- Email: [email protected]
SCHIZOPHRENIA AND ORGANIC DISEASE
776
additional diffuse airways obstruction and daytime hypoxaemia in such patients (sometimes only of mild-to-moderate severity) rather than obesity that
provokes CO2 retention, pulmonary hypertension, and cor pulmonale.24,26 The reasons are not clear. Small airways disease will tend to raise functional residual capacity (FRC) and residual volume, which to some extent offsets the expected airway closure and reduced gas exchange. In addition, a rise in FRC will increase the size of the pharynx27 (thus reducing the tendency to OSA) and the size of the O2 reserve during apnoea. However, obesity will push the FRC down again towards residual volume (particularly when the patient is supine) and airway resistance will be high at this lower lung volume.24,28 Thus the obese patient with mild airways obstruction will have a reduced daytime Pa02, small airway closure, and a lower FRC than expected-all factors worsening the degree of arterial desaturation for a given length of apnoea. 29 The presence of moderate airways obstruction may also limit the patient’s ability to hyperventilate and restore blood gases to normal between apnoeas: over many years this extra hypoxic and hypercapnic load may provoke resetting of Pa02 and PaC02 control mechanisms, 21,30 with consequent diurnal respiratory failure. The "pickwickian" patient is likely to be an obese individual having OSA with some CAWO and consequent diurnal respiratory failure. Thus, vigorous treatment of even moderate diffuse airways obstruction will lessen some of the physiological consequences of OSA by improving waking and sleeping oxygenation, though benefit in terms of symptoms such as sleepiness is uncertain. Fletcher et a131 have also shown that, if the primary problem of sleep apnoea is treated (by tracheostomy) in patients with associated moderate CAWO, then the raised pulmonary artery pressure and pulmonary vascular resistance improve. Another interesting possible relationship, recently reported to the British Thoracic Society, exists between asthma and OSA. Chan et al32 treated asthmatics with nocturnal asthma and OSA or very heavy snoring by continuous nasal positive airway pressure. The nocturnal asthma symptoms Bradley TD, Rutherford R, Lue F, Moldofsky H, Grossman RF, Zamel N, Phillipson EA. Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea. Am Rev Respir Dis 1986; 134: 920-24. 25. Weitzenblum E, Kneger J, Oswald M, Vallee E, Ehrhart M, Kurtz D. Pulmonary hypertension in patients with obstructive sleep apnea syndrome Clin Respir Physiol 1987; 23 (suppl 12): 419S. 26. Bradley TD, Rutherford R, Grossman RF, Lue F, Zamel N, Moldofsky H. Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1985; 131: 835-39. 27. Hoffstein V, Phillipson EA, Zamel N. Lung volume dependence of pharyngeal cross-sectional area in patients with obstructive sleep apnea. Am Rev Respir Dis 24.
1984; 130: 175-78. 28. Onal E, Leech JA, Lopata M. Relationship between pulmonary function and sleep-induced respiratory abnormalities. Chest 1985; 87: 437-41. 29. Bradley TD, Martinez D, Rutherford R, Lue F, Grossman R, Moldofsky H, Zamel N, Phillipson EA. Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnoea. J Appl Physiol 1985, 59: 1364-68. 30. Rapoport DM, Garay SM, Epstein H, Goldring RM. Mechanism of chronic hypercapnia in obstructive sleep apnea. Am Rev Respir Dis 1982; 125: A252. 31.
