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Central somatosensory conduction after head injury.

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ORIGINAL ARTICLES
Central Somatosensory
Conduction After Head Injury
Ann L. Hume, PhD, and B. R. Cant, MB, FRACP
In 94 patients with head injuries, conduction between the lower brainstem and the cerebral cortex was studied by
recording evoked potentials from the scalp and neck following stimulation of the median nerves. A conduction
time 3 SD or more above the normal mean (5.74 2 0.46 msec) or the absence of an evoked potential over one or both
hemispheres was considered abnormal. During successive periods in the first 35 days after injury, the evoked potenv2 days the
tials correlated with the outcome (classified as good or not good) in 75 to 84% of patients. Within 3
outcome was correctly predicted in 38 of 49 patients (78%). Six of the 7 surviving patients with persistent asymmetries of the cerebral evoked potentials remained hemiplegic. Serial studies over one year showed that both conduction time and amplitude recovered exponentially over many months, but differences persisted between the patients
who made a good recovery and those who remained disabled.
H u m e AL, Cant BR: Central somatosensory conduction after head injury. Ann Neurol 10:411-419, 1981
Normal data were obtained from 55 volunteers (26 men
and 29 women aged 12 to 57 years; mean, 32 years).
Ninety-four patients were studied following head injury
(75 men and 19 women aged 12 to 57 years; mean, 26
years). Thirteen were included in a previous study [19].
None had a history of alcoholism, cerebral disease, or prior
cerebral injury. Nineteen were unresponsive to command
for less than 6 hours after injury (median, 1 hour).
Twenty-two were unresponsive for 7 hours to 60 days
(median, 57 hours), and 53 were sedated, primarily with
phenobarbital, and artificially ventilated for 1 to 7 3 days
(median, 2 1 days) before they either became responsive or
died. Nine had a lucid interval before becoming unresponsive; six of these were subsequently sedated and artificially
ventilated. Somatosensory evoked potentials were recorded as soon as possible after admission (5 hours to 33
days; median, 21/2 days), and subsequent recordings were
usually made every 3 to 5 days during hospitalization and
then at longer intervals for up to 500 days. Rectal or oral
temperature was noted during each study while patients
were hospitalized, and serum phenobarbital level, arterial
blood gases, and pH were recorded for patients who were
sedated and artificially ventilated.
T h e outcome for surviving patients was ascertained 6 to
36 months after admission (mean, 13 months), except for 3
who made a rapid recovery and were lost to follow-up 1 to
4 months after injury. Outcomes were classified according
to the criteria of Jennett and Bond [20] as: good recovery
= resumption of normal life; moderate disability = disabled but independent; severe disability = conscious but
dependent; and death.
Square-wave pulses of 0.15 msec duration from a Grass
S48 stimulator were delivered at a rate of 4 per second
through a Singer S T 100 1 : 4 transformer to electrodes
over the median nerve at the wrist. The cathode was placed
3 cm proximal to the anode. Stimulus intensity was increased until a thumb twitch was produced or, in curarized
patients, until an evoked potential was recorded from the
neck.
Recordings were made from silver cup o r platinum alloy
needle electrodes placed over the central area of the scalp
From the Department of Clinical Neurophysiology, Auckland
Hospital, Auckland, New Zealand.
Received Aug 29, 1980, and in revised form Feb 23, 1981. Accepted for publication Mar 1 , 1981.
In patients sustaining head trauma, prediction of the
ultimate outcome soon after injury may be difficult
[ 5 , 7 , 16, 17,21, 26, 27, 37, 39,40,47, 501. Inaddition, the nature of the pathophysiological changes
following injury [ l , 14, 3 5 , 4 6 , 4 8 ] and the effects of
various types of early treatment [4, 8, 22, 28-30, 32,
41, 421 are not well understood.
A preliminary study of somatosensory evoked potentials in comatose patients showed that, within 10
days of the onset of coma, measurement of conduction time between the lower brainstem and cerebral
cortex provided prognostic information [ 191. Such
information could be obtained despite the institution
of positive-pressure ventilation and administration of
phenobarbital. The present study of patients with
head injuries was undertaken to assess in greater detail the principal conclusions of the previous report,
to determine how soon after injury the somatosensory evoked potentials could provide reliable prognoses, and to define more precisely the nature and
time course of changes that may occur in these potentials after head injury.
Materials and Methods
Address reprint requests to D r Cant.
