Feature

Neuromonitoring
Indications and Utility in
the Intensive Care Unit
CATHERINE HARRIS, PhD, MBA, CRNP

Information on the use of neuromonitoring in intensive care units is scattered but significant. Nurses who do
not care for neurologically impaired patients on a daily basis may not have a strong understanding of the util-
ity of various neuromonitoring techniques, why they are used, or how they are interpreted. Two main types of
neuromonitoring that are frequently seen but poorly understood are reviewed here: transcranial Doppler sono-
graphy and electrophysiology. Information on these 2 techniques tends to be either superficial with limited
applicability to the critical care setting or very technical. This review provides information about neuromoni-
toring to help guide critical care nurses providing care to neurologically impaired patients. {Critical Care Nurse.
2014;34[3]:30-40)

euromonitoring is an umbrella term used to describe the various invasive and nonin-

N vasive techniques that are available for monitoring functioning of the central nervous
system. Neuromonitoring techniques are essential tools used in evaluating patients with neu-
rological injury in critical care settings. Neuromonitoring is typically used when a clinical neurological
examination is either difficult or not practical to perform, such as during an operative procedure or
when the patient's mental status has deteriorated. Depending on the technique used, neuromonitoring
allows the health care staff to evaluate motor and sensory function, brain activity, blood fiow, and
intracranial pressures. Nurses must be able to use various neuromonitoring techniques and interpret
their results to provide the best care for their patients. However, useful and user-friendly information
on the indications and utility of neuromonitoring is scarce. In this article, I review 2 pertinent types of
noninvasive neuromonitoring techniques encountered in intensive care units, transcranial Doppler
monitoring and electrophysiology, for their indications, use, and applicability to patient care. Invasive
monitoring such as intracranial monitoring is not covered here.

CNE Continuing Nursing Education

This article has been designated for CNE credit, A closed-book, multiple-choice examination follows this article, which tests your knowledge
of the following objectives:

1, Describe neuromonitoring with transcranial Doppler monitoring and electrophysiology for the neurologically impaired patients
2, Identify normal and abnormal findings with transcranial Doppler monitoring and electrophysiology
3, Discuss the indications, use, and applicability of transcranial Doppler monitoring and electroencephalography in the neurocritical patient

©2014 American Association of Criticai-Care Nurses doi: http://dx,doi.org/10,4037/ccn2014506

3 0 CriticalCareNurse Vol 34, No, 3, JUNE 2014 www,ccnoniine,org

Transcranial Doppier Monitoring
Transcranial Doppler (TCD) monitoring is a nonin-
vasive technique that uses ultrasonic waves to measure
the velocity of blood fiow in the brain.' A pulsed Doppler
2-MHz portable ultrasound machine can be used at the
bedside to measure changes in blood fiow. TCD moni-
toring is most frequently used to detect and follow the
course of vasospasm in patients with aneurysmal sub-
arachnoid hemorrhage.^^ However, TCD monitoring can
be used any time that knowledge of cerebral circulation
and the state of blood fiow to the brain is of importance.
Table 1 lists both conventional and experimental uses of
TCD monitoring." Advantages of using TCD monitor-
ing include the following: it allows real-time detection
of changes in blood fiow, it is relatively inexpensive, it
can be repeated ñ^equently or used continuously if needed,
and most hospital systems already have an ultrasound
department.
In order to perform TCD monitoring, an ultrasound
probe is placed on specific locations on the skull where
the bone is very thin, called cranial windows. The 3 main
cranial windows are temporal, orbital, and occipital.
Each window allows access to different arteries. These
bony windows must be thin enough to allow insonation
of the artery. Insonation refers to the exposure of the
artery to ultrasound waves. Thick skull bones do not
allow passage of an ultrasound signal from the transducer.
In the case of no signal return, the technician reports that
there are "no windows" on TCDs. If the windows are acces-
sible, the TCD transducer will insonate or expose an artery
to an ultrasound signal through the bone (Figure 1).
The ultrasound beam bounces off erythrocytes in the
insonated artery and returns the signal to the transducer."
The signal is interpreted by software and presented as
a series of numbers, which are then used to determine
fiow velocity. There is also an auditory confirmation of
insonation of the artery, as the fiowing blood makes a
Author
Catherine Harris is an assistant professor atfefferson School of
Nursing and an acute care nurse practitioner in the neurocritical
care unit at Jefferson Hospital for Neuroscience in Philadelphia,
Pennsylvania.
Corresponding author: Catherine t-tarris, mi MM. CRNf. Thomas Jefferson University,
Schoot of Nursing, 901 Watnut Street, Suite 823, Philadetphia, PA 19107 (e-mait: blood fiow through
catherine.harris@jejferson.edu).
To purchase electronic or print reprints, contact the American Association ofCriticat-
Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Plume, (800) 899-1712 or (949)
362-2050 (ext532):fax, (949) 362-2049: e-mait, reprint.i@aacn.urg.
www.cononline.org
\3.U\Q 1 Uses for transcranial Doppler imaging^
Conventional Experimental
Assessment for intracranial Detection of cerebral venous
stenosis thrombosis
Detection of cerebral emboii Evaluation of autoreguiation
Assessment for collateral flow Evaluation of arteriovenous
patterns malformations
Assessment for cerebral blood Continuous monitoring
flow during angiography
Evaluation of stroke risk in chil- Evaluation of blood flow
dren with sickle cell disease during a migraine
ä Based on information from the American Institute of Ulfrasound in Medicine,'
Marshall ef al,' and rsivgoulis et al.'
swooshing sound corresponding to each heartbeat,
which the technician can hear and see on the TCD
screen (Figure 2). If the swooshing sound is dampened,
the technician may attempt to relocate the artery.
Table 2 provides important information regarding
normal values of TCDs. In the first column is the name
of the cranial window. The second column lists the asso-
ciated arteries that can be identified in that window, and
the third col-
umn shows at Neuromonitoring allows mofor and sensory
what depth function, brain activity, blood flow, and
the arteries intracranial pressures to be evaluated,
would be
expected. The last column is the anticipated mean fiow
velocity of the arteries. Higher values or no value may
indicate abnormal fiow or lack of fiow.
After performing TCD monitoring, the technician
prints out an output sheet of various numbers (Figure 3)
that indicate the difterent arteries that were insonated in
both hemispheres. Each artery may be repeated several
times on both the right and left sides because of the vari-
ation in fiow rates. The important numbers are the ones
that refiect the depth at which each artery was insonated
and the mean fiow velocities. If there is a large deviation
from normal depth or from the patient's baseline, the
TCD numbers should be viewed with some skepticism.
Findings on clinical examination should always take pri-
ority, and other imaging techniques such as computed
tomographic angiography may be warranted.
The mean fiow velocity refiects the average rate of
the artery. The peak fiow velocity is
significantly higher than the mean fiow velocity and is
subject to fiuctuations in the patient's heart rate and
blood pressure. Therefore, the peak now velocity varies
CriticalCareNurse voi 34, No. 3, JUNE 2014 3 1
 Suboccipital
window:
Vertebral artery
Basilar artery

