Activation Procedures
Hyperventilation (H.V.) (Fig. 71):
 Consists of 3-5 min of deep breathing (20/sec).
 Avoided in recent stroke or S.A. hemorrhage, recent M.I. and GOAD.
Normal and abnormal responses:
- No changes or
- Symmetrical slowness which may persist for up to 1 min or more;
- diffuse theta activity or
- more characteristic, intermittent or continuous 3-4 Hz high amplitude
(may be 250 µV) activity with frontal or occipital dominance.
- The amplitude and frequency of slowness are of no clinical importance
unless there is consistent asymmetry. The side that shows a slower
frequency and/or lower amplitude is usually considered the abnormal side.
- The most striking EEG abnormality seen during H.V. is 3 cps spike and
slow wave, but other abnormalities may be seen.
- H.V. effect is much more marked in children than in adults.
- Blood sugar level appears to influence the response to H.V.
Why H.V. induce slowness?
H.V.  hypocarbia (CO2)  V.C.  alters the metabolic rate of the
neurons  slowness.
Fig. 71 Gradual built up of bilateral symmetrical slow activity in a 10-yr old child after 2
min. of hyperventilation (Cal V 150 µV)
Intermittent Photic Stimulation (IPS) (Fig. 72):
 Each flash rate for 10 sec, eye closed for first 5 sec then opened.
 If there is a brief response repeat IPS.
 Red flashes are more effective in eliciting photoparoxysmal response.
 It is the most valuable in documenting photosensitivity which has a high
correlation with primary generalized epilepsy.
Photic driving:
 EEG activity that time-locked to the photic stimuli is often seen over the
posterior region.
 Photic driving is a physiologic response, usually symmetrical, observed in
all age groups. Absence of any response is not abnormal.
 Marked consistent asymmetry in amplitude or absence of driving to many
frequencies on one side is considered abnormal.
Fig. 72 Photic driving at 8, 12, and 15 flashes per second
Sleep:
 Whether natural or induced by chloral hydrate, 25-50 mg/kg body weight
with maximum of 2000 mg in adults and 1000 mg in children.
 Drowsiness and sleep are more effective in epilepsy.
 A dramatic increase in the number of spikes during sleep is a
characteristic feature of benign Rolandic epilepsy.
 In temporal lobe epilepsy, spikes may appear for first time during sleep.
 Sleep deprivation is still debated as an activation procedure.
Pharmacological activation:
 Used to differentiate between focal with secondary generalization from
primary generalized epilepsy.
 Drugs used are; metrazole, bemegride, barbiturates [thiopental I.V.].
EEG in Clinical Diagnosis
The aim is to give the physician an insight into the optimal use of EEG in
neurological diagnosis.
Role of EEG in diagnosis of neurological disorders (sensitivity and
specificity):
 It is a totally non-invasive procedure, useful in neurologic disorders in
which cerebral dysfunctions known to occur without an obvious structural
lesion.
 Intermittent e.g. epilepsy and sleep disorders.
 Persistent e.g. diffuse encephalopathies.
 Only rarely do we find a situation where the EEG is conclusively and
specifically diagnostic of a particular disease.
Seizure Disorder – General considerations
The EEG is the most important test in the evaluation of seizure disorder, as it
provides diagnostic and prognostic information in the majority of patients.
 Sensitivity
*Routine EEG +ve in  90% of absence
20-60% of generalized tonic-clonic (depend on
associated features like myoclonus)
*Normal EEG does not rule out genuine seizure disorder.
*Interictal abnormalities are more likely to occur with sleep, sleep deprivation
overnight, and sequential EEGs.
 Specificity
*Typical 3 cps spike & slow wave occur in absence seizures
1/3 of asymptomatic siblings of patients with absence may also show
3cps.
*Hypsarrhythmia and slow spike & wave occur in infantile spasms (West’s)
Lennox-Gastaut syndrome
 Recurrence
After first fit, probability of recurrence is twice with epileptogenic EEG.
 Primary vs. secondary
 Categorization of seizures




1.
Choosing the appropriate AED
Selecting suitable candidate for surgery in intractable epilepsy
Decisions regarding discontinuation of AEDs
Diagnosis of non-convulsive status
Febrile seizures
 Ictal  focal or generalized may persist for one week.
 Interictal  if persist  shift the diagnosis to seizure disorder.
2. Infantile spasms
 Hypsarrhythmia is the characteristic EEG pattern.
3. Lennox-Gastaut syndrome
 Petit mal variant is the typical EEG pattern with slow background.
4. Primary generalized epilepsy
Absence seizure
 Typically 3 cps (21/2-4) spike &slow wave with normal background.
 Prolonged discharges last more than 12 sec. Often lead to automatisms
and confusional states.
 If there is consistent asymmetry of the discharges or the onset of absence
occurs later in life, neuroimaging is recommended.
Generalized tonic- clonic seizures
Ictal pattern
Tonic phase  initially a repetitive discharge of spikes or fast rhythmic
Activity  progressive  rate and  amplitude.
Clonic phase  generalized spikes coinciding with the clonic jerks, often
followed by slow waves (periods of relaxation)
+ bilateral symmetrical synchronous muscle artifacts.
 Less frequent  stop abruptly.
Post-ictal  marked suppression of activity for varying periods.
Interictal
2-4 Hz or faster bilateral synchronous spike & wave complexes, spikes, in
generalized distribution, polyspikes, or polyspike and wave complexes.
5. Partial (focal) epilepsy
Rolandic benign epilepsy of childhood with rolandic spikes (BECRs) 25% of
childhood epilepsy.
Sylvian Epilepsy: centromidtemporal epilepsy
Spikes: central, mid-temporal or centroparietal, unilateral or bilateral.
Markedly accentuated in stages I and II sleep, may occur without an
accompanying seizures.
A similar syndrome with occipital or parietooccipital spikes or spike & slow
wave complexes.
Occipital spikes may occur in children with early-onset visual problems
without fits.
Simple partial seizure: EEG is not very sensitive.
Complex partial seizure: Sphenoidal leads may be necessary.
Higher incidence of spikes in sleep EEG.
Antro- and mesio-temporal spikes are considered more significant than
mid-temporal.
Frontopolar, orbito-frontal and temprooccipital; spikes may be also associated
with CPS.
6. Non-convulsive status epilepticus (NCSE)
Absence continuous generalized 2.5-3 cps spike & wave complexes.
CPS  repetitive focal or lateralized activity of spikes, sharp waves,
Spike & slow, rhythmic slow waves, or fast activity.
Sleep Disorders
Polysomnography  EEG, respiratory movements,
movements, muscle activity, and blood oxygen conc.
 Sleep apnea syndrome; obstructive, central or mixed.
 Narcolepsy: excessive sleepiness + REM-sleep.
air
flow,
eye
The Comatose Patient
Determine the patient’s level of consciousness
In unresponsive patient  passive opening of eyes + painful stimuli
 reactive tracing  more favorable prognosis.
Artifacts  monitoring.
EEG is complementary to neuroimaging in evaluation
EEG abnormalities seen in comatose patient are often non-specific
Encephalopathies
Delta activity may be intermittent and rhythmic or diffuse and polymorphic.
Hepatic
Uremic
Drug intoxication  diffuse slowness + generalized beta
Cerebral anoxia  diffuse slowness +
burst suppression or electrosilence,
or myoclonic jerks accompanying epileptiform activity,
or markedly attenuated background.
Supratentorial lesions 
focal or lateralized polymorphic delta.
Bilateral brain stem lesions (pontine tegmentum) 
alpha coma = activity in the alpha frequency
 unresponsive to passive eye opening.
 Greater amplitude in the anterior regions.
(also in cerebral anoxia and drug intoxication)
While responsive in locked-in-syndrome and psychogenic coma.
NCSE (non-convulsive status epilepticus) – causing coma
DD = Postictal state
Transient global amnesia
Drug intoxication
Electrolyte imbalance (diffuse slowness)
Psychogenic (normal EEG)
Elecrocerebral Silence (ECS)


Absence of electrocerebral activity above 2 µV.
Occurs in Brain death - Hypothermia – Drug intoxication.
Diffuse Encephalopathies