0364-5134/81/110411-09$01.25 @ 1981 by the American Neurological Association
411
ratio, 1.65 I
0.76. The mean difference between the
conduction times to each hemisphere was 0.25 -+
0.18 msec, and that between the amplitude ratios
over each hemisphere was 0.45 2 0.35.
All 19 patients unresponsive to command for less
than 6 hours after injury made a good recovery, and
all had normal central conduction times when first
tested (16 within 3 days of injury, 3 within 15 days).
The means during successive periods after injury
were also normal. In 1 patient only, the conduction
time to one hemisphere became abnormal, increasing to 7.1 to 7.2 msec berween days 7 and 66. The
amplitude ratios of individual patients within the first
few days after injury were usually low relative both to
later measurements and to the normal mean, although the differences were not statistically significant. The mean at day 2 was 1.18 -+ 0.61 (significantly lower than norma1,p < 0.05) and at day 12 it
was 1.57 2 1.00. The results from these patients are
excluded from further consideration, as it was apparent shortly after admission that all would make a
good recovery.
Details on the outcome, presentation, and treatment of the 75 patients unresponsive to command
for more than 6 hours after injury are contained in
Table 1. Figure 2 shows their results during successive periods after injury and illustrates the two major
findings of this study. First, the results correlated
with the outcome: most patients who made a good
recovery had normal conduction times before day 10,
contralateral to the stimulated wrist ( C , and C3, international 10-20 system) and over the second cervical vertebra.
The reference electrode was placed on the midforehead
(Fp,). The output from high-impedance differential amplifiers (bandpass 1 H t to 2.5 kHz) was averaged by a
PDP-8L computer either directly or after storage on a
Philips ANA-LOG tape recorder.
In all subjects, two or three series of 1,000 evoked potentials were averaged concurrently from neck and scalp
following stimulation of each wrist (bin width 150 psec).
The peak latencies of the major negative potential from the
neck, N14, and of the initial negative cerebral potential
from the scalp, N20, were measured. Voltages between the
baseline and peak of N14 and between the peak of N20
and subsequent maximal positivity in the 20 to 35 msec
range, P25, were also measured. The difference in peak
latency between N 1 4 and N20, the central conduction
time, and amplitude ratio, N20-P25/N 14, were calculated
for each series and averaged for each side. Abnormalities of
central conduction time and of differences between the
conduction time to each hemisphere and the amplitude
ratio over each hemisphere were defined as those 3 SD or
more above the mean for the normal subjects. T h e absence
of a cerebral evoked potential over one or both hemispheres was also defined as abnormal. All serial results presented for each patient are for stimulation of one wrist
only; these are for the right wrist unless results for the left
were more abnormal.
Results
An example of the somatosensory evoked potentials
recorded after head injury is shown in Figure 1. The
components analyzed in this study, the central conduction times, and the amplitude ratios are indicated.
This patient had asymmetrical conduction times and
amplitude ratios for more than a year, and she was
left moderately disabled with a right hemiplegia.
In the 55 normal subjects, the mean conduction
time was 5.74 -+ 0.46 msec and mean amplitude
F i g 1 . Somatosensory evoked potentials from the contralateral
scalp (upper tracing) and neck (lower tracing) d a patient 29
hours after head injury. Actual latencies (msec) of components
N20 and N14 and the difference between them, central conduction time, are indicated. The amplitude ratios, N20P25lNl4 (alb), are also shown.
R WRIST
L WRIST
N20
N20
I
Siimulus
1
0
412
Annals of Neurology
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t.
I
I
2o msec
Vol 10 No 5
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1
40
November 1981
J
60
Stimulus
0
2o msec
40
60
Table 1. Outcomes, Presenting Features, and Treatment of 75 Patients Unresponsive to Command
for more than 6 Hours after Head Injury
Patient Data
Good Recovery
Moderate Disability
Severe Disability
Died"
No. of patients
31 (41.3%)
0
9
10 (13.3%)
13 (17.3%)
8
3
8
2 1 (28%)
Residual hemiplegia
Skull fracture
Multiple trauma
Surgically treated
intracranial hematoma
Sedated and
artificially ventilated
5
4
10
5
8
1
12
9
I
11
. . .
16
11
11
21
"All within 37 days of injury; median survival, 9 days.
while most who remained disabled or died had more
persistently abnormal conduction times or absent
scalp evoked potentials. Second, the results changed
with time. Most strikingly, the conduction times in all
surviving patients decreased over the duration of the
study, although some increased temporarily.
