depersonalisation

2
851 To resolve such difficulties was the object of research at the British Industrial Biological Research Association. Safety-in-use established in animal experiments could be confirmed only by studies in man. Opinion in this country would probably be against the recruitment of volunteers from prisoners, Church groups, or Boy Scouts (as is done in America), but people would prob- ably come forward in suitable numbers if the case was put to them effectively. In the long run, human experience of the use of food treated with low practical levels of new additives was to be preferred to the analysis of artefacts induced in aging rats by astronomical dietary concentra- tions of these additives. DEPERSONALISATION DEPERSONALISATION means peculiar change in the aware- ness of the self, in which the individual feels unreal. It is often accompanied by a similar change in the awareness of the external world, to which the term " derealisation " was given by Mapother. I Ackner 2 has emphasised the unpleasant quality of depersonalisation experiences. Other symptoms, such as disturbances of the body schema, subjective time disorders, a lack of feeling, hypochondriacal preoccupation, and (more rarely) déjà vu, metamorphopsia, or autoscopy, may affect the same individual. Some of these symptoms, in particular body-schema disturbances, may be included under depersonalisation.3 4 The term has also been used in a quite different context to include schizophrenic " passivity " experiences.5 Both these uses are to be discouraged. Transient depersonalisation experiences are not un- common in normal subjects,! 6 particularly in fatigue, after drinking alcohol, in the half-waking state, in a variety of minor toxic states, or under conditions of sensory deprivation. It is debatable whether such experiences are phenomenologically the same as the severe and often intractable states of depersonalisation that the psychiatrist observes. There have been attempts to create a " depersonalisa- tion syndrome " 11-12 though the bulk of evidence suggests that it is a non-specific symptom in a variety of disorders, particularly in temporal-lobe epilepsy, affective states, the acute organic syndromes (especially associated with the psychotomimetic drugs), psychogenic reactions, and occasionally schizophrenia. There are cases, however, in which depersonalisation seems to be an almost isolated symptom and in which other setiological factors are not prominent. 13 It has long been known that certain types of personality are more liable to depersonalisation, and it has recently been shown by Sedman et al.’ 14-1’ that there is a statistically significant association between depressed mood, insecure (obsessional) personality, and depersonalisation in depres- sive states, in schizophrenia, under the effects of L.S.D.-25, in temporal-lobe epilepsy, and in the organic psychoses. Theories of depersonalisation abound; they may be 1. Mayer-Gross, W. Brit. J. med. Psychol. 1935, 15, 103. 2. Ackner, B. J. ment. Sci. 1954, 100, 838. 3. Fisher, S., Seidner, R. J. nerv. ment. Dis. 1963, 137, 252. 4. Von Mering, O., et al. Experimental Psychopathology. New York, 1957. 5. Langfeldt, G. Proc. R. Soc. Med. 1960, 53, 1047. 6. Dixon, J. C. Brit. J. Psychiat. 1963, 109, 371. 7. Reed, G. F., Sedman, G. Percept. Met. Skills, 1964, 18, 659. 8. Shorvon, H. J. Proc. R. Soc. Med. 1946, 39, 779. 9. Roth, M. ibid. 1959, 52, 587. 10. Roth, M. J. Neuropsychiat. 1960, 1, 293. 11. Roth, M., Harper, M. Compr. Psychiat. 1962, 3, 215. 12. Harper, M., Roth, M. ibid. p. 129. 13. Davison, K. Brit. J. Psychiat. 1964, 110, 505. 14. Sedman, G., Reed, G. F. ibid. p. 376. 15. Sedman, G., Kenna, J. C. ibid. p. 669. 16. Sedman, G., Kenna, J. C. Psychiat. Neurol., Basle, 1964, 147, 129. 