Brain (2001), 124, 1077–1090
Functional neuroanatomical correlates of hysterical
P. Vuilleumier,1,4C. Chicherio,2F. Assal,1S. Schwartz,3D. Slosman2and T. Landis1
Departments of1Neurology and2Nuclear Medicine and
Radiology, University Hospital of Geneva,3Institute of
Psychology, University of Lausanne, Switzerland and
4Institute of Cognitive Neuroscience, University College
Correspondence to: Dr P. Vuilleumier, MD, Institute of
Cognitive Neuroscience, University College London,
Alexandra House, 17 Queen Square, London WC1N 3AR, UK
Hysterical conversion disorders refer to functional
neurological deficits such as paralysis, anaesthesia or
blindness not caused by organic damage but associated
with emotional ‘psychogenic’ disturbances. Symptoms are
not intentionally feigned by the patients whose handicap
concomitants of their altered experience of sensation and
volition are still not known. We assessed brain functional
activation in seven patients with unilateral hysterical
sensorimotor loss during passive vibratory stimulation of
both hands, when their deficit was present and 2–4 months
later when they had recovered. Single photon emission
computerized tomography using99mTc-ECD revealed a
consistent decrease of regional cerebral blood flow in the
thalamus and basal ganglia contralateral to the deficit.
component statistical analyses converged to show that
Keywords: basal ganglia; conversion; hysteria; neuroimaging; thalamus
Abbreviations: AOI ? area of interest; BA ? Brodmann area; ECD ? ethylenecysteinate dimer; rCBF ? regional cerebral
blood flow; ROI ? region of interest; SPECT ? single photon emission computerized tomography; SPM ? statistical
parametric mapping; SSM ? Scaled Subprofile Model; T1? vibratory stimulation with symptoms present; T2? vibratory
stimulation after recovery
Patients with hysterical conversion disorders present with a
loss or distortion of neurological function that cannot be
fully explained by a known organic neurological disease
(American Psychiatric Association, 1994). Yet, their symp-
toms are not intentionally feigned, not adequately explained
by malingering, and may result in significant distress and
handicap (Merskey, 1995). In clinical neurological practice,
accounting for 1–3% of diagnoses in general hospitals
(Marsden, 1986), or even more in some neurological settings
(Binzer and Kullgren, 1998; Ron, 1994). Such symptoms
usually confront clinicians with several problems of
© Oxford University Press 2001
Importantly, contralateral basal ganglia and thalamic
hypoactivation resolved after recovery. Furthermore,
loweractivation incontralateralcaudate duringhysterical
conversion symptoms predicted poor recovery at follow-
may entail a functional disorder in striatothalamocortical
circuits controlling sensorimotor function and voluntary
motor behaviour. Basal ganglia, especially the caudate
nucleus, might be particularly well situated to modulate
motor processes based on emotional and situational cues
from the limbic system. Remarkably, the same subcortical
premotor circuits are also involved in unilateral motor
voluntary limb use may fail despite a lack of true paralysis
provide novel constraints for a modern psychobiological
theory of hysteria.
management due to difficulties with definition, diagnosis, and
therapeutic approaches (Ron, 1994), challenging a traditional
division between neurology and psychiatry (Marsden, 1986;
Hysterical symptoms long raised questions about mind–
body relationships. Described in early medical writings as
psychic disorders caused by bodily disturbances (e.g.
displaced uterus in Antiquity), they were later regarded as
the physical effect of violent impressions or passions (for
review, see Merskey, 1995). One century ago, Charcot
postulated a dysfunction of the nervous system produced by
psychological factors and ideas through mechanisms similar
P. Vuilleumier et al.
to hypnosis (Charcot, 1892). He classified hysteria as a
neurosis, together with epilepsy, chorea and parkinsonism,
in contrast to structural lesions. Janet further stated that ‘fixed
ideas’ can arise outside consciousness and cause hysterical
symptoms from a dissociation between cognitive and
of behaviour (Janet, 1894). The most influential contribution
came from Freud, who emphasized the primary role of
psychic motives, which he believed to be kept unconscious
by repression, related to childhood trauma and sexuality, and
transformed into symbolic physical complaints based on past
experiences (Freud and Breuer, 1895). Current designation
as ‘conversion disorder’ in modern psychiatric terminology
Association, 1994). However, conversion and other hysterical
conditions occur with a variety of psychosocial stressors not
necessarily related to childhood or sexual difficulties, and
their pathogenesis remains a matter of debate (Miller, 1987;
Merskey, 1995; Halligan and David, 1999). A role of neuro-
biological factors is suggested by the fact that symptoms are
more frequent on left-side limbs, pointing to possible right-
hemisphere involvement (e.g. Stern, 1983), and seem
occasionally facilitated by a real coexisting brain disease
(e.g. Eames, 1992).
However, specific functional brain correlates of conversion
symptoms have not been demonstrated, except for a few
recent pioneering studies (Marshall et al., 1997; Spence et al.,
2000). Over 100 years after Charcot and Freud, hysteria has
generated many speculations but still few novel observations
(for reviews, see Kihlstrom, 1994; Halligan and David,
1999). Purely psychodynamic accounts are now recognized
as insufficient, but a modern theoretical framework is still
lacking (Miller, 1987; Merskey, 1995; Halligan and David,
1999). Physicians, like philosophers, still often call upon a
‘disease of the will’ or ‘of the imagination’ (Merskey, 1995),
yet little is known about the neural functioning of motor will
or imagination, and how it may be affected in hysterical
patients (Spence et al., 2000). Demonstrating objective brain
correlates of hysterical symptoms may therefore help to
understand the mechanisms that underlie a subjective
experience of abnormal neurological function in these
mechanisms that subserve normal conscious experience of
sensation and volition. A variety of neuropsychological
findings (e.g. Flor-Henry et al., 1981) and neurophysiological
abnormalities (e.g. Tiihonen et al., 1995; Marshall et al.,
1997; Lorenz et al., 1998; Spence et al., 2000) have been
reported in patients with hysterical conversion. However,
many of these studies included only a few or single patients,
and provided relatively conflicting or inconclusive results
overall. Moreover, many other studies have emphasized
normal findings using standard neurophysiological measures
such as somatosensory or motor evoked potentials (e.g.
