Abstract
Self-enucleation of one eye
A 38-year-old divorced, bespectacled woman with a 20 year and family history of schizophrenia recently self-enucleated one eye at the Royal Hobart Hospital. She had been admitted to the general psychiatric ward from a clo-zapine clinic, when she presented in a floridly psychotic state, having reduced her recommended medications.
In the first 4 days of admission she was delusional (believing Saddam Hussain had been murdered in her flat, and that she was a man), hallucinating (hearing voices and seeing the face of God), and ceased taking food and fluids. She assaulted a staff member and was transferred to a psychiatric intensive care unit (PICU).
In PICU the patient grabbed and spat on staff, questioned whether she was a man or a woman and was disorganized in behaviour (repeatedly unmaking and making her bed). She expressed the delusion that she had cut her penis off, and that staff were planning to kill her. She assumed bizarre postures and slithered over the floor and lounge chairs as if she was a snake.
After 4 days in PICU, at a morning ward round, she stated that she believed she was a werewolf because she ‘couldn't see anything’, and staff discussed with her the possibility of obtaining a new pair of spectacles. That afternoon she was ‘irritable, abusive and menacing’. At 18.25 hours, while alone in her room, she removed her eye.
The patient was transferred to a surgical ward and physical and psychiatric recovery was gradual but uneventful.
Over the 8 days prior to the enucleation the patient refused clozapine and half the other offered oral anti-psychotic medication. On the day of, but prior to the enucleation, she was given, against her wishes, zuclo-penthixol acetate 150 mg, i.m., zuclopenthixol decanoate 200 mg, i.m., and midazolam 5 mg, i.m. Over the 4 days in PICU the patient was on 15 min nursing observations and was placed in audiovisually monitored seclusion on five occasions.
Krause et al. identified reports of 50 individuals who had removed one or both eyes between 1846 and 1985 [1]. Subsequently, on average, one new case has been reported annually. The majority of cases involved psychosis, including drug-induced psychosis.
Witherspoon et al. recommended the early identification of patients at risk, and stated that cases have been reported of patients enucleating a second eye despite increased precautions [2]. Kumar and Geist suggested a range of preventive methods, from the wearing of boxing gloves to tarsorrhaphy [3].
We examined the present patient's history and noted that at 3 days prior to the enucleation, the patient had believed she had cut her penis off (another form of serious self-mutilation), and on the day of the event she had mentioned her eyesight. These utterances, however, were in a setting of florid psychosis and we could not identify markers that could be taken as predictors of this grievous outcome. A recent naturalistic study suggested that if permission is forthcoming, repeated courses of electro-convulsive therapy may have a place in the prevention of self-harm by individuals with psychosis [4].
References
1. Krause H, Yee R, Foos R. Autoenucleation. Surv Ophthalmol 1984; 29:179–187.
2. Witherspoon D, Feist F, Morris R, Feist R. Ocular self-mutilation. Ann Ophthalmol 1989; 21:255–259.
3. Kumar A, Geist C. A case report of bilateral autoenucleation and its prevention. Orbit 2007; 26:309–313.
4. Hustig H, Onilov R. ECT rekindles pharmacological response in schizophrenia. Eur Psychiatry 2009 [Epub ahead of print].
Ti: myths about monoamine oxidase inhibitors perpetuated
It is disappointing to see Shaikh and Fuls perpetuating old myths in a pharmacologically naïve contribution about tranylcypromine (TCP) [1]. They state that amphetamine and methamphetamine are serotonin releasers, whereas they are noradrenaline and dopamine releasers [2]. Their claim that TCP also is a serotonin releaser is not referenced; indeed there is no such evidence, for one very simple reason: if TCP was a significantly potent 5-HT releaser then it would precipitate severe serotonin toxicity at therapeutic doses, which it patently does not do, see [3] for an explanation of why that is the case. If it was a noradrenaline releaser it would precipitate the sympathomimetic toxidrome (i.e. like the tyramine-mediated ‘cheese reaction’, and the amphetamine/TCP interaction), and cause hypertension: but it induces hypotension, both acutely and chronically, and even in overdose hypertension is only occasionally severe [4]. The notion that TCP is a 5-HT releaser is vacuous and facile: the simplistic comparison of TCP to amphetamine in 2-D representations of structure is outmoded science, if it ever was science [5]. More recent evidence does indicate that selegiline is metabolized into amphetamine [6,7]. The report by You-dim et al. of amphetamine metabolites of TCP is a key reference about which these authors, and your referees, appear ignorant [8]. But it is an observation not substantively validated since then; rather, subsequent evidence has tended to negate it [9]: caveat lector.
