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Current diagnostic criteria for guillain-barr syndrome.

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LETTERS
PET Imaging of
Brain Tumors
Lorcan A. O’Tuama, MD’ and Peter C . Phillips, MD?
Dr Mazziotta (April 1991 issue of Annals) has provided an
excellent account of the role of PET, especially f18F12deoxy-2-fluoro-~-g~ucose
(FDG) imaging, in the diagnosis of
brain tumors [l}. His review prompts us to comment on
another important aspect of PET imaging of brain tumors.
The study of amino acid metabolism in brain neoplasms
has made an important contribution to the characterization
of the functional activity of these lesions. The tracer L{methyl-11C)methionine (1 1C-MET) has shown uniformly
high sensitivity for detection of low-grade gliomas E2, 3 , 47
and a wide range of other histological tumor types [ S ] . 11CMET positivity for supratentorial lesions has been found to
exceed that of FDG [4]. 11C-MET also holds promise as a
valuable probe for the assessment of cerebral radiation injury
in vivo. As noted by Dr Mazziotta, decreased uptake of FDG
has been widely used I61 as an indicator of cerebral radiation
injury. Significant ambiguity may attend this method, however, since focal hypometabolism is found in a substantial
number of primary brain tumors 171, especially in low-grade
lesions [8]. 11C-MET, which was consistently elevated even
with low-grade lesions, might be expected to offer a clearer
choice between tumor and edema.
Further elucidation of radiation injury may be obtained
through study of the mechanism underlying increased concentration of 11C-MET in human brain tumors. Normal human brains show a competitive mechanism of transport for
neutral amino acids 197, which is retained by human brain
neoplasms [lo, 111, but not at sites of radation injury 1113.
We suggest consideration of the readily synthesized positron
radiopharmaceutical 11C-MET to play a primary role in the
functional imaging of human brain tumors.
*Departmentsof Radiology (NuclearMedicine) and Neuroloa
Children’s Hospital
Boston, M A
?Department of Neumiogy
Children’sHospital of Phikadelphia
Philadelphia, PA
RefeerenceJ
1. Mazziotta JC. The continuing challenge of primary brain tumor
management: the contribution of positron emission tomography. Ann Neurol 1991;29:345-346
2. Shishido F, Uemura K, Inugami A, Tomura N, Higano S, Fujita
H , Murakami M, Kanno I, Yasui N, Mineura K. Value of 11Cmethionine and PET in the diagnosis of low-grade gliomas.
Kaku Igaku 1790;27:273-302
3. Schober 0, Cruetzig H, Meyer GJ, Becker H, Schwarzrock R,
Dietz H, Hundeshagen H. 11C-Methionine-PET, IMPSPECT, CT, and MRI bei Hirntumoren. ROFO 1985;143:
133-136
4. Ericson K, Lilja A, Bergstrom M, Collins VP, Ericksson L, Ehrin
E, von Holst H , Lundqvist H , Langstrom B, Mosskm M. Positron emission tomography with (I1lC]methyl)-~-rnethionine,
I1 lCID-glucose, and 168GalEDTA in supratentorial tumors.
