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PARALYTIC POLIOMYELITIS
1154 excessive excretion of methylmalonic acid in rats exposed to nitrous oxide. This may be related to the short duration of the experiment since Schrauzer and Stadlbauer9 found by direct enzyme assay that the bacterial enzyme cthanolamine ammonia lyase, also dependent on coenzyme vitamin B12, was inactivated by nitrous oxide. J. F. BURMAN Department of Hæmatology, J. A. L. AMESS St Bartholomew’s Hospital, D. L. MOLLIN London EC1A 7BE
ANIMAL MODEL FOR SUBACUTE COMBINED DEGENERATION
SIR,-The pathogenesis of subacute combined degeneration of the spinal cord-as a result of vitamin-B12 deficiency is unresolved. The main obstacle is the absence of a suitable animal model on which to investigate the molecular basis of the myelin degeneration. Agamanolis et al. succeeded in producing’ neurological changes in monkeys, but only by keeping the animals on a vitamin-B12-deficient diet for 3-5 years. When Amess et al.23 observed haematological changes consistent with vitamin-B12 inactivation in man after exposure to nitrous oxide, we wondered if this gas might prove a realistic way to
study vitamin-B12-related neurological damage.
which finally resulted in inability to sit up or drink. The spinal cord of this animal revealed degeneration of both the myelin sheaths and axis cylinders in the posterior columns and also in the lateral corticospinal and spinocerebellar tracts. In several areas of the posterior columns, entire fibre tracts were replaced by groups of fatty macrophages. The characteristic spongy degeneration ("field of holes") was also evident around the periphery of the anterior columns (see figure). The central greymatter and the myelinated tracts bordering it were intact. These findings demonstrate that the monkey, while apparently resistant to hoematological damage, shows susceptibility to the neurological degeneration seen in man. We hope that future work will produce neurological change even more rapidly and thus facilitate the investigation of the biochemical defect in this lesion.
J. J. DINN S. MCCANN P. WILSON B. REED
Departments of Neuropathology, Medicine, and Biochemistry, Trinity College,
D. WEIR
Dublin 2, Ireland
J. SCOTT PARALYTIC POLIOMYELITIS
SIR,-May I correct an error in the figures given in your editorial of Nov. 11 (p. 1030). You state that there were 13 reports of paralytic poliomyelitis in 1976 and 26 in 1977. In fact there were 13 cases in each year-i.e., a total of 26. These 1 cases and the attendant circumstances have been described. Research Laboratory, Central Public Health Laboratory, London NW9 5HT
Epidemiological
T. M. POLLOCK
SERUM-POTASSIUM IN DELIRIUM TREMENS
SIR,-Dr Wadstein and
Dr Skude (Sept. 9, p. 549) report in delirium tremens. Unfortunately, platelethypokalsemia counts are-not given. During clotting, platelets liberate their
intracellular potassium, thereby increasing potassium concentrations. "Normal" values are based upon data obtained in patients -with normal platelet-counts. Thrombocytopenia may thus cause spurious hypokalsmia. Hematology Division, Montefiore Hospital and Medical Center, THEODORE H. SPAET
Bronx, N.Y. 10467, U.S.A. section of characteristic spongy
monkey spinal cord illustrating the degeneration of vitamin B12 deficiency. (Luxol fast-blue/cresyl-violet; x about 6.)
Transverse
***This letter has been shown
to
Dr Wadstein and Dr Skude,
whose reply follows.-ED.L In rats and mice exposed oxygen mixture biochemical
to
50% nitrous oxide and 50%
changes consistent with vitamin-B12 deficiency quickly developed--e.g., decreased folate uptake, decreased polyglutamate biosynthesis, abnormal deoxyuridine-suppression tests, and methylmalonicaciduria4 but there were no neurological or haematological changes after 8 months. However, a monkey placed in a similar gas mixture had both the biochemical changes and the neurological signs of vitamin-B12 deficiency. After only 2 months, the monkey became unsteady and uncoordinated with progressive ataxia, 9. Schrauzer, G. N., Staelbauer, E. A. Bioinorg. Chem. 1975, 4, 185. 1. Agamanolis, D. P., Chester, E. M., Victor, M., Kark, J. A., Hines, J. D., Harris, J. W. Neurology, 1976, 26, 905. 2. Amess, J. A. L., Burman, J. F., Greany, M., Nancekievill, D. G. International Society of Hæmatology (Istanbul, 1977); abstr. 614. 3. Amess, J. A. L., Burman, J. F., Rees, G. M., Nancekievill, D. G., Mollin, D. L. Lancet, 1978, ii, 339. 4. Scott, J. M., Reed, B., McKenna, B., McGing, P., McCann, S., O’Sullivan, H., Wilson, P., Weir, D. G. in Proceedings of 6th International Symposium on the Chemistry and Biology of the Pteridines. (in the press.)
SiR,—Thrombocytopenia in alcoholics (and rebound thrombocytosis after alcohol withdrawal) are well known. We did platelet-counts in five patients before and during delirium tremens, the mean values being 146 and 198x10/1, respectively. In our experience the mean difference between potassium concentrations in serum and plasma is about 0.3mmoVI at normal thrombocyte-counts. Thus, we agree with Professor Spaet that the low serum-potassium at admission could, partly at least, be due to this effect, but the rapid fall in serum-potassium before and the low concentration during delirium tremens cannot be explained in this way. Department of Alcohol Diseases, Malmö General Hospital, S-214 01 Malmö, Sweden
JAN WADSTEIN
Department of Clinical Chemistry, Central Hospital, Kalmar, Sweden 1.
