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Central somatosensory conduction time in comatose patients.

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Central Somatosensory Conduction Time
in Comatose Patients
A n n L. H u m e , PhD, B.
R. Cant, MB,
and N. A. Shaw, MA
Somatosensory conduction time between the dorsal column nuclei and the cerebral cortex may be measured
following median nerve stimulation by recording evoked potentials from both scalp and neck. Central conduction
times were significantly increased relative to normal (5.6 2 0.5 msec) in 11 of 24 comatose patients. Results within
10 and 35 days of onset of coma were correlated with the final clinical outcome. Conduction times were independent of serum phenobarbital (0 to 630 ymol per liter) and of central body temperature (35.0 to 38.5"C). Serial
studies in coma demonstrated (1) short-term increases during temporary metabolic disorders, and (2) sustained
increases with gradual recovery over many months, particularly after head injury.
Hume AL, Cant BR, Shaw NA: Central somatosensory conduction time
in comatose patients. Ann Neurol 5:379-384, 1979
The clinical evaluation of comatose patients is hampered by the sedative and paralyzing drugs used increasingly in some areas in t h e management of coma.
Methods of assessing brain function that are not
influenced by these drugs are required. This paper
describes a procedure for assessing o n e aspect of
brain function in comatose patients based o n a new
method of analyzing somatosensory evoked potentials [12].
W h e n the median nerve is stimulated at the wrist,
the initial component of the somatosensory evoked
potential recorded from the scalp has a latency of
about 20 msec. However, approximately 70% of t h e
latency of this component represents conduction in
the peripheral nerve and spinal cord; it therefore
varies with body size and limb temperature and is not
a useful measure of conduction within t h e brain.
Conduction time within the somatosensory pathways
of the brainstem and cerebrum (central conduction
time) can be measured by recording evoked potentials from both the upper cervical spine and the scalp.
tive shock, heat stroke, or barbiturate overdosage. All patients with nontraumatic coma and 9 with posttraumatic
coma were artificially ventilated for 4 to 105 days (median,
23 days), and all except the patient with barbiturate overdosage were sedated, primarily with phenobarbital. The
patients who were not sedated wcre unresponsive to command for 5 or more days.
When the evoked potentials were first recorded, all
patients were unresponsive to command and 20 were sedated, curarized, and ventilated. When possible, serial recordings were made at 3- to 5-day intervals until responsiveness was regained, and subsequently at longer intervals
for up to one year. The patients' outcomes were classified
according to the criteria of Jennett and Bond 1131 as follows: good recovery = resumption of normal life; moderate disability = disabled but independent; severe disability
= conscious but dependent; persistent vegetative state =
prolonged unresponsiveness; and death. A patient's outcome was ascertained three to twelve months after admission except for those who died or made a good recovery
within three months.
Procedure
The normal data were obtained from 21 volunteer subjects
(11 men and 10 women, aged 19 to 42 years).
Twenty-four patients were studied. Thirteen had coma
following head injury (11 men and 2 women, 16 to 35 years
old), and 1I patients had nontraumatic coma (7 men and 4
women, 19 to 49 years old). Of this latter group, 5 suffered
from diffuse cerebral ischemia, hypoxia, or both, 2 had
encephalitis, and the others had hypoglycemia, postopera-
Stimuli were square-wave pulses of 0.15 msec duration
from a Grass S48 stimulator; they were delivered at a rate
of 4 per second through a Singer ST 100 1:4 transformer to
electrodes over the median nerve at the wrist. The cathode
was 3 cm proximal to the anode. Stimulus intensity was
increased until a thumb twitch was produced or, in
curarized patients, an evoked potential was recorded from
the cervical area.
Recordings were made from the central area of the scalp
contralateral to the stimulated wrist (C4,C3, International
10-20 system) and from the second cervical vertebra. The
From the Department of Clinical Neurophysiology, Auckland
Hospital, Auckland, New Zealand.
Address reprint requests to Dr Hume, Department of Clinical
Neurophysiology, Auckland Hospital, Auckland, New Zealand.
Method
Normal Subjects and Patients
Accepted for publication Sept 11, 1978.
0364-5134/79/040379-06$01.25 @ 1978 by Ann L. Hume
379
A
reference electrode was o n the midforehead (Fp,). Silver
cup or platinum alloy needle electrodes were used, having
been found to produce identical results in normal subjects.
The output from high-impedance differential amplifiers
(bandpass 1 Hz to 2.5 kHz, -3 db) was either averaged
directly by a PDPdL computer or, during examinations at
the bedside, stored on a Philips ANA-LOG 7 tape recorder
(bandpass 0 to 5 kHz) for later off-line analysis.
