Correspondence
Psychotic depression, subcortical
arteriosclerotic encephalopathy and holocaustconditioned posttraumatic stress disorder
Stefan Kropp, Jann Schlimme, Udo Schneider, Department
of Clinical Psychiatry and Psychotherapy, Hanover
Medical School, Germany:

We report the case of a 79-year-old, white married
patient, who on admission revealed that she was weary of
life. On mental state examinations she was alert, clearthinking and orientated. Formal thinking was coherent, the
contents of which showed a marked delusion of poverty
without any indication of hallucination. The patient suffered a severe lack of motivation and showed only fleeting
signs of emotion. Psychomotor inhibition was prominent.
She admitted to continual suicidal thoughts, although
lacked the drive to carry out such an attempt. Hamilton
Depression Rating Score (HAMD) was 41 points on
admission. Relatives reported her screaming out in terror
while asleep. Medical history included chronic obstructive
lung disease, hyperthyroidism (now stable) and osteoporosis. A subcortical arteriosclerotic encephalopathy
was apparent in magnetic resonance imaging.
Throughout World War II, the patient was in hiding in
Germany because she was Jewish, and was in constant
fear of being detected and deported. Her father and all
other members of the family except her mother did not
survive the war and the extermination of the Jews.
Despite initial treatment with 30 mg mirtazapine and
2 mg risperidone her condition worsened. The patient
became distraught, withdrew into herself, refused to
accept any form of liquid or nourishment and became
incontinent. She lost orientation as to time, place or
person. She was preoccupied with the thought that someone was waiting to kill her. This disturbance of consciousness was most likely associated with flashbacks
which occur in patients with posttraumatic stress disorder (PTSD; meeting DSM-IV criteria) and which is
common in Holocaust survivors [1,2]. This was probably triggered off by dehydration, exacerbating the subcortical arteriosclerotic encephalopathy. Due to her poor
health, all medication was discontinued. She received
medical care and her condition stabilized. Then further
treatment was started with 75 mg of sertraline due to its
proven efficacy on delusional symptoms in depression
[3], combined with a kava-extract containing product.
After 2 weeks of symptoms such as anxiety and delusions improved, while no severe side-effects were
observed. She regained her sense of orientation and no
longer had suicidal ideas. She still suffered with a mild
degree of delusion of poverty; however, HAMD dropped
to 12 points and the patient was discharged home in a
satisfactory condition. In conclusion, selective serotonin

re-uptake inhibitor (SSRI) treatment of PTSD-associated
major depression seems to be effective and further study
might clarify the role of SSRIs in the treatment of this
disease.
References
1.
2.
3.

Kuch K, Cox BJ. Symptoms of PTSD in 124 survivors of the
Holocaust. American Journal of Psychiatry 1992; 149:337–340.
Beinsheim H. Die K.Z.-Neurose rassisch Verfolgter. Nervenarzt
1960; 31:462–469.
Zanardi R, Franchini L, Gasperini M, Perez J, Smeraldi E.
Double-blind controlled trial of sertraline versus paroxetine in
the treatment of delusional depression. American Journal of
Psychiatry 1996; 153:1631–1633.

Committal of a patient due to media influence?
A case report
Peter J. Dean, Herman E. Lombard, Steve Wilkes, Henry
Bennett Centre, Waikato Hospital, Hamilton, New Zealand:

