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Clinical and electrophysiological studies of human immunodeficiency virusЧseropositive men without AIDS.

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BRIEF COMMUNICATIONS
immunodeficiency virus (HIV) infection per se or the
immunodeficiency syndrome, we examined 15 HIVseropositive but otherwise healthy subjects. None of
the subjects had AIDS-related complex.
Clinical and
Electrophysiologicd
Studies-of Hum-an
Immunodeficiency
Virus-Serooositive Men
Without AfDS
Materials and Methods
T. Smith, MD,*J. Jakobsen, MD,t J. Gaub, MD,$
S. Helweg-Larsen, MD,T and W. Trojaborg, MD*
Motor weakness and ataxia of lower limbs and abnormalities of somatosensory evoked potentials occur in
many patients with the acquired immunodeficiency syndrome (AIDS). We studied 15 human immunodeficiency
virus-seropositive subjects without AIDS and found no
clinical neurological abnormalities. The mean latency of
the brainstem auditory evoked potential (peak V) was
increased, suggesting a central defect. Despite normal
peripheral nerve conduction along the tibial nerve, the
mean latency of the spinal cord potential of the twelfth
thoracic vertebra was increased compared with normal,
possibly indicating an incipient conduction defect at or
near the spinal root ganglion or lumbar spinal cord.
Smith T, Jakobsen J, Gaub J, Helweg-Larsen S,
Trojaborg W. Clinical and electrophysiological
studies of human immunodeficiency
virus-seropositive men without AIDS.
Ann Neurol 1988;23:295-297
Neurological complications are so common in the acquired immunodeficiency syndrome (AIDS) that they
may be regarded as concomitants of the immune disorder 12-5, 81.In a study of AIDS patients in Denmark,
we found that two-thirds had ataxia or motor weakness
of lower limbs. In 16 of 22 patients in whom somatosensory evoked potentials following tibial nerve stimulation could be obtained, latencies of spinal cord and
cortical potentials were prolonged. The defect could
be attributed partly to peripheral slowing, and partly to
central slowing, of conduction through the lower part
of the spinal cord 111.
To study whether the clinical and electrophysiological defects in AIDS were associated with human
From the Departments of *Clinical Neurophysiology, TNeurology,
and $Medicine (InfectiousDisease), R~gshospitalet,National Hospital, Copenhagen, Denmark.
Received Apr 30, 1987, and in revised form July 16 and Aug 21.
Accepted for publication Sept 10, 1987.
Address correspondence to Dr Smith, Department of Clinical
Neurophysiology NF, Rigshospitalet, Blegdamsvej 9, Copenhagen,
DK-2 100 Denmark.
Fifteen homosexual HIV-seropositive men gave informed
consent to the study, which was approved by the ethical
committee. Exclusionary criteria were a diagnosis of AIDS
and a history of other disorders that might cause neurological
dysfunction.
Subjects completed a standardized questionnaire and
underwent a neurologicalexamination in which special attention was given to lower limb performance in strength and
coordination tests. To estimate subclinical leg ataxia, hitmaking within a 2-cmz-squaretarget, precision of horizontal
drawings between two vertical lines, and amplitude of deviations in copying a circular form were measured.
The evoked potentials techniques used have been described in detail elsewhere [6,9]. In short, visual stimulation
of each eye in nun was performed at a rate of 2 stimulations
per second with a black-and-white checkerboard pattern.
The visual evoked potentials were recorded at 0 1 , 0,, and
0 2 , with a reference at F, (international 10-20 EEG electrode system). Monaural auditory stimulationwas performed
with magnetically screened earphones using a click of 0.1millisecond duration of approximately 7 5 decibels presented
at a rate of 10 clicks per second. The brainstem auditory
evoked potentials (BAEPs) were recorded at the vertex, referenced to the mastoid. The median and tibial nerves were
stimulated with surface electrodes placed at the wrist and the
ankle, respectively. Stimuli of 0.2-millisecond duration and
1.5 times above motor threshold were given at the rate of 2
stimulations per second. The somatosensory evoked potentials were recorded over the appropriate cortical hand and
foot areas, i.e., C3 or C4 for median nerve recording, and C,
for tibial nerve recording referenced to F,. Recordings were
also made over the supraclavicular fossa (Erb’spoint) and at
the C7 spinous process, following median nerve stimulation
(reference electrodes at the shoulder and at F, respectively),
and over the gluteal crease and TI2spinous process, following tibial nerve stimulation (reference electrode at the iliac
crest). Conduction distance was estimated using a tape measure. Findings in HIV-seropositive subjects were compared
to values from age- and sex-matched controls.
Differences between HIV-seropositive men and controls
were compared using the unpaired Student’s t test with a 5%
limit of significance ( 2 2 SD). Individual values were considered abnormal when they exceeded the control mean by two
standard deviations.
