Transcript No Slide Title

Neurological Systems
Mary Roche, RN, MSN, CS
Community College
of Rhode Island
July 17, 2015
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Credits
All materials for this presentation are based on:
Medical-Surgical Nursing Across the Health Care Continuum by
Ignatavicius, Workman, and Mishler - Volume 2 - 3rd Edition W.B. Saunders Company - 1991
This presentation was built for and is the copyrighted property of Mary
Roche, RN.
This presentation is publicly available for viewing under the Web
Developments section at http://www.stacyhouse.com
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Goals of this Course
Following attendance at this series of lectures, you should be:
– Familiar with the nomenclature and functions of the nervous system,
– In possession of a viable summary of the course textbook,
– Empowered to find information in a timely fashion, and
– Prepared to initiate nursing practice in neurological situations.
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Anatomy and Physiology Review
The nervous system is the basis for all human function. It is the center
of thinking, memory, judgment, sensation, movement, cognition,
communication, behavior, and personality.
In addition to its direct control over many processes, the nervous
system innervates many other body systems.
The major divisions of the nervous system are the Central Nervous
System and the Peripheral Nervous System.
The brain and spinal cord are the major components of the Central
Nervous System.
The Peripheral Nervous System is composed of 12 pairs of cranial
nerves, 1 pairs of spinal nerves and the autonomic nervous system.
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Anatomy and Physiology Review
Neurons
The Neuron Is the Basic Unit of the Nervous System.
When a neuron receives an impulse from another neuron, the effect may be excitation
or inhibition.
Neurons Function to Transmit Impulses.
Sensory – facilitate sensation.
Motor – facilitate movement.
Some process information; some retain information
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Anatomy and Physiology Review
Structure
Each neuron has a cell body, a short branching process called a dendrite and a
single axon.
Each dendrite synapses with another cell body, axon or dendrite.
Axons are covered by a myelin sheath.
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Anatomy and Physiology Review
Pathways
Dendritic process is called afferent pathway.
Axonic process is called efferent pathway.
Also called white matter.
Non-myelinated – gray matter.
Nodes of Ranvier – gaps in the myelin.
Terminal knob – large distal end of each axon.
Within the synaptic knobs are mechanisms for manufacturing, storing, and
releasing a transmitter substance.
Each neuron produces a specific substance. Either enhances or inhibits
impulses.
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Anatomy and Physiology Review
Nerve Impulse Conduction
Mechanism for nerve impulse conduction – the sodium and chloride ions.
Sodium and chloride are heavily concentrated outside the cell.
Intracellular concentration of potassium
Due to these different concentrations – a neuron is always charged.
Via stimulus – polarity changes = depolarization.
Proteins function as gates and open to either potassium or sodium (NOT
BOTH).
Sodium in – potassium out; then repolarization with sodium being actively
pumped back out. In the membranes this occurs as an action potential.
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Anatomy and Physiology Review
Synapse
Neuron to neuron / Muscle to muscle
Factors affecting transmission:
Strength of the stimulus
Inadequate supply of substance
Cerebrospinal Fluid (CSF) changes
Lack of oxygen
Acidosis/alkalosis
Drugs
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See Table 43-1,
page 993
Anatomy and Physiology Review
Transmitters
Chemical substances that enhance or inhibit nerve conduction.
Amines:
Acetylcholine
Brain, brain stem, basal ganglia, ANS
Nerve and muscle transmission.
Parasympathetic and preganglionic systems.
Excitatory, but some inhibitory.
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Anatomy and Physiology Review
Transmitters
Gamma-aminobutyric acid (GABA)
Brain, brain stem, Nerve and muscle basal ganglia, spinal cord,
cerebellum Possibly one-third of brain neurons.
Inhibitory.
Histamine / Serotonin
Brain, spinal cord, PNS Medial brain stem, hypothalamus, dorsal horn of
spinal cord.
Possible onset of sleep, mood control, pain pathway inhibitor.
Inhibitory.
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Anatomy and Physiology Review
Transmitters
Catecholamines:
Dopamine
Substantia nigra to basal ganglia. Complex movement, emotional response
regulation, attention.
Usually inhibitory.
Norepinephrine
Hypothalamus, brain stem, reticular formation, cerebellum, sympathetic
nervous system. Maintenance of arousal, reward system, dreaming sleep,
mood regulation.
Mainly excitatory.
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Anatomy and Physiology Review
Transmitters
Amino Acids:
Aspartic acid
Brain, spinal cord interneurons
Sensation.
Excitatory.
Glutamic acid
Sensory pathways
Sensation
Excitatory.
Glycine
Spinal cord interneurons Muscle control.
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Inhibitory.
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Anatomy and Physiology Review
Transmitters
Polypeptides:
Substance P
Brain, neurons in spinal cord
Pain transmission
Excitatory
Endorphins, enkephalins
Brain, neurons in spinal cord
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Pain transmission
Excitatory
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Anatomy and Physiology Review
Glial Cells
Glial cells – two main classes: Microglia and Macroglia
Microglia cells respond to infections or trauma in CNS.
Macroglia Cells are divided into four subsets:
Astroglia (star-shaped) cells provide physical support for neurons,
regulate chemical environment, nourish.
Oligodendrocyte and Schwann cells – form the myelin sheath.
Ependymal cells for lining of ventricles of the spinal cord. Also part
of blood-brain barrier.
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Central Nervous System
Central Nervous System
Components
Brain - directs regulation and function of the nervous system and other
systems of the body.
Spinal Cord - initiates reflex activity and transmits impulses to and
from the brain.
Cranium And Vertebral Column - Brain and spinal cord are
encased, respectively, in cranium and vertebral column.
Vertebrae - 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral, fused
coccygeal.
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Central Nervous System
The Brain
Meninges - form the immediate protective covering of the brain and
spinal cord.
• Pia Mater - thin, delicate and vascular membrane. Adheres to the
brain and spinal cord.
• Arachnoid - the next layer which is thin, delicate and fibrous. CSF
fills tissue.
• Dura Mater - The outer layer which is heavy, fibrous, nonelastic.
Subarachnoid - situated between arachnoid and pia mater is
subarachnoid space where CSF circulates.
Venous sinuses are between two layers of dura.
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Central Nervous System
Cerebrum
Lobes and Ventricles
Two hemispheres. Right and left lobes joined by corpus callosum.
Dominant hemisphere for most people is the left hemisphere.
Within the cerebrum are the right and left lateral ventricles.
Cerebral Cortex
Cerebral cortex divided into lobes by sulci and are named the same as
the overlying bones.
Speech Areas: Wernicke’s and Broca’s areas: higher brain functions
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Table 43-2,
Page 994
Central Nervous System
Brain Lobe Functions
Primary motor area. Broca’s speech center. Eye field, access
to current sensory data. Access to past info. Affective response. Behavior.
Judgment. Ability to develop long-term goals and to weigh pros and cons.
Frontal Lobe
Parietal Lobe
Understand sensation, texture, size, shape, and spatial
relations. Playing musical instruments. Processing nonverbal visual experiences.
Perception of body parts and body position awareness. Taste impulses for
interpretation.
Temporal Lobe Auditory center for sound interpretation. Complicated
memory patterns. Wernicke’s area for speech.
Occipital Lobe
Primary visual center.
Limbic Lobe
Emotional and visceral patterns connected with survival.
Learning and memory.
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Central Nervous System
Brain
Diencephalon - lies below the cerebrum and includes:
Thalamus – the ‘central switchboard’ for the CNS
Hypothalamus - intellectual function
Epithalamus - controls pineal gland
Hypophysis (pituitary gland) – situated in the sella turcica of the
ethmoid bone and is connected to the hypothalamus by the
hypophyseal stalk.
