Q 1998 Martin
Dunitz Ltd
InternationalJournal of Psychiatry in Clinical Practice 1998 Volume 2 Pages 57-59
57
A case of periodic catatonia, due to frontal lobe epilepsy
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of California Irvine on 11/07/14 For personal use only.
AFG LEENTJENS’ AND L PEPPLINKHUIZEN~ I Department of Psychiatry, Maastricht University Hospital; and 2Department of Psychiatry, Rotterdam University Hospital, The Netherlands
A case history is presented in which acute periodic catatonia was caused by frontal lobe epilepsy. This manifestation offrontal lobe epilepsy has not, to the authors’ knowledge, been described before. The authors mention the problems of diagnosis and discuss a possible pathogenetic mechunism for the capricious presentation in this patient. (IntJ Psych Clin Pract 1998; 2: 57-59)
Correspondence Address Dr Albert FG Leentjens, Department of Psychiatry, Maastricht University Hospital, PO Box 5800, 6202 AZ Maastricht, The Netherlands Tel: +31 43 3877443 Fax +31 43 3875444 Received 25 October 1997; accepted for publication 10 January 1998
INTRODUCTION cute recurrent or non-recurrent catatonic stupor a A rare psychiatric syndrome with an extensive differential diagnosis.’ Although catatonic stupor as a symptom is
in severe psychotic and affective disorders is well known, psychiatric causes have become less frequent as better treatment for these disorders has become available. The differential diagnosis mainly ‘includes a wide range of medical and neurological diseases. Better known aetiologies for recurrent catatonic stupor are metabolic diseases like acute intermittent porphyria, insulinomas, ACTH-secreting tumours, abnormal serine and glycine metabolism and Gjessings’ syndrome.’-3 All these disorders are rare and difficult to confirm. They usually require lengthy clinical observation and extensive investigations. In spite of the cost and effort, this is usually worthwhile, as most causes can be treated adequately. We present the case history of a patient with acute recurrent catatonic stupor that, after repeated clinical observation periods, could finally be attributed to frontal epilepsy.
CASE REPORT A 47-year-old sailor was admitted to our department in a
state of catatonic stupor. The history from a friend revealed that this condition had come about suddenly and had been preceded by 3 days of anxiety a>d bizarre behaviour. The patient was characterized as a friendly, hard-working and religious man who did not use any recreational drugs or
abuse alcohol. He was not known to have any physical illnesses and had no previous history of psychiatric illness. He lived modestly and supported a wife and seven children. On general physical and neurological examination no abnormalities were detected. At mental state examination we saw a mute man, lying motionless in bed. Features of catatonia were present in the form of severe hypertonia and waxy flexibility. His consciousness appeared to be clear. He stared into space for most of the time. His pupils were dilated and he perspired heavily. Sometimes this stupor was interrupted for brief periods in which the patient looked around himself in a state of fright. During these intervals the patient reacted in a dysphoric and paranoid manner, and at times violently, to his surroundings. He exhibited echolalia, echopraxia and mannerisms. After intramuscular injection of 5 mg haloperidol the patient calmed down and fell asleep. The next morning he was orientated and much improved. He only remembered fragments of what had happened over the previous days. He said that he hadn’t been able to sleep for several days because he had been troubled by voices in his head which threatened him. He denied the use of alcohol, recreational drugs or medication. Because of the acute onset of stupor and the absence of any previous psychiatric history, an organic cause was suspected. Extensive laboratory investigations were performed, but no abnormal results were found with regard to serum electrolytes, liver and kidney function tests, protein spectrum and full blood count. Fasting glucose levels and thyroid function tests were normal. Vitamins B1,Be, Blz and folic acid were normal. Urine
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of California Irvine on 11/07/14 For personal use only.