Temporal window
MCA
Transorbltai
ACA, PCA
window:
ICA
Ophthainnic artery

Jaw angle window: Vertebral

iCA artery
ECA, CCA

Figure 1 Transcranlal Doppier imaging windows and insonated arteries.

Abbreviations: ACA, anterior cerebral artery; CCA, common carotid artery; ECA, external carotid artery; ICA, internai carotid artery; MCA, middie cerebral artery;
PCA, posterior cerebral artery.

Reprinted trom Scheil et ai,' witb kind permission trom Springer Science+Business Media B.V,

2 Normai findings on transcraniai Doppier

imaging
Flow velocity,
Depth, mean (SD),
Window Artery mm cm/s
Temporal Middle cerebral 30-60 55(12)
Temporal Anterior cerebral 60-85 50(11)
Temporal Posterior cerebrai 60-70 40(10)
Temporal Terminal internal 55-65 39(9)
carotid
Orbital Internal carotid 60-80 45(15)
artery siphon
Orbital Ophthalmic 40-60 20(10)
Occipital Vertebral 60-80 38(10)
Occipital Basilar 0-110 41 (10)

Figure 2 Transcranial Doppier imaging output.

Abbreviations: BA, basiiar artery; Ex, external; iCA, internai carotid artery;
L, iett; MCA, middle cerebrai artery; OA, opbtbaimic artery; R, rigbt.
more widely than the mean flow velocity. The mean flow
velocity is considered more stable and thus a more reli-
able indicator of blood flow in the brain, so it has been
established as the criterion to follow.'
After subarachnoid hemorrhage, TCD monitoring
may be ordered daily or twice daily to assess the mean
flow velocity. Primary providers who order TCD moni-
toring will be most interested in the mean flow velocity
of the middle cerebral artery (MCA), the anterior cere-
bral artery (ACA), and the basilar artery because they
are the largest vessels and thus have the potential to
cause the most devastating strokes. They are also the 3