Howard and Dorfman, 1986; Meyer et al., 1992).
The present study sought to determine whether there are
specific neurophysiological markers associated with hysterical
motor deficits in a group of seven patients who were
prospectively selected from referrals to a general neurological
clinic. We measured regional cerebral blood flow (rCBF)
changes associated with the presence of strictly unilateral
symptoms, using single photon emission computerized
conditions. We selected patients with acute conversion
exhibit circumscribed deficits with good recovery and fewer
comorbidities than patients with long-lasting deficits (Ron,
1994; Binzer and Kullgren, 1998).
Our study design introduced two important methodological
features. First, cerebral activation was measured not only at
rest, but also during a controlled stimulation involving
bilateral vibration of both affected and unaffected limbs.
Passive vibration provides selective inputs within proprio-
ceptive pathways directly participating in motor control (e.g.
Lackner and Di Zio, 1984), and it is known to elicit
widespread activity in both sensory and motor areas through
such afferents, including primary and secondary cortex,
premotor areas and subcortical structures, even when subjects
are not required to undertake an active motor task (Seitz and
Roland, 1992; Coghill et al., 1994; Yousry et al., 1997).
Abnormal neural response to vibration can be observed in a
variety of neurological diseases that affect either sensory or
that are characterized by difficulties in voluntary motor
function without true paralysis (e.g. Tempel and Perlmutter,
1990). We expected that passive vibration might thus enable
us to probe the functional state of activity and responsiveness
of distributed motor and sensory circuits in a symmetric and
controlled manner, while avoiding some confounds due to
the possible variability or unreliability in performing an
active task. In contrast, previous studies required patients to
execute voluntary movements with their affected (paralysed
Although requiring active movements might be expected to
recruit more specifically volitional motor processes that are
presumably affected in hysterical paralysis (e.g. Halligan and
David, 1999), there are potential problems related to the
ambiguity of such instructions in patients who actually
complain of an inability to move, as well as to the many
possible differences in strategy, effort and conflict reaction
that may be brought into play by different individual subjects
in such conditions.
A second novel feature was that we compared brain
activation when the patients’ conversion deficit was present,
and then a few weeks later when it was resolved, so that the
patients could serve as their own controls and rCBF changes
could be directly correlated with the presence of hysterical
symptoms. Such a repeated test/retest design within the same
individuals has proved to be crucial in complex psychiatric
conditions in order to distinguish between state (symptom)
or trait (comorbidity) abnormalities (Ebert and Ebmeier,
1996; Frith and Dolan, 1998). In summary, our main goal
was to determine regions in motor and sensory systems that
Neural correlates of hysteria
would show asymmetric activation in response to vibratory
stimulation, specifically associated with the presence of
Seven patients admitted in our hospital were prospectively
selected during a 2-year period (1996–1997), including six
females and one male (age 16–54, mean 35.1 years, all right-
handed except one). Criteria for inclusion were a strictly
unilateral loss of motor function of recent onset (?2 months),
with or without concomitant sensory disturbances in the same
limb, clearly due to psychogenic factors, and in the absence
of any present or past neurological disease (American
Psychiatric Association, 1994). Patients with additional
complaints (e.g. bilateral deficits, vision disturbances,
vertigo), long-lasting deficits (?2 months), past medical
problems or other major psychiatric illness were excluded.
No patient was under psychotropic medication at the time
of presentation. Subjective paralysis and weakness were
predominant symptoms in all cases, but often accompanied
by superficial sensory disturbances such as numbness or
dysaesthesia (six out of seven patients, see Appendix I). The
upper limb (one case), lower limb (one case) or both limbs
(five cases) were involved on one side of the body (four left
and three right).
Neurological and psychiatric diagnoses were made by
physicians independent to the study. Organic pathology of
the central or peripheral nervous system was excluded in all
cases by negative neurological examination, as well as
detailed radiological imaging and electrodiagnostic investiga-
tions, including normal brain MRI (seven cases) or spine
MRI (threecases), normal
(somatosensory, motor and visual evoked potentials in seven,
five and five cases, respectively; EMG in three; carotido-
vertebral Doppler in three), normal laboratory and immuno-
logical tests (including CSF in five cases), and positive
psychiatric assessment suggesting a conversion disorder
Association, 1994). All patients faced stressful life events
noted acute or chronic stress factors (DSM-IV axis 4) in all
cases, depressed mood in five, and unspecified personality
disorder (DSM-IV axis 2) in one.
All patients were followed-up for 6–12 months after
initial admission. All of them improved with supportive
physiotherapy and psychotherapy. Four patients had no
symptom on follow-up 3–6 months after admission (V.U.,
T.A., V.A., B.R.), while three others had milder but persisting
or new complaints after 12 months (L.M., R.O., L.A.).
Informed consent was obtained from all subjects and the
study was approved by the University Hospital of Geneva.