58
AFG Leentjens and L Pepplinhhuizen
tests for cannabis, cocaine, opiates and amphetamines were negative. The 8-ALA and PBG in the urine, together with porphyrin concentration in the faeces, were determined in order to exclude porphyria. Repeatedly no abnormal results were obtained. There was no evidence of any recent viral infection. Lues reactions were negative, as were those for toxoplasmosis and borrelia. A thick blood film excluded malaria. Additional investigations were conducted in order to exclude a possible neurological cause. Examination of cerebrospinal fluid showed no abnormalities. The electroencephalogram (EEG) was normal. There was a well-developed reactive background pattern with a-rhythm between 10 and 11 Hz without focal abnormalities, peaks or peak wave complexes. The possibility of a reactive or hysterical psychosis was considered unlikely because of the absence of any previous history and the normal premorbid personality of the patient. Therefore the diagnosis remained obscure. The patient stayed well during the remainder of the observation period and was discharged after 3 weeks. Five days after discharge, i.e. 30 days after the initial period of catatonia, the patient was again admitted in a state of catatonic stupor. The clinical picture was largely the same. This time the patient was treated with 100 mg zuclopentixol IM. His condition improved gradually and his catatonic state disappeared completely after 2 days. All routine investigations were normal again. A glucose tolerance test (GTT) was performed and C-peptide was determined in order to exclude insulinoma. A dexamethasone suppression test (DST) was conducted in order to exclude ACTH-secreting tumours. The results of all these tests showed no abnormalities. The fasting amino acid spectrum in the plasma was normal. Amino acid loading tests were performed to exclude episodic acute polymorphous psychosis. Serine and glycine loading failed to induce symptoms in this patient.2 Again the EEG was normal. No abnormalities were seen on a CT scan. However, 30 days later (from the start of this episode), the patient again relapsed into a state of catatonic stupor, having shown no psychopathology in the intervening period. This sequence of events was repeated for a fourth and fifth time, again with an exact periodicity of 30 days. During this last event the patient was brought in by the police, having been arrested at the Central Railway Station for bizarre behaviour and unprovoked aggression towards passers-by. Upon admission, he presented in a catatonic stupor that was frequently intempted by clearly paranoid psychotic periods during which he sometimes became aggressive. Shortly after an injection of 5 mg haloperidol, the patient called for help. At that moment his consciousness was clear and his interaction adequate. He told the nurses that he had fallen out of his bed due to the fact that his head had turned away to the right and that his right hand had manifested involuntary clonic movements. There was no tongue bite or incontinence and he had remained fully conscious.
This time an EEG could be arranged without delay. It showed an excess of P-activity, which was considered a medication effect. Over the frontal leads one single peakwave complex was reported. In addition, bursts of sharp transients were observed, particularly during provoked hyperventilation. This may be interpreted as an arousal phenomenon, but an abnormal aetiology could not be excluded. Because of these abnormalities a repeat EEG after sleep deprivation was arranged for the next day. This showed clear disturbances of functions in the frontal areas. Using suborbital electrodes, paroxysms of waves with durations of 0.25-0.33 s and an amplitude of up to 60 pV were recorded in the prefrontal and frontal areas, superimposed with sharp waves with durations of 0.8-0.11 s and an amplitude of up to 65 pV. The EEG was strongly suggestive of temporal or frontal lobe epilepsy. The diagnosis of frontal epilepsia was considered consistent with the clinical presentation and was chosen as a working hypothesis. The patient was succesfully treated with carbamazepine. At this time, the patient has remained free of catatonic episodes for almost 2 years. An MRl scan, performed after discharge, did not show any anatomical abnormalities as a possible cause for epilepsy.
DISCUSSION This patient presented with five episodes of catatonic stupor, with an exact periodicity of 30 days. The episodes of stupor were intempted by brief periods of agitation, anxiety and aggression, during which the patient experienced auditory hallucinations. Intensive investigations were performed to exclude the many aetiologies of recurrent catatonia. Although frontal lobe epilepsy had already been rejected on the basis of repeated normal EEGs, this diagnosis again appeared possible when, during the final episode, the patient presented with motor symptoms. But even then, this diagnosis could only be confirmed with an EEG after sleep deprivation and the use of suborbital electrodes. Frontal epilepsy can manifest itself both clinically and electrophysiologically in many different ways.’-’ Several authors try to group the different symptoms in various ways, to distinguish different electroclinical ~yndrornes.’.~ Salanova et a1 describe supplementary motor seizures, focal motor seizures and psychomotor seizures.’ This patient would most closely fit the clinical description of frontal psychomotor seizures, except that in his case consciousness was maintained. Moreover, frequent alterations between stuporous states and non-stuporous overt psychotic states have not been described as part of this syndrome. Finally, strict periodicity in seizure frequency has, to the authors’ knowledge, never been reported. Progress has been made in linking clinical manifestations with epileptic activity in different anatomical structures of the frontal lobe. For instance, mutism and akinesia have been associated with stimulation of a negative
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of California Irvine on 11/07/14 For personal use only.