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Central Nervous System
Brain Stem
Midbrain
Contains the cerebral aqueduct or aqueduct of Sylvius. Location of periaqueductal
gray, which, when stimulated, may abolish pain. Cranial nerve nuclei III
(oculomotor) and IV (trochlear) located here
Pons
Cardiac acceleration and vasocontriction centers - pneumotaxic center helps
control respiration pattern and rate. - Four cranial nerves originate from the pons:
V (trigeminal), VI (abducens), VII (facial), and VIII (acoustic)
Medulla
Cardiac-slowing center - Respiratory center - Cranial nerves IX
(glossopharyngeal), X (vagus), XII (spinal accessory), and XII (hypoglossal) and
portions of VII (facial) and VIII (acoustic) emerge from the medulla
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Table 43-3,
Page 995
Central Nervous System
Diencephalon Functions
Hypothalamus
Regulates water metabolism, appetite, sleep-wake cycle, temperature
control, and thirst
Hormonal activity
Posterior pituitary hormones such as vasopressin and oxytocin
Anterior pituitary hormone excretion
Growth, thyrotropin, and follicle stimulating hormones, prolactin, and
corticotropin
Emotions and drives basic to self-preservation
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Central Nervous System
Diencephalon Functions
Thalamus
All sensation except smell
Sensation perceived at the thalamic level is crude and cannot be localized
or quantified
Epithalamus
By young adulthood often calcified and is radiopaque. Used as point of
reference on an x-ray or a CT scan
Subthalamus
Contains sensory tracts. Connections to basal ganglia
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Central Nervous System
Cerebellum
The Cerebellum receives instantaneous and continuous information
about the condition of muscles, joints, and tendons.
Cerebellar function enables a person to:
Keep a moving part from overshooting intended destination
Move in an orderly sequence
Predict distance, gauge speed of approaching object
Control voluntary movement
Maintain equilibrium
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Cerebral Circulation
Blood Distribution To The Brain
Cerebrospinal Fluid
Spinal Cord
Blood Distribution
Cerebral Circulation
Cerebral circulation originates from carotid and vertebral arteries.
Anterior, middle, and posterior cerebral arteries are joined together by
communicating arteries which for the circle of Willis.
Venous drainage occurs through cerebral veins into dural sinuses.
Cerebral veins have no valves therefore intracranial pressure can be
affected by central venous pressure.
Two sinuses are of particular importance: superior saggital sinus and
cavernous sinus.
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Blood Distribution
Internal Carotid Artery Distribution
Hypophyseal
Posterior pituitary.
Ophthalmic
Eye, frontal scalp, frontal and ethmoid sinuses.
Anterior chorioidal
Choroid plexus (lateral), optic tract, uncus, amygdaloid body,
hippocampus, globus pallidus, lateral geniculate nucleus, Internal
capsule.
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Blood Distribution
Internal Carotid Artery Distribution
Letinculostriate
Putamen, caudate nucleus, globus pallidus, internal capsule, corona
radiata.
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Internal Carotid Artery Distribution
Basilar Artery Branches
Anterior inferior cerebellar – Cortex and inferior surface cerebellum,
cerebellar nuclei, upper medulla, lower pons.
Internal auditory – Inner ear
Pontine – Pons
Superior cerebellar – Cortex, white matter and nuclei of cerebellum,
pons, superior cerebellar peduncle, inferior peduncle, inferior
colliculus.
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Internal Carotid Artery Distribution
Vertebral Artery Branches
Posterior cerebellar – Medulla. Posterior cerebellum, inferior vermis,
cerebellar nuclei, choroid plexus (fourth ventricle), posterolateral
medulla.
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Cerebrospinal Fluid Circulation
CSF surrounds and cushions the brain and spinal cord.
While circulating through the subarachnoid space, the fluid is
continuously reabsorbed by the arachnoid villi and then channeled
into the superior sagittal sinus.
The spinothalamic tracts begin in the spinal cord and end primarily in
the thalamus.
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Spinal Cord
Function
Controls body movement; regulates visceral function; processes sensory
information, and transmits information to and from the brain.
It contains gray matter (neuron cell bodies) that is H-shaped and surrounded
by white matter (myelinated axions).
White matter is divide into posterior, lateral, and anterior columns.
Gray matter divisions are posterior, intermediolateral, and anterior.
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Spinal Cord
Components
Ascending tracts – groups of cells in white matter – generally begin in the
spinal cord and end in the brain.
Three ascending tracts are important for understanding neurologic problems:
spinothalamic, spinocerebellar and fasciculi gracilis and cuneatus (posterior
white columns).
The spinothalamic tracts begin in the spinal cord and end primarily in the
thalamus.
The posterior and anterior spinocerebellar tracts begin in the spinal cord
and end in the cerebellum.
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Spinal Cord
Transmissions
Posterior white columns transmit to the thalamus:
The sensation of proprioception from muscles, joints, and
tendons.
Vibratory sense.
Light touch from the skin.
Discrete localization.
Two-point discrimination.
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Spinal Cord
Descending tracts
Begin in the brain and end in the spinal cord.
Pyramidal tract (lateral corticospinal) – of major importance in understanding
neurological problems.
Originates in the motor cortex of the frontal lobe and portions of the parietal
lobe.
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Spinal Cord
Circulation
Spinal cord circulation – comes from three main arteries:
Anterior spinal artery which originates from a branch of the vertebral arteries.
The two posterior spinal arteries originate from either the vertebral or
posterior inferior cerebellar artery.
Additional circulation is supplied by branches of the descending aorta.
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Peripheral Nervous System
The peripheral nervous system is composed of the
spinal nerves, the twelve cranial nerves, and the
autonomic nervous system (ANS).
Peripheral Nervous System
Spinal Nerves / Sensory Receptors
Spinal Nerves - There are 31 pairs (8 cervical, 12 thoracic, 5 lumbar,
5 sacral and 1 coccygeal) exiting from the spinal cord.
Each spinal nerve is responsible for the muscle innervation and
sensory reception of a given area of the body.
Sensory Receptors throughtout the body monitor and transmit
impulses of pain, temperature, touch, vibration, pressure, visceral
sensation, and proprioception, as well as those sensations of vision,
taste, smell,and hearing.
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Peripheral Nervous System
Lower Motor Neurons and Plexuses
Each motor neuron that leaves the spinal cord joins other nerves to
form plexuses.
Plexuses continue as trunks, cords, divisions and finally branch into
individual peripheral nerves.
The major plexuses are: cervical, brachial, lumbar and sacral. Here are
major concentrations of nerves.
The nerves of each plexus pass through or are surrounded by bone.
Injury to the area or entrapment of a nerve can cause multiple
problems.
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Peripheral Nervous System
Reflexes
Reflexes consist of sensory input from:
• The muscles, tendons, skin, organs, and special senses.
• Small cells in the spinal cord lying between the posterior and
anterior gray matter (interneurons).
• Anterior motor neurons, along with the muscles they innervate.
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Peripheral Nervous System
Cranial Nerves
There are 12 cranial nerves. The numbers, and names are listed below.
The type, origin and function of the cranial nerves are summarized will
be explained in the next few slides.
I. Olfactory
VII. Facial
II. Optic
VIII. Vestibulocochlear
III. Oculomotor
IX. Glossopharyngeal
IV. Trochlear
X. Vagus
V. Trigeminal
XI. Spinal accessory
VI. Abducens
XII. Hypoglossal
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Cranial Nerves
Assessment
Cranial Nerve I: Olfactory
With the client’s eyes closed, the nurse tests one of the client’s nostrils at a time; the
client occludes the other with a finger. The nurse asks the client to identify familiar
odors, such as coffee, tobacco, mint, or soap. Alcohol sponges and ammonia are not
used because they stimulate the trigeminal nerve rather than the olfactory nerve.
Cranial Nerve II: Optic
Each eye is tested individually, with the other eye covered but open. The nurse tests
central vision, or visual acuity, using the Snellen chart. Clients are tested with and
without glasses. Visual fields or peripheral vision are assessed by asking the client to
focus on the nurse’s nose. The nurse wiggles one finger of each hand in the superior
field, asking the client where the movement is. The client should see movement on both
sides. This is then repeated with the inferior field.