In all subjects, two or three series of 1,000 evoked potentials were averaged following separate stimulation of
each hand (bin width 150 psec). During each series,
evoked potentials were averaged concurrently from the
neck and from the contralateral scalp. The peak latencies of
the major negative potential from the neck, N14,and of
the initial negative potential from the scalp, N20, were
measured using a cursor on an oscilloscope.The difference
in the peak latency between these potentials, central conduction time, was calculated for each series and averaged
over the two or three series for each hand.
Results
Figure 1 shows somatosensory evoked potentials
from a normal subject and from a comatose patient.
The components analyzed in this study, N20 from
the scalp and N14 from the neck, and the central
conduction time, representing the difference in peak
latency between these components, are indicated.
In the 21 normal subjects the central conduction
times (5.6 2 0.5 msec) were independent of arm
length and of height. In all 24 patients N14 could be
recorded from the neck, but in 3 , N20 could not be
recorded from the scalp. N20 was unrecordable over
both hemispheres in 2 patients who had isoelectric
electroencephalograms; in the third patient, who had
a head injury, it remained absent over the right hemisphere for six weeks.
Central conduction times for the two groups of
patients are shown in Figure 2. Results were obtained
o n only one occasion from 6 patients who died
shortly after the first testing and from 2 who made a
rapid recovery. Serial examinations were made of the
remaining patients at varying intervals, depending o n
380 Annals of Neurology Vol 5 No 4
April 1979
B
Fig 1 . Somatosensory e7 nked potentials from the scalp and neck
of a normal sublect ( A ) and a comatose patient 7 days after
head rnlury ( B ) . Actual latencier Imsec) of components N20
and N 14 and the diflerence between them (central conduction
time) are indicated.
clinical progress. T h e results for these patients are
presented only from the first examination and from
either the first day that a normal result was obtained
or the last day of testing if previous results were
normal. Conduction times for stimulation of the right
wrist are shown unless the conduction time for left
wrist stimulation was significantly longer at the first
test. No central conduction time in a normal subject
was more than 2 standard deviations (SD) from the
mean, but because of the small numbers of subjects,
only values more than 3 SD from the mean were
defined as abnormal. T h e central conduction time
was abnormally prolonged or N20 could not be recorded at first examination in 8 patients with head
injuries and in 5 patients with nontraumatic coma.
Subsequent studies of 16 patients showed that the
central conduction times decreased in 9 with head
injuries and in 4 with nontraumatic coma.
Figure 3, containing all serial results from 3 patients, illustrates some of the different rates of decrease in central conduction time that were observed
and also shows the temporary increases that occurred
in some patients during periods of clinical deterioration.
PATIENT 1. A 29-year-old man sustained a head injury
and multiple facial fractures in a road traffic accident. On
admission he was breathing spontaneously and began
reacting to noxious stimuli 1 hour after injury. He then
deteriorated rapidly and was sedated and artificially ventilated. Sixteen hours after injury his conduction time was
10.7 msec, whereas at the next examination, 7 days later, it
was normal at 5.6 msec (Fig 3A). During a period of renal
failure (days 10 to 30), the conduction time increased to
t
1
"1
A
€1
M
-
*-=*m
F i g 2. Central conduction time i n 13 patients with coma following head injury (A) and in 9 patients with nontrarimatic
coma (B). Mean conduction time I* l S D ) for normal subjects
and the upper limit of normal I + 3 SD1 are indicated. Results
for right wrist stimulation are shown unless the conduction
time for left wrist stimirlation was sipzificanth longer at first
testing. V a l ~ eshown
s
are from the first day of testing and
either the first day on which a normal result was obtained or,
when the first value was normal. the last day of testing. (Days
are plotted logarithmically., 1 4 = no scalp potential 2 1 days
prior t o this reszilt.)
F i g 3 . Serial central condirction times in 2 patients follow in^
head injury (A,B)and in 1 patient aher heat stroke IC).
Mean conduction time ( & 1 SD) for normal .tubjects and the
upper limit of normal I + 3 SD) are shown. Periods of sedation
and artificial ventilation are indicated by a solid line and periods of renal failure by a broken line. (Days are plotted
logarithmically.)
6.6 msec and subsequently fell. At four months he had
made a good recovery.
PATIENT 2 . An 18-year-old woman suffered a head injury
with a depressed skull fracture in a boating accident. She
was not breathing after impact and was given mouth-tomouth resuscitation for 5 to 10 minutes. O n admission 1
hour after injury she responded only to noxious stimuli.
The skull fracture was elevated on day 2. Phenobarbital, 30
mg three times a day was given, and the patient was discharged from the hospital after 18 days. Two days after
injury her central conduction time was 7 msec, at the upper
end of the normal range (Fig 3B). It remained at about 6.5
msec until day 75, and five months after injury, when the
patient returned to work part-time, it was still 6.3 msec. At
the final examination, over 1 year after injury, the conduction time was 5.6 msec, 20% shorter than at admission.