17. Kenna, J. C., Sedman, G. Brit. J. Psychiat. (in the press). summarised as those which regard it as organic; those which regard it as a disturbance of a particular psycho- logical function; those which take it to be a form of schizophrenia; and the analytical theories. The " organic " theory largely stems from Mayer- Gross,! who looked upon the condition as a " preformed functional response of the brain ", which could be set in motion by various factors. Haug 18 believed that deper- sonalisation was always associated with a change in the level of consciousness, though this is not readily recognis- able when depersonalisation occurs in the functional psychoses. Seiman and Kenna 16 17 failed to demonstrate any relation between an altered level of consciousness and depersonalisation, though this by no means dismisses the hypothesis. The frequency of depersonalisation symptoms in temporal-lobe epilepsy has naturally been a fruitful source of reference for those who support the organic theory, and in particular those who support cerebral localisation. The experiments of Penfield and Jasper 19 have demonstrated that patients may experience feelings of unreality when various parts of the temporal lobe are stimulated, although similar experiences have been reported after stimulation of the amygdaloid nucleus 20 and after cooling the dura in the parietal region by ethyl chloride.21 Whether such experiences are the same as unprovoked depersonalisation is of course open to argument. Davison 13 has reported 7 cases of episodic depersonalisation arising as an almost isolated symptom. Psychological, otoneurological, and electrophysiological studies failed to demonstrate any organic cerebral lesion, though minor E.E.G. changes were detected during attacks. Davison supports the view that there was a disturbance of cerebral arousal mechanisms, as do Roth and Harper.10 11 Earlier workers 22-24 regarded depersonalisation as a disturbance of sense perception, other as an affective or emotional disorder ’25-21 while Janet 28 judged the hyper- activity of the memory to be the important factor. Like- wise Schilder 29-31 emphasised the importance of increased self-observation and, like I’Hermitte,32 he tried to relate depersonalisation to a disturbance of the body schema. Psychoanalytical writers 33-38 are in general agreed that depersonalisation is a defence against affect and sensations or against anxiety arising from threats to the ego, from the id or super ego. An existential view of depersonalisation has been discussed by Kimura 37 and by Goppert.38 Some workers s8-43 believe depersonalisation to be a forme fruste or prodromal phase of schizophrenia, but, though it is true that schizophrenia does occasionally 18. Haug, K. Die Störungen des Persönlichkeitsbewusstseins und verwandte Entfremdungserlebnisse. Stuttgart, 1936. 19. Penfield, W., Jasper, H. H. Ass. Res. nerv. Dis. Proc. 1946, 26, 252. 20. Jasper, H. H. Temporal Lobe Epilepsy. Springfield, Ill., 1958. 21. Hoff, H., Potzl, O. Jb. Psychiat. Neurol. 1935, 52, 173. 22. Krishaber. Gaz. Sci. méd. Bordeaux. 1872. 23. Ribot, T. Diseases of Memory. London, 1882. 24. Taine, H. De l’intelligence, 1870. 25. Pick, A. Arch. Psychiat. Nervenkr. 1904, 38, 22. 26. Oesterreich, K. Phaenomenologie des Ich. Leipzig, 1910. 27. Loevy, H. Prog. Med. Wschr. 1908, 33, 443. 28. Janet, P. Les obsessions et la psychasthénie. Paris, 1903. 29. Schilder, P. Selbstbewusstsein und Persönlichkeitbewusstsein. Berlin, 1914. 30. Schilder, P. Introduction to Psychoanalytical Psychiatry. 1928. 31. Schilder, P. The Image and Appearance of the Human Body. London, 1935. 32. L’Hermitte, J. L’Image de Notre Corps. Paris, 1939. 33. Freud, S. Almanach der Psychoanalyse, 1937, 9. 34. Fenichel, O. Int. Z. Psychoanal. 1928, 14, 61. 35. Sadger, I. ibid. p. 348. 36. Obendoff, C. P. ibid. 1950, 31, 1. 37. Kimura, B. Nervenarzt, 1963, 34, 391. 38. Goppert, H. Zwangskrankheit und Depersonalisation. Basle, 1960. 39. Lewis, N. D. C. Amer. J. Psychoterap. 1949, 3, 4. 40. Klein, M. Int. J. Psychoanal. 1946, 27, 99. 41. Rosenfeld, H. ibid. 1947, 28, 130. 42. Galdston, I. J. nerv. ment. Dis. 1947, 105, 25. 43. Winnik, H. Brit. J. med. Psychol. 1948, 21, 268

