hysterical conversion and brain function

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:

[email protected]

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


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


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


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


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-


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


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


8/21

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


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


10/21

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


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).


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


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)


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


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


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


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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