cord vasculature autoregulation occurs,
causing the blood flow to the spinal cord to be dependent on
the systemic blood pressure. Signs and symptoms include
hypotension, severe bradycardia, and loss of the ability to
sweat below the level of injury.
 Systemic effects of spinal cord injury
• The traumatic insult causing the spinal cord injury is
associated with an immediate stimulation of central and
peripheral sympathetic tone.
• Initially, the elevated sympathetic activity raises systemic
arterial blood pressure and induces cardiac arrhythmias.
• At the stage of spinal shock with loss of neuronal conduction,
the sympathetic excitation is closely followed by decreases in
systemic vascular resistance, arterial hypotension and venous
pooling..
• Spinal cord injury may produce respiratory failure.
• Injuries above the level of C4–C5 produce complete paralysis
of the diaphragm, with substantial decreases in tidal volume
and consecutive hypoxia.
• With lesions below C6, the function of the diaphragm is
maintained and there is incomplete respiratory failure due to
paralyzed intercostal and abdominal musculature.
• As a consequence, arterial hypoxia and
• hypercapnia occur, both of which promote neuronal and glial
acidosis, edema and neuroexcitation.
• Nursing Practice
• Spinal cord injury should be suspected in patients with neck
pain, sensory and motor deficits, unconsciousness,
intoxication, spondylitis or rheumatoid arthritis, head injury
and facial fractures.
• If spinal cord injury is suspected or cannot be excluded, the
patient must be placed on a spine board with the head and
neck immobilized in a neutral position using a rigid collar to
reduce the risk of neurological deterioration from repeated
mechanical insults.
• Spinal injury patients are susceptible to pressure insults, so
time must be considered when hard surfaces are used for
immobilization. Total neck immobilization should not
interfere with maintenance of the airway, and inadequate
respiratory function must be avoided
• Resuscitation
• Initial treatment aims for decompression of the spinal cord and reversal of
neurogenic shock and respiratory failure.
• Spinal shock is associated with decreases in systemic vascular resistance,
arterial hypotension, venous pooling, severe bradycardia and decreased
myocardial contractility.
• Treatment of neurogenic shock includes fluid replacement using
crystalloid or colloid solutions to maintain arterial blood pressure,
circulatory volume, renal function and tissue oxygenation.
• Infusion of free water must be avoided, as this decreases plasma
osmolarity and promotes spinal cord edema.
• Atropine may be administered to reverse bradycardia and increase cardiac
output. Administration of vasopressors (e.g. noradrenaline) prior to
correction of the intravascular volume status may increase systemic
vascular resistance (left ventricular afterload) and further impair
myocardial contractility.
• Therefore, volume replacement is the first step, and
administration of vasopressors the second step in the
treatment of arterial hypotension and low cardiac output
after acute cervical spinal cord injury.
• The major early cause of death in patients with acute cervical
SCI is respiratory failure. Tracheal intubation may be indicated
in unconscious patients, during shock, in patients with other
major associated injuries, and during cardiovascular and
respiratory distress. It is also indicated in conscious patients
presenting with the following criteria: maximum expiratory
force below +20 cmH2O, maximum inspiratory force below
−20 cmH2O, vital capacity below 1000 mL, and presence of
atelectasis, contusion and infiltrate.
• Investigations and alignment
• Following the initial assessment of the patient, detailed
diagnostic radiography defines the bone damage and
compression of the spinal cord.
• Collaborative Management
• Patients with acute cervical spinal cord injury require ICU
monitoring, observation and support of ventilation, a
nasogastric tube to reduce abdominal distension and risk of
aspiration, a urinary catheter and thermal maintenance.
• Tracheostomy is indicated in high cervical spine injury and
ischemia,
• Spinal alignment and immobilization requires careful
positioning with dedicated neck support by experienced
clinicians.
• l Shoulder and lumbar support pillows are often prescribed.
Pressure-relief mattresses must be suitably designed for spine
immobilization and when prescribed can be tilted to facilitate
ventilation.
• l Meticulous integument and bowel care are indicated with
daily protocols for regular stool softeners and peristaltic
stimulants essential for the prevention of autonomic
dysreflexia and autonomic nerve dysfunction.