SPECT scans were obtained in three different conditions on
separate sessions: during baseline resting state with subjective
deficit present (B scan, sevencases); during bilateral vibratory
stimulation with subjective deficit present (T1scan, seven
cases) a few days later (2–4 days, mean 2.8); and during the
same stimulation after recovery from deficit (T2scan, four
cases) 2–4 months later (8–18 weeks, mean 14.3). Three
patients who had persisting or new complaints at follow-up
after 6 months had no T2scan. In T1and T2scans, vibratory
stimulation (50 Hz) was symmetrically applied to both
affected and unaffected limbs (hands in six cases; feet in one
attached to the hands or feet. Patients lay down in the supine
position in a darkened and silent room, with eyes closed and
dimer (ECD) labelled with Technetium-99m (99mTc-ECD)
was injected for each of the three scan session; note that
ECD tracer is more reliable than others [e.g. HMPAO
(hexa-methyl-propylene-amino-oxime)] for discrete regional
changes and depends not only on CBF but also on cerebral
metabolism (Shishido et al., 1995). At T1and T2, vibration
was administered for 3 min before injection and lasted 3 min
more afterward. SPECT scans were obtained 20 min after
injection on a 3-heads Toshiba CGA-9300 camera with fan
beam collimators and simultaneous acquisition of the153Gd-
rod source for transmission and scatter correction (Billet and
Slosman, 1998). Data were acquired and reconstructed in a
128 ? 128 matrix. The whole brain volume was covered.
Scatter correction used a Shepp and Logan filter and
transmission correction was applied using the
transmission scan. Images were reconstructed in sagittal,
coronal and transaxial planes from the orbitomeatal line with
a slice thickness of 2 pixels (32 slices).
SPECT data were analysed using two different statistical
methods, allowing to combine inferential and descriptive
approaches suitable to a small sample size, and independent
cross-checking of the results without relying on an a priori
hypothesis (see Pawlik, 1991). Regional changes in perfusion
between conditions were first assessed by parametric analyses
on a voxel-by-voxel basis across the whole group of patients,
following standard statistical parametric mapping method-
ology (SPM; Friston et al., 1995), as described below. This
was supplemented by independent non-parametric analyses
applied to regions of interest on a multiple single case
basis, using Scaled Subprofile Model (SSM) (Alexander and
Moeller, 1994), also as described below. Since the side of
deficit differed across patients (left versus right limb deficits),
all analyses were done after realigning scans onto the side
of symptoms (contralateral versus ipsilateral hemisphere)
unless stated otherwise.
Statistical parametric mapping
Statistical parametric mapping was performed using SPM96
(Wellcome Dept of Cognitive Neurology, London, UK)
P. Vuilleumier et al.
(Friston et al., 1995) implemented in MATLAB (Mathworks
Inc., Sherborn, Mass., USA), after data from reconstructed
scans were spatially transformed and flipped according to
the side of deficit. The different images from each patient
were realigned to the first, creating a mean volume of
resliced scans, and applying a linear 9 parameters affine
transformation. Images were normalized into a standard space
(Talairach and Tournoux, 1988) and smoothed with an
isotropic Gaussian kernel (full-width half-maximum of 16
mm) to accommodate intersubject differences in gyral
anatomy and suppress high frequency noise. Analysis of
covariance was applied to count densities on a voxel by
voxel basis, with proportional scaling to remove differences
in global activity within and between patients. Changes in
rCBF were represented by a linear contrast of the means
across conditions on a voxel by voxel basis using the
t-statistic. The resulting sets of t-values constituted the
statistical parametric map SPM t. SPM t-values were
transformed to the unit normal distribution SPM(Z) with
Z scores ?3.09 (P ? 0.005 uncorrected for multiple
conditions, andonly activation
significance of P ? 0.01 at the cluster level were reported.
There were two planned comparisons of interest: (i) activation
during T1scan (with vibratory stimulation) versus baseline
(resting state), assessing the effect of bilateral vibratory
inputs in the presence of unilateral deficits in sensorimotor
function; and (ii) activation during T2 scan (symptoms
recovered) versus activation during T1 scan (symptoms
present), assessing the changes in cerebral activity associated
with changes in sensorimotor function.
Region of interest segmentation
Cerebral cortex and subcortical nuclei were segmented into
several small, symmetrical regions of interest (ROIs) by a
semi-automated procedure (see Hellman et al., 1989), and
mean count density, standard deviation and pixel size were
then measured in these ROIs. On each axial slice, a cortical
rim was first determined using a standardized threshold based
on whole brain median count value to define the outer edge
and a fixed width from the latter to define the inner edge, and
18 consecutive slices. Symmetrical elliptical ROIs were also
placed on other regions not captured by this procedure
(temporal poles, medial and orbital frontal lobes, thalamus,
caudate and lenticular nuclei; 3–6 ROIs per hemisphere each).
The resulting ROIs segments were subsequently grouped into
20 anatomically defined areas of interest (AOIs) and their
mean count densities were averaged, correcting for segment
size. The same ROIs matched across hemispheres and scans
in a given subject were selected for AOI analysis (about
equal number across subjects). In total, 180–186 segments in
each hemisphere were grouped in 20 cortical and subcortical
AOIs, including motor [Brodmann area (BA) 4, 10–13 ROIs],
premotor (BA 6, 9–11; BA 8, 8–10), prefrontal (BA 9–44,
8; BA 45, 8; BA 46, 8–10; BA 10, 6–9; BA 11, 4–8), medial
18–20), posterior parietal (BA 7, 14–16; BA 39–40, 18–19),
temporal (BA 37, 14–16; BA 22, 9–12; BA 20–21, 6–12;
BA 38, 8–10), occipital (BA 17–18–19, 8–10) and subcortical
regions (caudate, 5–6; lenticular nuclei, 3–4; thalamus, 5–6).
