259

GILLES DE LA TOURETrE'S SYNDROME
In our patient an acute akinetic state, which may
have reflected an acute reduction of functional
dopaminergic

activity, was followed by a sustained

improvement in the TS. This gives further support
to the hypothesis that dopaminergic
or other
functionally related pathways are involved in the
aetiology of TS.

MEYER, B. C. & Rosa,

D. (1986)

Runarks

on the etiology

of Gilles

de la burette's syndrome. Journal of Nervous and Mental
Disease, 174, 387—3%.
RASTOGNI,
R. B., LAPIERRE,Y. D. & SINGSIAL,
R. L. (1978) Some
neurochemical correlates of “¿rebound―
phenomenon observed
during withdrawal after long term exposure to l,4-benzo
diazepmes. P1'ogress in Neuro-Psychopharmacology, 2,43-45.
SHAPIRO, A. K. & SHAPIRO, B. (1988) Treatment
of Gilles de la
Tourette's
syndrome
with haloperidol.
British
Journal
of

Psychiatry, 114, 345-350.
SNYDER, S., TAYLOR, J. M.,

References
CAMPBELL, A. & BALDESSARINI, R. J. (1985)

diazepinesDivided(ed.
Wiley.

T. J., eta!

(1970)

The

role

of

psychotropicdrugs.AmericanJournalofPsychiatry,127,117-125.
Prolonged

pharmaco

VON Ecop@o,@io,
C. (1931) Encep'valitis

logicactivityof neuroleptics.Archivesof GeneralPsychiatry,
42, 637.
LADER, M. (1983) Benzodiazepine

Cois,

brain dopamine in behavioural regulation and the actions of

withdrawal states. In Benzo

f@g@g@•
its Seque!ae and

Treatment (trans. K. 0. Newman). Oxford: Oxford University
Press.
WOOD, P. L., ETIENNE, P.,

LAL, S., eta!

(1984)

Benzodiazepines

and GABAergicof nigrostriatal neurons: lack of tolerance.

M. R. Trimble), pp. 17-31. Chichester:

Progress in Neuro-Psychopharinacology, 8, 779-783.

Simon Wright, MB,ChB,MRCPsych,Registrar in Psychiatry; *Malcolm Peet, MB,ChB,MRCPSyCh,
Consultant
Psychiatrist, Northern General Hospital, Herries Road, Sheffield S5 7A U
5Correspondence

British Journal of Psychiatry (1989), 154, 259—261

Treatment of Mood Disorder Associated with Bmswanger's Disease
EILEENM. JOYCE and RAYMOND LEVY
Binswanger's disease is a cerebrovascular disorder affecting deep white matter and is
associated with dementia and affective disturbance. In the case reported, the mood
disorder was successfully treated with a combination of lithium and amitriptyline, resulting
in an improved quality of life despite continuing
cognitive decline. This underlines
the
importance
of treating the affective component
of organic dementing conditions on its own

merit.

Binswanger's

disease

disease

in which

is a variant

of cerebrovascular

the periventricular

and

deep

white matter bear the brunt of the neuropatho
logical

process

and in which

there

are athero

intellectual

processes,

memory

impairment

and

disorientation.
The advent of computerised tomography (CT) and
magnetic resonance imaging (MRI) has allowed

sclerotic changes in local nutrient arteries (Olzewski,
1962). The clinical accompaniment has been
reviewed by Caplan (1985) and consists of a

changes in the white matter to be identified in vivo,
and the neologism leuko-araiosis has been coined

progressive dementia with or without neurological
signs, beginning in middle or old age, and often

1987). Whether leuko-araiosis actually represents

associated with psychiatric disturbances such as
depression,

euphoria,

irritability

and anxiety. The

dementia takes the form of a generalised slowing of

to

describe

Binswanger's

such

a finding

(Hachinski

et al,

disease is under debate (Hachinski

et

al, 1987) because, while the latter used to be a
relatively rare finding at post mortem, the former
is becoming an increasingly

common

observation.

260

JOYCE AND LEVY

Nevertheless,

an

association

between

the

cardio

vascular indices of stroke and hypertension with
leuko-araiosis
has been described (Kinkel et a!,
1985; Inzitari et a!, 1987) and, indeed, one report
has convincingly
demonstrated
an association
between leuko-araiosis, as an isolated finding, and
intellectual impairment, suggesting that this might

/

/ I

be a marker for early dementia (Steingart eta!, 1987).

