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Loss of evoked potentials during spinal surgery due to spinal cord hemorrhage.

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dine was initiated in month 3 of receiving bromocriptine, and the dosage later was increased in month 4 of
receiving placebo.
Discussion
This study failed to demonstrate any beneficial effect
of bromocriptine on the symptoms of vascular dementia. In fact, on several of our measures, there was a
trend toward worse performance while on bromocriptine. In 4 patients, changes were made in other drugs
which might affect higher cortical function, but in our
judgment, these changes probably did not exert a substantial influence on the study outcome.
The considerable statistical power of the crossover
design makes it unlikely that the lack of significant
results favoring bromocriptine was due to small sample
size [S]. On the other hand, it is quite possible that our
sample was not representative of vascular dementia in
general or that we failed to include a subclass of vascular dementia patients that might benefit from the drug.
However, our experience with over 50 vascular dementia patients enrolled in a prospective diagnostic
study of dementia (unpublished observations) suggests
that the patients selected for the present study were
quite typical.
The finding that bromocriptine may actually be
harmful to patients with vascular dementia should lead
to a search for other agents of potential benefit; it also
increases the importance of making the sometimes
difficult clinical distinction between Parkinson's disease and vascular dementia. Theoretically, our negative
results suggest that the neurobehavioral features of
vascular dementia cannot be attributed to reduced
dopamine levels in the target organs of the midbrain
dopaminergic projections. Our results are also congruent with animal studies, which suggest that a fairly
narrowly defined range of tissue dopamine concentration is a necessary condition for normal function of the
basal ganglia {9, 101 (and, by inference, mesolimbic
and mesocortical systems). Increasing dopamine levels
may only add to, rather than compensate for, dysfunction stemming from damage to other aspects of frontal
lobe systems, such as may occur in vascuLar dementia.
We are indebted to Sandoz Pharmaceuticals, Inc, which provided
the drugs used in this study; to William Byrd, who managed drug
dispensing; to Opal Good and Linda Pritchett, who typed the manuscript; to Shulamit Verman, who did part of the neuropsychologicd
testing; and to Kenneth M. Hedman, who reviewed the manuscript
and provided much constructive criticism.
References
1. Babikian V, Ropper A H . Biswanger's disease: a review. Stroke
1987;18:2-12
2. Ross ED, Steward RM. Akinetic mutism from hypothalamic
damage: successful treatment with dopamine agonists. Neurology I 98 I ;3 1: 14 3 5- 143'9
3. Jackson .~
JA, Jankovic J, Ford J. Progressive supranuclear palsy.
clinical features and response to treatment in 16 patients. Ann
Neurol 1983; 13~273-278
4. Markham C H . The choreoarhetoid movement disorder incluced
by levodopa. Clin Pharmacol Ther 1'97 1;12:340-343
5. Fellows BJ. Chance stimulus sequences for discrimination tasks.
Psycho1 Bull 1967;67:87-92
6. Conover WJ. Practical nonpararnetric statistics. New York:
Wiley, 1971
7. Fleiss JL. The design and analysis of clinical experiments. New
York: John Wiley, 1986
8. Louis TA, Lavori PW, Bailar JC, Polansky M. Crossover and
self-controlled designs in clinical research. N Engl J Med 1084;
310:24-3 1
9. Rolls ET, Thorpe SJ, Boytim M, et al. Responses of srriatd
neurons in the behaving monkey, 3 . Effects of iontophoretically
applied dopamine on normal responsiveness. Neuroscience
1984;12:1201- 12 12
10. Toan DL, Schultz W. Responses of rat pallidum cells to cortex
stimulation and effects of altered dopaminergic activity. Ncuroscience 1984;15:683-694
Loss of Evoked Potentials
During Spinal Surgery
Due to Spinal Cord
Hemorrhage
R. Shukla, MB, ChB,* T. B. Docherty, RMN,
R. K. Jackson, FRCS, R. 0. Weller, FRCP,
and E. M. Sedgwick, M D
The cortical somatosensory evoked potential (SEP) clisappeared during corrective spinal surgery in a patient
with muscular dystrophy. The patient died 18 hours after surgery. Autopsy revealed an intramedullary hemorrhage 4 mm in diameter in the posterior horn of the
cervical spinal cord. Microscopically, hypoxic neurons
were seen adjacent to the hemorrhagic area, implying
that the lesion was at least 6 hours old. The hemorrhage
corresponded to the loss of SEPs and confirms that
spinal cord monitoring can detect such lesions.
