LETTERS

Thalamic Acalculia
SIR: Acalculia refers to impairments
in mathematical abilities from brain
injury.1 Acalculia can result from
language impairment, visuospatial
difficulties, or a primary anarithme-
tia for mathematical operations.1–3
Calculations also require working
memory as a temporary online buf-
fer necessary for complex computa-
tions. We report a patient with acal-
culia from a left thalamic stroke and
analyze his deficits.
Case Report
A 61-year-old right-handed carpet
salesman became acutely unable to
figure out how to perform the cal-
culations needed to determine the
amount of carpet for a floor area.
He denied trouble with other daily
calculations, such as making change
at the store, estimating quantities,
or using a calculator. His history
was significant for lacunar strokes,
two myocardial infarctions, hyper-
tension, hypercholesterolemia, and
heavy smoking.
Except for his acalculia, his exam-
ination was mostly normal. He
scored 29/30 on the Mini-Mental
State Examination, missing one re-
call item. His digit span was 6 for-
ward, but he was able to repeat
only one digit backward and had
difficulty on more complex serial
reversal tasks. Tests of language,
declarative memory, visuospatial
construction, praxis, right–left ori-
entation, finger naming, and alter-
nate programs were all normal.
Cranial nerves, gait, coordination,
and sensory examinations were
normal, but he had a slight right
upper extremity pronator drift and
his reflexes were brisker on the
right with a right upgoing toe.
On magnetic resonance imaging,
he had old lacunar infarcts in the
right caudate head and the genu of
the left internal capsule and a new
lacunar infarct in the anterior aspect
of the left anterior thalamus.
He underwent tests of his calcula-
tion ability. On 16 written prob-
lems, he made the following errors:
5Ⳮ6⳱36, 26Ⳮ17⳱53, 621ⳮ72⳱
541, 5⳯13⳱75, 78/13⳱5.5, and
carrying-over errors in 42⳯126. On
a word problem (18 books on two
shelves, put twice as many on top
shelf), he stated ”18 on the top and
none on the bottom.” On the EC301
Battery (Table 1),1,3 he made errors
in mental and written calculations
but did well on all other subtests.
The patient satisfactorily explained
each individual step involved in
calculating the sale of carpet but

TABLE 1. EC301 battery and additional math questions administered to patient

Score
Measure Max Patient
3
EC301 battery
Number sequences C1–C3: spoken verbal, arabic digital, written verbal 14 14
Dot counting C4–C8: two small sets, three medium sets 30 30
Transcoding C9–C15: oral, reading and writing, arabic-written verbal 84 83
Arithmetic signs C16–C18: naming and writing 16 16
Number comparison C18–C19: 16 pairs arabic, 16 pairs written verbal 32 32
Mental calculation C20–C21: spoken numbers and arabic 32 27a
Estimation of the result of an operation C22 16 16
Number positioning on a zero to 100 vertical scale C23–C24 20 20
Writing down an operation C25: spatial alignment 8 8
Written calculation C26–C28: addition, subtraction, multiplication 15 7a
Perceptive estimation of quantity C29 12 12
Contextual magnitude judgments C30 10 10
Precise number knowledge C31 12 12

Additional mathematical fact questionsb

How many degrees in a right angle? Patient’s answer: 90⬚
How many sides are there in a pentagon? Patient’s answer: 5
What do the angles of a triangle add up to? Patient’s answer: 180⬚
How many corners does a cube have? Patient’s answer: 8
What is the freezing point of water? Patient’s answer: 32⬚ F
a
Scores fall bellow tenth percentile for normal subjects.3
b
Modified from Crutch and Warrington, 2001.2