Periodic catatonia due to epilepsy
motor area, localized in the inferolateral frontal area, and .~ behavioural manifestations with the prefrontal c ~ r t e x In spite of this, the frequent changes in psychomotor function in our patient remain unexplained. Although of older date, the hypothesis proposed by Winters is interesting in this respect. He postulated a continuum of excitation states of the central nervous system (CNS). Using an experimental model in cats, he demonstrated that with increasing excitation, different psychomotor and sensory phases are passed in a well-defined order, viz (in order of increasing excitation): agitation, ataxia, bizarre catatonic movements, catalepsy, myoclonia and epileptic fits, In cats, the phase of ataxia is accompanied by euphoria and the phases of catatonia and catalepsy by visual hallucinations. All these phases may reversibly progress to an adjacent excitational stage, or to depression of the CNS with stupor and coma, and finally to death. 'In each of these phases, the EEG In a more philosophic shows specific approach, Fischer proposed a similar hypothesis for man, but this is less convincingly backed by clinical or electrophysiological
disorders. Sometimes, prolonged and repeated clinical observation is necessary to confirin a diagnosis. This is a worthwhile effort, as many of the the possible causes can be treated adequately. In this patient, acute periodic catatonic stupor could finally be atributed to frontal lobe epilepsy. This presentation of frontal lobe epilepsy has, to the authors' knowledge, not yet been described. The patient has been successfully treated with the anticonvulsant carbamazepine.
KEY POINTS 0
0
CONCLUSION The differential diagnosis of acute recurrent catatonia includes a large number of neurological and psychiatric
59
0
Recurrent catatonic stupor is a rare neuropsychiatric syndrome, with a range of causes Frontal lobe epilepsy may cause recurrent stupor, and can be treated successfully with anticonvulsants Abnormalities on the EEG may be only transient, but can be revealed by sleep deprivation
REFERENCES 1. Gelenberg AJ (1976) The catatonic syndrome. Lancet i: 133941. 2. Fekkes D. Pepplinkhuizen L, Verhey R et a1 (1994) Abnormal plasma levels of serine, methionine, and taurine in transient acute polymorphic psychosis. Psychiatry Res 51: 11- 18. 3. Gjessing RR (1976) The somatology of periodic catatonia. Pergamon, Oxford. 4. Broglin D,Delgado-Escueta AV, Walsh GO et a1 (1992) Clinical approach to the patient with seizures and epilepsies of frontal origin. Adv Neurol 57: 59 - 88. 5. Meierkord H (1992) Die klinischen und neurophysiologischen Merkmale von Epilepsien mit Frontallappenanfdlen bei einer mit Video-EEG-Telemetrie diagnostizierten Sene von Patienten. Nervenarzt 63: 485-91. 6. Fornazarri L, Farcnik K, Smith I et a1 (1992) Violent visual hallucinations in frontal lobe dysfunction: clinical manifestations of deep orbitofrontal foci. J Neuropsychiatr Clin Neurosci 4: 42 - 4.
7. Williamson PD (1992) Frontal lobe seizures: problems of diagnosis and classification. Adv Neurol 57: 289-309. 8. Salanova V, Morris HH, Van Ness P et a1 (1995) Frontal lobe seizures: electroclinical syndromes. Epilepsia 3 6 16- 24. 9. Watennan K, Wada JA (1990) Frontal lobe epilepsy. In: Comprehensive epileptology (ed M Dam, L Gram) 197-213. Raven Press, New York. 10. Winters WD (1975) The continuum of CNS excitory states and hallucinosis. In: Hallucinations: behavior, experience and theory (ed RK Siegel, LJ West) 53-70. John Wiley, New York. 11. Fischer R (1969) The perception-hallucination continuum: a reexamination. Dis Nervous System 30: 161- 71. 12. Fischer R (1986) Toward a neuroscience of self-experience and states of self-awareness and interpreting interpretations. In: Handbook of states of consciousness (ed B Wolman, M Ullman) 3-30. Van Nostrand Reinhold, New York.