The following sections describe the effects of some
of the variables associated with treatment on the
evoked potentials, the pattern of recovery of evoked
potentials, and the accuracy with which evoked potentials predicted the outcome.
Effects of Temperature, Blood Gases, and Phenobarbital
Cerebral evoked potentials could be recorded from
some patients throughout the observed ranges of
central body temperature, arterial blood gases and
pH, and serum phenobarbital levels (Table 2). Normal conduction times were recorded over similar or
slightly narrower ranges. A number of patients with
the longest conduction times had normal temperatures and blood gases and had levels of serum
phenobarbital up to 300 pmol/L. However, all 4 patients with temperatures below 35°C and l of the 3
with serum phenobarbital levels exceeding 500
pmol/L had abnormal conduction times.
Within the ranges over which cerebral evoked potentials could be recorded, the conduction time correlated inversely with central body temperature
(0.098 msec/OC, r = -0.15, p < 0.05) and directly
with serum phenobarbital levels (0.002 msecl
pmol/L, r = 0.23, p < 0.005). It was independent
of arterial blood gases and p H . The amplitude ratio
correlated inversely with serum phenobarbital
(O.OOl/pmol/L, r = -0.17,p < 0.05) and was independent of temperature, arterial blood gases, and
pH. As temperature and phenobarbital contributed
to only 4% of the variance in conduction time,
neither of these variables nor the others detailed in
Table 2 could account wholly for the absence of
cerebral evoked potentials or the increases in conduction time that were observed.
Recovery of Conduction Time and Amplitude
Thirty-three surviving patients had an abnormal central conduction time before day 35. Figure 3 compares the mean conduction times and amplitude
ratios of the patients who remained disabled with
those of the patients who made a good recovery at
different periods. The mean conduction times for
both groups were significantly lower than normal
during all periods ( p < 0.005). The amplitude ratios
of the patients who made a good recovery were lower
than normal ( p < 0.02) during the first four periods
only (days 2 through 13), while those of the disabled
patients remained lower than normal ( p < 0.005)
during all periods except the last (day 313).
Regression functions were fitted to each set of data
by the method of least squares. The logarithm of time
since injury was used to give appropriate weighting
to values obtained during the early periods, when
both conduction times and amplitude ratios changed
most rapidly. For both the disabled patients and
those who made a good recovery, conduction times
decreased ( r = -0.81, p < 0.02; r = -0.89, p <
0.005) and amplitude ratios increased ( r = 0.93,
0.95, p < 0.001) during recovery. However, during
all periods, the conduction times for the disabled patients were longer than those for the patients who
recovered completely. Hence, the elevations of the
regression functions for conduction time were
significantly different (7.93, 7.03 msec, F = 36.44,p
< 0.001, analysis of covariance) while the slopes
were similar (-0.71, -0.66 msedlog unit day). The
amplitude ratios of the disabled patients were lower
than those of the patients who made a good recovery,
and the differences were maximal during later periods. Hence, the elevations of the regression functions were significantly different (0.69, 1.17, F =
45.5,p < 0.001), and the slopes also differed (0.32,
0.59hog unit day, F = 11.0,p < 0.01). The regression functions for conduction time crossed the upper
limit of normal on day 13 for patients who made a
good recovery and on day 263 for the disabled pa-
Hume and Cant: Head Injury
413
GOOD RECOVERY
not sedated
---
51
L$
i.5
i
16
ii
ii
POST HEAD INJURV~days
tients. The amplitude ratios on these days were 1.09
and 1.06, respectively. Regression functions for each
group based on the results for all surviving patients,
including those with normal conduction times during
the first 35 days, were similar to those in Figure 3,
although the intercepts were nearer normal and the
slopes were less steep.
Sedation and artificial ventilation did not account
for the differences between the patients who remained disabled and those who made a good recovery. First, although more of the disabled patients
were still sedated and ventilated during the fifth and
sixth periods, similar proportions of each group remained sedated and ventilated during the seventh.