J Neuropsychiatry Clin Neurosci 15:1, Winter 2003 115

LETTERS
could not perform the actual series
of steps.
Comment
Acalculia commonly results from
disturbances in the left parietal cor-
tex but can result from abnormali-
ties in prefrontal and other loca-
tions.1 Infarction in the territory of
the left tuberothalamic artery can
produce acalculia from involvement
of the ventral lateral and dorsome-
dial thalamic nuclei with sparing of
other nuclei,4 similar to the findings
in our patient.
We analyzed our patient’s acalcu-
lia. There was no evidence of alexia
or agraphia for numbers or other
specific numerical problems. He
could perform most simple mathe-
matical operations, but he had diffi-
culty in performing complex or
multistep operations. Along with
his initial difficulty with serial re-
versal and mental control tasks, his
examination suggested a form of
acalculia stemming from difficulty
with working memory. Recent re-
search has documented the role of
working memory in performing
multistep, complex calculations,5
and lesions in the left thalamus, as
well as dorsolateral frontal regions,
could impair working memory.
MARIO F. MENDEZ, M.D., PH.D.
NORA C. PAPASIAN, M.D.
GERALD T.H. LIM, M.D.
Departments of Neurology and
Psychiatry & Biobehavioral Sci-
ences, University of California
at Los Angeles, VA Greater Los
Angeles Healthcare Center, Los
Angeles, CA
References
1. Kahn HJ, Whitaker HA: Acalculia: an
historical review of localization. Brain
Cogn 1991; 17:102–115
2. Crutch SJ, Warrington EK: Acalculia: def-
icits of operational and quantity number
knowledge. J Int Neuropsychol Soc
2001; 7:825–834
3. Dellatolas G, Deloche G, Basso A, et al:
Assessment of calculation and number
116
processing using the EC301 battery:
cross-cultural normative data and appli-
cation to left- and right-brain damaged
patients. J Int Neuropsychol Soc 2001;
7:840–859
4. Bogousslavsky J, Regli F, Assal G: The
syndrome of unilateral tuberothalamic
artery territory infarction. Stroke 1986;
17:434–441
5. Prabhakaran V, Rypma B, Gabrieli JDE:
Neural substrates of mathematical rea-
soning: a functional magnetic resonance
imaging study of neocortical activation
during performance of the necessary
arithmetic operations test. Neuropsy-
chology 2001; 15:115–127
Heroin and Malignant
Coprolalia in Tourette’s
Syndrome
SIR: Coprolalia, the involuntary
emission of socially unacceptable or
obscene sounds, words, and utter-
ances, is a typical symptom of Tou-
rette’s syndrome (TS).1 Rarely, cop-
rolalia can adopt a malignant
character because of the uncontrol-
lable emission of obscenities and re-
fractoriness to multiple pharmaco-
logical agents. We report the
emergence of malignant coprolalia
and motor tic exacerbation in a
woman with TS in association with
chronic heroin abuse.
Case Report
The patient was a 37-year-old
woman in whom repetitive phonic
tics (“ih”) had developed when she
was 9. Phonic tics had a fluctuating
course thereafter, and at the age of
15 she developed eye movements,
mouth opening, neck jerks, bilateral
shoulder shrugging, abdominal
tensing, touching rituals, and mild
self-injurious behavior. The patient
rarely pronounced obscene words,
and she added letters and changed
the accentuation of words to cam-
ouflage their obscene content. She
also had obsessive-compulsive be-
havior and borderline personality
disorder. She received haloperidol
J Neuropsychiatry Clin Neurosci 15:1, Winter 2003
for 3 years with partial control of
tics. At the age of 25 she began to
smoke heroin once a week to allevi-
ate puerperal dysphoria. Three
months later, she experienced an
uncontrollable increase in motor
tics and began to emit, for the first
time, loud phonic tics (cough) and
obscenities.
Obscene words and phrases
erupted in a distinctly louder tone
and with a lower pitch and more
obvious hoarseness than the patient
used in a normal conversation,
were unsuppressible voluntarily,
and occurred very frequently
(about 10 words or phrases per
minute). She was admitted to an in-
patient detoxification program for 6
months, during which she stopped
smoking heroin. However, coprola-
lia and motor tics did not improve,
and trials of haloperidol, sulpiride,
clonazepam, tetrabenazine, risperi-
done, and olanzapine were ineffec-
tive. An otolaryngologic examina-
tion revealed Reinke’s edema due
to vocal abuse, and microsurgical
decortication of the vocal cords was
performed. During the surgical pro-
cedure, 30 units of botulinum toxin
were injected in the left vocal cord,1
but this treatment failed to suppress
coprolalia. She continued to abstain
from illicit drugs, but 6 months
later she smoked a heroin mixture
and was readmitted in a tic status
(incessant coprolalia and violent
motor tics) that required sedation
with a propofol infusion. The pa-
tient’s condition partially improved,
and she was discharged on a re-
gime of sulpiride 600 mg/day and
clonazepam 4 mg/day without ade-
quate tic control.
Comment
Converging evidence suggests over-
lapping biological mechanisms be-
tween TS and associated drug
abuse.3,4 Motor tics and vocaliza-
tions in TS are thought to be the re-
sult of disinhibition of the dopami-
nergic system.1,3 Coprolalia has