We wish to present a case of committal against the recommendation of the Responsible Clinician, brought
about by pressure from the media and patient’s family.
With recent amendments to the New Zealand Mental
Health Act emphasizing consultation with families, we
speculate that more cases of this type may occur.
David has a 13-year history of schizophrenia. For
8 months he had a peripatetic lifestyle. On return to his
mother’s home, he was referred for assessment under the
Mental Health Act. David presented with loosening of
associations, delusions of identity, ideas of reference,
thought insertion, thought broadcast and auditory hallucinations. He expressed no suicidal ideation and no
thoughts of harm to others. In view of this, he was committed for further assessment.
David was no management problem, with appropriate
social interaction. Plans were made for discharge following trial leave. David declined ongoing psychiatric care.
A number of political agencies made contact to ask
about the ‘dangerous psychotic’ who was about to be
released into the community. A second opinion was
sought, which concurred with the view that there were
no grounds to suspect dangerousness. The Ministry of
Health strongly recommended that he remain an inpatient until at least the end of the assessment period, as
it was likely that the press would print the story.
Unfortunately, a sensationalist article appeared on the
front page of the local paper. An application to the District
Court for a Treatment Order was made in order to prevent further publication of the outcome.
The Court hearing was unusual in that the Responsible
Clinician and supporting clinicians recommended that
David be discharged from the Act. The judge ruled that
David should be detained as an inpatient on the grounds

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CORRESPONDENCE

of psychological distress to the family and seriously
diminished capacity to care for himself due to dysfunctional social interactions. Despite this extreme provocation, David presented himself in a dignified and
appropriate manner.
The media’s sensational report impacted on the clinical care of our patient. The article conveyed an impression that this psychotic individual was dangerous. It
included descriptions of unrelated homicides, while a
more balanced article was placed in a less prominent
position. Nairn has observed that journalistic devices for
creating ‘newsworthy’ items undermine positive portrayals of the mentally ill [1].
The implication of the judge’s ruling is that eccentric
social functioning could be grounds for detention under
the Mental Health Act. Despite ‘serious psychological
distress’, David’s family was very willing to have him
under their care for leave. Applebaum notes that judges,
across the world, have intuitive criteria and a moral sense
of involuntary commitment, allowing a bending of strict
interpretations of the law [2].
This case reflects an apparent trend within New
Zealand towards more paternalistic care and less autonomy in the care of the mentally ill; similar to that experienced in the UK [3]. There seems to be an increase in the
pressure from society, reflected in the media, to restrict
our patients, based on an assumption that psychiatric
patients are dangerous and community care is failing.
References
1.

2.

3.

Nairn R. Does the use of psychiatrists as sources of information
improve media depictions of mental illness? A pilot study.
Australian and New Zealand Journal of Psychiatry 1999;
33:583–589.
Applebaum PS. Almost a revolution: an international perspective
on the law of involuntary commitment. Journal of the American
Academy of Psychiatry and Law 1997; 25:135–147.
Hotopf M, Wall S, Buchanan A, Wessly S, Churchill R.
Changing patterns in the use of the Mental Health Act 1983 in
England 1984–96. British Journal of Psychiatry 2000;
176:479–484.

Signal transmission, schizophrenia and the
limits to biological psychiatry
N. McLaren, Darwin, Australia:

After an extensive review, Dean [1] left no doubt that
evidence for a specific neurochemical defect in schizophrenia was contentious at best, even contradictory.
He concluded: ‘Data from both neuroimaging and
post-mortem studies have identified changes in the
presynaptic proteins and/or function in the brains
of schizophrenic patients . . . Changes in functioning of
presynaptic processes could be a component of the
pathology . . . It would, therefore, seem that the focus

