1352
pia and
amnesia for the period between the accident and hospital admission. On admission the patient was conscious, capable of opening and closing his eyes in response to verbal commands, and had a normal conjugate gaze in all directions; blink occlusion was weak. He had tetraplegia and could not move his shoulders and neck. The pupils were equal, slightly mydriatic, and reacted to light. He had bilateral facial paresis with occasional trismus and paresis of the other motor cranial nerves with anarthria. Sensibility to pain was normal; the patient closed his eyes when he noticed the pain. Muscle tone was normal. Tendon reflexes were bilaterally symmetrical and hyperactive, particularly in the legs; Babinski sign and abdominal reflexes were absent. Vital signs, electrocardiogram, blood picture and chemistry were normal. A lumbar puncture showed normal pressure with c.s.F. glucose 67 mg/dl and protein 30 mg/dl. There were no cells in the c.s.F. and no xanthochromia. An electroencephalogram was normal The simple skull and cervical spine X-rays were normal. These data suggested a "de-efferented state" or "locked-in" syndrome.’ 4 h after the accident the patient began to recover speech and mobility, and 6 hours later neurological examination was normal. The pathophysiological mechanism of this de-efferented state is, we think, related to a transitory ischaemia at a ventral pontine level due to compression of the vertebral artery caused2 by the hyperextension rotation at the time of the accident. This hypothesis would be supported by the transitory ambly-
opia. We have not read of a case of transitory post-traumatic locked-in syndrome; the syndrome may be overlooked and misdiagnosed as true coma if vertical and horizontal conjugate gaze are not tested. Department of Neurology, Hospital de la Santa Cruz y San Pablo, Barcelona, Spain
J. L. MARTI-VILALTA C. ROIG-ARNALL
ADIPOSITY AND ADIPOSE CELLS
SIR,-Dr Whitelaw (Nov. 26,
p.
1098)
sets out to
exploit
a
hypothesis that does not exist-namely, a connection between adiposity in childhood, the number of adipose cells, and the outlook for obesity. I have never made this suggestion, nor did I refer3 to overnutrition in pregnancy, as Whitelaw avers. His data are important but not surprising in view of other published evidence indicating a lack of critical periods for fatness. New data being analysed in my department indicate that fatness in adult life is not well predicted by fatness in childhood. Nevertheless an individual obese person may well remain fat. We know nothing about the long-term effects of the number of adipose cells an individual possesses. I have just returned from two conferences in Washington. There is general agreement that the increase in adipose tissue which normally occurs during the first year of life is largely accommodated by an increase in adipose cell size. After this rapid increase is finished, increase in the adipose organ is probably achieved largely by increases in adipose cell numbers, and everyone agrees that once adipose cells have been formed they cannot be lost. There is mounting evidence that adipose cells can be recruited by the extreme stimulus of overnutrition and that this recruitment can probably take place at any time of life. Whether it arises from replication of existing adipose cells or from the formation of new fat cells is not known. An attractive hypothesis which would explain these facts is that adipose cell size is the trigger for adipose cell replication. Thus, during 1.
Plum, F., Posner, J. B. Diagnosis of Stupor and Coma; p. 93. Philadelphia, 1966.
2. Schneider, R. C., Crosby, E. C. Neurology, 3. Brook, C. G. D. Lancet, 1972, ii, 624.
1959, 9, 643.
the first year of life, whenever a critical adipose cell size is reached replication takes place, and that principle operates later, even if the critical size changes with age. Enormous fat cells are not found in the extremely obese who must, therefore, have an increased number of fat cells regardless of the age of onset.
