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8/17/2019 Hysterical Conversion and Brain Function
1/21
S.
Laurry:s
Ed.
Progress
n Rrailt
Researrh.
Vol. 150
lssN
0079-6123
Coplrighi
(C
2005
Elsevi::r J.V
All rights
rcserved
CHAPTER
23
HysterLcalonversionand brain
function
Patrik
Vuilleumier*
l-aboratorl,.for
Behatioral
Neurolagy
and
ltrwgingl
of Cognition,
Clfuic
of Neurology
&
Department
of Neurosciences,
Ltniuersit),"trteclical
Center,
Faatttli of
Psyainiy
& Educution
Sciences,
uniuersity
of
Geneua,
Genetta,
Switzerland
Abstract:
Hysterical
conversion
disorders
epresent
functional"
or
unexplained
neurological
deficits
such
as
paralysis
or somatosensory
osses
hat are
not explained
by
organic
esions
n the
nervous
system,
but
arise
n the
context
of
"psychogenic'n
tress
or emotional
conflicts.
After
more
than a
century
of
both
clinical and theoretical nterest,the exact nature of such emotional disordersresponsibleor hysterical
symptorus,
and
their functional
consequenes
on
neural
systems
n the
brain,
still
remain
argely
unknown.
Aor*u.r,
several
ecentstudies
have
used unctional
brain
imaging
echniques
such
as
EEG,
fMRI,
PET,
or SPECT)
in the attempt
to identify
specific
neural
correlates
associated
with
hysterical
conversion
symptoms.
This article
presents
general
overview
of these
indings
and of
previousneuropsychologically
based
accounts
of hysteria.
Functional
neuroimaging
haS revealed
selective
decreases
n the activity
of
frontal
and subcortical
circuits
nvolved
n motor
control
during
hysterical
paralysis,
decreases
n
somato-
sensory
ortic€s
during
hysterical
anesthesia,
r
decreases
n visual
cortex
during
hysterical
blindness.
Such
changes re
usually
not
accompanied
y
any signifrcant
changes
n
elementary
tages
of sensory
or
motor
processing
s measured
y evoked
potentials,although
some
changes
n
later stages
f
integration
(such
as
it:00
t"rplnses)
havebeen
eported.
On
the
other hand,
several
euroimaging
esults
have
shown ncreased
activation n limbic regions, uchascingulateor orbitofrontalcortexduring
conversion
symptoms
affecting
difl'erent
sensory
or motor
modalities.
Taken
together,
hese
data
generallydo not
support
previous
pro-
posals
hat
hysteria
rnight
involve
an
exclusion
of sensorimotor
epresentations
rom awareness
hrough
attentional
processes. he1,1a11t"t
eem
o
point
to
a modulation
of such
representations
y
primary
affective
or
stress-related
actors,
perhaps
nvolving
primitive reflexive mechanisms
of
protection and
alertness
hat are
partly
independent
of conscious
control.
and
mediated
by
dynamic
modulatory
inter-
actions
between
imbic
and sensorimotor
networks.
A better
understanding
of the
neuropsychr:biological
bases
f hysterical
conversion
disorder
might
therefore
be obtained
by t'uture
maging
studies
hat
compare
different
conversionsymptoms
and
employ
functional
connectivity
analyses.
his should
not
only
lead to
improve
clinical
management
f these
patients,
but
also
provide
new
insights
on the brain
mechanisms
f
self-awareness.
Introduction
Sincemore
than a
century,
hysteria
has
ctlntinu-
ousll'
fascinated
both
clinicians
and
theorists
n-
terestedn altercd
states
of self-consciousness.
s a
*Corrcsponding
author.
Tel.:
1-41
(0)22
379-s.381;
Far
*41
(0)223795.402:
E-mail:
DOI: 10.0l ti/S0079-6123(0ti0023-:
medical
condition
in
which
patients may
present
with various
somatic
symptoms
without
a
recog-
nized organic
illness,
hysteria
still
constitutes
a
poorly
understood
class
of disorders
at
the
border
between
psychiatryand
neurology,
with
many
dif-
ferent
appearances
nd
names.
A variety
of clas-
sifications
and
explanations
have been
proposed
over
the
years,
vith different
emphasison
psycho-
logical
or neurobiological
actors.
but
none is
still
309
8/17/2019 Hysterical Conversion and Brain Function
2/21
3 1 0
Fig.
l. Illustration
of
paraparesis
astasia-abasia) f hysterical
origin
(drawn
by
Jean-Martin
Charcot
n the
1870s).
entirely
satisfactory
see
Halligan
et al.,
2001 or a
recent
general
overview).
In some
r€spects,
he most
important
chang€
sinceclassical
descriptions
of
hysteria
by Charcot
and others
at theend
ofthe
l9th c€ntury
(see
Figs.
I and 2) is
related
to the
fact that
the term
"hys-
teria" was recently eliminated from the official
psychiatric
erminology.
Thus,
hysteria
s now
re-
ferred to as
"conversiondisorder"
in the
DSM-IV
classification
(American Psychiatric
Association,
1994,Diagnostic
and Statistical
Manual
of lfental
Disorders),
where
t is
definedas a
loss or
distor-
tion of a
neurological
unction
(e.g.,
paralysis
or
anesthesia)
hat is
not explained
by
an organic
neurological
esion or medical
disease, rising
in
relation
to some
psychological
stress
or
conflict'
Fig. 2.
"L'anesth6sie
yst6rique",
a cruel
demonstrationofan-
esthesian a patientat I-a Sal$triere, while n a stateof hysteria
(etched
rom
photograph
by
P. R6gnard,
1887,ks maladies
6pid6miques
e 'esprit
Sorcellerie,magn6tisme,
morphinisme,
d6lire des
grandeurs.
Plon-Nourrit, Paris).
but
not
consciously
produced
or intentionally
feigned.However,
although
he term'oconversion"
implies a
specific
mechanism
whereby
a
primary
psychological
disorder
is
converted
into bodily
s)imptoms,
he
exact
pr@esses
esponsible
or
trig-
gering
his
phenomenonand altering
the
patients'
awar€ness
f their
bodily state
still
remain un-
known. In fact, when considering he possiblene-
urobiological
changes
associated
with
hysterical
conversion
symptoms,
many
of the current
hy-
potheses
re
not very
different
from those
elabo-
rated
n the l9th
century.
Moreover,
n contrast
to
other
psychiatric
conditions
(such
as
depression,
anxiety,
compulsion,
or
phobia),
surprisingly
tbw
investigations
have
been
carried
out to examine
whether
the "functional"
symptoms
experienced
by
hysterical
patients
might
correspond to
any
8/17/2019 Hysterical Conversion and Brain Function
3/21
3 l l
underlying
"functional
changes"
n cerebral
activ-
ity,
as
can be evaluated
or
instance
sing
a variety
of
modern
neuroimaging
echniques.
The
aim of
this
chapter
s to
present
a
general
overview of the relationshipsbetweenhysterical
conversion
and
brain
function,
focusing
particu-
larly on
previous attempts
o
determine
some
ne-
urophysiological
correlates
of
hysterical
conversion
disorders.
This
review
will
primarily
concentrate
on
patients
with
unexplained
neuro-
logical
deficits
n
sensory
and/or
motor
functions
(i.e.,
hysterical
paralysisor anesthesia),
ince
such
disorders
are the
most
frequent
and most
easily
described
n terms
of
specifrc
neurological
path-
ways. Similar
approaches
n
other
domains
(e-g.,
visual loss, deafness,or amnesia)will also be
briefly
mentioned,
but
other
conversion
disorders
associated
ith more
oopositive"
symptoms
such
as
pseudo-seizure nd
abnormal
movem€nts
will
not
be
discussed
ere,
since
even
ess
s known
about
their
possible unctional
neural
correlates
for re-
view
see
Prigatano
et al.,
2002;
Reuber
et
al.,
2003).
