Abstract
Psychopathology in twins: ancient case study
In a letter to this journal Pridmore provided an account of the Aboriginal myth ‘The Jealous Twins’ Perindi and Harrimiah, which Pridmore suggests is likely to be 5000 years old, followed by his psychiatric diagnostic speculations about the figures of the myth [1].
Pridmore treats the myth as an historical account, and the characters involved as if they were real people, to whom psychiatric diagnoses may be applied, as for example, ‘the information that is provided on symptoms is presented in ordinary, clear language rather than technical terms’, and ‘Perindi may have suffered a paranoid psychosis and Harrimiah a major depressive disorder’.
When we consider the myth of Icarus and Daedalus we are unlikely to conclude that this father and son really fashioned wings with wax and feathers and really flew with them, or that the sun really did melt the wax of Icarus’ wings so that he fell to his death. We understand that the myth is a story of the imagination, a communication that represents something emotionally and culturally real, but not an account of real events or real people.
Possibly it was not Pridmore's explicit intention to convey the impression that Perindi and Harrimiah were real people, but if not then we are left with the conclusion that he has failed to grasp that psychiatric diagnosis is not applicable to the figures of myth. If one adopts the epistemological framework of psychiatric diagnosis, its potential validity must remain limited to real human beings; it cannot be logically or validly applied outside of this frame. It makes sense to suggest that the myth of Icarus and Daedalus deals with hubris, pride, and grandiosity, but it makes no sense to attribute a diagnosis of, say, narcissistic personality disorder to Icarus. Similarly it makes sense to consider, as Pridmore does, that the figures of Perindi and Harrimiah reflect elements of a split situation, and as reflecting psychotic and depressive aspects of the mind respectively, but this cannot be taken to support his conclusion ‘Perindi may have suffered from a paranoid psychosis and Harrimiah a major depressive disorder’. It would have made sense to consider the myth as an exploration of the nature of jealousy, as its name ‘The Jealous Twins’ suggests, but Pridmore makes no reference at all to this central theme.
The second disturbing aspect of Pridmore's analysis is the kind of psychiatric cultural imperialism that it conveys. I think it is unwise to simply superimpose a psychiatric perspective, which inevitably has significant cultural dimensions of its own, onto the imaginative creation of another culture. This is after all an Aboriginal myth, and in seeking to understand the meaning of this myth one might expect to begin by enquiring about the place of its origin, that is, in the Aboriginal culture and psyche.
It is, of course, quite possible to argue that the scientific perspective has potential application that transcends cultural perspectives. Even if this possibility is allowed, however, Pridmore's analysis remains invalid for the reasons outlined. It lies in the realm of pseudoscience rather than science.
Pridmore suggests that his diagnostic conclusions may be ‘parsimonious and reasonable’; I would suggest they are parsimonious in every sense of the word, and quite unreasonable. Myths, like fairy tales and poetry, exist in what Winnicott has called the ‘transitional area’ of relating [2]. They are no one's property and they defy reductionism.
Clozapine-withdrawal catatonia
Abrupt discontinuation of clozapine can potentially induce a rapid-onset psychosis. Clozapine-withdrawal catatonia, however, has not been well described. We report a case of catatonia occurring after sudden discontinuation of clozapine in a 58-year-old Caucasian woman with schizoaffective disorder, which had been well controlled on clozapine, 150 mg day–1, and sodium valproate, 1500 mg twice a day, for 4 years.
Three days prior to the presentation the patient was visited by the mental health nurse, who had reported that she was in remission and compliant with her medications. Subsequently, the Acute Crisis and Intervention Service (ACIS) was contacted by a friend of the patient, reporting that the patient was not answering phone calls or door bells and had been behaving in a bizarre manner for 2 days. She was found by ACIS team half naked, lying in bed in a fetal position. Her dosette showed that she had not taken her clozapine for 3 days.
On presentation to the emergency department she had diarrhoea and was incontinent of urine and faeces and became agitated on several occasions. Examination indicated fever, diaphoresis, autonomic instability (fluctuating blood pressure), mutism, stupor, posturing, mannerisms (repetitive blinking) and myoclonus in lower limbs. No other abnormalities were found on physical examination or investigations including computed tomography of the head. She was admitted to a medical ward and was regularly assessed by psychiatrists. She remained mute and refused to eat.