What we need now are large cohorts of infants, children, and their parents to be followed up prospectively, both for their fatness and for the number and size of their adipose cells. If we had such data we could answer the three outstanding questions. First, is it possible to have adipose hypercellularity and not be obese (does the number of fat cells an individual has matter to him)? Secondly, if the number does matter, can one exert a sufficiently strong environmental counter stimulus to alter the pattern of adipose-cell replication in an individual without otherwise harming him? Thirdly, do parents pass on their cellularity patterns like they seem to pass on the amount and shape of adipose tissue and, if so, are we to be lamarckian rather than darwinian and say that acquired hypercellularity can be passed on to the offspring? Middlesex Hospital, London WIN 8AA
C. G. D. BROOK
LIGNOCAINE AND DEEP-VEIN THROMBOSIS
SIR,-Dr Cooke and his colleagues (Oct. 15, p. 797) report that lignocaine lowers the frequency of deep-vein thrombosis after hip surgery. They attribute this effect to the inhibition of white-cell induced endothelial damage secondary to white-cell adhesion to vein walls and transendothelial migration. They cite the work of Stewart et al.l-3 as evidence that this occurs adjacent to or remote from sites of surgical trauma in dogs. Their explanation presumes that leucocyte-induced venous injury also occurs in surgery in man. This has been reported by Ts’ao et al.,4 who found intravascular and extravascular accumulation and disruption of neutrophils near venules of many tissues during cardiac surgery. They could not duplicate this finding in laboratory animals. Because of our own interest in leucocyte-induced thrombi’ we attempted to confirm Ts’ao’s work in patients undergoing elective abdominal surgery. We prepared standard paraffin sections of formalin-fixed subcutaneous tissues taken from the opening skin incision of patients having a cholecystectomy. A similar sample was removed from a remote subcutaneous site (the T-tube drain site) towards the end of the surgical procedure. A third specimen was taken from the original abdominal wound just before it was closed. We found neutrophil adhesion in 49% of venules in the specimen taken from the original abdominal wound at the end of the surgery. There was no neutrophil adhesion in specimens taken at the start of surgery nor in specimens from a remote site taken towards the end of surgery. We concluded that the neutrophil adhesion we saw was part of the local inflammatory response to surgical trauma and not a generalised effect which occurred at remote sites. Our findings suggest that some explanation other than leucocyte adhesion must be considered. One such explanation might be a platelet alteration, as proposed by Dr O’Brien (Oct. 29, p. 928) in his comment on Cooke’s paper.
New York Medical
College,
Flower-5th Avenue Hospital, New York, N.Y. 10029, U.S.A.
R. G. LERNER V. TCHERTKOFF I. KEMPNER J. C. NELSON R. GOLDSTEIN
Stewart, G. J., Ritchie, W. G. M., Lynch, P. R. in Proceedings of Workshop on Scanning Electron Microscopy in Pathology; p. 473. Chicago, 1973. 2. Stewart, G. J., Ritchie, W. G. M., Lynch, P. R. Am. J. Path. 1974, 74, 507. 3. Stewart, G. J., Lynch, P. R., Reichle, F. P., Ritchie, W. G. M., Smith, A., 1.
Schaulbo, R. G. Ann. N.Y. Acad. Sci. 1977, 283, 179. 4. Ts’ao, C. H., Lin, C. Y., Glagov, S., Replogle, R. L. Archs Path. 1973, 95, 357. 5. Lerner, R. G., Goldstein, R., Nelson, J. C. Thrombosis Res. 1977, 11, 11.
pia and
amnesia for the period between the accident and hospital admission. On admission the patient was conscious, capable of opening and closing his eyes in response to verbal commands, and had a normal conjugate gaze in all directions; blink occlusion was weak. He had tetraplegia and could not move his shoulders and neck. The pupils were equal, slightly mydriatic, and reacted to light. He had bilateral facial paresis with occasional trismus and paresis of the other motor cranial nerves with anarthria. Sensibility to pain was normal; the patient closed his eyes when he noticed the pain. Muscle tone was normal. Tendon reflexes were bilaterally symmetrical and hyperactive, particularly in the legs; Babinski sign and abdominal reflexes were absent. Vital signs, electrocardiogram, blood picture and chemistry were normal. A lumbar puncture showed normal pressure with c.s.F. glucose 67 mg/dl and protein 30 mg/dl. There were no cells in the c.s.F. and no xanthochromia. An electroencephalogram was normal The simple skull and cervical spine X-rays were normal. These data suggested a "de-efferented state" or "locked-in" syndrome.’ 4 h after the accident the patient began to recover speech and mobility, and 6 hours later neurological examination was normal. The pathophysiological mechanism of this de-efferented state is, we think, related to a transitory ischaemia at a ventral pontine level due to compression of the vertebral artery caused2 by the hyperextension rotation at the time of the accident. This hypothesis would be supported by the transitory ambly-
opia. We have not read of a case of transitory post-traumatic locked-in syndrome; the syndrome may be overlooked and misdiagnosed as true coma if vertical and horizontal conjugate gaze are not tested. Department of Neurology, Hospital de la Santa Cruz y San Pablo, Barcelona, Spain
J. L. MARTI-VILALTA C. ROIG-ARNALL
ADIPOSITY AND ADIPOSE CELLS
SIR,-Dr Whitelaw (Nov. 26,
p.