Hemispheric asymmetries (contralateral versus ipsilateral)
and recovery changes (T2 versus T1) were assessed by
pairwise non-parametric comparisons between homologous
AOIs, using regional count densities extracted from ROIs,
normalized to whole brain mean (Wilcoxon test with
P ? 0.01; all reported comparisons correspond to P ? 0.002
uncorrected using t-tests, P ? 0.05 corrected for multiple
comparisons; for advantages of non-parametric tests with
small sample size, see Pawlik, 1991). Asymmetry percentages
were computed using mean count differences between
homologous ROIs in the two hemispheres for each scan
[% ? (contralateral – ipsilateral)/(contralateral ? ipsilateral)
? 200], and change percentages were computed using count
differences between T1and T2scans in homologous ROIs
for each hemisphere [% ? (T2– T1)/(T2? T1) ? 200].
Scaled Subprofile Model
Raw data from all AOIs were entered into SSM analysis to
determine patterns of activation across scans and patients
(Alexander and Moeller, 1994). SSM is a statistically robust
method that applies a modified principal component analysis,
allowing detection of simultaneous networks of regions that
form significant covarying patterns (topographic profiles)
associated with a specific state, and to measure how the
expression of such regional patterns may differ not only
between different scans but also between hemispheres or
subjects (see Alexander and Moeller, 1994). Thus, when
different subjects (or hemispheres) manifest particular
covariance patterns to a greater or lesser degree, SSM can
compute loading scores that quantify the representation of
this pattern in each subject (or hemisphere). Such a method
is particularly suitable to assess patterns of activity and
temporal changes using repeated measures in a small sample
of subjects (see Eidelberg et al., 1996).
SSM was performed using data from our 20 AOIs to create
a 20 region ? 16 hemisphere matrix (each scan/subject), as
described in detail elsewhere (Alexander and Moeller, 1994).
Briefly, the SSM analysis comprises a series of 16
observations, including T1and T2data from all AOIs of the
two hemispheres, in the four subjects who recovered, entered
into the analysis without any a priori specification about the
possible relevant conditions (i.e. before or after recovery,
data in the matrix are log transformed, the mean values
across regions are first subtracted from each hemisphere
value, and the mean values across hemisphere are then
subtracted from each regional value, thus resulting in a
twice normalized matrix of residual profiles. The latter is
subsequently used to compute two separate region ? region
Neural correlates of hysteria
Table 1 Coordinates and magnitude of maximal rCBF changes in SPM analysis
Brain side Brodmann area
rCBF changes associated with bilateral vibrotactile stimulation
Contra Middle prefrontal gyrus (BA 6)
Contra Middle prefrontal gyrus (BA 8)
Contra Middle prefrontal gyrus (BA 8)
Contra Superior prefrontal gyrus (BA 9/46)
Contra Post-central gyrus (BA 1/2)
Contra Post-central gyrus (BA 5)
Contra Superior parietal lobule (BA 7)
Ipsi Superior prefrontal gyrus (BA 9/46)
Ipsi Middle prefrontal gyrus (BA 46)
Ipsi Superior prefrontal gyrus (BA 9)
Ipsi Superior prefrontal gyrus (BA 8)
Ipsi Paracentral lobule (BA 5)
Ipsi Post-central gyrus (BA 1/2)
B ? T1
Contra Cuneus/medial occipital gyrus (BA 19/18)
IpsiInferior occipital gyrus (BA 18)
IpsiLingual gyrus (BA 18)
Contra Inferior occipital gyrus (BA 18/19)
IpsiLingual gyrus (BA 18)
rCBF changes associated with unilateral sensorimotor symptoms
Contra Caudate nucleus
Ipsi Post-central gyrus (BA 1/3)
IpsiPrecentral gyrus (BA 6/4)
B ? baseline resting state with symptoms present; T1? vibratory stimulation with symptoms present;
T2? vibratory stimulation after recovery; contra/ipsi ? hemisphere contralateral/ipsilateral to
symptoms; BA ? Brodmann area; x, y and z (in millimetres) are coordinates in the stereotactic space
of Talairach and Tournoux (1988). *P ? 0.005 corrected for the cluster.
and hemisphere ? hemisphere covariance matrices. These
are then entered in a principal components analysis performed
without rotation to obtain a set of regional patterns and the
corresponding loading of each hemisphere/subject, respect-
ively. Here again, our goal was to identify whether any
patterns of regional activity changed with the presence or
absence of deficit.
We first assessed the effects of symmetric sensorimotor
stimulation at the time of unilateral conversion symptoms
using SPM across the whole group of patients (Table 1).
stimulation in the presence of subjective paralysis (T1)
produced significant rCBF increases in both hemispheres in
the parietal somatosensory cortex (bilateral BA 1/2/3 and 5,
contralateral BA 7), frontal premotor cortex (bilateral BA 8,
contralateral BA 6) and anterior prefrontal areas (bilateral
BA 9/46, contralateral BA 10; Fig. 1A). These activations
correspond to the locations found in PET studies using hand
vibration in normal subjects (Seitz and Roland, 1992; Coghill
et al., 1994; Yousry et al., 1997), and confirm that our
vibratory stimulation induced reliable activity in both sensory
and motor systems (Tempel and Perlmutter, 1990; Yousry
et al., 1997). There were no reliable asymmetries in cortical
activity elicited by vibration between hemispheres contra-
lateral and ipsilateral to the symptoms, except for slightly
greater responses in contralateral superior parietal cortex.
Visual areas showed bilateral rCBF decreases during
stimulation (Table 1).
We then examined the changes associated with recovery.
