Conference Proceeding

Somatosensory evoked potential monitoring

Georgene Singh

INTRODUCTION gracilis (first order fibres). It then decussates near

the cervicomedullary junction ascending via the
The somatosensory evoked potential (SSEP) monitoring contralateral medial lemniscus (second order fibres).
is the electrophysiological response of the nervous A second synapse occurs in the ventro‑posterolateral
system to sensory stimulation.[1] The peripheral mixed nucleus of the thalamus. The third order fibres from the
nerves are stimulated electrically, and the response is thalamus project to the frontoparietal sensory motor
measured along the sensory pathway. SSEP reflects the cortex.[2]
functional integrity of the somatosensory pathways.
They not only reflect specific sensory transmission but
also serve as more general indicators of neurological SENSORY PATHWAY
function in adjacent structures.

HOW IS A SOMATOSENSORY EVOKED

POTENTIAL GENERATED?
SSEPs are elicited by mechanical or thermal stimulation
of somatic sensory nerves. The most common stimulus
used is an electrical pulse. It is delivered to a peripheral
nerve which is a large mixed motor and sensory nerves
such as median nerve, ulnar nerve and common peroneal
or posterior tibial nerve.

The peripheral nerve stimulation activates the large

diameter fast conducting Ia muscle afferent and
Group II cutaneous nerve fibres. This produces a
neural transmission which proceeds both in the
normal direction (orthodromic) and in the reverse The waveform resulting from the stimulation of a
direction (antidromic). The orthodromic motor nerve is displayed as a plot of voltage against time
stimulation elicits a muscle response which is seen as and is characterised by measurements of post‑stimulus
a twitch and confirms stimulation. The orthodromic latencies (in milliseconds) and amplitudes (in
sensory stimulation produces the SSEP. The incoming microvolts) of particular peaks. According to
volley of neural activity from stimulation represents convention, deflections below the baseline are
primarily the pathway of proprioception and vibration labelled positive (P) and those above the baseline are
that ascends the ipsilateral dorsal column synapsing negative (N). Standard identification of waveforms is
in the dorsal column nuclei, nucleus cuneatus and by a letter designating the direction of the deflection
followed by a number representing the latency of the
Associate Professor, Department of Anaesthesiology, waveform.
Christian Medical College, Vellore, Tamil Nadu, India

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DOI:
10.4103/2348-0548.174745 How to cite this article: Singh G. Somatosensory evoked potential
monitoring. J Neuroanaesthesiol Crit Care 2016;3:97-104.

© 2016 Journal of Neuroanaesthesiology and Critical Care

| Published by Wolters Kluwer - Medknow | S97
 Generators of somatosensory evoked potential
after tibial nerve stimulation
Peak Generator Recording site
N20 Spinal root/cord Lumbar
P27 Nucleus gracilis Cervical spine
N35 Somatosensory cortex Scalp
P40 Somatosensory cortex Scalp

POST‑STIMULUS LATENCY
The post‑stimulus latency of an SSEP peak reflects the
time required for impulse transmission from the site of
sensory stimulation to the neurophysiological generator
of that peak. Thus, the latency depends on the length of
the sensory pathway and the speed of neural conduction.

Two measurements derived from the post‑stimulus

latencies are used to help characterise neurological
function, conduction velocity (CV) and central conduction
time (CCT).

CV can be estimated from the post‑stimulus latency

of evoked electrical activity and the distance from the
stimulus site to the recording electrode.

CCT is calculated by measuring the intervals between

the peaks and reflects pathophysiological alterations in
brain function.[1]

Generators of the somatosensory evoked potentials SSEPs consist of both short‑ (<40 ms) and long‑ (>120 ms)
after median nerve stimulation[3] latency evoked potentials. The primary cortical evoked
Peak Generator Recording site responses result from the earliest electrical activity
generated by the cortical neurons. They arise from
N9 Brachial plexus Erb’s point
the post‑central sulcus parietal neurons. These are the
N11 Posterior columns Cervical
short latency SSEPs that are most commonly studied
N13/P13 Dorsal column Cervical intraoperatively because they are less influenced by
nucleus cuneatus
anaesthetic factors.
N14, 15 Medial lemniscus Cervicomedullary
(brainstem) junction The secondary cortical potentials which are of longer
N18, 22 Parietal sensory cortex Scalp latency arise in the association cortex and are less
N20 Somatosensory cortex Scalp stable and have greater variability of waveform and
are extremely difficult to record in the operating room
environment.[4]

SSEP responses from the upper extremity primarily

represent activity in the posterior column pathway
whereas those from the lower extremity also include
additional components that pass in the spinocerebellar
pathway.

