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CASE REPORT Table of Contents  
Ahead of print publication
Functional and organic psychosis: Overlap or distinct phenomenon

1 Professor, Department of Psychiatry, P.E.S. Institute of Medical Sciences and Research, Kuppam, Andhra Pradesh, India
2 Junior Resident, Department of Psychiatry, P.E.S. Institute of Medical Sciences and Research, Kuppam, Andhra Pradesh, India

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Date of Submission11-Oct-2022
Date of Acceptance26-Nov-2022
Date of Web Publication28-Feb-2023


Organic and nonorganic/functional psychosis present with unique symptoms which can propel in differentiating these entities. Not always the distinction is clear-cut which poses challenges with the treatment approach to ensure that the patient responds to the medication. We are presenting a case with initial evidence suggestive of organic causation. On revaluation of the case, as no further pointers towards as organic basis was found. Futher management of case as functional psychosis showed clinical and functional improvement. This case report highlights the blurring of the distinction between organic and functional etiologies of psychosis.

Keywords: Atypical, functional, late-onset schizophrenia, organic

How to cite this URL:
Sreelatha P, Manickyam M. Functional and organic psychosis: Overlap or distinct phenomenon. Arch Ment Health [Epub ahead of print] [cited 2023 Mar 24]. Available from: https://www.amhonline.org/preprintarticle.asp?id=370759

  Introduction Top

The term organic psychosis is used to describe a cluster of symptoms attributable to a specific cerebral or systemic pathology, diagnosed through systemic examination and appropriate investigations.[1] Organic psychiatric disorders are now covered in the Diagnostic and Statistical Manual of Mental Disorders-5 and the International Classification of Diseases-10 (ICD-10) as secondary to or due to general medical conditions.[2] Organicity can be determined by the temporal relationship of neurophysiological insult to the onset of psychiatric symptoms. It can also be evaluated by observed improvement of the psychiatric symptoms on the treatment of the causal physical/neurological disorder.[3] Whereas functional implies no diagnosable pathophysiology contributing to the etiology of the psychiatric disorder. The organic-functional distinction establishes the causality of the psychiatric symptoms with further emphasis on the implementation of relevant treatment protocols and influence on the prognosis.

Psychotic disorders occurring in old age could be diagnosed with schizophrenia, dementia, delirium, delusional disorder, depression/mania, organic psychosis, and neuropsychiatric disorders like Parkinson's disease.[4] Late-life psychotic disorders occur due to the interplay of various biological, psychological, social, and environmental factors. Late-onset psychosis needs special attention due to the associated comorbid conditions, high morbidity, and mortality. Schizophrenia is considered to be a disorder of early adulthood onset. Late-onset schizophrenia first described by Martin Roth as “late paraphrenia” demonstrates that the disorder can present itself first in late life. Diagnosing late-life functional schizophrenia poses difficulty in differentiating it clinically from the most commonly occurring psychotic disorders in the elderly like organic psychosis among others. Presenting a case of late-onset schizophrenia initially considered being organic psychosis.

  Case Report Top

A 70-year-old male, married, a farmer came to the psychiatry outpatient department (OPD), with complaints of hearing voices, seeing images, talking to himself, and decreased sleep/appetite for 3 years with exacerbation of symptoms for 2 months. The patient's son reported that they had visited a private psychiatrist for the first time, with the same complaints, and was hospitalized for 10 days and treated with tablet risperidone 4 mg 0-0-1 and tablet trihexyphenidyl (THP) 2 mg 1-0-0 for 10 days. As there was no improvement noted. Magnetic resonance imaging (MRI) of the brain was suggested by a psychiatrist. MRI of the brain showed a ring-enhancing lesion in gray matter and white matter junction of the left parietal temporal lobe with adjacent perilesional edema – suggestive of neurocysticercosis. The patient consulted a neurologist, who advised a repeat MRI of the brain which showed T2 hyperdense well-defined lesion peripheral enhancement in the left middle temporal lobe with perilesional edema – suggestive of central nervous system (CNS) tuberculoma. The patient was initiated on tablet levetiracetam 500 mg 1-0-1. Further, based on the MRI findings, antitubercular regimen was started (tablet isoniazid 300 mg, tablet rifampicin 250 mg, tablet ethambutol 1000 mg, and tablet pyrazinamide 1500 mg). The patient was compliant with the medication which was supervised by his son and was regular for treatment follow-up and completed the course of antitubercular treatment. The patient's symptoms of hearing voices and seeing images had reduced in severity and sleep and appetite improved, but symptoms persisted even after the course of antitubercular treatment was completed by the patient. After 1 year of completion of antitubercular treatment, the patient consulted our psychiatry OPD with persistent and exacerbation of the same symptoms for the past 2 months. On detailed evaluation, the patient's son reported that for the past 3 years, he has observed a change in the patient's behavior in that patient stays aloof, his interaction with other family members had decreased, prefers to stay at home, and appears fearful in the presence of visitors. The patient was consuming less quantity of food; he neglected his self-care. He reported hearing voices and he was responding back to the voices and that no matter how much he tried the voices do not go away and that the voices are constantly disturbing him which were present throughout the day. The patient also reported that voices were clear and audible and commanded him to do certain activities which he obeys. The patient reported that he saw images of human beings, animals, snakes, and sometimes humans without clothes, and he was fearful after seeing these images, sometimes these animals, and snakes used to enter his body and he could feel the sensation of these creatures entering his body. His sleep was reduced with disturbance in the initiation of sleep.

