(Stroke. 1999;30:2651.)
© 1999 American Heart Association, Inc.
Original Contributions |
Primary Somatosensory Cortex Activation Is Not Altered in Patients With Ventroposterior Thalamic Lesions
A PET Study
From the CEA, Service Hospitalier Frédéric Joliot (P.R., M.Z., Y.S.), Orsay; Service de Neurologie, CHU Henri-Mondor (P.R., P.C., J-D.D.), Créteil; Service de Neurologie, CHU Lariboisière (P.A.), Paris; Urgences Cérébro-Vasculaires, CHU Pitié-Salpêtrière (Y.S.), Paris, France.
Correspondence to Dr Philippe REMY, CEA, Service Hospitalier Frédéric Joliot, 4, Place du Général Leclerc, 91401 Orsay Cedex, France. E-mail remy{at}shfj.cea.fr
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Abstract |
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Background and Purpose—We know remarkably little about the mechanisms underlying cortical activation. Such mechanisms might be better understood by studying the effect of well-localized lesions on the cortical activations in simple paradigms.
Methods—We used H215O and positron emission tomography to measure regional cerebral blood flow (rCBF) at rest and during hand vibration in 7 patients with unilateral thalamic lesion involving the ventroposterior (VP) somatosensory thalamic relay nuclei. We compared the results with those obtained in 6 patients with thalamic lesions sparing the VP nuclei and 6 healthy controls.
Results—The patients with VP lesions had a selective hypoperfusion at rest in the ipsilesional primary sensorimotor cortex (SM1). This hypoperfusion was significantly correlated with the degree of contralateral somatosensory deficit. This abnormality may reflect the deafferentation of SM1 from its somatosensory thalamic input. Despite this deafferentation, the ipsilesional SM1 was normally activated by the vibration of the hypesthetic hand.
Conclusions—The fact that a lesion of the somatosensory thalamic relay nuclei alters the rCBF at rest in SM1 but not its activation by hand vibration indicates that the mechanism of cortical activation is complex, even in the case of simple sensory stimulation. In addition, a dissociation may occur between obvious neurological deficits and apparently normal activation patterns, which suggests that activation studies should be interpreted cautiously in patients with focal brain lesions.
Key Words: cerebral blood flow • somatosensory cortex • thalamus • tomography, emission computed • vibration
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Introduction |
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Positron emission tomography (PET) and functional MRI are useful for mapping the functions of the human brain because they reveal the activation of precisely localized and often distributed cortical areas during sensory, motor, or cognitive tasks.1 2 However, we still know remarkably little about the mechanisms underlying cortical activation. For example, it seems obvious that moving the right hand would activate motor cortical areas in the left hemisphere, but it remains unknown how these areas are selectively activated when a subject decides to move. Yet, it has been recently shown that this process may be disrupted in many diseases, because abnormal patterns of cortical activations have been described in patients recovering from focal brain lesions3 4 5 6 7 and in a variety of diseases, ranging from Parkinson’s disease and dystonia8 9 10 to schizophrenia and autism.11 12 However, to interpret these abnormal activations it is necessary to better understand what leads to the activation of a specific cortical area. One way to address this issue is to investigate how well-localized lesions modify the cortical activations in simple paradigms.
One of the most simple activation paradigm studied is unilateral hand vibration, which normally results in a strong and robust activation of the contralateral primary sensorimotor cortex (SM1).13 14 15 16 17 These activations may simply reflect the processing of information conveyed to specialized somatosensory cortical areas by the ascending somatosensory pathways. A major subcortical relay of these pathways is the ventroposterior (VP) group in the thalamus, which receives many extralemniscal and almost all lemniscal ascending fibers.18 19 20 21 22 Accordingly, a lesion involving the VP nuclei may impair the somatosensory cortical activations during contralesional hand vibration. To investigate this issue, we studied the effects of thalamic lesions on the cortical activations induced by hand vibration in 2 groups of patients whose lesion involved or spared the specific somatosensory relays in the thalamus (ie, the VP group). Our results do not fit with the proposed model and suggest that cortical somatosensory activation do not depend on the VP integrity and may thus involve more complex and parallel systems.