414
Annals of Neurology
Vol 10 No 5
3;
GNAL
POST HEAD INJURY- days
F i g 2. Central conduction times irr 75 patients following head
injury. All were unresponsive t o command for more than 6
hours. Mean conduction time (? 1 SD) for normal subjects
and the upper limit of normal (+3 SD; dashed line) are indicated. Results are for right wrist stiniulation unlessfor left
wrist stimulation the conduction time was Jignz'jicantly longer
or there was no cerebral evokedpotential (EP) at first or on
subsequent tests. Results are from the last test within 3 1/2 days:
the longest conduction time (or no cerebral E P ) between days
4 - 7 , 8 - 1 0 , l l - 1 5 , 16-21, and 22-35: and from the final
test. ( 8 = conductioiz times for p~tientswith cerebral EPs over
both hemisphere.r at all tests: 0 = no cerebral EP recorded oiier
one or both hemispheres at all tests; other open symbols are for
indirlidualpatients who had no cerebral EP at some tests.)
November 1981
Table 2. Somatosensory Evoked Potentials and Central Body Temperature, Arterial Blood Gases and pH,
and Serum Phenobarbital Levels.in Patients with Head Injuty
Ranges When:
Observed
Range
Cerebral
Potentials
Recorded
Normal Conduction
Times Recorded
Conduction Times (msec)
Observed within Normal
Physiological Ranges
31.0-39.4
(37 .O)
50-484
(123)
2 1-93
(34)
7.16-7.64
(7.43)
0-686
(139)
31.0-39.4
35.0-39.4
4.8- 12.5 5
50-484
50-484
5.6-12.35
2 1-93
22-53
5.35-12.35
7.16-7.64
7.22-7.64
5.35-12.35
0-686
0-686
4.8-10.0
Determination
Temperature ("C)
Arterial Po, (rnm Hg)
Arterial PCo2 (mm Hg)
Arterial p H
Serum phenobarbital
(pnol/L")
aMeans are similar or identical.
bSee [2, 121.
'4.3 wmol/L = 1 wglml.
Second, in the group who made a good recovery, the
regression functions for conduction time and
amplitude ratio were similar for the patients who
were sedated and ventilated and for those who were
not.
Y
zI-
8-
z
P
I-
s 70
z
8 2
A "t,
B
O
k1
2
1
14
28
56
210
POST HEAO INJURY -days
Fig 3 . (A) Mean central conduction times and (B) mean
amplitub ratios forpatients with disability ( 0 ; N = 18) and
good recovery (m; N = 15) i n whom an abnormal conduction
time ( 37.12 msec) was recorded before duy 35. Regression
curues were fitted by the method of least squares. Mean conduction times are based on the longest recorded for each patient
witbindays 1-3$$,4-7,8-10, 11-15, 16-21,22-35,and
36-100 of injury, and at the final test. Mean amplitude
ratios are derived from the same tests. Means for disabledpatients include results of lefi wrist stimulation in 3 with no
cerebral evoked potentials following stimulation of the right
wrist. (Days are plotted logarithmically.)
Prediction of Outcome
During each successive period after injury, the results correlated with outcome in 75 to 84% of the
patients (Table 3 ) . After the first 3% days, both the
conduction time and the presence of a cerebral
evoked potential over both hemispheres correlated
independently with outcome.
Within the first 3% days, for example, 49 patients
were tested at least once. The last result during this
period was normal in 14 of the 20 patients who made
a good recovery and abnormal in 24 of the 29 who
died or were left disabled (x' = 11.74, p <
0.001). The absence of evoked potentials over both
hemispheres during any period was of uniformly
poor prognosis, and all 8 patients with this finding
died (4 hours to 7y2 days later). The presence or absence of a surgically treated intracranial hematoma
did not alter the correlation between evoked potentials and outcome.
The outcome was not correlated with the results
during every period in all patients. First, 10 patients
among the 44 who did not make a good recovery had
normal results during some periods. Three of these
who had normal results on all occasions were left disabled. Another 5 who remained disabled had normal
results during only some periods, and 2 who died had
normal results during early periods but not later.
Second, 15 patients in the group of 3 1 who made a
good recovery had abnormal results during some pe-
Hume and Cant: Head Injury
415
Table 3. Somatosensory Evoked Potentials and Outiome afrer Head Injury
Evoked Potentialsb
Outcomea
Prolonged
Conduction
Time(s)
No Cerebral
Significanced
Evoked
Potentials
Normal
SignificanceC
Significance"
14
p < 0.001
6
9
NS
0
I5
p < 0.001
21
5
p < 0.001
6
9
p < 0.05
0
12
p < 0.001
23
7
p < 0.001
6
P < 0.05
0
10
p < 0.001
24
p < 0.001
Days 1-3$'"
Good
N o t good
Days 4-7
Good
N o t good
Days 8- 10
Good
N o t good
Days 11-15
Good
N o t good
Days 16-21
Good
N o t good
5
9
6
25
p < 0.001
6
9
p < 0.05
6
p < 0.001
p < 0.05
0
p < 0.01
6
14
3
1
7
Days 22-35
Good
N o t good
27
5
p < 0.001
p < 0.001
4
14
0
7
p < 0.01
~
Good = resumption of normal life; not good = moderate to severe disability or death.
bLast result measured within the first 3% days after injury. For subsequent periods: normal = all results normal; abnormal = at least one
abnormal result. For surviving patients, if no results obtained, those from previous period used. Results for patients who died during each
period are excluded from subsequent periods.