Results
Two of the 15 HIV-seropositive men had dysesthesias
as the only complaints. All had a normal neurological
examination regarding reflexes, two-point discrimination, position sense, and quantitative rests for araxia
The table summarizes the results of the electrophysiological studies. For comparison, the normal values
for age- and sex-matched controls are given. The pat-
Copyright 0 1988 by the American Neurological Association 295
-
ELectrophysiological Findings"
Normal Controls
n
Mean
20
94
SD
AIDS Patientsb
n
Mean
6.0'
24
93
6.3 5 0.3'
2.0 ? 0.1
4.3 f 0.3'
24
24
24
n
Mean
98
f
SD
f
2.7
37
f
0.1
0.1
0.2
40
26
26
48
48
48
67 r 4.8
14.5 i 0.7
20.2 f 1.4
42
36
43
60
15.2
21.3
?
f
?
4.9'
1.0'
1.3'
30
29
67
14.8
20.4
48
48
48
56
24.2
35.4
30
32
42
51
26.6
40.6
2
?
f
6.1'
2.7'
4.5'
30
30
30
55
25.0
36.2
40
40
40
SEP Median nerve
CV wrist-supraclavical ( d s )
N 1 4 wrist-C7 (ms)
N20 wrist-cortex (ms)
SEP tibial nerve
CV ankle-gluteal crease (ds)
N 2 4 ankle-Tlz (ms)
Onset ankle-cortex (ms)
f
HIV-seropositive
Subjects Without AIDS
5.8
2.0
3.9
f
f
f
?
2
3.5
1.4
2.1
2
f
SD
r 4.8
6.1 i 0.3'
1.9 2 0.09
4.2 r 0.06'
2
f
f
f
f
-t
5.4
1.0
1.2
4.3
1.9'
2.3
"Values represent nerve conduction time in milliseconds (ms) or nerve conduction velocity in meters per second ( d s ) .
bValues were obtained from a study of Danish AIDS patients [l].
'p < 0.05; for statistical comparison, degrees of freedom are the number of individuals studied minus one.
AIDS = acquired immune deficiency syndrome; HIV = human immune deficiency virus; N = number of eyes, ears, or nerves studied; SD =
standard deviation; VEP = visual evoked potential; BAEP = brainstem auditory evoked potential; SEP = somatosensory evoked potential; CV
= conduction velocity, d s = meters per second; ms = milliseconds, conduction time.
6
Fig I . Individual latencies of peak V of brainstem auditory
wokedpotentialr (BAEPs) in 12 human immunodeficiencyvirus-seropositive subjects. There are two values f i r each patient,
rrpresenting the left and the right sides. The hatched area represents the range of normal values (mean 2 2 SD); the horizontal
line in the middle, the mean.
Fig 2. Latency of N24 of the somatosensory ewoked potential
(SEP) after tibial nerve stimulation recorded at TI2 as a function of the conduction distance in 15 human immunod&cieng
virus-seropositive subjects. There are two values for each patient,
representing the left and the right sides. The solid line in the
middle indicates the mean value of normal controls; the hatched
area, the m a n f 2 SD.
tern reversal visual evoked potential was normal in all
12 subjects tested. The BAEP was abnormal in 3 subjects, and most of the remaining subjects had latencies
(peak V) in the upper part of the normal range (Fig 1).
The mean latency of peak V and of the peak I-V
interval was significantly increased in HIV-seropositive subjects compared with controls @ < 0.05) (see
Table).
Somatosensory conduction along peripheral nerves
and the spinal cord to C7 and the cortex after median
nerve stimulation was normal in all subjects, as were
the mean values compared with controls (see Table).
The peripheral conduction velocity along the tibial
nerve from the ankle to the gluteal crease was normal
in all patients except one, and the mean value was
similar to that of controls. However, the mean value of
the thoracic N24 component after tibial nerve stimulation was significantly prolonged in the subject group
compared with controls (p < 0.05) (see Table, Fig 2).
The latency to the onset of the cortical somatosen-
296 Annals of Neurology Vol 23 N o 3 March 1988
sory evoked potential evoked by tibial nerve stimulation was increased beyond two standard deviations in 2
patients, bpt the differences between control and subject latency means were not statistically significant.
4.
Discussion
6.
The 15 healthy HIV-seropositive subjects of this study
had neither lower limb weakness nor ataxia, but mean
latencies of BAEPs and tibial nerve evoked potentials
at T12 were prolonged compared with controls. In
AIDS also, these electrophysiological abnormalities
are present, but the slowing of conduction is more
severe and the defects are more widespread in the
peripheral and the central nervous systems (see Table).
Therefore, the electrophysiological abnormalities reported here could represent the earliest detectable
neurological attack during HIV infection.