RECORDING OF SOMATOSENSORY
EVOKED POTENTIAL
The mode of stimulation is either the median nerve
at the wrist or the tibial nerve at the ankle. The
peripheral nerve is stimulated at a rate of 2–4 Hz with

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the duration of 0.2–2 ms depending on the type of RECORDING ELECTRODES
surgery. A sufficient number of repetitions must be
averaged to produce an interpretable SSEP. Generally,
100–500 repetitions are needed. The filters settings
should be kept constant during the procedure and
usually it lies in between 10 and 1000 Hz. The analysis
time for median nerve is 50 ms and for tibial nerve
is 100 ms.[5]

For the upper extremity, the evoked responses can be

measured from electrodes placed over the antecubital
fossa, supraclavicular fossa (brachial plexus), cervical
spine and cortex. For the lower extremity, they can Either standard disc electroencephalogram (EEG)
be recorded over the popliteal fossa, along the spinal electrodes or 12 mm twisted pair sub‑ dermal
cord (surface or epidural electrodes) and at cervical platinum‑iridium tip needle electrodes of 27‑gauge
and cortical locations. Response recordings are usually are commonly used. Skin preparation and the proper
recorded at multiple recording sites, to verify that
electrode placement are important. Either surgical
the nervous system is stimulated and to identify the
spirit or NuPrep Gel (Viasys Healthcare, US) is used.
location of neural compromise if the response is lost.
Electrodes need to be secured well or they may come
The cortical response is best recorded over the primary off during the procedure.[5]
somatosensory cortex appropriate for the nerve which
is stimulated. Recording electrodes are placed on the STIMULATION
scalp at C3’ or C4’ for median nerve and Cz’ or Cz’’ for
tibial nerve. The reference electrode is placed at Fpz. The When the median nerve is stimulated for SSEP
measuring peak latencies for median nerve are N20, P25 monitoring, the cathode should be placed between
and for tibial nerve are P37, N45. the tendons of the palmaris longus and the flexor
carpi radialis muscles, 2 cm proximal to the wrist
crease. The anode should be placed 2–3 cm distal to
the cathode or on the dorsal surface of the wrist. For
stimulation of the tibial nerve, the cathode should
be placed over the posterior portion of the medial
surface of the ankle, 1–2 cm distal and posterior to the
medial malleolus. The anode should be placed 2–3 cm
distal to the cathode. Gold‑plated stainless steel disc
electrodes with 9 mm diameters and 30 mm spacing
are used for stimulation.

International 10–20 system for electroencephalogram

It is helpful to record both brainstem and cortical SSEP

signals because though each can serve as a monitor
of dorsal column function, anaesthetic agents and
electrical interference in the  operating room affect the
two classes of signals differently. Cortical SSEPs are
relatively resistant to muscle noise and electrical artefact
but can be suppressed by anaesthetic agents. Brainstem CRITERIA FOR SIGNIFICANT CHANGE IN
SSEPs are much more susceptible to electrical noise SOMATOSENSORY EVOKED POTENTIAL
and electromyographic (EMG) artefacts but are largely
unaffected by anaesthetic drugs. Thus, both cortical and A 50% decrease in the amplitude and a 10% increase in
brainstem SSEPs complement each other. latency from the baseline is associated with injury to the

