S. Laurry:si Ed.

)
Progressin Rrailt Researrh.Vol. 150
lssN 0079-6123
Coplrighi (C 2005Elsevi::rlJ.V All rights rcserved

CHAPTER 23

HysterLcalconversionand brain function

Patrik Vuilleumier*
l-aboratorl,.for Behatioral Neurolagy and ltrwgingl of Cognition, Clfuic of Neurology & Department of Neurosciences,
& Educution Sciences, uniuersity of Geneua, Genetta, Switzerland
Ltniuersit),"trteclical Center, Faatttli of Psyainiy

Abstract: Hystericalconversiondisordersrepresent"functional" or unexplainedneurologicaldeficits such

as paralysisor somatosensorylossesthat are not explainedby organic lesionsin the nervous system,but
arise in the context of "psychogenic'nstressor emotional conflicts. After more than a century of both
clinical and theoretical interest, the exact nature of such emotional disorders responsiblefor hysterical
symptorus,and their functional consequeneson neural systemsin the brain, still remain largely unknown.
Aor*u.r, severalrecentstudieshave usedfunctional brain imaging techniques(suchas EEG, fMRI, PET,
or SPECT) in the attempt to identify specific neural correlatesassociatedwith hysterical conversion
symptoms.This article presentsa generaloverviewof thesefindings and of previousneuropsychologically
based accounts of hysteria. Functional neuroimaginghaS revealedselectivedecreasesin the activity of
in somatofrontal and subcorticalcircuits involved in motor control during hystericalparalysis,decreases
Such
blindness.
hysterical
during
cortex
in
visual
decreases
or
anesthesia,
hysterical
sensorycorticsduring
motor
or
of
sensory
stages
elementary
in
changes
any
signifrcant
by
accompanied
not
changesare usually
processingas measuredby evokedpotentials,although somechangesin later stagesof integration (such as
it:00 t"rplnses) havebeenreported.On the other hand, severalneuroimagingresultshaveshown increased
activation in limbic regions,suchas cingulateor orbitofrontal cortex during conversionsymptomsaffecting
difl'erent sensoryor motor modalities.Taken together,thesedata generallydo not support previous proposals that hysteria rnight involve an exclusionof sensorimotorrepresentationsfrom awarenessthrough
attentional processes.The1,1a11t"tseem to point to a modulation of such representationsby primary
affective or stress-relatedfactors, perhaps involving primitive reflexive mechanismsof protection and
alertnessthat are partly independentof consciouscontrol. and mediated by dynamic modulatory interactions betweenlimbic and sensorimotornetworks. A better understandingof the neuropsychr:biological
basesof hystericalconversiondisordermight thereforebe obtainedby t'utureimaging studiesthat compare
different conversionsymptomsand employ functional connectivityanalyses.This should not only lead to
improve clinical managementof thesepatients,but also provide new insightson the brain mechanismsof
self-awareness.
medical condition in which patients may present
with various somatic symptoms without a recognized organic illness, hysteria still constitutes a
poorly understoodclassof disordersat the border
betweenpsychiatryand neurology,with many different appearancesand names.A variety of classifications and explanations have been proposed
over the years,rvith different emphasison psychological or neurobiologicalfactors. but none is still

Introduction
Sincemore than a century, hysteria has ctlntinuousll' fascinatedboth clinicians and theorists inAs a
terestedin altercd statesof self-consciousness.
*Corrcspondingauthor. Tel.: 1-41 (0)22 379-s.381;
Far *41 (0)223795.402:
E-mail: patrik.vuilleumier@medecine.unige.ch
DOI: 10.l0l ti/S0079-6123(0ti0023-:

309

310

of hysterical
Fig. l. Illustration of paraparesis(astasia-abasia)
origin (drawn by Jean-Martin Charcot in the 1870s).

Fig. 2. "L'anesth6siehyst6rique",a cruel demonstrationofanesthesiain a patientat I-a Sal$triere, while in a stateof hysteria
(etchedfrom photograph by P. R6gnard, 1887,ks maladies
de I'esprit- Sorcellerie,magn6tisme,morphinisme,
6pid6miques
d6lire des grandeurs.Plon-Nourrit, Paris).

entirely satisfactory(seeHalligan et al., 2001for a

recent general overview).
In some rspects,the most important chang
sinceclassicaldescriptionsof hysteria by Charcot
and othersat theend ofthe l9th cntury (seeFigs.
I and 2) is related to the fact that the term "hysteria" was recently eliminated from the official
psychiatricterminology. Thus, hysteria is now referred to as "conversiondisorder" in the DSM-IV
classification (American Psychiatric Association,
1994,Diagnostic and Statistical Manual of lfental
Disorders),where it is definedas a loss or distortion of a neurological function (e.g., paralysis or
anesthesia)that is not explained by an organic
neurological lesion or medical disease,arising in
relation to some psychologicalstressor conflict'

but not consciously produced or intentionally

feigned.However,although the term'oconversion"
implies a specific mechanismwhereby a primary
psychological disorder is converted into bodily
s)imptoms,the exact pr@essesresponsiblefor triggering this phenomenonand altering the patients'
awarnessof their bodily state still remain unknown. In fact, when consideringthe possibleneurobiological changesassociatedwith hysterical
conversion symptoms, many of the current hypothesesare not very different from those elaborated in the l9th century. Moreover, in contrast to
other psychiatric conditions (such as depression,
anxiety, compulsion, or phobia), surprisingly tbw
investigationshave beencarried out to examine
whether the "functional" symptoms experienced
by hysterical patients might correspond to any

3ll

1:

i
!i

underlying "functional changes"in cerebralactivity, as can be evaluatedfor instanceusing a variety

of modern neuroimagingtechniques.
The aim of this chapter is to presenta general
overview of the relationshipsbetween hysterical
conversion and brain function, focusing particularly on previous attempts to determinesomenehysterical
urophysiological correlates of
conversion disorders. This review will primarily
concentrate on patients with unexplainedneurological deficits in sensoryand/or motor functions
(i.e., hystericalparalysisor anesthesia),sincesuch
disorders are the most frequent and most easily
describedin terms of specifrcneurological pathways. Similar approachesin other domains (e-g.,
visual loss, deafness,or amnesia) will also be
briefly mentioned,but other conversiondisorders
oopositive"symptomssuchas
associatedwith more
pseudo-seizureand abnormal movemntswill not
be discussedhere, sinceeven lessis known about
their possiblefunctional neural correlates(for review see Prigatano et al., 2002; Reuber et al.,
2003). Finally, a few studies have examined the
functional neuroanatomyof dissociationsinduced
by hypnosis (Maquet et al., 1999;Faymonville et
al., 2000; Halligan et al., 2000;Kupers et al., this
volume), but their implications for hystericaldeficits are still in part unclear and will be discussed
briefly
A better understandingof patientswith hysterical conversion has important implications for
severalreasons,both clinical and theoretical.First,
such disorders are very common in clinical practice, causing frequent problems in diagnosisand
therapy for neurologists as well as psychiatrists,
and resulting in important medical costs and major socio-economicburden for the patients and
their relatives.Second,conversiondisordersraise
important theoretical questions concerning the relationships between body and mind, and the neurobiological and psychological mechanisms
underlying self,-awareness.
From the perspective of clinical neurology,

diGdciatiitniffii@
performanceare not unusualin patientswith6f
.+.--_-__..-braln Fslons, a
organTc*t5iffi
organlc
osognosra,,
;tognOtit' *E-fg-bJ-F4!@

anlr

edgeand-evenexpligLgy_legya se]erl hanjgP

resulting from their brain lesion (Vuilleumier,

2000a, 2004; Marcel et al., 2004). Anosognosia
cannot be explainedby psychogenicfactors alone,
or by generalconfusion, but it is often associated
with a lack of emotional concern quite similar to
"la belle indifference" that has typically been describedin hysteria.Moreover, like anosognosiafor
hemiplegia,hystericalparalysisand hysterical anesthesiaare often thought to affect the letl more
than the right limbs, without this being entirely
accountedfor a more frequent dominance of the
right hand (Galin et al., 19771'Stern, 1983; Pascuzzi, 1994;Gaglieseet al., 1995),although a recnt mta-analysishas questionedthe existenceof
such an asymmetry(Stone et a1.,2002).It is also
intriguing io.tot" that theleurological @
ass@la

