Pseudoneurotic schizophrenia revisited

Karen O. Connor, Barnaby Nelson, Mark Walterfang, Dennis Velakoulis,

Andrew Thompson

Objectives: ‘Pseudoneurotic schizophrenia’ was a diagnostic term coined in the 1940s by

Hoch and Polatin. It described a subgroup of patients who presented with prominent
anxiety symptoms, which masked a latent psychotic disorder. Pseudoneurotic
schizophrenia as a diagnostic entity has fallen out of clinical use.
Methods: Described herein is a case that meets the Hoch and Polatin definition of
pseudoneurotic schizophrenia.
Results: The history of the concept is reviewed and a discussion is given of why it was
forgotten.
Conclusion: The concepts that underlie the diagnostic entity of pseudoneurotic
schizophrenia remain relevant to current practice. Recent findings in patients with an
emerging psychotic disorder lend modern support to the idea that schizophrenia may
present with significant neurotic symptoms
Key words: anxiety, borderline, pseudoneurotic, psychosis, schizophrenia.

Australian and New Zealand Journal of Psychiatry 2009; 43:873 876

‘Pseudoneurotic schizophrenia’ was a diagnostic Case report
term described in the 1940s by Hoch and Polatin to
describe a subgroup of patients who presented with The patient was a 22-year-old unemployed man
prominent anxiety symptoms, which masked a latent living with his brother. He was referred to the
psychotic disorder [1]. Pseudoneurotic schizophrenia psychiatric crisis team via the emergency department,
as a diagnostic entity, however, has fallen out of having presented with a panic attack.
clinical use and is not part of current classification At assessment he described a 6 month history of
systems. We describe a case that meets the Hoch and worsening low mood, insomnia, anhedonia, anergia,
Polatin definition of pseudoneurotic schizophrenia, poor concentration and memory. He reported a
review the history of the concept and why it was number of somatic concerns, including constant
forgotten. Significantly, recent findings in patients thirst, neck lumps, unsteadiness of gait and concerns
with an emerging psychotic disorder lend modern that he may have acquired immunodeficiency syn-
support to the idea that schizophrenia may present drome (AIDS) or cancer. He was preoccupied with
with significant neurotic symptoms. the idea that he was dying. His first panic attack,
which precipitated his referral, lasted 1 h and was
Karen O. Connor, Psychiatry Registrar (Correspondence); Barnaby
characterized by a discrete episode of sudden-onset
Nelson, Clinical Psychologist and Research Fellow; Andrew Thompson, shortness of breath, increased heart rate, diaphoresis
Consultant Psychiatrist and Honorary Senior Research Fellow
and perceived chest tightness.
ORYGEN Youth Health, Poplar Road, Parkville, Vic. 3052, Australia.
Email: karenoconnor2@hotmail.com Pre-morbidly, the patient was reported to be a very
Mark Walterfang, Consultant Neuropsychiatrist and Research Fellow; bright student but there had been a marked decline in
Dennis Velakoulis, Consultant Neuropsychiatrist and Clinical Director his functioning since his final year of schooling. He
Neuropsychiatry Unit, Royal Melbourne Hospital, Melbourne, Victoria, had been employed full-time as a shift worker in a
Australia
factory until 2 months prior to presentation but had
Received 29 April 2009; accepted 5 May 2009.