Shukla R, Docherty TB, Jackson RK, Weller RO,
Sedgwick EM. Loss of evoked potentials during
spinal surgery due to spinal cord hemorrhage.
Ann Neurol 1988,24 272-275
Spinal cord monitoring during corrective spinal surgery is now routinely done. Most workers in this field
From the Wessex Neurological Centrr, General Hospital, Southampton, U K SO9 4XY
Received Nov 30, 1987, and in revised form Feh 2, 1988 Accepted
for publication Feb 26, 1988
Address correspondence to D r Sedgwiik
"Present address Department of Neurology, King George's Mrdical College, Lucknow 226003 India
272 Copyright 6 1988 by the American Neurological Association
B.P.
Time
1343
(mmltigt
-
-
1325
1 OW64
13:ll
106/80
188166
130/66
13:02
12:59
12:28
11:55
128180
11:45
W
i+
1.25pV
10:15
f 1 10/80
109174
09:52
09:33
98/66
I
10
L
24
38
Fig 1 . Cortical somatosensoty evoked potential recorded following
stimulation of the right posterior tibial nerve at d;fferent stages
of surgey. The time is shown on the ldt and bloodpressure
(B.P.) on the right. There is a progressive increase in P40 latency from 1 1 5 3 t o 12:40 before the potential disappears completeb at 12.39.
have observed cases in which an attenuation or disappearance of the somatosensory evoked potential (SEP)
was followed by a postoperative neurological deficit C7,
121, but occasionally a deficit develops despite a normal SEP @]. The site of the lesion cannot usually be
ascertained and pathological confirmation of a lesion
has not previously been reported. We describe a patient whose cortical SEP disappeared during spinal instrumentation, and autopsy showed an appropriately
situated lesion in the posterior horn of the cervical
spinal cord.
Case Report
The patient was an 18-year-old male first seen at 3 years of
age when he had difficulty in walking. After a full investigation, he was diagnosed as suffering from muscular dystrophy
of the Emery-Dreifuss type 131. At 14 years he was seen with
a progressive extension deformity of the neck. At the age of
18 years he was admitted for posterior cervical release and
Luque's instrumentation. H e exhibited a marked cervical lordosis and limitation of neck flexion, with his head held facing
upward and tilted backward.
52
66
80 msec
Operative Procedure
A midline incision was made at the back of the neck, and
minimal correction was achieved when all soft tissues were
released. There was ankylosis at C3-4. Osteotomy and apical
laminectomy resulted in a further correction of the lordosis.
Spinal instrumentation was performed with two conjoined
Luque rods and sublaminar wiring from the atlas to T-2. A
graft was taken from the left iliac crest and laid in the lateral
gutters, though no formal facet excision was performed.
Blood loss was about 5,500 ml, which was replaced by 5,000
ml of whole blood during the operation. There was a dural
leak at C3-4 which ceased during the operation.
Electropbysiological Findings
Scalp SEPs were recorded from Cz'-Fz', following posterior
tibial nerve stimulation at the ankle on a Nicolet Pathfinder
II machine according to a previously described method 161.
The cortical P40 latency was 4 1.8 msec (right) and 4 1.5 msec
(left), with an amplitude of 2.90 FV bilaterally in the preoperative recordings the day before surgery. Anesthesia produced an 83% decrement in P40 amplitude. During the
procedure (from 9 0 5 to 11:45 AM) the latency of the P40 of
the SEP changed by only 1 msec but fluctuated in the amplitude by 28.5%. From 11:55 onward there was a progressive
prolongation of latency before the SEP disappeared completely at 12:59 (Fig 1). Just prior to this (at 12:28), the
blood pressure rose to 188/66 mm Hg, then fell to 110/80
mm Hg at 12:59. Sublaminar wires were being attached but
not tightened when the SEP disappeared. The SEP did not
Brief Communication: Shukla et al: Loss of SEP Due to Cord Hemorrhage
273
A
B
~~
Fig 2. Transversesections of the spinal cord viewed from above.
At the C-8 lael (top), there is a fresh hemorrhage, 4 mm in
diameter, in the ldt side ofthe cord. At the T-1 level (bottom),
there is gray discoloration in the left side of the cord medially.