The EEG abnormality is non-specific except in few circumstances.
In many of these conditions, when the EEG is grossly abnormal, the CT
may not reveal any specific changes.
Metabolic encephalopathies
Diffuse slowing of background rhythms resulting in theta or delta activity
commonly with FIRDA or sometimes OIRDA.
Hepatic  1/3 patients  triphasic delta (rare in Reye’s syndrome)
Hypoglycemia  accentuated EEG response to HV +
progressive slowing of background activity +/IRDA may appear +/enhance pre-existing epileptiform activity (reversible).
Hyperglycemia  non-specific slowing of the background activity.
Focal seizure activity is not uncommon.
Renal disorders
 Uremic encephalopathy  slowing + FIRDA +
photoparoxysmal or photomyogenic response
+ occasional triphasic waves.
 Dialysis disequilibrium syndrome  temporary worsening of the EEG
pattern.
 Following dialysis  the slow activity gradually disappear.
 Dialysis dementia  focal abnormality in the EEG pattern precedes the
onset of clinical dementia (predictive).
Infectious encephalopathies
In acute phase  diffuse slowing + often epileptiform abnormality.
 HSE  early focal slowing and epileptiform discharges over temporal or
frontotemporal regions, followed by periodic complexes (lateralized or
generalized).
 SSPE  generalized periodic complexes
*High voltage (100-1000 µV)
*At intervals of 4-14 sec.
*Often associated with myoclonus.
 Jackob-Creutzfeldt disease  periodic complexes recur at about 1 sec.
Dementia
 In suspected cases  the EEG is often quite informative. A decrease in
alpha rhythm, although non-specific, is a consistent finding.
 In advanced cases  very low-amplitude EEG with slow background
(classic in Huntington’s disease).
Focal Encephalopathies
The type of EEG abnormality depends on the site and size of the lesion.
Subcortical  disruption of the thalamocortical connection  PDA.
If there are multiple areas of slow activity, the site of lesion is likely to be
underneath the area that shows the slowest and most irregular activity,
irrespective of its amplitude.
Cortical and subcortical  PDA
But the amplitude is likely to be smaller in the area directly over the lesion.
Cortical  may be less striking, may be normal or only a decrease in
amplitude of the background activity, particularly beta, on the side of the
lesion.
Pseudtumor cerebri  normal EEG
Chronic recurrent headache  if there is focal slowing, CT is recommended
Seizure disorders  PDA  CT is needed.
Supratentorial tumors  while EEG correctly lateralizes the tumor, it is of
little value in differentiating type of the tumor.
PDA in EEG with normal CT:
 Recent non-hemorrhagic infarction.
 Recent episode of migraine.
 Post-ictal.
 Post-traumatic.
Cerebrovascular Disorders
Acute neurologic deficit with normal CT findings.
Large infarct (cortical and subcortical)  PDA + lack of fast activity +
PLEDs + suppression of sleep spindles.
Small cortical lesions  minimal changes if any
Deep lesions  minimal changes if any
TIAs transient focal or lateralized changes (if persist, impending infarction)
Subarachnoid hemorrhage  often non-specific slowing
focal abnormality  site of aneurysm??
AVM  focal or lateralized slowing +/- focal epileptiform abnormality
Moyamoya disease  excessive and prolonged slowing in response to H.V.
may occur.
Head Trauma
Concussion diffuse non-specific slowing.
Contusion  localized slowing.
 Normal EEG in symptomatic patient = psychogenic.
 Early EEG changes have shown no consistent predictive value for posttraumatic epilepsy.
Sophisticated and Advanced EEG technology
Special Electrodes (Fig. 5)
For inaccessible regions; basomedial parts of the temporal lobes and orbital
and medial parts of the frontal lobes.
Zygomatic Electrodes: For tips of temporal lobes.
Nasopharyngeal Electrodes: For uncus, hippocampus, and orbito-frontal
cortex.
Sphinoidal Electrodes: For basal and mesial temporal cortex.
Ethmoidal Electrodes: For orbito-frontal cortex.
Electrocorticography
Surgically placed electrodes; epidurally, subdurally, or depth electrodes for
seizure surgery.
Video/EEG Monitoring
(Short - & Long-Term)
It provides simultaneous recording of patient’s behavior and EEG, by the use
of a split-half T.V. screen; this is recorded on a magnetic tape (or computer
media) and can be played back later on a T.V. monitor for review and
evaluation.
System design:
A simple basic system consists of:
1. T.V. camera.
2. Electronics for displaying the video on one half of the T.V. monitor.
3. Patient hook up: standard EEG, cable telemetry, wireless telemetry and
electronics for filtering the EEG voltages to IRIG level.
4. Electronics for converting the EEG voltages to video signals suitable for
displaying on the other half of the T.V. monitor.
5. Digital clock.
6. Video-cassette recorder (or a computer storage media).
Time synchronization of data:
On video tape and analog tape.
Interpretation:
By observation made by patient (alarm clock), technician and by taken
samples from the record.
Disadvantages:
- Time consuming.
- Hospitalization (in long-term only, short-term can be done in out patient)
- Restriction of patient’s mobility.
Ambulatory EEG Monitoring (AEEG)
(Holter EEG)




No need for hospitalization.
Increases patient’s mobility.
Long-term recording without supervision.
With rapid video-audio play back device, 24 hours recording reviewed in
24 minutes.
System design
 Battery operated.
 Pre-amplifiers are secured to the scalp along with the electrodes.
 Output wires are fed to the recorder.
Patient hook up:
 Collodion electrodes.
 Electrode impedance should be less than 3 kohms.
 Not to use referential montages.
 Loop area between electrodes kept too minimum to avoid contamination
from the surroundings.
Operation:
 Electrodes applied and tested.
 Calibrate.
 Record while patient in various activities.
 On return back, do brief record again.
Brain Electrical Activity Mapping (BEAM)
Definition: It is a spatially oriented procedure for calculating amplitude and
frequency patterns of the EEG and EP on the basis of restricted number of
electrodes on the head and by subsequent interpolation methods.
Terminology: Brain mapping, EEG and EP topography, Brain electrical
activity mapping (BEAM), Quantitative EEG, Computerized EEG, EEG
cartography.
The rational for BEAM is that the traditional EEG or evoked potential (EP)
tracings contains too much data in a form not appreciated by the naked eye.
Methodology:
 General condition:
a) Room: sound proof, electromagnetically shielded.
b) Subject: comfortable position (to avoid muscle artifacts), maintained
alertness (if possible), free of medications (or documented).
 Calibration: at the start of each recording.
 Electrodes: International 10-20 system, minimum of 19 electrodes (+ 4
artifact electrodes).
Fig. 73 Electrodes jel injection (head cap)

Reference:
a) Single references as ear or mastoid, linked ears or mastoids, nasion or
chin (Disadvantage: may be electrically active)
b) Common average reference (CAR) (the most commonly used one)
c) Local average reference (LAR, Laplacian)

Baseline: is the technical zero line of EEG and EP, it can affect the
pattern of EP maps or spikes (time domain).
Fig. 74 Baseline correction options

Filters: high and low pass filters are determined
Fig. 75 Filter options

Artifacts: should be removed prior to analysis and mapping. Best done by
the human eye (for EEG) or automatically (for EP). Additional electrodes
should be applied for detecting eye blinks, horizontal and vertical eye
movements, and muscle and movement artifacts. Other artifacts are
caused by: heart, pulse-waves, perspiration, electrodes, cables, AC
interference, cautery, and neon lambs.
Fig. 76 A marked and rejected block of digital EEG with eye movement artifact
Data Acquisition and Signal Analysis:
 Analog to Digital Conversion (ADC): It is the process by which the
external analog EEG or EP signal is transformed into the digital equivalent.
Sampling rate: is the frequency at which the current signal amplitude is
measured.
Fig. 77 Signal amplitude sampling for analog to digital conversion

Time Domain (Amplitude mapping): (time vs. amplitude) the amplitude
values of an EEG at certain point in time are mapped. It is used in
mapping of epileptic features, focal disturbances and display of special
EEG patterns such as: K complexes, spindle activity…etc.
Fig. 78 Time domain epoch (time vs. amplitude)
Dipole Estimation: Dipole is a simplified equivalent of simultaneous
discharges of multiple neurons. In conventional EEG phase reversal
indicates focus location. In mapping dipoles may facilitate the search for
sources. If there are no dipoles the source may be directly under the
electrode.