That ‘sausage, salami, processed meat and beer’ are ‘tyramine-rich’ is now disproved. Modern food hygiene standards are such that meats do not have significant levels of tyramine and the food police have regulated against proper matured salami-style meat products in Australia, but even with European fermented salami-styles tyramine content is very rarely >200 mg kg −1 [10], and that amount is unlikely (in sensible portions) to elevate blood pressure at all, never mind seriously (for discussion and further references see http://www.psychotropical.com/maois_diet_full.shtml) Beers rarely go over 1 mg L −1 [11]. Even commonly available cheeses rarely have a high tyramine content: I recommend to your readers to the McCabe-Sellers et al. recent review of food and tyramine [12]. Hypertension from monoamine oxidase inhibitors seems to cause panic in most doctors, but there have been no documented deaths in Medline in 50 years, and most reported cases of ‘hypertension’ do not involve blood pressure increases any greater than those (hopefully) experienced when engaging in vigorously amorous pursuits with our partners [13], or weightlifting [14,15], or a combination of the two. As an exercise in perspective, these activities are by themselves associated with sub-arachnoid haemorrhage, as are ephedrine-related compounds that are over-the-counter drugs [16]. People do not commit suicide because of a runny nose, but no one has proposed banning those drugs or activities.
Phenelzine seems more popular because it is perceived as having a lower risk of hypertension (probably because it is given in subtherapeutic doses), but it causes more deaths from hepatic failure. So much better, or currently more acceptable, to get metabolic syndrome on antipsychotics such as olanzapine!
References
1. Shaikh W, Fuls K. Tranylcypromine dependence and withdrawal. Aust N Z J Psychiatry 2009; 43:580-581.
2. Rothman RB, Baumann MH. Monoamine transporters and psychostimulant drugs. Eur J Pharmacol 2003; 479:23-40.
3. Stanford SC, Stanford BJ, Gillman PK. Risk of severe serotonin toxicity following co-administration of methylene blue and serotonin reuptake inhibitors: an update on a case report of post-operative delirium. J Psychopharmacol 2009 [Epub ahead of print].
4. Whyte IM. Monoamine oxidase inhibitors. In: Dart RC, ed. Medical toxicology, 3rd edn. Baltimore: Lippincott Williams & Wilkins, 2004:823–834.
5. Wishart DS, Knox C, Guo AC, et al. DrugBank: a comprehensive resource for in silico drug discovery and exploration. Nucleic Acids Res 2006; 34:D668–672.
6. Heinonen EH, Anttila MI, Lammintausta RA. Pharmacokinetic aspects of l–deprenyl (selegiline) and its metabolites. Clin Pharmacol Ther 1994; 56:742–749.
7. Finberg JP, Gross A, Bar-Am O, Friedman R, Loboda Y, Youdim MB. Cardiovascular responses to combined treatment with selective monoamine oxidase type B inhibitors and L-DOPA in the rat. Br J Pharmacol 2006; 149:647–656.
8. Youdim MB, Aronson JK, Blau K, Green AR, Grahame-Smith DG. Tranylcypromine (‘Parnate’) overdose: measurement of tranylcypromine concentrations and MAO inhibitory activity and identification of amphetamines in plasma. Psychol Med 1979; 9:377–382.
9. Sherry RL, Rauw G, McKenna KF, Paetsch PR, Coutts RT, Baker GB. Failure to detect amphetamine or 1-amino-3-phenlypropane in humans or rats receiving the MAO inhibitor tranylcypromine. J Affect Disord 2000; 61:23–29.
10. Latorre ML. Biogenic amines in traditional fermented sausages produced in selected European countries. Food Chem 2008; 107:912–921.
11. Anli RE, Vura N, Demiray S, Mert B. Biogenic amine content of beers consumed in Turkey and influence of storage conditions on biogenic amine formation. J Inst Brew 2006; 112:267–274.
12. McCabe-Sellers BJ, Staggs CG, Bogle ML. Tyramine in foods and monoamine oxidase inhibitor drugs: a crossroad where medicine, nutrition, pharmacy, and food industry converge. J Food Comp Anal 2006; 19:S58–S65.
13. Landtblom AM, Fridriksson S, Boivie J, Hillman J, Johansson G, Johansson I. Sudden onset headache: a prospective study of features, incidence and causes. Cephalalgia 2002; 22:354–360.
14. MacDougall JD, Tuxen D, Sale DG, Moroz JR, Sutton JR. Arterial blood pressure response to heavy resistance exercise. J Appl Physiol 1985; 58:785–790.
15. Haykowsky MJ, Findlay JM, Ignaszewski AP. Aneurysmal subarachnoid hemorrhage associated with weight training: three case reports. Clin J Sport Med 1996; 6:52–55.
16. Cantu C, Arauz A, Murillo-Bonilla LM, Lopez M, Barinagarrementeria F. Stroke associated with sympathomimetics contained in over-the-counter cough and cold drugs. Stroke 2003; 34:1667–1672.