Finally,
a
few studies
have
examined
he
functional
neuroanatomy
of dissociations
nduced
by hypnosis
(Maquet et al.,
1999;
Faymonville
et
al.,
2000;
Halligan
et al.,
2000;Kupers
et al.,
this
volume),
but their
implications
for hysterical
def-
icits are
still
in
part
unclear
and
will
be discussed
briefly
A
better
understanding
of
patients with hyster-
ical conversion
has
important
implications
for
several
easons,
oth
clinical
and
theoretical.
First,
such
disorders
are
very common
in clinical
prac-
tice,
causing
frequent
problems
n
diagnosis
and
therapy
for
neurologists
as
well as
psychiatrists,
and
resulting
n important
medical
costs and
ma-
jor
socio-economic
burden
for
the
patients and
their
relatives.
Second,
conversion
disorders
aise
important theoretical questions concerningthe re-
lationships
between
body
and
mind,
and
the
ne-
urobiological
and
psychological
mechanisms
underlying
self,-awareness.
From
the
perspective of
clinical
neurology,
resulting
from
their
brain
lesion
(Vuilleumier,
2000a,
2004; Marcel
et al.,
2004).
Anosognosia
cannot
be
explained
by
psychogenicactors
alone,
or
by
general
confusion,
but
it is often
associated
with a lack of emotional concernquite similar to
"la belle
indifference"
that
has
typically
been
de-
scribed
n
hysteria.
Moreover,
ike
anosognosia
or
hemiplegia,
hysterical
paralysisand hysterical
an-
esthesia
re
often
thought
to affect
the
letl more
than
the
right
limbs,
without
this
being
entirely
accounted
or
a more
frequent
dominance
of
the
right
hand
(Galin et al.,
19771'
tern,
1983;
Pas-
cuzzi,
1994;
Gagliese
et al.,
1995),
although
a re-
c€nt m€ta-analysis
as
questioned he
existence
f
such
an asymmetry
Stone
et
a1.,2002).
t is also
intriguing o.tot"
that
theleurological
@
ass@la
osognosra,,togn
O it'
*E€-f -bJ-F4 @
lr
4
hvoiqt
[o- -esly--ttuila ele]-.
Sral$
Aa*ArcsareS6,^'but
lso
blindness,
mnesiq,.-of
idigoir
aphasid
O['enkei,"
-1995;
VriiliJumier,
20OOa).
tlhoGtr
such
similarities
do
not
indicate
any
clear
relationships
between
hese
different
dis-
orders,
hese
parallels
between
neurology
and
psy-
chiatry
highlight
the
fact
that
some
behavioral
abilities
may
dissociate
rom
the subjective
expe-
rience
of
these
abilities,
and
that
such
dissociations
are
likely to arise from specificchanges n brain
furrction
-
be
they
due
to
certain
types of
organic
damage
or
to
certain
psycho-affective
tates.
Incidence
and
evolution
Hysterical
conversion
disorders
are
thought
to
represent
4o/o
of all diagnoses
n
generalhospi-
tals
throughout
w€stern
countries.
This
frequency
has
remained
remarkably
stable
across
the
past
decades espitemany important changes n med-
icine.
Thus,
a retrospective
urvey
at
the
National
Hospital
of
Neurology
and
Neurosurgery
n
Lon-
don,
Queen
Square,
rom
1955
o 1975
evealed
a
relatively
constant
ate of
patients nvestigated
or
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
successive
utpatient
referrals
at Charing
Cross
diGdciatiitniffii@
6f
performance
re
not unusual
n
patientswith-
.+.--_-__..--
organlc
braln
Fslons,
a
rganTc*t5iffi
an-
edge
and-even
expligLgy_legy
se]erl
hanjgP
8/17/2019 Hysterical Conversion and Brain Function
4/21
312
Hospital
between
19'17and
1987
(Perkin,
1989),
which
revealed
a stable
ncidence
of 3.8%
of con-
version
disorders
over the
years.
In
Switzerland,
Frei
(1984)
also estimated
that the
proportion
andpresentation f hysterical onversiondisorders
among
patients
seen
n
a
large
public
hospital
was
similar
in the
1920s s compared
with the
1980s.
However,
it
is
important
to
emphasize
hat the
type ofconversion
disorders
may
significantly
vary
across
ifferent
medical
settings
and
referral
sourc-
es. This
might
explain
why
the incidence
of hys-
teria may appear
o vary in
somedomains
but not
are n€ver
seen
fto",
t9ggl.
Neurologists
probably seemany
more
patients with
relatively acute
and
limited
symp-
toms,
as
compared
with
psychiatristswho
tend
to
see
patients with more
chronic
and
multiform
dis-
orders
(Marsden, 1986).
Moreover,
although
there
is a
good
consensus
between
neurologists
as to
clinical
syndromes
eflecting
non-organic
diseases
(irrespective of which term
is actually
preferred
to
describe
these
syndrom€s,
e.g., hysterical,
func-
tional,
or
psychogenic),here
s
usually
ess
agree-
m€nt among
psychiatrists
(Mace
and
Trimble,
l99l).
Furthennore,
although
most n€urologists
would agree
with
the DSM-IV
statement
that
"typically, individual
conversion
symptoms
are of
short
duration'',
many
psychiatrist have
rather
observed
hat
conversionsymptoms
often
tend to
persist
or reoccur
in association
with
other
psy-
chiatric comorbidities
and
pathological personal-
ity traits
(Ron, 1994;
Binzer
and
Kullgren,
1998;
Stone
et al.,
2003).
However,
in most cas€s
seenby
neurologists,
a
rapid
remission
of initial
symptoms
is observed
after appropriate behavioral treatment. The like-
lihood of spontaneous
emission
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 even
gleater
(Folks et al.,
1984).
Among
young
patients
(< 27
year-old),
only 3Yo
have
symptoms
or more
than
I
month
(Turgay,
1990).
The
duration
ofeffective
behavi-
oral
treatment
in such cases
s usually
between
Personality
disorder
appears
as a
particularly-
@ C r i m l i s k e t a l .
1998;
Crimlisk
et al., 1998;
Stone
et al.,
2003).
[-qgs).
t is ilieiffiirnportant
to
identity
pot€n-
tial
risk factors
during
the
initial
evaluation
of
patients,
n
order
to
prevent he
development
of a
more
chronic
handicap.
Body,
mind, and
brain
diseases
A
potential
limitation
to
our
current understand-
ing of hysterical
conversion
comes
rom
a
lack of
clear definition
of the
boundaries
with sorne
elat-
ed disorders.
From
the
perspective f
psychiatry,a
number
of
problems
are still
unresolved
concern-
ing the terminology
and
classification
f functional
symptoms
without
an
organic
cause. n
DSM-IV,
the
concept of
hysteria
has
been broken
down
to
different disorders, including somatoform disor-
ders on one
hand
and
dissociative
disorders
on
the
other
hand,
with
conversion
disorders
being
considered
as
a
specific category
of somatoform
disorders
involving
sensorimotor
symptoms
or
pseudo-seizures,istinct
from
other somatization
symptorns
or
psychogenic
ain
disorders.
Further-
more, depression
and
chronic
fatigue
syndrome
would
fall
under
other diagnostic
categories
although
in clinical
practice there
is often
some
overlap
between
all
suchconditions.
For example,
. Furthermore.
version
disorders
are defined
as-d.gft"]q@'-@g
t - ' - - *
a
ibecffit neurological
Sl9lign-;gg[*qs---molQr
dtien.$h
or-
sbm€ttisGnsory
perception,
Py9. 9-
-
ioniiGreifTniiead--unde
enlc
memory
loss
ls consl(]€fe(l
_ll*:19._.--
ine-"ataEmytor-"dissoaaf
G-?1i-ofr
E-re''oq
:*
- : j
_
' -
- _ - r '
-
* : -
- ' : - c
"
t&G l
+emory
s
obviously.?lig
spe.sifrp
fain
fuiiiiion
(see
Markowitsch,
1999,
2003
for
a
--.--'-:--..-.: .--
associated
with
a favorable
prognosis,
acutenesS
f
presentation, nset
St
many patients recoveringfto-j,o y9lg 94
2 to X
weeks
(Speed,
1996).