of future drugs should change from blockade of the
post-synaptic receptor to modulation of presynaptic
function, that is, “modulate signal transmission” rather
than “reduce signal reception”’ (p.566).
At first glance, Dean would appear to have espoused
the extreme view of biological psychiatry, Maudsley’s
aphorism that ‘Mental disease just is brain disease’ (cited
in [2, chap.2]). At different points he stated: ‘. . . overactive dopaminergic neurones cause the psychoses
associated with schizophrenia’ (pp.560–561), or ‘As the
molecules in these processes are isolated and their function better understood, it should be possible to determine
if changes in a single protein common to all affected
presynaptic processes is the cause of schizophrenia’
(p566). That is, he adopts the reductionist concept of a
unitary biological cause of this complex disorder, with
all that that view entails. If he had not done so, his search
among the proteins of the presynaptic neurones would
become incoherent [2, chap.2].
The language of his review appears to soar beyond
mere detail. For example, ‘. . . the dopamine hypothesis
of schizophrenia still requires total validation . . ’
(p.562), or the case for an increase in GABA receptors is
only ‘less compelling’ after contradictory evidence,
while an inability to replicate results is a ‘paradigm’
(p.565). Such bold phraseology may induce the lesssceptical reader to believe that the vast outpouring of
research he reviewed amounts to something substantial,
but it does not. All Dean established was that the case for
a biological cause for schizophrenia is no stronger than
the case for psychological causation of this mysterious
condition. Now this, surely, is a bold claim?
Not really. In arguing that the ‘primary lesion’ is presynaptic, all he is saying is that input should be accorded
greater significance. But input is such a general term as
to be nearly meaningless: input from what to what?
Which synapses, in which brain nuclei? The brain is an
ineffably complex organ; part of its complexity arises
from its capacity to act upon itself. In this sense, one part
of the brain is presynaptic to another part, and acts upon
it as part of its normal function. Therefore, if we say that
the ‘primary lesion’ is presynaptic, we are allowing the
possibility that the disorder arises by virtue of the brain
acting back upon itself. That recursive action may in fact
be mentally determined, and is therefore not necessarily
pathological, even if its outcome is. For example, if I
decide to close one eye for the rest of my life, I would
eventually lose vision in that eye. I expect that the visual
pathways in my brain would show pathological changes
as a result. In this case, the receptor pathology would
clearly be the result of a presynaptic event, which is itself
just part of a very long chain of pre- and post-synaptic
elements. However, at their initiation, these are the result

CORRESPONDENCE

of a willed action for which there is no biological
substrate [2, chap.2]. Ultimately, such pathology as exists
can be traced back to a mental event. Of course, this is not
what biological psychiatry dictates, but I am utterly
unconvinced by the claims of biological psychiatry [3].
Biological psychiatry looks for pathological changes,
and most authors uncritically assume that such changes
as they find are necessarily primary. There is no reason
to believe this. Any change can be the result of an
earlier change; for the brain, since mental function has
a physical substrate, the initiating event may well be
the subject’s own mental state. There is no a priori
reason why this should not be the case. Think of programming or input errors in computers. These have a
physical substrate, but nobody is interested in the computer’s function at that level. What counts is its informational state, not the physical realisation of that state
[2, chap.12].
Dean’s error, of believing that any changes are necessarily primary, is not new. This type of error will keep on
happening because biological psychiatrists refuse to lift
their heads from their microscopes to look at the larger
issues in their field. The race is on to find the elusive
schizococcus; nobody has time to ask the obvious question of whether there can in fact be such a thing, which
is a metaphysical question and therefore not amenable
to an empirical answer [2, chap.15]. By refusing to
acknowledge that there may in fact be metaphysical
questions for which their research is incapable of generating answers, biological psychiatrists are placing themselves in the same class as psychoanalysts [2, chap.6]
and radical behaviourists [2, chap.4], not so much scientists as propagandists.
References
1.

2.
3.

Dean B. Signal transmission, rather than reception, is the
underlying neurochemical abnormality in schizophrenia.
Australian and New Zealand Journal of Psychiatry 2000;
34:560–569.
McLaren N. The future of psychiatry. Chaps 2–4, 12, 15.
www.futurepsychiatry.com. Established January 2000.
Guze SB. Why psychiatry is a branch of medicine. New York:
Oxford University Press, 1992.