Fletcher EC, Schaaf JW, Miller J, Fletcher JG Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease. Am Rev Respir Dis 1987; 135:
525-33. 32. Chan CS, Woolcock AJ, Sullivan CE. Nocturnal asthma: role of snoring and obstructive sleep apnoea (OSA). Presented at British Thoracic Society Meeting, Edinburgh, 1987
improved, as did the morning peak flows. The mechanism is far from clear, but these workers suggest that a pharyngeal reflex may be operative, although hypoxia itself can provoke bronchoconstriction. At present the clinical implications of these findings on the interrelations between CAWO and OSA are debatable. Most patients will have one or other, not both. A spectrum must exist within the small group having both-some predominantly CAWO, some predominantly OSA. Symptoms that may be due to OSA are worth investigation, whether or not CAWO is present as well. On existing evidence there is no case for routine sleep studies in all patients with CAWO. SCHIZOPHRENIA AND ORGANIC DISEASE SINCE
Kraepelin first introduced the term dementia describe the condition that subsequently became praecox schizophrenia there has been a constant debate about the relation between this condition and organic disease. Kraepelin1 was unequivocal in regarding it as an organic dementia "in which the faculty of comprehension and the recollection of knowledge previously acquired are much less affected than judgement, emotional impulses and acts of volition". Kraepelin’s views are now known to have been substantially correct, in that a significant proportion of patients with schizophrenia have cerebral abnormalities, particularly in the temporal lobe .2-6 Despite these findings the cause or causes of schizophrenia remain elusive. In these circumstances it is sometimes helpful to look carefully at coexisting diagnosable organic disease. Although such associations might be fortuitous or independent of the cause, the degree of association between organic disease and schizophrenia exceeds that expected by chance7,8 and it seems likely that at least in some cases the organic disease is of major aetiological importance. Interpretation of data is made more difficult by the prolonged course of schizophrenia and the development of secondary complications, including alcohol abuse,9 depression tardive dyskinesia," and personality change. Because there is dispute over whether these secondary features are part of the natural history of schizophrenia or a consequence of management there are merits in studying schizophrenia at first presentation. Results of such inquiries have shown that schizophrenia is associated relatively to
Kraepelin E. Lectures on clinical psychiatry. Revised and edited by T. Johnstone. London: Baillière, Tindall and Cox, 1906: 26. 2. Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L. Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet 1976; ii: 924-26. 3. Weinberger DR, Torrey EF, Neophytides A, Wyatt RJ. Structural abnormalities of the cerebral cortex in chronic schizophrenia. Arch Gen Psychiatry 1979; 36: 935-39. 4. Reveley AM, Reveley MA, Clifford CA, Murray RM. Cerebral ventricular size in twins discordant for schizophrenia. Lancet 1982; i: 540-42. 5. Weinberger DR, Wagner RL, Wyatt RJ. Neuropathological studies of schizophrenia a selective review. Schizophr Bull 1983; 9: 193-212. 6. Brown R, Colter N, Corselhs JAN, et al. Postmortem evidence of structural brain changes in schizophrenia: differences in brain weight, temporal hom area, and parahippocampal gyrus compared with affective disorder. Arch Gen Psychiatry 1986; 43: 36-42. 7. Davison K, Bagley CR. Schizophrenia-like psychoses associated with organic disorders of the central nervous system: a review of the literature. In: Herrington RN, ed. Current problems in neuropsychiatry. Ashford: Headley Bros, 1969: 1.
113-84. E, Beard AW, Glithero E. The
schizophrenia-like psychoses of epilepsy. Br J Psychiatry 1963; 109: 95-150. Freed EX. Alcoholism and schizophrenia: the search for perspectives. J Stud Alcohol 1975; 36: 853-81. Virkkunen M. Suicides in schizophrenia and paranoid psychoses. Acta Psychiat Scand 1974 (suppl 250). Crane GE. Persistent dyskinesia. Br J Psychiatry 1973; 122: 395-405.