Despite normal hearing and normal latency of peak
I, the mean latency of peak V of the BAEP was prolonged, suggesting an incipient conduction defect in
the brainstem. As the peripheral conduction along the
tibial nerve was normal, the delay of the potential recorded at the twelfth thoracic vertebra might reflect an
incipient defect in conduction in the vicinity of the
dorsal root ganghon.
The mean latency to the cortical response in subjects was not statistically different from that in controls. Similarly, the mean central conduction time from
TI* to cortex in subjects did not differ from that in
normal subjects (11.2 milliseconds in controls versus
11.2 milliseconds in the HIV-seropositive group).
Thus, it is likely that the delayed TI2 response is
caused by a defect between the gluteal region and the
twelfth thoracic vertebra.
A neuropathological study of the spinal cord in 89
AIDS patients revealed a vacuolar myelopathy caused
by swelling within myelin sheaths and affecting the
long tracts of the lumbar and lower thoracic cord in
one-fifth of the patients E7). There are no reports available of the pathology of the spinal root ganglia in
AIDS patients. Alternatively, the lack of a bloodneural tissue barrier in the ganglia enables the retrovirus to gain access to the nerve cell bodies and their
axons, producing edema and axonal damage. Our findings favor a defect of the myelin in the lumbar part of
the spinal cord, rather than a distal axonopathy with
dorsal root ganglion involvement.
5.
7.
8.
9.
experience at UCSF and review of the literature. J Neurosurg
62~475-495, 1985
Navia BA, Cho E-S, Petito CK, Price RW: The AIDS dementia
complex: 11. Neuropathology. Ann Neurol 19:525-535, 1986
Navia BA, Jordan BD, Price RW. The AIDS dementia complex:
I. Clinical features. Ann Neurol 19:517-524, 1986
Petersen L, Trojaborg W: Visual, auditory, and somatosensory
pathway involvement in hereditary cerebellar ataxia, Friedreich's
ataxia and familial spastic paraplegia Electroencephalogr Clin
Neurophysiol 521:283-297, 1981
Petito CK, Navia BA, Cho E-S, et al: Vacuolar myelopathy
pathologically resembling subacute combined degeneration in patients with the acquired immune deficiency syndrome. N Engl J
Med 312:874-879, 1985
Snider WD,Simpson DM, Nielsen S, et al: Neurological complications of acquired immune deficiency syndrome: analysis of 50
patients. Ann N e w 1 14:403-418, 1983
Trojaborg W, Petersen E: Visual and somatosensory evoked potentials in multiple sclerosis. J Neurol Neurosurg Psychiatry
42:323-330, 1975
CerebrosDinal Fluid
Antibodiis to Myelin Basic
Protein in Acute Idiopathic
Optic Neuritis
Kenneth G. Warren, MD, Ingrid Catz, MSc,
and Christopher Bauer
~
~~~
~~~~~~~~
Free and bound levels of anti-myelin basic protein
(anti-MBP) antibodies were measured by radioimmunoassay in the cerebrospinal fluid of 20 patients with
acute idiopathic optic neuritis, 133 patients with rnultiple sclerosis (MS) divided into three clinical subgroups,
and 76 normal control subjects. Patients with idiopathic
optic neuritis had elevated levels of anti-MBP predominantly in free form, resulting in an elevated (above
unity) freehound anti-MBP ratio similar to that of MS
patients with acute relapses. These data suggest that
acute idiopathic optic neuritis, like active MS, is associated with anti-MBP.
Warren KG, Catz I, Bauer C. Cerebrospinal fluid
antibodies to myelin basic protein in
acute idiopathic optic neuritis.
Ann Neurol 1988;23:297-299
Intrathecally produced autoantibodies to myelin basic
protein (anti-MBP) are detected in increased levels in
References
Helweg-Larsen S, Jakobsen J, Boesen F, et al: Myelopathy in
AIDS. A clinical, neuroradiological, and electrophysiological
study of 23 Danish patients with AIDS. Acta Neurol Scand
7764-73, 1988
Koppel BS, Wormser GP, Tuchman AJ, et al: Central nervous
system involvement in patients with acquired immune deficiency
syndrome (AIDS). Acta Neurol Scand 71:337-353, 1985
Levy RM, Bredesen DE, Rosenblum ML: Neurological manifestations of the acquired immune deficiency syndrome (AIDS):
From the Multiple Sclerosis Patient Care and Research Clinic, Division of Neurology, Department of Medicine of the University of
Alberta, Edmonton, Alberta, Canada.
Received May 13, 1987, and in revised form Jul 31 and Sep 8.
Accepted for publication Sep 11, 1987.
Address correspondence to Dr Warren, 9-101 Clinical Sciences
Building, University of Alberta, Edmonton, Alberta, Canada, T6G
2G3.
Copyright 0 1988 by the American Neurological Association 297
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