Case Report
Psychopathology 2003;36:218–220
DOI: 10.1159/000072793
Received: August 28, 2002
Accepted: April 10, 2003
Delusional Paralysis: An Unusual
Variant of Cotard’s Syndrome
Andreas Reif Waldemar M. Murach Bruno Pfuhlmann
Department of Psychiatry and Psychotherapy, University of Würzburg, Würzburg, Germany
Key Words
Coenaesthesic hallucination W Cotard’s syndrome W
Delusional disorder W Electroconvulsive therapy W
Nihilistic ideas W Nosology W Psychotic depression
Abstract
Cotard’s syndrome, a highly impressive psychopathological condition, occurs mainly in depressive disorders
and entails nihilistic delusions concerning the body and
the non-existing of the self as outstanding features,
accompanied by hypochondriacal delusions and ideas of
guilt as well as immortality. We here report on a female
patient presenting with an unusual variant of the syndrome: most prominently, she had the delusion to be
paralysed, although displaying psychomotor agitation,
and that neuroleptic agents had devoured her nerve ganglia. Upon ECT, symptoms rapidly improved. Psychopathological implications and the nosological position of
Cotard’s syndrome are discussed.
Copyright © 2003 S. Karger AG, Basel
Introduction
Among the generally astonishing uncommon psychiatric syndromes, Cotard’s syndrome (which he himself
termed ‘le délire de négation’, coming close to the English
translation ‘delusional nihilism’) is one of the most fascinating disorders in both psychological and philosophical
terms. Cotard listed the following symptoms of the syn-
ABC
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drome: anxious melancholy, ideas of damnation or possession, a tendency for self-mutilation or suicide, hypochondriac ideas about the non-existence or destruction of
inner organs or the whole body, and the idea that one cannot die [1]. The key feature, however, is the delusional
belief that parts of the patient’s body or organs are missing
or malfunctioning. This is often described with bizarre
comparisons, which can extent to the conviction of one’s
own death or non-existence. How can a person deny his
own existence? This question reflects the intriguing enigma of Cotard’s delusion, resembling an existentialist variant of Epimenides’s paradoxon (Epimenides was the Cretan who coined the famous sentence ‘All Cretans are
liars’). Thus, Cotard’s delusion is not the only self-verifying delusion as Pearn at al. [2] suggested, but in fact a
self-falsifying delusion and therefore a paradoxon.
Cotard’s syndrome can present in many and astonishing clinical pictures, and there is even a manic variant
incorporating megalomaniac ideas with bodily illusions of
enormity [3]. Depressive ideas, apart from the nihilistic
delusion of being dead, include the patients’ denial of the
world’s existence, the plea to be buried because the
patients believe they are a rotting corpse, the conviction
that their bowels and stomach are lacking or that even
most parts of their body do not work (examples taken
from Enoch and Ball [3]). Here we present a remarkable
case of delusional paralysis, which has so far not been
described in the literature to this extent and once more
demonstrates the amazing multi-facetted appearance of
Cotard’s syndrome.
Andreas Reif
Department of Psychiatry and Psychotherapy
University of Würzburg, Füchsleinstrasse 15
DE–97080 Würzburg (Germany)
Tel. +49 931 201 76000, Fax +49 931 201 77550, E-Mail a.reif@gmx.net
Case Report
Discussion
Ms P., a 71-year-old retired teacher, had no history of psychiatric
illness until the age of 69. Following a suicide attempt, she had been
admitted to hospital; she complained of sleep disturbances, restlessness and hypochondriac ideas, and she was described as lamenting. A
diagnosis of adjustment disorder and histrionic-anancastic disorder
was applied. Following anti-depressant and neuroleptic treatment,
she was discharged as almost recovered, however, she soon had to be
readmitted due to somatoform symptoms (mainly concerning pollakisuria), which she again described in an anxious and lamenting
manner. Furthermore, she worried about stiffness (which could not
be objectified), attributed by her to neuroleptic treatment, connected
with the fear that her hands had to be amputated and that medical
insurance would not pay for treatment. During in-patient treatment,
she attempted suicide twice (by means of intoxication and attempted
drowning), albeit rather demonstrative. As her condition did not
resolve following treatment with lorazepam, risperidone, mirtazapine and trimipramine, she was referred to our department for further diagnostic evaluation.