Frequency Domain (Frequency mapping): (amplitude vs. frequency)
data are transformed from the time domain into the frequency domain
(frequency spectra is calculated) using a special algorithm for Fourier
transformation (aided by special computer programs or microchips).This is
called FFT (fast Fourier transformation). The most common target
variables for EEG mapping are power (uV2) or mean amplitudes (uV) in
four to sex frequency bands (Delta 1-4 Hz, Theta 4-8 Hz, Alpha 8-12 Hz,
Beta 12-35 Hz).
Fig. 79 Frequency domain (frequency vs. amplitude) bar histogram

Spatial Domain (Map construction): Starting with a limited number of
actual data points an image consisting of thousands of data points (pixels)
is generated.

Interpolation is used to fill in the gaps. A) Linear interpolation uses the
three or four nearest electrodes (fast, but maxima & minima are always at
electrode sites) B) Surface spline interpolation (exhibits maxima &
minima, but slow)

Calibration (color or tone) bar: should accompany each map, it indicates
(a) amplitude (uV) or power (uV2) ranges of EP & EEG events in time
domain (b) activity ranges (uV or uV2) in EEG frequencies in frequency
domain (c) ranges of statistical values from z statistics (standard
deviations), t-test (t values), and significance levels (p values).
Fig. 80 Interpolation
Time domain spatial maps:
Fig. 81 On the left side (an EEG strip) the cursor is placed exactly on an area with a
positive alpha peak (at 178.99 seconds). On the right side the corresponding 2D brain
map of this particular moment of EEG activity. Electrodes locations are marked on the
map (black dots), each amplitude is represented by a color on the map (coded on the
attached color bar), the 2 dimensions of the head map are (1) The time point (178,99s)
or interval, and (2) the waves amplitudes in microvolts (uV). We note that alpha waves
have produced a crown of colors (grades of red) in the occipital, parietal and posterior
temporal areas.
Fig. 82. A spike presentation with a positive maximum activity at C3 (time domain map)
Frequency domain spatial maps:
Fig. 83 Frequency domain spatial maps showing the 4 main frequency bands (Delta,
Theta, Alpha and beta). The frequency domain represents: frequency vs. amplitude (no
time). The amplitudes (in uV) are represented by color grades (attached color bars
shows amplitudes color codes).
Statistical Procedures:
A. Standard tests:
1. Z statistics significant probability mapping (SPM): represents the
extent to which (in terms of standard deviation) an individual
observation differs from the mean of a reference set (a group)
Fig. 84 Z statistics SPM
2. T statistics significant probability mapping (SPM): quantifies extent
of difference between two sets of measures (two groups), taking into
account the difference between group means and the variance within
each group.
Fig. 85 T statistics SPM
B. Procedures used for group comparison:
a) Exploratory / descriptive methods:
1. Student’s t test (significant probability mapping)
2. Wilcoxon test, linear regression.
b) Confirmatory methods:
1. ANOVA (analysis of variance)
2. MANOVA (multivariate analysis of variance) and discriminant
analysis.
3. t test, Wilcoxon test, or Mann-Whitney U test (after data reduction)
Description of normal maps (frequency domain):
Delta and theta maps tend to be symmetrical and posterior, of medium
amplitude. Alpha tends to be of highest amplitude, better in the eye closed
state. There is a good symmetry and occipital dominance. The same pattern
is preserved in the eyes-open state. Beta is of low amplitude throughout, and
not well defined.
BEAM indications and important guidelines:
These are mainly the same indications of traditional EEG, keeping in mind
BEAM’s objectivity, increased sensitivity, its ability to measure many unique
additional parameters and the availability of a wide variety of statistical
methods which are stable over time. There is a list of many clinical conditions
in which BEAM was extensively tested. These were included in the following
“Report for BEAM assessment issued by the American Academy of Neurology
and American Neurophysiology Society”:
 BEAM should be used only as an adjunct to and in conjunction with
traditional EEG interpretation.
 It may be clinically useful only for patients who have been well selected on
the basis of their clinical presentation.
 It is considered established in:
1- Epilepsy: for screening for possible epileptic spikes or seizures in longterm EEG monitoring or ambulatory recording to facilitate subsequent
expert visual EEG interpretation
2- Operation room or intensive care unit monitoring: for continuous EEG
monitoring by frequency-trending to detect early acute intracranial
complications in the operation room or intensive care unit, and for
screening for possible epileptic seizures in high-risk ICU patients.
 It is considered possibly useful in:
1- Epilepsy: for topographic voltage and dipole analysis in presurgical
evaluations.
2- Cerebrovascular diseases: in expert hands may be possibly useful in
evaluating certain patients with symptoms of cerebrovascular disease
whose neuroimaging and routine EEG studies are not conclusive.
3- Dementia: it may be a useful adjunct to interpretation of the routine
EEG in evaluation of dementia and encephalopathy when used in
expert hands.
 It is considered investigational for clinical use in:
1- Postconcussion syndromes
2- Mild or moderate head injury
3- Learning disability
4- Attention disorders
5- Schizophrenia
6- Depression
7- Alcoholism
8- Drug abuse
 It is not recommended for use in civil or criminal judicial proceedings
 Because of the very substantial risk of erroneous interpretations, it is
unacceptable for any BEAM techniques to be used clinically by those who
are not physicians highly skilled in clinical EEG interpretation.
EVOKED POTENTIALS
When picked up by scalp electrodes, evoked electrical activity appears
against a background of spontaneous activity in mixture. The evoked activity
is the “signal” we desire to record while the background activity is the “noise”.
Signal is normally of much lower amplitude than the noise (signal-to-noise is
low). To detect an evoked potential, one can do either decrease amplitude of
noise (keep eyes open) or increase the amplitude of signal (averaging =
superimposition).
Visual Evoked Potentials
Anatomical Basis
Represent electrical activity induced in the visual cortex by lilght stimuli that
reach the macular and perimacular areas of the retina.
Light energy  cones in macula  electrical energy  axons of ganglion
cells of retina  optic nerve  optic chiasm (where nasal fibers cross)
LGB  optic radiation (subcortical P and T lobes)  visual cortex.
 Full-field stimulation of either eye  both visual cortices.
- More useful in evaluating the anterior pathway (optic nerve and chiasm).
 Half-field stimulation  separately stimulate one visual cortex.
- More useful in evaluating the retrochiasmal pathways (optic tract,
radiation and cortex).
Stimulus Parameters
Pattern visual stimuli
The most commonly used stimulus in clinical testing is the black and white
checkerboard (pattern VEP). On the screen the checkerboard patterns
reverse at regular intervals so that the white squares become black and the
black squares become white at a rate of 2/sec.
Flash visual stimuli
Photic stimulation at a distance of 30 – 45 cm with a rate of 0.5 – 1 /sec, used
in poor visual acuity, coma, and anaesthesia. It is less reliable for clinical use.
Factors affecting the waveforms
Patient-related
Age
 Several studies have reported an absence of significant age related
changes of the P100 latency in adults until fifth decade. After the fifth
decade, the P100 latency increase with age but with no major changes in
the amplitude.
Gender
 P100 latency has a shorter latency and greater amplitude in females than
in males.
Visual acuity
 Corrected with eye glasses. With deficiency use larger checks.
Visual fixation
 To ensure that the macula is stimulated.
 With poor fixation  smaller amplitude
Pupillary size
 Patient should not have mydriatics or cycloplegics at least 12 hours prior
to the test.
Stimulus-related
 Rate
1 – 2 /sec. is optimal for transient VEP (used clinically).
Exceeds 10 /sec.
Steady-state VEP.
Slower rate
time consuming – difficult fixation.
Faster rate
contamination.
 Luminance (stimulus intensity) and degree of contrast (difference
between bright and dark)
Reduction of the luminance and degree of contrast leads to reduction of the
amplitude and increase of the latency.
 Visual angle
Depends upon size of the checks and distance between screen and eyes.
VA = 57.3 (W/D in cm).
Recording parameters
 The patient in a sitting position, fixates on the small target in the middle of
the screen at a distance of one meter.
Filter sittings
low-frequency
0.2 – 2.0 Hz
High-frequency 100 – 500 Hz
Analysis time
250 msec., if no response repeat at 500 msec.
Number of trials averaged 100 – 200 or more
Recording electrodes (10-20 system)
Recording
Oz – O1 – O2
Reference
Fz
Ground
Fpz
Normal response
Pattern VEPs contain three main components,which are recorded in the mid
occipital region  Initially –ve peak = N75