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Cranial Nerves
Assessment
Cranial Nerve III: Oculomotor
Pupil constriction is tested with the room darkened. The nurse brings the penlight in
from the side or from above or below the client’s head and shines the light in the
client’s eye. The pupil should constrict and stay constricted. This is direct response. The
response in the other eye is consensual and is less than the eye being tested. Pupils
should be equal, round, regular, and react to light and accommodation. (PERRLA).
Cranial Nerve IV: Trochlear
Eye movement (inferior and medial) is tested with assessment of cranial nerve VI.
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Cranial Nerves
Assessment
Cranial Nerve V: Trigeminal
The nurse tests all three branches of the trigeminal nerve. Ophthalmic branch –
forehead; maxillary branch – cheek; mandibular branch – jaw. Using an object that has
sharp and blunt aspects (a safety pin), the nurse asks the client to indicate whether the
sensation is sharp or dull and then repeats the process. The motor aspect can be tested
with the eyes open. The nurse palpates the jaw muscles for strength and equality.
Cranial Nerve VI: Abducens
Cranial nerve VI control lateral eye movement. Together with cranial nerves III and IV,
cranial verve VI is tested by checking the six cardinal positions of gaze.
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Cranial Nerves
Assessment
Cranial Nerve VII: Facial
Only the motor portion of the facial nerve is tested. Taste on the anterior portion of the
tongue is tested with cranial nerve IX. The nurse asks the client to frown, smile puff out
cheeks looking for symmetry.
Cranial Nerve VIII: Vestibulocochlear (Acoustic)
Hearing is tested initially with the client’s eyes closed. The nurse rubs a thumb and
finger together next to the client’s ear and asks where sound is heard. The nurse then
repeats this maneuver for the other ear. The nurse may use the Weber and Rinne tests
(with the client’s eyes open) to check for conductive or sensorineural hearing loss.
Conductive hearing loss is caused by external-ear and middle-ear problems, such as
excessive cerumen , presence of pus, ossicle fusion, or a damaged eardrum.
Sensorineural hearing loss is due to cochlear or nerve damage.
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Cranial Nerves
Assessment
Cranial Nerve IX: Glossopharyngeal
The motor portion is tested with cranial nerve X assessment. Taste is often not tested
unless the client reports loss of taste.
Cranial Nerve X: Vagus
To test the motor portion, the nurse asks the client to say “Ah” when looking into the
throat. The uvula and palate should rise bilaterally and equally.
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Cranial Nerves
Assessment
Cranial Nerve XI: Spinal Accessory
The nurse assesses the strength of the client’s sternocleidomastoid and trapezius
muscles by having the client turn the head against resistance.
Cranial Nerve XII: Hypoglossal
The nurse tests motor innervation to the tongue by asking the client to stick out the
tongue. The nurse checks for deviation to one side or the other. The tongue deviates
toward the same side where the lesion has occurred in the brain.
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Autonomic Nervous System
The Autonomic Nervous System is composed of two parts:
Sympathetic Nervous System, and
Parasympathetic Nervous System.
Autonomic Nervous System
Sympathetic vs. Parasympathetic
Sympathetic
If almost any portion of the sympathetic nervous system is stimulated, the
whole system responds (the fight or flight response).
During periods of excessive sympathetic stimulation:
• Skeletal muscle vessels dilate
• The heart pumps faster
• The liver releases extra glucose
• The thyroid is stimulated
• Sweating increases
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Autonomic Nervous System
Sympathetic vs. Parasympathetic
Parasympathetic
The PAS nervous system conserves the body’s resources.
Parasympathetic fibers to the viscera have some sensory ability in addition
to motor function.
Sensations of irritation, stretching of an organ, or decrease in tissue
oxygen are transmitted to the thalamus through pathways not yet fully
understood.
Table 43-7 page 1003-1004 compares the action of
sympathetic and parasympathetic systems in the body.
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Neurological Changes
Associated with Aging
Motor / Sensory Ability
Mental Status
Diagnostic Assessment
Aging
Motor / Sensory Ability
Sensory changes in older people can affect their daily activities.
Pupils decrease in size and adapt more slowly.
Touch sensation decreases.
Vibration sense may be lost in ankles and feet.
Hearing also decreases.
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Aging
Mental Status
Memory is one of the most important criteria for neurologic
assessment. Loss of memory (esp. recent) tends to be an early sign of
neurologic problems.
Anxiety, insomnia, and depression may cause change in mental status.
Circadian rhythm disorders may alter normal sleep patterns.
Long term memory seems beter than recal or immediate memory.
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Assessment of Mental Status
Personal And Family History
Level of Consciousness
Lethargic
Demographic Data
Stuporous
Past Medical History
Comatose
Current History
Current symptoms
Social History
Activities
The client is also asked questions
to indicate orientation to person,
place, and time.
Habits
Other
Appropriateness
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Assessment of Mental Status
Abnormal Posturing
Decortication
is abnormal posturing seen in the client with lesions that interrupt the
corticospinal pathways.
The client’s arms, wrists, and fingers are flexed with internal rotation
and plantar flexion of the legs.
Decerebration
is abnormal posturing and rigidity characterized by extension of the
client’s arms and legs, pronation of the arms, plantar flexion, and
opisthotonos.
It is usually associated with dysfunction in the brain stem area.
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Assessment of Mental Status
Glasgow Coma Scale*
Eye Opening
Spontaneous
To sound
To pain
Never
Verbal Responses
4
3
2
1
Motor Responses
Obeys commands
Localizes pain
Normal flexion
Abnormal flexion
Extension
Nil
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6
5
4
3
2
1
Oriented
Confused Conversation
Inappropriate words
Incomprehensible Sounds
None
5
4
3
2
1
* The highest score is 15.
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Assessment of Mental Status
Diagnostic Assessment
X-rays of the Skull and Spine - x-rays are used to determine bony
fractures, curvatures,bone erosion, done dislocation, and possible
calcification of soft tissue.
Cerebral Angiography - illuminates the cerebral circulation. Contrast
medium is injected into an artery, and x-rays are taken as the medium
flows with the blood.
Digital Subtraction Angiography - (DSA) is used to evaluate the
carotid and other cerebral arteries.
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Assessment of Mental Status
Diagnostic Assessment
Myelography
Myelography enables the vertebral column, intervertebral disks, spinal
nerve roots, and blood vessels to be visualized. A contrast medium is
inserted into the subarachnoid space of the spine. A lumbar puncture is
the usual insertion site.
Contrast Media Method
A contrast medium is injected and x-rays are taken. Follow-up care
requires vital and neuro signs, bed rest for 6 hours, extremity used is
checked for adequate circulation demonstrated by skin color and
temperature, pulses distal to the injection site and capillary refill.
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Assessment of Mental Status
Diagnostic Assessment
Computerized Tomography - With the aid of a computer, pictures
are taken at many horizontal slices of the brain or spinal cord. The
nurse must ascertain if the client is allergic to iodine. The client must
be completely still for the procedure which takes 10 minutes or less.
Positron Emission Tomography / Single Photon Emission Computed
Tomography. PET scanning provides information about the function of
the brain.
Lumbar Puncture - (spinal tap) is the insertion of a needle into the
subarachnoid space between the third and fourth lumbar vertebrae.
Used to obtain pressure readings, obtain CSF, inject medium, inject
medication, reduce increased ICP.
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Spinal Cord Injury
Manifestations / Classifications/ Symptoms
Nursing Assessment
Nursing Diagnoses
Spinal Cord Injury
Manifestations / Classifications
SCI often result in loss of
– motor function
– sensation
– reflex activity, and
– bowel and bladder control
The client may experience significant behavior and emotional problems as
a result of changes in body image, role performance, and self-concept.
SCI are classified as complete or incomplete.
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Spinal Cord Injury
Symptoms
Specific syndromes seen after SCI and damage to the ANS are spinal shock and
autonomic dysreflexia.