P
3. A 23-year-old man suffered a heat stroke
B
during an athletic competition. He had a grand ma1 convulsion shortly after collapsing. O n admission 1 hour later his
rectal temperature was 41.6"C and he was unresponsive to
noxious stimuli. He was cooled, sedated, and ventilated.
Disseminated intravascular coagulation developed within
about 6 hours and was treated with intravenous heparin.
Three days after admission the central conduction time was
6.7 msec (Fig 3C).Renal failure developed o n the fourth day
and he received dialysis for 39 days. He also developed a
1'
PATIENT
;
i
1
(D
1
I
%
1
P
1
am
'1,-
H u m e et al: Central Conduction in Coma
381
Sonlatosensory CentralCondrrrtion TinzeandOritconie in Comaa
Outcome
Central Conduction Time
Within 10 days of coma onset
(N = 18)b
Normal
Abnormal
Within 35 days of coma onset
(N = 24)d
Normal
Abnormal
Good
Not Good
8
2
2
6c
11
0
11-
2
"Abnormal conducrion time >3 SD above normal mean.
"Association between conduction time and 0utcome.p = 0.030 by
Fisher exact probability test.
'Two had no scalp evoked potentials.
dAssociation between conduction time and outcome, xp = 13.9,p
< 0.001.
'One had no scalp evoked potential on the right.
probable gram-negative septicemia (day 8), which was
treated with antibiotics for 37 days. During this period the
conduction time increased to 7.4 msec before returning to
about 6.7 msec and remaining at this level, more than 2 SD
above the normal mean, until day 82. The patient made a
good recovery and was discharged after 69 days. At
follow-up seven months later the conduction time was 6.2
msec.
The patients' outcomes were compared with central conduction times recorded within two intervals.
In the Table, the last result obtained from each patient within 10 days and 35 days of the onset of coma
is analyzed. The results of the patients who made a
good recovery, as defined in the Method section, are
compared with those of the patients who did not.
Eighteen patients were tested at least once within 10
days of coma onset (9 trauma, 9 nontrauma). Eight of
the 10 who made a good recovery had normal conduction times at the end of this period, and 6 of the 8
who did not make a good recovery had either prolonged conduction times or no recordable N 2 0 component over either hemisphere (p = 0.030, Fisher
exact probability test).
All 24 patients were tested on one or more occasions within 35 days. All 11 who made a good recovery (5 trauma, 6 nontrauma) had normal results
within this period, and 11 of the 13 who did not
make a good recovery ( 6 trauma, 5 nontrauma) had
abnormal results (x2= 13.9,p < 0.001). T h e relationship between central conduction time and outcome
was also significant when each smaller group of
trauma and nontrauma patients was considered separately ( p = 0.016 and 0.002, Fisher exact probability). The results in 3 patients changed between days
10 and 35: the conduction times of 2 who made a
382
Annals of Neurology Vol 5
No 4
April 1979
good recovery became normal, whereas those from
the third patient, who deteriorated while under
treatment for enceDhalitis. became abnormal.
Serum phenobarbital levels of 0 to 630 pmol per
liter (0 to 146 pg/ml) were recorded during both the
first and later tests. T h e median level for patients
given phenobarbital was 240 pmol per liter (56
pglml). Conduction times were independent of these
levels for both trauma and nontrauma groups ( r =
0.13 and 0.10). They were also independent of central body temperature for both groups ( r = 0.09 and
0.06) if the results in 1 patient who had a temperature of 33.5"C and conduction times of 11.5 and 11.8
msec are excluded.
Discussion
The final outcome of coma depends on the amount of
permanent damage done to the central nervous system. This study demonstrates that the function of the
somatosensory pathways in the brain can be investigated in comatose patients by recording evoked potentials from the neck and scalp. The information
obtained by this method cannot be provided by clinical examination or by other neurophysiological techniq ue s.
Central conduction time at both 10 and 35 days
after the onset of coma correlated significantly with
the patients' outcomes. All 11 patients who made a
good recovery had normal conduction times at or
before the end of the 35-day period, whereas the
conduction time remained abnormal o r the cortical
evoked potentials could not be recorded in 11 of the
13 who did not make a good recovery.
Further study is required to determine how soon
after the onset of coma a useful prognosis can be
given. It is possible that central conduction time will
be no more accurate than clinical examination during
the first few days of coma [3, 141, but its particular
value may be that observations can be made after the
institution of positive-pressure ventilation and the
administration of phenobarbital. The benefit of
positive-pressure ventilation has not been proved,
although a number of workers have advocated its use
in head injuries [9], and it is widely used in the management of coma from other causes [3]. The value of
barbiturates in comatose patients is similarly uncertain [18], though they also have been used in the
treatment of head injuries [17, 211, cardiac arrest [7],
stroke [ 8 ] , and metabolic-toxic-infectious encephalopathy [22]. Although this study is not specifically
concerned with the effects of these methods of
treatment, it does describe a physiological measure
that is independent of serum phenobarbital levels
and unaffected by muscle paralysis, the effect of
positive-pressure ventilation remaining undefined.