Most prominent and consistent +ve peak = P100
+/- subsequent –ve peak = N145
Of these three components the positive one peaking at a latency of about 100
ms (P100) has the largest amplitude.
Origins of the pattern reversal VEPs
- N75  fovea or area 17.
- P100  either the striate area or area19.
- N145  area18.
Measurements and normative data
The clinical interpretation of pattern VEPs is based mainly on the
measurement of the P100 latency and inter-ocular latency difference.
 P100 normally at 90 – 110 ms (>110 is abnormally delayed).
 Inter-ocular latency difference is <10 ms
 Amplitude measured from the baseline or from peak to peak shows a
greater inter- individual variability than its latency. Values between 2 – 20
v fall into the normal range of most laboratories. For this variability, the
inter-ocular difference is crucial for interpretating the waveforms. The P100
latency and amplitude from each eye are almost identical. Inter-ocular
P100 latency and amplitude differences over 10 ms and 8 v respectively,
are reported as beyond the upper limits of normality.
 When pattern covers both the left and right half fields, both occipital visual
cortices are stimulated and the scalp recorded potentials reflects this
simultaneous activation. By contrast, half field stimulation permits separate
activation of only one hemisphere.
Interpretation of data and abnormalities of VEP
The most frequent abnormality is the delayed P100 latency and the most
severe abnormality is an absent VEP.
 Increased P100 latency from one eye  optic nerve lesion.
 Increased P100 latency from both eyes  it may indicate bilateral optic
nerve, extensive chiasmal or retrochiasmal lesions. Hemifield stimulation
may be helpful to differentiate between them. Increased P100 latency with
left hemifield stimulation may indicate lesion in the right optic tract.
 Interocular latency difference is more sensitive than absolute latency. (For
example, Rt = 97 and Lt = 110. The difference is > 10 ms which is
abnormal). Indicate pathology on the side with the longer latency.
 The absolute latency of each eye may be within normal but the difference
between them is more than 10 ms. For example, Rt = 97 and Lt = 110.
These are normal latencies but the difference is > 10 ms which is
abnormal. This indicates pathology on the side with the longer latency.
Side
P100 latency (N = 90-110 ms)
Lt
95
95
130
Rt
102
110
110
Normal P100 latency
on both sides
Rt optic nerve lesion
(The diference
>10ms)
Lt optic nerve lesion
(Delayed on the Lt)
Clinical applications
The best indication for VEP is a suspected disorder of the anterior visual
pathway. Optic tracts and radiations are best assessed by CT or MRI.
Optic neuritis
 Unilateral optic neuritis increases the P100 latency on the same side.
 Bilateral optic neuritis increases P100 latency on both sides.
 It is abnormal in 100% of patients with previous optic neuritis.
 Delayed P100 or absent VEPs have been reported in other disorders
affecting the optic nerve (SLE, ischemic optic neuropathy and toxic optic
neuropathy).
Multiple sclerosis
 The ability of VEPs to detect clinically silent optic nerve lesions is a very
useful tool for the diagnosis of MS. 70% of patients with MS have
abnormal VEPs.
 Abnormal VEP latency is present in approximately 40% of patient with MS
who do not have a history of optic neuritis.
Tumors
 Compressive lesions of the optic nerve or chiam (pituitary tumor or
invasion by glioma) almost always associated with abnormal VEPs.
Changes in latency are more reliable than amplitude changes.
Retrochiasmatic disorders
 VEPs to full field stimulation are usually normal in patients with unilateral
hemispheric lesion even in the presence of a dense homonymous
hemianopia.
 Half field stimulation may show abnormalities in some patients in the form
of absent potentials on the affected hemifield or gross distortion of the
amplitude.
 Bilateral retrochiasmatic lesions if extensive will produce cortical
blindness.
 VEPs are often normal in cortical blindness or bilateral hemianopia
(explanation for this is that VEPs originate in remnants of cortical area 17).
Functional disorders
 Normal VEP usually suggests continuity of the visual pathways in
functional visual loss but does not fully exclude cortical blindness.
Ocular and retinal disorders
 Retinopathies
 Macular degeneration
 Retinal infarcts
 Retinitis pigmentosa
*VEP is not ordinary used for the diagnosis of these disorders. Many of these
disorders cause abnormalities of VEP.
*ERG and VEPs may be useful in differentiating between disorders affecting
the retina or the optic nerve.
*In retinopathies and maculopathies, ERGs are usually absent or abnormal.
*In optic nerve lesions VEPs may be absent or prolonged but ERGs are
normal. In optic atrophy with large central scotoma, both ERGs and VEPs are
absent.
Ground (Fpz)
Reference (Fz)
Active (MO, RO and LO)
Fig. 1 Electrode placement for VEPs
Fig. 2 Pattern reversal
Fig. 3 Normal VEPs to pattern-reversal full-field stimulation of the right eye using a
checkerboard image of 16X16 checks at a distance of 1 m. Stimulation rate at 1.88/s.
The band-pass is at 1 to 1 Hz, and 250 trials were averaged. Two separate tests were
run, and the paired tracings show good replication. The downgoing arrow points to
N75, while the upgoing arrow indicates P100 (Cal H 50 ms, V 5 µV)
Brainstem Auditory Evoked Potentials (BAEPs)
Routine Procedure
Electrode placement
 In a supine position and supporting the head to minimize neck muscle
activity. Active recording electrode is placed at the vertex, usually at Cz.
 Reference electrode is placed close to the stimulated ear on the mastoid
or the ear lobe (A1).
 Ground electrode on the frontal region.
Stimulus
 Click sound at a rate of 8 – 10 /sec and intensity of 70 dB or more.
 White noise is similar to the hush sound made by a radio and is delivered
into the ear not being stimulated with clicks. This is called masking.
Without masking the ear not being tested could be stimulated by bone
conduction of the clicks delivered to the opposite ear.
Normal response
 BAEPs are composed of five successive peaks, labeled (I – V) in Roman
figures.
 These waves are reproducible; at least 2 separate trials should be
superimposed.
Measurements and calculations
 Latency is a more important measure than amplitude.
 The measurements and calculations routinely performed in clinical testing
include:
- Peak latencies (Wave I, III and V)
- Inter-peak latencies (I – III, I – V and III – V).
- Inter-ear latency difference (I – V latency).
Normative data
Wave I at 2 ms
Wave III at 4 ms
Wave V at 6 ms
I – III inter-peak latency 2.5 ms
III –V inter-peak latency 2.5 ms
I – V inter-peak latency 4.5 ms
Inter-ear I – V latency difference <0.5 ms.
Origin of waveforms
 Wave I originates from the peripheral portion of the cochlear nerve (similar
to CAP).
 Wave II originates from the proximal portion of the eighth nerve.
 Wave III has been localized in the pontine portion of the brainstem
auditory pathways.
 Wave V may be generated by projections from the pons to the midbrain. It
appears at approximately 6ms and is often combined with wave IV to form
a single IV/V complex.
Interpretation of data
Wave I latency (2.1 ms) increased if the most distal portion of the nerve is
affected. Absence of wave I with normal III and V may indicate a peripheral
hearing disorder. Absence of wave I with absence of waves III and V indicates
a defect of conduction in the eighth nerve along with the caudal pons.
Wave III latency (4.1 ms): absence of wave III with increased I – V latency
may indicate a lesion somewhere in the eighth nerve to the midbrain.
Wave V latency (6.1 ms): absence of wave V with normal I and III may
indicate lesion above the caudal pons (ipsilaterally).
Increased I – III interpeak latency (2.5 ms), indicate a defect in the pathway
from the proximal part of the nerve into the pons (common finding in acoustic
neuromas CPA).
III – V interpeak latency (2.3 ms) increase, indicate a defect in conduction
between the caudal pons and midbrain.
I – V interpeak latency (4.5 ms)
I/V amplitude ratio is usually <100%
Inter-ear I – V latency difference of more than 0.5 ms is abnormal
Clinical applications of BAEPs
Multiple sclerosis
 It is less sensitive than VEPs or SSEPs.
 The most important is to identify subclinical lesions in the brainstem.
 Patients with definite MS showed abnormal VEP in 70 - 80% and SSEP in
50 - 70% and BAEP in 30 - 50%.
 Probable or possible MS patients showed abnormal VEP in 50%, SSEP in
50% and BAEP in 20%.
 The usual abnormalities:
- Increased III - V inter-peak interval
- Increased I - V inter-peak interval
- Reduction in wave V amplitude
Intrinsic and extrinsic brainstem lesions
Acoustic neuromas
 Increased I – III inter-peak interval
Glioma and stroke
 Absent or delay of waves III and V
 Increased III – V inter-peak intervals
Coma and brain death
 In brain death there is absence of either all BAEPs or of all except wave I.
 In evaluating patients with coma, BAEPs provide an index of brainstem
function.
 BAEPs are relatively resistant to metabolic insults and drug overdose
(normal BAEPs may suggest reversibility of coma).
