Abstract
‘Pseudoneurotic schizophrenia’ was a diagnostic term described in the 1940s by Hoch and Polatin to describe a subgroup of patients who presented with prominent anxiety symptoms, which masked a latent psychotic disorder [1]. Pseudoneurotic schizophrenia as a diagnostic entity, however, has fallen out of clinical use and is not part of current classification systems. We describe a case that meets the Hoch and Polatin definition of pseudoneurotic schizophrenia, review the history of the concept and why it was forgotten. Significantly, recent findings in patients with an emerging psychotic disorder lend modern support to the idea that schizophrenia may present with significant neurotic symptoms.
Case report
The patient was a 22-year-old unemployed man living with his brother. He was referred to the psychiatric crisis team via the emergency department, having presented with a panic attack.
At assessment he described a 6 month history of worsening low mood, insomnia, anhedonia, anergia, poor concentration and memory. He reported a number of somatic concerns, including constant thirst, neck lumps, unsteadiness of gait and concerns that he may have acquired immunodeficiency syndrome (AIDS) or cancer. He was preoccupied with the idea that he was dying. His first panic attack, which precipitated his referral, lasted 1 h and was characterized by a discrete episode of sudden-onset shortness of breath, increased heart rate, diaphoresis and perceived chest tightness.
Pre-morbidly, the patient was reported to be a very bright student but there had been a marked decline in his functioning since his final year of schooling. He had been employed full-time as a shift worker in a factory until 2 months prior to presentation but had resigned, reporting that the work was too stressful. His father had a diagnosis of schizophrenia.
Mental state examination indicated a pleasant and cooperative young man who frequently appeared perplexed. His affect was flat. His speech was coherent but with increased latency of response, reduced rate and poverty of content. He was tangential with pessimistic thought content and overvalued almost delusional ideas of guilt, failure and physical ill health. There was no cognitive impairment evident on bedside assessment. He minimized the extent to which mental illness was contributing to his situation, and attributed his state to an unrecognized medical condition. The physical examination, neuroimaging, routine biochemical and serological screening were unremarkable.
The patient was diagnosed with a severe depressive disorder with possible psychotic symptoms and was commenced on fluoxetine 20 mg. The following weeks saw deterioration in his mental state with increased psychomotor retardation, increased preoccupation with somatic complaints and dying, and discrete periods of time when he was uncommunicative. He exhibited thought blocking and catatonic symptoms of posturing, motor stereotypies and echolalia. The dose of fluoxetine was increased to 60 mg and he was commenced on quetiapine (400 mg) and diazepam (5 mg bid). The quetiapine was changed to risperidone (0.5 mg) due to intolerable side-effects including dizziness, weakness and stiffness. The patient developed a dystonic reaction and risperidone was discontinued. He was discharged on fluoxetine 60 mg with improved mood but continued somatic concerns regarding headache, generalized numbness and leg weakness.
The patient's mental state continued to decline and he had a planned admission to a neuropsychiatry unit for assessment and diagnostic clarification given his reported neurological and catatonic symptoms. During this neuropsychiatric evaluation he was diagnosed with a primary psychotic illness with prominent anxiety symptoms, consistent with the Hoch and Polatin description of pseudoneurotic schizophrenia, and commenced on olanzapine, which was titrated up to 15 mg. The patient became more reactive and less anxious, with marked improvement in his ability to concentrate. His catatonic symptoms abated, as did his thought disorder. His somatic concerns remained but decreased in intensity. He has retained this improvement and currently reports no psychotic or depressive symptoms and his functioning has improved.
Over the course of his outpatient therapy sessions the patient described an array of anomalous subjective experiences during his catatonic episode, which he continued to experience in attenuated form and which he reported as having been present to some extent throughout his life. These experiences included prominent depersonalization experiences, such as not feeling present in his body or feeling as though his centre of experience was ‘20 cm behind’ his physical body. He described derealization experiences, including a sense that the world and people around him were not entirely real, but may have been figments of his imagination. He experienced enormous difficulty ‘thinking clearly’ and choosing between different options. Cognitive processes felt like they required ‘a lot more effort’, prompting him to ‘give up’ and remain immobile and unresponsive. The patient described a number of perceptual disturbances, such as focusing on parts of a scene rather than seeing it as a whole. For example, he saw faces as an assortment of individual features, rather than seeing them as unitary wholes. He explained that ‘it [faces] wasn't expression, wasn't human anymore, I couldn't know whether somebody was annoyed or happy, they were disconnected parts.’
In summary this 22-year-old man presented with prominent anxiety, panic attacks, fear about dying, overvalued hypochondriacal beliefs, thought blocking and low mood. Subsequently he developed catatonic symptoms with impaired ability to communicate with those around him, perplexity, limb posturing and echolalia. All of this occurred on a background of a 3 year functional decline in a previously bright intellectual young man with a family history of schizophrenia. His low mood responded to antidepressants but his anxiety symptoms, impaired concentration and thought disorder worsened and his somatic concerns reached delusional intensity. The addition of olanzapine resulted in a dramatic improvement in all symptoms, including his anxiety.