4 hvoiqt

pSral$
[o-!-esly--ttuila!ele]-.

amnesiq,.-of
Aa*ArcsareS6,^'butalso blindness,
-1995;-VriiliJumier,
aphasid
idigoir
O['enkei,"
AtlhoGtr such similarities do not indicate
20OOa).
any clear relationshipsbetweenthesedifferent disorders,theseparallelsbetweenneurologyand psychiatry highlight the fact that some behavioral
abilities may dissociatefrom the subjectiveexperienceof theseabilities,and that suchdissociations
are likely to arise from specificchangesin brain
furrction - be they due to certain types of organic
damageor to certain psycho-affectivestates.

Incidenceand evolution
Hysterical conversion disorders are thought to
representl4o/o of all diagnosesin generalhospitals throughout wsterncountries.This frequency
has remained remarkably stable across the past
decadesdespitemany important changesin medicine. Thus, a retrospectivesurvey at the National
Hospital of Neurology and Neurosurgeryin London, QueenSquare,from 1955to 1975revealeda
relativelyconstantrate of patientsinvestigatedfor
conversion or "functional" symptoms, ranging
from 0.85 to 1.55oh over decades (Trimble,
l98l). A similar result was found by another
study examining the diagnoses made on 7836
successiveoutpatient referrals at Charing Cross

312
Hospital between 19'17and 1987 (Perkin, 1989),
which revealeda stableincidenceof 3.8% of conversion disorders over the years. In Switzerland,
Frei (1984) also estimated that the proportion
and presentationof hystericalconversiondisorders
among patients seenin a large public hospital was
similar in the 1920sas comparedwith the 1980s.
However, it is important to emphasizethat the
type ofconversion disordersmay significantlyvary
acrossdifferent medicalsettingsand referral sources. This might explain why the incidence of hysteria may appearto vary in somedomains but not

are nver seen

fto", t9ggl. Neurologistsprobably seemany more
patients with relatively acute and limited symptoms, as comparedwith psychiatristswho tend to
seepatients with more chronic and multiform disorders (Marsden, 1986).Moreover, although there
is a good consensusbetween neurologists as to
clinical syndromesreflectingnon-organic diseases
(irrespective of which term is actually preferred to
describe these syndroms,e.g., hysterical, functional, or psychogenic),there is usually lessagreemnt among psychiatrists (Mace and Trimble,
l99l). Furthennore, although most nurologists
would agree with the DSM-IV statement that
"typically, individual conversionsymptomsare of
short duration'', many psychiatrist have rather
observedthat conversionsymptomsoften tend to
persist or reoccur in associationwith other psychiatric comorbidities and pathological personality traits (Ron, 1994;Binzer and Kullgren, 1998;
Stoneet al., 2003).
However, in most cassseenby neurologists, a
rapid remission of initial symptoms is observed
after appropriate behavioral treatment. The likelihood of spontaneousremission has repeatedly
been found to be -50-60Yo after I or 2 years
{Singh and I-ee, 199?;Binzer and Kullgren, 1998;
Crimlisk et al., 1998)or evengleater (Folks et al.,
1984). Among young patients (< 27 year-old),
only 3Yo have symptoms for more than I month
(Turgay, 1990).The duration ofeffective behavioral treatment in such casesis usually between
2 to X weeks (Speed, 1996).Soveralfactors are

associatedwith a favorable prognosis,

of presentation,onset
acutenesS
St

1998;Crimlisk et al., 1998;Stone et al., 2003).

Personality disorder appears as a particularly@Crimlisketal.
to identity potn[-qgs).lt is ilieiffiirnportant
tial risk factors during the initial evaluation of
patients,in order to preventthe developmentof a
more chronic handicap.

Body, mind, and brain diseases

A potential limitation to our current understanding of hystericalconversioncomesfrom a lack of
clear definition of the boundarieswith sornerelated disorders.From the perspectiveof psychiatry,a
number of problems are still unresolvedconcerning the terminologyand classificationof functional
symptomswithout an organiccause.In DSM-IV,
the concept of hysteria has been broken down to
different disorders, including somatoform disorders on one hand and dissociativedisorders on
the other hand, with conversion disorders being
consideredas a specific category of somatoform
disorders involving sensorimotor symptoms or
pseudo-seizures,
distinct from other somatization
symptornsor psychogenicpain disorders.Furthermore, depressionand chronic fatigue syndrome
would fall under other diagnostic categories,
although in clinical practice there is often some
overlap betweenall suchconditions. For example,
many patients recovering fto-j,o!y9lg!94
. Furthermore.
version disorders are defined as-d.gft"]q@'-@g
a ibecffit neurological Sl9lign-;gg[*qs---molQr
*ort-'--*

dtien.$h

sbmttisGnsory
. perception, Py9.!9-

consl(]fe(l _ll*:19._.-genlc memory loss ls ioniiGreifTniiead--under

6E-re''oqtt
rG-?1i-ofr
ine-"ataEmytor-"dissoaaf
-:

-_-r'

- *

:-

-':-c

"

bfain
t&G!l +emory is obviously.?ligu spe.sifrp
(see Markowitsch, 1999, 2003 for a
fuiiiiion
--.--'-:--..-.
*: .--'
:*

'-

313
associationsbetween hysterical conversion and
neurological diseasesare not only challenging
for current "dichotomous" classificationschemes,
but in fact might potentially provide valuableclues
about the neurocognitive mechanismsby which
awarenessof a function can be dissociatedfrom
actual abilities in a patient. However, the coexistenceof these neurological diseasesand conversionmight alsojust be a coincidence,purely due
to their high incidence or to any other general
stressfactors.
Nevertheless,despite these problems of definitions and associations,hysterical conversion is
only rarely falsely diagnosedfor an occult neurological condition. Although a few early studies
suggestedthat up to 20o/oof patients initially diagnosedwith motor conversiondeficits may subsequently develop a real organic neurological
diseaseexplaining their original symptoms (Slater, 1965;Mace and Trimble, 1996),severalrecent
*driii.3ig=.
studieshavenow clearlyestablishedthat suchrates
behavi6-i'
Itrsi-" de-"liy3fdifit:Ii'ld"*
overestimatedand that only l-5% of hysterwere
colifiFortIiii'rcnutmttti6n;aiqtF!-s99,-by--=qtipatients
ical
tol'ati"ratingscales-t+i9$'...[..1a-6.ffstq:*-s.dt-;C- may present with a underlying but
occult organic cause(e.g.,Crimlisk et al.' 1998;
hiviors' couiii-?ni'iiide exaggeration, secondary
Stoneet al., 2003).The rarity of organic diseases
gain expectancy,
oi non-ggSgigp"age$f offe
in current follow-up studies is probably
detected
patientsprefldTrlii.'InieiisfiriglyjhoTa[tyru-qf
due to severalfactors, including a better characterization of neurologicaldiseasesand the availadiffuse brain lesions
bility of more sensitive non-invasive diagnostic
procedures.

