788
LETTERS to the EDITOR
Age and surgery and intensive care SIR,-Your Jan 26 editorial (p 209) echoes concerns often expressed by US physicians about the exclusion of elderly patients from intensive care. As a warning against using age in decisions about rationing, American commentators sometimes point to what they see as unjustified age barriers limiting access to high technology in Britain. In fact, age limits for transplantation apply in all countries, whereas audits of surgery and intensive care in Britain show that the elderly feature prominently.z3 Only 14% of the UK population are over 65 but they account for 25% of all operations and 30% of admissions to intensive care and over 50% of admissions to coronary care units. Of admissions to acute hospitals in UK almost 40% of those over the age of 75 go to surgical wards. Well-selected elderly patients can benefit greatly from appropriate surgery and intensive care. Diagnosis, severity of illness, and previous health status are factors that predict outcome from surgery and critical illness at all ages, and are therefore important in selecting patients on the basis of expected benefit. Age also influences outcome because of the linear decrease in physiological reserve of most organs after the age oaf 30 4 For example, mortality increased by 3-6 % for each year after the age of 35 in a large international series of severely head injured patients, with no watersheds at 50, 60, or 70 yearsOlder patients are more likely to have multiple pathology, which can also adversely affect results. Good results reported for major surgery or intensive care in older patients are not evidence that age does not affect outcome. Instead they reflect good selection criteria, not all of which feature in widely used severity scores. It would therefore not be wise to follow your editorial suggestion to compare the results in treated patients with the outcomes of those whom doctors decided were unlikely to benefit from certain interventions. Nor does it help to refer to the latter as having been "refused" or "denied" treatment. It is also unjustified to report results that exclude patients who die within six months, or those for whom a definitive decision was made to withhold or withdraw certain therapies, because a trial of treatment had indicated that to persist would be futile. Although academic commentators may press for intergenerational equity in access to medical technologies,l elderly patients themselves may be less concerned about undertreatment than about overenthusiastic efforts to prolong their lives. A US report on life-sustaining technologies and the elderly in 1987 advised restraint.6 Yet in 1990 it was noted that "the very high suicide rate among older Americans is probably due partly to their concern that they may be unable to stop treatment if they are some people now fear living more than dying hospitalised because they dread becoming prisoners of technology"Britain has ten times fewer intensive-care beds per head than the US, but it would be unwise to regard inappropriate overtreatment of the elderly as a problem that does not occur in this country.8,9 Least of all should we accept uncritically exhortations from America to be less selective in treating seriously ill elderly patients. ...
Department of Neurosurgery, Institute of Neurological Sciences, Glasgow G51 4TF, UK
1. Schneider EL.
BRYAN JENNETT
Options to control the rising health care costs of older Americans. JAMA 1989; 261: 907-08. 2. Jennett B. High technology medicine and the elderly in Britain. Int J Tech Assess Health Care 1987; 3: 491-93.
Jennett B. The elderly and high technology therapies. In: Wells N, Freer C, eds. Health problems of an ageing population. London: Macmillan, 1988. 4. Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med 1980; 3.
303: 130. 5 Teasdale G, Skene A, Spiegelhalter D, et al. Age, severity and outcome of head injury In: Grossman RG, Gildenberg PL, eds. Head injury: basic and clinical aspects. New York: Raven Press, 1982. 6. US Congress, Office of Technology Assessment. Life-sustaining technologies and the elderly. Washington, DC: US Government Printing Office, 1987 7. Angell M. Prisoners of technology: the case of Nancy Cruzan. N Engl J Med 1990, 322: 1226-28. 8. Cume CT. Life sustaining technologies and the elderly: Amencans badly need geriatricians. Br Med J 1988; 297: 3-4. 9. Jennett B. Decisions to limit the use of technologies that save or sustain life. Proc R Coll
Physn Edin 1990; 20: 407-15.