8. Slater 9. 10. 11.
777
infrequently with other organic disease: fewer than 10% of patients have an identifiable illness at the time of initial presentation with schizophrenia.12,13 The most common8 organic states associated with schizophrenia are epilepsy, neurosyphilis/,13,14 and alcohol and drug abuse.9.13,15 A study by Johnstone and her colleagues13 also documented sarcoidosis in 2 of 268 cases of first-episode schizophrenia. These findings indicate that the pathological changes in the brain in schizophrenia are unlikely to be a consequence of another known organic disease. In any event, many patients with schizophrenia do not have any organic changes. Nevertheless, the common associations of neurosyphilis, alcohol abuse, and epilepsy with schizophrenia cannot be dismissed as chance findings or non-specific vulnerability factors-these conditions occur too often in the presentation and course of schizophrenic illness to be ignored. It is more likely that such disorders share some of the pathophysiological changes of schizophrenia and thereby simulate or provoke episodes of illness. In schizophrenia there is good evidence of abnormalities in dopamine and peptide metabolism16.17 and, although the significance of such findings is disputed, they are likely to be important in the generation of psychotic symptoms. The anatomical sites of these changes are also important. Most of the pathological changes in schizophrenia are found in the limbic system, particularly its temporal lobe componentsand since Flor- Henry18 noted that schizophreniform psychoses and temporal lobe epilepsy were associated with epileptic foci in the dominant hemisphere there has been constant debate about the significance of laterality in the pathogenesis of schizophrenia. As epilepsy is much more likely to lead to schizophrenia when it affects the temporal lobe, and as the temporal lobe is also implicated in the schizophreniform psychoses of syphilis, and alcohol and drug abuse 1’°l9 these associations might explain why schizophrenic-like symptoms are manifest during such disorders. When organic disorder creates a schizophreniform psychosis the condition is usually indistinguishable from other forms of schizophrenia. No amount of phenomenological exactitude can differentiate between the symptoms of a true schizophreniform psychosis caused by an organic disease and those of schizophrenia itself. However, schizophreniform psychoses caused by organic disease are rare and have no common organic basis. Although structural and biochemical abnormalities have been found in the brain of schizophrenic patients it is dangerous to assume that schizophrenia is therefore an organic psychosis. Cutting2O lately compared the symptoms of acute organic psychosis and those of schizophrenia and found striking differences between them, particularly in respect of visual hallucinations (more common in organic patients), auditory 12. Small
IF, Small JG, Field SP, Hayden MP. Organic cognates of acute psychiatric illness. Am J Psychiatry 1966; 122: 790-97. 13. Johnstone EC, Macmillan JF, Crow TJ. The occurrence of organic disease of possible or probable aetiological significance in a population of 268 cases of first episode schizophrenia. Psychol Med 1987, 17: 371-79. 14. Dewhurst K. The neurosyphilitic psychoses today. Br J Psychiatry 1969; 115: 31-38. 15. Victor M, Hope JM. The phenomenon of auditory hallucinations in chronic alcoholism: a critical evaluation of the status of alcoholic hallucinosis. J Nerv Ment Dis 1958; 126: 451-81. 16. Owen F, Cross AJ, Crow TJ, Longden A, Poulter M, Riley GJ. Increased dopamine-receptor sensitivity in schizophrenia. Lancet 1978; ii: 223-26. 17. Ferrier IN, Crow TJ, Roberts GW, et al. Alterations in neuropeptides in the limbic lobe in schizophrenia. In: Trimble MR, Zarifian E, eds. Psychopharmacology of the limbic system. Oxford: Oxford University Press, 1984: 244-54. 18. Flor-Henry P. Psychosis and temporal lobe epilepsy: a controlled investigation. Epilepsia 1969; 10: 363-95. 19 Cutting J. A reappraisal of alcoholic psychoses. Psychol Med 1978; 8: 285-95. 20. Cutting J. The phenomenology of acute organic psychosis: comparison with acute schizophrenia. Br J Psychiatry 1987; 151: 324-32.
hallucinations (more common in schizophrenics), and misidentification of others (more common in the organic patients). Patients with organic psychosis also had different delusions and in particular "share the common theme of imminent misadventure to others or bizarre happenings in the immediate vicinity". 20 Thus one man in a hospital ward insisted he was at home but was puzzled why his wife had bought so many beds for their personal use. This symptom differs from the typical delusions of schizophrenia which are less fantastic and show the typical features of external control of the patient’s mind. Unfortunately no organic disease can serve as even a rough model for schizophrenia, and extrapolation from conditions such as amphetamine psychosis to schizophrenia in general is unwarranted. Only a few unusual cases covering a spectrum of disease mimic true schizophrenia successfully. A productive area of research is to examine the pathophysiological differences between schizophreniform psychoses of organic origin and the organic psychoses of similar aetiology. The ability of organic disease to reproduce a complete repertoire of schizophrenic pathology is remarkable, but rare, and understanding the mechanism would be an important advance in our knowledge of
schizophrenia.