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851

To resolve such difficulties was the object of research atthe British Industrial Biological Research Association.Safety-in-use established in animal experiments couldbe confirmed only by studies in man. Opinion in thiscountry would probably be against the recruitment ofvolunteers from prisoners, Church groups, or BoyScouts (as is done in America), but people would prob-ably come forward in suitable numbers if the case was putto them effectively. In the long run, human experienceof the use of food treated with low practical levels of newadditives was to be preferred to the analysis of artefactsinduced in aging rats by astronomical dietary concentra-tions of these additives.

DEPERSONALISATION

DEPERSONALISATION means peculiar change in the aware-ness of the self, in which the individual feels unreal. It isoften accompanied by a similar change in the awareness ofthe external world, to which the term " derealisation " wasgiven by Mapother. I Ackner 2 has emphasised the

unpleasant quality of depersonalisation experiences. Othersymptoms, such as disturbances of the body schema,subjective time disorders, a lack of feeling, hypochondriacalpreoccupation, and (more rarely) déjà vu, metamorphopsia,or autoscopy, may affect the same individual. Some ofthese symptoms, in particular body-schema disturbances,may be included under depersonalisation.3 4 The term hasalso been used in a quite different context to include

schizophrenic "

passivity "

experiences.5 Both these usesare to be discouraged.Transient depersonalisation experiences are not un-

common in normal subjects,! 6 particularly in fatigue,after drinking alcohol, in the half-waking state, in a varietyof minor toxic states, or under conditions of sensorydeprivation. It is debatable whether such experiences arephenomenologically the same as the severe and oftenintractable states of depersonalisation that the psychiatristobserves.There have been attempts to create a

" depersonalisa-tion syndrome " 11-12 though the bulk of evidence suggeststhat it is a non-specific symptom in a variety of disorders,particularly in temporal-lobe epilepsy, affective states, theacute organic syndromes (especially associated with thepsychotomimetic drugs), psychogenic reactions, and

occasionally schizophrenia. There are cases, however, inwhich depersonalisation seems to be an almost isolatedsymptom and in which other setiological factors are notprominent. 13

It has long been known that certain types of personalityare more liable to depersonalisation, and it has recently beenshown by Sedman et al.’ 14-1’ that there is a statisticallysignificant association between depressed mood, insecure(obsessional) personality, and depersonalisation in depres-sive states, in schizophrenia, under the effects of L.S.D.-25,in temporal-lobe epilepsy, and in the organic psychoses.

Theories of depersonalisation abound; they may be1. Mayer-Gross, W. Brit. J. med. Psychol. 1935, 15, 103.2. Ackner, B. J. ment. Sci. 1954, 100, 838.3. Fisher, S., Seidner, R. J. nerv. ment. Dis. 1963, 137, 252.4. Von Mering, O., et al. Experimental Psychopathology. New York, 1957.5. Langfeldt, G. Proc. R. Soc. Med. 1960, 53, 1047.6. Dixon, J. C. Brit. J. Psychiat. 1963, 109, 371.7. Reed, G. F., Sedman, G. Percept. Met. Skills, 1964, 18, 659.8. Shorvon, H. J. Proc. R. Soc. Med. 1946, 39, 779.9. Roth, M. ibid. 1959, 52, 587.