32 CriticalCareNurse Voi 34, No, 3, J U N E 2014 www.ccnoniine.org

 Left Right

Label Depth Mean Peak Edv PI Rl Label Depth Mean Peak Edv PI Rl
2 MHz
L-EX-ICA 50 -24,6 -58,1 -14,9 1,73 0,74 R-EX-ICA 50 -23,5 -56,2 -4,21 2,21 0,91
L-EX-ICA 52 -23,5 -52,4 -14,2 1,61 0,72 R-EX-ICA 50 -22,7 -60,1 -4,17 2,40 0,92
L-OA 50 19,6 39,7 6,17 1,64 0,81 R-EX-ICA 52 -25,4 -69,3 -7,50 2,39 0,88
L-Siphon 60 32,7 62,8 18,1 1,34 0,71 R-OA 50 18,1 36,2 4,39 1,72 0,87
-20.4 -43,1 -5,87 1,68 0,77 R-OA 50 21,2 38,1 5,45 1,52 0,85
L-Siphon 60 25,4 53,5 7,09 1,79 0,85 R-Siphon 66 36,2 65,8 14,2 1,39 0,77
L-MCA 50 55,8 115 34,6 1.43 0,69 R-VA 60 -20,0 -34,6 -7,28 1,28 0,76
L-MCA 52 64.3 137 39,8 1,51 0,71 R-VA 62 -25,8 -65,8 -4,56 2,33 0,92
L-MCA 56 61,2 132 38,5 1,51 0,70 R-VA 66 -16,6 -57,4 -3,99 3,09 0,91
L-MCA 58 70,1 139 45,4 1,32 0,67 R-VA 66 -15,8 -58,9 -3,62 3,17 0,91
L-MCA 58 68.1 142 43,2 1,44 0,69 R-VA 66
L-MCA 58 73,2 139 46.6 1,26 0,66 R-MCA 50 42,7 89,3 25,4 1,47 0,71
L-MCA 58 62,8 133 39,1 1,48 0,70 R-MCA 52 33,9 69,3 14,5 1,58 0,78
L-MCA 58 70,8 139 44,1 1,33 0,68 R-MCA 54 40,8 79,7 22,3 1,39 0,71
L-MCA 60 66,6 134 44,3 1,34 0,67 R-MCA 54 55,8 104 29,0 1,29 0,70
L-MCA/ACA 66 71,6 184 44.1 1,95 0,75 R-MCA 54 65,8 131 41,2 1,34 0,68
-40,8 -67,4 -25,1 1,02 0,62 R-MCA 58 65,8 167 37,0 1,95 0,77
L-MCA/ACA 66 61,2 161 37,2 2,00 0,74 R-MCA/ACA 64 43,5 82,0 28,9 1,21 0,64
-40.0 -72,8 -25,9 1,16 0,62 -50,8 -97,4 -30,5 1,30 0,68
L-ACA 66 -42,4 -72,0 -28,0 1,03 0,57 R-MCA/ACA 66 46,6 85,5 26,6 1,20 0,66
L-ACA 66 -44,3 -77,8 -28,9 1,09 0,59 -37,0 -67,0 -20,4 1,23 0,68
L-ACA 70 -44,7 -80,1 -30,7 1,09 0,61 R-ACA 70 -43,1 -87,0 -27,4 1,36 0,68
L-T-ICA 50 23,1 62,0 3,05 2.50 0,94 R-ACA 68 -39,7 -75,5 -24,6 1,27 0,67
L-PCA P1 70 43,9 70,8 20,7 1,11 0,68 R-MCA 50 64,7 146 37,5 1,66 0,72
L-PCA P1 70 46,2 68,5 25,4 0,91 0,62 R-MCA 56 75,1 138 48,8 1,18 0,64
L-PCA P1 68 43,5 72,0 23,4 1,10 0,67 R-MCA 56 73,9 144 44,7 1,33 0,68
L-VA 60 -26,2 -76.6 -9,41 2,32 0.60 R-T-ICA 56 20,0 45,4 4,71 2,00 0,89
L-VA 64 -20,0 -30,4 -12,4 0,89 0,58 R-T-ICA 56 23,5 54,7 4,97 2,02 0,87
L-VA 60 -21,9 -31,2 -15,8 0,69 0,49 R-PCA P1 56 18,1 45,0 2,61 2,28 0,92
L-VA 64 -21,2 -30,0 -14,6 0,72 0,51 R-PCA P1 64 22,7 40,8 13,3 1,19 0,66
L-VA 66 -20,4 -32,0 -12,8 0,92 0,59 R-PCA P1 66 21,9 41,6 12,6 1,30 0.68
L-VA 66 -21,2 -31,2 -14,4 0,78 0,53 R-PCA P1 72 20,0 45,4 6,74 1,80 0,79

BA 80 -111 -57,4 -6,13 1,73 0,83

BA 80 -30,8 -66,6 -13,1 1,76 0,77
BA 80 -28,1 -68,1 -13,9 1,91 0,79
Left Lindegaard ratio = 2,97 Right Lindegaard ratio = 2,95

Figure 3 Transcranial Doppler imaging output numbers.

Abbreviations: ACA, anterior cerebral artery; BA, basilar artery; Edv, end-diastolic velocity; EX, external; ICA , infernal carotid arterv; L. lef; MCA, middle cerebral artery;
OA, ophthalmic artery; PI, tirst section of posterior cerebral arfery; PCA, posterior cerebral artery; PI, pulsafility index; Rl, resistance index; T, terminus; VA, vertebral artery.