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Subjects and Methods |
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Subjects
These studies were approved by the local Ethical Committee for Human Studies, and all subjects gave their informed consent. Handedness was assessed with the Edinburgh inventory.23
Patients
We studied 13 right-handed patients aged 25 to 83 years, with a
unilateral thalamic lesion (stroke in 12 subjects and abscess in 1)
demonstrated by CT scan or MRI. They were divided into 2 groups
according to the presence (n=7; 62±14 years old) or absence (n=6;
46±12 years old) of a lesion of the VP nuclei of the thalamus. The
existence of a lesion of the VP thalamus was supported by the following
criteria: (1) a somatosensory deficit contralateral to the thalamic
lesion, and (2) the reconstruction of the lesion obtained from
individual MRI performed on the day of the PET examination (see below).
As shown in Figure 1
, the VP was involved
in the lesion in all patients with a contralateral somatosensory
deficit (patients 1 through 7). The 6 patients who had no somatosensory
deficit but, rather, cognitive symptoms had lesions of more
anteromedial parts of the thalamus that always spare the VP (Figure 2). In Tables 1 and 2,
the main clinical details of all patients are indicated, including a
score of somatosensory deficit that is described below.
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Control Subjects
Six healthy right-handed male volunteers aged 20 to 40 years
(mean±SD, 29±8 years) were studied. All had a normal clinical
examination and a normal brain MRI.
Clinical Examination
On the day of the PET study, all patients had a bedside
examination carried out by a single examiner (P.R.) who used a fixed
protocol.17 The Canadian Neurological Scale24
score was used to measure the degree of motor deficit. In addition, we
used a standardized scale to determine the degree of permanent
somatosensory deficit.17 The total score ranges from 0 to
70, with increasing values indicating increasing deficit. The following
somatosensory modalities were tested. (1)
Discriminative touch (0–21): This included (a) measuring
stereognosia (0–3), by placing 3 common objects successively in each
hand of the subjects with each incorrect recognition scored as 1 point;
(b) graphesthesia (0–6), for which 3 numbers were drawn on the forearm
and 3 others on the thigh and each error in recognizing the number was
scored as 1 point; and (c) 2-point discrimination (0–12), assessed
using Weber’s compasses. Two different areas were tested for the upper
limb (fingertip of the third finger and forearm) and lower limb (dorsal
foot and anterior part of the thigh). The first distance at which 2
points were discriminated on at least 3 different trials was measured.
This distance was then compared for each cutaneous area tested with the
measures obtained in the intact side, and a percent difference was
determined as follows: 100x(impaired side-normal side)/normal side.
For each site examined, 1, 2 or 3 points were scored if this percentage
exceeded 30%, 50%, or 100%, respectively. (2) Vibration and
proprioception (0–24): The subject had to detect a vibratory
stimulus applied with a tuning fork at 3 different levels on the upper
and the lower limb. For each of these trials, the patients scored 1
point if the sensation was reported to be diminished compared with the
contralateral (intact) side and 2 points if they did not detect the
vibration. In addition, 1 point was scored if the vibrator used for the
PET stimulation was felt with less intensity in the hypesthetic hand
than in the normal hand and 2 points if the vibration was not
perceived. The perception of passive movements was assessed by asking
the patients to identify the directions of 5 up-down movements applied
to the second finger and first toe. Each error was scored as 1 point.
(3 ) Temperature (0–6): The thermal sense was assessed with
2 different test tubes filled with cold water (
5°C) or warm water
(40°C). The subject had to recognize the temperature ("cold"
or "warm"). Three trials were performed for each limb. The score
corresponds to the number of errors. (4) Pin-prick (0–10):
For each limb 5 stimulations were performed. The subject had to
identify the stimulus (pin or prick). The score corresponds to the
number of errors. (5) Pain (0–4): 1 point was scored if the
patient had transient pain in the hemibody contralateral to the brain
lesion; 2 points if the pain was permanent; 3 if the pain increased
during hand vibration; and 4 in the case of severe central pain, such
as complete Déjerine-Roussy syndrome. (6) Paresthesia
(0–5): Paresthesia was scored as 1 if transient and 2 if
continuous, for each limb. One point was added if paresthesia occurred
to the face.