Thus because, irrespective of their value, such forms
of treatment (when used) are commonly instituted
before a reliable clinical assessment is possible, the
measurement of central conduction time may help to
solve the type of controversy [ 191:hat followed publication of the study of patients with head injuries
who were investigated and treated prior to review at
6 hours [4], the minimum period of coma for inclusion in the Glasgow coma study [14 I.
A number of previous studies have described the
recording of evoked potentials in comatose patients
[2, 5, 6, 10, 11, 16, 24-26], but none has been
specifically concerned with delays of the initial cortical component of the somatosensory evoked potential. It is of interest, however, that Greenberg et a1
[ 113 using a different method of analysis found that
somatosensory evoked potentials provide a more
powerful prognostic tool than either visual or auditory evoked potentials.
In this study the serial observations of central conduction time followed courses that were mainly of
two types. First, decreases of central conduction time
were observed in 9 of the 10 patients studied serially
after head injury. In most, including 3 for whom the
initial measure fell within the normal range, the conduction time decreased gradually over many months
(e.g., Fig 3B). Second, comparatively short-term increases were observed in association with temporary
metabolic disturbances, for example those associated
with renal failure (e.g., Fig 3A,C).
It is thought that N14 and N20 represent the initial postsynaptic activity in the dorsal column nuclei
and the somatosensory cortex, respectively [ 12, 151.
There are therefore three factors that could contribute t o increases of the N14-N20 interval: the first is
a postsynaptic disorder of the pyramidal cells that
generate N20; the second is increased synaptic delay
in the thalamus, the cortex, or both; and the third is
slowed axonal conduction in the medial lemniscus,
the thalamic radiation, or both. Since the spread of
activity in the pyramidal cells is electrotonic, it is
unlikely that a delay of 2 to 5 msec in the generation
of N20, due to dysfunction of these cells alone,
would be compatible with their survival. Similarly,
since central synaptic delay is normally less than 1
msec, increases of 20 to 100% in conduction time
from increased synaptic delay alone are unlikely.
Failure of synaptic transmission is more probable.
Thus, although damage or dysfunction of the
pyramidal cells and increased synaptic delay may
contribute to increases of central conduction time, it
seems likely that slowed axonal conduction in the
medial lemniscus, the thalamic radiation, or both, is
the major factor.
This study was undertaken primarily to
gate the brain damage that may result from head injury. Such damage may be due to direct mechanical
factors, intracranial bleeding, raised intracranial pressure, or ischemialanoxia, none of which can be expected to have the same effect, if any, on central
conduction time. The gradual decrease in central
conduction time in most patients with head injuries,
even when the initial value was not abnormally prolonged, suggests some common cause, which could
be mechanical damage to the somatosensory pathways. In 1956, Strich first drew recent attention to
the tearing of nerve fibers in the brain following head
injury [23]. More recently, Adams et a1 [l] have provided further evidence for Strich’s view that nerve
fibers are torn by shear strains engendered at impact.
They speculate on the possibility of lesser damage in
surviving patients, stating: “If this explanation is true,
it is very easy to envisage a situation where the effects
of shear strains on axons throughout the brain are
such as to interfere with their conduction for varying
periods of time” [ 11. It is also relevant to the present
study that Adams et a1 found the medial lemnisci
were commonly damaged. The role of prethalamic
damage in the delays found in this study cannot be
determined, however, since activity originating in the
thalamus cannot be identified with certainty in recordings from the scalp.
The patients with nontraumatic coma were investigated to determine whether factors not directly associated with head injury could prolong central conduction time. Although the group is too small to
allow precise specification of such variables, it is
likely that ischemia contributed to delays of conduction time in at least 2 of the nontrauma patients, a
suggestion that is consistent with the demonstration
by Noel and Desmedt 1201 that vascular lesions of
the brainstem can delay the cerebral somatosensory
evoked potential. Such observations, as well as the
type of temporary increases in conduction time illustrated in Figure 3 and t h e rapid recovery of conduction time found in 1 patient with head injury (Fig 3 A )
indicate that a number of factors, in addition to direct
mechanical damage, can prolong central conduction
time. Their mechanisms, at present, are unknown.
Supported by the War Pensions Medical Research Trust Board.
The authors thank Drs R. Barker, M. Spence, and R. Trubuhovich
for facilitating patient examinations, and Miss Anne Booth and Mr
Richard Burgess for
assistance.
References
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Hume et al: Central Conduction in Coma
383
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