CONSERVATIVE MANAGEMENT OF THE RUPTURED SPLEEN AFTER splenic trauma, preservation of the spleen should be considered and the surgical journals have published many reports on means to this end. The methods vary from segmental resection of the damaged splenic tissue to repair of lacerations with ’Dacron’ or omental patches, together with topical haemostatic agents. Conservative (nonoperative) management seems feasible, especially in children and where there are facilities for close monitoring and computerised tomography to detect bleeding. As early as 1919 there was awareness of the excess incidence of late infection after splenectomy,l and in 1952 King and Schumaker defmed a specific entity, overwhelming post-splenectomy infection (OPSI), as an illness of sudden onset presenting with nausea, vomiting, and mental confusion, progressing to coma and death; it was commonly related to a pneumococcal infection and particularly affected children. The published work indicates that the incidence of OPSI is much greater in children who have undergone splenectomy for haematological reasons than in those who have had the operation for trauma. Di Cataldo and colleagues3 analysed the data from series reported since 1981 and found 12 cases of OPSI in 1816 patients-an overall incidence of 0.66%. On critical analysis, however, they judged that some of the patients with alleged OPSI had originally had multiple injuries and had died of gram negative infection that could have been associated with non-splenic injuries. When these doubtful cases were excluded the overall incidence fell to 0-28% of adult patients-much lower than the 1-2 % incidence of fatal cases reported in children after splenectomy for trauma.4 The importance of the spleen in resistance to infection. Ann Surg 1919; 70: 513-21. 2. King H, Schumaker HB. Splenic studies: susceptibility to infection after splenectomy performed in infancy. Ann Surg 1952; 136: 239-42. 3. Di Cataldo A, Puelo S, Li Destri G, et al. Splenic trauma and overwhelming post-splenectomy infection. Br J Surg 1987; 74: 343-45. 1. Morris DH, Bullock FD.
-
additional diffuse airways obstruction and daytime hypoxaemia in such patients (sometimes only of mild-to-moderate severity) rather than obesity that
provokes CO2 retention, pulmonary hypertension, and cor pulmonale.24,26 The reasons are not clear. Small airways disease will tend to raise functional residual capacity (FRC) and residual volume, which to some extent offsets the expected airway closure and reduced gas exchange. In addition, a rise in FRC will increase the size of the pharynx27 (thus reducing the tendency to OSA) and the size of the O2 reserve during apnoea. However, obesity will push the FRC down again towards residual volume (particularly when the patient is supine) and airway resistance will be high at this lower lung volume.24,28 Thus the obese patient with mild airways obstruction will have a reduced daytime Pa02, small airway closure, and a lower FRC than expected-all factors worsening the degree of arterial desaturation for a given length of apnoea. 29 The presence of moderate airways obstruction may also limit the patient’s ability to hyperventilate and restore blood gases to normal between apnoeas: over many years this extra hypoxic and hypercapnic load may provoke resetting of Pa02 and PaC02 control mechanisms, 21,30 with consequent diurnal respiratory failure. The "pickwickian" patient is likely to be an obese individual having OSA with some CAWO and consequent diurnal respiratory failure. Thus, vigorous treatment of even moderate diffuse airways obstruction will lessen some of the physiological consequences of OSA by improving waking and sleeping oxygenation, though benefit in terms of symptoms such as sleepiness is uncertain. Fletcher et a131 have also shown that, if the primary problem of sleep apnoea is treated (by tracheostomy) in patients with associated moderate CAWO, then the raised pulmonary artery pressure and pulmonary vascular resistance improve. Another interesting possible relationship, recently reported to the British Thoracic Society, exists between asthma and OSA. Chan et al32 treated asthmatics with nocturnal asthma and OSA or very heavy snoring by continuous nasal positive airway pressure. The nocturnal asthma symptoms Bradley TD, Rutherford R, Lue F, Moldofsky H, Grossman RF, Zamel N, Phillipson EA. Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea. Am Rev Respir Dis 1986; 134: 920-24. 25. Weitzenblum E, Kneger J, Oswald M, Vallee E, Ehrhart M, Kurtz D. Pulmonary hypertension in patients with obstructive sleep apnea syndrome Clin Respir Physiol 1987; 23 (suppl 12): 419S. 26. Bradley TD, Rutherford R, Grossman RF, Lue F, Zamel N, Moldofsky H. Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 1985; 131: 835-39. 27. Hoffstein V, Phillipson EA, Zamel N. Lung volume dependence of pharyngeal cross-sectional area in patients with obstructive sleep apnea. Am Rev Respir Dis 24.