10. Roth, M. J. Neuropsychiat. 1960, 1, 293.11. Roth, M., Harper, M. Compr. Psychiat. 1962, 3, 215.12. Harper, M., Roth, M. ibid. p. 129.13. Davison, K. Brit. J. Psychiat. 1964, 110, 505.14. Sedman, G., Reed, G. F. ibid. p. 376.15. Sedman, G., Kenna, J. C. ibid. p. 669.16. Sedman, G., Kenna, J. C. Psychiat. Neurol., Basle, 1964, 147, 129.17. Kenna, J. C., Sedman, G. Brit. J. Psychiat. (in the press).

summarised as those which regard it as organic; thosewhich regard it as a disturbance of a particular psycho-logical function; those which take it to be a form of

schizophrenia; and the analytical theories.The " organic " theory largely stems from Mayer-

Gross,! who looked upon the condition as a " preformed

functional response of the brain ", which could be set inmotion by various factors. Haug 18 believed that deper-sonalisation was always associated with a change in thelevel of consciousness, though this is not readily recognis-able when depersonalisation occurs in the functional

psychoses. Seiman and Kenna 16 17 failed to demonstrate

any relation between an altered level of consciousnessand depersonalisation, though this by no means dismissesthe hypothesis. The frequency of depersonalisationsymptoms in temporal-lobe epilepsy has naturally been afruitful source of reference for those who support the

organic theory, and in particular those who supportcerebral localisation. The experiments of Penfield andJasper 19 have demonstrated that patients may experiencefeelings of unreality when various parts of the temporallobe are stimulated, although similar experiences havebeen reported after stimulation of the amygdaloidnucleus 20 and after cooling the dura in the parietal regionby ethyl chloride.21 Whether such experiences are thesame as unprovoked depersonalisation is of course open toargument. Davison 13 has reported 7 cases of episodicdepersonalisation arising as an almost isolated symptom.Psychological, otoneurological, and electrophysiologicalstudies failed to demonstrate any organic cerebral lesion,though minor E.E.G. changes were detected during attacks.Davison supports the view that there was a disturbance ofcerebral arousal mechanisms, as do Roth and Harper.10 11

Earlier workers 22-24 regarded depersonalisation as a

disturbance of sense perception, other as an affective oremotional disorder ’25-21 while Janet 28 judged the hyper-activity of the memory to be the important factor. Like-wise Schilder 29-31 emphasised the importance of increasedself-observation and, like I’Hermitte,32 he tried to relatedepersonalisation to a disturbance of the body schema.

Psychoanalytical writers 33-38 are in general agreed thatdepersonalisation is a defence against affect and sensationsor against anxiety arising from threats to the ego, from theid or super ego. An existential view of depersonalisationhas been discussed by Kimura 37 and by Goppert.38Some workers s8-43 believe depersonalisation to be a

forme fruste or prodromal phase of schizophrenia, but,though it is true that schizophrenia does occasionally18. Haug, K. Die Störungen des Persönlichkeitsbewusstseins und

verwandte Entfremdungserlebnisse. Stuttgart, 1936.19. Penfield, W., Jasper, H. H. Ass. Res. nerv. Dis. Proc. 1946, 26, 252.20. Jasper, H. H. Temporal Lobe Epilepsy. Springfield, Ill., 1958.21. Hoff, H., Potzl, O. Jb. Psychiat. Neurol. 1935, 52, 173.22. Krishaber. Gaz. Sci. méd. Bordeaux. 1872.23. Ribot, T. Diseases of Memory. London, 1882.24. Taine, H. De l’intelligence, 1870.25. Pick, A. Arch. Psychiat. Nervenkr. 1904, 38, 22.26. Oesterreich, K. Phaenomenologie des Ich. Leipzig, 1910.27. Loevy, H. Prog. Med. Wschr. 1908, 33, 443.28. Janet, P. Les obsessions et la psychasthénie. Paris, 1903.29. Schilder, P. Selbstbewusstsein und Persönlichkeitbewusstsein.