.4

There are few studies of therapeutic strategies in
Binswanger's disease, and no evidence to suggest
that successful treatment of the cardiovascular
complications either arrests or improves the neuro
psychiatric features. Biemond (1970) reported that
the

cerebrovascular

dilator

hydergine

,1

improved

cognitive function in one patient. There is only one
case report, to our knowledge, of a beneficial effect
of psychotropic medication on the mood disorder
associated with Binswanger's disease (Summergrad,
1985). In this case, a monoamine

,@

it-

oxidase inhibitor,

tranylcypromine,
but not a tricyclic antidepressant,
produced a marked improvement in mood and day
to-day activities. However, this patient had a 14-year
history

of a relapsing

severe

depressive

illness

and

on admission was found to have hypopituitarism.
Thus the depressive illness may have been co
incidental but not integral to Binswanger's disease.
We report a case in which the first episode of an
affective

disturbance

arose

in the

context

of

a

diagnosis of Binswanger's disease, and which was
successfully treated with antidepressant drugs.

Case report
The patientwas a 70-year-old
man with a nine-month

history of social withdrawal, lethargy, intermittent dis
orientation and memory problems. On admission to
hospital he had psychomotor retardation, poor appetite and
weight loss; this picture was punctuated on at least two
occasions
by 48-hour episodes of hyperactivity
and
excitability.
Cognitively he was disorientated
in time
and displayed impairment
of recent memory. Physical
examination

revealed

dyspnoea,

fast

atrial

fibrillation

and hypertension.
Extensive investigations
confirmed
cardiovascular
disease but did not reveal any treatable
organic

cause for his mental state. A CT scan demonstrated

ventricular enlargement and patchy changes in the deep
white matter. An MRI scan was performed (Fig. 1), which
showed

periventricular

white-matter

lesions,

with

no

evidence of cortical infarction.
These findings suggested a diagnosis of Binswanger's
disease

in association

with cardiovascular

disease

successfully with a combination of digoxin and diuretics.
In view of the observed rapid cycling of mood, lithium
carbonate (800 mg/day) was initiated. Because of cardio
vascular risk, antidepressants
were initially withheld;
as there was no improvement

of mood

1.

Magnetic

resonance

image

(spin-echo)

demonstrating

months, mianserin was added, up to a dose of 120 mg/day.
After three months on this combination
of drugs his mood

improved, he became orientated and his memory appeared
normal. He then stopped attending hospital and failed to
take his medication. This resulted in rapid deterioration and
he became quite clearly depressed. A combination of lithium
carbonate

at the previous

dose and amitriptyline

up to a dose

of 150 mg/day was initiated, with subsequent and significant
improvement,

which

has continued

for over a year.

Although the impression was that cognitive function had
improved along with his mood, this was not borne out by
formal neuropsychological
tests. On admission there was

no evidence of general intellectual decline, but he performed
poorly on specific tests of memory (Wechsler logical
memory and associate learning (Wechsler & Stone, 1945),
Kendrick

object

learning

(Kendrick,

1985)).

After clinical

improvement,
he continued to perform badly on the
memory tests, and in addition his performance IQ estimated
by the Wechsler Adult Intelligence Scale (Wechsler, 1955)

had deteriorated, perhaps indicating the onset of a more
global dementing

process.

and

hypertension. The physical complications were treated

however,

FIG.

areas of high signal intensity within the white matter (focal) and
around the ventricles (confluent).

after two

Discussion
Several neurological disorders exist in which the
pathological
process mainly affects subcortical
structures, and in which there is a neuropsychiatric
component characterised by psychomotor slowing,

MOOD

DISORDER

AND BINSWANGER'S

memory impairment, difficulty with problem solving
and mood disorder. Examples are Parkinson's
disease, Huntington's chorea, and progressive supra
nuclear palsy - the so-called subcortical

dementias

—¿,

Binswanger's disease (Ron, 1985; Caplan, 1985).
Although there have been no systematic studies of
the management of the psychiatric aspects of these
diseases, the affective disorder is often considered
to parallel the cognitive decline and to reflect the

underlying neuropathological changes. In this report
we have described such a case in which the patient's
quality of life was improved, despite continuing
cognitive decline, by successful treatment of the

mood disturbance. This underlines the importance
of treating the psychiatric component of organic
dementing

conditions

on its own merit.