The patient's presentation initially appeared consistent with a depressive disorder with psychotic symptoms. But although his depressive symptoms responded to antidepressants his psychotic symptoms worsened, as did his anxiety symptoms. Furthermore his 3 year history of functional decline, social withdrawal, neurocognitive changes and deteriorating self-care were more in keeping with a schizophrenic illness rather than an affective one. Another differential diagnosis was that of a somatoform disorder with a comorbid depression, but his gender, the chronology and full profile of symptoms, neuropsychological changes plus the failed response to antidepressants but dramatic response to antipsychotics were not consistent with this diagnosis.
The view that the patient was suffering from a psychotic disorder, particularly a schizophrenia spectrum disorder, is further supported by his anomalous subjective experiences, as outlined in the previous section. Such experiences have been termed ‘basic symptoms’ and have been found to be present in prodromal, acute and remitted phases of psychotic disorders, particularly schizophrenia spectrum conditions [2–4].
Discussion
Diagnosis of pseudoneurotic schizophrenia
The present patient had symptoms in all three of the primary symptoms category including (i) thought disorder; (ii) low mood; and (iii) altered temperature perception and generalized weakness with prominent secondary symptoms including panic attacks, generalized anxiety and specific health anxieties.
Pseudoneurotic symptoms sit on the borderline between psychosis and neurosis [5]. Indeed by the late 1960s pseudoneurotic schizophrenia became almost synonymous with the term ‘borderline states’. Consideration of this synonymy and the evolution of the term ‘borderline states’ is key in explaining how the concepts underlying pseudoneurotic schizophrenia came to be neglected in modern diagnostic manuals.
‘Borderline’ was a term that originally arose in the late 1800s to denote conditions in the borderland between psychosis and the milder neurosis [6]. The evolution of the ‘borderline’ concept, however, has seen it largely lose this original meaning. In the 1920s ‘borderline’ was used to refer to the perceived unalysability of patients with psychosis versus those with a neurotic illness [7]. Only with the publication of Kernberg's paper ‘Borderline personality organization’ (BPO) in 1967 was the term ‘personality’ introduced [5]. Kernberg described a condition that was distinct from both higher neurotic functioning and lower psychotic functioning. In BPO, reality testing was preserved (albeit with a tendency to over-valued ideas in certain emotionally laden areas) but identity-sense was weakened. ‘Borderline’, and the terms with which it had become synonymous, including ‘pseudoneurotic schizophrenia’, had now become completely decoupled from psychosis and schizophrenia. When borderline personality disorder was finally introduced into the DSM-III in 1980 the diagnosis was formulated predominantly in terms of mood and behaviour, distinguished from subsyndromal schizophrenia, which was termed ‘schizotypal personality disorder’ [8].
Although many of those previously diagnosed with pseudoneurotic schizophrenia may have had a borderline personality disorder, a 10 year follow-up study published in 1962 showed that 20% of patients with pseudoneurotic schizophrenia transitioned to conventional schizophrenia [9]. It appears, however, that in the evolution of the concepts of pseudoneurotic and borderline this psychotic group became neglected. The operationalization of schizophrenia further compounded this neglect. Many features previously considered characteristic of subschizophrenic conditions disappeared from psychiatric literature [10]. These features including the ‘pseudo-neurotic’ symptoms were increasingly neglected by 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, functions as a driving force behind comorbidity studies, rediscovering and elaborating on the links previously described in the prototypical approach to diagnosis [11].
Freeman and Garety put forward a direct, non-defensive role for psychosis in emotional dysregulation, and the growing evidence for this hypothesis is such that researchers have proposed that distress, anxiety, depression and other forms of emotional disturbance may play a major role in determining whether young people with psychotic symptoms progress to develop a psychotic disorder [12].
Evidence emerging from UHR subjects has underlined an increasing interest in the role of emotional dysregulation in the emergence of psychosis [13]. The UHR subjects are help-seeking young people who are identified using well-validated screening instruments (the CAARMS) as being at particularly high risk of developing a psychotic disorder within a short time period based on experience of subthreshold psychotic symptoms and other risk factors [14]. Within the UHR subject group there are very high rates of affective and anxiety disturbance at baseline, and it is usual for emotional disturbance and emerging psychotic symptoms to co-occur especially early in the illness course [Phillips LJ et al: unpublished data, 2009]. In fact Hafner et al. argue that the prodrome of depressive and psychotic disorders is so similar in behavioural and symptom profiles that they cannot be distinguished from each other [15]. Early retrospective studies have shown that there is a prominent place for affective disturbance and anxiety in the psychosis prodrome [16, 17]. Within the UHR group 30–40% have been found to transition to first-episode psychosis within 12 months [18, 19]. Interestingly, high levels of emotional disturbance, in particular anxiety and depression, have been found to be more predictive of transition to psychosis in the UHR group than high levels of positive psychotic symptoms alone [20].
We propose that the present case meets criteria for pseudoneurotic schizophrenia and although it is unlikely that this diagnostic term will return to routine psychiatric vocabulary, the concepts that underlie its use are still relevant to modern practice. Individuals with a primary psychotic process may present with prominent emotional disturbance, affective and/or anxiety symptoms, which mask the underlying psychotic illness. Suspicion should be raised in patients who present with atypical affective and/or anxiety states, with a history of functional decline who do not respond or respond only partially to antidepressants or psychological interventions. The division drawn between neurotic and psychotic symptoms is an artificial one and consideration needs to be made of the complex interplay between psychotic and neurotic symptoms and their capacity to affect, obscure and possibly provoke one another.