Berlin, 1914.30. Schilder, P. Introduction to Psychoanalytical Psychiatry. 1928.31. Schilder, P. The Image and Appearance of the Human Body. London,

1935.32. L’Hermitte, J. L’Image de Notre Corps. Paris, 1939.33. Freud, S. Almanach der Psychoanalyse, 1937, 9.34. Fenichel, O. Int. Z. Psychoanal. 1928, 14, 61.35. Sadger, I. ibid. p. 348.36. Obendoff, C. P. ibid. 1950, 31, 1.37. Kimura, B. Nervenarzt, 1963, 34, 391.38. Goppert, H. Zwangskrankheit und Depersonalisation. Basle, 1960.39. Lewis, N. D. C. Amer. J. Psychoterap. 1949, 3, 4.40. Klein, M. Int. J. Psychoanal. 1946, 27, 99.41. Rosenfeld, H. ibid. 1947, 28, 130.42. Galdston, I. J. nerv. ment. Dis. 1947, 105, 25.43. Winnik, H. Brit. J. med. Psychol. 1948, 21, 268

852

present in this way, there is little to support this view.

Meyer 44 has attempted to separate depersonalisationfrom schizophrenic ego disturbance, on the grounds thatthe depersonalised patient looks into himself for thereason for his separation from the world and never puts itdown to outside agencies, as does the schizophrenic.The treatment of depersonalisation remains unsatis-

factory. In affective illness, treatment of the depressionquite often leads to remission of the depersonalisation. Inschizophrenia, however, it tends to be more intractable 1 11;and when depersonalisation arises in temporal-lobeepilepsy, the management is that of the underlying cause.There are, however, some cases in which depersonalisationseems more isolated, severe and permanent. Varioustreatment such as methylamphetamine, continuousnarcosis, intravenous thiopentone, and even leucotomyhave been advised (electroconvulsion therapy is said to becontraindicated). The therapeutic possibilities have beenreviewed by Davison.13 Despite the despondent feelingthat pervades the subject, it must be remembered thatthis distressing symptom can remit spontaneously.

COLONIC RECONSTRUCTION OF THE PHARYNX

AFTER RADICAL OPERATION

CANCER of the lower part of the pharynx and cervicaloesophagus is still very hard to cure; and despite all therecent therapeutic advances, even palliation is often

unsatisfactory. The aim must be to eradicate the growthor, if this is impossible, at least to allow the patient tobreathe and swallow comfortably and to spend the restof her life at home with the family. While a biologicalsolution to disordered tissue growth still eludes us, thechoice is between irradiation and surgery. Both methodshave a low cure-rate, but operation probably offers thebest chance of eradication or adequate palliation. Radio-

therapy is widely used, but the dysphagia is apt to persistbecause of oedema, stricture, or recurrence, and dyspnoeamay also result from various respiratory complications.Even with the newer supervoltage therapy, the full courseof treatment makes heavy demands on the patient, and, ifit is unsuccessful, operation may be difficult or impossiblebecause of fibrosis or recurrent growth. Thus, manypatients treated with radical irradiation alone spend theremainder of their lives as permanent inpatients, oftenwith a tracheostomy and a feeding fistula.45The disadvantages of radiotherapy are responsible for

the trend towards surgery in many centres. Operationmeans excision of the pharynx, larynx, and cervical

oesophagus in continuity with potentially involved

lymph-nodes. The problem here is the restoration of thegullet, and most attempts to solve it have been based on thepioneer work of Trotter 46 and Wookey,47 using skin flapsfrom the neck and elsewhere. Although some success hasbeen achieved, several operations are required and longperiods in hospital; and the growth often recurs beforereconstruction is complete. Strictures and fistuÍae are notuncommon, and there are technical limitations on theamount of cervical oesophagus which may be resected.Because of these drawbacks to the staged operations, variousmethods of excision and repair in one operation have beendevised. Tubes of tissue or plastic materials have beenused to replace the pharynx, such as split skin over a44. Meyer, J. E. Psychiat. Neurol. Basle, 1956, 132, 221.45. Fairman, H. D., Hadley, S. K. J., John, H. T. Brit. J. Surg. 1964,