Computed tomographic examination in minor head injury SIR,-Intracranial haematoma is the commonest cause of avoidable death and disability after head injury, and appropriate management of patients who initially seem at low risk is the most important factor in the reduction of mortality.1 Most of the 200-380 patients per 100 000 population admitted per year to hospital are only mildly injured (Glasgow coma score of 13 or more).2,3 The key to improved results is timely detection of haematoma by computed tomographic (CT) scanning, but this complication seldom arises in mildly injured patients. American proposals for scanning every patient with abnormal mental status’ or even every low-risk head injury5 could be applied only in Japan or some parts of the USA where there is one scanner per 23 000 and 50 000 of the population, respectively. In EC countries there was, in 1988, one scanner per 150 000-500 000 of the population, and some selection of patients for scanning is essential. Haematoma is seen in fewer than 10% of adults with skull fracture, but in less than 0-5% of those without such fracture; for children the figures are 1 in 157 to 1 in 12 500 .6 Skull fracture could therefore form the basis of selection for scanning in less severely injured patients, although British and American radiologists contest this suggestion.7,8 Such guidelines have been useful in the UK and in our region of Italy. 6,9 In our region the availability of CT scanners has changed from 1 per 2 million to 1 per 200 000 in the past 10 years and yet we have been able to scan all mildly injured patients with fracture.9 The wider use of CT scanners is not necessarily more costly, because patients with negative scans can be safely discharged,5,6 thus reducing the cost of hospital treatment. The policy of non-admittance of patients with full recovery after a brief loss of consciousness if they do not have a fracture, and of increased use of CT scanning, has led to early detection of more intracranial lesions without haematomas being missed.6 Optimum treatment of acute traumatic intracranial haematomas in patients who remain conscious but may be confused, calls for CT scanning before clinical deterioration occurs. The transfer of all patients with skull fracture to the nearest hospital with scanning facilities is a policy based on published data for risk factors. In the past 18 months, of 113 patients who were fully conscious on admission we have operated on 40 with important intracranial lesions. Apart from a 5-year-old child with a posterior fossa extradural haematoma, all had skull fracture. Division of Neurosurgery, Ospedale Bufalini, 47023 Cesena, Italy
FRANCO SERVADEI
789
1. Klauber RM, Marshall LF, Luerssen TG, Frankowski R, Tabbador K, Eisenberg HM. Determinants of head injury mortality: importance of low risk patients. Neurosurgery 1989; 24: 31-36. 2 Jennett B, MacMillan R. Epidemiology of head injury. Br Med J 1981; 282: 101-04. 3. Servadei F, Ciucci G, Piazza G, et al. A prospective clinical and epidemiological study of head injuries m Northern Italy: the Comune of Ravena. Ital J Neurol Sci 1988; 9: 449-57. 4. Fuermann T, Wackym PA, Gade GF, Becker DP. Value of skull radiography, head computed tomographic scanning and admission in cases of minor head injury. Neurosurgery 1988; 22: 449-453. 5. Stein SC, Ross SE. The value of computed tomographic scans in patients with low risk head injuries. Neurosurgery 1990; 26: 638-40. 6. Teasdale GM, Murray G, Anderson E, et al. Risks of acute traumatic intracranial haematoma in children and adults: implication for clinical managing of head injuries. Br Med J 1990; 300: 363-67. 7. Royal College of Radiologists. Cost and benefits of skull radiography for head injury. Lancet 1981; ii 791-95. 8. Masters SJ, McClean PM, Acarese JS. Skull X-ray examination after head trauma.
N Engl J Med 1987; 316: 84-91. 9. Servadei F, Ciucci G, Morichetti A, et al. Skull fracture as a factor of increased risk in minor head injury. Surg Neurol 1988; 30: 364-69.