Significant differences were observed between presence and
absence of conversion deficit in those four patients who had
no symptoms at follow-up (Fig. 1B–D). When patients
experienced their subjective motor deficits (T1), rCBF during
vibration was decreased in the contralateral thalamus and
basal ganglia (caudate and putamen) compared with when
the deficit was resolved (T2), while it was increased in the
ipsilateral somatosensory (BA 1/3) and premotor (BA 6)
P. Vuilleumier et al.
Fig. 1 Statistical parametric maps of significant rCBF changes. (A) Increased activity in bilateral frontal and parietal cortical regions
when bilateral vibration stimulation was compared with resting state during unilateral hysterical symptoms (T1? B). (B) Increased
activity in basal ganglia and thalamus contralateral to the deficit when bilateral vibration after recovery was compared with the same
stimulation during symptoms (T2? T1). (C) rCBF changes in the thalamus (y ? –2 mm) and basal ganglia (–6 mm, caudate; –12 mm,
putamen) superimposed on a coronal MRI template in normalized stereotactic coordinates (Talairach and Tournoux, 1988). (D) Adjusted
mean rCBF equivalents (grey bars) and individual data points (red dots) at the maxima of changes in the basal ganglia and thalamus in
the presence and after recovery of symptoms. Exact coordinates are given in Table 1.
Neural correlates of hysteria
Fig. 2 Illustration of SPECT data in two patients with hysterical sensorimotor loss in the left arm (A and B) and right arm and leg (C
and D), respectively. (A and C) Raw images (axial and coronal slices) obtained during bilateral vibratory stimulation of the hands show
lower activity in the thalamus and caudate contralateral to the symptoms (T1), resolving after recovery (T2). (B and D) Average regional
perfusion values measured from regions of interest (converted in Z-scores, normalized for each scan separately). Contra/ipsi ?
hemisphere contralateral/ipsilateral to subjective deficit. Similar results were obtained in other patients.
P. Vuilleumier et al.
Table 2 Topographical profiles in SSM analysis
Factor 1Factor 2 Factor 3
% variance explained
(A) Brain areas
(B) Hemisphere (mean across subjects)
Factors indicate overlapping functional networks of brain areas
whose activity is covarying across subjects and scan sessions (T1
and T2? bilateral hand vibratory stimulation during subjective
deficit and after recovery, respectively). Coefficients indicate the
degree to which brain regions (A) and individual hemispheres
(B) contribute to (or ‘weigh’ in) each topographical profile. For
clarity, factor loadings ?0.5 in topographical profiles are not
cortex (Table 1). Such changes in contralateral thalamic and
caudate activity associated with recovery from conversion
symptoms were found in each individual patient (Figs 1C
and 2; and see ROI analysis below).
For completeness, statistical parametric comparisons were
also performed on scans not realigned onto the side of
symptoms. This revealed no additional changes associated
with vibratory stimulation or presence of symptoms, which
might have been related to some general right versus left
hemispheric factors independent of the side of deficit.
ROI and SSM analysis
Consistent changes in thalamic and caudate activity,
contralateral to conversion symptoms were confirmed by
independent multiple single-case analyses in which we
compared T1 and T2 scans in individual subjects who
underwent both scanning sessions. SSM factorial analysis
was performed on 20 anatomically defined AOIs to determine
covarying topographic patterns of activity in the contralateral
and ipsilateral hemispheres across scans and across subjects
(see Methods). SSM extracted three main topographical
profiles accounting for 82% of the data variance (Table 2A).
The first factor reflects a predominant activation of primary
and secondary sensorimotor areas in frontal and parietal lobes
(BA 4, 6, 1–2–3, 5–7 and 39–40), with relative deactivation
of lenticular nuclei and temporal lobe (BA 37–38). Loading
on both sides except for the hemisphere contralateral to the
deficit in scan T1. The second factor also reflects a network
of prefrontal and parietal areas, loading more on the ipsilateral
hemisphere during scan T1. The third factor indicates a
regional pattern that includes the thalamus, caudate and
ventral frontal areas (BA 11, 44–45), which characterizes the
hemisphere contralateral to the deficit in scan T1.
To examine further the changes in activity and hemispheric
asymmetry across the different scan conditions, paired
performed within individual subjects using average count
densities in AOIs, normalized to whole brain mean. When
sensorimotor symptoms were present (T1), asymmetries in
significant in each subject, with a relative hypoactivation of
the contralateral thalamus (–9 to –19%, mean 12.6; Z ?
3.06, P ? 0.005 in each case, Wilcoxon paired rank test)
and contralateral caudate (–6 to –30%, mean 15.9; Z ? 2.81,
P ? 0.005), together with a relative hyperactivation of the
contralateral lenticular nucleus (?9 to ?11%, mean 9.9;
Z ? 2.58, P ? 0.01). Only one patient (T.A.) showed a
significant asymmetry in the post-central somatosensory
cortex (BA 1/2/3, Z ? 4.01, P ? 0.005) and precentral motor
cortex (BA 4, Z ? 3.06, P ? 0.005). In addition, a relative
hyperactivation of the contralateral anterior temporal pole
(BA 38, right hemisphere, Fig. 2B) was found in two cases
(Z ? 2.52, P ? 0.01).
None of these asymmetries were seen after recovery (T2).
Compared with T1, average normalized perfusion on T2
scans significantly increased for each patient in contralateral
thalamus (?7 to ?23%, mean 18%; Z ? 3.07, P ? 0.005
in each case) and contralateral caudate (?12 to ?36%, mean
22%; Z ? 2.81, P ? 0.005), much more than ipsilaterally
(thalamus –12 to ?14%, mean ?4.6%, and caudate –5 to
14%, mean ?7%, respectively). Two patients (T.A. and V.A.)
also showed slight but significant decreases in somatosensory
cortex (BA 1/2/3), both contralaterally (Z ? 2.58, P ? 0.01)
changes associated with recovery were observed in prefrontal
areas (BA 46 and/or 6), with moderate but systematic
increases (Z ? 2.66, P ? 0.01) contralateral to the deficit in
two patients (V.U. and T.A.) and ipsilateral in one (V.A.),
i.e. in the right hemisphere in all three cases. In fact, this
resulted in a significant prefrontal asymmetry with relative
left hypoactivation in all of these three patients after recovery
(Z ? 2.66, P ? 0.01), whereas no such asymmetry was
noted during symptoms. No other asymmetries or changes
brain areas were
Neural correlates of hysteria
Prediction of recovery
Since afew patientsshowed alack of significantimprovement
in their symptoms at follow-up, we examined whether the
degree of functional abnormalities in brain activation during
initial symptoms was correlated with differential recovery.