1984; 130: 175-78. 28. Onal E, Leech JA, Lopata M. Relationship between pulmonary function and sleep-induced respiratory abnormalities. Chest 1985; 87: 437-41. 29. Bradley TD, Martinez D, Rutherford R, Lue F, Grossman R, Moldofsky H, Zamel N, Phillipson EA. Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnoea. J Appl Physiol 1985, 59: 1364-68. 30. Rapoport DM, Garay SM, Epstein H, Goldring RM. Mechanism of chronic hypercapnia in obstructive sleep apnea. Am Rev Respir Dis 1982; 125: A252. 31.
Fletcher EC, Schaaf JW, Miller J, Fletcher JG Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease. Am Rev Respir Dis 1987; 135:
525-33. 32. Chan CS, Woolcock AJ, Sullivan CE. Nocturnal asthma: role of snoring and obstructive sleep apnoea (OSA). Presented at British Thoracic Society Meeting, Edinburgh, 1987
improved, as did the morning peak flows. The mechanism is far from clear, but these workers suggest that a pharyngeal reflex may be operative, although hypoxia itself can provoke bronchoconstriction. At present the clinical implications of these findings on the interrelations between CAWO and OSA are debatable. Most patients will have one or other, not both. A spectrum must exist within the small group having both-some predominantly CAWO, some predominantly OSA. Symptoms that may be due to OSA are worth investigation, whether or not CAWO is present as well. On existing evidence there is no case for routine sleep studies in all patients with CAWO. SCHIZOPHRENIA AND ORGANIC DISEASE SINCE
Kraepelin first introduced the term dementia describe the condition that subsequently became praecox schizophrenia there has been a constant debate about the relation between this condition and organic disease. Kraepelin1 was unequivocal in regarding it as an organic dementia "in which the faculty of comprehension and the recollection of knowledge previously acquired are much less affected than judgement, emotional impulses and acts of volition". Kraepelin’s views are now known to have been substantially correct, in that a significant proportion of patients with schizophrenia have cerebral abnormalities, particularly in the temporal lobe .2-6 Despite these findings the cause or causes of schizophrenia remain elusive. In these circumstances it is sometimes helpful to look carefully at coexisting diagnosable organic disease. Although such associations might be fortuitous or independent of the cause, the degree of association between organic disease and schizophrenia exceeds that expected by chance7,8 and it seems likely that at least in some cases the organic disease is of major aetiological importance. Interpretation of data is made more difficult by the prolonged course of schizophrenia and the development of secondary complications, including alcohol abuse,9 depression tardive dyskinesia," and personality change. Because there is dispute over whether these secondary features are part of the natural history of schizophrenia or a consequence of management there are merits in studying schizophrenia at first presentation. Results of such inquiries have shown that schizophrenia is associated relatively to
Kraepelin E. Lectures on clinical psychiatry. Revised and edited by T. Johnstone. London: Baillière, Tindall and Cox, 1906: 26. 2. Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L. Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet 1976; ii: 924-26. 3. Weinberger DR, Torrey EF, Neophytides A, Wyatt RJ. Structural abnormalities of the cerebral cortex in chronic schizophrenia. Arch Gen Psychiatry 1979; 36: 935-39. 4. Reveley AM, Reveley MA, Clifford CA, Murray RM. Cerebral ventricular size in twins discordant for schizophrenia. Lancet 1982; i: 540-42. 5. Weinberger DR, Wagner RL, Wyatt RJ. Neuropathological studies of schizophrenia a selective review. Schizophr Bull 1983; 9: 193-212. 6. Brown R, Colter N, Corselhs JAN, et al. Postmortem evidence of structural brain changes in schizophrenia: differences in brain weight, temporal hom area, and parahippocampal gyrus compared with affective disorder. Arch Gen Psychiatry 1986; 43: 36-42. 7. Davison K, Bagley CR. Schizophrenia-like psychoses associated with organic disorders of the central nervous system: a review of the literature. In: Herrington RN, ed. Current problems in neuropsychiatry. Ashford: Headley Bros, 1969: 1.