Intraoperative monitoring of BAEPs
To monitor the brainstem integrity during posterior fossa surgery (CPA
tumors):
 Loss of waveforms after I
 Decreased amplitude of III and V or
 Increased inter-peak latency (III – V).
Evaluation of hearing in children
 Absent BAEPs usually indicate severe high frequency hearing loss and
provide very little information about the extent of low frequency hearing.
 Delayed wave I and shortening I – V inter-peak latency occur in perceptive
but not in conductive hearing loss.
Factors affecting BAEPs
Age
 The increase of latencies with age is too small (<0.3ms) between the ages
of 15 – 95 years.
Sex
 The latencies are slightly shorter in females than in males (0.1 – 0.2).
Body temperature
 Hypothermia prolongs the interpeak latencies but hyperthermia has the
opposite effect.
Subject relaxation
 To avoid overlapping myogenic response or excessive muscle activity.
Stimulus intensity
 There is an inverse relation between intensity of the click and absolute
latencies. (the waves are better identified with intensities above 60 dB).
Stimulus rate
 Increasing the rate above 20/sec decreases the amplitude and increases
the latencies of all waves (it should be 8 – 10/sec).
Stimulus mode
 Click sound and white noise to mask the non stimulated ear to avoid cross
conduction of the click by boe and air to the contralateral ear.
Filter sittings
 Affect the amplitude more than interpeak latencies and should remain
fixed at the values used when collecting the normative data (100 – 3000
Hz). Low frequency <100 allows EMG and EEG signals. Higher frequency
should be at least 3000 Hz (if <1000 it prolongs the latencies)
Ground
electrode
Active electrode at vertex
Mastiod
reference
Head set
phnes
Fig. 4 Electrode placement for BEAP
Fig. 5 Brainstem lesion (prolonged III – V interpeak latency)
Somatosensory Evoked Potentials
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Evoked potentials are the electrical signals generated by the nervous
system in response to sensory stimuli. Auditory, visual, and
somatosensory stimuli are used commonly for clinical evoked-potential
studies. Somatosensory evoked potentials (SSEPs) consist of a series of
waves that reflect sequential activation of neural structures along the
somatosensory pathways following electrical stimulation of peripheral
nerves.
In clinical practice, SSEPs are elicited typically by stimulation of the
median nerve at the wrist, the common peroneal nerve at the knee, and/or
the posterior tibial nerve at the ankle and recorded from electrodes placed
over the scalp, spine, and peripheral nerves. The dorsal column-lemniscal
system is the major anatomical substrate of the SSEPs within the CNS.
SSEPs are used for clinical diagnosis in patients with neurologic disease
and for intraoperative monitoring during surgeries that place parts of the
somatosensory pathways at risk. Abnormal SSEPs can result from
dysfunction at the level of the peripheral nerve, plexus, spinal root, spinal
cord, brain stem, thalamocortical projections, or primary somatosensory
cortex. Since individuals have multiple parallel afferent somatosensory
pathways (eg, anterior spinothalamic tract, dorsal column tracts within the
spinal cord), recordings of SSEPs can be normal even in patients with
significant sensory deficits.
SSEPs depend on the functional integrity of the fast-conducting, largediameter group IA muscle afferent fibers and group II cutaneous afferent
fibers, which travel in the posterior column of the spinal cord. When a
mixed peripheral nerve (with both sensory and motor components) is
stimulated, both group IA muscle afferents and group II cutaneous
afferents contribute to the resulting SSEP. Selective ablation of the dorsal
column of the spinal cord abolishes the SSEPs generated rostral to the
lesion. Diseases of the dorsal columns in which joint position sense and
proprioception are impaired invariably are associated with abnormal
SSEPs.
The development of and easy access to sophisticated neuroradiologic
imaging have had a great impact on the usage of SSEPs in clinical
settings; fewer diagnostic SSEP studies are being performed now than in
the pre-MRI era. Nevertheless, SSEPs are valuable as a diagnostic test in
several clinical situations. Their role in the operating room has expanded,
and interest remains high in SSEPs as research tools for unraveling of
fundamental aspects of sensory physiology.
Stimulus location
 For recording median nerve SSEPs, the nerve is stimulated at the wrist.
The anode is placed just proximal to the palmar crease, and the cathode is
placed between the tendons of the palmaris longus muscle, 3 cm proximal
to the anode.
 Ulnar nerve SSEPs are preferred to median nerve SSEPs for assessing
the lower cervical spinal cord segment since the ulnar nerve originates
from spinal roots C8-T1, whereas the median nerve originates from C6-T1.
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For recording posterior tibial nerve SSEPs, the nerve is stimulated at the
ankle, with the cathode midway between the Achilles tendon and the
medial malleolus and the anode 3cm distal to the cathode.
For recording peroneal nerve SSEPs, the common peroneal nerve is
stimulated at the knee, with the cathode inferior to the leg crease just
medial to the tendon of the biceps femoris muscle and the anode 3 cm
distal to the cathode.
In the lower limb, posterior tibial SSEPs are preferred because of the
following:
 In clinical diagnostic use, they are larger and less subject to variability.
 In intraoperative settings, they produce smaller muscle contractions
with larger SSEP amplitudes.
 In intraoperative settings, electrodes at the ankle are more easily
accessible than those at the knee.
 The peripheral compound action potential (CAP) is recorded easily at
the popliteal fossa.
Stimulus intensity
 The selected nerves are stimulated with monophasic square pulses, 100300 microseconds in duration. Stimuli are delivered by using either a
constant voltage or a constant current stimulator.
 The contact impedances of the stimulating electrodes should be kept low
for the following reasons:
 To minimize patient discomfort
 For more effective nerve stimulation, if a constant voltage stimulator is
used
 To avoid electrical artifacts with constant current stimulation
 In the clinical setting, the stimulus intensity is set high enough to produce a
consistent muscle twitch, which usually is tolerable to the patient. Because
the patient is anesthetized during intraoperative SSEP monitoring, higher
stimulus intensities can be used and are advisable to provide a safety
margin in case the efficacy of nerve stimulation decreases during surgery.
Stimulus rate
 Rapid stimulus delivery rates should be avoided, as they degrade the
waveforms of SSEPs. In clinical settings, a rate of 3-6 stimuli per second
usually is used.
Recording technique
 SSEPs typically are recorded by using standard EEG electrodes affixed
with tape or collodion; electrode caps containing multiple recording
electrodes also can be used.
 Recording electrode impedances should be kept below 5000 ohms and
should be as uniform as possible across the electrodes to maximize
common-mode rejection and minimize noise pickup. Also, placing the
ground electrodes on the stimulated limb helps reduce the electrical
stimulant artifact.
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Typical recording amplifier filter settings for SSEPs are 30-3000 Hz.
Diagnostic SSEP studies should be performed using the same filter
settings used to record normative data.
Small-amplitude components of SSEPs are composed of both low and
high frequencies, and filtering can be problematic. A bandpass that is too
wide results in noisy SSEPs, but a bandpass that is too restrictive
attenuates either high- or low-frequency components, depending on the
settings chosen. For example, reducing the low-frequency filter setting
(low-cut, high-pass) from 30 to 5 Hz may produce a clearer SSEP
component but also may allow more noise into the SSEP waveforms.
A typical analysis time is 40 milliseconds for an upper limb SSEP and 6080 milliseconds for a lower limb SSEP.
Typically, SSEPs are not visible in the raw data recorded from surface
electrodes, and signal averaging is used to extract the SSEPs from the
other electrical signals picked up by the recording electrodes.
Measurement of Somatosensory Evoked Potentials
 Several characteristics of SSEPs can be measured, including onset
latency, interpeak latency, morphology (ie, presence and absence of
components), and dispersion. Onset latency is the easiest SSEP feature to
measure and standardize, but it gives rather limited information. Other
characteristics (i.e., morphology and dispersion) are more variable and
difficult to interpret.
 Absolute SSEP latencies vary with limb length. Interpeak (ie, transit) times
are reliable parameters that are independent of limb length and usually
independent of peripheral nerve disease. Aging is associated with some
prolongation of SSEP latencies.
 Latencies are considered abnormal when they are more than 3 standard
deviations above the mean of the normative data.
Recording electrodes sites
