Articles in PresS. J Neurophysiol (June 25, 2008). doi:10.1152/jn.90564.2008
Cold stimuli evoke potentials which can be recorded directly from parasylvian cortex in
humans.
J.D. Greenspan 2, S. Ohara1, P. Franaszczuk 4, D.S. Veldhuijzen2,3, F.A.Lenz1
1
Department of Neurosurgery, and Neurology4, Johns Hopkins Hospital, Baltimore, USA.
2
Department of Biomedical Sciences, University of Maryland Dental School, Program in
Neuroscience, Baltimore, USA.
3
Division of Perioperative Care and Emergency Medicine, University Medical Center
Utrecht, Utrecht, Netherlands.
Abbreviated title: Cold evoked potentials from parasylvian cortex.
Keywords: Cold evoked potential, cold sensation, insular cortex, parietal cortex, central
pain, Human insula, mechanical sensation, thermal sensation,.
The number of words
Abstract
Introduction
Discussion
Total
120
255
816
2653
Address all correspondence and proofs to:
Fred A. Lenz
Department of Neurosurgery, Johns Hopkins Hospital
Meyer Building 8-181
600 North Wolfe Street
Baltimore, Maryland, USA. 21287-7713
Telephone
- 410-955-2257
FAX
- 410-287-4480
Email
- [email protected]
Acknowledgement: This work was supported by the National Institutes of Health –
National Institute of Neurological Disorders and Stroke (NS38493 and NS40059 to FAL
NS-39337 to JDG). We thank C. Cordes and L. H. Rowland for excellent technical
assistance .
1
Copyright © 2008 by the American Physiological Society.
Abstract
Anatomic, imaging and lesion studies suggest that insular or parietal opercular
cortical structures mediate the sensation of nonpainful cold. We have now tested the
hypothesis that cold stimuli evoke electrical responses from these cortical structures in
humans. We recorded the response to cold stimuli from electrodes implanted directly
over parasylvian cortex for the investigation of intractable seizures. The results
demonstrate that slow potentials can be evoked consistently over structures adjacent to
the sylvian fissure in response to nonpainful cold. The polarity of these cold evoked
potentials (EPs) for electrodes above the sylvian fissure is opposite to those below.
These results suggest that the generator of cold EPs is close to the Sylvian fissure in the
parietal operculum or insula.
2
The cortical structures which mediate the sensation of cold in humans have not
been clearly identified. Imaging studies have implicated contralateral sensorimotor
cortex, S2, premotor cortex, anterior cingulate cortex, and insula in innocuous cold
sensations (Casey et al. 1996;Craig et al., 2000;Davis et al. 1998;Kim et al. 2007). Some
of these cortical areas receive input from thalamic nuclei containing neurons which
respond to cold stimuli in monkeys and humans (Davis et al. 1999; Lenz and Dougherty
1998b;Lee et al., 1999). Stimulation in the region of the human thalamic somatic
sensory nucleus (ventral caudal, Vc) at microampere currents (microstimulation) can
evoke the sensation of cold (Ohara and Lenz 2003; Davis et al. 1999). Subnuclear
thalamic lesions in humans, or injections of local anesthetic in monkeys, decrease
perception of cold stimuli (Duncan et al. 1993; Kim et al. 2007).
There is scant evidence of cortical electrical events evoked by cold stimuli, which
are basic evidence to identify cortical structures mediating the sensation of cold. A study
of cold evoked potentials (cold EPs) from scalp EEG (Duclaux et al. 1974) demonstrated
potentials with a maximum at the scalp location C4, possibly corresponding to the
location of sensorimotor cortex (Jasper 1958).
We have now tested the hypothesis that parasylvian cortical structures display
evoked responses to cold stimuli. We recorded the response to cold stimuli from
electrodes implanted directly over parasylvian cortex for the investigation of complex
partial seizures of temporal lobe onset. The results demonstrate that cold EPs can be
recorded consistently over structures adjacent to the sylvian fissure.
3
Methods
This study was carried out at the Johns Hopkins Hospital between 2005
and 2006. The study protocol was approved by the Institutional Review Board of the
Johns Hopkins University and the University of Maryland. All patients signed an
informed consent for inclusion in these studies. These protocols were carried out in two
female patients, aged 40 and 26 years old, who had subdural grids implanted for surgical
treatment of medically intractable complex partial seizures in the absence of generalized
seizures or previous brain surgery. The grids were implanted over left lateral frontoparietal cortex including the region shown in Figure 1B (Patient 1102).