Soveral
actors
are
8/17/2019 Hysterical Conversion and Brain Function
5/21
Eames
(1992) described
a
seriesgf
, 9Z,g,g.ge s
€ - > - * . -
fr65 were
ad'iiiittecl
d a
iEhebilitation
ward
4nd-
neuropsychological
perspective of
psychogenic
amnesia).
Therefore,
unlike
DSM-IV,
the
Interna-
tional Classification
of Diseases
ICD-10) of the
World Health
Organization
has
included
all
sen-
sorimotor and memory symptoms of presumed
psychogenicorigin
under
the same
general cate-
gory
of
dissociative
disorders.
conversron
casionally
be
a
"complication"
of
organic
brain
disease,
nd
Schilder
1935)
wrote that brain
dys-
function could sometimesnduce
"organic
neurot-
ic
attitudes".
More
recently,
1gi4tnggf$-$-9lp-U
patients
exhibited
at
diffuse brain lesions
(Eames,
1992).
Similarly,
Gould
et al.
(1986)
re-
ported that
among
a
prospective
eries
of 30
pa-
tients
with an
acute
hemispheric
stroke,
"atypical
signs"
usually
suspected
o
reflect
non-organic
"functional"
origin
were
observed
n
approximate-
ly
20% of
cases
e.g.,
changrng
deficit,
patchy sen-
sory 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
diseases
n
which
not
only
some
truly
"organic'o
manifestations
may
sometimes
e
difficult
to dis-
tinguish
from
non-organic
disorders,
but
some
pa-
tients
may
also
present with a
combination
of
apparently
both
"organic" and
"psychogenic"
manifestations
at
the
same
ime.
These
occasional
31 3
associations
between
hysterical
conversion
and
neurological
diseases
are
not
only
challenging
for current
"dichotomous"
classification
schemes,
but
in fact
might
potentially
provide valuableclues
about the neurocognitivemechanismsby which
awareness
f
a
function
can
be dissociated
rom
actual
abilities
in
a
patient.
However,
the
co-
existence
of these
neurological
diseases
nd
con-
version
might
also
ust
be a
coincidence,
urely
due
to
their
high
incidence
or
to any
other
general
stress
actors.
Nevertheless,
espite
hese
problems of
defini-
tions
and
associations,
hysterical
conversion
is
only
rarely
falsely
diagnosed
or an
occult
neuro-
logical
condition.
Although
a
few early
studies
suggested
hat
up
to 20o/o
f
patients
initially
di-
agnosed
with motor
conversiondeficitsmay sub-
sequently
develop
a
real organic
neurological
disease
xplaining
their
original
symptoms
(Slat-
er,
1965;
Mace
and
Trimble,
1996),
several
ecent
studies
have
now clearly
established
hat
such
ates
were
overestimated
nd
that
only
l-5%
of hyster-
ical
patients may
present with a
underlying
but
occult
organic
cause
e.g.,
Crimlisk
et al.'
1998;
Stone
et al.,
2003).
The rarity
of organic
diseases
detected
n current
follow-up
studies
s
probably
due
to
several
actors,
including
a
better
charac-
terizationof neurologicaldiseases nd the availa-
bility
of
more
sensitive
non-invasive
diagnostic
procedures.
History
and
theories
The
term of
"hysteria"
was forged
by the
ancient
Greeks
to
indicate
that
physical
disturbances
n
the
uterus
were
the
primary cause of
psychic
symptomsn women.By contrast,all modern the-
ories
of
conversion
disorders
acknowledge
hat
not
only
both
men
and
women
may
be
affected,
but
also
a
primary
psychological
disturbance
s
prob-
ably
responsible
or
triggering
subjective
physical
s5rmptoms,
nd
perhaps also
{br
triggering
some
associated
hanges
n the
neurophysiological
tate
of
the
central
nervous
system.
However,
the
exact
psychological
actors
to blame
still
remain
disput-
ed, and
the
possible implication
of a
particular
From
a neurological
perspective, tU -JgIl
ins that
conversion
may
sometimes
c6-eiist
with a
real
organ
;"*pluined-by
thit
brain
hsio.rtg
Gowers
.._+
.c
----#-re
6g9ij-already
recognized
hat hysteria
could
oc-
Itrsi-"
de-"liy3fdifit:Ii'ld"*
behavi6-i'
driii.3ig=.
ihb
colifi
FortIi€ii'rcnutmttti6n;aiqtF -s99,-by--=qti-
tol'ati"ratingscales-t+i9$'...[..1a-6.ffstq:*-s.dt-;C-
hiviors'
couiii-?ni'iiide
exaggeration,
secondary
gain
expectancy,
i
non-ggSgigp"age$f
offe
fldTrlii.'Inieiisf
riglyjhoTa[tyru-qf
patientspre-
8/17/2019 Hysterical Conversion and Brain Function
6/21
314
brain functions in
generating
an abnormal
phys-
ical'experience till remainsunresolved.
Since the l9th
century, a myriad
of different
theories have been
put
forward to explain
how
hysterical motor or sensorydeficitsmight be im-
plemented
n the brain in terms
of specific ana-
tomical
circuits, or in
relation
to
putative
cognitive
architectures.However,
most of these heories est
on
purely
speculative
rounds,
and little empirical
work has been conducted o
test theseneuropsy-
chological
hypotheses.Although
it is beyond
the
scope
of this chapter
o discuss ll of
these heories
in
great
detail
(for
more complete
reviews, see
Merskey,
1995;Halligan
et al.,
2001),a few con-
jectures
on the neural
substratesof hysteria
that
have been
proposed
by influential
neuroscientists
will be briefly
illustrated. Although many
old the-
ories
are susceptibleo misinterpretations
ased
on
our
current
knowledge, t is nteresting
o note
that
some of them
might still appear
attractive
f they
were rephrased
using more
modern concepts
and
terminologies
f.rom current
cognitive and
aflective
neurosciences.
n
fact, several ecent
hypotheses
about the
possible
cerebral
correlates
of hysterical
conversion,
proposed
on the basis
of new
func-
tional neuroimaging
esults,can be traced
back to
strikingly similar ideas hat
were elaborated
more
than
a century ago, but naturallyphrased n terms
of models of
brain
physiology
rom
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).
Giting
activity of motor
or sensory
a[h@
with-
out any
p€rmanent
structural damage.
Hysteria
was thus consideredas a "neurosis" among other
functional
llnesses uch as
epilepsyor
Parkinson's
disease.Charcot
suggested hat such
functional
changes n the
nervous system
could be induoed
by
particular
ideas, suggestions,
or
psychological
states,as
demonstratedby the
effect of hypnosis
on
hysterical
symptoms.
Thus,
hysterical
paralysis
could result from an
inability to
form a
oomental
image"
of movement,
or instead rom
an abnormal
"mental
image" of
paralysis.
n
essence"hese deas
are echoing
he more recent
proposals
of a
selective
impairment
n action
"representations" or inten-
tional
motor
planning
(e.g.,
Spence,
1999),
al-
though
both the terminology
and
concepts f brain
function haveconsiderably hangedsince hen.
At the same
ime as Charcot,
Jun:lj 9{)gbg
orooosed hat
hvstericaldehcitswere
the result of
- : - 4
"fixed
ideas"
that could take
control
over mental
dr motor
functions. Flowever.
he added
that such
between
distinct do-
way to the classical
heory of
Freud and
Breuer
(1895),
ater refined by Freud
alone
Freud,
1909),
who
formulated a
purely psychodynamic
ascount
with only minimal
reference
o the nervous
systern.