Campylobacter infections, Guillain-Barré syndrome, and parenteral gangliosides SIR,-Over the past decade several groups have reported a high of Campylobacter jejuni infections in patients with GuillainBarre syndrome (GBS). Japanese workers1 have provided evidence that C jejuni infections could produce GBS by stimulating the production of antibodies capable of reacting with myelin in peripheral nerves. To support this they showed that proteins associated with C jejuni had antigenic properties similar to the myelin-specific proteins PO and P2. Shortly after this another Japanese group’- found that the enterotoxin produced by Cjejuni had immunological and enzymatic activity similar to that of cholera toxin and Escherichia coli heat-labile enterotoxin and suggested that the homologous subunits identified might be responsible for toxin binding to the ganglioside receptors on the cell surface. Yuki et al report high titres of IgG antibody against the ganglioside GM, in 2 patients with GBS after C jejuni enteritis.3 They suggest that GM1 is a target in both acute and chronic motor rate
disorders and that a rise in antiGM1 antibodies after C jejuni infection could be implicated in the pathogenesis of axonal degeneration of motor nerves.33 Although the proposition that exogenous gangliosides can induce GBS has been addressed, the evidence against this is strong. For example, it is impossible to induce antiganglioside antibodies by injection of purified gangliosides, and it is necessary first to create a protein-ganglioside complex.4 Swedish workers5 have shown that parenteral administration of purified bovine brain-derived GM1 ganglioside for three months to Alzheimer’s patients failed to produce antiganglioside antibodies. Our retrospective evaluationb of the immunological risk of parenteral gangliosides, in over 300 patients, could not demonstrate any difference in the frequency of severity of side-effects between ganglioside-treated and placebotreated patients. We believe that this evidence supports the hypothesis that C jejuni may be at least one cause of GBS by virtue of the production of antibodies against myelin. In support of this it has been reported that patients with C jejuni have a severe form of GBS,’ the immune attack in GBS is confined to myelin in the peripheral nervous system, and animal models of GBS can be induced by peripheral nervous system myelin$ In a comparison of GBS patients and controls only 15% of the patient group had antibodies that reacted with GM1 and/or GD1b and not with GMz, GD1a, and GT Ib (Walsh F, Doherty P, personal communication). This indicates that the antibodies detected bind to the carbohydrate epitope Gal(pl-3)GaINAc. An American group9 has shown that antibodies reacting with this epitope, common to many glycolipids and glycoproteins, bind to the surface of motor neurons whereas antibodies specific for GM1 do not. This group has reviewed neurological diseases associated with antiGM1 antibodies and has suggested that patients with motor or sensorimotor peripheral neuropathy or lower motomeuron disease should be tested for antiGM1 or antiGal(pl-3)GalNAc antibodies.1o A raised frequency of previous C jejuni infection has been seen in GBS and a correlation between the presence of axon
glycoconjugate antibodies and campylobacter infection found (Walsh F, Doherty P, personal communication). Fidia Research Laboratories, 35031 Abano Terme,
Italy
was
also
L. CALLEGARO D. B. JACK J. C. SAMSON
Fujimoto S, Amako K. Guillain-Barré syndrome and Campylobacter jejuni infection. Lancet 1990; 335: 1350. 2. Daikoku T, Kawaguchi M, Takama K, et al. Partial purification and characterization of the enterotoxin produced by Campylobacter jejuni. Infect Immunol 1990; 58: 1.
2414-19. 3. Yuki N, Yoshimo H, Sato S, et al. Acute axonal polyneuropathy associated with anti-GM1 antibodies following Campylobacter enteritis. Neurology 1990; 40: 1900-02. 4. Doherty P, Walsh FS. Ganglioside GM1 antibodies and &bgr;-cholera toxin bind specifically to embryonic chick dorsal root ganglion neurons but do not modulate neunte regeneration. J Neurochem 1987; 48: 1237-44. 5. Svennerholm L, Fredman P. Antibody detection in Guillain-Barré syndrome. Ann Neurol 1990; 27 (suppl): S36-40. 6. Massarotti M, Cornelli U, Samson JC, Jack DB. An evaulation of the immunological nsk of ganglioside (CronassialR) injections. Drug Invest (in press). 7. Kaldor J, Speed BR. Guillain-Barré syndrome and Campylobacter jejum: a serological study. Br Med J 1984; 288: 1867-70. 8. Ledeen RW, Oderfeld-Nowak B, Bronsan CF. Gangliosides offer partial protection in experimental allergic neuritis. Ann Neurol 1990; 27 (suppl): S69-75. 9. Thomas FP, Thomas JE, Sadiq SA, et al. Human monoclonal IgM anti-Gal(&bgr;13)GalNAc autoantibodies bind to the surface of bovine spinal motoneurons. J Neuropath Exp Neurol 1990; 49: 89-95. 10. Sadiq SA, Thomas FP, Kilidireas K, et al. The spectrum of neurologic disease associated with anti-GM1 antibodies. Neurology 1990; 40: 1067-72.
