100 We feel that C.E.P. and S.C.E.P. offer a high degree of sensitivity and specificity. When factors such as technical simplicity, speed, low cost, and wide applicability are considered this technique would appear to be of considerable merit. Our application of S.C.E.P. for the detection of virus in vector mosquitoes and virsmic animals is a significant new use of this technique which opens many possibilities for its future use in ecologic studies of arboviruses. University of Texas Health Science Center, School of Public Health, Houston, Texas 77025, U.S.A.
JOHN F. JAMES P. S. SULLIVAN D. R. ROBERTS.
PROGNOSIS IN COMA SIR,-You drew attention (Nov. 30, p. 1302) to two papers 1,2 which reported the bad prognosis associated with coma after cardiac arrest. Prognosis in many other conditions likewise becomes unfavourable if coma develops, and the mortality-rate and the incidence of persisting disability increase with the depth and duration of coma. Investigations in our hospitals of patients with nontraumatic coma lasting more than six hours (excluding cases of poisoning) have indicated that more than half die and that many survivors have persisting disabilities; when coma is due to head injury the outcome is more favourable, but is still closely related to the degree of coma. If coma is such a significant feature it must be critically assessed.33 One of the papers1 was based on retrospective data and the depth and duration of coma could not be accurately defined. The other2 depended on recognising that motor responses were at the most " only reflex ", but this also can be difficult to define and observe consistently. Important clinical decisions of the kind you suggest must
be based
reliable
on a
assessment
of
coma
and its
Together with colleagues in the U.S.A. and the Netherlands we are engaged on a study which aims to establish this relationship, so that the probability of different outcomes can be calculated for individual patients after various types of brain damage. We zealous efforts to keep agree that in some circumstances the patient alive may be misplaced ". But a formal investigation is required to define what these circumstances are for coma in various conditions. Our study should provide relationship
to outcome.
physiological knowledge. Professor Ritchie Russell’s view that " a purely physical effect may mimic exactly a so-called psychogenic feature " is speculation. Department of Neurology, Karolinska Sjukhuset, S-104 01 Stockholm 60, Sweden.
HANS F. LIDVALL.
REYE’S SYNDROME
SiR—Dr Thaler and his colleagues described a patient with Reye’s syndrome who had a " protein tolerant" variant of ornithine transcarbamylase (o.T.c.).1 They suggest a link between Reye’s syndrome and heritable Others have found reduced levels of o.T.c. deficiency. both carbamyl-phosphate synthetase (c.p.s.) and o.T.c. in this disorder.2 Females with an isolated deficiency of O.T.c. requiring low-protein diets excrete 6-60 mg. of orotic acid per 24 hours while on the diet, and when ill (and more comparable to patients with Reye’s syndrome) excrete up to 190 mg. orotic acid per 24 hours.3,4 In order to evaluate the (functional) defect in ureagenesis in Reye’s syndrome we have determined urinary orotic-acid excretion in children with Reye’s syndrome and in controls. Urine was obtained from 9 patients with Reye’s syndrome, ranging in age from 1 to 12 years, during the acute phase of their illness, from 9 normal children aged 3 to 13 years, and from one child of 2 years, during the acute phase of an acute encephalopathy other than Reye’s syndrome. In 4 patients with Reye’s syndrome and 9 controls the urines were 12-hour or 24-hour collections. All patients with Reye’s syndrome had a raised
blood-ammonia level. For estimation of orotic acid 0-1 1. 2.
3. 4.
uCi
14C-orotic acid
was
Thaler, M. M., Hoogenraad, N. J., Boswell, M. Lancet, 1974, ii, 438. Brown, T., Brown, H., Lansky, L., Hug, G. New Engl. J. Med. 1974, 291, 797. Levin, B., Oberholzer, V. G., Sinclair, L. Lancet, 1969, ii, 170. Corbeel, L. M., Colombo, J. P., Van Sande, M., Weber, A. Archs Dis. Child. 1969, 44, 681.
"
not only that information but will also define when recovery can be expected from coma, so that maximum effort may be directed to such patients. Department of Neurosurgery, Institute of Neurological Sciences, Southern General Hospital, BRYAN JENNETT. Glasgow G51 4TF. New York HospitalCornell Medical Center.
FRED PLUM.
Royal Victoria Infirmary, Newcastle upon Tyne.
DAVID SHAW.
RECOVERY AFTER MINOR HEAD
INJURY
SiR,—Iagree with Professor Ritchie Russell (Nov. 30, p. 1315) that an exact general distinction cannot be made between cerebrolesional and mental dysfunction due to head trauma. Moreover, it seems reasonable to assume that even " minor " head injury may give rise to discrete cerebral damage. From this it must not be concluded that the term " psychogenic " should be avoided in referring to the pathogenesis of postconcussional symptoms caused by an emotional reaction to trauma. On the contrary, this a
1. 2. 3.
seems
to
be the
psychopathological
most
convenient way of denoting we have sparse
process of which
Bell, J. A., Hodgson, H. J. F. Brain, 1974, 97, 361. Willoughby, J. O., Leach, B. G. Br. med. J. 1974, iii, Teasdale, G., Jennett, B. Lancet, 1974, ii, 81.
added
437.