 Recordings were taken from a 7 mm diameter gold disc electrode filled with
electrode gel and attached to the skin with an impedance of less than 2 k.
Volleys were recorded from Erb’s points bilateral against a reference
electrode on the mastoid process, from the spinal process of the 5th cervical
vertebra (Cv5) and seventh cervical vertebrae (Cv7) referred to the suprasternal notch (SSN).
 We did not use Cv7-Fpz montage in recording of N13 cervical potential, but
we used Cv7-SSN (Suprasternal Notch), according to the paper of
Mauguiere and Restuccia in (1991), they mentioned these advantages of
anterior neck reference as: a better base line stability and larger amplitude of
N13, due to the activity generated by the transverse dipolar source of N13 is
recorded at its maximal amplitude by the anterior neck reference from
parietal scalp sensory areas C4` and C3` on both sides which referred to
mastoid process.
Components of SSEPs
 SSEP components typically are named by their polarity and typical peak
latency in the normal population. For example, N20 is a negativity that
typically peaks at 20 milliseconds after the stimulus. The normal latency
value for a component in a particular individual may be different from that
implied by the component's name, because the lengths of the peripheral
nerve and spinal conduction pathways, which vary with the patient's
stature and age, influence the latencies of the SSEP components.
Upper Limb Somatosensory Evoked Potentials
Peripheral nerve compound action potential
 During clinical diagnostic studies of the upper limb SSEP, a surface
electrode at the Erb point is used to record the peripheral nerve CAP as it
traverses the brachial plexus. N9, the initial negative peak, reflects the
CAP within the most rapidly conducting subset of the afferent fibers.
Multiple negative peaks, reflecting peripheral nerve fiber populations with
different conduction velocities, may be recorded in some subjects, most
often in children. When this occurs, the earliest negative peak should be
interpreted as the N9 peak. A smaller P9 far-field peak, which most likely
also arises within the brachial plexus, may be seen in scalp-to-noncephalic
recordings; it has a slightly shorter latency than N9.
 Erb point-recording electrodes have several disadvantages during
intraoperative monitoring that include proximity to the sterile field, ease of
dislodgment, and pickup of ECG artifact. A useful alternative recording site
is over the peripheral nerve in the antecubital fossa.
Cervical components
 An SSEP component that most likely arises in the first-order afferent
neuron at or near the dorsal root entry zone (i.e. in the dorsal root and/or
the dorsal column) can be recorded as a far-field P11 peak in scalp-tononcephalic reference recordings and as a near-field N11 peak in surface
recordings over the lower cervical spine. This component is small and is
not identifiable in all healthy subjects.
 A larger and more consistent component recorded over the lower cervical
spine (eg, at SC5 or SC7) is N13. N13 has a horizontally oriented voltage
field, negative dorsally and positive ventrally, and is generated by
postsynaptic activity of neurons in the gray matter of the lower cervical
spinal cord. It sometimes is called the stationary cervical potential,
because its latency is not affected by cervical recording electrode location.
Far-field components
 The stationary cervical potential overlaps in time with a far-field SSEP
component, P14. While the origin of P14 has been the subject of some
controversy, it most likely reflects activity in the dorsal column nuclei
and/or the caudal medial lemniscus within the lower medulla. When a
forehead (i.e. Fpz) reference is used, this far-field component becomes
negativity (N14) at the SC5/SC7 recording location and summates with the
near-field N13 negativity picked up by that dorsal neck electrode.
 For intraoperative monitoring, the cervicomedullary far-field potential may
be recorded at the inion, mastoid, or earlobe, referred to as Fpz. It appears
as a negative peak, N14, in these recording linkages and, importantly, it is
not contaminated by the N13 cervical near-field potential. N14 can be used
to determine whether activity in afferent somatosensory pathways reaches
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the level of the cervicomedullary junction. Since at least 2 more synapses
(in thalamus and cortex) intervene, the N14 component may permit SSEP
monitoring of the cervical spinal cord when cortical SSEPs are of poor
quality because of high anesthetic levels and/or preexisting neuronal
damage.
If the region of the nervous system in jeopardy is rostral to the
cervicomedullary junction, N14 can be monitored to determine whether
changes in the cortical SSEPs are due to rostral nervous system
dysfunction, to peripheral nerve, or to technical problems. This is similar to
the intraoperative use of the peripheral nerve SSEP component described
above.
Optimally, both components should be monitored for 2 reasons: (1) N14
provides an alternative way of differentiating the possible causes of a
cortical SSEP change if peripheral nerve SSEP recordings are suboptimal,
and (2) if peripheral nerve CAPs are interpretable and remain unchanged
while cortical SSEPs deteriorate, examination of the N14 recordings can
localize further the neural dysfunction responsible for the cortical SSEP
changes above or below the cervicomedullary junction.
Another far-field component, N18, overlaps in time with the primary cortical
SSEP and may account for multiple negative peaks in the cortical
recordings in some subjects. N18 has a wide bilateral distribution over the
scalp. It is best seen in recordings with a noncephalic reference, though it
also may be demonstrated with a frontal reference. While N18 has been
attributed to a thalamic generator, several patients have been reported in
whom N18 was still present despite the presence of thalamic lesions that
eradicated the primary cortical SSEP. N18 most likely reflects activity in
multiple subthalamic (ie, brain stem) structures that are activated by the
somatosensory stimulus. Thus, examination of N18 cannot be used to
localize the cause for cortical SSEP changes (ie, rostral versus caudal to
the thalamus).
Cortical components
 The primary cortical SSEP component following median nerve stimulation,
N20 is recorded as a near-field potential over the parietal area
contralateral to the stimulated median nerve. Since an electrode also is
within the scalp distribution of the far-field N18 component, a recording
with a noncephalic reference contains an admixture of N18 and N20.
 While a thalamic or subcortical origin for N20 has been suggested, most
authors believe that N20 predominantly reflects activity of neurons in the
hand area of the primary somatosensory cortex; multiple generators with
overlapping voltage topographies may contribute to this. N20
predominantly originates in primary somatosensory cortex in the posterior
bank of the central sulcus and thus displays a polarity inversion across the
central sulcus in epidural cortical surface recordings and some scalp
recordings. This polarity inversion may be used to identify the central
sulcus during surgery.
Lower Limb Somatosensory Evoked Potentials
Peripheral nerve compound action potential
 A surface electrode placed in the popliteal fossa in the midline can be
used to record the peripheral nerve CAP following posterior tibial nerve
stimulation at the ankle. To minimize both electrical stimulus artifact and
ECG pickup, a reference electrode on the same leg is used. Possible
linkages include a midline electrode 2 cm above the popliteal crease
referred to a midline electrode 5 cm above the popliteal crease and a
midline popliteal fossa electrode referred to an electrode placed at the
lateral aspect of the same knee.
 In patients in whom a clear foot twitch is not obtained, the presence of a
clear peripheral nerve CAP at the popliteal fossa demonstrates that the
posterior tibial nerve has been stimulated adequately. In this case, the
absence of more rostrally generated SSEP components is evidence of
abnormality within the neural somatosensory pathways. Without the
peripheral nerve recording channel, the absence of SSEPs also could
have been due to technical factors that prevented adequate nerve
stimulation.
Lumbar components
 An electrode placed over the lower thoracic or upper lumbar spine records
a combination of the CAP in the primary afferent neuron, propagating
within the cauda equina and fasciculus gracilis, and a stationary lumbar
potential (SLP) that is derived from postsynaptic neurons in the gray
matter of the spinal cord. Recordings with a distant reference, such as the
iliac crest, emphasize the SLP, which is analogous to the stationary
cervical potential (N13) recorded over the lower cervical spine following
median nerve stimulation. Bipolar recordings between a pair of
rostrocaudally separated electrodes over the lower spine record the
propagating CAP.
 However, they also contain a component derived from the SLP,
representing the difference in amplitude or the SLP between the 2
recording electrodes. The relative magnitudes of the CAP and SLP