The three patients who had persisting deficits or new
symptoms at follow-up had significantly lower activity in the
contralateral caudate nucleus AOI during T1scan (mean
normalized count densities ? SD were 67.97 ? 2.17) as
compared with the other four patients who had complete
recovery (mean 84.59 ? 8.09; Mann–Whitney U ? 12, P ?
0.034), while activity in the contralateral thalamus AOI was
also marginally lower (mean 89.67 ? 1.75 versus 95.84 ?
2.39; Mann–Whitney U ? 11, P ? 0.078). By contrast, there
was no significant difference in ipsilateral caudate activation
(mean 97.97 ? 6.39 versus 96.91 ? 4.64) and ipsilateral
thalamic activation (mean 96.53 ? 5.38 versus 106.08 ?
7.09) between the two groups of patients (Mann–Whitney
U ? 8, P ? 0.48 for both comparisons). These data suggest
that patients with a greater asymmetry in subcortical grey
nuclei during symptoms might be less likely to show rapid
recovery, although interpretation of this finding is clearly
limited by the small number of cases.
These results demonstrate a systematic neural correlate of
focal hysterical conversion disorder, involving the basal
ganglia and thalamus. This provides the first direct evidence
of functional abnormalities in sensorimotor pathways
specifically related to the presence of subjective neurological
symptoms. Both SPM and SSM findings converged to show
that transient unilateral sensorimotor loss of hysterical origin
was associated with a relative hypoactivation of contralateral
thalamus and basal ganglia circuits during bilateral hand
vibration (T1), regressing with recovery (T2). Complementary
evidence from independent statistical methods, involving
voxel-based group analysis and ROI-based multiple single-
case analysis, respectively, lends strong support to these
results, with both types of methods similarly indicating that
such significant subcortical changes were found in all of
our patients. Changes in contralateral basal ganglia activity
between T1and T2cannot be explained by sessional effects
due to repeated scans, since repetition effects would not
explain such asymmetrical changes. Also, lower activation in
contralateral caudate during hysterical conversion symptoms
predicted poor recovery at follow-up. In contrast, somato-
sensory and premotor cortical areas were still activated by
vibration relatively symmetrically on both sides despite the
presence of symptoms, consistent with objectively intact
neurological function and normal cortical responses in motor
or sensory evoked potentials, as typically observed in
hysterical patients (Howard and Dorfman, 1986; Meyer et al.,
1992). Only a mild asymmetry in the covariance patterns of
frontoparietal networks was indicated by SSM and SPM
analyses in the hemisphere contralateral to the deficit. Thus,
activations induced by vibration were slightly greater
contralaterally than ipsilaterally during symptoms (T1–B),
but decreased ipsilaterally more than contralaterally with
recovery (T1–T2), suggesting a lower baseline activity, but
preserved response to vibration in frontal and parietal cortex
during symptoms. This would be consistent with an abnormal
modulation from subcortical circuits in the thalamus and
basal ganglia (Steriade and Llina ´s, 1988; Tempel and
Perlmutter, 1990; Rossini et al., 1998), and possibly some
secondary interhemispheric imbalance (Ferbert et al., 1992;
Seyal et al., 1995).
Basal ganglia and thalamus are intimately connected within
neural circuits or ‘loops’ that subserve both motor and
cognitive functions (Alexander et al., 1986; Graybiel et al.,
1994). In particular, striatothalamocortical premotor loops
are critically involved in generating intentional movements
and learning adaptive motor programmes (Graybiel et al.,
of motor volition and effort (Gandevia, 1987). Neurological
dysfunction in these circuits can cause a variety of motor
and neuropsychiatric illnesses, such as parkinsonism, chorea,
tics or obsessive–compulsive disorders, all implicating
abnormal control of cortical function by basal ganglia–
thalamic systems (Alexander et al., 1986; Bhatia and
Marsden, 1994; Rauch and Savage, 1997). The thalamus is
also strategically placed to modulate sensory and motor
signals as it is the main relay of afferents to the cortex, and
it may control the selective engagement of cortical areas
involved in motor and cognitive functions via the intralaminar
and reticular nuclei systems (Steriade and Llina ´s, 1988;
Strafella et al., 1997).