There was no significant past psychiatry history with significant family psychiatry history (with mother diagnosed with psychosis when she was 28-year-old, was on irregular treatment) (no history of consumption of uncooked or raw meat) with no medical comorbid conditions, and no history of substance use with premorbid well-adjusted personality who was attending to work regularly and good social relationships. The patient had a hearing impairment for 15 years (the current symptoms were of 3 years duration so the possibility of psychotic symptoms due to hearing impairment was considered unlikely) and on Ear nose and throat (ENT) consultation and audiometry sensorineural impairment was confirmed. Mental status examination: patient conscious, oriented, agitated, rapport established with difficulty, with anxious affect, second person auditory hallucinations, command hallucinations, and visual/tactile hallucinations, with poor insight. Physical examination showed no evidence of neurological deficits. Positive and negative Syndrome Scale (PANSS) score of 76 and Mini–Mental State Examination score was 27 indicating no cognitive impairment. The patient was diagnosed with F06 – other mental disorders due to brain damage and dysfunction and physical disease (F06.0 organic hallucinosis) according to ICD-10. The patient was started on tablet risperidone 2 mg 0-0-1, tablet THP 2 mg 1-0-0, and tablet clonazepam 0.5 mg 0-0-1. All blood investigations were within normal limits including a repeat MRI brain, which showed no evidence of CNS tuberculoma and no other CNS pathologies. In view of persisting psychotic symptoms after completion of antitubercular medication for a diagnosis of CNS tuberculoma and physical/neurological examination uneventful and blood investigations and neuroimaging showing no further organic pathology, the diagnosis was revised to F20.0 Paranoid schizophrenia as per ICD-10. Tablet risperidone 2 mg was hiked to 1-0-3 for 45 days with weekly follow-ups and monitoring of response and development of side effects. No tremors, slowness, rigidity, or slurring of speech was noted, and tablet clonazepam was tapered gradually to 0-0-1/2 and stopped. Over the next 2 months of treatment, the patient reported improvement in hearing voices, seeing images, sleep, and appetite. The repeat PANSS score after 1 month was 54. In the next 2 months, his psychotic symptoms completely resolved. At the end of 6 months of treatment with antipsychotics, the patient was observed to be maintained well and resumed his work as a farmer.

  Discussion Top

Late-onset functional schizophrenia, although depicted by various terminologies has a distinct and consistent clinical presentation. It has notable differences from its early onset counterpart and also organic psychosis. Patients with late-life schizophrenia present with predominant well-organized delusions and hallucinations of various modalities most common being auditory and visual, running commentary, and persecutory and partition delusions with a relative absence of disorganized thought, negative symptoms, and catatonia.[5] Although the current psychiatry diagnostic systems do not include any age specifiers for diagnosis the International Late-Onset Schizophrenia Group recommended the term very late-onset schizophrenia for psychotic symptoms developing after 60 years as is our index case.[6] The family history of schizophrenia patients with late-onset psychosis is higher than in the general population, but the risk is lesser when compared to relatives of patients with early-onset schizophrenia and the genetic associations are much weaker in very late-onset psychosis.[7] Sensory deficits pose an additional risk for late-onset psychosis. The clinical picture of organic psychosis includes an atypical age of onset, atypical clinical features, absence of past psychiatric history, predominant visual hallucinations, associated cognitive disturbances, neurological deficits, substance abuse, and presence of other medical conditions significant enough to contribute to psychotic phenomena.