neuropsychological perspective of psychogenic

amnesia).Therefore,unlike DSM-IV, the International Classification of Diseases(ICD-10) of the
World Health Organization has included all sensorimotor and memory symptoms of presumed
psychogenicorigin under the same general category of dissociativedisorders.
From a neurological perspective, tU!-JgIl!
conversionmay sometimes
ins that
c6-eiistwith a real organ
conversron
;"*pluined-bythit brain hsio.rtg
Gowers
occould
6g9ij-already recognizedthat hysteria
brain
organic
of
casionally be a "complication"
disease,and Schilder(1935)wrote that brain dysfunction could sometimesinduce "organic neurotic attitudes". More recently, 1gi4tnggf$-$-9lp-U
Eames (1992) described a seriesgf ,!9Z,g,g.ge!!s
fr65 were ad'iiiittecltd a iEhebilitation ward 4ndat
patients exhibited
-ihb
.._+

.c

----#-re

- > - * . -

(Eames, 1992). Similarly, Gould et al. (1986) reported that among a prospectiveseriesof 30 patients with an acute hemispheric stroke, "atypical
signs" usually suspectedto reflect non-organic
"functional" origin were observedin approximately 20% of cases(e.g.,changrngdeficit, patchy sensory loss, or "give-away" weakness). Finally,
multiple sclerosis (e.g., Nicolson and Feinstein,
1994) and epilepsy (e.g., Devinsky and Gordon,
1998) constitute two other frequent neurological
diseasesin which not only some truly "organic'o
manifestationsmay sometimesbe difficult to distinguish from non-organicdisorders,but somepatients may also present with a combination of
apparently both "organic" and "psychogenic"
manifestations at the sametime. These occasional

History and theories

The term of "hysteria" was forged by the ancient
Greeks to indicate that physical disturbancesin
the uterus were the primary cause of psychic
symptomsin women. By contrast, all modern theoriesof conversiondisordersacknowledgethat not
only both men and women may be affected, but
also a primary psychologicaldisturbanceis probably responsiblefor triggering subjectivephysical
s5rmptoms,and perhaps also {br triggering some
associatedchangesin the neurophysiologicalstate
of the central nervous system.However, the exact
psychologicalfactors to blame still remain disputed, and the possible implication of a particular

314
brain functions in generatingan abnormal physical'experiencestill remainsunresolved.
Since the l9th century, a myriad of different
theories have been put forward to explain how
hysterical motor or sensorydeficits might be implementedin the brain in terms of specific anatomical circuits, or in relation to putative cognitive
architectures.However,most of thesetheoriesrest
on purely speculativegrounds,and little empirical
work has been conducted to test theseneuropsychological hypotheses.Although it is beyond the
scopeof this chapterto discussall of thesetheories
in great detail (for more complete reviews, see
Merskey, 1995;Halligan et al., 2001),a few conjectures on the neural substratesof hysteria that
have been proposed by influential neuroscientists
will be briefly illustrated. Although many old theoriesare susceptibleto misinterpretationsbasedon
our current knowledge,it is interestingto note that
some of them might still appear attractive if they
were rephrasedusing more modern conceptsand
terminologies f.rom current cognitive and aflective
neurosciences.In fact, severalrecent hypotheses
about the possiblecerebralcorrelatesof hysterical
conversion, proposed on the basis of new functional neuroimagingresults,can be traced back to
strikingly similar ideas that were elaboratedmore
than a century ago, but naturally phrasedin terms
of models of brain physiologyfrom that time.
One of the first and best known hypothesison
the cerebral mechanismsof hysterical conversion
was proposed by Charcot in the early 1890s(see
Charcot, 1892; Widlocher, 1982; White, 1997).

ons within the central nervous system,afGiting activity of motor or sensorypa[h@ without any prmanent structural damage. Hysteria
was thus consideredas a "neurosis" among other
functional illnessessuch as epilepsyor Parkinson's
disease.Charcot suggestedthat such functional
changesin the nervous systemcould be induoed by
particular ideas, suggestions,or psychological
states,as demonstratedby the effect of hypnosis
on hystericalsymptoms.Thus, hystericalparalysis
oomental
could result from an inability to form a
image" of movement,or insteadfrom an abnormal
theseideas
"mental image" of paralysis.In essence"

are echoingthe more recentproposalsof a selective

impairment in action "representations"for intentional motor planning (e.g., Spence, 1999), although both the terminologyand conceptsof brain
function have considerablychangedsincethen.
At the same time as Charcot, Jun:lj!!9{)gbg
orooosedthat hvstericaldehcitswere the result of
- : - 4

"fixed ideas" that could take control over mental

dr motor functions. Flowever.he added that such

iZ-eaicould ariseat an u
inducing a dissocia

between distinct do-

eftry-o:!--ftltgEt (one becomingdominatedby

the unconscious fixed idea). Such views paved the

way to the classicaltheory of Freud and Breuer

(1895),later refined by Freud alone(Freud, 1909),
who formulated a purely psychodynamicascount
with only minimal referenceto the nervoussystern.
In brief. accordinsto Freud and Breuer.hvsterical
d"
and

transformedinto bodilv complaintswith symbolic

did not
vhlues.For this reasbn.hvstericaldef-rcits
obey anatomical constraints as observedwith organic neurologicallesions.This view has then naturally led to the term of "conversion disorder",
and in many respectsis still prevailingtoday. Only
later did Freud emphasizethat the unconscious
affectivemotives usually had their origin in sexual
concernsfrom early childhood.
An attempt to integrate thesedifferent cerebral
and psychologicalperspectiveswas made by the
FrenchneurologistBabinski in 1912,who also first
described anosognosia a,fter brain damage two

sequent interpretation stage. A more sophisticated

neuro-anatomical scheme was later proposed by

1933),who
Pavlov (1,928-1941,

315
cerebralcenters(possiblymediatingemotionalor
----rearncdcondrtronedresp!!!gql_!q!!d lelg to a re-

lsignals from limbic systemswithin orbitofrontal

,,and cingulatecortex during volitional movements
active inhibition of cortical inputs imposed by_l!he_ i (Marshall et al., 1997).Again, such inhibition was

_---ffi

lascribed to unconscious motivational factors

frontal corte>i This inhibition was responsible for

Finallv- from the mid-1970sto mi,

ing to the influence of the researchin split-brain

fitGtrffifalysis
or anesthesia,whose duration
was proportional to the amount of resourcesdepleted in the individual.
A number of more recent accounts based on
neurophysiological speculations have similarly
proposeda role for inhibitory or "filtering" mechanismsas a likely neural substratefor generating
hysterical conversion deficits. Thus, in line with
Babinski and Favlov, Sackeimet al. (1979)-arld
Stern ( I 983) hvooth"sizffffiT6iilor
motivational processesmight induce a selectiveblock----+--:-.__-.%
ase(or clrstortlon)oI sensoryand/ormotor rnpglls,
=#
resultlngln therr exclusronlrom conscrousawaren"rr. i greater involvement of the right hemisphere in emotion might account for more
frequent symptoms on the left side of the body
observedin some series(Stern, 1983;seeStone et
suchas
t972
a1.,2002).Other researchers

ical

r
(Galin et al.. 1977). The greater occurrence of left
r#
hemrbodV drsorders led to the ldea that the trans#
IEiof sensory or motor inputs mieht btimpairg!
between t
uvsrygg-_in_e-qg-

impairment in the rigbt (Stern, 1983)or left hem-

l*i;tt"."*fpm:H;itiffi..._-=4

uncuons
mechanisms
the level of thalamic mrclei.under the influence

gt-qt!g!@-&iqq-(*s 4-lo-$sttaeq4..&:ri
gl.