contributions vary across subjects; therefore, referential recordings show
less intersubject latency variability and should be used for clinical
diagnostic SSEP testing.
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The normal amplitude maximum of the SLP is at the T10-T12 vertebral
level but may be fairly restricted. Thus, referential recordings from multiple
electrodes over the lumbar and lower thoracic spine may be useful in
demonstrating the SLP.
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In patients with tethered spinal cords, recordings from such an array of
electrodes often demonstrate caudal displacement of the maximal
amplitude of the SLP, reflecting the anatomical displacement of the lower
spinal cord, or may show no identifiable SLP. The lumbar SSEP
components are sometimes not identifiable in unsedated healthy subjects,
especially if they are obese.
Far-field components
 When referred to a frontal scalp reference, electrodes over the cervical
spine record a biphasic waveform that was labeled originally as a cervical
potential but is believed now to reflect predominantly far-field potentials
generated in subcortical elements of the lemniscal somatosensory
pathways. If the inputs are connected so that the cervical lead is input 1
(i.e. C5S-Fpz), the waveform consists of a negativity followed by a
positivity.
 A near-field origin within the cervical spinal cord had been proposed for
some smaller and earlier peaks that can be picked up by the recording
electrodes placed on the posterior part of the neck. Like the lumbar SSEP
components, the far-field SSEP components elicited by lower limb nerve
stimulation may be difficult to identify in recordings from unsedated
subjects because of noise, particularly electromyography (EMG) artifact
from paraspinal musculature. Under surgical anesthesia, and especially
with the use of neuromuscular blocking agents, they are usually clearly
identifiable and reproducible.
 The cortically generated SSEPs due to stimulation of lower limb nerves
are far more sensitive to the effects of anesthesia than the far-field
components. During operations in which the cortically generated SSEPs
are markedly attenuated or completely suppressed by anesthesia or in
which they show a degree of anesthetic-related variability such that
changes related to surgical manipulations might not be recognized, the farfield SSEPs may be used to monitor the dorsal column pathways of the
spinal cord.
Cortical components
 The primary cortical SSEPs following lower limb stimulation are recorded
as near-field positivities: P37 following posterior tibial nerve stimulation
and P27 following peroneal nerve stimulation. In contrast to the N20
cortical component of the median nerve SSEP, which is maximal over the
lateral parietal area, the cortical SSEPs to lower limb nerve stimulation
often are maximal near the midline, reflecting the more medial location of
the foot and leg areas of the somatosensory homunculus.
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When the equivalent dipole of the cortical generator is oriented vertically,
the maximum positivity is in the midline. When the cortical generator is
located in the mesial wall of the hemisphere, the dipole assumes a more
horizontal orientation, producing a paradoxical maximum positive cortical
SSEP over the hemisphere ipsilateral to the stimulus In such situations, a
negative cortical SSEP may be recorded over the contralateral
hemisphere, and a midline electrode may pick up a much smaller and less
well-defined cortical SSEP. Rarely, the activated cortex is on the
dorsolateral convexity, producing a scalp positivity maximum over the
hemisphere contralateral to the stimulated leg. To cover all of these
possibilities.
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When the dipole is oriented horizontally, producing an ipsilateral positivity
and a contralateral negativity, however, the latencies of the ipsilateral
positivity and the contralateral negativity may not be identical.
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With both peroneal nerve and posterior tibial nerve stimulation, longer
latency cortical SSEP components follow the primary cortical P27 or P37
components. The second cortical positivity, which typically has a latency of
50-60 milliseconds after posterior tibial nerve stimulation, may be
substantially larger than the primary cortical SSEP. In noisy recordings
with a limited montage, a low-amplitude P37 component may not be
recognized, and the secondary cortical positivity may be identified
erroneously as a markedly delayed cortical SSEP. Thus, cortical SSEPs to
lower limb nerve stimulation should be interpreted with caution when their
peak latencies appear to be delayed abnormally to this latency range.
Spinal cord pathways mediating the somatosensory evoked potentials
 The large-fiber, rapidly conducting afferent somatosensory pathways that
sustain the primary cortical SSEPs to stimulation of mixed sensorimotor
limb nerves travel predominantly in the dorsal columns within the spinal
cord. In experimental animals, transection of the dorsal column pathways
almost completely obliterates the earliest cortical SSEPs to stimulation of
more caudally located peripheral nerves, while ventrolateral funiculus
lesions usually have only minor effects on these SSEPs.
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Thus, significant damage to descending motor systems can occur without
causing changes in the SSEPs used for intraoperative monitoring. Such
false-negative cases are fortunately rare, but they have occurred. In
contrast to the cortical SSEPs, near-field SSEPs recorded over the spinal
cord may contain components reflecting large-fiber afferent activity in both
the dorsal columns and the spinocerebellar tracts.
Clinical Application of Somatosensory Evoked Potentials
Cervical Myelopathy:
Median Nerve Somatosensory Evoked Potentials:
 As discussed before cervical spondylotic myelopathy is a common
condition that typically occurs in middle age and elderly subject. The
diagnosis is based on three clinical findings: Painful stiff neck, brachialgia,
and/or spastic paraparesis associated with variable degree of ataxia (Brain
et al, 1952).
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MRI of the cord can show several types of signal abnormalities at the level
of cord compression (Mehalic 1990) but gives no information on the
functional state of cervical cord. Therefore, it is of the utmost clinical
relevance to develop complementary investigations for assessing cord
dysfunction at the cervical level.
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Abnormal N13 potential was observed with preserved P14 and N20
potentials patients by stimulation of ulnar, median, and radial. The
preservation of P14 and N20 potentials reflect the activity of the dorsal
column systems with the absence of the clinical signs of dorsal column
dysfunction in their patients; nevertheless, abnormal scalp response in
cervical spondylotic myelopathy patients with normal sensation
(preclinical) are more frequently observed for the lower than for the upper
limb somatosensory evoked potential.
Posterior Tibial Nerve Evoked Potentials in Cervical Spondylosis:
 Posterior tibial somatosensory evoked potential is a good prognostic
indicator for patients undergoing spinal tumor removal, if they were
recorded pre and postoperatively. Good recovery was indicated in patients
a less pronounced posterior tibial somatosensory evoked potential
abnormality than clinical findings would indicate prior to surgery, and in
patients who showed a rapid somatosensory evoked potential
improvement postoperatively.
 Using posterior tibial somatosensory evoked potential to investigate
subjects with suspected spinal non-space occupying lesion, in addition to
prolonged latency, low amplitude and disturbed waveform.
Cervical Spinal Cord Syringomyelia:
 The major finding in this disorder is abnormal or absent N13 component
and it was correlated well with a segmental loss of pain and temperature
sensation and absent tendon reflex in the upper limb. With preserved
scalp P14 and N20 potentials
Intramedullary Cervical Cord Tumors:
 Somatosensory evoked potentials in cervical cord tumors is essential
either, preoperative or postoperative.
 Preoperative findings due to, impaired cervical dorsal horn postsynaptic
activity (abnormal N13 potential), with preserved dorsal columns
transmission up to the cortex (normal P14 and N20 potentials), or both,
dorsal horn activity and dorsal columns transmission are impaired.
 Postoperative follow-up helps in functional recovery assessment of those
patients.
Multiple Sclerosis:
 Initial neurophysiological recordings and clinical follow up on patients with
suspected multiple sclerosis found that evoked potential testing of three
modalities (visual, brain stem auditory, and somatosensory evoked
potential) increased the likelihood of detecting a silent lesion with only a
reasonable amount of time required to perform the test. Because of the
physiological properties of the nerve fibres are dependent on their myelin
sheaths.