Dr Joyce is currently a Welcome Trust Lecturer in Mental Health.
performance of an MRI scan at the National Hospital for
was typed by Mrs Maja Fisher.

References

&

WILLIS,

A.

BIEMOND, A. (1970) On Binswanger's
encephalopathy
and the possibility

L.

(1974)

The

‘¿subcortical

subcortical
arteriosclerotic
of its clinical recognition.

Psychiatria Neurologia Neurochirurgia, 73, 413-417.

CAP@, L. R. (1985)Binswanger'sdisease.Handbookof Clinical
Neurology, 46, 317—321.
HACHINSKI, V. C., PO-i-mR, P. & MERSKEY, H. (1987) Leuko
araiosis.
Archives
of Neurology,
44, 21-23.
INzrrARI, D., DIAZ, F., Fox, A., ci al(1987)
Vascular

risk factors

and leuko-araiosis. Archives of Neurology, 44, 42-47.
KENDRICK, D. C. (1985)

Kendrick

Cognitive

Tests for

the Elderly.

KINKEL, W. R., JACOBS, L., POLACHINI, I., ci a! (1985)

Subcortical

Windsor: NFER-Nelson.
arteriosclerotic encephalopathy (Binswanger's disease): com
puted tomographic, nuclear magnetic resonance and clinical
correlations. Archives of Neurology, 42, 951-959.
MCHUGH, P. R. & FolsrEIN,

M. F. (1975) Psychiatric

syndrome

in Huntington's chorea: a clinical and phenomenologic study.

In PsychiatricAspectsof NeurologicDisease(edsD. F. Benson
& D. Blamer), 267-286. New York, Grune and Stratton.
OI.zEwsKI,J. (1962) Subcortical arteriosclerotic encephalopathy.
WorldNeurology,
3,359—375.
RoN, M. A. (1985) Multiple sclerosis: psychiatric and psychometric

and neurologic findings in subjects with diffuse white matter
lucencies on computed tomographic scan (leuko-aralosis).
Archives
ofNeurology,
44,32-35.
Sua,aemo@, P. (1985) Depression in Binswanger's encephalo
pathy responsive to tranylcypromine: case report. Journal of
Clinical Psychiatry, 46, 69—70.
WECHSLER,

dementia.

0.

3—Il.
STEINGART,A., HACHINSKI,V. C., LAU, C., ci a! (1987) Cognitive

We are grateful to Dr Maria Ron for making possible the

ALBERT, M. L. (1978) Subcortical

R.

abnormalities. Journal of Psychosomatic Research, 30,

Acknowledgements

Nervous Diseases. The manuscript

FELDMAN,

dementia' of progressivesupranudearpalsy. JournalofNeurology,
Neurosurgery and Psychiatry, 37, 121-130.

(Albert et a!, 1974; McHugh & Foistein, 1975;
Albert, 1978). Furthermore, diseases predominantly
affecting cerebral white matter can also develop this
clinical picture, for example multiple sclerosis and

261

DISEASE

Disease: Senile Dementia andRelated Disorders (edsR. Katzman,

R. D. Terry& K. L. Bick),173-180.NewYork: RavenPress.

D. (1955)

Wechsler

Adult

Intelligence

Scale

Manual.

New York: The PsychologicalCorporation.

In Alzheimer's
—¿

&

STONE,

C.

P.

(1945)

WecMer

Memory

Scale

Manual.

New

York: The PsychologicalCorporation.

5Eileen M. Joyce, MA, PhD, MRCP, MRCPsych,Weilcome Trust Lecturer in Mental Health, Institute of
Psychiatry, De Crespigny Park, London SES 8AF; Raymond Levy, PhD, DPM,FRCP,FRCPsych,Professor
of OldAge Psychiatry, Section of OldAge Psychiatry, Institute of Psychiatry, L)e Crespigny Park, London
SES 8AF
Correspondence

British Journal of Psychiatry (1989), 154, 261—262

Wernicke's Encephalopathy

in an 18-Year-Old Woman

STUART TURNER, LYNN DANIELS and STEVEN GREER

An unusually young woman (18 years old) who misused alcohol and developed Wernicke's

encephalopathy is described.
Wemicke's encephalopathy

is an infrequent but well-

recognised complication of alcohol misuse in men

over the age of 20. We describe the clinical syndrome

in a young woman who misused alcohol.