Dunitz Ltd
InternationalJournal of Psychiatry in Clinical Practice 1998 Volume 2 Pages 57-59
57
A case of periodic catatonia, due to frontal lobe epilepsy
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of California Irvine on 11/07/14 For personal use only.
AFG LEENTJENS’ AND L PEPPLINKHUIZEN~ I Department of Psychiatry, Maastricht University Hospital; and 2Department of Psychiatry, Rotterdam University Hospital, The Netherlands
A case history is presented in which acute periodic catatonia was caused by frontal lobe epilepsy. This manifestation offrontal lobe epilepsy has not, to the authors’ knowledge, been described before. The authors mention the problems of diagnosis and discuss a possible pathogenetic mechunism for the capricious presentation in this patient. (IntJ Psych Clin Pract 1998; 2: 57-59)
Correspondence Address Dr Albert FG Leentjens, Department of Psychiatry, Maastricht University Hospital, PO Box 5800, 6202 AZ Maastricht, The Netherlands Tel: +31 43 3877443 Fax +31 43 3875444 Received 25 October 1997; accepted for publication 10 January 1998
INTRODUCTION cute recurrent or non-recurrent catatonic stupor a A rare psychiatric syndrome with an extensive differential diagnosis.’ Although catatonic stupor as a symptom is
in severe psychotic and affective disorders is well known, psychiatric causes have become less frequent as better treatment for these disorders has become available. The differential diagnosis mainly ‘includes a wide range of medical and neurological diseases. Better known aetiologies for recurrent catatonic stupor are metabolic diseases like acute intermittent porphyria, insulinomas, ACTH-secreting tumours, abnormal serine and glycine metabolism and Gjessings’ syndrome.’-3 All these disorders are rare and difficult to confirm. They usually require lengthy clinical observation and extensive investigations. In spite of the cost and effort, this is usually worthwhile, as most causes can be treated adequately. We present the case history of a patient with acute recurrent catatonic stupor that, after repeated clinical observation periods, could finally be attributed to frontal epilepsy.
CASE REPORT A 47-year-old sailor was admitted to our department in a
state of catatonic stupor. The history from a friend revealed that this condition had come about suddenly and had been preceded by 3 days of anxiety a>d bizarre behaviour. The patient was characterized as a friendly, hard-working and religious man who did not use any recreational drugs or
abuse alcohol. He was not known to have any physical illnesses and had no previous history of psychiatric illness. He lived modestly and supported a wife and seven children. On general physical and neurological examination no abnormalities were detected. At mental state examination we saw a mute man, lying motionless in bed. Features of catatonia were present in the form of severe hypertonia and waxy flexibility. His consciousness appeared to be clear. He stared into space for most of the time. His pupils were dilated and he perspired heavily. Sometimes this stupor was interrupted for brief periods in which the patient looked around himself in a state of fright. During these intervals the patient reacted in a dysphoric and paranoid manner, and at times violently, to his surroundings. He exhibited echolalia, echopraxia and mannerisms. After intramuscular injection of 5 mg haloperidol the patient calmed down and fell asleep. The next morning he was orientated and much improved. He only remembered fragments of what had happened over the previous days. He said that he hadn’t been able to sleep for several days because he had been troubled by voices in his head which threatened him. He denied the use of alcohol, recreational drugs or medication. Because of the acute onset of stupor and the absence of any previous psychiatric history, an organic cause was suspected. Extensive laboratory investigations were performed, but no abnormal results were found with regard to serum electrolytes, liver and kidney function tests, protein spectrum and full blood count. Fasting glucose levels and thyroid function tests were normal. Vitamins B1,Be, Blz and folic acid were normal. Urine
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of California Irvine on 11/07/14 For personal use only.