vvww,ccnonline,org CriticalCareNurse Voi 34, No. 3, JUNE 2014 33

 arteries that are large enough for endovascular interven-
tion if warranted. Significant increases or decreases in
the mean flow velocity should be reported to the primary
provider, as they may reflect important changes in circu-
lation in the brain. A significant increase in mean flow
velocity may be due to increasing severity of vasospasm
or hyperemia. A significant decrease in mean flow veloc-
ity may reflect an impending or completed stroke. An
extremely important change to report is when a previ-
ously high mean flow velocity is no longer detectable,
again possibly indicating a stroke. Patients with consis-
tently high mean flow velocity in the MCA should be
monitored very closely for potential stroke.
Another very important number to follow is the Lin-
degaard ratio. This ratio is the mean flow velocity in the
MCA divided by the mean flow velocity in the ipsilateral
internal carotid artery (ICA).'" This ratio helps to distin-
guish between true vasospasm and hyperemia. Hyperemia
is an increase in blood flow, which increases mean flow
velocity, possibly as a result of hypervolemia, but does not
indicate
Changes in the mean flow velocity of the vasospasm. In
rTiiddle or anterior cerebral artery and the hyperemia,
basilar artery are signs of trouble. the mean flow
velocity in the
MCA increases to more than 200 cm/s, but the Linde-
gaard ratio does not increase because an associated
increase in blood flow to the ICA also occurs. Table 3
shows the criteria for various degrees of vasospasm.
The output numbers on TCDs should not be used by
themselves as the sole criteria for making clinical deci-
sions and should always be correlated with findings on
the patient's neurological examination. Technical errors
are common, especially if the technician does not per-
form TCD often. Results may be dependent on the skill
of the technician. Often, results can change dramatically
when the only diièrence is that a different technician is
performing the TCD monitoring. Alternatively, errors
may occur if the bone windows are thickened or the ves-
sels are difficult to access and/or the patient is uncoop-
erative, confused, or combative.
TCD: Nursing Implications
Nurses at the bedside are responsible for ensuring
that TCD monitoring is done in a timely fashion and for
making sure that the patient is in optimal condition for
the technician to perform the procedure. Patients who
34 CriticalCareNurse voi 34, No. 3, JUNE 2014
Tsblö 3 Mean flow velocities and Lindegaard ratios
by severity of vasospasm
Vasospasm Flow velocity, Lindegaard
severity mean (SD), cm/s ratio^
None <120 <2
Mild 120-150 2-3
Moderate >150-200 >3-6
Severe >200 >6
' Ratio of flow velocity in middle cerebral artery to flow velocity in internal
carotid artery.
are combative and conñised may need behavioral or
pharmacological intervention before the start of the pro-
cedure. Nurses who are aware of the timing of the study
can make sure that patients are in bed and prepared.
Nurses might also consider having a patient care assistant
stay with the patient to help assuage fears or redirect the
patient's attention. Because the procedure can be limited
by movement or agitation, nurses can greatly facilitate
the situation by using their organizational skills and some
forethought about how the patient might respond. After
the procedure is completed, the nurse should review the
mean velocities of the MCA and compare those values
with valuesfi-omthe previous day. If there are any signif-
icant categorical differences, such as an increase fi:om
mild to moderate spasm or moderate to severe spasm,
the nurse should alert the provider. Also if there is an
increase in the Lindegaard ratio above 2 or loss of the
ability to find the artery, the nurse should alert the
provider.
Electrophysiology
Neurological electrophysiology includes monitoring
of various electrical impulses in the body. In the intensive
care unit, the most frequently encountered neuroelectro-
physiology techniques are electroencephalography (EEG)
and one of its derivatives, bispectral (BIS) monitoring.
Other derivatives of EEG include somatosensory evoked
potentials (SSEPs) and brainstem auditory evoked poten-
tials (BAEPs). These last 2 studies are more frequently
used in the operating room; however, they may be used
as adjunctive studies in assessing for brain damage and
brain death. SSEPs and BAEPs can be used to evaluate the
extent of brain damage and assist providers in discussing
prognoses with patients' families. Some experimental
studies" '^ have also been done to evaluate the utility of
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SSEPs and BAEPs in the intensive care unit, but at this
time those 2 techniques are not the standard of care.
An EEG is the evaluation of spontaneous electrical
activity in the brain used to guide seizure management,
assess level of consciousness, detect cerebral ischemia,
and monitor effects of medications such as barbiturates
in coma induction. The brain consists of billions of neu-
rons, all of which release an electrical charge. Neurons
are charged by the constant fiux of ions such as sodium
and potassium across their membranes. The ions are
transferred in and out of the cell body by membrane
transport proteins. Neurons send electrical impulses
(action potentials)firomthe cell body via myelinated
axons, which provide the signal to release neurotrans-
mitters from synaptic vesicles. This process is how the
neurons communicate with the body to perform various
functions. Although the electrical charge of 1 neuron is
too small for EEG to pick up alone, the synchronous
activity of millions of neurons generates a measurable
charge. Scalp electrodes can be used to monitor the fiuc-
tuations of the electrical charges of neurons. Evidence of
seizure activity can be seen on an EEG in the form of
abnormal fiuctuations of voltage displayed as spikes and
ñuctuating waveforms. EEG features do not correspond
to specific anatomy; rather, they correspond to territo-
ries of brain activity that cluster together. Therefore,
EEG is often used as an adjunctive technique to validate
results of other diagnostic tests.
EEG features are measured in terms of amplitude,
latencies, frequency, symmetry, and patterns (Table 4).
The amplitude of a variable is a measure of its change over
time. The amplitude of an EEG feature is compared with
either known norms or a person's baseline. The highest
value of an amplitude is called the peak. Latencies are a
Table 4 Electroencephalography attributes
Attribute Measures Evaluation
Ampiitude Microvolts (mV) Low or high
Latency Milliseconds (ms) Fast or slow
Frequency Hertz (Hz) Fast or slow
measure of a time delay between a stimulus and its
response. The latency comes just before the amplitude
on the EEG. Erequencies are oscillations that are syn-
chronized activity corresponding to a series of neuronal
networks." Some commonly known frequency bands are
delta, theta, alpha, beta, gamma, and mu waves (Table 5)."
Symmetry is assessed visually on EEGs to ascertain if
both hemi-
spheres are Pafienfs wifh consistenfly high mean flow
roughly velocify in fhe middie cerebral artery should
equivalent. be monitored very cioseiy for potential stroke.
Einally, pat-
terns can be identified, such as burst suppression, status
epilepticus, or brain death (Eigure 4). Nurses can and
should be taught to identify these 3 patterns, all of which
are extremely important in treatment of patients.
Status epilepticus can be either convulsive or non-
convulsive, so interpretation of EEG waves can be diffi-
cult and beyond the purview of bedside nurses.
However, any change in mental status of a patient may
prompt the nurse to look at the EEG if it is being contin-
uously monitored. Typical markings of status epilepti-
cus are spikes in amplitude, although such spikes vary
widely depending on the type of seizure. Movement of
the EEG leads may also cause artifact that may mimic
the look of seizure activity, so the nurse may receive a