Spinal Shock
occurs immediately after injury and is characterized by flaccid paralysis, loss of
reflex activity below the level of the lesion, bradycardia, hypotension and
occasionally paralytic ileus.
Autonomic Dysreflexia
is usually seen in injuries above the level of the sixth thoracic vertebra. It
generally occurs after the period of spinal shock is completed. Key features are:
severe, rapidly occurring HTN, bradycardia, flushing above level of lesion,
severe, throbbing headache, nasal stuffiness, sweating, nausea, blurred vision.
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Spinal Cord Injury
Nursing Assessment
Respiratory Status
Assess the client’s respiratory status; monitor for atelectasis, pneumonia, and
pulmonary embolus.
Vital Signs
Take vital signs q1h or more often if clinically indicated; monitor for
orthostatic hypotension.
Neurologic Status
Perform neurologic status checks q1h or more often if clinically indicated.
Notify physician immediately of a deterioration of motor status.
Watch for and immediately treat autonomic dysreflexia.
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Spinal Cord Injury
Nursing Assessment
Assess Bladder Function
Palpate for distention.
Begin retraining as appropriate.
Assess intake and output.
Assess Bowel Function
Auscultate bowel sounds.
Palpate for distention.
Chart stool frequency.
Begin a bowel program as
appropriate.
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Spinal Cord Injury
Nursing Assessment
Medical
Give pain medication as ordered;
Document the client’s response.
Prevent immobility complications.
Have the client TCDB q2h.
Use pneumatic boots or compression stockings.
Check skin for breakdown.
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Spinal Cord Injury
Nursing Assessment
Monitor Nutritional Status
including a calorie count, and collaborate with dietitian to identify an
appropriate diet.
Assess Psychological Status
Communicate with the client.
Answer questions honestly; refer questions you can’t answer to
someone who can.
Assess for signs of depression or anger.
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Emergency Care
Autonomic Dysreflexia
Positioning
Raise the head of the bed to a high Fowler position.
Loosen tight clothing on the client.
Physical Care
Monitor blood pressures every 10-15 minutes
Check the Foley catheter tubing (if present) for kinks or obstruction.
If a Foley is not present, check for bladder distention and catheterize
immediately.
Check the client for fecal impaction; if present, disimpact immediately
using anesthetic ointment.
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Emergency Care
Autonomic Dysreflexia
Notification
Call the physician and notify him or her of the emergency.
Environment
Check the room temperature to ensure that it is not too cool or drafty.
Medication
Give nitrates or Hydralazine (Apresoline, Novo-Hylazin) as ordered.
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Spinal Cord Injury
Common Cord Syndromes
Complete Lesion – total loss of motor sensory, and reflex activity.
Anterior Cord Syndrome – Loss of motor function with preservation of
position, vibration, and touch senses.
Brown-Sequard Syndrome – Loss of pain, temperature, and light touch on
opposite side. Loss of motor function and vibration, position, and deep touch
sensation on same side as the cord damage.
Central Cord Syndrome – Loss of motor function and incomplete loss of
motor function.
Conus Medullaris and Cauda Equina Syndromes – Loss of motor
and/or sensory function in various patterns, with potential for recovery of
function with regeneration of peripheral nerves; neurogenic bowel and bladder.
Please see text Figure 5-5 for the above common cord syndromes
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Spinal Cord Injury
Assessment
Respiratory Pattern
Initial assessment is respiratory
pattern to assure adequate
airway.
Sensation
Muskuloskeletal
Psychosocial
Laboratory
Diagnostic
Motor Ability
Cardiovascular
GI/GU
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Spinal Cord Injury
Assessment Of Motor Function
C-5 apply downward pressure while the client shrugs his shoulders
upward.
C5-6 apply resistance while the client pulls up his arms.
C7
apply resistance while the client straightens his flexed arms.
C-8 make sure that the client is able to grasp an object and form a fist.
L2
apply resistance while the client lifts his legs from the bed.
L5
apply resistance while the client dorsiflexes his or her feet.
S1
apply resistance while the client plantar flexes his feet.
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Spinal Cord Injury
Nonsurgical Management
Vital Signs and Neuro Signs
Nurse assesses vital signs and neuro signs every hour. In the first 2-hours after injury
the client is at risk for neurogenic shock which is manifested by bradycardia and
hypotension (most often associated with cervical spine injuries).
Fixed Skeletal Traction
The client with a cervical spine injury is usually placed in fixed skeletal traction to
realign the vertebrae, facilitate bone healing and prevent further injury.
Immobilization – Cervical Injuries
Most commonly used is the halo fixator and cervical tongs. Halo fixator is a static
traction device.
Immobilization – thoracic and lumbar/sacral injuries. Bed rest, immobilization with a
body cast.
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(See page 1070 in
text for illustration
of these devices).
Spinal Cord Injury
Use Of A Halo Device
Be aware that the weight of the halo device alters balance. Be
careful when leaning forward or backward.
Wear loose clothing preferably with Velcro fasteners.
Bath in the tub or sponge bathe.
Wash under lamb’s wool liner to prevent rash; use powders or
lotions sparingly under vest.
Have someone change liner if it becomes odorous.
Support head with small pillow when sleeping.
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(See page 1070 in
text for illustration
of these devices).
Use Of A Halo Device
Try to resume activities to the extent possible. Avoid contact sports,
swimming.
Do not drive, vision is impaired with the device.
Use straws to drink fluids.
Cut food into small pieces to facilitate chewing and swallowing.
Have someone clean pin sites according to hospital protocol.
Observe pin sites daily for drainage or redness.
Increase fluid and fiber in the diet to prevent constipation.
Use a position of comfort during sexual activity.
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Spinal Cord Injury
Drug Therapy
Solu-Medrol - in high dosages within first 8 hours of injury is the first
course of treatment. Clients receiving this medication show significant
improvement in motor and sensory function.
Dextran - a plasma expander, may be used to increase capillary blood
flow within the spinal cord and to prevent or treat hypotension.
Atropine sulfate - is used to treat bradycardia.
Dopamine and Isoproterenol - used to treat severe hypotension.
Dantrium [Bacolfan] - may be used to treat spasticity.
Didronel - may be ordered for patient with heterotopic ossification.
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Spinal Cord Injury
Surgical Management
Emergency Surgery
Emergency surgery may be indicated if there is evidence of spinal
cord compression. It may be necessary to remove bone fragments
from a vertebral fracture, evacuate a hematoma, or remove penetrating
objects.
Compressive laminectomy allows for cord expansion from edema.
Additional typical procedures include: Harrington rods to stabilize
thoracic spinal injuries. Postop the client usually wears a brace or
TLSO to keep operative area immobile.
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Spinal Cord Injury
Surgical Management
Postop Care
The nurse assesses the client’s neurological status and vital signs at
least every hour. Complications of surgery, such as hematoma and
edema, are manifested by a deterioration in neurologic status.
The client is at risk for cardiovascular instability because of the loss of
sympathetic innervation. Logrolling is used when moving the patient.
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Some Nursing Diagnoses
Associated With Spinal Cord Injury
Ineffective Airway Clearance;
Ineffective Breathing Pattern;
Impaired Gas Exchange
Expectations
The client is expected to maintain a patent airway and not experience
respiratory complications, such as pneumonia, atelectasis, and aspiration.
Interventions
Turn the client every 2 hours.
Instruct the client to breathe as deeply as possible.
Assist cough.
Use incentive spirometer.
Possible use of suction.
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Impaired Physical Mobility;
Self-Care Deficit
Expectations
The client is expected to be free from complications of immobility and learn
to perform activities of daily living as independently as possible.
Interventions
The client with an SCI is especially at risk for pressure ulcers, contractures,
and deep venous thrombosis or pulmonary emboli.
Preventing Complications of Immobility
Reposition or teach client to reposition every 2 hours. Use of special pressure
relief pads. ROM exercises at least once every 8 hours. The nurse collaborates
with PT and OT to determine the most appropriate positioning and exercise
techniques, to assess need for hand splints, to develop plan for foot drop.