(Fixedpostmortem specimen x 4.)
return during the remaining 45 minutes of surgery. Equipment and electrode impedance checks revealed no technical
reason for the loss of signal, and there was no change in
anesthetic drugs at that time.
Postoperative Progress
The following day at 1:OO AM, 12 hours after surgery, the
patient suffered cardiac arrest, but his pupils remained fixed
and dilated. A second cardiac arrest occurred at 3:53 AM the
same day and the patient died.
Autopsy Findings
There was a 3-mm-thick layer of fresh extradural hematoma
anteriorly and longitudinal ridging of the anterior ligaments.
A thickened circular band of ligament passed across the posterior aspect of the dura at the T-1 level and was divided
before removal of the cord; it was at this level that the cord
showed maximal curvature.
The isolated cord showed marked extension curvature,
and a linear depression 2 to 3 mm deep in the dorsal columns extended from the C-8 to T-2 cord level. Sections at
this level revealed a recent hemorrhage, 4 mm in diameter,
274
Annals of Neurology
Vol 24
No 2 August 1988
Fig 3. (A)Hypoxic neurons in the rrtrodorsolateralportion o f
the ldt anterior horn at C-8 adjacent to the hemorrhage. The
neurons are shrunken and eosinophilic; a dark4 staining pyknotic nucleus is seen in one cell (lower right). (B) N o m d
neurons from the retrodorsolateralnucleus of the right side ofthe
cord at C-8. The neurons have vesicular nuclei with prominent
nucleoli; granular Nissl substance is .reen in the cytoplasm.
( H 6 E ; x 230 before 33% reduction.)
on the left side of the cord, extending 10 mm caudally from
C-8 (Fig 2). At T-1 the cord was shrunken, gray, and soft on
the left side. Some discoloration was seen at the T-2 level,
but at T-4 and above C-8 the cord was normal.
Histological examination showed no abnormality at C-2
and T-4. The hemorrhage o n the left side at C-8 and T-1 had
disrupted the dorsal horns of the gray matter with the major
effect at C-8. Here, fresh extravasated blood had collected in
the central part of the dorsal horn and in the intermediate
portion of gray matter. Pallor of neural tissue was seen in the
surrounding areas due to recent infarction, but, apart from
occasional polymorphonuclear leukocytes, there was no invasion of inflammatory cells. The ventral three-fourths of the
nucleus proprius had been destroyed, together with the medial portion of the intermediolateral nucleus at this level.
Hypoxic, shrunken, eosinophilic neurons were seen in the
intermediolateral, retrodorsolateral, and dorsolateral nuclei
of the ventral and intermediate gray matter at C-8 (Fig 3 ) . In
addition, there was vacuolation of the ventrolateral portion
of the dorsal columns of white matter and of the ventromedial portion of the lateral column of white matter on the left.
Discussion
Neurological complications developing as a result of
scoliosis surgery are thought to be due to vascular
damage to the spinal cord [l}; however, this has not
been histologically confirmed in humans. Experiments
involving distraction with recording of SEPs in cats
have shown that distraction that continued after the
SEP was abolished prevented blood flow to an area up
to 20 mm caudal to the distraction zone. The cord in
these animals revealed only a few small hemorrhages
121. Because SEPs are conducted by fibers in the posterior and dorsolateral columns [ 5 , 61, the hemorrhagic lesion in the posterior horn of the spinal cord,
with damage to the ventrolateral aspect of the dorsal
column and ventromedial aspect of the lateral column
of white matter seen at C-8, is appropriately situated to
cause abolition of these SEPs. The presence of hypoxic
neurons surrounding the hemorrhagic area indicates
that the lesion was at least 6 hours old. However, it
was on the left side only, although the SEPs were being recorded from the right lower limb. Such lesions
can lead to impairment of function on the opposite
side of the cord due to edema. We have found that
unilateral changes following distraction are small (less
than a 0.5-msec increase in latency and a 20% decrease
in amplitude). Larger changes than this would be observed bilaterally [ 111. There was neither a technical
nor an anesthetic reason for the loss of the SEP. Sublaminar wires were being attached at the time, and we
presume that the lesion resulted from pressure on the
cord during that maneuver. We believe the marked
rise in blood pressure, followed by a fall 30 minutes
later, just prior to the SEP's disappearance, was due to
sympathetic stimulation [4, 9, lo}.