CAssociationbetween evoked potentials and outcome.
dAssociation between conduction times and outcome.
'Association between presence/absence of cerebral evoked potentials and outcome.
NS = not significant.
riods. Four had abnormalities only shortly before o r
after operation for an intracranial hematoma, and 1 of
these had no cerebral evoked potential over the affected hemisphere on one occasion (see Fig 2). Four
had abnormal conduction times only within 3 days of
injury, and 3 others had an abnormal conduction
time to one hemisphere within the first 10 days.
Bilateral delays of conduction occurred during renal
failure in 1 patient (days 14 to 58) and during renal
and pulmonary infection in another (days 14 to 33).
The remaining 2 patients had abnormal conduction
times to both hemispheres for 7 months and results
which were just within the normal range after one
year. Both of these patients recovered very slowly
and did not resume employment until 6 and 8
months after injury, respectively.
Asymmetry and Prediction of Hemiplegia
Persistent asymmetries during the first 35 days were
observed in 7 surviving patients, 6 of whom remained hemiplegic. No evoked potential could be
recorded over the left hemisphere for the duration of
study ( 5 and 10 months) in 2 who had an intracranial
hematoma evacuated from the left side shortly after
admission, and until 10 months in another who had a
contused right frontal pole and overlying subdural
hematoma removed. All 3 remained severely disabled with a right hemiplegia. The other 3 patients
with a persistent right hemiplegia and moderate disability had a significantly longer conduction time to
the left hemisphere and a lower amplitude over it.
One of these patients had suffered occlusion of the
left carotid artery in a crushing head injury. Another
had an initial clinical presentation suggesting right
hemispheric damage (see Fig l), and the third presented with signs of a left pontine lesion. The seventh
patient who made a full recovery had increased
amplitudes over a craniotomy for 9 months.
Of the other 7 patients who remained hemiplegic,
1 had normal results from day 1. Two others had abnormal results, but their relationship to the patients'
disabilities was complicated by a fracture-dislocation
of C2 in 1 instance and by a penetrating injury to the
skull and brain in the other. The remaining 4 patients
had too few studies for reliable correlation with the
hemiplegia, although 2 who were first tested 1 month
416 Annals of Neurology Vol 10 No 5 N o v e m b e r 1981
after injury had significantly longer conduction times
to the affected hemisphere and lower amplitudes on
this side. Asymmetries were observed on one or two
occasions only in 22 other surviving patients, in 8
shortly before or after surgery for an intracranial
hematoma. None of these asymmetries could be related to focal neurological sequelae.
Discussion
The best measure of the severity of a head injury
is the final outcome. That outcome is generally
achieved within 6 months after injury, and in most
patients cognitive function recovers within 12
months [20,40]. Clinical examination within 24 to 72
hours can usually discriminate between patients
likely to make a very poor or a very good recovery
but is less reliable in the remainder [21, 37, 39, 471.
More importantly, clinical assessment may be limited
by sedation and neuromuscular paralysis.
This study shows that in patients with posttraumatic coma, the conduction time within the central
somatosensory pathways and the presence or absence
of a cerebral evoked potential over both hemispheres
predicted outcome. Thus, three-fourths of the patients showing normal conduction times within 3y2
days of injury made agood recovery, while consistent
asymmetries of amplitude and conduction time or the
long-term absence of an evoked potential over one
hemisphere predicted a hemiplegia, and evoked potentials were absent over both hemispheres only in
patients who died.
These general relationships were not affected by
sedation and neuromuscular paralysis. However, correlations were found between the conduction time
and both central body temperature and serum
phenobarbital level that were not demonstrated in
the previous smaller series [19], and between the
amplitude ratio and serum phenobarbital. A working
rule now used is that abnormal conduction times are
interpreted cautiously if a patient’s central temperature is below 35°C or the serum phenobarbital level
exceeds 300 pmol/L.
