Journal of Geriatric Mental Health

: 2014  |  Volume : 1  |  Issue : 2  |  Page : 60--70

Late-life psychosis: An overview

Naresh Nebhinani1, Vrinda Pareek1, Sandeep Grover2,  
1 Department of Psychiatry, All India Institute of Medical Science, Jodhpur, Rajasthan, India
2 Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
Dr. Naresh Nebhinani
Department of Psychiatry, All India Institute of Medical Science, Jodhpur - 342 005, Rajasthan


There could be multiple causes for late-life psychosis, such as chronic conditions, like early-onset schizophrenia, late-onset schizophrenia, delusional disorder, psychosis associated with various dementias, various neuropsychiatric disorders, delirium, and secondary to organic causes. This article will provide an overview of late-life psychosis by elaborating different types of psychotic disorders usually seen in the elderly population. Psychosis associated with dementia and delirium is usually accompanied by cognitive symptoms. Organic Psychosis is usually characterized by higher prevalence of visual hallucination. There are few well-designed randomized controlled evaluating the efficacy of atypical antipsychotics for management of various forms of psychosis in elderly and there is a black box warning for using atypical antipsychotics in elderly patients with dementia.

How to cite this article:
Nebhinani N, Pareek V, Grover S. Late-life psychosis: An overview.J Geriatr Ment Health 2014;1:60-70

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Nebhinani N, Pareek V, Grover S. Late-life psychosis: An overview. J Geriatr Ment Health [serial online] 2014 [cited 2021 May 13 ];1:60-70
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Historically, schizophrenia has been considered a disease of younger adulthood. However, literature suggests that approximately 23% of patients with schizophrenia have an onset of illness after 40 years of age with 3% being older than 60 years at the time of onset of the illness. [1] Kraepelin initially had coined the term "paraphrenia" to describe a group of symptoms matching with those of dementia praecox, characterized by a cognitive decline with hallucinations and delusions, without any negative symptoms such as emotional dullness or loss of volition. [2],[3],[4],[5] Moreover, in these patients, there was no long-term deterioration of personality while hallucinations and delusions were experienced in clear consciousness without bothersome sequelae. These findings were in sharp contrast to the majority of early-onset schizophrenia (EOS) cases studied during the early part of 20 th century. Kraepelin used the term paranoia to describe the patients who had chronic, well-organized delusions, but did not manifest perceptual disturbances, personality deterioration, or a formal thought disorder. In many ways, this later term is similar to the diagnostic and statistical manual (DSM-IV-TR) construct of delusional disorder. The work of Eugen Bleuler's son, Manfred Bleuler, on late-onset schizophrenia (LOS), demonstrated that the illness could first present later in life. [6],[7]

Feighner et al. [8] criteria for schizophrenia are restricted for its onset before 40 years of age. Similarly, the DSM-III did not allow for the diagnosis of schizophrenia if the onset of illness was after the age 45. Subsequently, the DSM-III-R permitted the diagnosis of schizophrenia late-onset type after age 45, and the subsequent revisions of DSM contain no diagnostic restrictions for age of onset. [8] It is still a debatable issue whether to consider LOS as a separate diagnostic entity or same as EOS. However, over the years, it has been realized that psychotic symptoms can occur in old age and can be part of various disorders like schizophrenia, dementia, delirium, delusional disorder, depression, organic psychosis, etc. This article provides an overview of current understanding about psychotic symptoms in late life. For this, a literature search using the keywords, elderly, psychosis, late-life psychosis, schizophrenia, delusional disorder, delirium, depression, organic psychosis, etc., was carried out in PubMed and Google Scholar search engines. Some of the key articles were selected to provide an overview on the topic.

 Late Life Schizophrenia

The term "late-life schizophrenia" refers to older individuals with schizophrenia, irrespective of the age of onset. [8] Based on the age of onset, The International LOS Group [9] suggests that if schizophrenia-like psychotic symptoms start after the age of 40 years, then should be called late-onset schizophrenia-like psychosis (LOSLP) and if the onset is after the age of 60 years, it should be called very late-onset schizophrenia-like psychosis (VLOSLP).