58
AFG Leentjens and L Pepplinhhuizen
tests for cannabis, cocaine, opiates and amphetamines were negative. The 8-ALA and PBG in the urine, together with porphyrin concentration in the faeces, were determined in order to exclude porphyria. Repeatedly no abnormal results were obtained. There was no evidence of any recent viral infection. Lues reactions were negative, as were those for toxoplasmosis and borrelia. A thick blood film excluded malaria. Additional investigations were conducted in order to exclude a possible neurological cause. Examination of cerebrospinal fluid showed no abnormalities. The electroencephalogram (EEG) was normal. There was a well-developed reactive background pattern with a-rhythm between 10 and 11 Hz without focal abnormalities, peaks or peak wave complexes. The possibility of a reactive or hysterical psychosis was considered unlikely because of the absence of any previous history and the normal premorbid personality of the patient. Therefore the diagnosis remained obscure. The patient stayed well during the remainder of the observation period and was discharged after 3 weeks. Five days after discharge, i.e. 30 days after the initial period of catatonia, the patient was again admitted in a state of catatonic stupor. The clinical picture was largely the same. This time the patient was treated with 100 mg zuclopentixol IM. His condition improved gradually and his catatonic state disappeared completely after 2 days. All routine investigations were normal again. A glucose tolerance test (GTT) was performed and C-peptide was determined in order to exclude insulinoma. A dexamethasone suppression test (DST) was conducted in order to exclude ACTH-secreting tumours. The results of all these tests showed no abnormalities. The fasting amino acid spectrum in the plasma was normal. Amino acid loading tests were performed to exclude episodic acute polymorphous psychosis. Serine and glycine loading failed to induce symptoms in this patient.2 Again the EEG was normal. No abnormalities were seen on a CT scan. However, 30 days later (from the start of this episode), the patient again relapsed into a state of catatonic stupor, having shown no psychopathology in the intervening period. This sequence of events was repeated for a fourth and fifth time, again with an exact periodicity of 30 days. During this last event the patient was brought in by the police, having been arrested at the Central Railway Station for bizarre behaviour and unprovoked aggression towards passers-by. Upon admission, he presented in a catatonic stupor that was frequently intempted by clearly paranoid psychotic periods during which he sometimes became aggressive. Shortly after an injection of 5 mg haloperidol, the patient called for help. At that moment his consciousness was clear and his interaction adequate. He told the nurses that he had fallen out of his bed due to the fact that his head had turned away to the right and that his right hand had manifested involuntary clonic movements. There was no tongue bite or incontinence and he had remained fully conscious.
This time an EEG could be arranged without delay. It showed an excess of P-activity, which was considered a medication effect. Over the frontal leads one single peakwave complex was reported. In addition, bursts of sharp transients were observed, particularly during provoked hyperventilation. This may be interpreted as an arousal phenomenon, but an abnormal aetiology could not be excluded. Because of these abnormalities a repeat EEG after sleep deprivation was arranged for the next day. This showed clear disturbances of functions in the frontal areas. Using suborbital electrodes, paroxysms of waves with durations of 0.25-0.33 s and an amplitude of up to 60 pV were recorded in the prefrontal and frontal areas, superimposed with sharp waves with durations of 0.8-0.11 s and an amplitude of up to 65 pV. The EEG was strongly suggestive of temporal or frontal lobe epilepsy. The diagnosis of frontal epilepsia was considered consistent with the clinical presentation and was chosen as a working hypothesis. The patient was succesfully treated with carbamazepine. At this time, the patient has remained free of catatonic episodes for almost 2 years. An MRl scan, performed after discharge, did not show any anatomical abnormalities as a possible cause for epilepsy.
DISCUSSION This patient presented with five episodes of catatonic stupor, with an exact periodicity of 30 days. The episodes of stupor were intempted by brief periods of agitation, anxiety and aggression, during which the patient experienced auditory hallucinations. Intensive investigations were performed to exclude the many aetiologies of recurrent catatonia. Although frontal lobe epilepsy had already been rejected on the basis of repeated normal EEGs, this diagnosis again appeared possible when, during the final episode, the patient presented with motor symptoms. But even then, this diagnosis could only be confirmed with an EEG after sleep deprivation and the use of suborbital electrodes. Frontal epilepsy can manifest itself both clinically and electrophysiologically in many different ways.’-’ Several authors try to group the different symptoms in various ways, to distinguish different electroclinical ~yndrornes.’.~ Salanova et a1 describe supplementary motor seizures, focal motor seizures and psychomotor seizures.’ This patient would most closely fit the clinical description of frontal psychomotor seizures, except that in his case consciousness was maintained. Moreover, frequent alterations between stuporous states and non-stuporous overt psychotic states have not been described as part of this syndrome. Finally, strict periodicity in seizure frequency has, to the authors’ knowledge, never been reported. Progress has been made in linking clinical manifestations with epileptic activity in different anatomical structures of the frontal lobe. For instance, mutism and akinesia have been associated with stimulation of a negative
Int J Psych Clin Pract Downloaded from informahealthcare.com by University of California Irvine on 11/07/14 For personal use only.