J Comput Assist Tomogr 1985;9:683-689
5. O’Tuama LA, Phillips PC, Strauss LC, Uno Y,Smith QR, Dan-
nals RF, Wilson AA, Ravert HT, LaFrance ND, Wagner H N
Jr. Two-phase [l lC]~-methioninePET scanning in diagnosis of
childhood brain tumors. Pediatr N e w 1 1990;6:163-170
6. Di Chiro G. Positron emission tomography using fl8F1fluorodeoxyglucose in brain tumors: a powerful diagnostic and prognostic tool. Invest Radio1 1987;22:360-371
7. Alavi JB, Alavi A, Chawluk J, Kushner M, Powe J, Hickey W,
Reivich J. Positron emission tomography in patients with &oma: a predictor of prognosis. Cancer 1988;15:62:1074-1078
8. Francavilla TL, Miletich RS, Di Chiro G, Patronas NJ, Rizzoli
HV, Wright DC. Positron emission tomography in the detection
of malignant degeneration of low-grade gliomas. Neurosurgery
1989;24:1-5
9. OTuama LA, Guilarte TR, Douglass KH, Wagner HN Jr,
Wong DF, Dannals RF, Ravert HT, Wilson AA, LaFrance ND,
Bice AN, Links JM. Assessment of 11-C-L-methioninetransport
into the human brain. J Cereb Blood Flow Metab 1988;8:
341-345
10. Bergstrom M, Ericson K, Hagenfeldt L, Mosskin M, von Holst
H , Noren G, Eriksson L, Ehrin E, Johnstrom P. PET study
of methionine accumulation in glioma and normal brain tissue:
competition with branched chain amino acids. J Comput Assist
Tomogr 1987;11:208-213
11. OTuarna LA. Methionine transport in brain tumors. J Neuropsych Clin Neurosc 1989;1:S37-S44
Current Diamostic Criteria
for Guillain-garre
Syndrome
F. G. A. van der Mech6, MD, PhD, J. Meulstee, MD, and
R. P. Kleyweg, MD, PhD
Guillain-BarrC syndrome is an inflammatory, predominantly
demyelinating polyneuropathy with an often severe course.
At present this condition can be treated to decrease morbidity and to improve outcome. The first proven treatment was
plasma exchange [ 11. Plasmapheresis is especially effective if
applied early in the course of the disease 11). In this early
phase, therefore, diagnostic criteria are becoming increasingly important, compared to 1978, for example, when the
criteria were originally described to improve epidemiological
studies. Recently, the criteria have been reconfirmed and
expanded by Asbury and Cornblath {27. Detailed criteria may
result, however, in delay of the diagnosis and, hence, appropriate treatment, especially if physicians who are less familiar
with the problem look for laboratory confirmation of an essentially clinical diagnosis.
It is our experience that sometimes a definite diagnosis is
postponed until the protein content of the cerebrospinal fluid
is raised above normal values or until electrodiagnostic signs
suggesting demyelination are found. We wish to warn against
such a practice. The diagnosis, as discussed in the criteria,
should be based primarily on the development of more o r
less symmetrical motor weakness over a period ranging from
days to 4 weeks. As a general rule, myotatic reflexes decrease
or disappear but may be present up to grade 3 weakness
(MRC-scale) if the sensory fibers are uninvolved 131. We
fully agree, therefore, with the clinical criteria as confirmed
Copyright 0 1991 by the American Neurological Association 851
by Asbury and Cornblath [2]. In our view laboratory studies
are-especially early in the disease-of primary importance
to exclude other conditions, but they are not necessary to
confirm the clinical diagnosis.
Furthermore, a general comment on electrodiagnostic criteria for demyelination may be worth considering. Demyelination distributed along the whole nerve may result in both
dispersion of motor unit potentials and conduction block.
Both mechanisms result in a decrease of the CMAP amplitude if the stimulating electrode is progressively moved to
more proximal stimulation sites. However, it is impossible
to separate these two mechanisms on the basis of the duration
of the CMAP amplitude [43. For diagnostic purposes, however, it is not necessary to separate dispersion and conduction
block because both result from demyelination. It is for this
reason that we suggested the descriptive term length&pendent amplitude reduction [31. The artificial separation of
CMAP amplitude with or without a 15% or higher increase
in duration will not be necessary, then, as criteria for demyelination. At present the electrodiagnostic studies in the Dutch
immunoglobulin trial, performed at entry, after 1, and after
4 weeks, are being analyzed to compare these different approaches.