been associated with increased met-
abolic activity of the left language-
related corticosubcortical network
(perisylvian cortex, cingulate gyrus,
basal ganglia, thalamus), which is
modulated by dopaminergic projec-
tions from the ventral tegmental
area (VTA).3 The mesolimbic sys-
tem also has a key role in the acqui-
sition of addictive behaviors,4,5 and
PET studies in opiate addict males
during heroin injections or expo-
sure to heroin-related visual cues
showed activation of reward cir-
cuitry, including the VTA and its
target regions (dorsal raphe, nu-
cleus accumbens, extended amyg-
dala, insula, dorsolateral prefrontal
cortex, and cingulate gyrus),4
which themselves are also critical
for the clinical expression of tics
and impulsive-compulsive behav-
iors in TS.3 Thus, uncontrollable
coprolalia, motor tic exacerbation,
neuroleptic refractoriness, and re-
lapse to heroin-seeking behavior in
our patient might be due to opiate-
induced long-term changes in me-
socorticolimbic systems.3–5
Based on the evidence from pre-
vious cases reporting temporary ex-
acerbation or recurrence of tic
symptoms after cocaine use2 and
from the long-term consequences in
our case even after heroin discon-
tinuation, it seems that having TS
entails an inherent vulnerability for
addictive, impulsive, and compul-
sive behaviors (reward deficiency
syndrome)6 and exacerbation of
motor-phonic tics after illicit drug
exposure. Individuals with TS
should be advised about the devas-
tating effect that heroin and other
illicit drugs may have on the sever-
ity and long-term evolution of tic
symptoms.
MARCELO L. BERTHIER, M.D.
VICTOR M. CAMPOS, M.D.
JAIME KULISEVSKY, M.D.
JUAN A. VALERO, M.D.
University of Malaga School of
Medicine (M.L.B.) and Services of
J Neuropsychiatry Clin Neurosci 15:1, Winter 2003
Neurology (V.M.C.) and Otolar-
yngology (J.A.V.), Clinic Univer-
sity Hospital, Malaga; Depart-
ment of Neurology, Sant Pau
Hospital and Autonomous Uni-
versity of Barcelona (J.K.), Spain
References
1. Scott BL, Jankovic J, Donovan DT: Botu-
linum toxin injection into vocal cord in
the treatment of malignant coprolalia as-
sociated with Tourette’s syndrome. Mov
Disord 1996; 11:431–433
2. Cardoso FE, Jankovic J: Cocaine-induced
movement disorders. Mov Disord 1993;
8:175–178
3. Stern E, Silbersweig DA, Chee K-Y, et al:
A functional neuroanatomy of tics in
Tourette syndrome. Arch Gen Psychia-
try 2000; 57:741–748
4. Sell LA, Morris J, Bearn RS, et al: Acti-
vation of reward circuitry in human opi-
ate addicts. Eur J Neurosci 1999;
11:1042–1048
5. Spanagel R, Weiss F: The dopamine hy-
pothesis of reward: past and current
status. Trends Neurosci 1999; 22:521–527
6. Comings DE, Blum K: Reward defi-
ciency syndrome: genetic aspects of be-
havioral disorders. Prog Brain Res 2000;
126:325–341
On Bresch’s Glossary of
Eponyms
SIR: Mark Twain famously wrote,
“The reports of my death have been
greatly exaggerated.” Equally exag-
gerated is David Bresch’s claim1
that “no one has ever composed a
glossary of psychiatry’s numerous
eponyms.” After many years of
work, in 1999 we published a book
on the subject.2 In writing this book
we used the principal medical and
psychiatric dictionaries in English,
French, German, and Spanish, as
well as varied bibliographical
sources and the main biomedical
(MEDLINE, Embase, etc.) and ge-
netic (OMIM) databases. We also
traveled to the main Spanish librar-
LETTERS
ies and newspaper archives and
ended up visiting the rich Cam-
bridge University Library in En-
gland. The methodology we used
yielded a total of 811 eponyms, al-
though we did not include some
whose use is not yet established.