Reply to Dr McLaren
Brian Dean, Mental Health Research Institute, Melbourne,
Australia:

I would first like to thank Dr McLaren for acknowledging the extensive nature of my recent review [1]. It
would seem that Dr McLaren then goes on to conclude
that my interpretation of the data in this review is without value. This is because I have made the ‘error of
believing that any [physical] changes are necessarily

131

primary [in causing the symptoms of mental illness]
. . . [and this] will keep on happening because biological psychiatrists refuse to lift their heads from their
microscopes to look at the larger issues’. Dr McLaren
has put this argument previously [2], along with the
argument that the ‘biopsychosocial model’ of psychiatry
is of no value [3].
To most of us in medical research, science is an inclusive rather than exclusive exercise in attempting to
improve the lifestyle of those with illness. As such,
rather than simply refuting Dr McLaren’s position that
the answers to the causation of mental illness lie in the
‘mental’ rather than ‘biological’ state of the brain, it
would seem better to assess where these two hypotheses
may overlap. Dr McLaren rightly points out that the
human brain is a complex organ, the function of which is
dependent on complex interactive processes. The
research I describe in my review is designed to understand how the components of the brain that allow it to
carry out many of its function may be deranged in mental
illness. It does not exclude the possibility that mental
illness is due to a derangement of higher brain function.
Like the great Australian neuroscientist, John Carew
Eccles [4], Dr McLaren suggests that mental processes
may affect the operational integrity of the brain. While
this is an excellent working theory, there is a paucity of
data on whether an abstract ‘mind’ exists and how it
functions, let alone enough data to allow the study of its
abnormalities in mental illness. Even despite this paucity
of data, I do view research designed to understand the
complex ‘mind/brain’ relationship [5] to be of value,
even though the immediate benefits of such research are
not clear. However, until this research generates some
convincing and testable hypothesis as to the cause of
mental illness, I believe there is also great value in
continuing to study the structure of the human brain
and how it may be altered in these illnesses. Surely,
Dr McLaren would agree that all efforts must be made
to reduce the burden that mental illness places on sufferers of those illnesses.
Those committed to a single point of view can take
many statements out of context. Unfortunately, Dr
McLaren is perhaps over-zealous in taking quotations
from my review to support his position. For example, a
quote he references back to my review is ‘. . . the
dopamine hypothesis of schizophrenia still requires total
validation . . .’ Dr McLaren states that this indicates an
idea of ‘certainty which soars above mere detail’.
Importantly, the sentence quoted actually states that
‘While the dopamine hypothesis of schizophrenia still
requires total validation, studies using brain tissue
obtained at autopsy and PET suggest there are changes
in the functioning of the dopaminergic systems in

132

CORRESPONDENCE

subjects with schizophrenia’. The key word in the sentence being ‘suggest’, not a word associated with certainty. Dr McLaren also chooses to totally ignore my
closing remark that the most important outcome from the
acceptance of my hypothesis that presynaptic abnormalities are important in the pathology associated with
schizophrenia would be to re-direct drug design programmes to targets other than postsynaptic receptors.
Given the need to develop better drugs with which to
treat schizophrenia, I would have thought even Dr
McLaren would be in favour of ideas being developed
and discussed in this important area of pharmacology.
In closing, I would like to correct another error made
by Dr McLaren. I am not a psychiatrist, I am a biologist who chooses to use my expertise in attempting to
understand the processes that precipitate schizophrenia.
Unfortunately, I have not looked down a microscope in
many years, but I have certainly looked away from whatever technology I am using in an attempt to appreciate
and understand the views of others. Perhaps this would
be a good ethos for the ‘mind over brainers’ to adopt
when reading reviews of other areas within the broad
horizons of psychiatric research.
References
1.

2.

3.

4.

5.

Dean B. Signal transmission, rather than reception, is the
underlying neurochemical abnormality in schizophrenia.
Australian and New Zealand Journal Psychiatry 2000;
34:560–569.
McLaren N. Is mental disease just brain disease? The limits to
biological psychiatry. Australian and New Zealand Journal of
Psychiatry 1992; 26:270–276.
McLaren N. A critical review of the biopsychosocial model.
Australian and New Zealand Journal of Psychiatry 1998;
32:86–92.
Eccles JC. Do mental events cause neural changes analogously
to the probability of quantum mechanics? Proceedings of the
Royal Society of London, Series B, Biological Science 1986;
227:411–428.
Eccles JC. Evolution of consciousness. Proceedings of the
National Academy of Sciences 1992; 89: 7320–7324.

