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Electrophysiological studies in the Guillain-Barr syndrome.

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Electrophysiological Studies
in the Gdain-Barr6 Syndrome
J. G. McLeod, MB BS, D Phil
~
Electrophysiological studies were performed on 114 patients with Guillain-Barre syndrome and t h e literature was
reviewed. Abnormalities of motor and sensory conduction were present in about 90% of the patients. Because of the
patchy distribution of demyelinating lesions, the likelihood of detecting electrophysiological abnormalities increases with the number of nerves studied. Marked slowing of conduction or an abnormally prolonged distal motor
latency consistent with demyelination was found i n one or more nerves in about 50% of the patients. Abnormalities
of conduction not present in t h e early stages of t h e illness may become evident at t h e peak of disability or during
the recovery phase. T h e application of F-wave studies and somatosensory evoked potential recordings may assist in
detecting demyelinatiori in roots and proximal segments of the peripheral nervous system. T h e r e is no correlation
between the degree of slowing of conduction and the duration of illness or the long-term prognosis. Abnormalities
of conduction at follow-up d o not correlate with the clinical disability. O n the other hand, electromyographic
findings of abundant spontaneous fibrillation and other evidence of axonal degeneration are associated with a poor
prognosis for complete recovery and also with a slower rate of recovery from the initial illness.
McLeod JG. Electrophysiologlcal studies in the Guillain-Barri. syndrome. Ann Neurol9(supp1).20-27, 198 1
Electrophysiological studies in the Guillain-BarrC
syndrome (GBS) have been reported by a number of
workers and have been found useful in diagnosing
the condition [2-4, 11, 14, 16-19, 2 5 , 26, 32, 34,
38, 4 3 , 441. Measutenent of F-wave conduction has
also been helpful in detecting lesions in the proximal
segments of nerves and in the roots [21-241. T h e r e
have been conflicting reports about t h e correlation of
electrophysiological abnormalities and the clinical
disability and lofig-term prognosis [ 1 1 , 14, 27, 32,
3 4 , 3 8 , 4 2 ] . I n the present paper our own experience
with electrophysiological studies in GBS and that of
other workers is reviewed.
Materials and Methods
Clinical assessment and electrophysiological studies were
performed on 114 subjects who presented with an acute
monophasic illness characterized by a predominantly motor
neuropathy that developed to a maximum disability within
21 days [39, 401. There were 61 male and 53 female patients, and ages ranged from 3 to 78 years (mean, 32
years). The results in 50 of these patients have already been
reported [ 3 2 ] ; the remainder have been investigated in
our department since 1975. Diabetes mellitus, infectious
mononucleosis, chronic renal failure, vitamin B,2 deficiency, and acute porphyria were excluded by laboratory
investigations, and subjects were omitted from the study if
there was evidence of alcoholism or nutritional deficiency
From the Department of Medicine, University of Sydney, and Deparunent of Neurology, Royal Prince Alfred Hospital, Sydney,
Australia.
or if malignancy or toxic causes were suspected. The electrophysiological studies performed on these patients
were compared with those obtained from 35 control subjects.
Electromyography was performed in most instances on
the intrinsic muscles of the hand and the distal muscles of
the legs using a concentric needle electrode. Nerve conduction study techniques have been described fully
elsewhere 132, 451. Motor conduction velocities were
measured in the median, ulnar, and lateral popliteal nerves.
Muscle action potentials were recorded with a concentric
needle electrode or with surface recording electrodes from
the abductor pollicis brevis, abductor digiti minimi, and
extensor digitorum brevis muscles, respectively, following
supramaximal stimulation of the nerve at two sites, and
conduction velocity was calculated after measuring the latency of the responses from photographic records. Sensory
action potentials were recorded with surface electrodes
from the median and ulnar nerves at the wrist on stimulating the index and fifth fingers, respectively, through ring
electrodes. Mixed nerve action potentials were recorded
with subcutaneous needle electrodes from t h e lateral popliteal nerve at the neck of the fibula on stimulating the anterior tibia1 nerve at the ankle. Latency to peak and the
amplitude of sensory and mixed nerve action potentials
were measured from photographic records. The stimulus
was a square wave with a duration of 0.2 or 0.5 msec and
amplitude of up to 500 v derived from the Disa Ministim.