Urinary orotic-acid excretion in Reye’s syndrome.
JOHN F. JAMES P. S. SULLIVAN D. R. ROBERTS.
PROGNOSIS IN COMA SIR,-You drew attention (Nov. 30, p. 1302) to two papers 1,2 which reported the bad prognosis associated with coma after cardiac arrest. Prognosis in many other conditions likewise becomes unfavourable if coma develops, and the mortality-rate and the incidence of persisting disability increase with the depth and duration of coma. Investigations in our hospitals of patients with nontraumatic coma lasting more than six hours (excluding cases of poisoning) have indicated that more than half die and that many survivors have persisting disabilities; when coma is due to head injury the outcome is more favourable, but is still closely related to the degree of coma. If coma is such a significant feature it must be critically assessed.33 One of the papers1 was based on retrospective data and the depth and duration of coma could not be accurately defined. The other2 depended on recognising that motor responses were at the most " only reflex ", but this also can be difficult to define and observe consistently. Important clinical decisions of the kind you suggest must
be based
reliable
on a
assessment
of
coma
and its
Together with colleagues in the U.S.A. and the Netherlands we are engaged on a study which aims to establish this relationship, so that the probability of different outcomes can be calculated for individual patients after various types of brain damage. We zealous efforts to keep agree that in some circumstances the patient alive may be misplaced ". But a formal investigation is required to define what these circumstances are for coma in various conditions. Our study should provide relationship
to outcome.
physiological knowledge. Professor Ritchie Russell’s view that " a purely physical effect may mimic exactly a so-called psychogenic feature " is speculation. Department of Neurology, Karolinska Sjukhuset, S-104 01 Stockholm 60, Sweden.
HANS F. LIDVALL.
REYE’S SYNDROME
SiR—Dr Thaler and his colleagues described a patient with Reye’s syndrome who had a " protein tolerant" variant of ornithine transcarbamylase (o.T.c.).1 They suggest a link between Reye’s syndrome and heritable Others have found reduced levels of o.T.c. deficiency. both carbamyl-phosphate synthetase (c.p.s.) and o.T.c. in this disorder.2 Females with an isolated deficiency of O.T.c. requiring low-protein diets excrete 6-60 mg. of orotic acid per 24 hours while on the diet, and when ill (and more comparable to patients with Reye’s syndrome) excrete up to 190 mg. orotic acid per 24 hours.3,4 In order to evaluate the (functional) defect in ureagenesis in Reye’s syndrome we have determined urinary orotic-acid excretion in children with Reye’s syndrome and in controls. Urine was obtained from 9 patients with Reye’s syndrome, ranging in age from 1 to 12 years, during the acute phase of their illness, from 9 normal children aged 3 to 13 years, and from one child of 2 years, during the acute phase of an acute encephalopathy other than Reye’s syndrome. In 4 patients with Reye’s syndrome and 9 controls the urines were 12-hour or 24-hour collections. All patients with Reye’s syndrome had a raised
blood-ammonia level. For estimation of orotic acid 0-1 1. 2.
3. 4.
uCi
14C-orotic acid
was
Thaler, M. M., Hoogenraad, N. J., Boswell, M. Lancet, 1974, ii, 438. Brown, T., Brown, H., Lansky, L., Hug, G. New Engl. J. Med. 1974, 291, 797. Levin, B., Oberholzer, V. G., Sinclair, L. Lancet, 1969, ii, 170. Corbeel, L. M., Colombo, J. P., Van Sande, M., Weber, A. Archs Dis. Child. 1969, 44, 681.
"
not only that information but will also define when recovery can be expected from coma, so that maximum effort may be directed to such patients. Department of Neurosurgery, Institute of Neurological Sciences, Southern General Hospital, BRYAN JENNETT. Glasgow G51 4TF. New York HospitalCornell Medical Center.
FRED PLUM.
Royal Victoria Infirmary, Newcastle upon Tyne.
DAVID SHAW.
RECOVERY AFTER MINOR HEAD
INJURY
SiR,—Iagree with Professor Ritchie Russell (Nov. 30, p. 1315) that an exact general distinction cannot be made between cerebrolesional and mental dysfunction due to head trauma. Moreover, it seems reasonable to assume that even " minor " head injury may give rise to discrete cerebral damage. From this it must not be concluded that the term " psychogenic " should be avoided in referring to the pathogenesis of postconcussional symptoms caused by an emotional reaction to trauma. On the contrary, this a
1. 2. 3.
seems
to
be the
psychopathological
most
convenient way of denoting we have sparse
process of which
Bell, J. A., Hodgson, H. J. F. Brain, 1974, 97, 361. Willoughby, J. O., Leach, B. G. Br. med. J. 1974, iii, Teasdale, G., Jennett, B. Lancet, 1974, ii, 81.
added
437.
Urinary orotic-acid excretion in Reye’s syndrome.