• Early nutritious feeding is essential, whether oral or enteric; however,
aspiration must be prevented. The supplementation of feeding with
high-energy protein fluids to match the catabolic state assists with
recovery
• Hyperglycaemia is associated with increased inflammation and must be
controlled to less than 10 mmol/Hg, avoiding hypoglycaemia.
• The concept of pain relief and sedation in patients with spinal cord injury
is based on the maintenance of coupling between metabolism and spinal
cord blood flow while achieving hypnosis, analgesia and a ‘relaxed cord’.
This concept includes maintenance of normal to high systemic perfusion
pressures, normoxia and normocapnia.
• Psychological and empathetic support is essential and appropriate referral
for grieving and stress is paramount. Rehabilitation counselling and
planning starts at the acute stage in order to give the family unit some
future focus and hope.
• CEREBROVASCULAR DISORDERS
• Cerebral vascular disorders include cerebrovascular disease
and cerebral vascular accidents (stroke). A stroke (acute brain
injury of vascular origin) may be either ischemic or
hemorrhagic and is defined as an interruption of the blood
supply to any part of the brain, resulting in damaged brain
tissue.
• Etiology
• Hypertension is the leading risk factor for stroke.
• Other risk factors include diabetes, cardiac disease, previous
cerebrovascular disease (transient ischemic attack or stroke or
myocardial infarction), age, sex, lipid disorders, excessive ethanol
ingestion, elevated haematocrit, elevated fibrinogen and cigarette
smoking. Cerebral arteriosclerosis predisposes individuals to both
ischaemic and hemorrhagic stroke.
• Smoking is the strongest risk factor for aneurysmal SAH.
• Atrial fibrillation, endocarditis and medications containing
supplemental estrogen are risk factors for embolic stroke.
• Seizures develop in approximately 10% of cases, usually appearing
in the first 24 hours and more likely to be focal than generalized.
• Most patients with aphasia will have a cerebral infarction in the
distribution of the left middle cerebral artery
• Ischaemic Stroke
• Ischemic stroke compromises blood flow and energy supply to the
brain, which triggers mechanisms that lead to cell death.
• Infarction occurs rapidly in the region of most severe ischemia
(termed ischemic penumbra) and expands at the expense of the
surrounding hypoxic tissue, from the center to the periphery.
• Therapeutic strategies in acute ischemic stroke are based on the
concept of arresting the transition of the penumbral region into
infarction, thereby limiting ultimate infarct size and improving
neurological and functional outcome. Ischemic stroke can be
further categorized as middle cerebral artery occlusion, acute
basilar occlusion, and cerebellar infarcts
• The management of an ischemic stroke comprises four
primary goals: restoration of cerebral blood flow
(reperfusion), prevention of recurrent thrombosis,
neuroprotection, and supportive care.
• Haemorrhagic Stroke
• Hemorrhagic strokes are caused by bleeding into the
brain tissue, the ventricles or the subarachnoid space.
• Primary intracerebral hemorrhage from a spontaneous
rupture of small vessels accounts for approximately 80%
of hemorrhagic strokes and is primarily caused by
uncontrolled hypertension.
• Secondary intracerebral hemorrhage is associated with
arteriovenous malformations (AVMs), intracranial
aneurysms, or certain medications (e.g. anticoagulants
and amphetamines).
• Symptoms are produced when an aneurysm or arteriovenous
malformation (AVM) enlarges and presses on nearby cranial
nerves or brain tissue or, more dramatically, when a blood
vessel, aneurysm or AVM ruptures, causing intracerebral or
subarachnoid hemorrhage.
• When an aneurysm ruptures, arterial pressure forces blood
into the subarachnoid space between the arachnoid mater
and the surface of the brain. Free blood then travels through
the fissures into the basal cisterns and across the surface of
the brain.
• When clotted, this blood can interfere with the circulation
and reabsorption of cerebrospinal fluid (CSF), potentially
causing obstructive hydrocephalus and raised intracranial
pressure.