The responses were recorded and displayed on a Medelec
M-Scope. Room temperature was maintained at 26°C.
Presented at the Conference o n Guillain-Bar& Syndrome sponsored by the Kroc Foundation, Santa Ynez Valley, CA, Sept
22-26, 1980.
Address reprint requests to Dr McLeod, Department of Medicine,
University of Sydney, Sydney, NSW 2006, Australia.
20
0364-5 134/8l/SlOO20-0S$Ol.25 @ 1980 by the American Neurological Association
Results
Nerve conduction studies were performed in all
cases usually close to the time of peak disability. T h e
mean interval from onset of symptoms to the time of
nerve conduction studies in the group was 23.7 2
18.1 (SD) days (range, 1 to 128 days). T h e mean
values for the GBS group are given in the Table and
are compared with the mean values for the 35 control
subjects. The patients with GBS had increased terminal motor latency and slowing of motor conduction in the median, ulnar, and lateral popliteal nerves
as well as reduction in amplitude of the sensory action potentials of the median and ulnar nerves and of
the mixed nerve action potential of the lateral popliteal nerve.
The terminal motor latency in the median nerve
was greater than 7.0 msec in 38 patients and motor
conduction velocity was below 40 m/sec in 34 (Fig 1).
There was a significant correlation between the terminal motor latency and motor conduction velocity
in the forearm segment (Y = 0.61). However, in 3
subjects in whom the terminal motor latency in the
median nerve was greater than 7.0 msec, the median
motor conduction velocity was within the control
range (Fig 2). The median terminal motor latency
and median motor conduction velocity fell within
two standard deviations of the mean for controls
in 46 and 54 subjects, respectively, and in 31 patients ( 2 7 % ) both were within two standard deviations of control values. In the lateral popliteal nerve,
the terminal latency was above 10 msec in 22 patients
and motor conduction velocity was less than 30 m/sec
in 19 (Fig 3). In 4 patients in whom the distal motor
latency was greater than 10 msec, motor conduction
velocity was within the control range. In 56 subjects
(49%), motor conduction velocities and terminal
latencies in one or more nerves were in the range
characteristic for demyelination (terminal latency
>7.0 msec in median nerve or >10 msec in lateral
popliteal nerve; motor conduction velocity <40
mlsec in median or ulnar nerve or <30 misec in lateral popliteal nerve).
T h e degree of impairment of conduction varied in
different nerves of the same subject; some patients
had marked abnormalities in one o r more nerves with
normal conduction in others. In 34 of the 114 patients (30%),abnormalities were found in one o r two
but not all three nerves studied. Abnormalities of
sensory conduction in the median or ulnar nerve or
both were detected in 87 patients (76F). All nerve
conduction studies were within normal limits in 10
subjects (996). The mean motor conduction veloci-
Nerre Conduction Studies in Guillain-Barre Syndrome
GBS (N
Determination
Mean
k
SD
=
114)
Range
Control (N = 3 5 )
Mean t SD
Range
Significance"
MOTOR CO N D U CTI O N
Median nerve
Latency (msec)
Velocity (mlsec)
Ulnar nerve
Latency (msec)
Velocity (m/sec)
Lateral popliteal nerve
Latency (msec)
Velocity (m/sec)
6.1
13.6
2.0-28 .0
4-70
3.4 I 0.5
56.9 +- 5.0
2.5-4.9
49-66
p < 0.001
p < 0.001
4.0
13.6
1.9-24.0
6-70
2.58 ? 0.4
55.7 t 4.6
2.1-3.7
47-69
p < 0.001
p < 0.001
9.2 t 1.3
36.5 ? 11.4
2.0-31.0
5-56
4.6 ? 1.0
47.3 1 4 . 9
3.3-7.7
38-56
p < 0.001
p < 0.001
7.6
43.9
?
5.2
43.5
I
?
&
SENSORY ACTION POTENTIALS
~
Median nerve
3.2 t 0.7
6.6 t 8.3
2.2-6.7
0-34
3.0
17.9
?
2.9
3.4
0.5
5.0
I .9-4.5
0-24
2.5
13.7
I
6.5 I 1.2
2.2
2.7
aSignificance of difference by Studenc's t tesc.