The epidemiologic catchment area study reported a lifetime prevalence of schizophrenia among people aged 45-64 to be 1.0% and among people aged 65 years and older to be 0.3%. [10] The healthcare costs of late-life schizophrenia are estimated to be as high as the amount spent on teenagers and young adults with schizophrenia. Nursing home care accounts for the maximum of these expenditures. [8],[11]

Early-onset schizophrenia in later life

In spite of higher mortality rates in general and suicide and homicide rates in particular, among individuals with schizophrenia than in general population, [12],[13],[14] many of the patients with EOS are now living into older adulthood.

Longitudinal follow-up studies of patients with EOS indicate considerable variability of outcome. A minority of patients experience remission of both positive and negative symptoms. [15],[16],[17] Auslander and Jeste [18] reported that nearly 10% of community-dwelling older patients with schizophrenia meet strict research criteria for sustained remission. The course of illness in most of the patients remains unchanged, [19],[20],[21] although there is an improvement in positive symptoms. [22]

Factors associated with poor prognosis for EOS are chronicity, insidious onset, premorbid psychosocial or functional deficits, and prominent negative symptoms. [23] In a sample of chronically institutionalized patients with schizophrenia, older age was associated with lower levels of positive symptoms and higher levels of negative symptoms. [24] Available literature also suggests the presence of more cognitive deficits in patients with EOS compared to healthy subjects, particularly in the areas of learning, abstraction, and cognitive flexibility. Cognitive performance tends to remain stable in this subgroup. [25],[26]

Functional capacity varies considerably among older patients with schizophrenia. In a study of a group of middle-aged and older schizophrenia outpatients, Palmer et al. [27] found that 30% had been employed at least part time since the onset of psychosis. In general, worse neuropsychological test performance, lower educational level, and negative symptoms but not positive symptoms are associated with poorer functional capacity in older outpatients with schizophrenia. [28] Vahia et al. [29] observed self-assessed lower quality-of-life to be associated with depression, positive and negative symptoms, cognitive deficits, financial strain, poor social support, and poor social skills.

Late-onset schizophrenia-like psychosis

Risk factors and clinical presentation associated with LOS are similar to those associated with EOS. [30],[31] Similar proportion of individuals with EOS or LOS report having a family history of schizophrenia (10-15%) and no consistent link has been found between age of onset and genetic risk of schizophrenia. [6],[32] Levels of childhood maladjustment, measured retrospectively were similar in LOS and EOS patients but higher in both the groups than in healthy subjects. [33] Patients with LOS have increased rates of minor physical anomalies relative to healthy subjects, but rates of these anomalies are similar to those with EOS. [34]

Neuroimaging studies show that compared to patients with EOS patients with LOS have more nonspecific structural abnormalities such as enlarged ventricles and increased white matter intensities [35] and a larger volume of the thalamus on magnetic resonance imaging. [36] Finally, long-term neuropsychological follow-up of a group of patients with LOS revealed no evidence of cognitive decline, suggesting a neurodevelopmental rather than a neurodegenerative process. [26]

Women predominate among individuals with onset of schizophrenia in middle to late life. [6],[37] It has been speculated that estrogen may serve as an endogenous antipsychotic, masking symptoms of schizophrenia in vulnerable women until after menopause. [38] However, investigations on efficacy of hormonal replacement therapy as an adjunct treatment for postmenopausal women with psychosis [39],[40] have not had promising results.

Jeste et al. [6] found a higher prevalence of the paranoid subtype of schizophrenia in patients with LOS (75%) compared to EOS (50%). Patients with LOS tend to have more organized delusions, auditory hallucinations or hallucinations with a running commentary and persecutory delusions with or without hallucinations. [9] Patients with LOS also have lower levels of negative symptoms than patients with EOS; however, they have higher levels of negative symptoms than healthy subjects. [6],[41]

On neuropsychological testing, patients with LOS tend to have less impairment in learning, abstraction and flexibility in thinking than patients with EOS. [6] Compared to patients with EOS, a greater proportion of patients with LOS have successful occupational and marital histories and generally have better premorbid functioning. Sensory deficits, particularly hearing loss, are associated with psychotic symptoms in late life and have been proposed as a risk factor for LOS. [42]

