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Letters to the Editor Acute Onset of Schizophrenia Following Autocastration Dear Editor: Autocastration is a rare form of genital self-mutilation traditionally associated with patients suffering from acute psychosis, especially those harbouring religious delusions and having other risk factors (1). We present a case of autocastration occurring during the prodrome of schizophrenia, with florid psychosis emerging only after the act. We discuss possible neuroendocrinal and neurotransmitter interactions underlying the appearance of this schizophrenia-like psychosis after castration.
The patient, a 26-year-old married man, was admitted with a recent psychotic exacerbation of a 5-year illness characterized by suspiciousness, hearing sounds, unprovoked irritability, unpredictable violence, inappropriate mood states, awkward postures, and progressive personality deterioration. He was diagnosed with undifferentiated schizophrenia according to the ICD-10 criteria. Although he had a history of sexual abuse and pedophilic behaviour dating from early adolescence, he did not display any traits suggesting a personality disorder. The first changes in his demeanour were noticed when, following the loss of his job in 1995, he became sad and aloof. He also experienced sleep disturbance that gradually worsened over the next 6 months. Toward the end of this 6-month period, he became more religious as well. During this time, however, there was no depressive cognition or overt psychosis. As his sleep deteriorated, he consulted many general practitioners, but without much relief. One day, distressed because of this lack of sleep, the patient impulsively decided to commit suicide. He went to a lonely hill, where he first thought of stabbing himself but then instead castrated himself, believing this to be more lethal. Using a knife, he completely excised the scrotum at its base and then threw the testes away, but left his penis untouched. He felt no pain during the act. Fortunately, he was rescued and the remaining part of the scrotum was sutured. Following recuperation in a hospital, he was discharged after 15 days. The testes were not reattached, nor was he started on testosterone. As assessed by a psychiatrist, the patient had no psychotic symptoms during the hospital stay, and his only reason for committing the act was a genuine wish to die, precipitated by sleeplessness. There was no evidence of sexual conflicts over past experiences, and there was no history of self-injury or family history of psychiatric illness. A couple of days after reaching home, the patient started behaving abnormally. He suspected his neighbours of plotting to kill him so that they could have intercourse with his wife, since he no longer felt like a “normal male.” Intermittently, he would hear sounds of someone banging at the door and, on hearing these sounds, would become irritable and violent. Referred to a psychiatrist, he was diagnosed with schizophrenia in 1996 and started on antipsychotics. To date, he has had a fluctuating course, with remissions and exacerbations, without reaching his premorbid state.
No reports explicitly describe castration occurring during the prodromal phase of schizophrenia, with such a rapid emergence of psychosis after the act. However, a single report describes a patient with schizotypal personality disorder who developed schizophrenia about 3 years after autocastration (2). Most patients with schizophrenia who commit genital self-mutilation are found to be psychotic either during the act or immediately following it (1). Although patients without psychosis who display genital self-mutilation usually have a disturbance in sexual identity or a personality disorder (1), our patient did not have anything to suggest these. An interesting finding was the rapid emergence of psychosis following the castration. It can be argued that the patient followed the natural course of illness, but the striking temporal correlation between the castration and the emergence of psychopathology set us to explore whether neuroendocrinal factors consequent to decrease in testosterone contributed to the onset of the schizophrenia-like psychosis. There are conflicting reports about the role of testosterone per se in
schizophrenia, with reports demonstrating decreased (3), normal (4), and
higher levels (5). More relevant in explaining psychopathology is the
effect of testosterone on catecholamines and serotonin. Although exogenous
testosterone may not affect dopamine receptor function in the human male
(6), animal studies provide supporting evidence that testosterone manipulates
serotonergic transmission in rats (7). This in turn may regulate the dopaminergic
function. This latter study found that castration decreased the 5-HT2A-receptor
binding sites, the content of 5-HT2A messenger ribonucleic acid (mRNA),
and the serotonin-transporter binding sites in the brain, thus decreasing
the serotonergic transmission. Conversely, administration of testosterone
had the opposite effect. When viewed in light of the well-chronicled inhibitory
role of the serotonergic system over the dopaminergic system, especially
in the frontal areas, this indicates that falling testosterone levels
consequent to castration cause a hyperdopaminergic state. These observations
thus indirectly support the hypothesis that testosterone protects against
schizophrenia by modulating the neurotransmitters implicated in the disorder.
A similar role for estradiol is more accepted in the literature; whether
testosterone exerts its protective action via conversion to estradiol
(7) is a question that opens new avenues for elucidating its impact on
the psychopathology of schizophrenia.
1. Nakaya M. On background factors of male genital self-mutilation. Psychopathology 1996;29:242–48. 2. Myers WC, Nguyen M. Autocastration as a presenting sign of incipient schizophrenia. Psychiatr Serv 2001;52:685–6. 3. Hirasawa H, Asakawa O, Koyama K, Takahashi Y, Atsumi Y, Kumakura T. A case of Klinefelter’s syndrome with schizophrenia-like symptoms. Nippon Ronen Igakkai Zasshi 2000;37:495–8. 4. Brown AS, Hembree WC, Friedman JH, Kaufmann CA, Gorman JM. The gonadal axis in schizophrenia. Biol Psychiatry 1991;29:457–66. 5. Mason JW, Giller EL, Kosten TR. Serum testosterone differences between patients with schizophrenia and those with affective disorder. Biol Psychiatry 1988;23:357–66. 6. Lal S, Nair NP, Thavundayil JX, Tawar V, Guyda H, Ayotte C. The effect of methyltestosterone on the growth hormone response to the dopamine receptor agonist, apomorphine. Prog Neuropsychopharmacol Biol Psychiatry 1991;15:263–8. 7. Fink G, Summer B, Rosie R, Wilson H, McQueen J. Androgen actions on central serotonin neurotransmission: relevance for mood, mental state and memory. Behav Brain Res 1999;105:53–68. Harpreet S Duggal, DPM
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