T a b l e 5 Frequency bands^

Type Location Hertz (Hz) Amplitude Normal occurrence Pathological occurrence

Delta Frontal <4 High Slow-wave sleep Metabolic encephalopathy, diffuse
injury
Theta Random 4-8 High Drowsiness Metabolic encephalopathy
Alpha Posterior head 8-13 Low Eye closing, relaxed Coma
Beta Symmetrical 13-30 Alert, active, concentration Benzodiazepines
Gamma Somatosensory cortex 30-100 Cross-modal sensory Cognitive decline
Mu Sensorimotor cortex 8-13 Rest-state motor neurons Autism, social and cognitive deficits
^ Based on information from Bianco ef al."

www.ocnoniine,org CriticalCareNurse voi 34, No, 3, JUNE 2014 35

 Normal EEG
•J
1
.'•••y/,-"''»-!'-

'„•-. • „ ' ' , . •---

• " \ "
.••'.•V-V--1V '•Af.'-'..'-••"•.•
"/•• .'vA-^"'

Status epileptícus

Burst suppression
/I

Brain death

Figure 4 Electroencephalography (EEG) pafferns.

cali from the epileptologist who is monitoring the patient
for clarification.
Burst suppression is evidenced by voltage attenua-
tion with bursts of generalized activity. Burst suppres-
sion is seen in clinical states such as anoxic brain injury
or prolonged resuscitation or it can be induced with
medications such as pentobarbital or propofol. When
burst suppression is pharmacologically induced.
providers will typically ask the nurses to titrate the med-
ications to a certain number of bursts per minute. For
example, in an induced coma, the order may read to
titrate either a pentobarbital or propofol infusion to 4 to
6 bursts per minute. If a standard EEG screen displays 15
seconds of information, the nurse should see a minimum
of 1 burst of electrical activity on the screen at any given
time, but no more than 2. An accurate assessment of