The subjects were blindfolded during all testing. Each hemibody was similarly tested, and the score is given for 1 side.
Brain Imaging Studies
These studies were performed 1 to 37 months (mean±SD, 11±10
months; n=13) after the occurrence of the lesion. This delay did not
significantly differ between the groups (with somatosensory deficit,
10±9 months; without somatosensory deficit, 13±12 months).
Brain imaging studies consisted of MRI and PET images acquired on the same day for each subject. The detailed information obtained from the MRI allowed us to perform an individualized anatomic localization of brain regions for the functional PET image analysis for each subject.17 25
Anatomic Images
MR images were obtained with a 0.5-T MR imager (MRMAX, General
Electric). Each subject was positioned so that MRI axial slices
were parallel to the bicommissural line (AC-PC),26 which
was verified on a midsagittal image. Skin marks were applied where
indicated by the MR imager positioning laser. Contiguous T1-weighted
3-mm-thick axial slices and 5-mm-thick coronal T2-weighted slices were
then obtained throughout the entire brain.
Functional Images
Scanning was performed with a LETI-TTV03 tomograph (CEA), the
characteristics of which have been described elsewhere.27
Briefly, this scanner collects 7 parallel transaxial planes, 9 mm
thick and 12 mm apart, with a reconstructed 7-mm in-plane
resolution (full width at half maximum).27 We used the
skin marks drawn on the subjects’ face in the MR imager to ensure an
exact repositioning of the head in the PET session. In addition, the
crossed laser beams permanently attached on the PET tomograph allowed
us to monitor the subjects’ head position throughout the examination.
During each PET scan, the room was darkened and the only ambient noise
was the cooling system. The effects of radiation attenuation by the
head were corrected using a transmission scan collected during exposure
to a [68Ge]germanium source. In each condition,
an rCBF study was performed with a method derived from the
H215O
autoradiographic method, except no arterial
catheters were used.28 We injected an
intravenous bolus of 3 mL of saline containing 2960 to 3700
MBq 15O-labeled water, and an 80-second scan was
initiated when the tracer bolus entered the brain. The first frame
showing the arrival of radioactivity in the brain was identified. From
this time point the radioactive counts for the ensuing 80 seconds were
summed to generate rCBF images.17 25 There was a 15-minute
interval between each rCBF measurement.
Tasks
Three different conditions were studied: (1) rest (subjects were
asked to remain in a resting awake state), (2) vibration of the right
hand, and (3) vibration of the left hand. The order of conditions (2)
and (3) was counterbalanced across subjects. One of the 6 controls
received stimulation only on the left hand. The stimulations were
performed by a single examiner using a vibrator that produces
2-mm-amplitude movements with a frequency of 130 Hz
(Daito),13 and involved all the fingers. The subjects were
asked not to grasp the vibrator, but instead to let the examiner
maintain their fingerpads in contact with the vibrator.29
To avoid any surprised reaction to the task, subjects were acclimated
to the vibrator before the PET session, and stimulation began 30
seconds before tracer injection.17
Data Analysis
Regions of Interests
We focused our interest on the primary sensorimotor cortex and
used an individual anatomic analysis to take into account the
anatomic variability between brains of different
subjects.30 PET and MRI data were transferred to a VAX
computer (Digital Equipment Corporation) and the MRI-PET images put in
register as described previously.17 25 Briefly, 3
digitized 3-mm-thick axial slices of the MRI were combined to obtain
images with the same thickness as the PET slices (9 mm). MRI and
PET were coregistered with isodensity contours and custom software
allowing in-plane translation and rotation. Using this software, MRI
isocontours were then superimposed on PET images in all slices. The
accuracy of this registration was assessed by checking that a
successful superimposition was simultaneously obtained at
all brain levels. Such a simultaneous superimposition
cannot be achieved if registration error exceeds 5 millimeters in any
of the x, y, and z axes. This procedure was
repeated for each set of rCBF images to rule out head movements between
rCBF measurements.