1999),whereasSpiegel(1991)insteademphasized
f_e_

__

anattentlonalmechailsm_..l+e^4_!Atg4*b:"tb9=*a!!ejr-

or cingllatg.-aql[er.Likewise,KLtpjryn"1[!$CI
aiEriCii-thaiconversiondisordersmlelt'ilGlve t

dysfunction in the 'omonitoring and controlli4g

.,.#,*.-**@

@..->===*

nEsf'. idulrin'sil i disso

diiaaifif b:r?o;sri5G
ciafivtiltilFtil,t imffi
"ff"ffi voluntary actlon,
nence ot' perceptron a-nd/or
-.,-.."ry

presumably tnrough abnorrnal coordlnatlon oI

particular neurocognitive modules. Oakley (1999)

also referred to neuropsychologicalmoAels6ffitentlon to suggestthat dunng hystena,an lntern4l

motor
tation
from awarenessbv a
i"ioiuine
atten
oenti6f-Effi
ontif
excutive
ffi;GtiotiITiste-

uiiud.[r nuir rfi rin; ; J1

f6ritaFnntcifr'su6i6
"
""
(1997)
D='dvit
rq99)
a-nifMurrii,a-ll"una
f

"oil"ugu;
and colleaguesf
, as well as Spence(1999)and Spence
. (2000) also speculated that representationsof N
i motor action miebt b inhibited in patients with I
I hystericalparalysis,with activation in their motor I
\ cortex being actively suppressedby abnormal \

D:-fiowevei,oniy

"FrqS performance on
very l
n-urop-pfiological tests was otTeredin support
of theseinterhemispherichypotheses(Flor-Henry
et al., 1981).
In sum, most theoretical models trying to link
hystericaldisorderswith specificneuropsychological or neurophysiologicalmechanismshave essentiallybeeninspiredby speculativeargumentsor
analogieswith general models of the brain and
mind, rather than by the convergenceof systematic
empirical research.It is striking that relatively few
studissover the past decadeshave exploited neurophysiologicaltechniques(seebelow) that provide objectiverneasuresofbrain functions (suchas
electroencephalogram(EEG) or brain imaging),
allowing a better identification of neurobiological
factors associatedwith hystericalconversion.This
is all the more surprising since the well-defined
neurological-like symptoms of conversion (e.g.,
paralysis, anesthesia,blindness,etc.) should potentially be amenable to a precise investigation
with well-definedpredictions about the site and
type of neurophysiologicaldysfunction. In particular, the advent of new tirnctional imaging techniques should now allow a refine assessmentof
functional correlates in brain activity potentially
associatedwith hysterical conversion, and thus
go beyond the dichotomousquestionof "organic"
versus "non-organic" disease. A better knowledgeof such functional correlatesmight provide

316
important constraints on psychodynamictheories
of conversion,with greater biological and neurological plausibility, and might also improve the
clinical assessment
and managementof patients.

results suggesting a paradoxical amplification

rather than attenuation of tactile evoked responses during hysterical anesthesia(Moldofsky and
England,1975).Taken
the common

correlatesof conversion
Electrophysiological
disorders
SinceEEG provided one of the first tools to measure brain activity, a number of studies from the
1960sto 1970sonward have used this technique
and other related:electrophysiologicalmeasuresto
investigatebrain functions in patientswith hysterical conversion. These studies can generally be
consideredin two broad categories:those aiming
at demonstrating intact electrophysiologicalresponsesdespite subjective functional losses,and
those trying to determinesomeabnormal pattern
correlating with functional symptoms.

or instance" standard soma

potentials (SEPs),visual evokedpotentials
effi
(VEPs), or brainstem auditory evoked potentials
(BAEPs) are usually found to disclosenormal amplitudes and latenciesin the prsenceof subjective
anesthesia,blindness, or deafness, respectively
(e.g.,Howard and Dorfman, 1986;Drake, 1990).
These findings clearly indicatejhalpd_mety sens-ry pathwaysare both qtnrcjurally-andftuqtiqoallfi-n6Et in the patients. In the somatosensory
been studied using
@
(MEG) in order to dismagnetoencephalography
tinguish activationsin primary (SI) and secondary
(SII) cortical areas (Hoechstetter et al., 2002),
since data from healthy people typically show a
differential modulation of SII but not SI activity
by attention and ra-sk-relatedfactors. However,
MEG results in patients with hyrloig[tpg@
loss 6i5o showe6; ndffiaf patter":of rfiponse r"t
the characteristicconpprr"nt. g"oeruiediiiU"otn Sf
and-Sil, controlaterally and ipsilaterally to the
daficii:'I
pafrlats relative to
sponffi-wli?bservedG-tire

rieaft[yCn{eclT,inTotfr-Srant su@-ffiCiGr
eiEl- 2002I.TFGiddaialirnneigewithearlierEEG

b_,
ly early
stagesof cortical processing.Moreover, theseearly
SEPsmay not necessarilycorrelatewith subjective
perceptualexperience,since SI responsescan still
be elicited by unperceivedstimuli in patients with
brain tumors involving the parietal lobe but sparing SI @reisslet al., 2001).Also, in patientsin a
vegetativestate, devoid of any consciousperreption, preservedSI activation has beenshown using
functional imaging and simultaneouslyrecorded
SEPs(Laureyset al., 2002).Thesedata emphasize
that SI activation does not necessarilymean conperception.
scioussomatosensory
On the other hand. a few other studies have reported subtle changes in paradigms that were
slightly more sophisticatedthan just detection of
simple tactile stimuli. For instance,tactile stimuli
closeto percepual threshold may fail to produce
normal evokedpotentials in patients with sensory
conversion s)mptoms, even when stimuli above
threshold still produce normal responses(Levy
and Mushin, 1973). In addition, anomalies in
the rate of habituation to repeatedstimulations
were observedin hystericalconversionusing SEPs
(Moldofsky and England, 1975)as well as skinconductanoe reactivity (Horvath et al., 1980).
In normal subjects, responseswere found to decreaseover time when comparing late blocks of
stimuli relative to initial blocks. Such habituation
could also be observedin patientswith high levels
of anxiety (Horvath et al., 1980), but was not
present in patients with hysterical conversion,
indicating that the latter tended to process
frequent and exprcted stimuli as if they were
still novel.
-case stud
rted
Another rcent
evoked Dotentia

ri5e P500 conBonent (Lorenz et al.,

component is typically elicited by

Tery""tfra

317
novelstimuli in an "oddball" task or by infrequent
targets within a stream of successivestimuli, and
presumablyreflectsa normal orienting responseto
relevant stimuli. Lorenz et al. (1998) designedan
elegant EEG paradigm in which they repeatedly
stimulated the unaffectedleft hand of a man with
hysterical sensoryloss on the right hand, and occasionallyapplied a "deviant" stimuli on either the
affected right hand, or on another finger of the
same unaffected left hand. The patient sbowed a

normal P300response
for dEfr6-ntJtffii-on:iG

ffid*painful tactile stimuli, demonst

$P*qlilg !e:seje:

infrequent stimuli on that side (i.e., Iike the conversion patient), a P300was still normally evoked
oy tnese o"uran@
hand, indicating that a reduction of P300 in the
patient was not due to malingering or control by
voluntary inhibition.
Interestingly, reducedP300 responsesto tactile
"oddball" stimuli have also been observedin patients who present with a "segmental exclusion
syndrome" (Beis et al., 1998).Thesepatientsexhibit an abnormally prolongedunder-useand pain
of their upper limb after sufferinga relatively minor injury to peripheral body tissuesin one hand
or one finger, and such functional exclusionof the
limb cannot be explainedby the severityof injury.
Although this syndromeis different from conversion disorder, it has similarly beenconsideredas a
maladaptive deficit with a partly psychogenicorigin, and abnormal P300responseswre interpreted as reflectingsomekind of attentional inhibition
or hemineglect in motor behavior (Beis et al.,
1998).Accordingly, anomaliesin P300 have been
f,oundfor undetectedstimuli not only in patients
with spatial hemineglectafter right parietal lobe
lesions(Lhermitte et al., 1985),but also in patients
with Parkinson's diseasewith impairments in intentional motor planning (Kropotov and Ponomarev, l99l; Sohnet al., 1998).