36 CriticalCareNurse voi 34, No. 3, JUNE 2O14 www.ccnonline.org

 burst suppression clearly depends on the time sequence
of the computer screen, which should be verified and
documented.
Brain death is the cessation of any activity on EEC
In this scenario, the nurses can alert providers that no
activity has been seen on EEG for an extended period.
This information may prompt providers to initiate other
evaluation methods to conflrm brain death.
Despite an effort to identify the meaning of patterns,
their interpretation remains largely elusive and it is diffi-
cult to correlate EEG patterns with clinical condition.
One derived measure of EEG has been interpreted to
correlate with level of consciousness. The BIS monitor
detects a slowed pattern of electrical activity and corre-
lates to depth of anesthesia.'^ BIS monitoring uses statis-
tically based and complex equations to derive a sum of
EEG parameters that include time and frequency. These
composite measures are then assessed in relation to
various signal components. This process allows the BIS
monitor to detect certain patterns, which can then be
correlated with depth of anesthesia. In an awake patient,
the BIS monitor would detect a small amplitude with a
fast frequency, whereas in moderate sedation, the BIS
monitor would detect an increase in amplitude at a slower
ñ-equency. In a patient under general anesthesia, the BIS
monitor would detect a large amplitude at a very slow
frequency. In a patient under deep anesthesia, the BIS
monitor would detect an isoelectric charge that looks
similar to an EEG consistent with brain death (Eigure 4).
BIS monitoring is commonly used in intensive care
units to ascertain the level of consciousness of the patient.
Sedative and anesthesia can be titrated on the basis of the
BIS monitoring, depending on the needs of the patient.
The lower the number on the BIS monitor, the deeper
the level of anesthesia'" (Table 6).
BAEPs and SSEPs are also derivatives of EEG that
correlate with specific electrical impulses. SSEPs are used
to monitor spinal cord ascending pathways and their
functional integrity. Tiny needle electrodes are placed in
the skin along the medial nerve and the posterior tibial
nerve. Scalp electrodes capture the response of an elec-
trical stimulation that is generated through the needles.
Once the stimulus is given peripherally, there is a certain
amount of time that is expected to elapse before the scalp
electrodes record the response. If there is a delay or no
response is recorded, a break in the integrity of the ascend-
ing pathways of the spinal cord is indicated. A break in
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Table 6 Index for bispectrai monitoring device^
Index range Clinical state
>90-100 Awake
>60-90 Light to moderate sedation
>40-60 General anesthesia
20-40 Burst suppression
<20 isoelectric electroencephalogram
" Based on information trom Keiiy."
T a b l G 7 Waves seen in brainstem auditory evoked
potentials
Wave Probable anatomic correlate
P1 (wave 1) Distal acoustic wave
P2 (wave 11) Proximal acoustic nerve/cochlear nucleus
P3 (wave ill) Lower pons
P4 (wave IV) Mid/upper pons
P5 (wave V) Lower midbrain
the function of the system could be due to a malfunction
in the neuromonitoring system, the presence of central
nervous system depressants/paralytic agents, or spinal
cord injury or brain injury. SSEPs might be used in the
intensive care unit in a patient who does not wake up
after surgery or as an adjunctive diagnostic tool in deter-
mining brain death. In brain death, no response would
be captured through the scalp electrodes despite an
intact spine.
BAEPs are used to evaluate the function and integrity
of the brainstem. BAEPs also entail the placement of
electrodes on the scalp. BAEPs are elicited by the appli-
cation of brief transient stimuli such as audible clicks in
the ears. The response is then received and recorded via
electrodes. Eive
common types The lower the number on the BIS monitor,
of waves that the deeper the level of anesthesia,
are recorded
from BAEPs corre.spond to anatomic locations (Table 7).
BAEPs are more robust than SSEPs because BAEPs are
more resistant to effects of medications or anesthesia.
Disorders of the ear such as labyrinthitis do not affect
BAEPs. Even hearing loss does not preclude the use of
BAEPs. Wave V is used to assess hearing loss in the clini-
cal setting; however, waves I through IV can still be
assessed for a baseline. BAEPs are largely affected only
CriticalCareNur.se Voi34, No. 3, JLiNE20t4 37
by a structural abnormality such as a stroke, tumor, or
cerebral edema in the brainstem. Signal changes may
start to occur when intracranial pressures exceed 30 mm
Hg." The presence of BAEPs will disappear in more than
80% of patients who are clinically brain dead. Because
BAEPs are not 100% sensitive and specific for brain
death, they can be used as an adjunctive diagnostic tool,
but they cannot be used alone to declare brain death.
Electrophysiology: Nursing Implications
Nurses are typically not responsible for reading or
interpreting EEG, SSEPs, or BAEPS; however, they do
monitor continuous EEG for burst suppression and fol-
low BIS recordings to determine a patient's level of con-
sciousness. Therefore, it is important for nurses to
understand how these techniques work. Furthermore,
knowledge of these techniques assists nurses in explain-
ing to patients' families what is going on and educating
them on what it all means. Nurses are instrumental in
this process, but educating patients' families requires a
solid understanding of the technology.
Summary
This article reviewed 2 important noninvasive neu-
romonitoring techniques that are commonly used in
neurocritical care settings. Eor nurses who work in a
general critical care setting and do not encounter neuro-
critical care patients on an everyday basis, understand-
ing key techniques in neurocritical care is essential. EEG
and TCD play a major role in understanding a patient's
overall neurological status and prognosis. Nurses must
understand the importance of these techniques, how
they work, and how to interpret their meaning in the
context of the individual patient. Understanding neu-
romonitoring is an essential aspect of working with criti-
cally ill neurological patients. CCN
Financial Disclosures
None reported.
3 8 CriticalCareNtirse Voi 34, No, 3, JUNE 2014
Now that you've read the article, create or contribute to an online discussion about
this topic using eLetters, Just visit www,ccnonline,org and select the article you want
to comment on. In the full-text or PDF view of the article, click "Responses" in the
middle column and then "Submit a response,"
To learn more about neuromonitoring, read "Intracranial Pressure
Waveform Morphology and Intracranial Adaptive Capacity" by Fan
et al in the American Journal of Critical Care, November 2008;17:545-
554. Available at wtvw.ajcconline.org.
References
1, Aaslid R, Markwalder TM, Normes H, Noninvasive transcranial Doppler
ultrasound recording offlowvelocity in basal cerebral aiteries. J Neurosiirg.
1982;57:769-774,
2, Treggiari-Venzi MM, Suter PiVl, Romand JA, Review of medical prevention
of vasospasm after aneurysmal subarachnoid bemorrhage: a problem of
neurointen,sive care, Neurosurgery. 2001;48:249-261,
3, Oyama K, Criddle L, Vasospasm after aneurysmal subarachnoid hemorrhage,
Crit Care Nurse. 2004;24:58-60,62,64-67,
4, American Institute of Ultrasound in Medicine, AIUM practice guideline
for the performance of a transcranial Doppler ultrasound examination for
adults and children,/ UltrasoundMed. 2012;31:1489-1500,
5, Marsball SA, Nyquist P, Ziai WC, Tbe role of transcranial Doppler ultra-
sonography in the diagnosis and management of vasospasm after aneury.s-
mal subaracbnoid hemorrhage, Neurosurg Clin North Am. 2010;21;29f-303.
6, Tsivgoulis G, Alexandrov AV, Sloan MA, Advances in transcranial
Doppler ultrasonongraphy, Curr Neurol Neurosei Rep. 2009;9;46-54,
7, Scbell R, Cole D, Lichtor JL, Miller RD, Neurophysiologic monitors. In:
Miller RD, Licbtor JL, eds. Atlas of Anesthesia. Vol, 3, New York, NY:
Springer Publishing; 2002:chap 10,
8, Padayachee TS, Kirkbam FJ, Lewis RR, et al, Transcranial measurement of
blood velocities in tbe basal cerebral arteries using pulsed Doppler ultra,sound:
a method of assessing tbe circle of Willis, Ultrasound Med Biol. 1986;12:5-14,
9, Sloan MA, Alexandrov AV, Tegeler CH, et al, Transcranial Doppler ultra-
sonograpby in 2004: a comprehensive evidence-based update. Neurology.
2004;62(9):1468-148I,
10, Lindegaard KF, Nornes H, Bakee SJ, Sorteberg W, Nakstad P, Cerebral
vaso,spasm after subarachnoid haemorrhage investigated by means of tran-
scranial Doppler ultrasound, Aeta Neuroehir SuppI (Wien). 1988;42:81-84,
11, Amantini A, Amadori A, Fossi S, Evoked potentials in the ICU, EurJ
Anaesthesiol SuppI 2008;42:196-202,
12, Emerson RG, Pedley TA, Clinical neuropbysiology: electroencephalograpby
and evoked potentials. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J,
eds. Neurology in Clinieal Practice. 6th ed, Philadelphia, PA: Butterworth-
Heinemann: 2012:cbap 32A,
13, Andrade-Valenca LP, Dubeau F, Mari F, Zelmann R, Gotman J. High-frequency
oscillations recorded on scalp EEG, Neurology. 2011;77:524-531,
14, Blanco JA, Stead M, Krieger A, et al. Data mining neocortical bigb-fVequency
oscillations in epilepsy and controls. Brain. 2011;134(10):2948-2959,
\b. Olson D, Chioffi SM, Macy GE, Meek LG, Cook HA, Potential benefits of
bispectral index monitoring in critical care: a case study. Crit Care Nurse.
2003:23C4):45-52,
16, Kelly SD, Monitoring Consciousness: Using the Bispectral Index during Anes-
thesia. 2nd ed. Boulder, CO: Covidien; 2010,
17, Im JJ, Park BR, Does oxygen deficit to tbe cerebral blood flow caused by
subdural hematoma and/or increased intracranial pressure affect tbe vari-
ations in auditory evoked potentials in white New Zealand rabbits? Nra-
rosriie«, 2002:317:139-142,
www,ccnoniine,org
 CCN Fast Facts CriticalCareNurse
The journal for high acui;,'. progressive, and critical care nursing