The primary sensorimotor cortex (SM1) was a priori defined in each hemisphere for analysis. In addition, a global cortical area was defined in each hemisphere, including all cortical areas that were not analyzed for their involvement in sensorimotor function (we excluded the parietal cortex). This global cortical area (mainly temporal, frontal, and occipital cortex) was defined as a cortical ribbon having a 14-mm thickness. All regions of interest (ROIs) were drawn on individual MR images and copied onto corresponding PET images. Their boundaries were determined according to the identification of the main sulci.17 25 29 31 32
Data Analysis
Since the change in local tissue radioactivity is linearly
related to blood flow, relative changes in tissue activity are taken to
indicate relative changes in blood flow.28 One should
note, however, that the relationship between rCBF increase and
neuronal activation is not necessarily linear.33 To
correct for intercondition changes in the global activity of the brain,
all PET images were normalized so that for each emission scan, each
pixel of each slice was divided by the mean pixel value of all
slices.28 34 The analysis based on individual ROIs
and comparison of normalized activity values in each subject avoids any
bias induced by different levels of atrophy in the 3 groups.
Our main analysis aimed at detecting abnormal somatosensory
cortical activations induced by the vibration of the hand contralateral
to the thalamic lesion. The relative changes in rCBF induced by hand
vibration were determined for each subject by calculating the
difference in the normalized activity between each somatosensory task
and rest using the formula 
%=100x(activation-rest)/rest. For the
6 controls the data obtained during right and left hand vibration were
considered, but 1 of the controls had a stimulation of the left hand
only. The statistical significance of the activations was
analyzed with a 1-sample Student’s t test. We then
compared the activations obtained in the 3 groups of subjects
(controls, patients with, and patients without VP lesions) using a
2-way ANOVA with the group as intersubject variable and the brain
side (lesioned and nonlesioned for the patients and right and left for
the controls) as intrasubject variable. Post hoc analysis
was performed with the Fisher protected least significant difference
test.
Finally, the rCBF asymmetry in the resting state determined whether some of the selected ROIs were hypoperfused in the lesioned hemisphere independent of any stimulation. This was measured by calculating for each region an asymmetry index: AIrest=100x(normal hemisphere-lesioned hemisphere)/normal hemisphere. In controls, the AIrest was determined as follows: 200x(right side-left side)/(right side+left side). The statistical significance of this asymmetry was analyzed with a Student t test. The rest asymmetries (AIrest) in the 2 groups of patients were compared by an ANOVA with the Scheffé S post hoc test. Finally, we made a correlation analysis between clinical scores and the rCBF parameters.
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Results |
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Activations Induced by Hand Vibration
Control Subjects
In control subjects, hand vibration strongly and significantly (P<0.001, Student t test) activated the contralateral SM1 when compared with rest: left SM1, +12.8±4.6%; right SM1, +12.7±4.0%. The asymmetry between activation obtained in left and right SM1 was 0.0±4.5% (range -6.8% to +5.5%, n=5; Figure 3
).
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Patients
Patients With VP Lesion
The vibration of the hypesthetic hand significantly
activated the contralateral SM1 (+9.2±6.2%,
P<0.01). SM1 activation in the lesioned hemisphere did not
significantly correlate with any of the somatosensory scores. More
specifically, the vibratory score was not significantly correlated with
the asymmetry of response in SM1 (Avib,
r=0.48, P=0.29) or with the amplitude of
activation in SM1 in the lesioned hemisphere (r=-0.15,
P=0.76). In addition, there was no correlation between the
level of activation in SM1 and the degree of rCBF asymmetry measured at
rest (r=0.27, P=0.57).