3.6-7.6
0-10
Latency (msec)
Amplitude (pv)
Ulnar nerve
Latency (msec)
Amplitude (pv)
?
?
NS
0.3
7.5
2.2-3.8
9-40
p < 0.001.
0.3
6.4
2.0-3.4
5-36
p < 0.001
6.3 t 0.7
5.2 ? 3.9
5.1-8.1
0-15
p < 0.001
?
?
NS
MIXED NERVE ACTION POTENTIALS
Lateral popliteal nerve
Latency (msec)
Amplitude ( p v )
*
NS
McLeod: Electrophysiological Studies in GBS
21
'L
16
14
801
.
12
-m
5
-
10
.
8
t
U
z
5
c
4
::
0
6
30.
.
3
n
Z
2
4
e
e
K
20
2
5
0
t
20.
-
.
.
10.
.*
i
C
20
40
60
80
AGE
IN Y E A R S
Fig 1 . LateniJi of the muscle action potential on .stimulating
the median nerve at the uiriJt und median newe motor conduction celocity in GBS. The solid 1ine.r represent mean control
value.^: dashed lines indicate t w o standard dwiatiom from the
meun.
70
60
2
z
I-
6
s
.
50
40
8
Y
>
z
30
0
I-
U
3
n 20
z
0
U
.
K
10
0
z
.
0
0
.
i
I
-
0
5
10
15
20
25
30
L A T E N C Y (MS)
F i g 2. Relationhip of terminal motor Iutency to motor conduction wlority i n the forearm .segment of the median nerz'e in 107
patient5 with G B S .
22
Annals of Ncurologv
Supplement to Volume 9, 1981
16
..
14
b
12
**
10
*.
h
In
E
8
U
+
U
5
6
I-
4
4
. . .
* : -__--____---___----
-
L: **
* *
.*
*
*
*
*2*
**
I
*
*
a
**
-------- _ _ _ _ _ _ _--*
A
0
*
20
40
*
4
60
a0
AGE
0
40
20
60
80
IN Y E A R S
F i g 3. Latency of the muscle action potential on stimulating
the lateral popliteal newe near the ankle and lateralpojditeal
nerwe motor condmtion velocity. The solid lines represen1 mean
control calzles; dashed lines indicate t w o standard deriatinns
from the mean.
701
$
z
5
I
60
(i i
Y
2
50
U
ties were significantly greater ( p < 0.001) in the median, ulnar, and lateral popliteal nerves of the patients with GBS than in a group of 23 patients with
subacute or chronic relapsing demyelinating neuropathy [41](Fig 4 ) .
In 50 patients there was no correlation between
motor conduction velocity when the electrodiagnostic studies were first performed and maximum clinical
disability (Fig 5 ) .
Discussion
Patients were included in the present study only if
they experienced acute onset of a predominantly
motor neuropathy in which no specific etiological
factor was found and which reached its maximum
severity within three weeks 132, 39, 401. Patients
with a subacute onset or chronic relapsing course
were excluded since they may have a different clinical
syndrome [41].However, other authors who have
reported electrophysiological studies in GBS have
included patients with a subacute onset [11, 14, 2 9 ,
40
Z
-0
3
30
0
z
...
....
:..
0
"
2
20
g
...
...
.:..
....
..:...
01
10
a
-
MEDIAN
..:..
+:.:
...
...
...
...
...
...
...
....
...
....
...
..:...
....
....
....
....
:..
...
-
U LNAR
-
.:...
:...
..
...
...
...
...
...
......
..'
...
....'.
LATERAL POPLITEAL
F i g 4. Mean motor c.oriduction wlorities in the median, ulnar,
and lateral popliteal n e r m of control subjects (open bars) and
patients with GBS (hatched bars) or chronic relapsing denryelinrrting neuropathy [41] (stippled bars). Mean z?aluesare
shozcln with one .rtandard dmiation.
34, 381.
McLeod: Electrophysiological Studies in GBS 23
MEDIAN
LATERAL POPLITEAL
Fig 5 . Relationship between motor conduction zdorities i t i median and lateral popliteul newer and maximum clinical diiability. Grade I1 = mild motor and sensory synzptom, no
signs: I11 = moderate disability; IV = ussistance needed with
walking: V = unable t o uwlk. No patients were grade 0 (normal) o r I (signs but TZO symptomsl. (Modifiedfrom McLeod et a l
1321.)