Evoked potentials in other sensory modalities

such as vision and audition have been less often
studiedbeyondelementarysensoryresponses,perhaps becauseconversiondisordersin such modalitiesare lessfrequent,more variable,and/or seenby
physiciansother than neurologists.In patientswith
functional blindness,a P300 was still evoked by
unreported visual stimuli but with smaller ampli
tude (Towle et al., 1985).By contrast,a study of
auditory processing in patients with hysterical
deafnessrsported a reducedP300 response,with
preservation of earlier Nl and N2 auditory responses(Fukuda et al., 1996).Some anomalies
were also reported in patients with various somatization symptoms for the auditory mismatch
negativity (MM1.0, which is normally evoked by
deviant stimuli in a series of repetitive sounds
(Jameset al., 1989). Still other studies reported
more generalchangesin EEG spectrain patients
with conversionand somatoformdisorders.includdistribution over
right and lefllrontal
y, motor conversiondisordershave been
investigatedby transcranial magnetic stimulation
(TMS), typically
6voked
tials
-+_* :+/

over the motor co

ffisfiis et a\., 1999).Again,

suchresultsare usually taken to indicate that motor pathways are structurally and functionally intact in thesepatients.Only one recentstudv &und
a decreasedexcitabilitffit

*g*yU--.t'"e-q,e_e_;"r'!r?F
Fgt-q$p-ry:.:1ygf
(Foong
eral left hystericalweakness

bffih6sC"cb

et al., 1997b),

slds"did-rat

changewhen pa_treats
recoveredfla$.qh-eil lveakness.There is also anecdotal evidencethat conpatients may show an abnormal
ffin
contingent negative variation (CI.W) component
in EEG, which is normally evoked during motor
preparation in responseto a cue prior to an expectedto-be-judgedstimulus (Drake, 1990).
Considered all

are

ical dat
af-

absenceof
Iectrngth_p-!ngg-sensoryor pnmary motol$-Instead.
#
Ems
anv chan-sesln-biain function

318
associatedwith conversion misht involve hipher
_

flow changesduring a restingstateor during a task

l_"dlo{.-pl-o-9"-e..s_s.lug,93._lppJLe$eg=*.1-_*F!irq
period. The first of such SPECT studieswas carf---i

sensoryandJ_q_1-mo.Jpr.--SiSnal$._=.a1q._.ig!-e"g"r.p"!_ej
ried out by Tiihonen and colleagues(Tiihonen et
di'tli moie'ioriipir*' information related to the
al., 1995)in a woman who had a long history of
meaningi nd-l.q1i-rer.e-i-drleft hemisensorydisturbancesof presumedhysterf-;ji!sdi-asa;eld;,
(e.g.,motivational significanc,novelty, expectedical origin, and reported both decreasesirytg4
ness, etc.). This might relate to the reduced
p_gg"t"i"9tt""{y-."Afg9'_".g'*
A
P300 responsefound in a few different studies
tivity when the affected hand of the patient was
..r::"'l-.-:-*;
--*i.-*.*--"..--.
using different paradigms. However, EEG and
s!,iuulateClascompaEd=-ffilFilffiiF sym'metiiC
MEG investigations still remain remarkably
patternafter recovery).However,this singleobscarce, and reported findings have too rarely
servationwas mor qualitative than truly quantibeen replicated to allow firm conclusionsabout
tative, and not statistically analyzed. Similarly,
any putative neural correlatesofrspecifrcconveranother SPECT study reported a seriesof five pasion symptoms.
tients with heterogeneousconversion symptoms,
including not only limb weaknessbut also vertigo
and gait disturbances $anci and Kostakoglu,
Hemodynamicbrain imaging
1998),in whom brain scansat rest showed a reduction in activity for several cortical regions,
Over the past l0 years, functional brain imaging
predominantly in left parietal and left temporal
has literally exploded into innumerable paths of
lobes,but with a great variability acrosspatients.
new researchon the cerebralbasesof various beA more systematicSPECT study was conducted
havioral functions in humans, including not only
in our own center, in a group of sevenpatients
perceptualand motor processesaccessibleto exwho wereprospectivelyselectedbasedon the presternal objective assessment,
but also much more
enceof an isolated and oofocal"motor conversion
complex mental operationsrelated to internal afdisorder, with a recent onset and short duration
fective states(Damasio et al., 2000),perceptualor
(< 2 months)(Vuilleumieret al., 2001).Strict semotor imagery(Kosslynet al., 1995;Ehrssonet al.,
lection criteria were used including: unilateral
2003),and ven unconsciousprocessingor prelbrweaknessin upper and lower limb, with or withences(Elliott and Dolan, 1998).This functional
out sensoryloss in the sameterritory, but without
brain mapping approachhas.alsoboensuccessfully
any other psychogenicor neurological symptoms
extendedto a variety of psychiatricconditionssuch
(such as headache,vertigo, blurred vision, etc.),
asdepression,obsessive-compulsive
disorders.phowithout any past history of major psychiatric or
bia, pos{-traumaticstressdisorders,schizophrenia,
neurologicaldisease,and without any organic leor hallucinations (e.g., Frith and Dolan, 1998;
sion as determinedby extensivemedical investigaParsey and Mann, 2003; Kircher, this volume).
tions (i.e., brain and spine MRI, SEPs.MEPs,
Surprisingly, however, very few neuroimaging
VEPs, EMG, etc.). These patients were followed
studies have been performed in patients with
up for 6 months after the onsetof their symptoms,
conversion symptoms. despite the fact that sucb
and underwent brain SPECT scanning in three
symptomsmight often be very well suited to neurodifferent conditions: (l) a baselinerest condition
imaging investigations.
(To), with eye closed and no stimulation, rvhen
Most neuroimaging studiesof conversionused
motor symptomswere present;(2) a passiveactiSPECT (single photon emission computerized
vation condition (Tl), with bilateral vibrotactile
tomography) or PET (positron emission tomostimuli (50 Hz) applied to both the affected and
graphy),and t-ocusedon motor rather than sensory
unaffected limbs simultaneously, when motor
conversionsymptoms.Thesetechniquesallorv onsymptomswere prsent;and (3) the sameactivaly a few brain scansto be taken and provide an
tion sondition (T2), again with bilateral vibrotacestimateof activity averagedover severalminutes,
tile stimulation of the affected and unaffected
indirectly obtained by a measureof cerebralblood
limbs, after motor symptoms had recovered