Compression stockings or boots are used. Coumadin is used to prevent DVT.
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Impaired Physical Mobility;
Self-Care Deficit
Preventing Orthostatic Hypotension
Clients with cervical cord injuries are especially at high risk for orthostatic
(postural) hypotension. If the client moves from a lying to a sitting or a
standing position quickly, he may experience hypotension which could result
in dizziness and falls because of autonomic innervation in which blood
vessels do not respond quickly enough to push blood up to the brain. To help
prevent this, the nurse instructs the client to move slowly. Thigh high
embolism stockings also help.
Promoting Self-Care
The most important thing is to set realistic goals. The nurse collaborates with
PT and OT to do this and maximize self-care.
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Impaired Physical Mobility;
Self-Care Deficit
Preventing Orthostatic Hypotension
Clients with cervical cord injuries are especially at high risk for orthostatic
(postural) hypotension. If the client moves from a lying to a sitting or a
standing position quickly, he may experience hypotension which could result
in dizziness and falls because of autonomic innervation in which blood
vessels do not respond quickly enough to push blood up to the brain. To help
prevent this, the nurse instructs the client to move slowly. Thigh high
embolism stockings also help.
Promoting Self-Care
The most important thing is to set realistic goals. The nurse collaborates with
PT and OT to do this and maximize self-care.
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Altered Urinary Elimination;
Constipation
Expectations
The client is expected to achieve continence of stool and urine.
Interventions
Clients with SCIs have reflex or neurogenic loss of bowel and bladder control.
Many clients can become continent if they rigorously adhere to an established
program.
The type program depends on whether the injury involves upper motor
neurons or lower motor neurons.
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Altered Urinary Elimination;
Constipation
Establishing a Bladder Retraining Program - Catheterization
Client typically is catheterized every 3 hours and more frequently if output is
greater than 500 cc. Over time intervals between catheterizations are increased
and adjusted to intake and sleep times.
Other techniques may be used. Urecholine may be prescribed. To
ascertain effectiveness of these maneuvers, the nurse catheterizes the
client for residual urine after voiding.
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Altered Urinary Elimination;
Constipation
Establishing a Bowel Retraining Program
The essential elements of a bowel program are:
• A consistent time for bowel elimination.
• A high fluid intake (at least 2000 cc a day).
• A high fiber diet.
• Rectal stimulation with or without suppositories.
• If needed, a stool softener.
If the client has sustained an LMN injury, the resulting flaccid large bowel
may require the client to perform or to have manual disimpaction.
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Impaired Adjustment
Expectations
The client is expected to demonstrate the ability to cope with the changes caused by the
injury and verbalize his or her feelings about the injury and changes in lifestyle.
Interventions:
The nurse encourages the client to discuss his perception of the situation and what
coping skills can be used. Referrals to clergy, rabbis, or other spiritual leaders or a
psychologist are offered. Support groups are available to family and friends. Social
workers can help with insurance status and appropriate social service agencies as
necessary.
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Spinal Cord Injury
Home Care Management
If the client is discharged home or returns home for a weekend visit
from the rehab setting, the environment must be assessed to ensure
that it is free from hazards and can accommodate the client’s special
needs. OT or PT works in collaboration with rehab in the home
setting.
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Spinal Cord Injury
Health Teaching
The teaching plan for the client with an SCI includes:
Physical mobility and activity skills
ADL skills
Bowel and bladder retraining program
Skin care
Medication regimen
Sexuality education
The information should be reinforced with handouts.
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Spinal Cord Injury
Health Teaching
Learning mobility skills is important so that the client can negotiate
movement on sidewalks and carpeting and other flooring surfaces. The client
must also be able to negotiate sidewalk curbs while walking independently
with crutches, cane, or in a wheelchair.
Some clients are discharged to home with a halo vest that has a significant
physical and psychological impact on clients. Clients find it difficult to
perform mobility skills and ADLs independently.
ADL training includes a structured exercise program to promote strength and
endurance.
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Spinal Cord Injury
Psychosocial Preparation
Nurse teaches name and purpose of medication and side effects. Client
should understand possible interaction of prescribed medication with
OTC and illegal drugs and alcohol.
Psychosocial adaptation is one of the critical factors in determining
the success of rehab. The nurse should prepare the client for reactions
of others outside the rehab. For example, the client can practice
answering questions about why he is in a wheelchair.
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Spinal Cord Injury
Health Care Resources
The nurse or case manager refers the client to appropriate
organizations.
There is a National Spinal Cord Injury Association and hotline.
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Spinal Cord Tumors
Key Features
Manifestations
Spinal Cord Tumors
Key Features
Occur most frequently in the thoracic area. Venous occlusion by the
tumor may lead to spinal cord congestion and infarction.
The appearance of neurologic signs and symptoms is related to the
rate of tumor growth. The spinal cord can often accommodate a slow
growing tumor. On the other hand, a fast growing tumor quickly leads
to spinal cord compression.
Anatomically, spinal cord tumors may be extramedullary or
intramedullary, i.e. originate within or out of the spinal cord.
Spinal cord tumors account for about 1% of all tumors in adults.
The majority of tumors are benign.
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Spinal Cord Tumors
General Symptoms
Pain
Quadriparesis
Sensory loss or impairment
Stiff neck
Motor loss or impairment
Nystagmus
Sphincter disturbance (bladder
before bowel)
Cranial nerve dysfunction
Cervical
Pain in the arms and shoulders
High cervical
Respiratory distress
Diaphragm paralysis
Occipital headache
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Low cervical
Weakness
Paresthesia
Motor loss
Horner's syndrome
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Spinal Cord Tumors
Specific
Thoracic
Lumbosacral
Sensory loss
Low back pain
Spastic paralysis
Paresis
Positive Babinski’s sign
Spastic paralysis
Bladder and bowel dysfunction
Sensory loss
Pain in the chest and the back
Bladder and bowel dysfunction
Muscle atrophy
Sexual dysfunction
Muscle weakness in the legs
Decreased-to-absent ankle and
knee reflexes
Foot drop
See Table
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1, p. 1077 inCopyright
text for -Location
of Spinal Cord Tumors
Mary Roche,and
RN -Treatment
2002
Spinal Cord Tumors
Assessment/Clinical Manifestations
Clinical manifestations depend on the location of the tumor and its
rate of growth.
The nurse assesses for weakness, clumsiness, spasticity, and
hyperactive reflexes and compares the responses on both sides of the
body.
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Problems Of The
Peripheral Nervous System
Peripheral Nervous System
Guillain-Barre Syndrome (GBS)
is an acute inflammatory process characterized by varying degrees of motor
weakness and pathology.
In GBS the immune system starts to destroy the myelin sheath that surrounds
the axons.
Etiology
cell mediated immunologic reaction.
Lab Assessment
No single finding confirms diagnosis. Physician does a lumbar puncture to
evaluate CSF. Peripheral blood tests may show leukocytosis early in the
illness. ESR is typically WNL.
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Peripheral Nervous System
Myasthenia Gravis (MG)
Myasthenia Gravis means ‘grave muscle weakness’ or weakness of the
voluntary or striated muscles.
May take many forms, from mild ocular muscle disturbance to severe
weakness leading to death from respiratory failure.
Clients with MG develop specific antibodies to one or more ACh receptor
sites, possibly because of autoimmune injury.
Etiology
Research suggests that MG is caused by antibodies to ACh receptors.
Evidence also suggests a relationship between MG and hyperplasia of the
thymus gland.
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Myasthenia Gravis (MG)
Assessment
Subjective complaints are noted. Inquiry re: eye problems, ability with
performing ADLs, respiratory difficulty, presence of paresthesia or
aching, weakened muscles.
Any history of thymus gland tumor is elicited.
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Myasthenia Gravis
Clinical Manifestations
Progressive paresis, ocular palsies, ptosis, diplopia, weak or
incomplete eye closure.
Diagnostic assessment - Response to cholinergic drugs. Thyroid
function should be tested. Assessment for thyoma by CT.