For every eponym, we list a de-
scription of the symptom, syn-
drome, illness, sign, test, or com-
plex; the original reference where it
is described for the first time; a
brief biography of the author; the
synonymy and the eponym’s En-
glish, French, and German ver-
sions; and, finally, bibliographical
references to descriptions of the ep-
onym.
In view of the above, we feel that
Dr. Bresch’s work is worthy of
praise in that it attempts to recover
a tradition that has proven its prac-
tical usefulness, but at the same
time we believe that its approach is
reductionist, dealing with a small
number of eponyms in just two or
three lines and failing to provide
any biographical information on the
authors. Another major defect is
what Lain Entralgo3 calls an atti-
tude of “Adamism” (the researcher
enters a scientific field as Adam
would enter Eden: as a place where
no man has gone before): the au-
thor did not bother to check the
statement with which he starts his
work, either by consulting the usual
bibliographical indices or the well-
known ISBN. Needless to say, if
one is to do an appropriate job, one
must start by being exhaustive in
one’s use of sources.
LORENZO LIVIANOS-ALDANA
ANTONIO REY-GONZÁLEZ
Valencia, Spain
References
1. Bresch D: Beyond Wernicke’s: a lexicon
of eponyms in psychiatry. J Neuropsy-
chiatry Clin Neurosci 2002; 14:155–160
2. Rey González A, Livianos Aldana L: La
Psiquiatrı́a y sus nombres: Diccionario
117
LETTERS
de epónimos. Madrid, Editorial Médica
Panamericana, 1999
3. Lain Entralgo P: Historia de la medicina.
Madrid, Editorial Labor, 1999
In Reply
SIR: I submitted my article in May
2000. Dr. Livianos-Aldano’s book
was printed in Spain in December
1999. I was not aware of his book
when I finished my article. Had I
been, I would have included La-
segue-Falret Syndrome (folie à deux)
but no other entry from this work,
because the remainder fail one or
several of my article’s inclusion cri-
teria. The book includes Zelig Syn-
drome (from Woody Allen) and an
eponym named for and by one of
the authors, which uses only that
author as a citation (“Rey-Livianos
Syndrome”). On the other hand, he
and his co-author failed to include
Waxman-Geschwind (behavioral
complex of epilepsy), Martin-Bell
(fragile X), Landau-Kleffner (epi-
lepsy-related aphasia), and numer-
ous other signs and syndromes that
are relatively important, current, or
useful for psychiatrists, but man-
aged to include numerous entries
on vampirism and lycanthropy. I
think Drs. Livianos-Aldana and
Rey-Gonzalez’s work is interesting,
but not particularly helpful to the
practicing psychiatrist or trainee.
DAVID BRESCH, M.D.
Atypical Antipsychotic Use
Among Acute Schizophrenic
Inpatients
SIR: The introduction of atypical
antipsychotics has triggered the re-
evaluation of treatment strategies in
schizophrenia.1–3 However, little in-
formation is available about the
118
prescribing of novel antipsychotic
drugs, in general or in different set-
tings, or about the differential char-
acteristics of patients on novel anti-
psychotics. The aims of this study
were both to elucidate the prescrib-
ing practices for atypical antipsy-
chotics among acute schizophrenic
inpatients in Athens and to reveal
the differential characteristics of
schizophrenic patients on atypical
antipsychotics.
The subjects of this prospective
study were 63 schizophrenic pa-
tients (39 males), consecutively ad-
mitted at Eginition Hospital, De-
partment of Psychiatry, Athens,
from February 1997 to March 1998.
Their mean age was 30.2Ⳳ8.8 years.
All patients were diagnosed on the
basis of DSM-IV criteria.4 Written
informed consent was obtained