Very-late-onset schizophrenia-like psychosis

Very-late-onset schizophrenia-like psychosis may be difficult to diagnose clinically because its clinical picture can be confused with other conditions such as dementia, delirium, and psychosis due to underlying medical illness. In a prospective study comparing individuals with VLOSLP to a gender-matched sample of individuals with EOS, the patients with VLOSLP were distinguished by higher rates of marriage, higher education levels, better responses to treatment with risperidone, and more pronounced cerebellar atrophy. [28],[43] Overall, VLOSLP may be a neurodegenerative process in contrast to LOS that develops before age 60 which is theorized to be a neurodevelopmental process. [9]

Factors distinguishing patients with VLOSLP from "true" schizophrenia include a lower genetic load, less evidence of early childhood maladjustment, a relative lack of thought disorder and negative symptoms (including blunted affect); a greater risk for tardive dyskinesia and evidence of a neurodegenerative rather than a neurodevelopmental process. [44],[45] VLOSLP has been noted to be more common in immigrant populations, suggesting that psychosocial factors might play a role. [46] Imaging studies have shown underlying focal white matter abnormalities in cerebral tracts. [47] A study by Mazeh et al. [48] suggested that patients with VLOSLP may have somewhat more stable cognitive and everyday functioning than do chronically institutionalized elderly patients with schizophrenia. [Table 1] compares risk factors and clinical features of EOS, LOS, and VLOSLP.{Table 1}

There are very few studies from India on LOS. One of the studies reported female preponderance and high prevalence of persecutory delusion (83%). [49] Jayaswal et al. [50] and Adityanjee et al. [51] reported that 2.04% patients with the clinical diagnosis of schizophrenic have onset after the age of 40 years. Among those who had onset after the age of 40 years, 62.5% were females giving a male and female ratio of 1:1.67. In another study, on clinical characteristics of LOS, the age of onset of illness was 47.97 years for males and 51.54 years for females, indicating women have onset later than men. There was no evidence suggestive of cognitive impairment in any of the patient. [52] Kulhara et al. [53] compared patients with LOS (13 subjects) and EOS (30 subjects, with two subgroups of 15 subjects of the current age <40 years and >40 years). Overall profile was comparable among both the groups except LOS group scored greater on persecutory delusions compared to EOS group.

Most of the studies of pharmacological treatments for late-life schizophrenia focus on individuals with early-onset, rather than late-onset or very-LOS-like psychosis. Although certain discrepancies exist, majority of studies support the efficacy of various atypical antipsychotics including clozapine, risperidone, olanzapine, and aripiprazole in the treatment of late-life psychosis. Thus, first-line treatment for psychosis in the elderly is atypical antipsychotics. In general, atypical antipsychotics are preferred in elderly due to less extrapyramidal side effects, but at the cost of metabolic side effects compared to typical antipsychotics. [54],[55],[56]

Use of low-dose risperidone has relatively more positive data in controlled trials. [57],[58] Similar rates of efficacy for the treatment of older persons with chronic schizophrenia were found for risperidone (2 mg) and olanzapine (10 mg) in a randomized controlled trial (RCT), but olanzapine was associated with greater metabolic side effects. [22] A Cochrane review [59] reported lack of the evidence base for antipsychotics among patients with LOS or VLOSLP. Open studies of typical antipsychotics used for the treatment of LOS and VLOSLP indicated that 48-61% of patients demonstrated full remission of psychotic symptoms. [9]

The high-potency (haloperidol) and low-potency (chlorpromazine) typical antipsychotics are associated with various extrapyramidal and anticholinergic side effects. A review suggests that there is significantly greater cumulative incidence of tardive dyskinesia in elderly populations receiving typical antipsychotics compared to adult population (as after 3 years of therapy 63% incidence among elderly vs. 15% among adult population). [60]

Due to various pharmacodynamic and pharmacokinetic changes among the elderly population, psychotropic prescription should follow "start low, go slow" principle. [61]