Tensilon testing - This test can be used to evaluate myasthenic crisis
(under medication with cholinesterase inhibitors).
EMG – electrical testing to detect defective neuromuscular
transmission.
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Myasthenia Gravis
Interventions
Assistance with activities. Active
or passive ROM. Turn q. 2 h.
Self-care.
Nutritional support.
Drug therapy: Three groups of
drugs used – anticholinesterases
(Prostigmin), Corticosteroids
(Prednisone),
immunosuppressants (Imuran).
Plasmapheresis is a method by
which offending autoantibodies
are removed from the plasma.
Assistance with communication.
Eye protection.
Surgical management
(thymectomy) .
Lifestyle changes.
Respiratory support.
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Myasthenia Gravis
Crisis
Sudden increases in weakness and the inability to clear secretions, swallow, or breathe
adequately indicate that the client is experiencing crisis. There are two types of crisis:
Myasthenic crisis
an exacerbation of the myasthenic symptoms caused by under medication with
anticholinesterase drugs. Myasthenic crisis is often preceded by some type of infection.
Cholinergic crisis
an acute exacerbation of muscle weakness caused by overmedication with cholinergic
(anticholinesterase) drugs.
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Characteristics of Crises
Increased pulse and
respiration.
Nausea, vomiting,
diarrhea.
Restlessness.
Rise in blood pressure.
Anoxia.
Abdominal cramps.
Dysphagia.
Blurred vision.
Dysarthria.
Pallor.
Increased lacrimation.
Facial muscle
twitching.
Increased salivation.
Cyanosis.
Bowel and bladder
incontinence.
Decreased urinary
output.
Absence of cough and
swallow reflex.
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Pupillary miosis.
Hypotension.
Apprehensio
n.
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Dyspnea.
Diaphoresis.
Generalized weakness.
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Myasthenia Gravis
Treatment
In either crisis, an adequate airway and artificial respiration must be
maintained.
Because both have many common characteristics, the type of crisis the
client is experiencing must be identified for effective treatment to be
provided.
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Myasthenia Gravis
Improving Nutrition In Clients
Assess the client’s gag reflex and
ability to chew and swallow.
Keep the head of the bed elevated
during meals and for 0 minutes after.
Provide frequent oral hygiene as
needed.
Avoid liquids as they can easily cause
choking and aspiration. Provide a soft
diet.
Collaborate with the dietitian, speech
and language pathologist, to plan and
implement a meal the client can enjoy.
Monitor food intake carefully.
Weigh the client daily.
Offer small, frequent meals.
Observe client for choking, nasal
regurgitation, and aspiration.
Provide high-calorie snacks or
supplements such as puddings
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Monitor serum transferring and
albumin levels.
Administer anticholinesterase drugs, as
ordered: 0-60 minutes before each
meal.
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Peripheral Nervous System
Polyneuritis and Polyneuropathy
Manifestations
Systemic diseases, infections, trauma, vascular or metabolic disturbances,
alcohol, medications, heavy metals may damage cranial and peripheral nerves.
Although the term polyneuritis implies an inflammatory process, it may
denote noninflammatory lesions as well.
Hallmarks
Terms polyneuritis, polyneuropathy, and peripheral neuropathy may describe
syndromes whose clinical hallmarks are muscle weakness with or without
atrophy, pains and paresthesia, impaired reflexes, or a combination of these
symptoms.
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Polyneuritis and Polyneuropathy
Assessment
Interventions:
Examination of sensory and motor
ability. Position sense, pain, signs
of injury of which the client may
be unaware. The nurse also
assesses the client for:
Removal of the underlying
cause.
Supplementation of diet.
Client teaching.
Orthostatic hypotension
Abnormal sweating
Miosis
Sphincter disturbances.
Other dysfunctions that may
accompany neuropathy.
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Peripheral Nervous System
Restless Leg Syndrome
The client complains of intense “crawling-type” sensations in the
limbs and subsequently feels the need to move the limbs repeatedly.
Diagnosis is made on history and there is no known etiology.
Management is symptomatic.
Antiembolism stockings may be helpful.
Some medications that may help include: Catapres, Tegretol,
Clonidine.
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Peripheral Nervous System
Trigeminal Neuralgia
Also called tic douloureux.
Entails a type of facial pain, which occurs in abrupt, intense paroxysms.
Usually provoked by minimal stimulation of a trigger zone. Is unilateral and
confined to the area innervated by the trigeminal nerve, most often the second
and third branches.
Usually in persons over 50.
Cause is thought to be related to impaired inhibitory mechanisms in the brain
stem.
Approximately 70% respond to carbamazepine (Tegretol).
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Peripheral Nervous System
Facial Paralysis (Bell’s Palsy)
Onset is acute.
Cause remains obscure.
Management consists of prednisone and analgesics.
Nursing care is directed toward managing the major neurologic
deficits and providing psychosocial support.
80% of clients recover fully within a few months.
Approximately 20% have residual weakness; a few have permanent
neurologic deficits.
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Interventions For Critically Ill Clients
With Neurologic Problems
Some neurologic problems, such as cerebrovascular accident (CVA),
head injury, brain tumor, can cause increased intracranial pressure
(ICP), a life-threatening complication.
Through prompt recognition and aggressive management of this
complication, permanent neurologic dysfunction or death may be
prevented.
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Cerebrovascular Accident
– “stroke”, is a disruption in the normal blood supply to the brain. It
often occurs suddenly and produces focal neurologic deficits.
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Cerebrovascular Accident
Pathophysiology
Through the process of cerebral autoregulation, blood flow to the brain
is maintained at a fairly constant rate of 1000mL/min. In the event of a
CVA, ischemia occurs in the brain tissue supplied by the affected artery.
Ischemia leads to hypoxia or anoxia and hypoglycemia.
These processes then cause infarction or death of the neurons, the glia,
and the involved area of the brain. In addition, brain metabolism after
stroke is affected in the involved area as well as in the contralateral
hemisphere.
Small lacunar infarcts may also occur. Lacunae are small, deep cavities
within the brain that result from occlusion of a small vessel.
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Cerebrovascular Accident
Classifications
CVAs are generally classified as ischemic (occlusive) or hemorrhagic.
Ischemic strokes are further divided into thrombotic strokes and
embolic strokes.
Ischemic Stroke – caused by occlusion of a cerebral artery by either
a thrombus or an embolus.
Hemorrhagic Stroke - In this type of stroke, the integrity of the
vessel is interrupted. Hemorrhage into the brain tissue generally
results from a ruptured saccular (berry) aneurysm, rupture of an AV
malformation or, hypertension. A ruptured cerebral aneurysm is
another cause of hemorrhagic stroke.
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Transient Ischemic Attack
TIA and Reversible Ischemic Neurologic Deficit – RIND. Warning
signs or silent strokes.
Etiology – Strokes are caused by an occlusion in an artery from a
thrombus or an embolus; also from hypertension.
Risk factors include: smoking, substance abuse (particularly
cocaine), obesity, sedentary lifestyle, high stress levels, elevated
cholesterol, lipoprotein, triglycerides, previous CVA or TIA, heavy
alcohol use.
Sudden discontinuation of antihypertensive medications can cause
hemorrhagic stroke.
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Transient Ischemic Attack
African-Americans affected more frequently as a result of high
frequency of diabetes and HTN in this group.
Prevalence – Estimated million stroke survivors in U.S.
The number of strokes occurring in the younger population is
increasing as a result of IV drug abuse.
Those using crack cocaine experience increased incidence of stroke
due to changes in clotting mechanism caused by the drugs or sudden
increase in systolic BP.
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Key Features of
Transient Ischemic Attack
Visual Deficits
Sensory Deficits
Blurred vision
Diplopia
Transient numbness (face, arm,
or hand)
Blindness in one eye
Vertigo
Tunnel vision
Speech Deficits
Motor Deficits
Transient weakness (arm, hand,
or leg)
Aphasia
Dysarthria (slurred speech)
Gait disturbance
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Monitoring for
Increased Intracranial Pressure
Client is at most risk for increased intracranial pressure (ICP) resulting
from edema during the first 72-hours after the onset of the stroke.