Maintenance electroconvulsive therapy in
schizophrenia
John Stevens, Peter Cheung, Tim Lambert, Melbourne,
Australia:

The role of electroconvulsive therapy (ECT) is recognized in acute schizophrenia, and as an alternative to
antipsychotics in patients with treatment-resistant schizophrenia [1]. However, the use of maintenance electroconvulsive therapy (M-ECT) is less well defined. Our
Index Medicus/Medline search found only 12 reports of
M-ECT in schizophrenia; only six of them specifically
describe its use in schizophrenia [2], and only two are
systematic research studies.

One study compared continuation electroconvulsive
therapy (C-ECT) alone, with combination C-ECT and
flupenthixol, and flupenthixol alone [2]. In this study, a
significant relapse rate of 93% was noted with the use of
either flupenthixol or C-ECT alone compared with only
a 40% relapse rate following combination of C-ECT
and flupenthixol. It should be noted that C-ECT was
only given weekly for 4 weeks, and then bi-weekly
for 5 months (total 14 C-ECT treatments), which may
explain the high rate of relapse with C-ECT.
The other study was a retrospective study with a mixed
sample [3]. However, those with a diagnosis of schizophrenia alone (three patients) received a longer course of
M-ECT than patients in the previous study [2], in the
order of 35–88 ECT treatments. The three patients were
reported to have made significant improvement in the
areas of level of functioning, discharge after prolonged
hospitalization or reduction in aggression. We would like
to report a patient who has required ongoing ECT treatment to avert deterioration of his mental state.
Mr L was a 50-year-old, separated man on a disability
support pension living in supported accommodation.
He had a 34-year history of chronic, paranoid, treatment-resistant schizophrenia with significant history of
violence. He was first diagnosed at age 16, and required
multiple prolonged admissions during his late teens and
first 10 years of his adult life. He was reasonably stable
between the ages of 28 and 38 with regular fluphenazine decanoate. However, following the transfer
of his care to his general practitioner, he missed his
depot medication and deteriorated rapidly, presenting
with acute psychotic symptoms, disinhibition, verbal
and physical aggression.
Over the next 6 months, he was admitted on five occasions to acute psychiatric units. Multiple agents including atypical antipsychotics in combination with depot
antipsychotics were utilized with virtually no response.
However, he did respond satisfactorily, albeit briefly, to
short courses of ECT (usually 5–6 treatments) with disappearance of psychotic symptoms and physical aggression. The latter were important target symptoms as there
was considerable concern over the potential for violence
in this situation of manifest treatment resistance.
During his last admission, Mr L was transferred to a
secure extended care ward with the aim of commencing
him on clozapine. He remained there for the next
12 months. Unfortunately, he developed clozapineinduced neutropenia and clozapine was ceased. The
patient, in addition to his already established treatmentresistant schizophrenia, then developed a super-sensitivitylike exacerbation of his psychosis on withdrawal of the
clozapine. Over this period, he received regular short
courses of ECT, but deteriorated rapidly each time upon

CORRESPONDENCE

cessation. Hence, he was prescribed M-ECT, initially
weekly. He suffered from confusion (for a couple of days
after ECT) and short-term memory impairment, but no
other side-effects of the M-ECT.
Mr L was successfully discharged after receiving 42
treatments. He lives alone with intensive case management, and receives M-ECT 4-weekly (66 treatments to
date). His improvement has been sustained. He no longer
has confusion or memory impairment.
In conclusion, M-ECT has substantially improved
Mr L’s function and independence. Questions are how
long to continue M-ECT and at what frequency? Mr L
himself is keen to have ECT treatment terminated.
References
1.
2.

3.