Erasmus Uniuersiteit Rotterdam
The Netherlands
Refereences
1. Guillain-Barre Syndrome Study Group. Plasmapheresis and acute
Guillain-Barre syndrome. Neurology 1985;35:1096- 1104
2. Asbury AK, Cornblath DR. Assessment of current diagnostic
criteria for Guillain-Barre syndrome. Ann Neurol 1990;27:
S2 1-24
3. Van der Mechk FGA, Meulstee J, Vermeulen M, Kievit A. Patterns of conduction failure in the Guillain-Barri. syndrome. Brain
1988;111:405-416
4. Rhee EK, Sumner AJ. A computer simulation of conduction
block effects produced by actual block versus interphase cancellation. Ann Neurol 1990;28(2):146-156
Reply
David R. Cornblath, M D
Dr van der Mech6 and associates raise an important point
about applying diagnostic criteria in studies of Guillain-Bar6
syndrome. Early on, patients may not meet all diagnostic
criteria, yet they clearly have Guillain-Barr&syndrome, which
becomes better defined over time. This does not imply that
patients cannot enter therapeutic trials until all diagnostic
criteria have been met. Rather, based on a tentative diagnosis
by experienced clinicians, patients could enter a therapeutic
trial as long as there was a review of the original symptoms
to be certain that patients indeed had the proper diagnosis.
In the North American study of Guillain-Bard syndrome,
for example, this was an effective method of ensuring proper
diagnosis. In fact, no patient who was entered into the study
based on clinical criteria was subsequently found to have
another disorder (Dr J. Griffin, personal communication).
This would allow for relatively rigd criteria to be applied in
studies as long as the criteria were applied post hoc.
Johm Hopkins Hospital
Baltimore, M D
852
Annals of Neurology
Vol 30
An Alternative Amea Test
for the Evaluatioiof
Brain Death
David H. Gutmann, MD, PhD,”
and Paul L. Marino, MD, PhDt
Recent experience with the apnea test for brain death reveals
serious complications that can pose a threat to patient safety
and to the success of organ donation [l}.The problems arise
from the use of prolonged apnea (10 minutes or longer)
to promote CO, retention to excitatory levels, because the
complete cessation of breathing movements eliminates the
ability to provide oxygen by inhalarion and creates a risk for
severe hypoxemia. Inhalation of 100% oxygen prior to the
apnea period has not eliminated the problem; in fact, a recent
report demonstrated an average arterial pOz of 26 mm Hg
after 10 minutes of apnea despite pretest inhalation of 100%
oxygen for 15 minutes 111. Continuous flow oxygen insufflation into the trachea during the apnea period has been associated with adequate oxygenation; however, insufflation may
lead to tracheal disruption and barotrauma 11). Another
drawback is the lack of effective blood gas monitoring during
the test. The current practice is to obtain a blood sample for
blood gas measurement at the end of the apnea period and
resume mechanical ventilation pending these results. This
“hit or miss” approach is not designed to identify the endpoint pC02, and this can produce either unwanted hypercapnia (overshoot) or inadequate C 0 2 retention (undershoot).
The undesirable features of the apnea maneuver can be
circumvented by employing hypoventilation to promote CO,
retention. The presence of breathing movements allows oxygen ro be inhaled during the test, which should reduce or
eliminate the risk for hypoxemia. Breathing movements also
create the ability to measure exhaled CO,, and the CO, at
end-exhalation (end-tidal CO,) can be used as an indirect
measure of arterial pC02. This on-line type of monitoring
helps to identify the end-point of the test, thereby preventing
unwanted overshoot or undershoot in the target pC0,.
The clinical performance of the hypoventilation test for an
adult male with no spontaneous respirations is shown in the
Figure. At zero minutes, the ventilation is abruptly decreased
to 1.0 L/min. The upper panel represents the arterial 0,
saturation measured noninvasively with a pulse oximeter
placed on one of the digits. The patients should receive
100% oxygen during the hypoventilation period, and the 0,
saturation should be maintained at 90% or higher. Pulse
oximetry has proved reliable in a variety of clinical settings
and over a wide range of hemoglobin levels 121, but the
accuracy in any individual patient must be determined by
blood gas measurement. The lower panel in the Figure represents the end-expiratory p C 0 2 (pETC02) measured with an
infrared CO, probe placed along the expiratory ventilator
tubing. When lung function is normal, the pETC0, is equivalent to the arterial pC02. However, when cardiopulmonary
pathology produces ventilation-perfusion inequalities in the
lung, the pETC0, decreases relative to the arterial CO, by
an amount dictated by the severity of the abnormality [31.
Nevertheless, the difference between the arterial and endtidal pC0, remains constant as long as the clinical condition
N o 6 December 1991
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