Honey poisoning in Turkey SIR,-Food poisoning associated with honey is not uncommon in the Black Sea region of Turkey. Nectar from some plants in the area is toxic. This form of poisoning is mentioned in Xenophon’s Anabasis’ but published reports are very rare. We describe here a large series. We have evaluated retrospectively 23 cases from two parts of the Black Sea region of Turkey seen between 1983 and 1986. A report on 16 of them, diagnosed in Trabzon in the eastern Black Sea region, has been published in a Turkish medical journa1.1 Most of the other 7 lived in Inebolu in the middle Black Sea region. Clinical information is not always complete and signs and symptoms are given as percentages of the number of patients evaluated:
The youngest of the 23 patients was 7 months old and the oldest 61-year-old. 21 were males. The amounts of toxic honey consumed ranged between two teaspoonsful and five tablespoonsful. Symptoms began within 30 min if large amounts were ingested or if honey was taken in the form of sherbert, the longest interval being 2 h. The most striking symptoms and signs
was a
nausea, vomiting, sweating, dizziness, hypotension, bradycardia, and impairment of consciousness. On electrocardiography (ECG) (16 patients) 63% had bradycardia, 31% junctional rhythm, 6% complete atrioventricular block, and 6% Wolff-Parkinson-White syndrome with sinus bradycardia. were
Patients regained consciousness or felt better after between half an hour and 6 hours, and they had recovered completely in 1 or 2 days. ECGs were normal within 24 h. Intravenous fluids, atropine, and vasopressive agents were sufficient for therapy. Isoproterenol was given to a patient who had complete atrioventricular block. The toxic substances are thought to come from rhododendrons found in the forests of northern Anatolia. There are five species of rhododendron in Turkey, the most found being Rhododendron ponticum and R flavum.2 Grayanotoxins present in these plants cause intoxication. These diterpenoids are present in leaves and flowers of rhododendrons and some other plants. Eighteen forms of grayanotoxin have been isolated, three being especially important. Grayanotoxin I and II have been found in honey and in the leaves and flowers of R ponticum and R flavum but grayanotoxin III has
LETTERS to the EDITOR
Age and surgery and intensive care SIR,-Your Jan 26 editorial (p 209) echoes concerns often expressed by US physicians about the exclusion of elderly patients from intensive care. As a warning against using age in decisions about rationing, American commentators sometimes point to what they see as unjustified age barriers limiting access to high technology in Britain. In fact, age limits for transplantation apply in all countries, whereas audits of surgery and intensive care in Britain show that the elderly feature prominently.z3 Only 14% of the UK population are over 65 but they account for 25% of all operations and 30% of admissions to intensive care and over 50% of admissions to coronary care units. Of admissions to acute hospitals in UK almost 40% of those over the age of 75 go to surgical wards. Well-selected elderly patients can benefit greatly from appropriate surgery and intensive care. Diagnosis, severity of illness, and previous health status are factors that predict outcome from surgery and critical illness at all ages, and are therefore important in selecting patients on the basis of expected benefit. Age also influences outcome because of the linear decrease in physiological reserve of most organs after the age oaf 30 4 For example, mortality increased by 3-6 % for each year after the age of 35 in a large international series of severely head injured patients, with no watersheds at 50, 60, or 70 yearsOlder patients are more likely to have multiple pathology, which can also adversely affect results. Good results reported for major surgery or intensive care in older patients are not evidence that age does not affect outcome. Instead they reflect good selection criteria, not all of which feature in widely used severity scores. It would therefore not be wise to follow your editorial suggestion to compare the results in treated patients with the outcomes of those whom doctors decided were unlikely to benefit from certain interventions. Nor does it help to refer to the latter as having been "refused" or "denied" treatment. It is also unjustified to report results that exclude patients who die within six months, or those for whom a definitive decision was made to withhold or withdraw certain therapies, because a trial of treatment had indicated that to persist would be futile. Although academic commentators may press for intergenerational equity in access to medical technologies,l elderly patients themselves may be less concerned about undertreatment than about overenthusiastic efforts to prolong their lives. A US report on life-sustaining technologies and the elderly in 1987 advised restraint.6 Yet in 1990 it was noted that "the very high suicide rate among older Americans is probably due partly to their concern that they may be unable to stop treatment if they are some people now fear living more than dying hospitalised because they dread becoming prisoners of technology"Britain has ten times fewer intensive-care beds per head than the US, but it would be unwise to regard inappropriate overtreatment of the elderly as a problem that does not occur in this country.8,9 Least of all should we accept uncritically exhortations from America to be less selective in treating seriously ill elderly patients. ...