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large fibre dorsal column pathways.[6] SSEP responses which suppress or enhance the primary monitored
being very low in amplitude require prolonged pathway, global effect of anaesthetics on cortical and
averaging. Therefore, it may take 3–5 min to determine spinal cord neural processing.[9]
a significant change depending on the ambient noise
level. EFFECTS OF SPECIFIC ANAESTHETIC
In intraoperative spinal cord injury, loss of SSEP
AGENTS ON SOMATOSENSORY EVOKED
amplitude and degradation of the signal morphology POTENTIAL
are commonly noticed due to conduction block and
desynchronisation. The changes in latencies are less
Inhalational anaesthetic agents
Halogenated volatile anaesthetics are shown to reduce
prominent. Ignoring an amplitude change in the event of
SSEP amplitude and prolong their latencies. Isoflurane
normal latencies can therefore be disastrous. Moreover,
has the most potent effect and halothane the least.
50% decrease in the amplitude and a 10% increase in
Sevoflurane and desflurane are less soluble, and hence
latency alarm criteria is empirically based and are best
the anaesthetic effects on SSEP changes, rapidly when
used as a guide rather than a strict threshold above
their concentrations are changed making them ideal for
which it can be assumed that no adverse effect can
monitoring.[10]
happen. It is therefore prudent to inform even small
changes in the SSEP that exceed the prior variability. Nitrous oxide
This will facilitate more accurate identification of the Nitrous oxide (60–70%) decreases the cortical amplitude
cause and alerts the surgeon who will decide to either by about 50% but does not alter the cortical latency and
act or wait and observe. sub‑cortical waveform. This is because of its potent effect
on neuronal nicotinic acetylcholine receptors. Hence, it
The use of amplitude criteria is associated with better
is prudent to avoid nitrous oxide.[9]
sensitivity for detecting neurologic injury than latency
criteria. The SSEPs have high specificity and low Propofol
sensitivity to injury.[7] At high doses, it decreases the amplitude and
prolongs the latency but its combined use with other
OPTIMAL CONDITIONS FOR sedative‑analgesic agents allows for the use of lower
SOMATOSENSORY EVOKED POTENTIAL concentrations which preserve evoked potential.
MONITORING Because of its rapid metabolism, it allows easy titration
which makes it an anaesthetic of choice in SSEP
An anaesthetic technique that does not markedly monitoring.[9,10]
depress the cortical SSEP recording should be used. The
anaesthetic depth and physiological state of the patient Thiopentone sodium
should remain as constant as possible during critical A transient decreased amplitude and increased latency
periods of monitoring when there can be potential of evoked potentials are observed after induction with
surgical injury to the monitored pathway such as thiopentone. The effect lasts <10 min.[27] Minimal effects
during carotid clamping, aneurysm clipping or induced are seen on sub‑cortical and peripheral responses. It
hypotension. Major changes in the anaesthetic gas influences synaptic transmission more than axonal
levels and boluses of intravenous anaesthetics should conduction.[10]
be avoided during critical periods. Reliable baseline
Etomidate
tracings should be obtained during any intervention.
Etomidate causes an increase in the amplitude of cortical
Electrical interference due to cautery etc., should be
SSEPs. After a bolus, there is prolongation of the latency
reduced.[8]
and CCT. However, etomidate infusions have been used
to enhance SSEP recording in patients in whom it was not
ANAESTHETIC FACTORS WHICH ALTER possible to obtain reliable recordings due to pathologic
THE SOMATOSENSORY EVOKED findings.[10]
POTENTIAL RECORDING
Ketamine
Since anaesthetic agents depress the synaptic function, Although ketamine increases the cortical SSEP amplitude,
the more synapses in the monitored neurological it can increase intracranial pressure (ICP) in patients with
pathway, the more marked the effect on latency and cortical abnormalities and thus affect the SSEP. It has
amplitude of SSEPs. SSEPs are affected by altered minimal effects on sub‑cortical and peripheral SSEP
synaptic function, altered ancillary neural pathways responses.[10]

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Midazolam Hypoxia
Midazolam causes mild suppression of cortical SSEPs at Hypoxia leads to decreased amplitude similar to
doses used for induction of anaesthesia (0.2 mg/kg).[10] ischaemia.