113-84. E, Beard AW, Glithero E. The
schizophrenia-like psychoses of epilepsy. Br J Psychiatry 1963; 109: 95-150. Freed EX. Alcoholism and schizophrenia: the search for perspectives. J Stud Alcohol 1975; 36: 853-81. Virkkunen M. Suicides in schizophrenia and paranoid psychoses. Acta Psychiat Scand 1974 (suppl 250). Crane GE. Persistent dyskinesia. Br J Psychiatry 1973; 122: 395-405.
8. Slater 9. 10. 11.
777
infrequently with other organic disease: fewer than 10% of patients have an identifiable illness at the time of initial presentation with schizophrenia.12,13 The most common8 organic states associated with schizophrenia are epilepsy, neurosyphilis/,13,14 and alcohol and drug abuse.9.13,15 A study by Johnstone and her colleagues13 also documented sarcoidosis in 2 of 268 cases of first-episode schizophrenia. These findings indicate that the pathological changes in the brain in schizophrenia are unlikely to be a consequence of another known organic disease. In any event, many patients with schizophrenia do not have any organic changes. Nevertheless, the common associations of neurosyphilis, alcohol abuse, and epilepsy with schizophrenia cannot be dismissed as chance findings or non-specific vulnerability factors-these conditions occur too often in the presentation and course of schizophrenic illness to be ignored. It is more likely that such disorders share some of the pathophysiological changes of schizophrenia and thereby simulate or provoke episodes of illness. In schizophrenia there is good evidence of abnormalities in dopamine and peptide metabolism16.17 and, although the significance of such findings is disputed, they are likely to be important in the generation of psychotic symptoms. The anatomical sites of these changes are also important. Most of the pathological changes in schizophrenia are found in the limbic system, particularly its temporal lobe componentsand since Flor- Henry18 noted that schizophreniform psychoses and temporal lobe epilepsy were associated with epileptic foci in the dominant hemisphere there has been constant debate about the significance of laterality in the pathogenesis of schizophrenia. As epilepsy is much more likely to lead to schizophrenia when it affects the temporal lobe, and as the temporal lobe is also implicated in the schizophreniform psychoses of syphilis, and alcohol and drug abuse 1’°l9 these associations might explain why schizophrenic-like symptoms are manifest during such disorders. When organic disorder creates a schizophreniform psychosis the condition is usually indistinguishable from other forms of schizophrenia. No amount of phenomenological exactitude can differentiate between the symptoms of a true schizophreniform psychosis caused by an organic disease and those of schizophrenia itself. However, schizophreniform psychoses caused by organic disease are rare and have no common organic basis. Although structural and biochemical abnormalities have been found in the brain of schizophrenic patients it is dangerous to assume that schizophrenia is therefore an organic psychosis. Cutting2O lately compared the symptoms of acute organic psychosis and those of schizophrenia and found striking differences between them, particularly in respect of visual hallucinations (more common in organic patients), auditory 12. Small
IF, Small JG, Field SP, Hayden MP. Organic cognates of acute psychiatric illness. Am J Psychiatry 1966; 122: 790-97. 13. Johnstone EC, Macmillan JF, Crow TJ. The occurrence of organic disease of possible or probable aetiological significance in a population of 268 cases of first episode schizophrenia. Psychol Med 1987, 17: 371-79. 14. Dewhurst K. The neurosyphilitic psychoses today. Br J Psychiatry 1969; 115: 31-38. 15. Victor M, Hope JM. The phenomenon of auditory hallucinations in chronic alcoholism: a critical evaluation of the status of alcoholic hallucinosis. J Nerv Ment Dis 1958; 126: 451-81. 16. Owen F, Cross AJ, Crow TJ, Longden A, Poulter M, Riley GJ. Increased dopamine-receptor sensitivity in schizophrenia. Lancet 1978; ii: 223-26. 17. Ferrier IN, Crow TJ, Roberts GW, et al. Alterations in neuropeptides in the limbic lobe in schizophrenia. In: Trimble MR, Zarifian E, eds. Psychopharmacology of the limbic system. Oxford: Oxford University Press, 1984: 244-54. 18. Flor-Henry P. Psychosis and temporal lobe epilepsy: a controlled investigation. Epilepsia 1969; 10: 363-95. 19 Cutting J. A reappraisal of alcoholic psychoses. Psychol Med 1978; 8: 285-95. 20. Cutting J. The phenomenology of acute organic psychosis: comparison with acute schizophrenia. Br J Psychiatry 1987; 151: 324-32.