from the subjects and their rela-
tives. All patients were assessed on
admission with the Positive and
Negative Syndrome Scale (PANSS)5
by the same psychiatrist-investiga-
tor, who was blind to the patients’
antipsychotic medications. Another
independent psychiatrist performed
analysis of patients’ case notes, sur-
veying the prescribing of antipsy-
chotic drugs on the first week after
their admission.
Of the total 63 patients, 22 (35%)
were on atypical antipsychotics; of
these, 12 (54%) used atypical anti-
psychotics as monotherapy, and 10
(46%) used atypical antipsychotics
concurrently with conventional an-
tipsychotics. Patients on atypical
antipsychotics were evenly divided
between men and women (50%)
and had a mean age of 32.9 years
(SD⳱9.0). The most often used
atypical antipsychotics were risperi-
done (54%), clozapine (23%), olan-
zapine (18%) and sertindole (5%). It
is worth noting that risperidone
and olanzapine were introduced in
Greece in May 1994 and December
1997, respectively. Clozapine was
reintroduced in July 1990, and ser-
J Neuropsychiatry Clin Neurosci 15:1, Winter 2003
tindole was introduced in Decem-
ber 1997 but was withdrawn in De-
cember 1998. Quetiapine and
ziprasidone were not yet available
in the Greek market during the pe-
riod of the study.
Patients on atypical antipsychot-
ics (as monotherapy or in combina-
tion with conventional antipsychot-
ics, n⳱22, Group A) were
compared with those on conven-
tional antipsychotics (n⳱41, Group
B). For the statistical evaluation,
Mann-Whitney U-tests, Student’s t-
tests, or chi-square tests were used.
There were no statistically signifi-
cant differences between Group A
and Group B patients on many so-
ciodemographic and clinical-psy-
chopathological parameters such as
age (32.9 vs. 30.9 years), sex (men,
50% vs. 61%), family status (single,
70% vs. 87%), duration of illness
(years, 6.7 vs. 7.6), PANSS-total
score (73.2 vs. 76.0), PANSS-posi-
tive subscale score (18.1 vs. 18.4),
PANSS-negative subscale score
(18.7 vs. 18.8), and PANSS-general
psychopathology subscale score
(36.3 vs. 38.3). There were no statis-
tically significant differences be-
tween Group A and Group B pa-
tients regarding the PANSS item
scores with one exception. Schizo-
phrenic patients on atypical anti-
psychotics showed a trend for sig-
nificantly lower scores on item G14
of the PANSS (poor impulse con-
trol, 1.5 vs. 2.2; U⳱168, P⳱0.07).
In summary, acute schizophrenic
patients on atypical antipsychotics
were differentiated from those on
conventional antipsychotics in that
they had better impulse control.
VASSILIS P. KONTAXAKIS, M.D.
BEATA J. HAVAKI-KONTAXAKI, M.D.
COSTAS T. KOLLIAS, M.D.
MARIA M. MARGARITI, M.D.
SOPHIA S. STAMOULI, M.D.
GEORGE N. CHRISTODOULOU, M.D.,
F.I.C.P.M., F.R.C.PSYCH.
Department of Psychiatry,
 LETTERS

University of Athens, Eginition
Hospital, Athens, Greece
References
1. Tamminga CA: The promise of new
drugs for schizophrenia treatment. Can J
Psychiatry 1997; 42:265–273
2. Peuskens J: Good medical practice in an-
tipsychotic pharmacotherapy. Int Clin
Psychopharmacol 1998; 13 (suppl
3):S35–S41
3. Frangou S, Lewis M: Atypical antipsy-
chotics in ordinary clinical practice: a
pharmaco-epidemiologic survey in a
South London service. Eur Psychiatry
2000; 15:220–226
4. American Psychiatric Association:
Diagnostic and Statistical Manual of
Mental Disorders, 4th ed. Washington,
DC, American Psychiatric Association,
1994
5. Kay SR, Fiszbein A, Opler LA: The Posi-
tive and Negative Syndrome Scale
(PANSS) for schizophrenia. Schizophr
Bull 1987; 13:261–267

J Neuropsychiatry Clin Neurosci 15:1, Winter 2003 119