In brief. accordins
o Freud
and Breuer.hvsterical
d"
and
eftry-o: --ftltgEt
(one
becoming ominated
y
the unconscious
fixed
idea). Such views
paved
the
transformed
nto
bodilv
complaints
with symbolic
vhlues.For
this reasbn.
hvsterical
ef-rcitsid
not
obey anatomical
constraints
as observed
with or-
ganic
neurological
esions.
This view has then
nat-
urally
led to
the
term
of
"conversion disorder",
and n many
respectss still
prevailing
oday.
Only
later
did Freud emphasize
hat the
unconscious
affectivemotives usuallyhad their origin in sexual
concerns
rom early childhood.
An attempt to
integrate hese
different cerebral
and
psychological
perspectives
was made by the
Frenchneurologist
Babinski
n
1912,
who
also
irst
described anosognosia
a,fter
brain damage two
sequent interpretation
stage.
A more sophisticated
neuro-anatomical
scheme
was later
proposed
by
iZ-eai ould ariseat an
u
inducing
a dissocia
ons within
the central
nervous system,
af-
Pavlov
1,928-1941,
933),
who
8/17/2019 Hysterical Conversion and Brain Function
7/21
cerebral enters
possibly
mediatingemotionalor
-----
rearncdcondrtroned esp gql_ q d
lelg
to a re-
_---ffi
active
inhibition
of
cortical
inputs
imposed
by_l he_
frontal corte>i This inhibition was responsible or
fitGtrffifalysis or anesthesia, hose duration
was
proportional
to the amount
of
resources e-
pleted
n the individual.
A number of more recent
accounts based on
neurophysiological speculations have
similarly
proposed
a role for inhibitory
or
"filtering"
mech-
anismsas a likely neural
substrate or
generating
hysterical
conversion
deficits. Thus, in line with
Babinski and Favlov,
Sackeim
et
al.
(1979)-arld
Stern
(
I
983) hvooth"sizffffiT6iilor moti-
vational
processes
might induce
a
selectiveblock-
----+--:-.__-.%
ase
or
clrstortlon) I sensory nd/ormotor rnpglls,
=#
resultlng
n
therr
exclusronrom conscrous
ware-
n"rr.
i
greater
involvement
of
the right hemi-
sphere in emotion might
account
for more
frequent symptoms on the left side
of the body
observed
n
some
series
Stern,
1983;seeStone et
t972
uncuons mechanisms
the level
of thalamic
mrclei.under the influence
315
lsignals
from
limbic systems
within orbitofrontal
,,
and cingulate
cortex during volitional movements
i
(Marshall
et al., 1997).Again, such nhibition
was
lascribed
to unconscious
motivational factors
Finallv- from the mid-1970so mi,
ing to the influenceof the
research n split-brain
ical
between t
uvsrygg-_in_e-qg-
impairment in the
rigbt
(Stern,
1983)or left hem-
l*i;tt"."*fpm:H;itiffi-
"FrqS
D:-fiowevei,
oniy
aiEriCii-thai onversion isordersmlelt'ilGlve
t
.,.#,*.-**@
@..->===*
dysfunction in the
'omonitoring
and controlli4g
diiaaifif
b:r?o;sri5GEsf
.
idulrin's l
-
i disso
ciafivtiltilF
il,t imffi
"ff"ffi
. , - . . " r y
gt-qt g @-&iqq-(*s
4-lo-
stta
eq4..&:ri
l.
1999),
whereas
Spiegel
1991)
nsteademphasized
f _ e _
__
anattentlonalmechailsm_..l+e^4_ Atg4*b:"tb9=*a ejr-
or cingllatg
-aql[er.
Likewise,KLtpjryn"1[ $CI
nence ot'
perceptron
a-nd/or voluntary
actlon,
4
presumably
tnrough abnorrnal coordlnatlon
oI
particular
neurocognitive
modules. Oakley
(1999)
also referred
to neuropsychologicalmoAels6ffi-
tentlon o
suggesthat dunng hystena, n lntern4l
very
l
performance
on
..._-=4
n-urop-pfiological tests
was otTered n support
of these nterhemispheric
ypotheses
Flor-Henry
et
al . , 1981).
In sum, most
theoretical models trying to link
hystericaldisorders
with
specific
neuropsycholog-
ical or neurophysiologicalmechanisms
have es-
sentiallybeen
nspired by speculative rguments
or
analogies
with
general
models
of the brain and
mind, rather than by the convergence f systematic
empirical
research. t is striking
that relatively few
studissover
the
past
decades
have exploited ne-
urophysiological
echniques
see
below) that
pro-
vide objective
neasures
fbrain
functions
(such
as
electroencephalogram
EEG)
or
brain imaging),
allowing
a better identification
of neurobiological
factors associated
with hystericalconversion.
This
is
all
the more surprising
since the
well-defined
neurological-like symptoms
of conversion
(e.g.,
paralysis,
anesthesia,
lindness,etc.)
should
po-
tentially be amenable o a precise nvestigation
with
well-defined
predictions
about
the site and
type of neurophysiological
ysfunction.
In
partic-
ular, the advent
of new
tirnctional
imaging tech-
niques should now
allow a refine
assessment f
functional correlates
in brain activity
potentially
associated
with
hysterical conversion,
and thus
go
beyond he
dichotomous
question
of "organic"
versus
"non-organic"
disease.
A better
know-
ledge
of such
functional correlates
might
provide
tation
oenti6f- ex€cutive
atten
from awareness v a
motor
ontif Effi ffi;GtiotiITiste-
i"ioiuine
f6ritaFnnt
ifr'su6i6iiud.
r
nuir
""
rfi
ri
n;
"
; J
1
D='dvitrq99)a-nifMurrii,a-ll"una
"oil"ugu;
(1997)
\
,
as well as Spence
1999)
and Spence
nd colleagues
f
.
(2000)
also speculated that
representationsof
N
i
motor action miebt b€ inhibited
in
patients
with
I
I
hysterical
paralysis,
with activation n their
motor
I
\
cortex being actively suppressed
by abnormal
\
r
(Galin
et
al.. 1977). The
greater
occurrence of
left
r #
hemrbodVdrsorders ed to the ldea that the trans-
#
IEiof sensory
or motor
inputs
mieht
btimpairg
a1.,2002).
Other researchersuchas
8/17/2019 Hysterical Conversion and Brain Function
8/21
6
constraints on
psychodynamic
heories
conversion,
with
greater
biological and neuro-
plausibility,
and might also improve the
assessment
nd management f
patients.
orrelates
of conversion
EEG
provided
one
of
the first tools to meas-
n activity, a number of studies from the
o
1970sonward
have
used this
technique
lectrophysiologicalmeasureso
patients
with hyster-
conversion. These studies can
generally
be
n two broad categories: hose aiming
intact electrophysiological e-
despite subjective unctional
losses,and
rying to determinesomeabnormal
pattern
with functional symptoms.
or brainstem auditory evoked
potentials
are
usually found to disclose ormal am-
and latencies n the pr€sence f subjective
blindness, or deafness, respectively
Howard and Dorfman,
1986;
Drake,
1990).
results suggesting a
paradoxical
amplification
rather than attenuation of tactile evoked respons-
es during hysterical anesthesia
Moldofsky
and
b _ ,
ly early
stages f cortical
processing.
Moreover,
hese arly
SEPsmay not necessarily orrelate
with
subjective
perceptual
experience, ince
SI
responses an still
be
elicited by unperceived timuli in
patients
with
brain tumors involving the
parietal
lobe but spar-
ing SI
@reissl
t al.,
2001).
Also, in
patients
n a
vegetative
state, devoid of any
conscious
perrep-
tion,
preserved
I activation
has
been
shown using
functional imaging and simultaneously
ecorded
SEPs
Laureys
et al., 2002).Thesedata emphasize
that
SI
activation does not necessarilymean con-
scious omatosensory
erception.