hallucinations (more common in schizophrenics), and misidentification of others (more common in the organic patients). Patients with organic psychosis also had different delusions and in particular "share the common theme of imminent misadventure to others or bizarre happenings in the immediate vicinity". 20 Thus one man in a hospital ward insisted he was at home but was puzzled why his wife had bought so many beds for their personal use. This symptom differs from the typical delusions of schizophrenia which are less fantastic and show the typical features of external control of the patient’s mind. Unfortunately no organic disease can serve as even a rough model for schizophrenia, and extrapolation from conditions such as amphetamine psychosis to schizophrenia in general is unwarranted. Only a few unusual cases covering a spectrum of disease mimic true schizophrenia successfully. A productive area of research is to examine the pathophysiological differences between schizophreniform psychoses of organic origin and the organic psychoses of similar aetiology. The ability of organic disease to reproduce a complete repertoire of schizophrenic pathology is remarkable, but rare, and understanding the mechanism would be an important advance in our knowledge of
schizophrenia.
CONSERVATIVE MANAGEMENT OF THE RUPTURED SPLEEN AFTER splenic trauma, preservation of the spleen should be considered and the surgical journals have published many reports on means to this end. The methods vary from segmental resection of the damaged splenic tissue to repair of lacerations with ’Dacron’ or omental patches, together with topical haemostatic agents. Conservative (nonoperative) management seems feasible, especially in children and where there are facilities for close monitoring and computerised tomography to detect bleeding. As early as 1919 there was awareness of the excess incidence of late infection after splenectomy,l and in 1952 King and Schumaker defmed a specific entity, overwhelming post-splenectomy infection (OPSI), as an illness of sudden onset presenting with nausea, vomiting, and mental confusion, progressing to coma and death; it was commonly related to a pneumococcal infection and particularly affected children. The published work indicates that the incidence of OPSI is much greater in children who have undergone splenectomy for haematological reasons than in those who have had the operation for trauma. Di Cataldo and colleagues3 analysed the data from series reported since 1981 and found 12 cases of OPSI in 1816 patients-an overall incidence of 0.66%. On critical analysis, however, they judged that some of the patients with alleged OPSI had originally had multiple injuries and had died of gram negative infection that could have been associated with non-splenic injuries. When these doubtful cases were excluded the overall incidence fell to 0-28% of adult patients-much lower than the 1-2 % incidence of fatal cases reported in children after splenectomy for trauma.4 The importance of the spleen in resistance to infection. Ann Surg 1919; 70: 513-21. 2. King H, Schumaker HB. Splenic studies: susceptibility to infection after splenectomy performed in infancy. Ann Surg 1952; 136: 239-42. 3. Di Cataldo A, Puelo S, Li Destri G, et al. Splenic trauma and overwhelming post-splenectomy infection. Br J Surg 1987; 74: 343-45. 1. Morris DH, Bullock FD.
-