This case highlights the difficulties and challenges faced by the clinician in diagnosing a case of functional psychosis initially presenting as organic psychosis. With the information provided by the family, a diagnosis of organic psychosis was made with the evidence of MRI findings of CNS tuberculoma and the onset of psychotic symptoms temporally related to CNS pathology. Owing to the first-time consultation of the patient with us, we reinvestigated and re-evaluated to establish the diagnosis. Points clinching toward a diagnosis of functional psychosis were repeated MRI reports showing normal findings, persistent psychotic symptoms after the treatment for tuberculoma, absence of cognitive/neurological deficits, no significant past psychiatric history, family history of psychiatric disorder, no substance use clinical picture of positive psychotic symptoms, and absence of negative/catatonic features, hearing impairment contributing to sensory deficit elevating the risk.

Female preponderance, absence of cognitive disturbances, absence of weak genetic association, and nonresponse to low doses of antipsychotics goes against very late-onset schizophrenia.[8] Although the patient was not initiated on antipsychotics with the diagnosis of CNS tuberculoma, it can be predicted that organic psychosis would improve with treating the causative neurological disorder. This was not observed in this report, and the persisting psychotic symptoms responded after the initiation of antipsychotics. This case also enlightens the overlap of the functional-organic distinction and that each of these entities cannot be clearly delineated. The clinical presentation, in this case, cannot be attributed to a “purely functional” or “purely organic” causality or “true schizophrenia” being very late onset.[9] The organic-functional dichotomy undermines the dynamic relationship of CNS/systemic pathology, behavior, perception, affect, and cognition. Another argument is that although there is definite evidence of CNS pathology through investigative procedures, with what certainty can it be linked to the psychiatric disorder etiologically. Detecting the causality may have relevance in ensuring appropriate and adequate management of the case with referrals to other specialties if required.

  Conclusion Top

A better clinical understanding of the organic-functional psychosis and its perception among the treating clinicians can be helpful in planning an adequate care plan for the patient. At the phenomenology level, some differentiation can be postulated which can be confirmed by physical examination, laboratory parameters, and neuroimaging. However, it can be concluded that the complex interactions of pathophysiology and psychological experiences of the patient cannot be simplified with the organic-functional dichotomous approach.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kendler KS. The dappled nature of causes of psychiatric illness: Replacing the organic-functional/hardware-software dichotomy with empirically based pluralism. Mol Psychiatry 2012;17:377-88.  Back to cited text no. 1
Tyrer P. A comparison of DSM and ICD classifications of mental disorder. Adv Psychiatr Treat 2014;20:280-5.  Back to cited text no. 2
Bell V, Wilkinson S, Greco M, Hendrie C, Mills B, Deeley Q. What is the functional/organic distinction actually doing in psychiatry and neurology? Wellcome Open Res 2020;5:138.  Back to cited text no. 3
Tampi RR, Young J, Hoq R, Resnick K, Tampi DJ. Psychotic disorders in late life: A narrative review. Ther Adv Psychopharmacol 2019;9:1-13: 2045125319882798.  Back to cited text no. 4
Nebhinani N, Pareek V, Grover S. Late-life psychosis: An overview. J Geriatr Ment Health 2014;1:60-70.  Back to cited text no. 5
  [Full text]  
Howard R, Rabins PV, Seeman MV, Jeste DV. Late-onset schizophrenia and very-late-onset schizophrenia-like psychosis: An international consensus. The international late-onset schizophrenia group. Am J Psychiatry 2000;157:172-8.  Back to cited text no. 6
Howard RJ, Graham C, Sham P, Dennehey J, Castle DJ, Levy R, et al. A controlled family study of late-onset non-affective psychosis (late paraphrenia). Br J Psychiatry 1997;170:511-4.  Back to cited text no. 7
Chen L, Selvendra A, Stewart A, Castle D. Risk factors in early and late onset schizophrenia. Compr Psychiatry 2018;80:155-62.  Back to cited text no. 8
Palmer BW, McClure FS, Jeste DV. Schizophrenia in late life: Findings challenge traditional concepts. Harv Rev Psychiatry 2001;9:51-8.  Back to cited text no. 9

Correspondence Address:
P Sreelatha,
Department of Psychiatry, P.E.S. Institute of Medical Sciences and Research, Chittoor District, Kuppam - 517 425, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/amh.amh_160_22


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