Collingham, K. E., Pollock, T. M., Roebuck, M.
G. SKUDE O. Lancet, 1978, i, 976.
ANIMAL MODEL FOR SUBACUTE COMBINED DEGENERATION
SIR,-The pathogenesis of subacute combined degeneration of the spinal cord-as a result of vitamin-B12 deficiency is unresolved. The main obstacle is the absence of a suitable animal model on which to investigate the molecular basis of the myelin degeneration. Agamanolis et al. succeeded in producing’ neurological changes in monkeys, but only by keeping the animals on a vitamin-B12-deficient diet for 3-5 years. When Amess et al.23 observed haematological changes consistent with vitamin-B12 inactivation in man after exposure to nitrous oxide, we wondered if this gas might prove a realistic way to
study vitamin-B12-related neurological damage.
which finally resulted in inability to sit up or drink. The spinal cord of this animal revealed degeneration of both the myelin sheaths and axis cylinders in the posterior columns and also in the lateral corticospinal and spinocerebellar tracts. In several areas of the posterior columns, entire fibre tracts were replaced by groups of fatty macrophages. The characteristic spongy degeneration ("field of holes") was also evident around the periphery of the anterior columns (see figure). The central greymatter and the myelinated tracts bordering it were intact. These findings demonstrate that the monkey, while apparently resistant to hoematological damage, shows susceptibility to the neurological degeneration seen in man. We hope that future work will produce neurological change even more rapidly and thus facilitate the investigation of the biochemical defect in this lesion.
J. J. DINN S. MCCANN P. WILSON B. REED
Departments of Neuropathology, Medicine, and Biochemistry, Trinity College,
D. WEIR
Dublin 2, Ireland
J. SCOTT PARALYTIC POLIOMYELITIS
SIR,-May I correct an error in the figures given in your editorial of Nov. 11 (p. 1030). You state that there were 13 reports of paralytic poliomyelitis in 1976 and 26 in 1977. In fact there were 13 cases in each year-i.e., a total of 26. These 1 cases and the attendant circumstances have been described. Research Laboratory, Central Public Health Laboratory, London NW9 5HT
Epidemiological
T. M. POLLOCK
SERUM-POTASSIUM IN DELIRIUM TREMENS
SIR,-Dr Wadstein and
Dr Skude (Sept. 9, p. 549) report in delirium tremens. Unfortunately, platelethypokalsemia counts are-not given. During clotting, platelets liberate their
intracellular potassium, thereby increasing potassium concentrations. "Normal" values are based upon data obtained in patients -with normal platelet-counts. Thrombocytopenia may thus cause spurious hypokalsmia. Hematology Division, Montefiore Hospital and Medical Center, THEODORE H. SPAET
Bronx, N.Y. 10467, U.S.A. section of characteristic spongy
monkey spinal cord illustrating the degeneration of vitamin B12 deficiency. (Luxol fast-blue/cresyl-violet; x about 6.)
Transverse
***This letter has been shown
to
Dr Wadstein and Dr Skude,
whose reply follows.-ED.L In rats and mice exposed oxygen mixture biochemical
to
50% nitrous oxide and 50%
changes consistent with vitamin-B12 deficiency quickly developed--e.g., decreased folate uptake, decreased polyglutamate biosynthesis, abnormal deoxyuridine-suppression tests, and methylmalonicaciduria4 but there were no neurological or haematological changes after 8 months. However, a monkey placed in a similar gas mixture had both the biochemical changes and the neurological signs of vitamin-B12 deficiency. After only 2 months, the monkey became unsteady and uncoordinated with progressive ataxia, 9. Schrauzer, G. N., Staelbauer, E. A. Bioinorg. Chem. 1975, 4, 185. 1. Agamanolis, D. P., Chester, E. M., Victor, M., Kark, J. A., Hines, J. D., Harris, J. W. Neurology, 1976, 26, 905. 2. Amess, J. A. L., Burman, J. F., Greany, M., Nancekievill, D. G. International Society of Hæmatology (Istanbul, 1977); abstr. 614. 3. Amess, J. A. L., Burman, J. F., Rees, G. M., Nancekievill, D. G., Mollin, D. L. Lancet, 1978, ii, 339. 4. Scott, J. M., Reed, B., McKenna, B., McGing, P., McCann, S., O’Sullivan, H., Wilson, P., Weir, D. G. in Proceedings of 6th International Symposium on the Chemistry and Biology of the Pteridines. (in the press.)
SiR,—Thrombocytopenia in alcoholics (and rebound thrombocytosis after alcohol withdrawal) are well known. We did platelet-counts in five patients before and during delirium tremens, the mean values being 146 and 198x10/1, respectively. In our experience the mean difference between potassium concentrations in serum and plasma is about 0.3mmoVI at normal thrombocyte-counts. Thus, we agree with Professor Spaet that the low serum-potassium at admission could, partly at least, be due to this effect, but the rapid fall in serum-potassium before and the low concentration during delirium tremens cannot be explained in this way. Department of Alcohol Diseases, Malmö General Hospital, S-214 01 Malmö, Sweden
JAN WADSTEIN
Department of Clinical Chemistry, Central Hospital, Kalmar, Sweden 1.
Collingham, K. E., Pollock, T. M., Roebuck, M.
G. SKUDE O. Lancet, 1978, i, 976.