The vibration of the normal hand of these patients induced comparable
activations in the contralateral SM1 (+9.3±3.9%,
P<0.001). The activations were thus symmetrical in the
normal and lesioned hemisphere, because the amplitude of asymmetry in
SM1 (Avib) was 0.1±4.8% (range -7.4% to
+6.5%). This asymmetry was comparable with that observed in controls
(0.0±4.5%, range -6.8% to +5.5%; Figure 3
and 4).
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Patients Without VP Lesion
In patients without somatosensory deficit, the SM1 activation
induced by contralateral hand vibration was significant in the lesioned
(+13.5±4.4%, P<0.001) and in the normal (+12.1±5.6%,
P<0.01) hemispheres.
Between-Group Comparisons
No significant difference or interaction was found when comparing
the activations observed in SM1 of the different groups, using an ANOVA
with the group as intersubject variable and the hemisphere as
intrasubject variable (F2,15=1.3,
P=0.3). In addition, since the SD value of the activation of
SM1 in the lesioned hemisphere is higher than in the other groups, we
compared these SD values with an F test. This test demonstrated no
significant difference in the SD values of SM1 activation between
patients with VP lesion and patients without VP lesion
(F56=1.82) or controls
(F56=1.99). Finally, in controls
and in the normal hemisphere of the patients, there was no correlation
between age and SM1 activation induced by hand vibration
(df=17, r=-0.3, P=0.2).
Asymmetry at Rest
We found no significant asymmetry at rest in the control subjects.
The patients with VP lesion had a slight rCBF asymmetry in the cortical
ribbon (AIrest=2.7±1.5%, P<0.01,
Student t test), and a marked asymmetry in SM1 (7.3±5.2%,
P<0.01). The patients without VP lesion had a marked rCBF
asymmetry in the cortical ribbon
(AIrest=6.6±2.1%, P<0.001). The
comparison of asymmetries between the 2 groups of patients showed a
significant interaction between patients and regions
(F1,11=15.2, P<0.005), because the
AIrest was higher in the SM1 region of patients
with VP lesion than in the patients without VP lesion, whereas the
reverse was found for the cortical ribbon (7.3±5.2% and 1.4±3.4%,
respectively).
The rest asymmetry in SM1 of patients with VP lesion was significantly
correlated with the vibration-proprioception subscore of the
somatosensory scale (df=5, r=0.96,
P<0.0005; Figure 5), the
lemniscal score (r=0.85, P=0.01), and the total
score of somatosensory deficit (r=0.80,
P=0.03).
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Discussion |
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The main result of this study is that patients with thalamic lesions involving the VP thalamic somatosensory relays have a normal activation of somatosensory cortical areas during the vibration of the contralesional, hypesthetic hand. The activation of SM1 is symmetrical to the activation during the vibration of the normal hand in the same subjects and lies in the range of activations observed in controls or in patients with thalamic lesions outside the VP somatosensory relays. The normal response to hand vibration in patients with VP lesion occurs despite the deafferentation of somatosensory cortical areas demonstrated by the clinical somatosensory deficit and the decreased rCBF observed in the somatosensory cortical areas during the resting state. These findings will be discussed below.
In this study, the thalamic lesions appear to have little effect on the rCBF SM1 activation provoked by hand vibration but induce different patterns of rCBF abnormalities at rest in the 2 groups of patients. The patients without VP lesion had a widespread cortical hypoperfusion ipsilateral to the thalamic lesion, as evidenced by a significant rCBF asymmetry in the cortical ribbon. This widespread effect is a well-known consequence of thalamic lesions involving nonspecific activating thalamic nuclei,35 36 37 which were likely damaged in these patients. This widespread cortical hypoperfusion contrasts with the selective hypoperfusion at rest of the ipsilesional SM1 found in the patients with VP lesion. The latter indicates the local reduction of the synaptic activity at rest in this region, confirming its partial deafferentation from the specific somatosensory thalamic inputs due to the VP lesion.38 39 40 Accordingly, we found a significant correlation between the SM1 rCBF asymmetry at rest and the somatosensory deficit in these patients.