Seizures in patient 1102 were treated chronically with Phenobarbital 60 mg once
per day, and Lamotrigene 225mg twice per day. Patient 1122 was treated chronically
with Oxcarbazepine 1200mg in the morning 1050 in the evening, Zonisamide 300mg
twice per day. Both patients had been off these medications for at least 24 hours at the
time of this testing. The half life of these drugs is in the range of 14 to 24 hours in patient
1102 and 14 to 60 hours in patient 1122, so that both patients had substantial drug levels
at all time points relevant to this study (PDR 2008).
In both patients a standard neurological examination, including a sensory testing
protocol, disclosed no abnormality (Adams et al. 1996; Lenz et al. 1993b). Brain
magnetic resonance imaging (MRI) revealed no abnormality in patient 1102, and mesial
temporal atrophy in patient 1122 which is consistent with the diagnosis of temporal lobe
epilepsy, but not with sensory abnormalities (Adams et al. 1996; Gloor 1997).
As a part of the sensory protocol sites on the face, and on the dorsum of the hand,
and foot were stimulated with a battery of stimuli including: camel hair brush, brass
4
probe at room temperature (23 degrees Centigrade), brass probe kept in ice water, plastic
probe at room temperature, tuning fork (128 Hz) (Lenz et al. 1993b)(Essick 1992;Kim et
al. 2007). The description of these stimuli using a standard questionnaire was examined
to determine whether responses were different from those determined in a population of
patients with movement disorders and no identified sensory abnormality (Lenz et al.
1993b). By this protocol neither patient had any abnormality of cold sensation, although
the protocol provides only an approximate measure of sensory function (Lenz et al.
1993b).
Standard techniques were used to identify cortical gyri and sulci from the 3D-MRI
scan (Lenz et al. 1998a;Boatman et al. 1997;Vogel et al. 2003). The central sulcus (CS)
was identified relative to both the deep symmetrical, approximately medial-lateral sulcus
with the inverted omega sign on axial scan (Figure 1B), and the marginal branch of the
cingulate sulcus (not shown)(Lenz et al. 1998b;Naidich et al. 1995). The CS was also
identified by the inferior frontal gyrus (IFS) and superior frontal sulcus (SFS), each of
which forms a T-junction with the precentral sulcus (PreCS). The postcentral sulus
(PostCS) and Sylvian fissure (SF) are also labeled (Naidich, 1991;Naidich et al., 1995).
This anatomy was confirmed by intraoperative photos of electrode position relative to the
cortical structures as determined by intraoperative computerized guidance system
(Brainlab, Munich, FRD).
- Place Figure 1 about here The cold stimulus was produced by a system of temperature controlled waterbaths
and pumps. This cold stimulator was constructed at the University of Maryland Dental
School (JDG). It consisted of three water baths (Neslab RTE-111), each of which held
5
7.0 liters of water, and could be set to maintain any given temperature between -25
to100°C with 0.1°C stability. Each bath was outfitted with a suction pump (March Mfg.
Inc. LC 3CP MD), capable of pumping 32 liters/min. Water from each bath was directed
through insulated Tygon® tubes to a switching station. The switching station allowed for
each bath’s water flow to be directed either a) back to the same bath directly, or b) to the
stimulator head before returning to the same bath. For this experiment, only two different
temperatures were required: 31°C and 5°C.
The stimulator itself was a flat copper conduit with a stimulator surface of 1.5 by
4 cm which was placed on the skin. This copper piece was 0.5mm thick, so as to rapidly
conduct the temperature from the circulating water to the skin’s surface. The temperature
at the probe surface-skin surface was monitored using a Physitemp (Clifton, NJ, USA)
IT-1E thermister, capable of measuring temperature accurate to 0.1°C, with a time
constant of 5ms. The output of that thermister signal was sent as an analog input signal
recorded along with the local field potentials (LFP) signals from the cortex.
The skin was maintained at an adapting temperature of 31 degrees centigrade
prior to the cold stimuli. The water flow to the stimulator was manually switched from a
waterbath at 31 degrees to flow from the refrigerated water (5 degrees). The cooled
water was directed through the stimulator for two seconds before being switched back to
the output of the 31 degree waterbath (Figure 1). Between one and three minutes was
allowed between successive stimuli. With each stimulus, the stimulator was moved to a
different location on the dorsum of the hand or forearm contralateral to the grid
electrodes.
6
LFPs were recorded from 64 subdural electrodes the properties and location of
which were as previously described (Ohara et al. 2004).