Pathophysiological Implications
The results shown in Figures 2 and 3 demonstrate
that the central somatosensory pathways were more
severely damaged at the time of injury in the disabled
patients than in those who made a good recovery,
that the conduction time decreased exponentially
after injury and at a similar rate in both groups, and
that the amplitude of the cerebral evoked potential
increased exponentially but at different rates in the
two groups.
The pathophysiological mechanisms underlying
these results are speculative. An increase in conduction time and decrease in amplitude ratio both reflect
an abnormality of the initial cerebral potential,
N20-P25, generated by neurons in sensorimotor
cortex (for review, see [ 151). Three basic physiological abnormalities, each operating at any level rostra1
to the origin of N14 in the lower brainstem [ 11, 18,
231, could delay or reduce the amplitude of N20P25. A uniform slowing of conduction would delay
N20-P25 without affecting its amplitude while a decrease in the number of active neurons could reduce
the amplitude without affecting the latency, an effect
seen in normal subjects when stimulus intensity is
decreased [ 18, 441. Nonuniform slowing resulting in
asynchrony of conduction could both delay and reduce the amplitude of the cerebral potential.
The amplitude ratios in patients with abnormal
conduction times did not exceed 67% of normal until
the conduction times fell to the upper limit of normal
(see Fig 3). This observation suggests that a common
mechanism, such as asynchrony of subcortical conduction, could underlie both the delays and the
amplitude reduction of N20-P2 5. Conduction times
of up to 9 to 12 msec with recovery over varying periods in individual patients also indicate that axonal
conduction must be slowed since, although both
synaptic and cortical neuronal dysfunction are likely
to contribute to abnormalities of N20-P2 5, these
factors alone could not account for a doubling of
conduction time. The total synaptic delay at the
thalamus and cortex has recently been estimated as
0.9 msec [ l l ] . It is improbable that this delay could
be increased by up to 5 msec without total failure of
transmission. Similarly, it is unlikely that such an increase could result solely from a delay in electrotonic
spread through the cortical neuropil. A major part of
the conduction delay in these patients may be due to
a milder form of the damage to medial lemnisci that
has been demonstrated at autopsy [ 11.
The 30% reduction of amplitude ratio soon after
injury in patients with normal conduction times, including those unresponsive for less than 6 hours, indicates that, at least in the immediate posttraumatic
period, slowing of conduction cannot be the only
mechanism underlying changes in N20-P25. The
amplitude reduction in this group may have reflected
temporary cortical dysfunction, and this is consistent
with the suggestion that relatively mild head in juries
affect cortical but not subcortical function [35]. Altered activity in efferent systems to thalamic and dorsal column nuclei may also be involved [34, 43, 531.
Finally, although pathological demonstrations of
diffuse neuron loss after head injury [ 1 , 4 6 , 4 8 ] indicate that slowing of subcortical conduction cannot be
the only pathophysiological change, it may be the abnormality most amenable to recovery.
Mechanical trauma to neurons as well as ischemia, anoxia, intracranial hypertension, and other
H u m e and Cant: Head Injury 417
metabolic disturbances may each have contributed to
the delays and amplitude reduction of N20-P25.
Other clinical [16, 17, 24, 36, 381 and experimental
[ 10, 2 5 , 351 studies describing somatosensory
evoked potentials after head injury, and during experimental ischemia [ 3, 61 and intracranial hypertension [ 313, have shown that various components of the
cerebral evoked potential may be reduced in
amplitude or abolished. None of these investigations
monitored delays of the primary cortical component,
although other clinical studies have demonstrated increases in central somatosensory conduction time
and reduction o r loss of N20 in patients with multiple sclerosis [9, 13, 18, 44, 451, vascular lesions of
the cerebral hemispheres and brainstem [33, 49, 5 1 ,
521, and nontraumatic coma [ 191.
The results shown in Figures 2 and 3 suggest that
the major damage to central somatosensory pathways
in the patients included in this study occurred within
a day or two of injury and that, in general, complications arising later in the first one or two weeks were
of lesser importance. These complications could,
however, result in short-term abnormalities of conduction time such as those illustrated in a previous
study [19] and more recently described during decreased hemispheric blood flow after subarachnoid
hemorrhage [49].
Supported by the War Pensions Medical Research Trust Board
and the Medical Research Council of New Zealand.
The authors thank Drs R. Barker, M. Spence, and R. Trubuhovich
for facilitating patient examinations, and Miss Amanda James for
technical assistance.
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