On the other
hand.
a few other
studies have re-
ported
subtle changes in
paradigms
that were
slightly
more
sophisticated han
just
detection of
simple actile stimuli.
For instance, actile stimuli
close o
percepual
threshold
may fail to
produce
normal evoked
potentials
n
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 repeated
stimulations
were observedn hysterical
onversionusing SEPs
(Moldofsky
and
England, 1975)as well
as
skin-
conductanoe reactivity
(Horvath
et
al.,
1980).
In
normal subjects, responseswere
found to de-
creaseover time
when comparing late blocks
of
stimuli relative o initial blocks. Such
habituation
could also be observed n
patients
with 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.
Another
r€cent
rted
ri5e
P500
conBonent
(Lorenz
et al.,
component
is typically elicited by
clearly indicatejhalpd_mety
sen-
pathways
are both
qtnrcjurally-andftuqtiqo-
in the
patients.
In
the
somatosensory
been studied
using
MEG)
in order to dis-
activations
n
primary (SI)
and
secondary
cortical areas
(Hoechstetter
et
al.,
2002),
data from healthy
people
typically show a
modulation of SII but not SI activity
ra-sk-relatedactors. However,
in
patients
with hyrloig[tpg@
showe6; ndffiaf
patter":of
rfiponse
r"t
characteristic onpprr"nt.
g"oeruied
iiU"otn
Sf
controlaterally and ipsilaterally to
the
pafrlats
relative to
Cn{eclT,
nTotfr-Srant su@-ffiCiGr
FGid aialirnneige
ithearlierEEG
England,1975). aken
the common
or instance"
standard soma
potentials
(SEPs),
visual
evoked
potentials
-case
stud
evoked Dotentia
Tery""tfra
8/17/2019 Hysterical Conversion and Brain Function
9/21
novel
stimuli
n an "oddball"
taskor by
infrequent
targets within
a stream
of successive
timuli,
and
presumably
eflects
a normal orienting
responseo
relevant
stimuli.
Lorenz et
al.
(1998)
designed
an
elegantEEG paradigm in which they repeatedly
stimulated he
unaffected eft
hand of a man
with
hysterical sensory
oss
on the right hand,
and oc-
casionally
applied a "deviant"
stimuli on
either he
affected right
hand, or on
another finger of the
$P*qlilg e:seje:
infrequent stimuli
on that side
(i.e.,
Iike
the con-
version
patient),
a P300was
still normally evoked
oy tnese o"uran@
hand, indicating that
a reduction of P300
n the
patient
was
not due
to malingering or control by
voluntary
inhibition.
Interestingly,
reducedP300 responseso
tactile
"oddball" stimuli
have also been observed
n
pa-
tients
who
present
with
a
"segmental
exclusion
syndrome"
(Beis
et al., 1998).These
patients
ex-
hibit
an abnormally
prolonged
under-use nd
pain
of
their upper limb
after sufferinga relatively
mi-
nor injury
to
peripheral
body tissues
n one hand
or one finger,
and such unctional exclusion
of the
limb cannot
be explainedby the severity
of
injury.
Although this syndrome
s different from conver-
sion disorder, t has similarly
beenconsidered
s a
maladaptive
deficit
with a
partly psychogenic
r-
igin, and abnormal P300 esponses €re nterpret-
ed as
reflecting
some
kind of attentional nhibition
or hemineglect
n motor
behavior
(Beis
et al.,
1998).Accordingly,
anomalies n P300
have been
f,ound or undetected
stimuli not
only in
patients
with spatial hemineglect
after right
parietal
lobe
lesions
Lhermitte
et al., 1985),but
also
n
patients
with
Parkinson's
diseasewith
impairments n in-
tentional
motor
planning
(Kropotov
and Ponoma-
rev,
99l; Sohnet al., 1998).
317
Evoked
potentials
in other sensory
modalities
such as vision and
audition have been
ess often
studied
beyondelementary
ensory esponses,
er-
haps
because onversion
disorders n
such modali-
tiesare ess requent,more variable,and/or seenby
physicians
ther than
neurologists.n
patients
with
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
n
patients
with
hysterical
deafness sported
a reducedP300
response,with
preservation
of earlier Nl
and N2 auditory
re-
sponses Fukuda
et al., 1996).
Some anomalies
were also reported
in
patients
with
various som-
atization symptoms
for the auditory
mismatch
negativity(MM1.0, which is normally evoked by
deviant
stimuli in
a series of repetitive sounds
(James
et
al., 1989).
Still other studies
reported
more
general
changes n EEG
spectra
n
patients
with conversion
nd somatoformdisorders.
nclud-
distribution
over
right
and lefllrontal
- + _ * : + /
y,
motor conversion
disordershave
been
investigated
by transcranial
magnetic stimulation
bffih6sC"cb
slds"did-rat
changewhen
pa_treats
ecovered
la$.qh-eil
lveak-
ness.There is
also anecdotal evidence hat con-
ffin patients may show an abnormal
contingent negative variation (CI.W)
component
in
EEG, which is normally
evoked
during
motor
preparation
in response o a cue
prior
to
an ex-
Considered all ical
da-
t
absenceof
af-
such
esultsare usually aken to indicate
hat mo-
tor
pathways
are structurally
and functionally in-
tact in
these
patients.
Only one recent
studv
&und
a decreased xcitabilitffit
Fgt-q$p-ry:€.:1ygf
g*yU--.t'"e-q,e_e_;"r'
eral left
hystericalweakness
Foong
et al., 1997b),
same unaffected
left hand.
The
patient
sbowed
a
normal P300
esponseor
dEfr6-ntJtffii-on:iG
ffid*painful tactile stimuli, demonst
(TMS),
typically
6voked
tials
over the motor co
ffisfiis
et a\., 1999).Again,
pected
o-be-judgedstimulus
(Drake,
1990).
are
Iectrng
h€_p- ngg-sensoryor
pnmary
motol$-
#
Ems
-Instead.
anv
chan-sesln-biain
function
8/17/2019 Hysterical Conversion and Brain Function
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3 1 8
associatedwith
conversion
misht involve
hipher
f - - - i
_
h
l_"dlo{.-pl-o-9"-e..s_s.lug,93._lppJ€Le$eg=*.1-_*F irq
sensoryandJ_q_1-mo.Jpr.--SiSnal$._=.a1q._.ig -e"g"r.p" _ej
di'tli
moie'ioriipir*'
information
related to the
meanng nd-.q i-rer.e-i-dr--;ji sdi-asa;eld;,
(e.g.,
motivational
significanc€,
ovelty, expected-
ness,
etc.). This might
relate
to
the
reduced
P300 response
ound in
a
few
different studies
using different
paradigms.
However,
EEG and
MEG
investigations
still remain remarkably
scarce,
and reported findings
have too rarely
been replicated to
allow firm conclusions
about
any
putative
neural
correlates
ofrspecifrcconver-
sion
symptoms.
Hemodynamic
rain imaging
Over
the
past
l0
years,
functional
brain imaging
has literally exploded into
innumerable
paths
of
new research
on the cerebralbases
of
various
be-
havioral functions
in
humans, ncluding not only
perceptual
and motor
processes
ccessibleo ex-
ternal
objective assessment,
ut also much more
complex mental
operations elated
to internal af-
fective
states
Damasio
et
al.,
2000),
perceptual
or
motor magery
Kosslyn
et
al.,
1995;
Ehrsson t al.,
2003),and €ven unconscious rocessing r prelbr-
ences
Elliott
and Dolan, 1998).This functional
brain
mapping approachhas.also
oensuccessfully
extended o
a
variety
of
psychiatric
conditions
such
asdepression,
bsessive-compulsive
isorders.
ho-
bia,
pos{-traumatic
stressdisorders, chizophrenia,
or hallucinations
(e.g.,
Frith
and
Dolan,
1998;
Parsey and Mann,
2003; Kircher, this volume).