Multichannel LFP signals were
remontaged using an average reference to minimize the influence of location and activity
of the reference electrode (Crone et al. 1998;Lehmann 1987). The time of onset of the
cold stimulus was determined by the first change in temperature as determined by visual
inspection of the temperature trace (Figure 1A)(Ohara et al. 2001). Evoked potentials
were averaged across cold stimuli zeroed to the first change in temperature.
A time window of 2.1 s with 0.1-s prestimulus period was used the cold EPs.
Responses to individual trials with artifacts or large baseline fluctuation were excluded
before averaging. A total of 30-50 responses were used for averaging. Peak latencies and
amplitudes were measured from averaged waveforms. Peak amplitudes were measured
from the baseline value, which was defined as the average value during the prestimulus
period. All latencies were measured at the time of the peak amplitude. Descriptive
statistics are given as Mean +/- 1 Standard deviation; differences between parametric
variables were tested with T-tests, and tests of proportions included Fisher or Chi-square,
as appropriate.
Results
Figure 1A shows the temperature trace (upper panel) and one EP in the same time
scale, which applies throughout the figure. The temperature of the conduit was dropped
from an average adapting temperature of 31 degrees to approximately 27 degrees
centigrade within 0.5 seconds, and to 21 degrees within 2 seconds. The variance of the
temperature signal increased progressively from the onset of the stimulus to the
7
temperature nadir. Both patients described this stimulus as a nonpainful, surface, cold
sensation. LFP recordings in both subjects demonstrated a slow negative potential over
the frontal and parietal lobes in response to this stimulus. The maximal evoked potential
for subject 1122 is shown in A lower panel.
- Place Table 1 about here The location of the electrodes in subject 1102 are shown in figure 1B while the
EPs for this subject along the three rows of electrodes are shown in figures 1C, 1D, and
1E, as appropriate. The recordings from the fronto-parietal lobe (Figure 1C) showed
slow negative potentials while those over the temporal lobe were positive (Figure 1D and
1E). In patient 1122 EPs were all negative and only recorded over the frontoparietal lobe.
Table 1 shows peak amplitudes and maxima for negative waves (subjects 1102
and 1122) and positive waves (Subject 1102 only). Peak amplitudes were calculated
from all electrodes for which EPs were recorded, as indicated by n. Peak amplitudes
were approximately 30µV, and occurred at a latency of approximately 800 ms (Table 1).
Differences between patients 1102 (Figure 1B-E) and 1122 (maximum shown in Figure
1A) were significant for amplitudes (P=0.021, t-test), but not significant for latency
(P=0.35, t-test).
- Place Table 1 about here In subject 1102, negative potentials were recorded from the row of electrodes on
the frontal and parietal lobes as shown in Figure 1C. Positive potentials were recorded in
the two rows of electrodes over the temporal lobe in Figure 1D and 1E. It is notable that
the mean latencies of the positive waves below the sylvian fissure and negative waves
above the fissure are identical (Figure 1) in this patient, suggesting that they are produced
8
by the same generator. Spatial reproducibility of the response over cortical recording
from electrodes separated by 1 cm are shown in the overlays located in the lowest row of
C, D, and E. It seems unlikely that volume conduction explains these results since the
slow waves are reproducible, while the noise is different, particularly in C and E.
Discussion.
Overall, the peak of the cold evoked potentials occurred with a mean amplitude of
30 µA, and with a latency of approximately 800 ms. This is consistent with the late
response to cold stimuli which occurs in human thalamic neuronal activity (Lenz and
Dougherty 1998). In a previous study of scalp cold evoked potentials (Chatt & Kenshalo
1979) the peak latency was 325 ms, which is much shorter than the present results. One
major difference between the previous scalp EEG study and the present study is that the
earlier scalp study apparently achieved a faster rate of temperature change, thereby
producing faster and more robust activation of afferents responding to cold stimuli. At
the same time, rapid cooling of the skin evokes mechanoreceptor activation (Duclaux et
al. 1974; Burton et al. 1972), which may be the source of the higher velocity inputs and
the shorter EP latencies in the scalp study. The location of the maximum cold evoked
response in the Duclaux et al. study was at contralateral C4, possibly corresponding to the
location of the sensorimotor cortex (Jasper 1958). This also suggests mechanoreceptor
activation in the scalp study since sensorimotor cortex is the primary cortical locus for
mechanoreceptive input.
Localization of the generators of evoked potentials by subdural recordings are
more reliable than that by scalp recordings. When event related potentials are recorded
9
from the scalp, they are limited by low pass and spatial filtering at the scalp, skull, and
CSF (Cooper et al. 1965;Pfurtscheller and Cooper 1975;Gevins et al. 1994), and by large
inter-electrode distances (Gevins et al. 1994). The present subdural recordings avoid all
these sources of error and clearly indicate that cold evoked potentials can be recorded
over to the parasylvian cortex (Figure 1 cf (Duclaux et al. 1974)).