Nurse elevates the HOB to 0-5 degrees and maintains the client’s head
in a midline position.
Avoid clustering activities and nursing procedures.
Hyperoxygenate the client prior to suctioning.
Quiet environment in presence of headache.
Lights lowered for clients with photophobia.
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Key Features of
Increased Intracranial Pressure
Decreased LOC (lethargy to coma).
Behavior changes; restless, irritable,
and confused.
Cranial nerve dysfunction.
Headache.
Ataxia.
Nausea and vomiting.
Change in speech pattern.
Seizures.
Cushing’s triad: increased BP, widening
of pulse rate and decreased heart rate.
Aphasia.
Slurred speech.
Change in sensorimotor status.
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Pupillary changes; dilated and
nonreactive or constricted and
nonreactive pupils.
Abnormal posturing: Decerebrate (latest
stage) or decorticate (latest stage).
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Head Injury
Craniocerebral Trauma
commonly referred to as head trauma, is a traumatic insult to the brain
caused by an external physical force that may produce a diminished or
altered state of consciousness.
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Head Injury
Direct vs. Indirect Injury
Various terms are used to describe brain injuries that are produced
when a mechanical force is applied either directly or indirectly to the
brain.
A force produced by a blow to the head is a direct injury.
A force applied to another body part with a rebound effect to the brain
is an indirect injury.
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Head Injury
Shearing Injuries
The brain may also rebound or rotate on the brain stem, causing
diffuse axonal injury (shearing injuries).
This moving brain may be contused or lacerated as it moves over the
inner surfaces of the cranium, which is irregularly shaped and sharp.
Damage most frequently occurs to the frontal and temporal lobes of
the brain, especially the raised surfaces of the summits of the gyri.
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Primary Brain Injury
Results from the physical stress (force) within the brain tissue caused
by open or closed trauma.
Open Head Injury
occurs when there is a fracture of the skull or the skull is pierced. The
integrity of the brain and the dura is violated and there is exposure to
the outside. Damage may occur to underlying vessels, dural sinus,
brain, and the cranial nerves.
Closed head injury is the result of blunt trauma; the integrity of the
skull is not violated. It is the more serious of the two types of injury.
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Primary Brain Injury
Open Head Injury
Four types of fractures associated with open head injuries.
linear fracture - A linear fracture is a simple, clean break in which
the impacted area of bone bends inward, whereas the area around it
bends outward. Linear fractures account for about 80% of head
fractures.
depressed fracture - In a depressed fracture the bone is pressed
inward into the brain tissue to at least the thickness of the skull.
open fracture - In an open fracture, the scalp is lacerated, creating a
direct opening to the brain tissue.
comminuted fracture - involves fragmentation of the bone, with
depression of the bone into the brain tissue.
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Primary Brain Injury
Unique Fracture
A unique fracture is the basilar skull fracture.
It occurs at the base of the skull and results in CSF leakage from the
nose or ears. Of significance with this fracture is the potential
development of hemorrhage caused by damage to the internal carotid
artery; damage to cranial nerves I, II, VII, and VIII; and infection.
The majority of penetrating injuries to the skull are caused by gunshot
wounds and knife injuries. The degree of injury to the brain tissue
depends on the velocity, mass, shape, and direction of impact.
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Primary Brain Injury
Closed Head Injury
Caused by blunt trauma and lead to concussions, contusions, and
lacerations of the brain.
Concussion - is characterized by a brief LOC. Damage occurs to
the gray matter of the cerebral cortex or possibly to the diencephalon
or brain stem. The damage to the axons is functional, not structural,
which is why permanent neurologic dysfunction is generally not seen.
Contusion - Contusion is bruising of the brain tissue.
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Primary Brain Injury
Types of force
Acceleration Injury
An acceleration injury is caused by the head in motion.
Deceleration Injury
A deceleration injury occurs when the head is suddenly stopped or hits
a stationary object.
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Primary Brain Injury
Secondary Responses and Insults
The most frequently occurring response is the development of
increased Intracranial pressure (ICP) attributable to edema,
hemorrhage, hematoma development, impaired cerebral
autoregulation, or hydrocephalus.
Hypoxemia, hypercapnia, or systemic hypotension may precipitate
increased ICP.
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Secondary Responses and Insults
Increased Intracranial Pressure
The brain is composed of brain tissue, blood, and cerebrospinal fluid
encased in a rigid skull. Through the processes of accommodation and
compliance, the ICP is maintained at its normal level of 10-15 mmHg
despite transient increases in pressure that occur.
Increased ICP is the leading cause of death from head trauma in
clients who reach the hospital alive. It occurs when compliance no
longer takes place.
As the ICP increases, cerebral blood flow decreases, leading to tissue
hypoxia, a decrease in serum pH level, and an increase in CO2 levels.
This process causes cerebral vasodilation, edema, and a further
increase in the ICP, and the cycle continues.
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Secondary Responses and Insults
Increased Intracranial Pressure
If not treated, the brain herniates downward toward the brain stem,
causing irreversible brain damage and possible death.
Two types of edema may cause ICP: vasogenic and cytotoxic. A third
type (interstitial edema) occurs in the presence of acute brain swelling.
Vasogenic edema - is seen most often as a cause of increased ICP in
the adult. Fluid accumulates mostly in the white matter.
Cytotoxic or cellular, edema - may occur as a result of a hypoxic
insult, which causes a disturbance in cellular metabolism, the
sodium pump, and active ion transport. This results in an abnormal
amount of fluid in the brain cells. Cytotoxic edema may lead to
vasogenic edema and further increase in ICP.
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Focus on the Elderly: Head Injury
It is the fifth leading cause of death. 65-75 year old group has second
highest incidence of head injury of all age groups. Falls and motor
vehicle accidents are most common cause.
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Focus on the Elderly: Head Injury
High Mortality Factors
The following factors contribute to high mortality:
Falls causing subdural hematomas – especially CSH.
Poorly tolerated systemic stress.
Medical complications, such as hypotension, hypertension, and
cardiac problems.
Decreased protective mechanisms, which make clients
susceptible to infections (especially pneumonia).
Decreased immunologic competence, further diminished by head
injury.
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Physical Assessment
Clinical Manifestations
The goals of nursing assessment are the establishment of baseline data
and the early detection of and prevention of increased ICP, systemic
hypotension, hypoxia, or hypercapnia.
Because it is estimated that 5% to 20% of clients with head trauma
have associated cervical spinal cord injuries, all clients with head
trauma are treated as though they have spinal cord injury until
radiographic studies prove otherwise.
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Nursing Assessments
The nurse makes the following assessments:
Airway and breathing pattern
Vital signs
Neurologic
Eye
Motor
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Other Assessments
The following assessments are also made:
Laboratory – there are no laboratory tests to diagnose primary brain
injury; however, several tests are used to prevent secondary damage.
ABGs, CBC, serum glucose, electrolytes and osmolality.
Radiography.
Other – Magnetic Resonance Imaging is particularly useful.
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Common Respiratory Patterns in
Comatose Clients
PATTERN
LOCATION OF LESION
Cheyne-Stokes
Usually bilateral in cerebral
Respiration
hemispheres. Cerebellar
sometimes. Midbrain. Upper pons
Central neurogenic
Hyperventilation
Low midbrain. Upper pons.
Apneustic breathing
Mid pons. Low pons.
Cluster breathing
Low pons. High medulla.
Ataxic breathing
Medulla.
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Minor Head Injury
If the person is sleeping, wake him every - hours for the first two
days,asking name, where the client is, and identification of caregiver.
Expect the person to complain of headache, nausea, or dizziness for at
least 2-hours. If these symptoms are severe or do not improve, contact the
physician immediately or take the person back to the ER.