Rakesh Shukla is a Commonwealth Universities Medical Fellow.
References
1. Dastur DK, Wadia N H , Desai AD, Sinh G: Medullospinal
compression due to atlanto-axial dislocation and sudden haematomyelia during decompression. Brain 882397-924, 1965
2. Dolan EJ, Transfeldt EE, Tator CH, et al: The effect of spinal
distraction on regional spinal cord blood flow in cats. J Neurosurg 531756-764, 1980
3. Emery AEH, Dreifuss FE: Unusual type of benign X-linked
muscular dystrophy. J Neurol Neurosurg Psychiatry 29:338-
342, 1966
4. Greenhoot JH, Mauck H P The effect of cervical cord injury on
cardiac rhythm and conduction. Am Heart J 83:659-662, 1972
5. Jones SJ, Edgar MA, Ransford AO: Sensory nerve conduction
in the human spinal cord: epidural recordings made during scoliosis surgery. J Neurol Neurosurg Psychiatry 45:446-45 1,
1982
6. Katifi HA, Sedgwick EM: Somatosensory evoked potentials
from posterior tibial nerve and lumbosacral dermatomes. Electroencephalogr Clin Neurophysiol65:249-259, 1986
7. Koht A, Sloan T, Ronai A, Toleikis J R Intraoperative deterioration of evoked potentials during spinal surgery. In SchrammJ,
Jones SJ (eds): Spinal Cord Monitoring. Berlin, Springer Verlag,
1985, pp 162-166
8. Lesser RP, Raudzens P, Luders M, et al: Postoperative neurological deficits may occur despite unchanged intraoperative somatosensory evoked potentials. Ann Neurol 19:22-25, I986
9. Muelheims GH, Walter KE, Billy L Catecholamine release after spinal cord section. Proc Soc Exp Biol Med 130:574-576,
1969
10. Satomi K, Nishimoto GI: Effects of selective spinal cord transection on evoked spinal potentials in cats. In Homma s, Tamaki T (eds): Fundamentals and Clinical Application of Spinal
Cord Monitoring. Tokyo, Saikon, 1984, pp 87-98
11. Shukla R, Docherty TB, Jackson RK, Sedgwick EM: Comparison of epidural responses from right and left posterior tibial
nerves during surgery for scoliosis. Paper presented at the 3rd
International Evoked Potentials Symposium, West Berlin, September 28 to October 1, 1986, p 18 (Abstract)
12. Young W, Berenstein A: Somatosensory evoked potential monitoring of intraoperative procedures. In Schramm J, Jones SJ
(eds): Spinal Cord Monitoring. Berlin, Springer Verlag, 1985,
pp 197-203
Inflammatory Lesions of
Peripheral Nerve in a
Patient with Human TLymphotropic Virus Type
I-Associated Myelopathy
GCrard Said, MD, Catherine Goulon-Goeau, MD,
Catherine Lacroix, MD, Anaic Feve, MD,
HCkne Descarnps, MD, and Marie Fouchard, MD
In a patient with tropical spastic paraparesis associated
with a positive titer for human T-lymphotropic virus
type I, electrophysioIogical study detected a mixed, axonal and demyelinating, multifocal neuropathy. Perineural and perivascular infiltrates, moderate axon loss,
wallerian degeneration, and demyelinating lesions of
isolated fibers were present in the nerve biopsy specimen. These inflammatory lesions resembled those found
in the central nervous system of patients with tropical
spastic paraparesis.
Said G, Goulon-Goeau C, Lacroix C, F6ve A,
Descamps H, Fouchard M. Inflammatory lesions of
peripheral nerve in a patient with human
T-lymphotropic virus type I-associated
myelopathy. Ann Neurol 1988;24:275-277
Spastic paraparesis with slight involvement of the posterior columns has consistently been associated with
infection with the human T-lymphotropic virus type I
From the Service de Neurologie, HBpital de Bicktre (UniversitC
Paris XI), BicCtre, France.
Received Dec 29, 1987, and in revised form Mar 9, 1988. Accepted
for publication Mar 9, 1988.
Address correspondence to Dr. Said, Service de Neurologie, Centre
Hospitdier Universitaire de BicCtre, 94275 BicEtre Ckdex, France.
Copyright 0 1988 by the American Neurological Association 275
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