319
(in four patients; three others had persisting or
new symptoms at 6 months follow-up). The
rationale of vibrotactile stirnulation was to provide an indirect activation of both sensory and
motor areas in the brain (since such stimuli
provide inputs not only to cutaneous but also
deep tendon fibers), in a completelypassive,symmetric, and reproduciblemanner. All voxel-based
analyses in this study were done on a group
basis using statistical parametric mapping (SPM)
(Friston et al., 1995).
A first analysis comparing activation by bilateral vibrotactile stimulation to resting baseline
(Tl >T0) revealedrelatively symmetricincreasein
cerebral blood flow in frontal and parietal areas
involved in somatosensoryand motor functions,
both ipsilaterally and contralaterallyto the motor
conversion symptoms (Vuilleumier et a-1.,2001).
This result convergeswith previouselectrophysiological data indicating intact sensorimotorpathways in such patients.A second,more interesting
analysis compared activation by bilateral vibrotactile stimulation after recovery relative to the
samestimulationduring symptoms(T2>Tl), providing a direct measurof changesin brain activity
specificallyassociatedwith hystericalmotor weakness,irrespectiveofany other distinctivepattern of
brain function in these patients (e.g., related to
depression,anxiety, or other personality characteristics). This

rPPhYsrsJ-oCY

4!l'_l"eg9l_tggl9!.9:f
ffinot;eem

gry_qetgg_grthese
supprsre'
ffa:-

(as preniouslfffr]oSul:-Iiidwig,
1972; Sierra
and Berrios, 1999)but instead appearsenhanced
(Moldofsky and England, 1975: Hoechstetter
er a1.,2002).
These selectiveanomalies in subcortical brain
regions during motor conversion (Vuilleumier et
al., 2001)are intriguing sincetheseregionsare interconnectedinto functional loops forming a cortico*striato-thalamo-cortical circuit which is
critical for voluntary motor action (Alexander et
al., 1986) and since the striatum (especiallycaudate nucleus) constitutes an essentialneural site
within such loops where motivational signalscan
modulate motor preparation activity (Mogenson
et al., 1980;Kawagoeet al., 1998;Haber,2003;see
Fig. ). It is therefore conceivablethat thesecircuits might becomefunctionally suppressedduring
hystericalmotor conversionunder the influenceof
a particular affective or motivational states, resulting in an impaired "motor readiness"or impaired "motor intention" for the affccted limb(s).
Notably, in humans,focal tesions(e.g.,stroke) affecting the basal ganglia (Watson et al., 1978;
Healtonet al., 1982)and thalamus(Laplaneet al.,
1986;von Giesenet al., 1994)are implicatedin a
syndrome of unilateral motor neglect, in which
patients present with impairments in motor use
that cannot be explainedby primary weaknessbut
crases ln
rather reflect a lack of motor intention or planin the
ning. Sucha lossof motor intentionhas also been
motor defrcit" rv
implicated in the failure of some brain-damaged
patientsto becomeaware of their (real) paralysis,
her, the degreeof decreases
in caudatenuu"dJE
i.e., anosognosia for hemiplegia (Gold et al.,
"l""S
with ilii-oqlation oF
1994;Vuilleumier, 2000b),suggestingthat subjecwa-J-ffififfim-"laGd
tive experience of conscious motor action and
"Uf'gsfi.{';iffittre*t'"
volition might be linked to basal ganglia or
regions in patients who did not rcovr6 months
thalamus function. Also in support of this, direct
later, relative to thosewho subsequentlyrecovered
(Fig. 3B). This reducedactivation in contralateral
electric stimulation of lateral thalamic nuclei
by depth electrodes may trigger contralateral
basal ganglia-thalamic circuits might therefore
provide a plausible substrate for the subjective
movementswith a subjectiveexperienceof voluntary action (H6caenet al., 1949).Finally, changes
motor conversion deficits. Finally, we also perin basal ganglia activity have also been impliformed a reversecomparisonof vibrotactile stim.cated in immobilization behaviors exhibited by
ulation during symptoms relative to recovery
jnssjn-sJess.e.$.
animals to protect an injured limb (De Ceballos
Ol>T2).Tfril_rbpy_qd."o-ply-1gdd.
m1!o!ep=9.{y,_cp$-er_a"an!rp!4Je$l_ts-t}ssgmp.l.oms,et al., 1986).

o:=

320
Decreasedactivation d uring co n0alatelal sensorlmotor symptoms
relative to recovery (T2 > Tl)

Putamen/Pailidum

Caudde

Thalamus
o
o
6
dl

P
E
(D
o

Deficit

Dffcit Flecovery
(r2)
$1)

(A)

(rl)

Recovery

{r2)

Deficit
(r1)

Recovery
ff2)

symptoms{scanTl)
Ilecreasedacdvafiondurlngconoalateral
predicfing clinicalevolution

s0
sfier4montfts:
Symptoms
lt
d)

80

g
70

$!

eenistentln=3palienG)

ffi

(n=4 patients)
lmproved

60
(B)

50
Cilc,/e Thalamus

Fig. 3. Changesin brain activity associatedwith hysterical paralysis. (A) Selectivedecreasesin activity were found in the thalamus,
caudate, and putamen (upper row) in the hemispherecontralateral to the limb affected by sensorimotor symptoms. Measures of
regional cerebral blood flow (rCBF) were obtained by SPECT scans in seven patients (ower row) during bilateral sensorimotor
stimulation by vibrotactile stimuli when their symptoms were present(f I scan),and in four patients when their symptoms had abated
3-4 months later (I2 scan).Brain activity was decreasedin all thesesubcortical regionsin all patients in T'l as compared with the same
regions in T2 or with homologous regions in the bcmisphereipsilateral to the symptomsin T1. (B) Such decreasesin the thalamus and
caudate (but not in the putamen) were more severein the initial scan(fl) in the three patients who had persisting symptoms at followup 4 months tater, as compared with.four other patients who had recovered,suggestingtlat the severity of decreaseat the time of
initial symptoms, may predict the duration of their symptoms. (From Vuilleumier et al., 2001).

321

(r

Motor
commands

Modulations
bymofivafon f,
or emotlon

,/
(f

ffi

\\

Sbiatum

Thalamus

\\\

\t-*

Motor
execut'on

r-'r

\-*"(
it[[[E\

---)/;

\ ---'',-'
|

fVL-z
fi)

)-

TUIUIIETI

& oallidum

prinErymotorarea

E Supdemertarymotorarea
ffi Prsmotorarea
lffi Preftontalcortex
Linbicarea
I

Fig. 4. Schematic illustration of cortico-subcortico-cortical loops. These circuits link various areas in frontal cortex to the caudate
nucleus,putamenand pallidum, thalamus,and then back to the cortex,allowing a modulation and coordination of motor commands
initiated in the cortex during movementexecution-but presumablyalso during more complex cognitive operations. Such loops provide
severalneural sites, particularly in the striatum/caudate, where neural signalscan be modulated by allective and motivational inputs
from many other brain regions (such as orbitofrontal cortex, cingulate cortex, or amygdala), constituting a cerebral systemthought to
be critical for the integration of volitionally guided and emotionally triggered expressionsof behavior.