On admission, we saw a well-nourished lady with no prominent
cognitive-mnestic deficits or major physical disease apart from severe
presbyacusis. Her family history was positive in that her brother had
suffered from depression and committed suicide. She complained constantly that both her legs and arms were paralysed, resulting in an
inability to move, so that she feared that her extremities had to be
amputated and that thereafter she would be damned to live as a ‘helpless torso’. She claimed that the cause for this were neuroleptics still
circulating in her blood vessels and devouring her nerve cells, which she
could sense in her arms; she stated that she was no longer sure whether
she was still alive. The only treatment possible would be instant dialysis. These delusional beliefs were held with unshakable conviction; in a
letter, she wrote: ‘My feet and legs, my hands, my cervical vertebra
head and my back are paralysed by drugs. Paralysis of the back of the
head is yet sensible. If the paralysis progresses, I fear my hands, feet and
legs will have to be amputated.’ In striking contrast to her complaints,
she was psychomotorically agitated and far from being paralysed. Further psychopathological symptoms were logorrhea, lamenting and
depressive mood, although she stated not to suffer from depression.
Other depressive ideas were present, e.g. that she had to be imprisoned
because of tax fraud and that she was afraid of being entombed alive
with a plug in her mouth.
Extended laboratory tests, including auto-antibodies, GAD-IIantibodies and amphyphysine-antibodies (to rule out stiff-man syndrome), did not reveal gross abnormalities, neither did ECG, EEG,
SEP and cranial MRI. The patient refused lumbar puncture and PET
scanning. We initiated treatment with amitryptiline and olanzapine,
which slightly relieved her agitation but brought about no change
with respect to her delusions of being paralysed. Thus electroconvulsive therapy (ECT) was applied, which was well tolerated and proved
to be effective: following 8 treatments, Ms P. stated not to suffer any
longer from paralysis, and other delusional contents or depressive
ideas had also disappeared. Her mood was well, and she proved to be
a witty and charming lady, sharply contrasting her personality on
admission. She received maintenance therapy with olanzapine and
mirtazapine after ECT discontinuation, and her situation had not
deteriorated by the 5-week follow-up. Slight cognitive deficits could
be observed, such as affective lability, loss of distance and mental
rigidity, so we applied the ICD-10 diagnosis of organic affective disorder.
To the best of our knowledge, this is the first report on
delusional paralysis in medical literature. Strikingly, the
delusion was held with unshakable belief against all overt
evidence, i.e. psychomotor agitation. We feel that it is justified to regard the symptomatology of Ms P. as a variant
of Cotard’s syndrome: the delusional content was of the
nihilistic and hypochondriacal type (she thought that
parts of her body did not function well, feared to be buried
alive, and was at times not sure whether she was still living or not), accompanied by ideas of guilt and agitated
depression. Characteristically, the syndrome had been of
sudden onset, without a previous history of psychiatric
disorder but a typical period of initial anxiety. Thus our
patient featured the most frequent symptoms of Cotard’s
syndrome as reported by Berrios and Luque [4]. A predominance of women in their later years has been reported [3], as was Ms P., and she presented with clinical
evidence of the organic substrates suggested to play a role
in Cotard’s delusion [5]. As suggested by other authors
[6–8], ECT proved to be an efficient and well-tolerated
treatment with sustained efficacy.
There is considerable debate whether Cotard’s delusion is syndromal in nature or a distinct nosological entity. Based on a literature survey of 100 cases, Berrios and
Luque [4] reported three basic factors of nihilistic delusion by means of a factor analysis, arguing for nosological
unspecificity: psychotic depression, Cotard type I (which
resembles a pure form of the syndrome, closer to delusional than to affective disorder) and Cotard type II (which
constitutes a mixed group, displaying symptoms of the
schizophrenic spectrum as well as of affective psychoses).
Following this factor-analytic approach, our patient most
likely belongs to the ‘psychotic depression’ type. The
authors agree with Enoch and Ball [3] that Cotard’s delusion, defined narrowly, represents a highly specific and
clear-cut syndrome, not a distinct nosological entity.
However, the most challenging question concerns the
neurobiological underpinnings of nihilistic delusions.
There are two psychopathological key symptoms that
might help to elucidate this. First, there appears to be a
connection between Cotard’s syndrome (in its narrower
definition) and depression, which is primarily a disorder
of the thymopsyche. Depressive patients often claim to
feel nothing at all, a condition which bears some similarity to the negation of one’s own existence; furthermore,
depression often goes along with somatic symptoms. Second, Cotard’s delusion is accompanied by erroneous beliefs about the own body, often including inner organs,
Delusional Paralysis
Psychopathology 2003;36:218–220
219
but – as our case demonstrates – also extremities and thus
visible body parts. These misperceptions do not seem to
be of the coenaesthetic-hallucinatory type seen in schizophrenic disorders: the patient states that his organs do not
function, have disappeared, etc., but usually he does not
claim to actually feel this, which raises the question
whether the patient suffers from wrong perceptions or
from wrong judgements about his somatic state. This very
specific symptom of Cotard’s syndrome differentiates it
from coenaesthetic schizophrenia, and it suggests that the
biological substrate of the delusion does not primarily
involve the sensory perception of the body. Rather, it
seems to involve a disordered somatopsyche, a term
coined by Wernicke [9] to designate the concept of an
integrating self-consciousness of the body. This prompts
the question which associations between malfunctions of
the somatopsyche and thymopsyche exist, and if and how
both play a part in Cotard’s syndrome.