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Head Injury
Altered Cerebral Tissue Perfusion
Expectations
The client is expected to maintain a normal ICP, maintain appropriate
vital signs and ABGs, and improve LOC.
Interventions
Severe head injuries – admitted to CCU or trauma center.
Minor head injuries – either admitted to general nursing unit for 2hour observation or sent home with instructions.
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Head Injury
Nonsurgical Management
Interventions are directed toward preventing or detecting increased
ICP, promoting fluid and electrolyte balance, and monitoring the
effects of treatments and medications.
Vital signs are assessed q. 1-2 hours.
Nurse positions client to avoid extreme flexion or extension of the
neck and maintain the head in midline position.
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Head Injury
Nonsurgical Management
Prophylactic hyperventilation during the first 20 hours after injury is
usually avoided as it may produce ischemia.
Induction of barbiturate coma: for clients whose ICP cannot be
controlled by other means, the client may be given Nembutal to
decrease metabolic demands of the brain and cerebral blood flow, thus
decreasing edema.
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Head Injury
Drug Therapy
Mannitol used as an osmotic diuretic.
Codeine or Sublimaze may be used with ventilated clients to decrease
agitation and control restlessness.
Narcan reverses these.
Neuromuscular blocking agents such as Pavulon help decrease
cerebral metabolic rate and must never be used without sedation.
Anticonvulsants such as Dilantin are given for seizures.
Tylenol or aspirin are given to reduce fever.
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Head Injury
Surgical Management
The physician may elect to insert an intracranial pressure monitoring
device. Various types are used.
Craniotomy
In extreme cases where ICP cannot be controlled, the physician may
elect to perform a craniotomy. Removal of nonvital brain tissue allows
expansion of brain tissue. A craniotomy may also be performed to
removed epidural or subdural hematomas.
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Brain Tumors
Key Features
Cerebral Tumors
Hypokinesia
Headache (most common
feature)
Hyperesthesia, paresthesia,
decreased tactile discrimination
Vomiting unrelated to food
intake
Seizures
Aphasia
Changes in visual acuity and
visual fields; diplopia
Changes in personality and/or
behavior
Hemiparesis or hemiplegia
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Brain Tumors
Brain Stem Tumors
Hearing loss (acoustic neuroma)
Facial pain and weakness
Dysphagia, decreased gag reflex
Nystagmus
Hoarseness
Ataxia and Dysarthria (cerebellar tumors)
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Brain Tumors
Key Features of Brain Tumors
Complications of Tumors
Cerebral edema results from changes in capillary endothelial tissue
permeability which allows plasma to seep into the extracellular
spaces.
This leads to increased ICP, and herniation of brain tissue may occur.
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Brain Tumors
Key Features
A variety of focal neurologic deficits result from edema, infiltration,
and compression of surrounding brain tissue.
Increased ICP may also result from obstruction of the flow of CSF or
displacement of the lateral ventricles by the expanding lesion.
Typically, a tumor obstructs the aqueduct of Sylvius or one of the
ventricles or encroaches on the subarachnoid space.
Posterior fossa tumors may obstruct the flow of CSF from the fourth
ventricle to the foramen of Luschka of Magendie.
With any brain tumor, the obstruction of normal CSF flow causes
hydrocephalus and eventually leads to increased ICP.
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Brain Tumors
Classifications
Malignant
Benign
Acoustic neuroma
Astrocytoma (grades 2, , )
Meningioma
Oligodendroglioma
Pituitary adenoma
Ependymoma
Astrocytoma (a grade 1 may
become malignant)
Medulloblastoma
Chondroma
Chondrosarcoma
Glioma
Craniopharyngioma
Lymphoma
Hemangioblastoma
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Brain Tumors
Incidence / Assessment
Incidence/Prevalence
Brain tumors account for % of
all cancer deaths.
Each year 6,000 primary cases
are diagnosed and 18,000
secondary cases are found.
Brain tumors in the adult
population are seen primarily
in clients 0-60 years old.
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Assessment
Clinical manifestations vary.
Diagnosis based on history,
neuro assessment, clinical
exam and testing.
Noninvasive diagnostic studies
CT and MRI and done first.
Additionally EEG and PET
may be indicated.
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Interventions
Nonsurgical:
Surgical:
drug therapy,
Craniotomy.
radiation,
chemotherapy,
radiosurgical procedures.
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Surgical Management
after Craniotomy
Focus of Postop care is to monitor the client to detect changes in status
and prevent or minimize complications.
Positioning based on type of surgery. NPO status for 2-hours.
Monitoring the dressing: check for drainage (typical amount is 0-50 cc
per shift). Excessive amounts of drainage should be reported to
physician immediately.
Monitoring lab values: CBC, electrolytes, osmolality, coag studies and
ABGs. HCT and HGB
Drug therapy: Routinely given meds include anticonvulsants,
histamine blockers and corticosteroids.
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Continuing Care
after Craniotomy
The client with a brain tumor is managed at home if possible.
Seizures are a potential complication that can occur at any time for as
long as a year or more postoperatively.
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Preventing
Postoperative Complications
Increased ICP is the major postop complication of cranial surgery.
Symptoms include severe headache, deteriorating LOC, restlessness,
irritability and dilated or pinpoint pupils.
Treatment includes placing the client supine with HOB elevated 0-5
degrees. Osmotic diuretics may be given to decrease edema. Surgery may
be necessary.
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Preventing
Postoperative Complications
Hydrocephalus - caused by obstruction of the normal CSF pathway
from edema, an expanding lesion such as a hematoma, or blood in the
subarachnoid space. A surgical shunt may be placed for treatment.
Respiratory Problems - Complications include atelectasis, pneumonia,
and neurogenic pulmonary edema. Frequent deep breaths, movement,
incentive spirometry are useful in preventing these complications.
Wound infection - Occur more in debilitated clients. If infection occurs
the wound will be red and puffy. The nurse may treat a localized infection.
For more severe infection, systemic antibiotic treatment is given.
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Preventing
Postoperative Complications
Meningitis
an inflammation of the Meninges and may occur as a result of wound
infection, CSF leak or contamination during surgery.
Fluid And Electrolyte Imbalance
Complications include diabetes insipidus and syndrome of
inappropriate antidiuretic hormone (SIADH). Clients are on strict
I&O. The nurse assesses the client carefully for indications of fluid
overload or dehydration during treatment. Serum electrolyte levels and
osmolality are measured daily or more often if indicated clinically.
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Brain Abscess
A brain abscess is a prurulent infection of the brain in which pus forms
in the extradural, subdural, or intracerebral area of the brain.
Organisms enter from the ear, sinus, or the mastoid area.
Organisms cause a local infection.
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Brain Abscess
Physical Assessment/Clinical
Manifestations
Clinical manifestations are insidious.
Mild lethargy, some confusion.
Pupillary response is normal in the early stage.
As increased ICP progresses, the pupils dilate and become
nonresponsive.
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Key Features
of Brain Abscess
Early Manifestations
Late Manifestations
Headache
Confusion
Fever
Increased intracranial pressure
(ICP)
Focal neurologic deficits
Lethargy
Dilated and nonresponsive
pupils
Visual field deficits
Cushing’s triad
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Antibiotics Used
To Treat Brain Abscesses
Streptococcus
Enterobacteriaceae
Toxoplasma
Penicillin
Cefotaxime
Chloramphenicol
Pyrimethamine
Anaerobes
Staphylococcus
Sulfonamides
Metronidazole
Trimethoprimsulfamethoxazole
Nafcillin
Methicillin
Clindamycin
Fluconazole
Vancomycin
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Presentation Credits
This presentations was developed for Mary Roche under
contact with Peter Martin, dba Stacy House Designs.
The presentation is the sole, copyrighted property of Mary
Roche.
Copies of this and other presentations can be seen on the
Internet at http://www.StacyHouse.com. Please fill out the
guestbook selection when visiting that site.
Thank you.
Mary Roche & Peter Martin
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The End
Mary Roche, MSN, RN, CS