Other functional changesin brain areasrelated

to voluntary motor control havebeensuggestedby
two PET studiesin patientswith hystericalmotor
deticits (Marshall et al., 1997; see also Spence,
1999;Spenceet al., 2000;for review).Marshall et
al. (1997)studied a singlepatient with a history of
unilateral left leg weaknesspersistingmore than 2
years, in a task requiring either to prepare or to
execute movements with either the left (affected)

produced i nclqglgd_agUyalrp:Lof--:rentroge&l
fiffiffi*Aortex, including right anterior cingulate
dndTEmbrbitttfibii&l cbffi;*fii"h
.I,.
duiill| irioVeinnt-biEtlirtion- ilith the "inorr"*
unaffected
ri-ghtEg. II ivasccincludCtiihat during initiation of
m6ttii"action on the affected side, some signals
might be generated in the limbic ventro-medial
frontal and cingulate cortex due to affective or
motivational factors, and that such signalsmight
actively inhibit the activation of motor cortex,
preventing the execution of normal movements
(Konishi et a1.,1999;Paus,2001).However,it is
possiblethat this increasein frontal ;ndqlguEg

afnvationmghr
grqnifr pncm tneseregions
JricTr-as-diffig-ulty-,
tbimE-oTleilure_-&us-gt-al-.--lt9-8;van.V.een.et
200-a)-or
itiriflict (Dehaene
et al., 2003;Badreand
WeEner,ZO0+;due to ambiguoustask demands

ti
ti
ll
.jl
I

(i.e., "try to move even if you cannot"). In any

-

_- - __J_

- - - a -

te cortex actlvatlon.) was

study examining a single

healthy subject who perfonned the same motor

preparation and executiontask as in the preceding
study, but now 49. hlp1ggg_qUgglstiol of unilateral paralysis (Halligan et al., 2000).Although
this result suggestssome similarity betweenhypnotic suggestionand conversion symptoms, this
classicrelationship (entertainedsince Charcot by
many others: see Bliss, 1984; Spiegel, l99l;
Oakley, 1999)may still not be firmly established
(see,e.g.,Persinger,1994;Foonget al.,1997a).
A subsequentPET study therefore compared
three patients who had hysterical weakness(two
patients in left arm and one patient in right arm),
with four healthy control subjectswho were instructedto feign motor weaknessof the right hand
(Spenceet al., 2000).All participants had to perform regularly paced movementswith a joystick
held in their affected(or pseudo-affected)
hand. As

Patientswit! co
1I9!P,
-+

dgglgl*4activity in left prefrontal cortex relative

to the
decreasedactivity in-rignt "prefroiittfE6itex-rEti ve t o converSi6-fr
T-tfi 6if ilTlie aut hors suglEildd
that leTtfionlatd66ffiIffi*n
in hysteria may reflect
the role of thesecortical areasin motor planning
(Spence,1999).However.lqft frontal hypoactivity
^.-ru
is also frequently seenin other
conditions such as
-Ali"patfiil
-2T031

@evueis,
SpryssEu-

hystericalconversion,concerningde{icitsin somatosensoryprocessing(Mailis-Gagnoner al., 2003)

and visualpejgpption(Werringet al., 2004).MailisGagnon et al. (2003) studied four patients with
chronicdeficitsin sensationof touch and/or chronic
pain a"ffectingone or more limbs on one or both
sides,while they undenvent fMRI scanning during
blocks of brush and mildly noxious stimulation on
their affected and unaffected body parts. Results
revealeddifferent patterns for different brain areas.
First, unlikestimulationon intact limbs (whichwere
alwaysperceivedand reported),both noxious and
non-noxious stimuli on the une"Al;u-f*rri"r,

in t[i"

Study had a history of depression,although none

neededtreatrnent at the time of scanning.Moreover, theseleft frontal anomaliesdid not provide a
direct functional substrate for the contralateral
motor deficit itself, sincethe affectedside differed
acrossthe patients.But nevertheless,
someimpairment in internal representationsof voluntary
movementsis likely to be presentin thesepatients,
as also suggestedby purely behavioralstudiesthat
comparedmental motor imagerywith the affected
and unaffected hands in individuals with motor
conversion(Maruff and Velakoulis,2000; Roelofs
et al.,2002).
Finally, only two recent studies used functional
magneticresonan@imaging (fMRI) to examinethe
functional patterns of brain activity associatedwith

.+-

---.---"-g_\

ye!@&t}djgp-t!:e!e
thethalamus,
insular,
inferiorfrontal,
andposterior
-"-SeCoid,-'
-Coitic<ii.
-arenl:iingnlatb'
sbme
tCfititd
.!--;-..fu
Dy percelved qtlmul! qp_tq_e_4tag!lunb were apparently deactivated during stimulation on the affected

linb (ieltaiv,tto a iestingbtiafieTithout;t

stimulation).includinsoartsof contralateralSI and
SII as well as bilatelal pfefrgg!4!_qrys. Thir.d,
anGrioi cinzulatecortei showtr;GtG;
ictivation
during unpeiceived/unreported
stimulation
on the
"iFan -duriiiE
affected linib
bfriiEinfl sfrfriliffi-n
on the"unaffldat6dsida:'Fiffi iV; sefefr f ft$ffifi
in prefrontal addp-arietalcortex (includinga superior part of SI) appearedsimilarly responsiveto
unperceived and peroeived stimuli, although the
commonalitiesof such activations was not formally
tested.
vation reported for some arasmay correspond to
inhibitory effects,or be more
app4lqnllh4luq4"L{U
ion. [n
sensory symptoms in these patients might have
partly resulted tiom objective neurobiological
changesin a distributed somatosensorynetwork,
which the authors tentatively attributed to attentional and emotional processestriggered by mild
injuries or painful conditions, and perhaps
exacerbatedby a preexisting wlnerability (MailisGagrronet al., 2003).The complex resultsfrom this
study might partly reflect the heterogeneity of
patients and the fixedeffect statistical analysis
used in a small sample, but it is notable that increasedactivity in cingulate cortex was also found
in the critical condition involving stimulation of
the aflix,ted limb, as previously found during

an attempt to move the parulyzed limb in

motor conversion or hypnosis (Marshall et al.,
1997;Halhganet a1.,2000).Likewise,a recentfMRI

other hand. increasedactivity was found

cortex,
=#-----@

temporal poles as well q;

on
fitrs"Tftffi

different from previous findings for sensorimotor

deficits, this pattern was again interpreted as generallyconsistentwith the ideathat conversionmight
involve inhibitory modulation of visual processing
through increasesin the activity of limbic areas.
Altogether, thesenew functional neuroimaging
data provide compelling evidencethat "functional" symptoms in patients with hysterical conversion may at least in part correspond to specihc
componentsin brain function, potentially underlying an abnormal awarenessof perceptualand/or
motor abilities. Here again, there are still too few
studies, using different paradigms in different
types of patients, such that no definite conclusion

tivation as

r, further systematicstudies are neededto

better teaseapart the neural correlatesassociated
with subjectivedet'icitsthemselvesfrom other aspcts potentially associatedwith coexistingdisorders, such as changes in mood or anxiety"
personalitycharacteristics,expectations,attention,
coping reactionsaswell asany activity conceivably
related to unconsciousaffectivemotives and conflicts that were postulatedby Freudian psychodynamic accounts.