Department of Neurosurgery, Institute of Neurological Sciences, Glasgow G51 4TF, UK
1. Schneider EL.
BRYAN JENNETT
Options to control the rising health care costs of older Americans. JAMA 1989; 261: 907-08. 2. Jennett B. High technology medicine and the elderly in Britain. Int J Tech Assess Health Care 1987; 3: 491-93.
Jennett B. The elderly and high technology therapies. In: Wells N, Freer C, eds. Health problems of an ageing population. London: Macmillan, 1988. 4. Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med 1980; 3.
303: 130. 5 Teasdale G, Skene A, Spiegelhalter D, et al. Age, severity and outcome of head injury In: Grossman RG, Gildenberg PL, eds. Head injury: basic and clinical aspects. New York: Raven Press, 1982. 6. US Congress, Office of Technology Assessment. Life-sustaining technologies and the elderly. Washington, DC: US Government Printing Office, 1987 7. Angell M. Prisoners of technology: the case of Nancy Cruzan. N Engl J Med 1990, 322: 1226-28. 8. Cume CT. Life sustaining technologies and the elderly: Amencans badly need geriatricians. Br Med J 1988; 297: 3-4. 9. Jennett B. Decisions to limit the use of technologies that save or sustain life. Proc R Coll
Physn Edin 1990; 20: 407-15.
Computed tomographic examination in minor head injury SIR,-Intracranial haematoma is the commonest cause of avoidable death and disability after head injury, and appropriate management of patients who initially seem at low risk is the most important factor in the reduction of mortality.1 Most of the 200-380 patients per 100 000 population admitted per year to hospital are only mildly injured (Glasgow coma score of 13 or more).2,3 The key to improved results is timely detection of haematoma by computed tomographic (CT) scanning, but this complication seldom arises in mildly injured patients. American proposals for scanning every patient with abnormal mental status’ or even every low-risk head injury5 could be applied only in Japan or some parts of the USA where there is one scanner per 23 000 and 50 000 of the population, respectively. In EC countries there was, in 1988, one scanner per 150 000-500 000 of the population, and some selection of patients for scanning is essential. Haematoma is seen in fewer than 10% of adults with skull fracture, but in less than 0-5% of those without such fracture; for children the figures are 1 in 157 to 1 in 12 500 .6 Skull fracture could therefore form the basis of selection for scanning in less severely injured patients, although British and American radiologists contest this suggestion.7,8 Such guidelines have been useful in the UK and in our region of Italy. 6,9 In our region the availability of CT scanners has changed from 1 per 2 million to 1 per 200 000 in the past 10 years and yet we have been able to scan all mildly injured patients with fracture.9 The wider use of CT scanners is not necessarily more costly, because patients with negative scans can be safely discharged,5,6 thus reducing the cost of hospital treatment. The policy of non-admittance of patients with full recovery after a brief loss of consciousness if they do not have a fracture, and of increased use of CT scanning, has led to early detection of more intracranial lesions without haematomas being missed.6 Optimum treatment of acute traumatic intracranial haematomas in patients who remain conscious but may be confused, calls for CT scanning before clinical deterioration occurs. The transfer of all patients with skull fracture to the nearest hospital with scanning facilities is a policy based on published data for risk factors. In the past 18 months, of 113 patients who were fully conscious on admission we have operated on 40 with important intracranial lesions. Apart from a 5-year-old child with a posterior fossa extradural haematoma, all had skull fracture. Division of Neurosurgery, Ospedale Bufalini, 47023 Cesena, Italy
FRANCO SERVADEI
789
1. Klauber RM, Marshall LF, Luerssen TG, Frankowski R, Tabbador K, Eisenberg HM. Determinants of head injury mortality: importance of low risk patients. Neurosurgery 1989; 24: 31-36. 2 Jennett B, MacMillan R. Epidemiology of head injury. Br Med J 1981; 282: 101-04. 3. Servadei F, Ciucci G, Piazza G, et al. A prospective clinical and epidemiological study of head injuries m Northern Italy: the Comune of Ravena. Ital J Neurol Sci 1988; 9: 449-57. 4. Fuermann T, Wackym PA, Gade GF, Becker DP. Value of skull radiography, head computed tomographic scanning and admission in cases of minor head injury. Neurosurgery 1988; 22: 449-453. 5. Stein SC, Ross SE. The value of computed tomographic scans in patients with low risk head injuries. Neurosurgery 1990; 26: 638-40. 6. Teasdale GM, Murray G, Anderson E, et al. Risks of acute traumatic intracranial haematoma in children and adults: implication for clinical managing of head injuries. Br Med J 1990; 300: 363-67. 7. Royal College of Radiologists. Cost and benefits of skull radiography for head injury. Lancet 1981; ii 791-95. 8. Masters SJ, McClean PM, Acarese JS. Skull X-ray examination after head trauma.
