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Bilateral damage to the head of the caudate nuclei.

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2. Ridolfi RL, Bell WR. Thrombotic thrombocytopenic purpura:
report of 25 cases and review of the literature. Medicine
3. Hazeltine M, Rauch J, Danoff D, et al. Antiphospholipid antibodies in systemic lupus erythematosus: evidence of an association with positive Coombs’ and hypocomplementia J Rheumatol
4. Harris EN, Asherson RA, Gharavi AE, et al. Thrombocytopenia
in SLE and related autoimmune disorders-association with anticardiolipin antibodies. Br J Haematol 1985;59:227-230
5. Deleze M, Oria CV, Alarcon-Segovia D. Occurrence of both
hemolytic anaemia and thrombocytopenic purpura (Evan’s syndrome) in systemic lupus erythematosus. Relationship to antiphospholipid antibodies.J Rheumatol 1988;15:611-615
6. Harris EN, Asherson RA,Hughes GRV. Antiphospholipid antibodies-autoantibodies with a difference. Ann Rev Med 1988;
7. Asherson RA, Derksen RHWM, Harris EN, et al. Large vessel
occlusion and gangrene in systemic lupus erythematosus and
“lupus-like” disease. A report of six cases. J Rheumatol 1986;
Orrin Devinsky, MD, Carol K. Petito, MD,
and Daniel Alonso, M D
We thank Dr Asherson and colleagues for their comments
regarding our recent paper. In our patients, the diagnosis of
thrombotic thrombocytopenic purpura (TTP) was not supported by either increased fibrin split products or prolongation of the partial thromboplastin time. We agree that a positive Coombs’ test and hemolytic anemia may be found in
patients with antiphospholipid antibodies. However, identification of microangiopathic hemolytic anemia-not Coombs’
positive hemolytic anemia-is a critical feature for the recognition of TTP in patients with systemic lupus erythematosus
(SLE). As we discussed, antiphospholipid antibodies may
play a role in the development of TTP in patients with SLE.
Because our study was retrospective, extending over 20
years, antiphospholipid antibodies were assayed in only a
minority of patients. Therefore, we were unable to study the
relationship of these antibodies to either TTP or LibmanSacks endocarditis.
University of Medicine and Dentistry of New Jersey
Newark, NJ
New York Hospital-Cornell University Medical Center
New York, N Y
Bilateral Damage to the
Head of the Caudate
B. Croisile, MD, D. Tourniaire, MD, C. Confavreux, MD,
M. Trillet, MD, and G. Aimard, M D
Richfield and colleagues {l] describe a patient with bilateral damage to the head of the caudate nuclei. We report a
56-year-old right-handed woman who experienced apathy,
word-finding difficulties and incoherent writing in Septem-
Contrast computed tomographic scan (A, March 1986) and TI weighted magnetic resonance image (B, April 1987) show bikzteral abnormal low density of the head of the caudate nuclei, putamen, and anterior limb of the internal capsule.
ber 1985. All symptoms disappeared in a few days. A computed tomographic (CT) scan one month later showed infarction of the head of the left caudate nucleus. On November 2,
the same symptoms occurred again. CT scan and magnetic
resonance imaging showed bilateral low-density areas in the
heads of the caudate nuclei, in the putamen, and in the anterior limb of internal capsule (Figure). Since then, the patient
has demonstrated obsessional behavior with jaw movements,
chewing, skin scraping, and compulsive counting of objects
such as books or table-napkin folds. Initially she counted
during the night. These stereotyped activities were permanent. She could not stop by herself but could do so if commanded; in this case she did not feel any anxiety. She was
apathetic with general slowing (her breakfast took 4 hours)
and evidenced a decrease in initiative for housework, shopping, and social activities. There was a lack of emotional
reactivity, hyposexuality, and sometimes inappropriate tears
Annals of Neurology Vol 25
No 3 March 1989 313
or laughter. Initially she had an increased appetite, even for
her neighbor’s meals. She lacked spontaneous speech and
spoke only short sentences with a slow and whispered voice.
There was an alteration of spontaneous writing with misspellings, agrammatism, and verbal stereorypies. Psychometry showed an IQ of 115 (verbal I Q = 114, performance IQ
= 108). Otherwise language, intelligence, and orientation
were not altered. Her neurological examination was normal,
without motor frontal signs apart from bradykinesia and
bladder incontinence, her only complaint. Cerebral blood
flow (Xe 133) showed a decrease in the frontal lobes.
As Richfield and colleagues suggest 111, knowledge of
functions of the caudate nuclei in humans is based on study
of cases with degenerative or vascular disorders. In our patient the disturbances after the first infarct were transient.
Persistent obsessional behavior, apathy, and speech disturbances occurred only when infarction of the caudate nucleus
was bilateral. This is consistent with studies in animals 121
but not in humans in whom unilateral lesions may be associated with persistent dysfunction 131. Obsessive compulsivity
in the psychiatric sense (with intense anxiety) is known in
only one case, after bilateral pallidal lesions 141. Compulsive
finger activity has been described in bilateral cavitation of the
caudate nucleus also involving the right putamen 151. The
Note of Explanation
In the December 1988 issue of the Annals of Neurology, the
article by Friedland and colleagues on “Motor Vehicle
Crashes in Dementia of the Alzheimer Type” contains a
recommendation “that patients with a diagnosis of DAT not
drive a motor vehicle.” In the manuscript accepted for publication, that sentence ended with the phrase “under any circumstances.” The accompanying editorial by Drachman addresses some of the consequences and implications of the
phrase “under any circumstances.” Friedland and colleagues,
unaware of the editorial accompaniment, edited out this
phrase in the proofing process. The meaning of this change
in proof was not appreciated in the offices of the publisher,
and the matter did not come again to editorial attention. We
apologize to Dr Drachman and to the readership for this
A. K. Asbury, M D
314 Annals of Neurology Vol 25 No 3 March 1989
bilateral decrease in frontal cerebral blood flow in our patient
suggests disconnection between frontal cortex and caudate
nucleus. The case of Richfield and colleagues and the present
one show cognitive abnormalities consistent with a prefrontallcaudate disconnection.
Department of Neurology
Hspital Neurologique
Lyon, France
1. Richfield EK, Twyman R, Berent S . Neurological syndrome following bilateral damage to the head of the caudate nuclei. Ann
Neurol 1987;22:768-7 7 1
2. Iverson SD. Behaviour after neostriatal lesions in animals. In:
Divac I, Oberg RGE, eds. The neostriatum. New York: Pergamon, 1979
3. Cambier J, Elghozi D, Strube E. Hkmorragie de la t2te du noyau
caud6 gauche. Rev Neurol (Paris) 1979;135:763-774
4. Laplane D, Boulliat J, Baron JC, et al. Comportement compulsif
d’allure obsessionnelle par Iksion bilatkrale des noyaux lenticulaires. L’Encephale 1988;XIV:27-32
5. Williams AC, Owen C, Heath DA. A compulsive movement
disorder with cavitation of caudate nucleus. J Neurol Neurosurg
Psychiatry 1988;51:447-448
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head, nuclei, damage, caudata, bilateral
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