Dexmedetomidine Increased intracranial pressure

At low doses, SSEPs are preserved but these are Because of the pressure‑related effects on cortical
suppressed at higher doses. It is best used in combination structures, reduced amplitudes and increased latencies
with other agents to decrease the doses of total are noticed with elevation in ICP.[10]
intravenous anaesthesia.[9]
Ventilation
Opioids The vasoconstrictive effects of hypercapnoea may
The latencies are preserved at high doses. However, modify spinal and cortical blood flow which may alter
there is a dose‑dependent decrease in amplitude. Even SSEP at PaCO2 <20 mmHg.[10]
at high doses (60 mcg/kg) the use of fentanyl results
in reproducible SSEPs making it an ideal agent during Changes in the neurochemical milieu also affect
SSEP recordings. Morphine causes dose‑dependent SSEPs. Blood glucose levels and electrolytes should be
suppression of SSEPs. Pethidine increases the amplitude monitored and kept within normal limits.
of SSEPs. Although remifentanil has a dose‑dependent
effect on evoked potentials, its rapid metabolism allows WHEN DO WE MONITOR
for titration.[4] SOMATOSENSORY EVOKED POTENTIAL?
Muscle relaxants To achieve maximal benefit from intraoperative SSEP
SSEPs are unaffected by muscle relaxants since SSEPs do monitoring, it is important to ascertain that the neural
not arise from muscle activity. The use of neuromuscular structures/pathways which are potentially at risk are
antagonists may improve the quality of recording amenable to reliable monitoring. There must be an option
by reducing EMG interference near the recording for either surgical or anaesthetic intervention should there
electrodes.[10] be a suspected dysfunction or trespass of the pathway so that
it minimises the chances of permanent damage. It should
PHYSIOLOGICAL FACTORS AFFECTING provide information about the nervous system under
SOMATOSENSORY EVOKED POTENTIAL anaesthesia as would be obtained by clinical examination
of conscious patients. SSEPs are monitored only if the site
Blood flow and blood pressure of stimulation and recording are accessible during surgery
The amplitude of cortical SSEPs decreases when the and reliable equipment and neurophysiologist are available
regional cerebral blood flow falls below 20 ml/min/100 g for accurate interpretation of recorded signals.[1]
and is completely lost below 15 ml/min/100 g. SSEPs
are more sensitive to hypoperfusion. Even an acceptable SURGICAL PROCEDURES MONITORED
blood pressure at the lower limit of normal autoregulation
may cause a decline in SSEPs. Further, SSEPs may be
WITH SOMATOSENSORY EVOKED
decreased by the local pressure effects due to retraction, POTENTIAL
positioning.[11]
Surgeries of the spine
Sub‑cortical regions, such as the brainstem, spinal cord • Correction of scoliosis with instrumentation[12]
and nerve, appear to be less sensitive to hypoperfusion. • Spinal cord decompression and stabilisation after
Hence, SSEP persists at blood pressures below which the acute spinal cord injury[13]
EEG routinely disappears. • Spinal fusion[14]
• Release of tethered cord[15]
Haematocrit • Resection of spinal cord tumour/cyst/vascular
Decreased oxygen delivery associated with anaemia lesion[15]
during isovolemic haemodilution results in • Correction of cervical spondylosis.[15]
progressives in the latencies of SSEP which is marked at
haematocrit <15%. At very low haematocrits, amplitude Surgeries of the brain
of all waveforms is decreased.[10] • Localisation of the sensorimotor cortex[15]
• Clipping of intracranial aneurysms[16]
Temperature • Resection of intracranial vascular lesions involving
Hypothermia causes an increase in latency and decrease the sensory cortex and arteriovenous malformation[17]
in amplitude. With increase in temperature, there are • Resection of thalamic tumour
decreases in amplitudes and loss of SSEP at 42°.[10] • Brainstem surgeries.

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Vascular surgery
• Carotid endarterectomy (CEA)[18]
• Abdominal and thoracic aortic aneurysm repair[19]
• Repair of coarctation of the aorta.[20]
Intensive Care Unit
• Prognostication in hypoxic‑ischaemic encephalopathy/
traumatic brain injury (TBI)[23]
• Acute neurological deteriorations.
Others
• Brachial plexus exploration after injury[20]
• Positioning during surgeries of the skull base[21]
• Chronic pain[22]
• Herpetic neuralgia.[4]

LOCALISATION OF THE SENSORIMOTOR

CORTEX SURGERIES OF THE SPINE
Precise localisation of the motor cortex is important to The earliest form of electrophysiological monitoring
minimise the risk of contralateral motor deficits resulting for scoliosis surgery was SSEP monitoring. A survey of
from the surgical procedures which occur in close the scoliosis research society and the European spinal
proximity to the motor cortex. Very often, the anatomical disorder society showed that there was a decrease in
and radiological landmarks of sensorimotor cortex are injury from 0.7% to 4% in the pre‑SSEP era to <0.55%
distorted by the pathological lesion. The signal of SSEPs with SSEP monitoring.[7]
after stimulation of the contralateral median/tibial
nerve is recorded from a sub‑dural strip electrode However, some patients had SSEP monitoring that failed
placed on the sensorimotor cortex across the central to detect significant spinal cord injury. The primary
sulcus. High‑amplitude potentials are recorded from the conduction pathway of the SSEP in the spinal cord is the
electrodes lying on the post‑central gyrus corresponding dorsal column. The blood supply of the dorsal column is
to N20/P40. Inverted potentials (potentials which are different from that of the anterior two‑third of the spinal
mirror images of each other) are recorded from the cord which derives its blood supply from the anterior
electrodes positioned on the primary motor cortex. spinal artery. Loss of blood flow through the anterior
The central sulcus is then neurophysiologically spinal artery would place the anterior two‑third of the
identified between the two electrodes which show spinal cord at risk while the dorsal column remains
the phase reversal (inversion of post‑central negative intact. Hence, it is advisable to monitor both SSEP and
and pre‑central positive peak) of the SSEPs. A phase motor evoked potential.
reversal across central sulcus is a highly reproducible
characteristic that helps in the localisation of the primary The level of surgery determines the choice of stimulation
motor cortex.[15] and the recording sites. If the surgical site is the cervical
spine, median nerve SSEP is monitored and if the SSEP
is below the cervical level, tibial SSEPs are monitored.
Recording over a popliteal or supraclavicular space
provides a control.