1098)
sets out to
exploit
a
hypothesis that does not exist-namely, a connection between adiposity in childhood, the number of adipose cells, and the outlook for obesity. I have never made this suggestion, nor did I refer3 to overnutrition in pregnancy, as Whitelaw avers. His data are important but not surprising in view of other published evidence indicating a lack of critical periods for fatness. New data being analysed in my department indicate that fatness in adult life is not well predicted by fatness in childhood. Nevertheless an individual obese person may well remain fat. We know nothing about the long-term effects of the number of adipose cells an individual possesses. I have just returned from two conferences in Washington. There is general agreement that the increase in adipose tissue which normally occurs during the first year of life is largely accommodated by an increase in adipose cell size. After this rapid increase is finished, increase in the adipose organ is probably achieved largely by increases in adipose cell numbers, and everyone agrees that once adipose cells have been formed they cannot be lost. There is mounting evidence that adipose cells can be recruited by the extreme stimulus of overnutrition and that this recruitment can probably take place at any time of life. Whether it arises from replication of existing adipose cells or from the formation of new fat cells is not known. An attractive hypothesis which would explain these facts is that adipose cell size is the trigger for adipose cell replication. Thus, during 1.
Plum, F., Posner, J. B. Diagnosis of Stupor and Coma; p. 93. Philadelphia, 1966.
2. Schneider, R. C., Crosby, E. C. Neurology, 3. Brook, C. G. D. Lancet, 1972, ii, 624.
1959, 9, 643.
the first year of life, whenever a critical adipose cell size is reached replication takes place, and that principle operates later, even if the critical size changes with age. Enormous fat cells are not found in the extremely obese who must, therefore, have an increased number of fat cells regardless of the age of onset.
What we need now are large cohorts of infants, children, and their parents to be followed up prospectively, both for their fatness and for the number and size of their adipose cells. If we had such data we could answer the three outstanding questions. First, is it possible to have adipose hypercellularity and not be obese (does the number of fat cells an individual has matter to him)? Secondly, if the number does matter, can one exert a sufficiently strong environmental counter stimulus to alter the pattern of adipose-cell replication in an individual without otherwise harming him? Thirdly, do parents pass on their cellularity patterns like they seem to pass on the amount and shape of adipose tissue and, if so, are we to be lamarckian rather than darwinian and say that acquired hypercellularity can be passed on to the offspring? Middlesex Hospital, London WIN 8AA
C. G. D. BROOK
LIGNOCAINE AND DEEP-VEIN THROMBOSIS
SIR,-Dr Cooke and his colleagues (Oct. 15, p. 797) report that lignocaine lowers the frequency of deep-vein thrombosis after hip surgery. They attribute this effect to the inhibition of white-cell induced endothelial damage secondary to white-cell adhesion to vein walls and transendothelial migration. They cite the work of Stewart et al.l-3 as evidence that this occurs adjacent to or remote from sites of surgical trauma in dogs. Their explanation presumes that leucocyte-induced venous injury also occurs in surgery in man. This has been reported by Ts’ao et al.,4 who found intravascular and extravascular accumulation and disruption of neutrophils near venules of many tissues during cardiac surgery. They could not duplicate this finding in laboratory animals. Because of our own interest in leucocyte-induced thrombi’ we attempted to confirm Ts’ao’s work in patients undergoing elective abdominal surgery. We prepared standard paraffin sections of formalin-fixed subcutaneous tissues taken from the opening skin incision of patients having a cholecystectomy. A similar sample was removed from a remote subcutaneous site (the T-tube drain site) towards the end of the surgical procedure. A third specimen was taken from the original abdominal wound just before it was closed. We found neutrophil adhesion in 49% of venules in the specimen taken from the original abdominal wound at the end of the surgery. There was no neutrophil adhesion in specimens taken at the start of surgery nor in specimens from a remote site taken towards the end of surgery. We concluded that the neutrophil adhesion we saw was part of the local inflammatory response to surgical trauma and not a generalised effect which occurred at remote sites. Our findings suggest that some explanation other than leucocyte adhesion must be considered. One such explanation might be a platelet alteration, as proposed by Dr O’Brien (Oct. 29, p. 928) in his comment on Cooke’s paper.
New York Medical
College,
Flower-5th Avenue Hospital, New York, N.Y. 10029, U.S.A.
R. G. LERNER V. TCHERTKOFF I. KEMPNER J. C. NELSON R. GOLDSTEIN
Stewart, G. J., Ritchie, W. G. M., Lynch, P. R. in Proceedings of Workshop on Scanning Electron Microscopy in Pathology; p. 473. Chicago, 1973. 2. Stewart, G. J., Ritchie, W. G. M., Lynch, P. R. Am. J. Path. 1974, 74, 507. 3. Stewart, G. J., Lynch, P. R., Reichle, F. P., Ritchie, W. G. M., Smith, A., 1.
Schaulbo, R. G. Ann. N.Y. Acad. Sci. 1977, 283, 179. 4. Ts’ao, C. H., Lin, C. Y., Glagov, S., Replogle, R. L. Archs Path. 1973, 95, 357. 5. Lerner, R. G., Goldstein, R., Nelson, J. C. Thrombosis Res. 1977, 11, 11.