Psychosocial interventions

Growing evidence supports the adjunctive use of psychosocial interventions to treat late-life schizophrenia. In the arena of functional improvement, psychosocial interventions, used in conjunction with pharmacotherapy, show promise as an adjunctive treatment modality in older adults with schizophrenia. For example, functional adaptation skills training, a group-format manualized therapy that targets everyday life skills, improves the functional adaptation of older adults with schizophrenia [62],[63] and decreases their short-term use of emergency medical services. [64]

Cognitive-behavioral therapy and social skills training are evidence-based adjunctive therapies to psychopharmacologic treatment in younger adults with schizophrenia. [65] RCTs of the combination of above techniques called cognitive behavioral social skills training, for adults with late-life schizophrenia indicated that CBBST led to better skills acquisition and self-reported functioning than did participation in standard care, [66] with benefits persisting at 1-year follow-up. [67] Cognitive training or cognitive remediation improves their neuropsychological functioning with subsequent improvement in their overall functioning, symptom profile, and cognitive performance, especially with pharmacotherapy. [68],[69]

 Delusional Disorder

A dearth of literature exists about delusional disorder in older adults. Studies often do not distinguish between delusions, in general, which can be present in a multitude of disorders, and delusional disorder more specifically. At least 6% of older adults have paranoid symptoms like persecutory delusions, but most of these individuals have dementia. [70],[71] Delusional disorder accounts for 1-4% of inpatient psychiatric hospital admissions and is seen more frequently in lower socioeconomic status and immigrant populations. [72]

Among the various subtypes of delusional disorders, delusional parasitosis is seen more frequently in the elderly population, especially in females. [73] It is a persistent condition in which the patient falsely believes that small insects (fleas, vermin or maggots) have infested his/her skin. The syndrome is classified as a subtype of monosymptomatic hypochondriacal psychosis. [74] This is best-characterized as a primary delusion though it is sometimes described as an elaboration of a primary pathological experience such as tactile hallucination, paresthesia or pruritus. [75] In general, the description of delusional parasitosis mentions only the involvement of the skin and the tissues underneath.

Tandon et al. [76] found majority of patients with delusional parasitosis over were 50 years of age with the male:female ratio of 5:7. Psychiatric assessment revealed obsessional personality traits in more than one-third of the patients though surprisingly none of them ever had frank obsessive-compulsive neurosis. Srinivasan et al. [77] and Chaudhary et al. [78] reported delusional parasitosis in elder males, who showed good response with trifluoperazine and pimozide. In another study by Hebbar et al. [79] (N = 45), majority of the patients (46%) reported somatic delusions-infestation followed by delusions of jealousy and persecution.

To diagnose delusional disorder the clinician must rule out delirium, dementia, psychotic disorders due to general medical conditions or substance use, schizophrenia, mood disorders with psychotic features, significant organic brain syndrome or physical illnesses like pellagra. [80] Risk factors for delusional disorder include a family history of schizophrenia or avoidant, paranoid or schizoid personality disorder. [81]

Depression with psychotic features

Late-onset psychotic depression deserves special attention. Meyers et al. [82] reported more delusions in depressed patients with illness onset at age 60 years or later than those with an early onset. Individuals with delusional depression tended to be older and responded to ECT as opposed to tricyclic antidepressants. Delusions of persecution or of having an incurable illness are more common than delusions associated with guilt. If the guilt predominates the delusional picture, it usually involves some relatively trivial issue that occurred many years before the onset of the depressive episode, was forgotten over time, but presently is being considered as a major problem. [83] Nihilistic delusions may occur more commonly in late life. Focus on the abdomen is common among elderly patient with a delusional or psychotic depression, however, hallucinations are uncommon.

Thakur et al. [84] compared the profile of psychotic and non-psychotic depression in a tertiary care sample of 674 elderly and younger patients. In this study, younger age, psychomotor retardation, guilt, feelings of worthlessness, a history of delusions in the past, and increased suicidal ideation and intent were found more commonly in psychotic than in nonpsychotic patients, and these associations were largely confirmed when demographic variables were controlled. Psychotic depression also tended to be associated with poor social support and not surprisingly, bipolar illness.