Spatial resolution of SPECT does not permit definite
demonstration of which part of the thalamus was more
specifically affected in our patients. Notably, however,
stimulation of central thalamic nuclei can trigger movements
experienced as volitional by the subject (He ´caen et al., 1949),
or inhibit voluntary action (Strafella et al., 1997), whereas
their lesion (e.g. strokes) often cause ‘intentional’ motor
neglect (Watson et al., 1978; Laplane et al., 1986; von Giesen
et al., 1994) in which patients fail to use their affected limbs
or behave like hemiplegics despite normal strength and
sensation. Motor neglect is thought to reflect a dysfunction
in striatothalamic circuits mediating motor preparation and
intention (Watson et al., 1978; Laplane et al., 1986; von
Giesen et al., 1994), and if associated with real paralysis,
such a loss of intention may impede awareness of motor
function and contribute to anosognosia for hemiplegia (Gold
et al., 1994; Vuilleumier, 2000). In this respect, our findings
in patients with hysteria (who experience a deficit in the
absence of physical damage) offer an intriguing counterpart
to the findings in neurological patients with anosognosia
(who lack awareness of deficit following brain damage): in
both instances, there is a discrepancy between awareness in
striatothalamic disturbances are implicated in the abnormal
P. Vuilleumier et al.
conscious behaviour, independent of an integrity of primary
previous theoretical proposals suggesting that attentional or
motivational mechanisms might operate at the level of
thalamus or basal ganglia to influence sensorimotor processes
in hysterical conversion (Ludwig, 1972; Trimble, 1996), as
well as in other disorders of intentional motor behaviour
(Mogenson et al., 1980; Schultz, 1999; Brown and Pluck,
Remarkably, the basal ganglia have a unique position
within premotor pathways in that their activity is especially
dependent on environmental context cues and reinforcing
motivational values (Graybiel et al., 1994; Kawagoe et al.,
1998). The caudate nucleus receives prominent limbic inputs
from the amygdala and orbitofrontal cortex, encoding
emotional significance ofevents in relation topast experience,
and thus contributes to elicit or suppress specific patterns of
motor behaviour in response to emotional states (Rolls, 1995).
Direct limbic inputs from amygdala and orbitofrontal cortex
are also provided at the thalamic level, allowing the
modulation of striatocortical loops based on affective cues
(Mogenson et al., 1980). An influence of limbic signals on
striatothalamocortical circuits has been implicated in motor
or cognitive inhibition associated with several neurological
or psychiatric disorders, such as apathy and depression
(Bhatia and Marsden, 1994; Rauch and Savage, 1997; Brown
and Pluck, 2000). In animals, alert states with inhibition of
and protective limb immobility after an injury (De Ceballos
et al., 1986) are also known to implicate inhibitory processes
in striatal and thalamic control of motor function. A role of
these subcortical circuits in hysterical conversion therefore
lends strong support to the view that they may derive
from primitive psychobiological adaptive mechanisms or
stereotyped illness behaviour with self-preservation value
(Miller, 1987; Merskey, 1995), somehow similar to instinctive
freezing or immobilization reaction in response to perceived
threats (Kretschmer, 1948; Ludwig, 1972). We would suggest
that hysterical paralysis might build upon such neural
mechanisms to establish a selective inhibition of action
through the modulation of specific basal ganglia and
thalamocortical systems, with such inhibition being possibly
triggered outside conscious will by various emotional
stressors, through limbic inputs from amygdala and orbito-
frontal cortex (Graybiel et al., 1994; Marshall et al., 1997).
Decreased activity in basal ganglia–thalamic circuits might
set the motor system in a functional state characterized by
impaired motor readiness and initiation, resulting in abnormal
Our patients were all selected on the basis of limited
sensory disturbances in the same limb, mostly dysaesthesia
or hypoaesthesia. Such sensory symptoms are commonly
associated with conversion paralysis (Marsden, 1986;
Merskey, 1995; Trimble, 1996). Therefore, our findings might
reflect not only motor but also sensory hysterical deficits in
these patients. Further research is needed to determine
whether sensory and motor symptoms may relate to distinct
thalamic or basal ganglia abnormalities. Recent studies have
shown that both the thalamus (e.g. Iadarola et al., 1995;
Tracey et al., 2000) and basal ganglia (e.g. Tempel and
Perlmutter, 1990; Chudler and Dong, 1995; Rossini et al.,
1998; Tracey et al., 2000) are implicated in normal or
abnormal sensory integration and pain processing. Notably,
combined changes in thalamic and basal ganglia activity are
associated with an alteration of subjective sensation in
patients with fibromyalgia (Mountz et al., 1995) and during
acupuncture treatment (Hui et al., 2000), two conditions
where both physiological and motivational factors are
One limitation of recovery findings in our study is that
they applied to only four subjects who eventually recovered
from their symptoms during a 2-year follow-up. However,
our study includes the largest series of patients with a
conversion disorder hitherto reported in a controlled
neurophysiological investigation. Studies using evoked
potentials have shown normal motor responses (Meyer et al.,
1992) and early sensory components (Howard and Dorfman,
1986), but non-specific alteration in later components, such
as P300 or CNV (Lorenz et al., 1998), consistent with normal
elaboration of response to stimuli. Only a few imaging studies
using HMPAO-SPECT (Tiihonen et al., 1995; Yazici and
Kostakoglu, 1998) or PET (Marshall et al., 1997; Spence
et al., 2000) have been performed in patients with conversion
symptoms, demonstrating inconstant abnormalities such as
hyper- or hypoactivation in sensorimotor, parietal and/or
frontal areas. These discrepancies may be due to a number
of factors (e.g. small number of subjects, heterogeneous
associated deficits or conditions of activation during
scanning). A PET study (Marshall et al., 1997) performed in
a single patient with long-lasting hysterical problems reported
no activation of primary motor cortex when the patient
attempted to move the affected leg (as can be expected given
the lack of movement), together with an increased activity
in right orbitofrontal and cingulate cortex that was interpreted
as the source of active inhibition exerted on primary motor
cortex. However, orbitofrontal and cingulate activity might
also influence motor function through their inputs into basal
ganglia and thalamic circuits (Graybiel et al., 1994; Kawagoe
et al., 1998), or alternatively reflect monitoring of movement
failure or motivational conflicts (Ebert and Ebmeier, 1996;
Frith and Dolan, 1998; Fink et al., 1999). In two of our
patients, we found increased activity in the right temporal
pole (BA 38) during symptoms, possibly corresponding to
limbic areas close to the amygdala and orbitofrontal cortex,
but no such changes were observed in the remaining patients.