Surprisingly,
however,
very
few neuroimaging
studies have been
performed
in
patients
with
conversion symptoms. despite
the fact that sucb
symptomsmight often be very well suited to neuro-
imaging nvestigations.
Most
neuroimaging studies
of
conversion
used
SPECT
(single
photon
emission computerized
tomography)
or PET
(positron
emission tomo-
graphy),
and t-ocused
n motor rather than sensory
conversion
symptoms.These
echniques llorv on-
ly
a
few
brain scans o
be taken and
provide
an
estimateof activity
averaged ver severalminutes,
indirectly
obtained
by a measure f cerebralblood
flow
changes uring
a restingstateor during a task
period.
The
first of such SPECT studies
was car-
ried
out by Tiihonen
and colleagues
Tiihonen
et
al.,
1995)
n
a
woman who
had a long history
of
left hemisensory isturbances f presumedhyster-
ical origin,
and reported both decreases
rytg4
p_gg"t"i"9tt""{y-."Afg9'_".g'*
A
tivity when
the affected hand of the
patient
was
. . r : : " ' l - . - : - * ; - - * i . - * . * - - " . . - - .
s ,iuulateClas
compaEd=-ffilFlffiiF sym'metiiC
pattern
after recovery).
However, his singleob-
servation
was mor€
qualitative
than truly
quanti-
tative,
and not statistically analyzed.
Similarly,
another SPECT study reported a seriesof five
pa-
tients with
heterogeneous onversion symptoms,
including
not only limb weakness ut
also
vertigo
and
gait
disturbances
$anci
and Kostakoglu,
1998), n whom
brain scansat rest showed
a re-
duction in
activity for several cortical regions,
predominantly
in left
parietal
and left temporal
lobes,
but with a
great
variability across
patients.
A more systematic
SPECT study
was
conducted
in our
own center, n a
group
of seven
patients
who
were
prospectively
elected asedon the
pres-
enceof
an isolated and
oofocal"
motor conversion
disorder, with
a
recent
onset and short duration
(<
2 months)
Vuilleumier
et al., 2001).Strict se-
lection
criteria
were
used including: unilateral
weaknessn upper and lower limb, with or with-
out sensory oss n the same erritory, but without
any other
psychogenic
or
neurological symptoms
(such
as headache,vertigo, blurred vision, etc.),
without
any
past
history of major
psychiatric
or
neurologicaldisease, nd without any
organic
le-
sion
as
determinedby
extensivemedical nvestiga-
tions
(i.e.,
brain and spine MRI, SEPs.MEPs,
VEPs,
EMG, etc.). These
patients
were
followed
up for 6 months after the onsetof their symptoms,
and underwent brain SPECT scanning in three
different conditions: (l) a baseline est condition
(To),
with eye closed
and no stimulation,
rvhen
motor symptomswere
present;
2)
a
passive
acti-
vation
condition
(Tl),
with bilateral vibrotactile
stimuli
(50
Hz)
applied
to both
the
affected
and
unaffected limbs simultaneously,
when
motor
symptomswere
pr€sent;
and
(3)
the
sameactiva-
tion sondition
(T2),
again with bilateral vibrotac-
tile stimulation of the affected and unaffected
limbs,
after motor symptoms
had recovered
8/17/2019 Hysterical Conversion and Brain Function
11/21
(in
four
patients;
three others
had
persisting
or
new symptoms at
6 months follow-up).
The
rationale of vibrotactile stirnulation
was to
pro-
vide
an
indirect activation of both sensory and
motor areas in the brain (since such stimuli
provide
inputs
not only
to
cutaneous but also
deep endon fibers), n a completely
passive,
ym-
metric, and
reproducible
manner.
All voxel-based
analyses n this study were
done on a
group
basis using statistical
parametric
mapping
(SPM)
(Friston
et al.,
1995).
A first analysis comparing activation
by bilat-
eral
vibrotactile
stimulation
to resting baseline
(Tl
>T0) revealed elatively symmetric
ncreasen
cerebral blood
flow in frontal and
parietal
areas
involved in somatosensory nd motor functions,
both
ipsilaterally and contralaterally
o the motor
conversion symptoms
(Vuilleumier
et a-1., 001).
This result
converges
with
previous
electrophysio-
logical data indicating
intact sensorimotor
path-
ways in
such
patients.
A second,more
interesting
analysis
compared activation by bilateral
vibro-
tactile stimulation after
recovery relative to the
same timulation
during symptoms
T2>Tl), pro-
viding
a
direct measur€ f changes
n
brain
activity
specificallyassociated
ith hystericalmotor weak-
ness, rrespective fany other distinctive
pattern
of
brain function in these
patients (e.g.,
related to
depression,
anxiety, or other
personality
charac-
teristics). This
cr€ases ln
in the
motor defrcit"
rv
her, the degreeof decreasesn caudate
nu-
"l""S
u"dJE
wa-J-ffififfim-"laGd
with
ilii-oqlation
oF
"Uf'gsfi.{';iffittre*t'"
regions n patientswho did not r€cov€r6 months
later, relative to thosewho
subsequently
ecovered
(Fig.
3B). This reducedactivation
n contralateral
basal
ganglia-thalamic
circuits
might therefore
provide
a
plausible
substrate for the subjective
motor conversion deficits. Finally,
we
also
per-
formed a reversecomparisonof
vibrotactile stim-
ulation
during symptoms relative to recovery
Ol>T2).Tfril_rbpy_qd."o-ply-1gdd.
n-sJess.e.$.
nss-
m1 o ep=9.{y,_cp$-er_a"an rp 4Je$l_ts-t}ssgmp.l.oms,
4 l'_l"eg9l_tggl9 .9:f
gry_qetgg_grthe
ffinot;eem
suppr€sre
f f a : -
(as preniouslfffr]oSul:-Iiidwig,
1972; Sierra
31 9
rPPhYsrsJ-oCY
and Berrios, 1999)but instead appearsenhanced
(Moldofsky
and England,
1975: Hoechstetter
er
a1.,2002).
These
selectiveanomalies n
subcortical brain
regions
during motor conversion
(Vuilleumier
et
al.,
2001)are intriguing since
hese egionsare in-
terconnected
nto functional
loops forming a cor-
tico*striato-thalamo-cortical
circuit
which is
critical
for voluntary motor action
(Alexander
et
al., 1986)
and since the striatum
(especially
cau-
date
nucleus)
constitutes an essentialneural
site
within such oops wheremotivational signalscan
modulate motor
preparation
activity
(Mogenson
et
al., 1980;
Kawagoeet al., 1998;Haber,
2003;see
Fig.
).
It is
therefore conceivable
hat thesecir-
cuits might become unctionally
suppressed uring
hystericalmotor
conversionunder the
influenceof
a
particular
affective
or motivational states,
re-
sulting
in an impaired "motor
readiness"or
im-
paired
"motor intention" for
the
affccted
imb(s).
Notably, in humans, ocal
tesions
e.g.,
stroke) af-
fecting the
basal
ganglia
(Watson
et
al.,
1978;
Healtonet al., 1982) nd
thalamus
Laplane
et al.,
1986;
on Giesenet al., 1994)are implicated
n a
syndrome of unilateral motor neglect,
n which
patients present
with impairments in motor
use
that cannot be explained
by
primary
weakness ut
rather
reflect
a lack of motor intention
or
plan-
ning. Sucha lossof
motor intentionhasalsobeen
implicated
in
the failure of some brain-damaged
patients
o becomeaware of their
(real) paralysis,
i.e., anosognosia
for hemiplegia
(Gold
et al.,
1994;
Vuilleumier, 2000b),suggesting hat subjec-
tive experience
of conscious motor action
and
volition might be linked to basal ganglia or
thalamus unction. Also
in support of this, direct
electric
stimulation of lateral thalamic nuclei
by depth
electrodes may trigger
contralateral
movementswith a subjective
experience f volun-
tary action
(H6caen
et al., 1949).Finally, changes
in basal
ganglia
activity
have also been impli-
.cated
n immobilization
behaviors exhibited by
animals to
protect
an injured limb
(De
Ceballos
et al., 1986).