The use of selective serotonin reuptake inhibitors (SSRIs) has been growing in elderly patients (with or without medical illness). Citalopram, [85] escitalopram, [86] fluoxetine, [87] paroxetine, [88] and sertraline [89] have been shown to be effective in depressed older patients. Efficacy has also been seen among those with depression in the background of stroke [90] or who have vascular disease, in general [91] or Alzheimer's disease. [92] Tricyclic antidepressants are the agents of choice for some patients with more severe forms of major depression which can tolerate the side effects and do not respond to the medications mentioned above. ECT continues to be the most effective form of treatment for patients with more severe major depressive episodes. [93] It is primarily effective in patients having melancholic symptoms as well as psychotic symptoms associated with agitation or withdrawal. Many older patients with such syndromes either fail to respond to antidepressant medications or experience toxicity (usually postural hypotension) when taking antidepressants.

Psychosis of Alzheimer's disease

Behavioral and psychological symptoms of dementia (BPSD) is a heterogeneous range of psychological reactions, psychiatric symptoms, and behaviors occurring in people with dementia. [94] Diagnostic criteria for psychosis associated with Alzheimer's disease are elaborated in [Table 2]. [95] {Table 2}

Unlike positive psychotic symptoms of schizophrenia, the delusions of AD tend to be simpler (e.g., the delusion of theft, infidelity etc.). Visual hallucinations may be more frequent than auditory. [96] Comparative features of psychosis with Alzheimer's dementia and schizophrenia are detailed in [Table 3].{Table 3}

Several Indian studies have reported greater prevalence of BPSD in patients with Alzheimer's disease than patients with vascular dementia (VaD). [97],[98] They were rated as troubling to most caregivers, and it has adverse effects on the mental health of the caregivers. [98]

The frequency of delusion varies between 10% and 73%. [99] The most commonly reported delusions are persecutory or paranoid. Broadly, five types of delusions have been described: People stealing things; house is not one's home (misidentification); spouse (or other caregiver) is an impostor-capgras phenomenon; abandonment; and infidelity. [100]

The frequency of hallucinations (predominantly visual) with dementia is reported in the range of 12-49%, [101] which can be up to 80% in patients with Lewy body dementia (LBD). [102]

A community study from western India found lesser prevalence of hallucination (8.1%) and suspiciousness (2.3%) [103] compared to other community survey in southern India which reported greater prevalence of hallucinations (41%) and delusions (65%). [98] Greater caregiver stress and burden were reported with patients with psychotic symptoms. [98]

Nonpharmacological management plays a crucial role in BPSD along with judicious use of medications. The first step in the management involves the thorough evaluation and correction of abnormalities, triggers, or perpetuating factors in the genesis of BPSD. [104]

Following medications have grade-A recommendations for delusions/hallucinations/agitations in dementia: Risperidone (starting dose 0.5 mg/day and maximum dose 2 mg/day), Olanzapine (starting dose 2.5 mg/day and maximum dose 10 mg/day), Quetiapine (starting dose 25 mg/day and maximum dose 100 mg/day), and Aripiprazole (starting dose 2 mg/day and maximum dose 15 mg/day). [105] In line with Food and Drug Administration of United States of America black-box warning for "Cerebrovascular adverse events, including stroke, in elderly patients with dementia," low doses should be used over short periods of time with the eventual goal of discontinuation whenever possible.

Psychosis associated with other dementias

Psychosis is a common complication in other non-AD dementias. Three common disorders in that category are VaD, Parkinson's disease dementia (PDD), and LBD. No association was found between degree of dementia severity and presence of psychotic symptoms in VaD, contrasting the pattern found in AD wherein the probability of psychosis increases with worsening severity of AD up to a certain stage of illness.