Another recent PET study described reduced activation of
left frontal regions in three patients with hysterical weakness
of left limbs (Spence et al., 2000). However, in the absence
of repeated measures after recovery, left frontal hypoactivity
might also be related to antecedents of depression (Ebert and
Neural correlates of hysteria
Ebmeier, 1996; Elliott et al., 1997; Frith and Dolan, 1998),
commonly observed in these patients (Marsden, 1986; Ron,
1994; Trimble, 1996). Test–retest designs are important to
differentiate state from trait abnormalities in neuroimaging
studies of complex psychiatric disorders (Ebert and Ebmeier,
1996; Frith and Dolan, 1998). In our patients, left frontal
hypoactivity was inconstant but seen after recovery in three
cases (BA 46 and/or 6). Several of our patients had depressed
mood. Taken together, these findings may converge with
other psychological, epidemiological and biological results
(Merskey, 1995; Trimble, 1996; Tunca et al., 1996),
suggesting a relationship between depressive disorders and
conversion symptoms. Our results indicate that decreased
activity in subcortical structures might be more directly
related to the presence of contralateral conversion deficits
themselves, rather than to other comorbid traits, which may
coexist and outlast such transient deficits. It is also possible
that abnormal striatal and thalamic activity might represent
orbitofrontal, cingulate or prefrontal cortex, allowing for the
actual ‘implementation’ of motor inhibition associated with
These findings provide novel constraints for a modern
psychobiological theory of hysteria. Given the role of striatal–
thalamic circuits in many cognitive and affective domains
(Alexander et al., 1986; Graybiel et al., 1994; Rauch and
Savage, 1997), they also raise an intriguing question of
whether similar mechanisms might participate in other non-
motor hysterical disorders (e.g. memory). Future studies
using newer techniques such as functional MRI are needed
to extend these findings and explore other modalities of
hysterical deficits. Functional connectivity analyses (e.g.
Friston, 1994) might prove of particular interest in this
context. Importantly, while hysterical disorders are usually
defined by exclusion of an organic disease, the present
findings of specific neurophysiological correlates may
contribute to support a more positive diagnosis. In our recent
clinical experience, this may help to reassure both patients
and medical carers that hysterical symptoms are indeed
functional, but nonetheless real, rather than mere imagination
or malingering (Merskey, 1995). William James remarked
long ago (James, 1896): ‘Poor hysterics. First they were
treated as victims of sexual trouble . . . then of moral
perversity and mediocrity . . . then of imagination. Among
the various rehabilitation which our age has seen, none are
more deserving or humane. It is a real disease, but a
and A. Nahory for their support and helpful assistance,
F. Vingerhoets for advice with SSM analysis, and R. Rafal,
J. Kihlstrom, P. Halligan and R. Dolan for helpful comments
and suggestions. P.V. was supported by a grant from the Swiss
National Science Foundation. Part of this work was presented
at the 51st Annual Meeting of the American Academy of
Neurology, Toronto, April 1999, and at the European Meeting
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Received November 8, 2000. Revised January 31, 2001.
Accepted February 8, 2001
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P. Vuilleumier et al.
Brief patient histories
Forty-year-old, right-handed woman who fled from Algeria
during childhood, escaping a shooting where relatives were
killed. Chronic neck pain with left arm irradiation for several
years after a car accident with no injury, but no previous
somatoform or psychiatry diagnosis. Left arm weakness and
numbness 2 months after moving furnitures when being
forced to move home to Switzerland. She could not raise
and maintain the left arm outstretched, only slight and slow
movements of fingers. Decreased sensation to light touch on
the whole arm without radicular distribution.
Sixteen-year-old, right-handed woman, born in Portugal, in
conflict with parents since they moved to Switzerland. Sexual
assault from a cousin 2 years before. Transient gait
disturbances after breaking-up with her boyfriend 1 year
before, reported by relatives, but no previous somatoform or
psychiatry diagnosis. Sudden paralysis of both legs, then
in school. Complete absence of spontaneous movement and
lack of report of any sensory stimulation (touch, pain,
position) on the left side of the body.
Fifty-one-year-old, right-handed woman, divorced, whose
son died from heart disease 1 year prior to the study.
Heaviness, weakness and loss of dexterity of right limbs
after her new companion suffered myocardial infarction
while wrongly suspected of abusing a teenager. No sensory
Twenty-one-year-old, right-handed woman, with history of
misconduct at school during teenage, but no psychiatric
diagnosis. Pain with complete anaesthesia and weakness of
the right leg a few months after surgery for suspected
appendicitis. Unable to walk, stand or raise the leg from the
bed, give-away weakness, diffusely decreased sensation to
touch on entire right lower limb, without specific distribution,
no sensory loss on the abdomen. Abdominal CT scan, X-rays
and echography of hip joints were normal.
Twenty-nine-year-old, right-handed woman, born in east
Africa, precarious immigration condition since moving to
Switzerland 8 years ago, currently about to lose employment.
Inability to move left arm and leg, which can be raised from
the bed but uplift cannot be maintained. Can move fingers
and grasp, with sudden give-away weakness. Preserved
sensation except for dysaesthesia to light touch on whole left
hemibody, including trunk, with straight-cut demarcation
Thirty-six-year-old, right-handed woman, overworked from
familial and professional duties. Fatigue and depression for
2 months, progressive weakness of left limbs with loss of
dexterity and difficulty walking. Slightly decreased sensation
of left touch on left limbs and left trunk, with patchy
distribution on limbs and trunk.
conflict at work due to younger employees taking over. Back
pain after a benign fall without loss of consciousness, then
diffuse weakness of right hemibody, inability to move arm
or leg except for brief uncoordinated jerky attempts. Patchy
decreases of tactile sensation on right limbs.