Fink M, Sackheim HA. Convulsive therapy in schizophrenia?
Schizophrenia Bulletin 1996; 220:27–39.
Chanpattona W, Chakrabhand MLS, Sackheim HA et al.
Continuation ECT in treatment-resistant schizophrenic:
a controlled study. Journal of ECT 1999; 15:178–192.
Stiebel VG. Maintenance electroconvulsive therapy for chronic
mentally ill patients: a case series. Psychiatric Services 1995;
46:765–268.

Uncommon self-mutilation in a borderline
personality disorder patient
Jens D. Rollnik, Department of Neurology and Clinical
Neurophysiology, Udo Schneider, Felix Wedegaertner,
Thomas J. Huber, Hinderk M. Emrich, Department of
Clinical Psychiatry and Psychotherapy, Medical School of.
Hanover, Hanover, Germany:

Self-mutilation (SM) might be understood as a morbid
self-help effort providing rapid but temporary relief from
feelings of depersonalisation, guilt, rejection and
boredom, as well as hallucinations, sexual preoccupations and chaotic thoughts [1]. Self-mutilation in patients
suffering from borderline personality disorder is common,

133

occurring in up to 50% [2]. Therapeutic approaches to
self-injurious behaviour employ opioid antagonists [3],
neuroleptics such as clozapine and risperidone [4], and
behavioural treatment [5].
We report on a 26-year-old woman with a borderline
personality disorder associated with anorexia nervosa and
substance abuse (diazepam, alcohol) for 7 years. Selfmutilation started in 1996 with a delusion of dermatozoonosis. She started scratching only one place on her
head. Several dermatologic consultants could not find an
organic cause. Wound infections and an osteomyelitis of
the skull bone lead to a large tissue defect in 1998 (about
5 × 2 cm). In April 2000 our patient experienced a minor
head injury. She was admitted to a neurologic clinic with
symptomatic focal epilepsy, global aphasia and right
hemiparesis. Magnetic resonance imaging revealed the
large tissue defect with skull bone damage and intracerebral air inclusion left frontoparietal (Fig. 1). The patient
underwent surgery to cover the wound. Hemiparesis and
aphasia improved and she was discharged after wound
healing. Further therapy was refused.
The bad course of the disease in our patient underlines
the necessity of further scientific work to improve the
understanding of SM. Dermatologists should be aware of
symptoms such as delusion of dermatozoonosis to enable
early psychiatric intervention.
References
1.
2.

3.

Favazza AR. The coming age of self-mutilation. Journal of
Nervous and Mental Disease 1998; 186:259–268.
Dulit RA, Fyer MR, Leon AC, Brodsky BS, Frances AJ.
Clinical correlates of self-mutilation in borderline personlity
disorder. American Journal of Psychiatry 1994;
151:1305–1311.
Thompson T, Hackenberg T, Cerutti D, Baker D, Axtell S. Opiod
antagonist effects on self injury in adults with metal retardation:
response from and location as determinants of medication
effects. American Journal of Mental Retardation 1994;
99:85–102.

Figure 1. Magnetic resonance imaging of the patient’s head. The skull bone is damaged and there are intracerebral
air inclusions

134

4.

CORRESPONDENCE

Chengappa KN, Ebeling T, Kang JS, Levine J, Parepally H.
Clozapine reduces severe self-mutilation and aggression in
psychotic patients with borderline personality disorder. Journal
of Clinical Psychiatry 1999; 60:477–484.

5.

Bloxham G, Long CG, Alderman N, Hollin CR. The behavioral
treatment of self-starvation and severe self-injury in a patient
with borderline personality disorder. Journal of Behavioral
Therapy and Experimental Psychiatry 1993; 24:261–267.

Note
Last year we published a letter ‘Neuroleptic rechallenge following neuroleptic malignant syndrome’ by
Raju GVL, Ramesh Kumar TC and Khanna S (p.700). Our apologies to the authors of this letter for the
incorrect presentation of their names.