N Engl J Med 1987; 316: 84-91. 9. Servadei F, Ciucci G, Morichetti A, et al. Skull fracture as a factor of increased risk in minor head injury. Surg Neurol 1988; 30: 364-69.
Campylobacter infections, Guillain-Barré syndrome, and parenteral gangliosides SIR,-Over the past decade several groups have reported a high of Campylobacter jejuni infections in patients with GuillainBarre syndrome (GBS). Japanese workers1 have provided evidence that C jejuni infections could produce GBS by stimulating the production of antibodies capable of reacting with myelin in peripheral nerves. To support this they showed that proteins associated with C jejuni had antigenic properties similar to the myelin-specific proteins PO and P2. Shortly after this another Japanese group’- found that the enterotoxin produced by Cjejuni had immunological and enzymatic activity similar to that of cholera toxin and Escherichia coli heat-labile enterotoxin and suggested that the homologous subunits identified might be responsible for toxin binding to the ganglioside receptors on the cell surface. Yuki et al report high titres of IgG antibody against the ganglioside GM, in 2 patients with GBS after C jejuni enteritis.3 They suggest that GM1 is a target in both acute and chronic motor rate
disorders and that a rise in antiGM1 antibodies after C jejuni infection could be implicated in the pathogenesis of axonal degeneration of motor nerves.33 Although the proposition that exogenous gangliosides can induce GBS has been addressed, the evidence against this is strong. For example, it is impossible to induce antiganglioside antibodies by injection of purified gangliosides, and it is necessary first to create a protein-ganglioside complex.4 Swedish workers5 have shown that parenteral administration of purified bovine brain-derived GM1 ganglioside for three months to Alzheimer’s patients failed to produce antiganglioside antibodies. Our retrospective evaluationb of the immunological risk of parenteral gangliosides, in over 300 patients, could not demonstrate any difference in the frequency of severity of side-effects between ganglioside-treated and placebotreated patients. We believe that this evidence supports the hypothesis that C jejuni may be at least one cause of GBS by virtue of the production of antibodies against myelin. In support of this it has been reported that patients with C jejuni have a severe form of GBS,’ the immune attack in GBS is confined to myelin in the peripheral nervous system, and animal models of GBS can be induced by peripheral nervous system myelin$ In a comparison of GBS patients and controls only 15% of the patient group had antibodies that reacted with GM1 and/or GD1b and not with GMz, GD1a, and GT Ib (Walsh F, Doherty P, personal communication). This indicates that the antibodies detected bind to the carbohydrate epitope Gal(pl-3)GaINAc. An American group9 has shown that antibodies reacting with this epitope, common to many glycolipids and glycoproteins, bind to the surface of motor neurons whereas antibodies specific for GM1 do not. This group has reviewed neurological diseases associated with antiGM1 antibodies and has suggested that patients with motor or sensorimotor peripheral neuropathy or lower motomeuron disease should be tested for antiGM1 or antiGal(pl-3)GalNAc antibodies.1o A raised frequency of previous C jejuni infection has been seen in GBS and a correlation between the presence of axon
glycoconjugate antibodies and campylobacter infection found (Walsh F, Doherty P, personal communication). Fidia Research Laboratories, 35031 Abano Terme,
Italy
was
also
L. CALLEGARO D. B. JACK J. C. SAMSON
Fujimoto S, Amako K. Guillain-Barré syndrome and Campylobacter jejuni infection. Lancet 1990; 335: 1350. 2. Daikoku T, Kawaguchi M, Takama K, et al. Partial purification and characterization of the enterotoxin produced by Campylobacter jejuni. Infect Immunol 1990; 58: 1.