# 2009 The Royal Australian and New Zealand College of Psychiatrists

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874 PSEUDONEUROTIC SCHIZOPHRENIA REVISITED

resigned, reporting that the work was too stressful. Over the course of his outpatient therapy sessions
His father had a diagnosis of schizophrenia. the patient described an array of anomalous sub-
Mental state examination indicated a pleasant and jective experiences during his catatonic episode,
cooperative young man who frequently appeared which he continued to experience in attenuated
perplexed. His affect was flat. His speech was form and which he reported as having been present
coherent but with increased latency of response, to some extent throughout his life. These experiences
reduced rate and poverty of content. He was tangen- included prominent depersonalization experiences,
tial with pessimistic thought content and overvalued such as not feeling present in his body or feeling as
almost delusional ideas of guilt, failure and physical though his centre of experience was ‘20 cm behind’
ill health. There was no cognitive impairment evident his physical body. He described derealization experi-
on bedside assessment. He minimized the extent to ences, including a sense that the world and people
which mental illness was contributing to his situation, around him were not entirely real, but may have been
and attributed his state to an unrecognized medical figments of his imagination. He experienced enor-
condition. The physical examination, neuroimaging, mous difficulty ‘thinking clearly’ and choosing be-
routine biochemical and serological screening were tween different options. Cognitive processes felt like
unremarkable. they required ‘a lot more effort’, prompting him to
The patient was diagnosed with a severe depressive ‘give up’ and remain immobile and unresponsive. The
disorder with possible psychotic symptoms and was patient described a number of perceptual distur-
commenced on fluoxetine 20 mg. The following bances, such as focusing on parts of a scene rather
weeks saw deterioration in his mental state with than seeing it as a whole. For example, he saw faces
increased psychomotor retardation, increased preoc- as an assortment of individual features, rather than
cupation with somatic complaints and dying, and seeing them as unitary wholes. He explained that ‘it
discrete periods of time when he was uncommunica- [faces] wasn’t expression, wasn’t human anymore, I
couldn’t know whether somebody was annoyed or
tive. He exhibited thought blocking and catatonic
happy, they were disconnected parts.’
symptoms of posturing, motor stereotypies and
In summary this 22-year-old man presented with
echolalia. The dose of fluoxetine was increased to
prominent anxiety, panic attacks, fear about dying,
60 mg and he was commenced on quetiapine (400 mg)
overvalued hypochondriacal beliefs, thought block-
and diazepam (5 mg bid). The quetiapine was chan-
ing and low mood. Subsequently he developed
ged to risperidone (0.5 mg) due to intolerable side-
catatonic symptoms with impaired ability to commu-
effects including dizziness, weakness and stiffness.
nicate with those around him, perplexity, limb
The patient developed a dystonic reaction and
posturing and echolalia. All of this occurred on a
risperidone was discontinued. He was discharged on background of a 3 year functional decline in
fluoxetine 60 mg with improved mood but continued a previously bright intellectual young man with a
somatic concerns regarding headache, generalized family history of schizophrenia. His low mood
numbness and leg weakness. responded to antidepressants but his anxiety symp-
The patient’s mental state continued to decline and toms, impaired concentration and thought disorder
he had a planned admission to a neuropsychiatry unit worsened and his somatic concerns reached delu-
for assessment and diagnostic clarification given his sional intensity. The addition of olanzapine resulted
reported neurological and catatonic symptoms. Dur- in a dramatic improvement in all symptoms, includ-
ing this neuropsychiatric evaluation he was diagnosed ing his anxiety.
with a primary psychotic illness with prominent The patient’s presentation initially appeared con-
anxiety symptoms, consistent with the Hoch and sistent with a depressive disorder with psychotic
Polatin description of pseudoneurotic schizophrenia, symptoms. But although his depressive symptoms
and commenced on olanzapine, which was titrated up responded to antidepressants his psychotic symptoms
to 15 mg. The patient became more reactive and less worsened, as did his anxiety symptoms. Furthermore
anxious, with marked improvement in his ability to his 3 year history of functional decline, social with-
concentrate. His catatonic symptoms abated, as did drawal, neurocognitive changes and deteriorating
his thought disorder. His somatic concerns remained self-care were more in keeping with a schizophrenic
but decreased in intensity. He has retained illness rather than an affective one. Another
this improvement and currently reports no psychotic differential diagnosis was that of a somatoform
or depressive symptoms and his functioning disorder with a comorbid depression, but his gender,
has improved. the chronology and full profile of symptoms,