So the somatosensory evoked potentials can reflect the integrity of the
sensory pathway at different sites. One of the diseases, which can affect
the myelin, is multiple sclerosis. The abnormalities of N13 and/or N20,
recorded after median nerve stimulation, were significantly correlated with
MRI abnormalities located in the posterior half of the cervical cord.
Abnormalities of P40 following posterior tibial nerve stimulation were less
well correlated with MRI findings.
SSEPs in Children
 The cortical SSEP to posterior tibial nerve stimulation may be absent in
healthy infants as old as 3 months. The cortical SSEP to median nerve
stimulation also may be absent at birth but most likely is present
consistently in healthy infants at an earlier age than the corresponding
component of the lower limb SSEP. SSEP component latencies are, in
general, shorter in infants and children than in adults and change
progressively with growth and maturation.

The latency changes predominantly reflect linear growth with elongation of
the peripheral nerves and central somatosensory pathways. These effects
are counterbalanced partially by myelination and increase in the fiber
diameters, which produce faster conduction velocities, and partially by
maturation of synaptic transmission. The latter effects operate until age 68 years, at which time central conduction times have reached adult levels
and further latency changes are due to changes in stature.

During spinal surgery in children in whom cortical SSEPs are absent or
easily attenuated by anesthesia, the far-field SSEP components may be
used to monitor the dorsal column pathway of the spinal cord. However,
many patients with lumbar meningomyeloceles have conduction
abnormalities (e.g., conduction blocks, temporal dispersion) at the level of
the neural plaque so that both far-field and cortical SSEPs are absent; this
precludes intraoperative assessment of their dorsal column pathways.
N9
Erb’s
point
N13
Cv7
N20
P9
C4’
P14
Fig. 6 Median nerve somatosensory evoked potentials
P40
Fig. 7 Posterior Tibial somatosensory evoked potentials
MAGNETIC STIMULATION
Magnetic Stimulation as a Clinical Technique:
Magnetic stimulation is based on the scientific principle of mutual inductance,
which was discovered by Michael Faraday in 1831. He showed that current
was induced in a secondary circuit when it was brought near to a primary
circuit in which a time-varying current was flowing. In the case of magnetic
stimulation, electrically conductive tissue forms the secondary circuit; the
primary is being the stimulating coil through which the stimulator drives
current pulses. The magnetic field is proportional to current through the coil
and the current induced in the tissue is proportional to the rate of change of
the magnetic field. The first example of a physiological effect of a time varying
magnetic field was reported by d’Arsonval (1896) who observed that
phosphenes (flicking lights seen by a subject) and vertigo were produced
when a volunteer’s head was placed inside a coil driven at 42 Hz. Thompson
(1910) and others subsequently confirmed this finding.
Bickford and Freeming (1965) reported non-invasive magnetic stimulation of
human and animal peripheral nerves in 1965. They used a 500 Hz damped
sinusoidal magnetic field with a peak amplitude of 4 Tesla decaying to zero
over approximately 40 msec, and a stimulating coil of mean diameter
approximately 3cm. However a revolution in transcranial stimulation occurred
when Anthony Barker and colleagues used the first magnetic stimulator
(Barker et al, 1985)
Physiological Basis Of Motor Effect Of Transcranial Stimulation:
The aim of transcranial magnetic stimulation is to produce Electromyographic
responses on the target muscle This electromyographic response differ from
Electromyographic responses to peripheral nerve stimulation in that, The
motor evoked potentials are smaller and have a longer duration than the
compound muscle action potential elicited by supramaximal peripheral nerve
stimulation.
Now, magnetic stimulation is an increasingly popular technique for evaluation
of motor pathway conduction properties by means of MEP. It is easy to handle
technique, which does not cause any pain to the subject. It has almost
replaced electric high voltage stimulation. Magnetic stimulation has found its
place in the diagnosis of demyelinating disease, in the operating room for
itraoperative motor pathway monitoring, as well as the assessment of the
spinal disorders affecting the spinal cord or its nerve roots (Jiri et al, 1992).
Following Transcranial magnetic stimulation, pyramidal tract cells in the motor
cortex are excited either directly or trans-synaptically via tangentially oriented
afferent fibres.
Clinical Uses of Magnetic Stimulation:
Cervical Spondylosis:
In cervical spondylotic myelopathy the lateral cortico-spinal tracts are the first
to suffer from minor compression.
Central motor conduction time of the thenar were abnormal by using cortical
magnetic stimulation and these abnormalities were correlated with upper
motor neurone signs and MRI evidences. Abnormalities were also noticed in
the amplitude, latency and /or duration of the compound muscle action
potential after cortical stimulation.
These central motor conduction abnormalities may be due to several factors:
Slowed conduction, conduction block, and temporal dispersion of the
pyramidal tract action potentials in the cervical cord.
Central motor conduction time abnormalities in cervical spondylotic
myelopathy were closely related to the distal upper limb muscles while the
proximal muscles are normal.
Cervical Spondylosis and Preclinical Myelopathy:
Outcome after surgery is better in patients with recent cord compression than
with long-standing illness. These results gave a chance to detect and treat
these patients with cervical spondylotic myelopathy as early as we can in the
course of the disease.
Unfortunately, radiological findings of cervical spondylotic myelopathy
occurred with irreversible neurological deficit when the value of surgical
intervention is limited.
The value of the magnetic stimulation to elicit the cortico-spinal tract lesions in
radiculopathic patients with no clinical or radiological manifestations of spinal
cord involvement.
Multiple Sclerosis
The value of transcranial magnetic stimulation in the diagnosis of multiple
sclerosis is increasing in the central motor conduction time either in remission
or preclinical state.
Behçet’s Disease:
Magnetic stimulation also has the advantage to detect preclinical myelopathy
in various conditions. In Behçet’s disease patients had central motor
conduction time and threshold abnormalities.
Amyotrophic Lateral Sclerosis:
Many authors studied amyotrophic lateral sclerosis using transcranial
magnetic stimulation in different ways. Barker et al, In 1986 and 1985, found
no significant prolongation in central motor conduction time. But, Kohara et al,
in 1996, studied the effect of transcranial magnetic stimulation on discharge
characteristics of single motor unit during voluntary contraction. He found
abnormal excitability of the corticospinal pathways.
Parkinson's disease:
Marked decrease in Silent period is important tool in diagnosis and prognosis
tool of Parkinson's disease.
Psychiatric disorders:
Obsessive convulsive disorder and depression.
Other disorders:
Diagnosis of vitamin B12 deficiency by using magnetic stimulation, and also in
syringomyelia
Clinical Safety of Transcranial Magnetic Stimulation:
Since introduction of the Transcranial magnetic stimulation in 1985 (Barker et
al, 1985) several thousands of patients and normal subjects have been
subjected to such stimulation without significant side effects.
Barker et al, 1987 discussed that the phenomenon of kindling unlikely to be
caused by magnetic stimulation. As regarding to the seizures induction by
magnetic stimulation, is extremely rare, even in patients with epilepsy
(Tassinari et al, 1990). In the other hand Homberg and Netz, 1989. Induced a
generalised tonic-colonic seizure following magnetic brain stimulation in a
man 6 months after a large right hemispheric infarction. Hufnagel et al, 1990
activated the epileptic focus in 12 of 13 patients with medically intractable
epilepsy.
EEG examination after magnetic brain stimulation in normal subjects by
Bridgers and Delaney (1989) Krain et al, (1990) And Levy et al, (1990)
showed essentially no changes before and after brain stimulation except for a
marginal slowing lasting for 5 seconds only in one patient by levy et al, (1990)
Chokroverty et al, (1995); examined the EEG not only visually but also by
using power spectral analysis and brain mapping and found no short term or
long term EEG changes.
Thomas et al, (1991); noticed that there was no significant changes in serum
prolactin or cortisol level after magnetic brain stimulation and this is similar to
Chokroverty S. (1995). These results suggest that magnetic brain stimulation
does not have documented adverse effects on the hypothalamic-limbic
structures and this suggestion agree with Roth et al, (1991).
By using positron emission tomography Toshiaki et al, (1993) measured the
cerebral blood flow before and within 50 sec after transcranial magnetic
stimulation in normal subjects and he found no significant changes.
Several groups have investigated the possibility of pulsed magnetic fields
causing ventricular fibrillation in animal models. Polson et al, in 1982 studied
the effect of magnetic stimulation on rats sensitized by digitalis. McRbbie and
Foster in 1985 investigated the effects of field strength, frequency, and coil
configurations up to peak field of 2.4 T on rats. No incidences of ventricular
fibrillation have been reported.
6
5
4
3
2
1
0
-1
-2
-3
0
0.01
0.02
0.03
0.04
0.05
0.06
0.07
0.08
0.09
0.1
Fig. 8 First dorsal interosseous response to transcranial magnetic stimulation
Fig. 9 Tracing recorded from first dorsal interosseous muscle & tibialis anterior after
transcranial magnetic stimulation