The pathological changes in peripheral nerves in
GBS are those of primary demyelination 11, 6, 32,
35, 40, 461. Marked slowing of motor conduction
velocity (<40 mlsec in median and ulnar nerves or
<30 m/sec in lateral popliteal nerves, or prolongation
of terminal motor latency in median nerves beyond
7.0 msec) is characteristic of segmental demyelination 1311 and was found in 4996 of the patients in the
present study. Lambert and Mulder [26] found that
61% of their patients had values for conduction velocity that were less than 705% of the control mean.
In 25% of additional patients they recorded prolongation of distal latency and duration of the muscle
action potential, with slight or no reduction in conduction velocity in the fastest fibers. While diffuse
slowing of conduction was the most common pattern
encountered, the slowing was most pronounced at
common sites of nerve compression. Other workers
have also found greatly prolonged distal motor latencies in some patients in whom motor conduction velocities in more proximal sites of the nerve were
normal or only mildly slowed 13, 4 , 11, 17, 22, 32,
341. Complete block in conduction and dispersion of
the muscle action potentials were noted in some pa-
24
Annals of Neurology
Supplement to Volume 9, 1981
tients in the present series, as they have been in
others L2, 3, 7, 11, 251.
In the present study, normal nerve conduction was
found in 9%) of all subjects. The figure is less than
that of 14% from our earlier study 1321. Lambert and
Mulder [26] found normal conduction in 1 4 9 of 98
patients studied. McQuillen 1341 reported normal
motor conduction in 7 of 22 patients (41%), but only
2 of these had a muscle action potential of normal
amplitude. %sen and Humphreys [ 11J reported
normal conduction in 5 of 25 patients, and normal conduction was also found in some patients
by earlier workers [ 4 , 161. It is important in the investigation of patients with suspected GBS to study
several different nerves. In our earlier study, 9 of 50
subjects (18%) had normal conduction in some
nerves but impaired conduction in others [32]. In the
present larger series, 34 of the 114 (30%) had normal conduction in some nerves and abnormalities in
others.
A number of our patients had electromyographic
evidence of sparse spontaneous fibrillation. Eisen and
Humphreys [ 1 11 found electrical evidence of ongoing denervation in 23% of their patients, and the
electrical findings are consistent with the pathological
observations that axons as well as the myelin sheath
may be damaged [l, 6, 12, 15, 35, 36, 401. Quantitative electrophysiological studies of the number and
dimension o f motor units in the extensor digitorum
brevis muscle have confirmed the presence of definite axonal damage in the majority of patients with
GBS [291.
Abnormalities of sensory conduction in median o r
ulnar nerves or both were present in 87 (76%) of our
114 patients. Eisen and Humphreys [ 111 found absent sensory action potentials in one or both of these
nerves in 58% of their subjects.
In 1 of our patients, conduction velocities were
normal when first measured at the onset of the illness
but became abnormal subsequently. The fact that
motor conduction velocity may not be affected in the
early stages of the disease has been noted by many
workers [5, 11, 14, 16, 20, 22, 26, 371.
Correlution between Electrophysiologicul Studzes
and Clinicul Disubility
No apparent correlation exists between the degree of
impairment of conduction and maximum clinical disability in patients with GBS [14, 321. This finding reflects the variability in the nature and distribution of
pathological changes in the peripheral nervous system 111. Patients with segmental demyelination in
proximal portions of nerves o r in roots may be severely paralyzed but have normal peripheral nerve
conduction, and conduction may be only very mildly
slowed in patients in whom axonal degeneration occurs. B y contrast, only minor disability may be present in some patients who have severe slowing of
conduction. There is no statistical correlation between the degree of impairment of conduction and
the period of disability [32]. However, Eisen and
Humphreys [ 111 found that patients with electrophysiological abnormalities were slower to recover than those without, although McQuillen [34]
found the reverse. Some workers [ 1I , 421 have reported that spontaneous fibrillation and other electromyographic evidence of denervation are associated with a prolonged recovery time. These
electromyographic findings indicate that severe axonal degeneration has occurred, and the correlation
with a long period of disability is consistent with
our own observations [32].