An interesting, albeit highly speculative hypothesis to
resolve this issue is based on Damasio’s theory of emotion
and consciousness [10, 11]. Briefly (and very much simplified), Damasio proposes that sensory input from the
body is represented in neuronal maps which are inter alia
the basis for emotions, which, in turn, assist in generating
what Damasio terms ‘extended consciousness’. Damasio
pointed out a remarkable functional cross-over of the
brain stem and cingulate cortex in regulating homeostasis,
body perception, emotion, arousal, learning and consciousness. According to his theories, any disturbance of
those second-order neuronal maps of body perception –
the functional basis of the ‘somatopsyche’ – will lead to
specific changes in the subject’s emotions (the ‘thymopsyche’) and, eventually, in the person’s consciousness or
self-awareness. In terms of classic psychopathology (along
the lines of Wernicke) one could here postulate a specific
association between the somatopsyche and the auto-
psyche representing the consciousness of one’s body and
personal integrity – in contrast to the allopsyche, which
represents the consciousness of the external world. We
thus hypothesise that, in Cotard’s syndrome, the primary
defect is a functional disturbance in sensory second-order
neuronal maps or their integration, i.e. a somatopsychic
disturbance, leading to emotional disorder and, in severe
cases, to specific changes in consciousness – which psychopathologically imposes as the conviction to be nonexisting. Therefore, the most interesting anatomical target
structure for Cotard’s delusion would be, in our opinion,
the cingulate gyrus, integrating input from visceral organs
and the musculoskeletal system as well as playing a role in
emotions and consciousness.
Independently of the postulated neurobiological correlates, Cotard’s syndrome seems to be a nosologically
inconsistent condition. In the majority of cases, it could
be interpreted as a form of depressive delusional ideas
associated with other depressive symptoms. In some
cases, an association with megalomaniac ideas (délire
d’énormité) is described, where the megalomaniac ideas
are typically of a very extreme character, including absurdities like the merging of one’s body with the whole universe [3]. Such symptoms can typically be seen in specific
forms of schizophrenic psychoses, e.g. phantastic paraphrenia according to Leonhard’s differentiated nosology
[12]. On the other hand, in anxiety psychosis, a subform
of Leonhard’s cycloid psychoses, states of extreme anxiety, with ideas of threat and annihilation, may occur,
leading to transient nihilistic delusions. Thus Cotard’s
syndrome, in our opinion, represents a symptomatologically highly impressive and interesting but nosologically
non-specific condition. However, its investigation should
be pursued as it could yield important insights into the
psychobiological underpinnings of psychopathological
symptoms.
References
1 Cotard J: Du délire des négations. Arch Neurol
(Paris) 1882;6:209–295.
2 Pearn J, Gardner-Thorpe C: Jules Cotard
(1840–1889): His life and the unique syndrome
which bears his name. Neurology 2002;58:
1400–1403.
3 Enoch D, Ball H: Uncommon Psychiatric Syndromes, ed 4. London, Arnold, 2001.
4 Berrios GE, Luque R: Cotard’s syndrome:
Analysis of 100 cases. Acta Psychiatr Scand
1995;91:185–188.
220
5 Joseph AB, O’Leary DH: Brain atrophy and
interhemispheric fissure enlargement in Cotard’s syndrome. J Clin Psychiatry 1986;47:
518–520.
6 Petracca G, Migliorelli R, Vazquez S, Starkstein SE: SPECT findings before and after ECT
in a patient with major depression and Cotard’s syndrome. J Neuropsychiatry Clin Neurosci 1995;7:505–507.
7 Lohmann T, Nishimura K, Sabri O, Klosterkotter J: Successful electroconvulsive therapy
of Cotard syndrome with bitemporal hypoperfusion. Nervenarzt 1996;67:400–403 [in German].
Psychopathology 2003;36:218–220
8 Yamada K, Katsuragi S, Fujii I: A case study of
Cotard’s syndrome: Stages and diagnosis. Acta
Psychiatr Scand 1999;100:396–398.
9 Wernicke C: Grundriss der Psychiatrie in klinischen Vorlesungen, ed 2. Leipzig, Thieme,
1906.
10 Damasio AR: The Feeling of What Happens:
Body and Emotion in the Making of Consciousness, ed 1. London, Heinemann, 2000.
11 Damasio AR: Descartes’ Error: Emotion, Reason, and the Human Brain, ed 1. New York,
Putnam, 1994.
12 Leonhard K: The Classification of Endogenous
Psychoses, ed 5. New York, Irvington, 1979.
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