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 K.O. CONNOR, B. NELSON, M. WALTERFANG, D. VELAKOULIS, A. THOMPSON 875

neuropsychological changes plus the failed response ‘Borderline’ was a term that originally arose in the
to antidepressants but dramatic response to antipsy- late 1800s to denote conditions in the borderland
chotics were not consistent with this diagnosis. between psychosis and the milder neurosis [6]. The
The view that the patient was suffering from a evolution of the ‘borderline’ concept, however, has
psychotic disorder, particularly a schizophrenia spec- seen it largely lose this original meaning. In the 1920s
trum disorder, is further supported by his anomalous ‘borderline’ was used to refer to the perceived
subjective experiences, as outlined in the previous unalysability of patients with psychosis versus those
section. Such experiences have been termed ‘basic with a neurotic illness [7]. Only with the publication of
symptoms’ and have been found to be present in Kernberg’s paper ‘Borderline personality organiza-
prodromal, acute and remitted phases of psychotic tion’ (BPO) in 1967 was the term ‘personality’
disorders, particularly schizophrenia spectrum condi- introduced [5]. Kernberg described a condition that
tions [2
4]. was distinct from both higher neurotic functioning
and lower psychotic functioning. In BPO, reality
testing was preserved (albeit with a tendency to
Discussion over-valued ideas in certain emotionally laden areas)
but identity-sense was weakened. ‘Borderline’, and the
Hoch and Polatin proposed that a subgroup of terms with which it had become synonymous, includ-
patients may present with a constellation of symp- ing ‘pseudoneurotic schizophrenia’, had now become
toms, which initially appear to be neurotic in nature completely decoupled from psychosis and schizophre-
but occur in the context of a psychotic disorder. They nia. When borderline personality disorder was finally
described that a diagnosis of pseudoneurotic schizo- introduced into the DSM-III in 1980 the diagnosis
phrenia was warranted in the presence of primary was formulated predominantly in terms of mood and
clinical symptoms of schizophrenia and secondary behaviour, distinguished from subsyndromal schizo-
symptomatology (Table 1). Not all symptoms needed phrenia, which was termed ‘schizotypal personality
to be present for the diagnosis. disorder’ [8].
The present patient had symptoms in all three of Although many of those previously diagnosed with
the primary symptoms category including (i) thought pseudoneurotic schizophrenia may have had a bor-
disorder; (ii) low mood; and (iii) altered temperature derline personality disorder, a 10 year follow-up
perception and generalized weakness with prominent study published in 1962 showed that 20% of patients
secondary symptoms including panic attacks, gener- with pseudoneurotic schizophrenia transitioned to
alized anxiety and specific health anxieties. conventional schizophrenia [9]. It appears, however,
Pseudoneurotic symptoms sit on the borderline that in the evolution of the concepts of pseudoneuro-
between psychosis and neurosis [5]. Indeed by the tic and borderline this psychotic group became
late 1960s pseudoneurotic schizophrenia became al- neglected. The operationalization of schizophrenia
most synonymous with the term ‘borderline states’. further compounded this neglect. Many features
Consideration of this synonymy and the evolution of previously considered characteristic of subschizo-
the term ‘borderline states’ is key in explaining how phrenic conditions disappeared from psychiatric
the concepts underlying pseudoneurotic schizophre- literature [10]. These features including the ‘pseudo-
nia came to be neglected in modern diagnostic neurotic’ symptoms were increasingly neglected by
manuals. clinicians and researchers trained in the era of DSM-
III and beyond. But this progressively spreading
amnesia coupled with the emerging interest in the
groups at ultra-high risk (UHR) for psychosis,
Table 1. Diagnosis of pseudoneurotic schizophrenia
functions as a driving force behind comorbidity
studies, rediscovering and elaborating on the links
Primary clinical symptoms previously described in the prototypical approach to
1. Disorders of thinking and association: process; content diagnosis [11].
2. Disorders of emotional regulation: form; content
3. Disorders of sensorimotor and autonomic functioning Freeman and Garety put forward a direct, non-
Secondary clinical symptoms defensive role for psychosis in emotional dysregula-
1. Pan-anxiety tion, and the growing evidence for this hypothesis is
2. Pan-neurosis: neurotic symptomatology, acting out
such that researchers have proposed that distress,
behaviour and character disorder symptoms
3. Pan-sexuality anxiety, depression and other forms of emotional
disturbance may play a major role in determining

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876 PSEUDONEUROTIC SCHIZOPHRENIA REVISITED

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