More questionsand nervdirections

A better understandingof functional changesin
brain activity during hystericalconversion is certainly important not only becausethis may yield
new insights into neural correlates of subjective
experienceand awareness,but also becausethis
may provide new constraints on theoretical accounts of conversion,in a neurobiologicallyplausibleframework, and thereforelead to improve the
diagnosisand managementof patients.There is no
doubt (and perhaps no surprise) that an altered
experienceof bodily functions might be associated
with specific modifications in the brain networks
normally responsiblefor generatingour conscious
experienceof such functions,as also demonstrated
for even more extreme disturbances in bodily
awareness(Vuilleumier et al., 1997;Blanke et al.,
2004;Blanke,this volume).Demonstratingspecific
neural correlatesof hystericalconversionmay also
help reassurethe patients as well as their caretakers, including nursesand doctors who sometimes
show negative or unsympathetic reactions when
confronted with complaints unaccompanied by
visible organic pathology. As already suggestedby
James(1896), this may eventually help convince
someskepticsthat hysteriais a "real disease,but a
mental disease".
Importantly, neurobiological findings should
lead to refine our current psychopathologicalexplanations of conversion, by suggestingpossible
mechanisms by which the mind can produce
changesin the brain and body functions. Such
mechanismsare likely to involve dynamic interactions between neural systemsmediating specific
functions (e.g., motor, somatosensory,or visual
processing)and neural systemsresponsiblefor affectiveevaluationsand reactions,basedon current
(e.g.,limbic areasin the
as well as past experiences
broad sense,such ascingulate gyrus, orbitofrontal
cotrtex,or amygdala). Such interactions between
distributed brain areas might be usefully investigated by neuroimaging studiesusing connectivity
analysis (e.g., Friston, 1994; Mclntosh and
Gonzalez-Lima, 1994). Various statistical tools
now exist to describehow neural activity in one or
severalregions can either influence,or instead be
contingent upon, neural activity in other regions.

324
subjectedto threats or forced restraints(Rougeul
-Buseret al., 1983;Gray, 1993;Klemm,2001).Indeed,motor arrest and protective immobility (including behaviors such as "freezing", "sham
death", or'oalert state") seemto constitutefundamental and stereotypedmodesof reactivity to environmental eventsthat are perceivedas stressful
and hostile, where animals can sometimesadopt
awkward fixed postures while waiting for termination of the unfavorable situation (Klemm,
2001).It has already been proposedthat such reflexive behaviorsmight provide a possibleprimitive mechanism underlying more complex
hysterical and "illness" behaviors in humans
(e.g.,Kretschrner,1948;Whitlock, 1967).Hysterical conversion is typically trigggred by psychological stressorsoand sometimesminor physical
injuries, which may be experiencedas potentially
more harmful in the context of a subjectivelack of
It is therefore plausible
control and helplessness.
that in some individuals (perhaps due to predisposition or past history) a kind of primitive protection or avoidancemechanismsmight be induced
and abnormally maintained, resulting in a pathobffirD@y
logical state of alertnessand attention that can
6fnled dunns Daralvsrsln tfle contralateral nemmodulate their sensoryor motor experience,and
rk'*"' rffi
iWneru.
sao-nt='G;i?fr"tffiffi
(e.g.,
that is reflectedin neural activity within specific
arand sensorycorticalareas
iiifrFhotor
brain areas such as cingulate cortex and sensoriin all coneasl-2-3, 4-6), whichwerecoactivated
networks. It is also possible that similar
paralysis
the
motor
in
ditions, but less so during
psychobiological
responsesmay induce behavioral
sr
contralateral hernisphere;whereasa third
modalities (e.g., blindness,deafchanges
in
other
cant network i
or in more complex cognitive
ness,
dysphonia)
.--40-)--anil-ruas
(e.g.,
dependingon someintermemory)
domains
ni-ainltacaitatedintheipq1lqlgral-bq{lisp-ber.e-duteventsand prior expethe
causal
actions between
idgF'tiely$SfTliLougli Gry indirect,this network
given
In all such cases,
individual.
riencesin a
d{alysis sriggeststhat hystericalparalysis did not
often found in
in
neural
activity
changes
these
arise in associationwith reducedactivation of the
cortex
orbitotiontal
of
cingulate
or
area's
limbic
basalganglia-thalamiccircuits alone. bgljbis*rubpatprimary
dysfunction
coma
"core"
indica'te
might
with a distinct
inducing
disorders,
conversion
different
mon
to
with inferior
tern of l-u
secondaryfunctional changesin other brain areas
itforbitofronta I cortex
pattern
more directly with the symptoms.Howconnected
this
more
work will be necessaryto confirm such
ver,
s i n basal
that cha
different paradigms and to compare
in
changes
mnl an lni
them with other conditions such as feigning or
ve or stressful
hypnosis. Note, however, that many conversion
representedin
patients presentwith relatively complex and mulKringelbach and Rolls.
f(NfogenSon.rtt
tiform symptoms, making homogenous group
2004). Such inhibitory effects might be akin to
studied difflcult, and unfortunately limiting the
"behavioral arrst" observed in animals when

New methodsallowing inferencesabout the directionality of suchinfluences(suchas dynamic causal modeling,seeFriston et al., 2003)might prove
particularly valuablein this context.
Thus, in our own study of hysterical paralysis
(Vuilleumieret al., 2001) demonstratingreduced
activation in the contralateral basal gangliathalamic circuits, which becamenormal again after recovery from paralysis,we were also able to
show that such changesco-varied with concomitant changesin other distant brain areas, where
activity was not globally reduoedor enhancedbut
rather appeareddifferentially coupledwith the basal ganglia-thalamiccircuits during paralysis.This
was demonstratedusing a type of principal component analysis(scaledsubprofile modeling; Moeller and Strother, l99l) that allowedus to identify
three distinct networks of regions whose activity
tended to covary together acrossall subjectsand
all sessions,irrespectiveof their absolute level of
activity. Critically, this analysis identified a net-and thalamus,together
work includingthe cau<Iate
ffith inferior liontal regions lareas 44145)tnd or-

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325
generalizationof the findings from one study to
another.
Future studies might therefore fruitfully compare patterns of brain activity in conversion patients showing different types of deficits (e.g..
motor or somatosensoryloss) to determinemore
directly what are the changesrelated to specific
symptoms,and conversivereactionsin general(for
instance,testing whether someeffects in anterior
cingulate and frontal cortex may ariseirrespective
of the type of deficit). New studiesshould also use
different possibleapproaches,f,or instanceby examining brain function more systematicallyduring
and after conversiondeficits in the same individuals; by manipulating more explicitly factors related to attention, expectationor inhibitiory and
by investigatingany differencesin brain reactivity
to stressfulprobespresentedto thesepatientseven
when they haverecoveredfrom specificconversion
symptoms. In addition, we need to btter understand the cerebral mechanismsinvolved in other
psychiatric disturbancescharacterizedby dissociative symptoms, such as psychogenicamnesiaor
"mnestic block" (Markowitsch,2003;Glisky et al.,
2004), or depersonalization disorders affecting
prception of the self and/or of the environment
in stressfulsituations(Laniuset a1.,2002;Reinders
et al., 2002).New imagingdata may help to clarify
the possible relationships of these disorders
with conversiondisordersand other types ofpsychogenic "block" affecting conscioussensoryand
motor functions. Interestingly,functional neuroimaging correlatesof dissociativeresponseshave
also highlighted a key role of medial prefrontal
areas for integrating perceptual or motor representations with a subjective senseof conscious
control (Lanius et a1.,2002;Reinderset al., 2003).

Conclusions
In summary, although hysterical conversion has
rernained a common and fascinating disorder at
the border betweenneurologyand psychiatry,f,ew
systematicand controlled studies have yet been
conductedusing modern neuroimagingtools. This
is surprising given the variety of currently available techniques(ERPs,MEG, PET, SPECT,fMRI)

the rich productivity of imaging researchin

neuropsychiatricdomains. A better undering of functional changesin brain activity
ing hystericalconversionwill undoubtedlyprounique insights into neural mechanismsot
but should also improve the
consciousness,
gnosis,management,and assessmentof prog;is in thesepatients. Finally, further researchin
field might certainly contribute to strengthen
links betweenpsychiatry and brain sciences.

thanks to F. Assal, C. Chicherio,T. Landis,

S. Schwartz for their precious collaboration,
to P. Halligan for many valuable discussions.
of this work was supported by grants from
SwissNational Foundation.
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