• The commonest cause is a leaking aneurysm in the
area of the circle of Willis or a congenital AVM of the
brain. Blood in the subarachnoid space is a powerful
meningeal irritant, and it is this irritation that causes
most of the initial signs and symptoms of SAH.
• In intracerebral hemorrhage the bleeding is usually
arterial and occurs most commonly in the cerebral
lobes, basal ganglia, thalamus, brainstem (mostly the
pons) and cerebellum.
• Normal brain metabolism is disrupted by the brain being
exposed to blood. The sudden entry of blood into the
subarachnoid space or brain parenchyma results in a rise in
ICP, which then leads to compression and ischaemia resulting
from the reduced perfusion pressure and vasospasm that
often accompany intracerebral and subarachnoid
haemorrhage.
• Depending on the severity, clinical findings include severe
headache, nuchal rigidity, photophobia, nausea and vomiting,
hypertension, ECG changes, pyrexia, cranial nerve deficits,
visual changes, sensory or motor deficits, fixed and dilated
pupils, seizures, herniation and sudden death.
• Subarachnoid Haemorrhage
• Admission to ICU is indicated for subarachnoid haemorrhage
Hunt-Hess SAH severity Scale III (see Table 17.5) and greater
to manage systemic complications, recognize and treat
clinical deterioration, investigate the cause of the
haemorrhage and to treat any underlying aneurysm or
arteriovenous malformation.
• Resuscitation is directed towards maintaining cerebral
perfusion pressure by ensuring adequate arterial blood
pressure (often with the use of inotropes to produce relative
hypertension although reactive hypertension is often
present), ensuring a relatively high circulating blood volume
(hypervolaemia), and producing relative haemodilution
(’triple H therapy’).
• Hypovolaemia occurs in 30–50% of patients, as does excessive
hyponatraemia in 30% of patients. In the first six days, plasma
volume decreases of greater than 10% can occur following
SAH, thus increasing the risk of vasospasm and ischaemia.
Women have been found to have more significant drops in
blood volume than men following SAH. ‘Third space’ loss,
insensible losses and blood loss account for this drop in fluid
volume, as well as electrolyte disturbances.
• ICP monitoring and drainage of CSF via ventriculostomy is indicated in SAH
but not in cerebral haemorrhage.
• SAH causes increased sympathetic activation from the presence of
haemoglobin in the subarachnoid space. This results in elevated
catecholamine levels, which may result in focal myocardial necrosis,
explaining the presence of inverted T waves, ST depression, prominent U
waves, and Q-T intervals in more than 50% of patients.
• As cardiac function is one of the determinants for adequate cerebral blood
flow, it is essential to identify such occurrences early and treat them
accordingly.
• Hyponatraemia occurs from alterations in atrial natriuretic factor (ANF) in
response to sympathetic nervous system activation. The syndrome of
inappropriate secretion of antidiuretic hormone (SIADH) is primarily
responsible for hyponatraemia in those with SAH, as is cerebral
salt-wasting syndrome; however, both mechanisms are still relatively
misunderstood
• Collaborative Management of Stroke
• Expected outcomes for patients with acute ischaemic and
haemorrhagic stroke include prevention of secondary injury,
of airway and respiratory complications, and the maintenance
of haemodynamic stability.
• Timely assessment and intervention is paramount in the
management of ischaemic stroke, especially regarding
interventional pharmacology and prevention of cerebral
haemorrhage.
• Atrial fibrillation and deep vein thrombosis (DVT) prevention
(in ischaemic stroke) requires anticoagulation control. In
haemorrhagic stroke, sequential compression device and
stockings are indicated for DVT prophylaxis as anticoagulants
are a risk factor for rebleeding. Maintenance of bowel and
bladder function and prevention of integument
complications, malnutrition, seizures and increasing
neurological deficits are important goals. Environmental
precautions are implemented to provide a non-stimulating
environment, preventing rises in ICP and further bleeding.
• Sensory perceptual and motor alterations need to be
assessed in regard to effective communication and pain
management. Rehabilitation and psychological support for
the patient and significant others are integrated into the
acute care phase for a smooth transition.