The present cold potentials had longer latency and smaller amplitude than the first
potentials evoked by electrical stimulation of the median nerve (22 + 1ms, 26 + 3µA),
vibration of the distal palmar surface of the index finger (93 + 2ms, 29 + 11µA), or laser
applied to the dorsum of the hand (136-140ms, 54-71µA)(Ohara et al. 2004). The
variability of both latency and amplitude was much higher in the case of cold evoked
potentials than any of the other potentials (Table 1).
These potentials may reflect many sources of variability, such as the uncertainty
in identifying the onset of the temperature stimulus (Figure 1), and the variance in that
stimulus as 500 ms, the last temperature capable of influencing the EP, given conduction
delays. In addition, the variability of these potentials may result from the staggered onset
of activity and conduction velocities of Abeta/fast Adelta mechanoreceptors, and Adelta
specific cold receptors which may transduce and transmit the cold signal (Chatt and
Kenshalo, Sr. 1979;Burton et al. 1972;Duclaux and Kenshalo 1972). Finally this slow
potential could be the result of attention or novelty evoked by the cold stimulus, as in the
case of the cutaneous laser stimulus (Lenz et al. 2000;Legrain et al. 2002).
In the previous scalp study, the averager was triggered by the signal that began
cold water flow to the stimulator, which occurred before the present trigger from the
change in temperature (Duclaux et al. 1974). The present EPs do not seem to be the
10
result of input from the ‘high threshold’ cold receptors or deep cold receptors which are
located around veins in the skin (Klement and Arndt 1992). Neither of these types of
receptors would be activated in time to contribute to the cold EP since the temperature at
500 ms was 27 degrees, much too high to activate these receptors (Lamotte and
Thalhammer 1982;Kenshalo and Duclaux 1977). Whatever their origin these delays are
consistent with the slow dynamic phase of human thalamic cells to a cold stimulus (Lenz
and Dougherty 1998).
The widespread distribution of cold EPs on either side of the sylvian fissure may
be explained by a generator described by a vector tangential to the surface of the brain,
possibly in the insular or parietal cortex. This latter suggestion is consistent with the
apparent phase reversal about the sylvian fissure, on the assumption that thalamocortical
volleys produce cortical surface positivity (Andersen et al. 1964;Vogel et al. 2003). This
phase reversal suggests that the generator is described by a vector pointing across the
sylvian fissure at right angles to the cortical surface, consistent with a generator in the
parietal operculum.
A wide range of imaging data suggests that parasylvian structures show
bloodflow or BOLD activation in response to nonpainful cold stimuli. An early fMRI
study demonstrated that the insula was activated in one half of subjects, although
localization within the insula was variable (Davis et al. 1998). The parietal operculum
was not activated in that study, although a strong parietal opercular activation was
observed in a PET study employing a larger cold stimulus (Craig et al. 1996). In total,
these results are consistent with the hypothesis that parasylvian cortical structures display
11
evoked responses to cold stimuli, and so implicate these structures in the sensation of
cold.
12
Figure 1: Potentials recorded directly from the brain in response to a nonpainful cold
stimulus applied to the contralateral hand. A (upper), shows the profile of the average
temperature stimulus while the lower panel shows the maximal potential recorded over
the parietal operculum in subject 1122. B, the location of electrodes in subject 1102.
EPs recorded from the three rows of electrodes labeled C, D, and E in panel B are shown
in Figures 1C, 1D and 1E. Electrodes in these three rows are numbered from 1 to 6 in B,
and EPs recorded from those electrodes in any row are also numbered from 1 to 6, as
appropriate. Overlays of potentials recorded from two adjacent electrodes with large
EPs for each row is shown as the bottom tracing in the corresponding panel C, D and E.
13
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17
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Subject identifier
1122 negative
potentials (n= 6)
1102 negative
(n= 9)
Negative overall
1102 positive
potentials (n= 8)
Latency
Seconds
0.92 +/- 0.08
Amplitude
microamperes
24 +/- 5
Amplitude maxima
among recorded EPs.
- 31
0.80 +/- 0.10
39 +/- 10
- 60
0.85 +/- 0.10
0.81 +/- 0.28
32 +/- 14
40 +/- 14
+58
Table 1: Latency and amplitude for cold evoked potentials (Mean +/- SD) in the two
subjects studied in this report.