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
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