Despite the clear-cut effect on rCBF at rest, the thalamic lesions
appear to have little effect on the rCBF cortical activations induced
by hand vibration. The SM1 activation was normal in the 2 groups of
patients, even in the patients with VP lesion during the vibration of
the hypesthetic hand, which was much less perceived than the vibration
of the normal hand. Despite this clear asymmetry of perception, the
level of activation was symmetric in both hemispheres of patients with
VP lesion (Figures 3 and 4). Thus, the interruption of
the somatosensory input at the VP level alters the perception of
vibration and the synaptic activity at rest in SM1 but does not impede
the activation of this region by hand vibration. These results might be
limited by the lack of absolute rCBF quantitation, since this normal
activation is associated with a lower absolute rCBF in this region both
during rest and hand vibration. However, the subjects with VP lesion
still have a preserved ability to activate their ipsilesional
SM1 despite the lesion of the somatosensory relays at the thalamic
level. One possible explanation is that the SM1 region is only
partially deafferented. Although somatosensory evoked potentials could
not be performed in our patients to assess the amount of residual
connectivity between VP thalamus and SM1, it is evident that none of
the patients had a complete anesthesia. However, this
hardly explains the normal SM1 activation, because the level of this
activation did not correlate with the score of somatosensory deficit.
For example, patient 7, who had the most severe deficit of
vibration/position sense (score 21/24), still had a 7.7% increase of
blood flow in SM1 during vibration of the hypesthetic hand. In
addition, the SM1 rCBF increase induced by hand vibration is
symmetrical in both hemispheres of patients with VP lesion despite the
clear asymmetry of perception. These results are finally in line with
those of a previous report41 which show that the complete
section of the lemniscal pathways at the spinal cord level does not
abolish the SM1 activation induced by vibration. Taken together, these
data indicate that the cortical activation caused by contralateral
vibration does not require the integrity of the well-identified VP
thalamocortical circuitry. They suggest that other ascending systems
may play a role in specific cortical activation. In line with this
hypothesis, we recently reported17 that SM1 activation
induced by hand vibration is abolished in patients with tactile
extinction who present considerably fewer somatosensory
deficits than patients with VP lesion. Thus, even in this simple
paradigm, cortical activation emerges as a complex phenomenon that
might be viewed as a cortical "gating" mechanism: the light-up of
specialized cortical areas will allow them to process the flow of
information conveyed by modality-specific thalamic relay nuclei.
Although hypothetical, this view is consistent with the effects
of selective attention on the level of cortical activation, which are
now established in different sensory activation paradigms, including
hand vibration.14 42 43 Little is known about the
underlying neuroanatomic bases of these activation mechanisms. Here,
some parallel lemniscal ascending pathways44 might have
been spared by the VP lesion. Alternatively, the extralemniscal system
might be involved, since, unlike the lemniscal system, it sends
divergent fibers (ie, spinoreticulothalamic and spinomesencephalic) to
extrathalamic targets, which were not damaged in our patients. But how
some of these collaterals are able to activate specific
somatosensory cortical maps— through either dedicated pathways or
interactions with different cortical activating systems—remains to be
investigated. This will become an important field of clinical research,
since understanding the mechanisms of cortical activation may be a
major step to link localization and function in the human brain. Here
for example, the preserved activation of SM1 contrasting with its
hypoperfusion at rest might be an important cue to understand the
dissociation between preserved awareness and decreased perception of
somatosensory stimuli, which is a typical clinical feature of patients
with VP lesion.
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Acknowledgments |
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The authors thank Ken Moya, Dr V. Biousse, Dr F. Bolgert, Pr J.-C. Willer, M. Crouzel, L. Laurier, and B. Martins for their help.
Received August 9, 1999; revision received September 24, 1999; accepted September 24, 1999.
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