Prevalence of mental illness in older Australians
There appears a pressing need to clarify the reliability and validity of current mental health epidemiological methods applied to older people. The 2007 National Survey of Mental Health and Wellbeing (NSMHWB) reported a significant decline in prevalence of mental illness with age [1], with those aged above 74 years found to have approximately one-quarter the prevalence to those aged 16–24 years. The same survey found higher rates of mental health disorders (28% vs 17.6%) in those people with chronic medical conditions [2], which are known to increase with age. There is no discussion of the reasons for these conflicting trends.
NSMHWB estimates will have significant impact on planning and availability of services for older Australians. Consistent with other studies, the 2007 NSMHWB found that rates of service use for those with identified mental health problems declined with age [3]. NSMHWB prevalence estimates influence the limited attention this has received in mental health service reform.
O’Connor suggested that the 1997 NSMHWB findings regarding older people were impacted upon by sampling and case ascertainment bias, and exclusion of those within aged residential care [4]. Considering other evidence, he concluded that ‘functional mental disorders almost certainly rise in frequency in advanced old age, often in conjunction with dementia’. Sampling appears to have been modified in the 2007 NSMHWB to include more older people, but other concerns raised by O’Connor were not adequately addressed.
Standardized interview schedules can have signifi-cant problems in estimating depression prevalence in the elderly [5]. A review of the CIDI, upon which the NSMHWB is based, stated ‘The need for further procedural validity studies of the CIDI …. is emphasized. The latter should focus on specific aspects, such as the use of standardized questions in the elderly ….’ [6]. I have been unable to find literature examining the impact of older age on the reliability or validity of the CIDI. Action is required.
References
1. Slade T, Johnston A, Oakley-Browne MA, Andrews G, Whiteford H. 2007 National Survey of Mental Health and Wellbeing: methods and key findings. Aust N Z J Psychiatry 2009; 43:594–605.
2. Teeson M, Slade T, Mills K. Comorbidity in Australia: findings of the 2007 National Survey of Mental Health and Wellbeing. Aust N Z J Psychiatry 2009; 43:606–614.
3. Burgess PM, Pirkis JE, Slade TN, Johnston AK, Meadows GN, Gunn JM. Service use for mental health problems: findings from the 2007 National Survey of Mental Health and Wellbeing. Aust N Z J Psychiatry 2009; 43:615–623.
4. O’Connor DW. Do older Australians truly have low rates of anxiety and depression? A critique of the 1997 National Survey of Mental Health and Wellbeing. Aust N Z J Psychiatry 2006; 40: 623–631.
5. Knauper B, Wittchen HU. Diagnosing major depression in the elderly: evidence for response bias in standardized diagnostic interviews? J Psychiatr Res 1994; 28:147–164.
6. Wittchen HU. Reliability and validity studies of the WHO Composite International Diagnostic Interview (CIDI): a critical review. J Psychiatr Res 1994; 28:57–84.
Lycanthropy in alcohol intoxication
Hannover Medical School, Clinic for Psychiatry, Social Psychiatry and Psychotherapy, Hannover, Germany
Lycanthropy is the delusional belief of metamorphosis into an animal. It is has been defined by Keck et al. as being either verbalized by the patient or an obvious animal behaviour [1]. Lycanthropy has been reported in schizophrenia and affective disorders as well as in organic causes such as intoxication with cannabinoids or alcohol [2].
Reported herein is the case of a 43-year-old patient who was picked up by the police while trying to provoke an accident on a busy crossing, who was convinced that he had the identity of a wild boar and who was acting as such. The symptomatology lasted for 2 h and the patient could remember the delusional idea the day after. He reported that some days before he had seen some wild boars in a wildlife park and felt an ‘esoteric’ bond with a certain pig. At that tine there were media reports in Germany about wild boars leaving the forests and entering towns, being potentially dangerous to people. Psychopathologically there were no other symptoms beside agitation and aggression.
The patient's blood alcohol concentration was 0.28%. The patient has a known bipolar disorder but there was no hint of a current manic episode. On examination there were no pathological findings beside the intoxication signs. Diagnostically alcohol intoxication was stated.
To our knowledge this is the first report of a lycanthropy involving transformation into a wild boar. The symptomatology was triggered by preoccupation and real contacts with those animals before the occurrence. It was based on an alcohol intoxication and was short in duration. This is congruent with cases mentioned in the literature, and lycanthropy may occur more often in alcohol-related mental states than has yet been reported.
References
1. Keck PE, Pope HG, Hudson JI, McElroy SL, Kulick AR. Lycanthropy: alive and well in the twentieth century. Psychol Med 1998; 18:113–120.
2. Garlipp P, Gödecke-Koch T, Dietrich DE, Haltenhof H. Lycanthropy: psychopathological and psychodynamical aspects. Acta Psychiatr Scand 2004;109:19–22.