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Diagnostic criteria for multiple sclerosis An addendum.

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4. Paty D, Asbury A, Herndon R, et al. Use of magnetic resonance
Diagnostic Criteria
for Multiple Sclerosis:
An A d d i n d m
imaging in the diagnosis of multiple sclerosis. Neurology
C W e s M. Poser, M D
Perusal of a number of recent articles in the neurological
literature has made it clear that Poser and colleagues’ [I)
diagnostic criteria for multiple sclerosis (MS) have not always
been clearly understood: Dissemination in space is stressed
but dissemination in time is often ignored.
The differential diagnosis from acute disseminated encephalomyelitis (ADEM) remains a crucial and taxing problem; dissemination in space is extremely common, while recurrences are quite rare. Abnormalities of evoked potentials
127 and the presence of oligoclonal bands in cerebrospinal
fluid [3] are not infrequently found in ADEM, as well as in
many other diseases of the nervous system. Magnetic resonance imaging (MRI) has contributed to the confusion because the white matter changes of ADEM are indistinguishable from those of MS, although in the former the areas of
increased signal intensity have less of a tendency to be
periventricular in location and are somewhat more likely to
involve gray matter. Attention is called to the excellent and
clearly enunciated policy statement regarding the use of MRI
in the diagnosis of MS by Paty and associates [4]. Requirements that could usefully be added to this statement are that
there should be at least four areas of increased signal intensity in the white matter (Paty D: Personal communication,
1987), at least two of which should be periventricular in
location, but not including the symmetrical involvement of
the anterior angles of the lateral ventricles.
With the possible exception of serial MRI examinations
demonstrating the appearance of new plaques, the absolutely
mandatory criterion of dissemination in time will have to
remain based upon the clinical history subjected to critical
evaluation in order to attempt to distinguish true exacerbations, i.e., the appearance of new symptoms or the extension
of old ones, from what might be called pseudoexacerbations
caused by an alteration of the patient’s internal milieu by
changes in body temperature, infection, dehydration, and
other factors.
In summary, both dissemination in space and dissemination
in time are required for the diagnosis of MS.
Haruard Medical School
Beth Israel Hospital
Boston. MA
1. Poser C, Paty D, Scheinberg L, et al. New diagnostic criteria for
multiple sclerosis. Ann Neurol 1983;13:227-231
2. Cohen S, Synddko K, Tourtellone W. Visual evoked potentials
in the diagnosis of multiple sclerosis. In: Poser C, Paty D, Scheinberg L, et al, eds. The diagnosis of multiple sclerosis. New York:
Thieme-Suatton, 1984:103-119
3. Ebers G. Cerebrospinal fluid electrophoresis in multiple sclerosis.
In Poser C, Paty D, Scheinberg L, et al, eds. The diagnosis of
multiple sclerosis. New York: Thieme-Stratton, 1984:179-184
Clonidine in Gdes
de la Tourette’s Syndrome
R. A. C. Roos, MD,* R. B. Mirideraa, MD,t
A. P. Cohen, MD,S B. J. M. Van de Wetering, MDJ
and T. C. A. M. Van Woerkom, MDS
Goett and colleagues [I) presented the first randomized,
double-blind, placebo-controlled trial with clonidine in
Gilles de la Tourette’s syndrome (GTS). They did not find
any effect of clonidine. Some comments seem appropriate
concerning the evaluation method, certainly the most
difficult part in such studies. We cannot agree with the statement that two 1-minute video clips “provide a representative
sample of symptomatic behavior.” In the inclusion criteria of
DSM-111123 for the diagnosis of GTS, both the suppression
of tics for minutes to hours and the waxing and waning
course over weeks to months are main criteria. One-minute
video clips are too short to evaluate frequency of tics.
Awareness by patients that they are being watched or filmed
may well suffice to suppress the tics. Our experience includes
several patients who, at the moment they thought, erroneously, that the video session had ended, showed a burst of
tics. In our view, the assessment method of Goetz and associates [I] is not a valuable objective method. The method
of choice is a video clip of 3 to 5 minutes obtained while the
patient is unaware of the recording. The presence of other
persons in the room will certainly influence the tics, and
short periodic recording will bias the outcome as a consequence. In our opinion the results of video monitoring with
the other persons in the room also should have been presented.
One additional point is that the effect of clonidine becomes apparent in some patients only after three months of
regular drug intake 13). It has been reported that after even
brief discontinuation of clonidine, its reinstitution may become effective only after a period of two weeks to four
months 141. Therefore, a drug period of only six weeks does
not allow a final judgment to be made about the efficacy of
clonidine in the treatment of GTS.
In conclusion, we stress that there is still a need for a longterm double-blind clonidine-placebo clinical trial in GTS.
*Department of Neurology
University Hospital Leiden
Leiden, The Netherlands
$Department of Child Psychiatry
Sophia Children’s Hospital
Erasmus University
Rotterdam, The Netherlands
$Department of Neuropsychiatty
Psychiatric Centre Rosenburg
The Hague, The Netherlands
§Department of Psychiatty
University Hospital Rotterdam
Rotterdam, The Netherlands
Copyright 0 1987 by the American Neurological Association 773
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criterias, sclerosis, multiple, diagnostika, addendum
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