A recent consensus panel [106] has proposed the term Lewy body disorders as an umbrella term for Parkinson's disease (PD), PDD, and dementia with Lewy bodies (DLB). PDD is diagnosed when the dementia starts after 1-year or more after the onset of Parkinsonism. In contrast, LBD is diagnosed when the dementia onset occurs within 1-year of the onset of motor symptoms of parkinsonism. [107]

Patients with Parkinsonism and psychosis (both LBD and PDD) can be classified as experiencing "benign hallucinosis" or complex psychotic symptoms. "Benign hallucinosis," is commonly observed in PD without dementia, implying nontroubling mild visual perceptual disturbances for which patients usually maintain insight and which often do not warrant treatment. [108] In contrast, people with PDD and LBD more often experience frightening complex psychotic symptoms for which they lack insight, which are associated with behavioral changes, and which often warrant treatment. [108]

In a prospective study of 239 community-based patients with PD followed over 12 years, [109] 60% had psychotic symptoms and the incidence rate of psychosis was 79.7/1000 person-years. Proposed diagnostic criteria for psychosis in PD include having at least illusions, hallucinations, delusions, or a false sense of presence on a recurrent or continuous basis for one month with possible associated features of insight, dementia, and treatment for PD. [110] Visual hallucinations are the most frequent psychotic symptom present in PDD, [111] occurring in nearly half of patients. [112] As with PDD, visual hallucinations are the most frequent psychotic symptom in LBD and serve as one of the core diagnostic features. [107] Misidentifications in LBD range from simple misidentifications of people to "delusional misidentification syndromes," such as Capgras syndrome and the "phantom boarder" delusion. [113],[114] A recent study found that 78% of patients with LBD had hallucinations, 56% had misidentifications, and 25% had delusions. [115] Since the psychotic symptoms with LBD occur earlier in the course of the disease and are more frequent than in AD, they tend to cause more caregiver distress at the early stages of illness. [55]

Special pharmacologic treatment decisions need to be considered with the psychosis of PDD and LBD. Worsening Parkinsonism with the use of antipsychotics merits careful attention, especially since sensitivity to antipsychotic medications is one of the suggestive diagnostic features of LBD, and dopaminergic blockade can worsen parkinsonian symptoms in both conditions.

For psychosis in patients with PD, the first step involves evaluation for delirium and relationship of psychosis with antiparkinsonian medications. In absence of delirium and if the psychosis is possibly related to use of antiparkinsonian medications, then efforts should be made to reduce these medications to the lowest effective dose, in the order of anticholinergics, selegiline, amantadine, dopamine receptor agonists, catechol-O-methyltransferase inhibitors and finally levodopa. However, if the reduction in anti-PD medications to the lowest dose tolerable without exacerbation of motor symptoms does not improve the psychosis then use antipsychotic medication is warranted. [116]

Randomized controlled trials indicate that low-dose clozapine (25-150 mg) is efficacious without worsening parkinsonism symptoms, although clozapine is challenging to use in older adults because of its risk for agranulocytosis (necessitating frequent lab draws) and its potent anticholinergic properties. [117] Quetiapine is anecdotally the first-line treatment for psychosis in PD, but interestingly, RCTs comparing it to placebo do not strongly support its efficacy. [118],[119] Quetiapine was found to be just as effective as clozapine in one study, [120] and its use has been supported by open-label trials. Although not commonly considered for treating the psychosis associated with PD, small doses of risperidone (0.25-1.25 mg/day) have been shown to improve hallucinations without worsening Parkinsonism in a limited number of patients. [121]

Psychotic symptoms as part of delirium

As a neuropsychiatric syndrome, delirium typically occurs in medical, surgical illnesses and has an acute onset and fluctuating and reversible course. Patients with delirium have a worse prognosis than patients without delirium and are at an increased risk of developing long-term cognitive and functional decline [122],[123] which in turn leads to additional post hospitalization, rehabilitation services and home health care. [122] Delirium broadly has two types of symptoms: "Core" symptoms-disturbances of attention, memory, orientation, language, thought processes, and sleep-wake cycle; and "associated" features-psychotic symptoms, affect disturbances, and different motor profiles. [124]

In India, delirium is the most common diagnosis among general psychiatric referrals (30-39%) as well as for the elderly population (49%). [125] A recent Indian study on 98 elderly patients with delirium reported significantly greater prevalence of behavioral and cognitive symptoms compared to psychotic symptoms (delusion and hallucinations). [126] Psychotic symptoms such as delusions and hallucinations are more common reported in hyperactive and mixed subtype compared to hypoactive subtype. [126],[127]