Neuromonitoring Indioations and

Utility in the Intensive Care Unit
Facts depth the arteries would be t.ipected. 1 he last column is the
Neuromonitoring techniques are essential tools used anticipated mean flow velocity of the arteries. Higher val-
in evaluating patients with neurological injury in critical ues or no value may indicate ahiiormai ' i(iw or lack of flow.
care settings. Nurses must be able to use various neu- • Nurses should ensure that T' D mon loring is done in a
romonitoring techniques and interpret their results in timely fashion and make sui ;hat t^i.' patient is in optimal
order to provide the best care for their patients. condition for the technician o per orm the procedure
After the procedure is comp ^ reel, the nurse should review
Transcranial Doppler Monitoring the mean velocities of the n itidle cerebral artery and com-
• Transcranial Doppler (TCD) monitoring is a nonin- pare those values with valu, s tb »m the previous day. If
vasive technique that uses ultrasonic waves to meas- there are any significant caiigur ^al differences, the nur;e
ure the velocity of blood flow in the brain. A pulsed should alert the provider. A 'so ii here is an increase in t le
Doppler 2-MHz portable ultrasound machine can be Lindegaard ratio above 2 or os.s ''the abflity to find th.
used at the bedside to measure changes in blood flow. artery, the nurse should aler tht ; ovider.
• To perform TCD monitoring, an ultrasound probe
is placed on specific locations on the skull where the Electrophysiology
bone is very thin, called cranial windows. The 3 main • In the intensive care unit, the .mo.M frequently encountered
cranial windows are temporal, orbital, and occipital. neuroeiectrophysiology techniques are electroencephak'g-
Each window allows access to different arteries. raphy (EEG) and one of its di rival ves, bispectral (BIS)
• The Table provides important information regarding monitoring.
normal values of TCDs. In the first column is the • An EEG is the evaluation of spontaneous electrical activity
name of the cranial window. The second column in the brain used to guide seizure management, assess
lists the associated arteries that can be identified in level of consciousness, detect cerebral ischemia, and mon-
that window, and the third column shows at what itor effects of medications such as barbiturates in coma
induction.
T a b l e Normal findings on transcranial Doppler imaging • EEG features are measured in terms of amplitude, latencies,
frequency, symmetry, and patterns.
Flow velocity,
• It is difficult to correlate EEG patterns with clinical corn '• -
Depth, mean (SD),
Window Artery mm cm/s tions. One derived measure of EEG has been interprete«.^
to correlate with level of consciousness. The BIS monito
Temporal Middle cerebral 30-60 55(12)
detects a slowed pattern of electrical activity and corréis i s
Temporal Anterior cerebral 60-85 50(11) to depth of anesthesia.
Temporal Posterior cerebral 60-70 40 (10) • Nurses are typically not responsible for reading or intei -
Temporal Terminal internal 55-65 39 (9) preting EEGs; however, they do monitor continuous EEG
carotid for burst suppression and follow BIS recoi dings to determine
Orbital Internal carotid 60-80
a patient's level of consciousness. Knowledge of these
45 (15)
artery sipbon techniques assists nurses in explaining to patients' families
Orbital
what is going on and educating them on what it all means.
Opbtbalmic 40-60 20(10)
Nurses are instrumental in this process, but educating
Oc:ipital Vertebral 60-80 38(10) patients' families requires a solid understanding of the
Occipital Basilar 80-110 41 (10) technology. CCN