2414-19. 3. Yuki N, Yoshimo H, Sato S, et al. Acute axonal polyneuropathy associated with anti-GM1 antibodies following Campylobacter enteritis. Neurology 1990; 40: 1900-02. 4. Doherty P, Walsh FS. Ganglioside GM1 antibodies and &bgr;-cholera toxin bind specifically to embryonic chick dorsal root ganglion neurons but do not modulate neunte regeneration. J Neurochem 1987; 48: 1237-44. 5. Svennerholm L, Fredman P. Antibody detection in Guillain-Barré syndrome. Ann Neurol 1990; 27 (suppl): S36-40. 6. Massarotti M, Cornelli U, Samson JC, Jack DB. An evaulation of the immunological nsk of ganglioside (CronassialR) injections. Drug Invest (in press). 7. Kaldor J, Speed BR. Guillain-Barré syndrome and Campylobacter jejum: a serological study. Br Med J 1984; 288: 1867-70. 8. Ledeen RW, Oderfeld-Nowak B, Bronsan CF. Gangliosides offer partial protection in experimental allergic neuritis. Ann Neurol 1990; 27 (suppl): S69-75. 9. Thomas FP, Thomas JE, Sadiq SA, et al. Human monoclonal IgM anti-Gal(&bgr;13)GalNAc autoantibodies bind to the surface of bovine spinal motoneurons. J Neuropath Exp Neurol 1990; 49: 89-95. 10. Sadiq SA, Thomas FP, Kilidireas K, et al. The spectrum of neurologic disease associated with anti-GM1 antibodies. Neurology 1990; 40: 1067-72.
Honey poisoning in Turkey SIR,-Food poisoning associated with honey is not uncommon in the Black Sea region of Turkey. Nectar from some plants in the area is toxic. This form of poisoning is mentioned in Xenophon’s Anabasis’ but published reports are very rare. We describe here a large series. We have evaluated retrospectively 23 cases from two parts of the Black Sea region of Turkey seen between 1983 and 1986. A report on 16 of them, diagnosed in Trabzon in the eastern Black Sea region, has been published in a Turkish medical journa1.1 Most of the other 7 lived in Inebolu in the middle Black Sea region. Clinical information is not always complete and signs and symptoms are given as percentages of the number of patients evaluated:
The youngest of the 23 patients was 7 months old and the oldest 61-year-old. 21 were males. The amounts of toxic honey consumed ranged between two teaspoonsful and five tablespoonsful. Symptoms began within 30 min if large amounts were ingested or if honey was taken in the form of sherbert, the longest interval being 2 h. The most striking symptoms and signs
was a
nausea, vomiting, sweating, dizziness, hypotension, bradycardia, and impairment of consciousness. On electrocardiography (ECG) (16 patients) 63% had bradycardia, 31% junctional rhythm, 6% complete atrioventricular block, and 6% Wolff-Parkinson-White syndrome with sinus bradycardia. were
Patients regained consciousness or felt better after between half an hour and 6 hours, and they had recovered completely in 1 or 2 days. ECGs were normal within 24 h. Intravenous fluids, atropine, and vasopressive agents were sufficient for therapy. Isoproterenol was given to a patient who had complete atrioventricular block. The toxic substances are thought to come from rhododendrons found in the forests of northern Anatolia. There are five species of rhododendron in Turkey, the most found being Rhododendron ponticum and R flavum.2 Grayanotoxins present in these plants cause intoxication. These diterpenoids are present in leaves and flowers of rhododendrons and some other plants. Eighteen forms of grayanotoxin have been isolated, three being especially important. Grayanotoxin I and II have been found in honey and in the leaves and flowers of R ponticum and R flavum but grayanotoxin III has