Periodic catatonia due to epilepsy
motor area, localized in the inferolateral frontal area, and .~ behavioural manifestations with the prefrontal c ~ r t e x In spite of this, the frequent changes in psychomotor function in our patient remain unexplained. Although of older date, the hypothesis proposed by Winters is interesting in this respect. He postulated a continuum of excitation states of the central nervous system (CNS). Using an experimental model in cats, he demonstrated that with increasing excitation, different psychomotor and sensory phases are passed in a well-defined order, viz (in order of increasing excitation): agitation, ataxia, bizarre catatonic movements, catalepsy, myoclonia and epileptic fits, In cats, the phase of ataxia is accompanied by euphoria and the phases of catatonia and catalepsy by visual hallucinations. All these phases may reversibly progress to an adjacent excitational stage, or to depression of the CNS with stupor and coma, and finally to death. 'In each of these phases, the EEG In a more philosophic shows specific approach, Fischer proposed a similar hypothesis for man, but this is less convincingly backed by clinical or electrophysiological
disorders. Sometimes, prolonged and repeated clinical observation is necessary to confirin a diagnosis. This is a worthwhile effort, as many of the the possible causes can be treated adequately. In this patient, acute periodic catatonic stupor could finally be atributed to frontal lobe epilepsy. This presentation of frontal lobe epilepsy has, to the authors' knowledge, not yet been described. The patient has been successfully treated with the anticonvulsant carbamazepine.
KEY POINTS 0
0
CONCLUSION The differential diagnosis of acute recurrent catatonia includes a large number of neurological and psychiatric
59
0
Recurrent catatonic stupor is a rare neuropsychiatric syndrome, with a range of causes Frontal lobe epilepsy may cause recurrent stupor, and can be treated successfully with anticonvulsants Abnormalities on the EEG may be only transient, but can be revealed by sleep deprivation
REFERENCES 1. Gelenberg AJ (1976) The catatonic syndrome. Lancet i: 133941. 2. Fekkes D. Pepplinkhuizen L, Verhey R et a1 (1994) Abnormal plasma levels of serine, methionine, and taurine in transient acute polymorphic psychosis. Psychiatry Res 51: 11- 18. 3. Gjessing RR (1976) The somatology of periodic catatonia. Pergamon, Oxford. 4. Broglin D,Delgado-Escueta AV, Walsh GO et a1 (1992) Clinical approach to the patient with seizures and epilepsies of frontal origin. Adv Neurol 57: 59 - 88. 5. Meierkord H (1992) Die klinischen und neurophysiologischen Merkmale von Epilepsien mit Frontallappenanfdlen bei einer mit Video-EEG-Telemetrie diagnostizierten Sene von Patienten. Nervenarzt 63: 485-91. 6. Fornazarri L, Farcnik K, Smith I et a1 (1992) Violent visual hallucinations in frontal lobe dysfunction: clinical manifestations of deep orbitofrontal foci. J Neuropsychiatr Clin Neurosci 4: 42 - 4.
7. Williamson PD (1992) Frontal lobe seizures: problems of diagnosis and classification. Adv Neurol 57: 289-309. 8. Salanova V, Morris HH, Van Ness P et a1 (1995) Frontal lobe seizures: electroclinical syndromes. Epilepsia 3 6 16- 24. 9. Watennan K, Wada JA (1990) Frontal lobe epilepsy. In: Comprehensive epileptology (ed M Dam, L Gram) 197-213. Raven Press, New York. 10. Winters WD (1975) The continuum of CNS excitory states and hallucinosis. In: Hallucinations: behavior, experience and theory (ed RK Siegel, LJ West) 53-70. John Wiley, New York. 11. Fischer R (1969) The perception-hallucination continuum: a reexamination. Dis Nervous System 30: 161- 71. 12. Fischer R (1986) Toward a neuroscience of self-experience and states of self-awareness and interpreting interpretations. In: Handbook of states of consciousness (ed B Wolman, M Ullman) 3-30. Van Nostrand Reinhold, New York.