The prevalence of delusion (35-40%) and hallucinations (78-80%) remained substantially high in elderly patients with delirium. [128],[129] In another Indian study of 321 consecutive patients with delirium comparable prevalence of delusion (46% vs. 40%) and hallucinations (79% vs. 80%) were reported in adults as well as the elderly population. [129]

Correction of physical/metabolic abnormalities and nonpharmacological strategies (e.g. reorientation and behavioral intervention, etc.) is the first-line treatments for all patients with delirium including elderly. [130] Haloperidol has been the most widely used antipsychotic agent with proven effectiveness in randomized, controlled clinical trials. Now, atypical antipsychotics (risperidone, olanzapine, and quetiapine) are also being used to treat agitation in patients with delirium, with comparable efficacy to haloperidol. [130],[131],[132]

Recently, Wang et al. [133] reviewed six prospective, randomized controlled studies to compare amisulpride (mean dose 156 mg/day), quetiapine (mean dose 40-113 mg/day), olanzapine (mean dose 1.8-4.5 mg/day), risperidone (mean dose 0.6-1 mg/day), and haloperidol (mean dose 0.8-6.5 mg/day) in treating delirium. They found comparable efficacy and safety profile among all atypical antipsychotics and low-dose haloperidol.

Psychosis associated with general medical conditions, drugs of abuse or prescription drugs

Varity of medical diseases can present with psychotic symptoms (i.e., delusions, hallucinations) in elderly. A secondary psychosis is more likely if psychotic symptoms first appear at an atypical or older age and if there is no personal or family history of primary psychotic disorders. The temporal pattern of the symptoms onset remains the most important factor in making the diagnosis. If the course of the psychotic symptoms parallels the course of the medical disorder suspected as the cause, a diagnosis of secondary psychosis is more likely. Medical conditions commonly causing psychotic symptoms are metabolic disorders (e.g., vitamin B12 deficiency, hepatic encephalopathy, uremia, acute intermittent porphyria, thyroid and adrenal disorders, etc) or brain disorder (e.g., stroke, Wilson disease, tumor, epilepsy etc). [134]

Secondary psychosis is also seen as a side effect of medications like corticosteroids, dopaminergic drugs (e.g. L-dopa, amantadine), interferons, stimulants, anticholinergics etc. and rarely with antiarrhythmics, digitalis, anesthetics, antimalarial drugs: Mefloquine, antituberculous drugs: D-cycloserine, ethambutol, isoniazid, antibiotics: Ciprofloxacin, antivirals: Efavirenz, acyclovir, antineoplastics (especially ifosfamide). [134]

Alcohol, sedative-hypnotics, and recreational drugs also cause psychosis. Alcohol and sedative hypnotics can lead to psychosis during intoxication (rare), as well as during withdrawal (common). Alcoholic hallucinosis or pathological jealousy (othello syndrome) can develop with long-term alcohol abuse. Stimulant drugs (e.g., cocaine, methamphetamine) and psychotomimetics (e.g., lysergic acid diethylamide, phencyclidine as well as cannabis commonly causes psychosis. [135]

Therefore, a thorough differential diagnosis of possible medical and toxic causes of psychosis is necessary to avoid the mistaken attribution of psychosis to a primary psychiatric disorder. Ruling out secondary causes of psychosis is important because the causation of psychosis by a medical disorder or substance can dramatically change management and prognosis. For diagnosing drug-induced psychosis, one should ascertain proper medical history, thorough physical examination and investigations with a specific focus to clinical details and drugs which are prevalent in particular geographic areas and clinical subpopulations.


As summarized in this article, late-onset psychosis is an under-researched subject, especially in India. Research is required to understand the epidemiology, phenomenology, and other bio-psycho-social issues associated with this clinical entity. By now, we do not have well-established specific treatment guidelines for late-life psychosis. Although psychosocial interventions for psychosis in dementia are being carried out, more evidence-based data are required for its widespread implementation. This calls for a need of novel, safe, well-tolerated pharmacotherapy, and effective psychosocial approaches for late-life psychosis.


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