Long-term Follow-up Studies
Pleasure et a1 [38] found a correlation between the
severity of residual clinical disability and the extent
of electromyographic abnormalities and impaired
nerve conduction studies at follow-up. However,
they included in their studies patients with relapsing
neuropathies and neuropathies with subacute onset
in which persistently slow conduction velocities may
be expected [41] (Fig 4). McLeod et a1 [32] reexamined 18 patients at intervals from 6 months to 595
years after the onset of illness (mean, 3 years). There
was no relationship between the degree of slowing of
motor conduction at the time of diagnosis and the
clinical disability at follow-up examination. However,
the most severely disabled patient was one who had
clinical evidence of marked distal muscle wasting and
electromyographic evidence of chronic partial denervation although motor conduction was only mildly
impaired. Abnormalities of nerve conduction were
demonstrated at the initial examination in 1 7 of our
18 patients, but at follow-up all measurements were
within the control range in 11 subjects. Some abnormalities were demonstrated in the remaining 7
subjects, but in all cases improvement had occurred
from the initial studies. There was no relationship
between the residual clinical disability and nerve
conduction velocities at the time of final follow-up.
Three of the patients without clinical disability had
abnormalities of motor or sensory conduction; 5 of 9
patients with clinical disabilities had entirely normal
motor conduction studies. This lack of correlation
between the clinical state and electrophysiological
findings at follow-up has been confirmed in another
recent study [ 141. Our finding that most patients with
GBS have normal nerve conduction studies at
follow-up examination is consistent with the observations of Kaeser [20].
In the few patients in the present study in whom
serial electrophysiological studies were carried out
during the acute and recovery phases of the illness,
improvement slowly occurred. These findings are
consistent with the reports of others [2, 3, 16, 17,
341.
F -watle
The F-wave is a late evoked muscle response that occurs after the muscle action potential (M-responie)
on supramaximal stimulation of the nerve [28] and
results from antidromic activation and backfiring of
the motor neurons [8, 30, 331. It has beeh used by
several workers as a means of measuring proximal
motor conduction velocity in GBS [21-241. Kimura
and Butzer [22] used the F-wave as a measure of
proximal conduction betweed axilla and spinal cotd
in 9 patients with GBS. They studied only mildly affected patients since the F-wave was nearly always absent or difficult to detect if the M-response was
substantially delayed or diminished. In 4 of their 9 patients, motor conduction velocity was normal or only
mildly slowed in the first four weeks but F-waves
were abnormal. In a later study [21] the P-wave
findings were described in 45 patients with GBS, including 14 previously reported. The F-wave latency
was significantly increased. The F-wave conduction
velocity was slowed when motor conduction velocity
in distal segments was normal or borderline in nerves
of upper and lower limbs in a number of cases.
Slowing of conduction tended to be localized to
proximal segments and to terminal portions of motor
fibers.
King and Ashby [23], using techniques Similar to
Kimura’s, also studied the F-wave in motot. fibers of
the ulnar nerve in 11 patients with GBS. They found
that conduction velocity was reduced to a similar extent in both proximal and distal segments, but conduction in the proximal segment was disproportionately reduced in 2 of their patients, and in 1 of these
patients the distal conduction velocity remained
normal.
Lachman, Shahani, and Young [24] measured the
F-wave latencies to the abductor pollicis brevis and
the H-reflex latency to the soleuS muscle in tontrols
and in patients with GBS and other neuropathies.
Their technique of measuring the F-wave latency and
relating it to the subject’s height is preferable to the
less accurate method of attempting to estimate an
F-wave conduction velocity [21-231. Of 11 patients
with GBS, there were 2 in whom the late responses
were abnormal while motor conduction velocities in
distal segments were within the normal range. In 1
patient there were normal late responses while distal
conduction velocities were abnormal, and in 8 pa-
McLeod: Electrophysiological Studies in GBS
25
tients the late responses and distal conduction velocities were both abnormal.
Somatosensory Evoked Potentzals
Somatosensory cerebral and spinal evoked potentials
may be useful in evaluating slowing of conduction in
the peripheral nervous system [9, 10, 131 and may
be particularly helpful in evaluating lesions of proximal nerves and roots [lo]. A comparison of F-wave
and evoked potential techniques in the diagnosis of
predominantly root lesions in GBS is in progress in
our laboratory.
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McLeod: Electrophysiological Studies in GBS
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