51, 663.46. Trotter, W. Lancet, 1913, i, 1075.47. Wookey, H. Surg. Gynec. Obstet. 1942, 75, 499.

plastic tube,48 laryngeal mucosa,49 tracheal 11 and vasculargrafts,5l as well as polyethylene, nylon, and tygon. Thesemethods permit low excision of the oesophagus, and suc-cesses have been reported; but there has been a high rateof stenosis and fistula formation. Other workers havetherefore used a mucosa-lined viscus for direct anasto-mosis to a divided oropharynx. Such replacement of thepharynx has been achieved with stomach, 52 53 oesophagus,64jejunum,55 and the right or left colon. 56-59

Usually these new techniques have been described inonly one or two cases. The latest paper from Bristol 4sreports 9 patients with carcinoma of the pharynx or

cervical oesophagus in whom the defect in the pharynxafter excision was bridged at the same operation by a longloop of colon passing from the oropharynx to the stomachvia the anterior mediastinum. Palliation was the primaryaim, and swallowing was rapidly restored in most cases.Furthermore, the long-term results may be better becausethe needs of reconstruction can be ignored during theexcision. The method needs little special equipment orskills, and it should have a useful place in the treatment ofcancer of the pharynx or cervical oesophagus, but becauseof its magnitude it should probably be restricted to theyounger and fitter patients. The importance of collabora-tion between laryngologists, surgeons, and radiotherapistsin selecting the primary treatment with the greatest chanceof success should not need further emphasis.

PATTERNS IN MISMANAGEMENT

Stein and Susser 60 discuss the circumstances in whichcertain patients’ illnesses were mismanaged. Some wereseen in hospital practice, others in general practice. Wasthere any recurring pattern which might make suchfailure of care predictable and therefore preventible?They suggest that " failures in personal care will be thecharacteristic failures in hospital practice " and that" failures in technical competence will be the character-istic failures in general practice ".They set out hospital case-histories which illustrate

how social or personal factors have been ill considered;how communication has been at fault (sometimes betweenthe hospital and the patient or his relatives, sometimesbetween different members of the hospital unit); how therules and procedures of hospital organisation overrodethe patient’s needs; and how the hospital staff did notalways resolve their disagreements about treatment.The mistakes in general practice included failures in

routine examination and in simple diagnosis and failuresattributable to the doctor’s woeful inexperience in a par-ticular aspect of medicine or ignorance of recent importantdevelopments in diagnosis or treatment.The cases quoted came from many parts of the country,

which suggests that the problems they illustrate are

general and not local. Though the numbers are small (tencases from hospital and ten from general practice) there isno doubt that further similar studies would be justified-and equally salutary.

48. Negus, V. E. Proc. R. Soc. Med. 1950, 43, 157.49. Wilkins, S. A. Cancer, 1955, 8, 1189.50. Guidice, A. T. Cited by Iskeceli, O. K. Surgery, 1962, 51, 496.51. Roux, G. Cited by Iskeceli, O. K. ibid.52. Ong, G. B., Lee, T. C. Brit. J. Surg. 1960, 48, 193.53. Butler, T. J. Cited by Fairman et al. (footnote 45).54. Wooler, G. Proc. R. Soc. Med. 1952, 45, 264.55. Yudin, S. Surg. Gynec. Obstet. 1944, 78, 561.56. Goligher, J. C., Robin, I. G. Brit. J. Surg. 1954, 42, 283.57. Beck, A. R., Baronofsky, R. Surgery, 1960, 48, 499.58. Mustard, R. A. Surg. Gynec. Obstet. 1960, 111, 577.59. Sherman, C. D., Scanlon, E. F. ibid. p. 349.60. Stein, Z., Susser, M. Med. Care, 1964, 2, 162.