8/17/2019 Hysterical Conversion and Brain Function
12/21
320
o: =
Decreased
activation
d urin
g
co n0alatelal
se
nsorlmotor
sym
ptoms
relative
o recovery
(T2
>
Tl)
Caudde
oo
6
dl
P
E
(D
o
?
(A )
D€ffcit
Flecovery
$1)
(r2)
Deficit
Recovery
(rl)
{r2)
Deficit
Recovery
(r1)
ff2)
lt
d)
g
(B)
s0
80
70
60
50
Ilecreased
cdvafion
urlng
conoalateral
ymptoms
scan
Tl)
predicfi
g clinical
evolution
Symptoms
fier4
montfts:
$
eenistentln=3palienG)
ffi
lmproved
n=
4
patients)
Fig. 3. Changes
n brain activity
associated
with
hysterical
paralysis.
(A)
Selective
decreases
n activity
were found
in the thalamus,
caudate, and
putamen
(upper
row)
in the hemisphere
contralateral
to the
limb affected
by sensorimotor
symptoms.
Measures
of
regional cerebral blood
flow
(rCBF) were obtained
by SPECT scans
n 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
decreased
n all these
subcortical
regions n all
patients
n T'l as
compared
with the same
regions
n T2 or with homologous
regions n the
bcmisphere psilateral
to the
symptoms n
T1.
(B)
Such
decreases
n the thalamus
and
caudate
(but
not in the
putamen)
were
more severe
n the initial scan
fl)
in the
three
patients
who had
persisting
symptoms
at
follow-
up
4 months tater, as compared
with.four other
patients
who had
recovered,suggesting
lat the
severity of
decrease
at the time of
initial
symptoms, may
predict
the
duration of their
symptoms.
(From Vuilleumier et al.,
2001).
Thalamus
Putamen/Pailidum
Cilc€,/e
Thalamus
8/17/2019 Hysterical Conversion and Brain Function
13/21
321
Motor
commands
Modulations
bymofivafon
f,
or emotlon
\ \ \
z
\t-* r-'r ---)/;
\-*"(
\
---'',-'
it[[[E\ | -
f f i ) ) -
VL-z
m
prinErymotorarea
TUIUIIETI
& oallidum E
Supdemertary otor rea
ffi
Prsmotor
area
lffi
Preftontalcortex
I
Linbicarea
Fig. 4.
Schematic llustration of cortico-subcortico-cortical loops.
These circuits link
various
areas n frontal cortex
to
the caudate
nucleus,
putamen
and
pallidum,
halamus,and
then back o the cortex,allowing a modulation and coordination of motor commands
initiated in the cortex during movement
execution- but
presumably
also during more complex
cognitive
operations. Such oops
provide
several neural sites,
particularly
in
the striatum/caudate,
where
neural signals can be modulated by allective and motivational inputs
from many other brain regions
(such
as
orbitofrontal cortex, cingulate cortex, or amygdala), constituting a cerebral system hought
to
be critical for the integration of volitionally guided and emotionally triggeredexpressionsof behavior.
,/
Motor
(f
execut'on
\\
S
halamus
prod
uced i nclqglgd_agUyalrp:Lof--:rentroge&l
fiffiffi*Aortex, including
right anterior cingulate
dndTEmbrbitttfibii&l cbffi;*fii"h
.I,.
"inorr"*
duiill|
irioVein€nt-biEtlirtion- lith
the unaffected
ri-ghtEg. II ivasccincludCtihat 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,
t
is
possible
hat this increase n frontal ;ndqlguEg
afnvationmghr
fr
pncm
tnese
egions
ricTr-
as-diffi
-ulty-,
rqni-
tbimE-oTleilure_-&us-gt-al-.--lt9-8;van.V.een
200-a)-ortiriflict
(Dehaene
t al.,
2003;Badre
and
WeEner,
O0+; ue to ambiguous
ask demands
(r
ffi
biatum
Other functional changes
n brain areas elated
to voluntary motor control havebeensuggested
y
two PET
studies
n
patients
with
hystericalmotor
deticits
(Marshall
et
al.,
1997;
see also Spence,
1999;
Spence t al.,
2000; or
review). Marshall et
al.
(1997)
studied
a single
patient
with a history of
unilateral
left
leg
weakness
ersisting
more than 2
years,
n a
task requiring
either to
prepare
or to
execute movementswith either the left (affected)
8/17/2019 Hysterical Conversion and Brain Function
14/21
(i.e.,
"try
to move even
f
you
cannot").
In any
healthy subject who perfonned the same motor
preparation
and execution
ask as n the
preceding
study, but now
49.
hlp1ggg_qUgglstiol
of uni-
lateral
paralysis
(Halligan
et al., 2000).
Although
this result suggests
ome similarity
betweenhyp-
notic suggestionand conversion
symptoms,
this
classic elationship
(entertained
since Charcot by
many others:
see Bliss, 1984;
Spiegel, l99l;
Oakley, 1999)may
still not be firmly established
(see,
.g.,
Persinger, 994;Foong
et al.,1997a).
A subsequent
PET study therefore
compared
three
patients
who had
hysterical weakness
two
patients
n
left arm and
one
patient
in right
arm),
with four healthy
control subjectswho
were in-
structed o feign
motor weakness f the right
hand
(Spence
t al., 2000).
All
participants
had to
per-
form regularly
paced
movementswith
a
joystick
held
n
their affected
or pseudo-affected)
and. As
1€I9 P,
Patients
it
co d
-+
dgglgl*4activity in
left
prefrontal
cortex relative
to the
decreased
activity
in-rignt
"prefroiittfE6itex-r€E-
ti ve t
o co
n
ve
Si6-fr
-tfi
6if ilTlie au h
o rs su
glEildd
that leTtfionlatd66ffiIffi*n in hysteria may reflect
the role of these
cortical areas n motor
planning
(Spence,
999).However.
qft frontal hypoactivity
^ . - r u
is also frequently
seen n other conditions
such as
SpryssEu-
evueis,
2T031
Ali"patfiil
in t[i"
Study had a history of
depression, lthough none
needed reatrnent
at the time of scanning.More-
over, these eft frontal anomalies id
not
provide
a
direct functional
substrate for the contralateral
motor
deficit
itself, since he
affectedside differed
across
he
patients.
But nevertheless,ome
mpair-
ment in internal representationsof voluntary
movements s likely to be
present
n these
patients,
as also suggested y
purely
behavioral
studies hat
compared
mental 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
magnetic resonan@maging
(fMRI)
to examine he
functional
patterns
of brain
activity associatedwith
hysterical
conversion,concerning
de{icits n somato-
sensory
processing Mailis-Gagnon
er
al.,
2003)
_- - __J_
.+-
-
---.---"-g_\
and visual
pejgpption
Werring
et
al., 2004).
Mailis-
Gagnon et al.
(2003)
studied
four
patients
with
chronicdeficits n sensation f touch and/or chronic
pain
a"ffecting
one
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
revealed
different
patterns
for different brain
areas.