Harris C. Neuromonitoring Indications and Utility in the Intensive Care Unit. Critical Care Nurse. 2014;34(3):30-40.

www.ccnonline.org CriticalCareNurse Voi 34, No. 3, JUNE 2014 3 9

CNE T e s t Test ID C143: Neuromonitoring Indications and Utility in the Intensive Care Unit
Learning objectives: 1, Describe neuromonitoring with transcranial Doppler monitoring and electrophysiology for the neurologically impaired patients
2. Identify normal and abnormal findings with transcranial Doppler monitoring and electrophysiology 3, Discuss the indications, use, and applicability of
transcranial Doppler monitoring and electroencephalography in the neurocritical patient

1. Which of the following is an experimental use of transcranial Doppler 7, Which of the following is not a derivative of electroencephalography (EEG)?
(TCD) imaging? a, Bispectral monitoring
a. Assessment for collateral flow patterns b, Somatosensory evoked potentials
b. Assessment for cerebral blood flow c, Brainstem auditory evoked potentials
c. Detection of cerebral emboli d, Transcutaneous nerve stimulation
d. Evaluation of arteriovenous malformations
8, An EEG is the evaluation of spontaneous electrical activity in the brain
?.. Which of the following is not a cranial window for TCD monitoring? used to guide which of the following?
a. Temporal a. Nutritional management
b. Orbital b. Seizure management
c. PariPtal c. Vasopressor therapy
d. Occipital d. Hypothermia therapy

3. Which of the following velocities are established as the criterion to follow 9, Which of the following are the typical markings of status epilepticus on
to assess blood flow in the brain? the EEG?
a. Meanflowvelocity a. Amplitude spikes
b. Peak now velocity b. Latency spikes
c. Modeflowvelocity c. Frequency spikes
d. Median flow velocity d. Delta spikes

4, A significant decrease in mean flow velocity may reflect which of the 10, What can an EEG help diagnose when there is cessation of any activity?
following complications? a. Level of sedation
a. Increasing severity of vasospasm b. Brain death
b. Impending or competed stroke c. Level of anesthesia
c. Increasing severity of hyperemia d. Brain hypoxia
d. Rupture of a cerebral aneurysm
11, What does the bispectral monitoring device indicate if the index range
5, The Lindegaard ratio examines the mean flow velocity in which of the number is 20-40?
following? a. Awake
a. Middle cerebral artery divided by the mean flow velocity in the ipsilateral b. Light to moderate sedation
internal carotid artery (ICA) c. General anesthesia
b. Anterior cerebral artery divided by the mean flow velocity in the ipsilateral d. Burst suppression
ICA
c. Posterior cerebral artery divided by the mean flow velocity in the ipsilat- 12, Brainstem auditory evoked potentials may show signal changes when the
eral ICA patient s intracranial pressure is at what level?
d. Basilar cerebral artery divided by the meanflowvelocity in the ipsilateral ICA a, 15-19 mm Hg
b, 20-24 mm Hg
6. A Lindegaard ratio of >3-6 indicates which degree of vasospasm severity? c, 25-29 mm Hg
a. None d, >30 mm Hg
b. Mild
c. Moderate
d. Severe
Test answers: Mark only one box for your answer to each question. You may photocopy this form,
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•b üb Qb Qb Ub Uh Ub Qb Qb Qb üb Ub
•c Qc Qc Qc ac ac üc ac Qc Qc Qc Qc
•d ad Qd Qd Qd Qd Dd Qd Ud Qd Qd Qd
Test ID: C143 Form expires: June 1, 2017 Contact hours: 1,0 Pharma hours: 0,0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%)
Synergy CERP Category A Test writer: Lynn C, Simko, PhD, RN, CCRN

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