On the basis of these observations the patient was thought to be in a catatonic state. Clozapine regimen could not be reintroduced because the patient was refusing to take oral medications. She was commenced on i.m. lorazepam for 48 h with no response. Electroconvulsive therapy (ECT) was then considered but was delayed due to the patient's significant autonomic instability. Her blood pressure was ultimately controlled with i.m. clonidine and glyceryl trinitrate patches.
It was noted that the patient had a similar presentation 4 years previously after being non-compliant with clozapine for 1 week, which responded well to a course of ECT. On this admission her catatonic features and autonomic instability started to respond after the fourth ECT. By the 10th ECT session the patient was able to walk and eat indenpendently. She was then transferred to the psychiatry ward and clozapine was reintroduced.
Clozapine is an atypical antipsychotic that is widely used in treatment-resistant psychosis. Clozapine has complex pharmacological actions on different neurotransmitter systems. It has an antagonist action at dopaminergic, serotonergic, α-adrenergic and cholinergic receptors. Long-term administration of clozapine is believed to cause receptor upregulation in these neurotransmitter systems [1].
It has been shown that abrupt clozapine cessation, given the short duration of action and its rapid dissociation from the receptors, could provoke rapid onset of a somatic withdrawal syndrome [1], mainly caused by ‘cholinergic rebound’ and serotonergic hyperactivity. There is also strong evidence that clozapine withdrawal is associated with rapid onset of psychotic symptoms, known as ‘rebound psychosis’, which is now believed to be distinct from the relapse of the underlying disorder and due to increased dopamine activity in the limbic system [2].
Catatonia is a neuropsychiatric syndrome with a combination of psychomotor and behavioral signs and symptoms. Although the aetiology of catatonia is not fully understood, neurochemical studies suggest that the γ-aminobutyric acid (GABA)ergic system plays a central role, which explains the efficacy of lorazepam in treatment of acute catatonia [3]. Disequilibrium in the dopaminergic and serotonergic systems are also contributing factors in the pathophysiology of catatonia [4].
We believe that the present patient may have experienced rebound psychosis, which could be indicative of dopaminergic hyperactivity prior to becoming catatonic. Her agitation, diarrhoea and diaphoresis may have been due to cholinergic rebound. The pyrexia, autonomic dysfunction and myoclonus could be explained by serotonergic disequilibrium. Given that she did not respond to lorazepam, one could also speculate that her catatonia was not related to the GABAergic system.
Abrupt discontinuation of psychotropic drugs is not uncommon in the clinical setting; mostly because of side-effects or patient non-compliance. Clinicians, patients and their caregivers should be aware of the possibility of clozapine discontinuation-related symptoms and catatonia as a potentially-life threatening withdrawal syndrome.
Transsexualism in Australia: a further statistic
In reporting on the prevalence of transsexualism among New Zealand passport holders Jaimie Veale appealed for further research to be done on the male-to-female (MF): female-to-male (FM) ratio in Australasia [1].
Over the past decade in my private psychiatric practice in Sydney and Wollongong there have been 310 people presenting as transsexual referred to me for assessment or management. Of these, 227 were biologically male and 83 biologically female, yielding a ratio of, say, 2.7:1. This proportion is closer to general findings worldwide and contrasts with Veale's ratio of 6.1:1 and the identical figure found by Ross et al. in Australia [2].
Veale wonders whether social or biological factors may have contributed to a greater proportion of MF transsexualism in Australia, compared with Sweden. The Ross et al. work, however, was done some 30 years ago. If other contemporary statistics come to light similar to mine, we may have to turn to historical factors to explain the Ross et al. figure.
Whatever biological or social factors may influence the general finding that MF transsexualism greatly outnumbers the FM, a psychodynamic explanation has long been to hand in the work of the late Robert Stoller [3]. He pointed out that girls and boys alike go through a protracted early dependence on – and identification with – a mother figure. Psychologically (as it does embryologically) masculinity differentiates out of a feminine Anlage. Hence it is not surprising that male gender identity can prove in some cases a relatively fragile structure.