First,
unlike stimulation
on intact imbs
(which
were
always
perceived
nd
reported),
both noxious
and
non-noxious
stimuli
on
the
une"Al;u-f*rri"r,
ye @&t}djgp-t :e e
the
halamus,nsular,
nferior rontal,
and
posterior
iingnlatb'
Coitic
8/17/2019 Hysterical Conversion and Brain Function
15/21
an
attempt
to move
the
parulyzed limb
in
motor
conversion
or hypnosis
(Marshall
et
al.,
1997;Halhgan
t a1.,2000).
ikewise,
recent
MRI
cortex,
temporal
poles
as
well q;
on
fitrs"Tftffi
#-----@
different
from
previous
findings
for sensorimotor
deficits,
this
pattern
was again
interpreted
as
gen-
erallyconsistent
with the dea
hat
conversion
might
involve inhibitory modulationof visual processing
through
increases
n the activity
of limbic
areas.
Altogether,
these
new functional
neuroimaging
data
provide
compelling
evidence
hat
"function-
al"
symptoms
n
patients with hysterical
conver-
sion
may at
least in
part
correspond
to
specihc
components
n brain
function,
potentially
under-
lying
an abnormal
awareness
f
perceptualand/or
motor
abilities.
Here
again,
here are
still
too
few
studies,
using
different
paradigms
in
different
types
of
patients,
such
hat no
definite
conclusion
tivation
as
r, further systematicstudies are needed o
better
tease
apart the neural
correlates
associated
with
subjective
det'icits
hemselves
rom
other
as-
p€cts potentially associated
with
coexisting
disor-
ders, such
as changes
in
mood
or anxiety"
personality
characteristics,
xpectations,
ttention,
coping
reactions
as
well asany activity
conceivably
related
to unconscious
affective
motives
and
con-
flicts
that
were
postulated
by
Freudian
psychody-
namic accounts.
More
questions
nd
nerv
directions
A better
understanding
of
functional
changes n
brain
activity
during
hysterical
conversion
s cer-
tainly important not only becausehis may yield
new
insights
into neural
correlates
of
subjective
experience
and
awareness,
ut also
because
his
may
provide new
constraints
on
theoretical
ac-
counts
of
conversion,
n a
neurobiologically
plau-
sible
ramework,
and
therefore
ead
o improve
the
diagnosis
and
management
f
patients.
There
s
no
doubt
(and
perhaps
no surprise)
hat an
altered
experience
f
bodily
functions
might
be associated
with specific
modifications
n the
brain
networks
normally
responsible
or
generating
our
conscious
experience f such unctions,asalso demonstrated
for
even
more
extreme
disturbances
n bodily
awareness
Vuilleumier
et
al.,
1997;Blanke
et al.,
2004;Blanke,
his volume).
Demonstrating
specific
neural
correlates
of hysterical
onversion
may also
help
reassure
he
patients
as
well as
their
caretak-
ers, ncluding
nursesand
doctors
who sometimes
show
negative
or
unsympathetic
reactions
when
confronted
with complaints
unaccompanied
by
visible organic
pathology.
As
already
suggested
y
James
1896),
this may
eventually
help convince
some
skeptics
hat
hysteria
s a
"real disease,
ut a
mental disease".
Importantly,
neurobiological
findings
should
lead
to
refine our
current
psychopathologicalex-
planations of conversion,
by
suggesting
possible
mechanisms
by
which
the
mind can
produce
changes
n
the brain
and body
functions.
Such
mechanisms
re likely
to
involve
dynamic
nterac-
tions
between
neural
systems
mediating
specific
functions
(e.g.,
motor,
somatosensory,
r visual
processing) nd neural
systems
esponsible
or af-
fective
evaluations
and
reactions,
based
on current
aswell aspastexperiencese.g., imbic areasn the
broad
sense, uch
ascingulate
gyrus,
orbitofrontal
cotrtex,
or amygdala).
Such
interactions
between
distributed
brain areas
might
be usefully
investi-
gated
by neuroimaging
studies
using
connectivity
analysis
(e.g.,
Friston,
1994;
Mclntosh
and
Gonzalez-Lima,
1994).
Various statistical
tools
now
exist o
describe
ow
neural activity
in one
or
several
egions
can
either
influence,
or
instead
be
contingent
upon,
neural
activity
in other
regions.
other
hand.
increased
activity
was found
S
8/17/2019 Hysterical Conversion and Brain Function
16/21
324
New methods
allowing
inferences
bout
the
direc-
tionality
of such
nfluences
suchas dynamic
caus-
al
modeling,
see
Friston et
al., 2003)
might
prove
particularly valuable n
this context.
Thus, in our own study of hystericalparalysis
(Vuilleumieret al.,
2001)demonstrating
educed
activation
in the
contralateral
basal
ganglia-
thalamic
circuits,
which
became
normal
again af-
ter
recovery
rom
paralysis,we were
also
able to
show
that such
changes
o-varied
with concomi-
tant changes
n other
distant
brain areas,
where
activity
was not
globally
reduoed
or enhanced
but
rather appeared
differentially
coupled
with
the ba-
sal
ganglia-thalamic ircuits
during
paralysis.This
was
demonstrated
using
a type of
principal
com-
ponent analysis scaledsubprofilemodeling;Mo-
eller
and Strother,
99l) that
allowed
us to
identify
three
distinct
networks
of regions
whose
activity
tended
o covary
together across
all
subjects
and
all sessions,
rrespective
of their absolute
evel of
activity.
Critically,
this
analysis
dentified a
net-
- -
work including
he cau
8/17/2019 Hysterical Conversion and Brain Function
17/21
generalization
of the
findings
from one
study to
another.
Future studies might
therefore
ruitfully
com-
pare patterns
of brain
activity in
conversion
pa-
tients showing different types of deficits (e.g..
motor or
somatosensory
oss)
to
determine
more
directly
what are the
changes elated
to specific
symptoms,and
conversive
eactions n
general
for
instance, esting
whether some
effects n anterior
cingulate and
frontal cortex may
arise
rrespective
of
the type
of deficit).
New studies
should also
use
different
possible
approaches,
,or instance
by ex-
amining
brain function
more systematically
uring
and after
conversion
deficits in
the same ndivid-
uals; by manipulating
more
explicitly
factors re-
lated to attention, expectationor inhibitiory and
by investigatingany
differences
n brain reactivity
to stressful
probes
presented
o these
patients
even
when hey have
ecovered rom
specificconversion
symptoms.
In addition,
we need to
b€tter under-
stand the
cerebral mechanisms
nvolved
in other
psychiatric
disturbances
haracterized
by dissoci-
ative symptoms,
such as
psychogenic
amnesia
or
"mnestic
block"
(Markowitsch,
2003;
Glisky et al.,
2004), or depersonalization
disorders
affecting
p€rception
of the
self and/or
of the environment
in stressful ituations
Lanius
et a1.,2002;
Reinders
et al., 2002).
New imagingdata
may help to clarify
the
possible
relationships of these
disorders
with conversiondisorders
and other types
ofpsy-
chogenic
"block"
affecting
conscious ensoryand
motor functions.
Interestingly, unctional neuro-
imaging
correlatesof dissociative
esponses ave
also highlighted
a key role of
medial
prefrontal
areas for integrating
perceptual
or motor
repre-
sentations
with a subjective sense
of 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
between
neurologyand
psychiatry,
,ew
systematic and controlled
studies have
yet
been
conducted
using modern neuroimaging
ools.
This
is
surprising
given
the variety of
currently availa-
ble techniques
ERPs,
MEG,
PET, SPECT, MRI)
325
the
rich
productivity of imaging
research n
neuropsychiatric
domains.
A better
under-
ing of functional
changes
n brain activity
ing hysterical
conversion
will undoubtedly
pro-
unique insights into neural mechanismsot
consciousness,
ut should
also
mprove the
gnosis,
management,
and assessment
f
prog-
;is n these
patients. Finally,
further research
n
field might certainly
contribute
to strengthen
links between
psychiatry
and
brain sciences.
thanks
to F. Assal,
C. Chicherio,
T. Landis,
S. Schwartz
for their
precious
collaboration,
to P. Halligan for manyvaluable discussions
of this
work
was supported
by
grants
from
Swiss
National Foundation.
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