ANEURYSM SURGERY
Median nerve SSEP is generated by the primary
somatosensory cortex which sub‑serves the arm
and receives blood supply from the middle cerebral
artery (MCA). Hence, it is useful to monitor the
ischaemic insult associated with cerebral aneurysm
surgery, especially during temporary occlusion of the
MCA/internal carotid artery. Similarly, tibial nerve SSEP
has been used to monitor ischaemic events associated
with anterior cerebral artery aneurysm. Thalamic

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sub‑cortical activity supplied by the posterior cerebral ROLE OF SOMATOSENSORY EVOKED
artery can also be monitored using median nerve POTENTIAL IN THE INTENSIVE
SSEPs. The rationale for employing SSEP is the strong
correlation between electrophysiological changes and
CARE UNIT
regional cerebral blood flow. Ischaemia also prolongs Clinical neurophysiology plays a vital role in the
the CCT.[16] diagnosis, prognosis and monitoring in the Intensive Care
The CCT of more than 9–10 ms correlates with the Unit (ICU). EEGs and SSEPs are the most informative
neurological deficits whereas that below 10 ms was neurophysiological tests in the ICU. EEG is highly
associated with good outcome. Posterior circulation variable and sensitive to neurosedation whereas SSEPs
aneurysms require dual monitoring with SSEP and are resistant to sedation and metabolic derangement
brainstem auditory evoked potentials.[24] and have waveforms that are easily interpretable and
comparable. However, SSEPs are sensitive to structural
Monitoring during temporary clipping in aneurysm hypoxic/ischaemic damage. Bilateral absence of cortical
surgery has shown that a very prompt loss of cortical SSEPs recorded on the day 1 following cardiac arrest
SSEP response (<1 min after clipping) is associated accurately predicts poor outcome. Since SSEP amplitudes
with development of permanent neurological deficit. do not decrease during mild hypothermia (34–32°C),
However, a delayed loss with prompt recovery after it can be used in prognostication even in the cases of
the release of the clip is associated with the presence of therapeutic hypothermia. In coma induced by TBI,
collateral circulation with a markedly reduced incidence the SSEPs are able to predict both the poor and the
of neurological morbidity. When the N20 of the median favourable prognosis. Continuous SSEP monitoring is
nerve disappears slowly, 10 more minutes of occlusion able to detect neurological deterioration in acute brain
may be tolerated safely. Thus, SSEPs help us to guide in injury. Prolongation of the CCT in comatose patients
determining the duration of temporary clipping.[2] has been associated with worse long‑term prognosis.
The CCT is the difference between the latencies of the
SSEP monitoring can also be used to: responses recorded over the cervical spine and that
• Identify ischaemia from vasospasm recorded over the sensory cortex. In subarachnoid
• Unexpectedischaemia(retractorpressure,hypotension, haemorrhage, prolongation of the CCT is associated
temporary clipping and hyperventilation)
with transient neurological deficit and it precedes the
• Monitoring during neuroradiology procedures
development of these deficits. The changes in CCT are
• Streptokinase dissolution of blood clots.
related to cerebral ischaemia.[23]
Carotid endarterectomy
Intraoperative SSEP changes are used as an indicator for In summary, intraoperative monitoring of SSEPs
shunt placement and to predict post‑operative morbidity. have many valuable application. Correlation between
SSEP and EEG in CEA are complementary. Since SSEP is intraoperative SSEP and post‑operative functions are
able to detect ischaemia in the deep cortical structures, good. The scoliosis research society has developed a
EEG assesses a wider area of the surface cortex.[25] position statement that ‘neurophysiological monitoring
can assist in the early detection of complications and
Aortic aneurysm possibly prevent post‑operative morbidity in patients
Reversible changes in SSEP were not significantly undergoing surgery on the spine’. [26] Hence, SSEP
associated with immediate neurological deficit whereas monitoring has become a standard of care during a wide
irreversible changes in SSEP are associated with variety of procedures.
significant neurological deficit.[19]
Financial support and sponsorship
Positioning Nil.
Upper extremity stress during positioning has been
detected in real time using SSEP in patients undergoing Conflicts of interest
skull base surgery.[21] There are no conflicts of interest.

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