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CASE REPORT |
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Year : 2018 | Volume
: 5
| Issue : 2 | Page : 162-164 |
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First-episode psychosis in a 101-year-old male
Sayantani Mukherjee
Department of Psychiatry, Chaitanya Institute for Mental Health, Pune, Maharashtra, India
Date of Web Publication | 27-Dec-2018 |
Correspondence Address: Dr. Sayantani Mukherjee A1-707, Runwal Seagull Township, Handewadi Road, Hadapsar, Pune - 411 028, Maharashtra India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jgmh.jgmh_4_18
An elderly gentleman, age 101 years, was brought in with first episode of onset of psychotic features, diagnosed with paranoid schizophrenia [ICD F20.0] as well as VLOSLP (Very Late Onset Schizophrenia Like Psychosis). He responded well to treatment and achieved complete remission. Remarkable in his case was his advanced age coupled with the lack of any the usual cognitive detriment prevalent in geriatric population. Notably, he had mildly elevated CRP (C- Reactive Protein) levels, which could both lend validity to neurodegenarative theory of schizophrenia and possibly indicate imminent onset of cognitive decline, but more longitudinal data is needed to be conclusive. Furthermore, despite satisfying the primary criterion of VLOSLP i.e. age of onset, his presentation and recovery does not fit its typical narrative, perhaps calling for more diversification in characterization of old age psychosis.
Keywords: Elder psychosis, first-episode, geriatric psychosis, schizophrenia, very late-onset schizophrenia-like psychosis
How to cite this article: Mukherjee S. First-episode psychosis in a 101-year-old male. J Geriatr Ment Health 2018;5:162-4 |
Introduction | |  |
As human longevity increases, number and variety of psychiatric disorders manifesting in the elderly rise alongside. Very late-onset schizophrenia-like psychosis (VLOSLP) is one such diagnosis coming to fore, characterized by the first-time onset of psychotic symptoms in individuals aged >60 years; more in females; with primarily persecutory, referential, or grandiose delusions; usually with hallucinations, in the absence of primary affective, cognitive, or neurological features.[1],[2],[3]
Below detailed is one such case, where the novelty lies in the very advanced age of the patient (101 years). A literature search has yielded only one such example of a centenarian first-onset psychosis.[4]
Case Report | |  |
An elderly gentleman, Mr. X, was brought to outpatient department accompanied by his family. At the time of presentation (September 2016), he was 101 years old (born in April 1915), thin built and walked with the aid of a stick due to slight kyphosis. For the past 6 weeks, he had been observed to have become increasingly unduly suspicious, muttering and gesticulating by himself, poor sleep, and bouts of verbal and physical aggression. The symptoms had escalated in the last 2 weeks. There was no apparent stressor. He was initially hostile toward his interviewer, paced around the interview room constantly, and assaulted his wife twice during the interview. His mental status examination revealed suspicious and fearful mood, instances of tangentiality, delusions of persecution and reference against family members, impaired judgment and complete lack of insight. He displayed hallucinatory behavior and explained that he could hear an unknown male voice, continually abusing him, commenting on his actions, and saying that his family was plotting to kill him, which made him feel extremely fearful and he reacted by abusing back and being aggressive with his family, especially when they denied hearing any such voice.
The family was sanguine that this was the first time in his life he was displaying such symptoms. His wife (married for 82 years) was 8 years younger than him and cognitively sound. There was no past history of mental disorders or substance abuse. There has been no history of any organicity in past or in relation to the presenting complaints. His vision was adequate with spectacles to correct refractive error. He had been hypertensive, taking amlodipine 5 mg on and off for approximately last 30 years. He was also on multivitamin and calcium supplements. There was no other history of medical illnesses or significant sensory impairment. His routine blood investigations were unremarkable (complete hemogram, blood sugar levels, liver and renal function tests, thyroid hormone levels, serum B12, and homocysteine levels were normal) except C-reactive protein (CRP) level, which was mildly raised at 1.78 mg/L (1–3 mg/L = average risk).[5] Magnetic resonance imaging of brain showed age-related cerebrocortical atrophy. He initially did not cooperate for cognitive testing in form of mini-mental state examination (MMSE). His first rating on the Brief Psychiatric Rating Scale (BPRS) was 92.[6]
He was diagnosed with paranoid schizophrenia (ICD code F20.0) [Table 1] after adequately ruling out other neuropsychiatric disorders [Table 2].
He was treated with olanzapine 5 mg BD for the psychotic features and diazepam 5 mg HS to manage sleep. His aggression, suspiciousness, and hallucinations all gradually reduced and insight improved with psychoeducation that was regularly offered to both him and family. After 1 month, the BPRS score had reduced to 54, and insight had improved to 4/6. MMSE was 28/30 (losing 1 point in recall and serial calculation each). After 2 months, he displayed no active psychotic symptoms, insight improved to 5/6, BPRS score reduced to 24, and MMSE improved to 29/30 (losing 1 point in recall). Subsequently, as the patient continued to maintain this improvement, diazepam was tapered off and olanzapine was continued in the reduced dose of 5 mg HS.
Clinical neurological evaluation revealed his motor and sensory systems, reflexes, cranial nerve and cerebellar functions to be unremarkable; higher mental functions including attention, memory (immediate, recent and remote), language comprehension and expression, praxis, gnosis, computing, and reasoning were assessed and found to be within normal limits. Neuropsychiatric batteries were advised but were not done due to nonaffordability.
In further follow-up sessions, the patient was well-adherent to treatment and did not display any sign of relapse, any new psychiatric symptoms, drug-related side effects, or cognitive decline. He achieved clinical remission, and his general health remained unchanged.
He was lost to follow-up after 9 months as his family relocated.
Discussion | |  |
Originality of this case lies in the age of the patient at onset of first episode of psychosis and his apparent lack of any other preexisting or subsequent neuropsychiatric issues.
It is unique to be so well preserved, whereas cases of age-related neurodegenerative diseases are on the rise. Factors which are likely in preserving his faculties would be no major medical or previous neuropsychiatric issues, no positive family history, higher level of education (a college graduate), cognitively and physically active lifestyle, no substance abuse, no significant sensory impairment, steady course of life, good social support, as well as sound genetics.[7]
Concerned studies of such cases show that persons possessing certain genetic variants such as a 32 base-pair deletion allele in chemokine receptor CCR5 and cerebral D2 dopamine receptor polymorphism have the onset of psychosis very late in life.[8] Certainly, for this case, such testing could not be availed, leaving a lacuna in etiopathological data.
Coming to biochemical markers, raised CRP level in this patient could be due to a combination of inflammaging (mild inflammation associated with increased rates of attrition, i.e., aging tissues and organs),[5] mild hypertension, and maybe psychosis too. Although not tissue specific, increased CRP can give credence to neurodegenerative theory of schizophrenia.[5],[8],[9] The psychosis perhaps, due to obvious underlying neurotransmitter dysregulation, is pointing to an initial functional microdegeneration which may herald gross changes that result in a wider neuropsychiatric symptomatology. This is in concurrence with previous research, which has repeatedly shown that those elderly whose first psychosis occurs very late in life, usually follow-up with cognitive degeneration within the next 5 years.[1],[2],[3],[5] Here, no cognitive symptoms have surfaced yet so that it could be a combination of the patient's unusually robust constitution and that the continuing antipsychotic medication is holding off further decline by minimizing neurotoxicity.[10] Or possibly for Mr. X, as of now, it is just too early in the course of the disease to show clinical cognitive decline. Lack of objective evidence in form of a neuropsychiatric battery becomes a limitation here. Hence, further longitudinal follow-up (for at least the said 5-year period) would be required to draw satisfactory conclusions.
Should this case have been labeled VLOSLP? Along with the coded ICD criteria for paranoid schizophrenia, this case does satisfy the chief VLOSLP criterion in that the first onset of psychosis is after 60 years of age and corroborates with adjunct characteristics such as largely positive symptoms (in the form of persecutory and referential delusions and auditory hallucinations), no affective flattening and preserved capacity for learning. However, bearing disparity to the case presented here, VLOSLP, as recorded in literature, is associated with occurrence in women more than men, no formal thought disorders, hallucinations more in the visual modality, noticeable cerebellar atrophy on neuroimaging, some degree of sensory and cognitive impairment and often difficult symptom amelioration with psychotropics, with more burden of drug-induced complications.[1],[2],[10] However, VLOSLP itself is an evolving diagnosis at present, which allows for latitude and inclusivity in terms of symptomatological and other parametric variation. Thus, in conclusion, by the current terms embodying VLOSLP, this case is on its spectrum, but not utterly representative.
This seems to imply that nosological expansion is required for the diagnosis of old age psychosis, as the geriatric are an increasingly diverse population. Increased reporting of cases such as this would further the emergence of newer and more specific etiological and diagnostic characterizations as well as prognostic indicators.
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 identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2]
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