Pseudodelirium: Psychiatric Conditions to Consider on the Differential for Delirium
Abstract
Objective:
The phenotypes of several psychiatric conditions can very closely resemble delirium; the authors describe such presentations as pseudodelirium. However, because the clinical management of these conditions differs markedly from that of delirium, prompt differentiation is essential. The authors provide an educational review to assist clinicians in identifying and managing psychiatric conditions that may be especially challenging to differentiate from delirium.
Methods:
Based on clinical experience, the authors identified four psychiatric conditions as among the most difficult to differentiate from delirium: disorganized psychosis, Ganser syndrome, delirious mania, and catatonia. An overview of each condition, description of clinical features, differentiation of specific phenotypes from delirium, and review of clinical management are also provided.
Results:
The thought and behavioral disorganization in disorganized psychosis can be mistaken for the clouded sensorium and behavioral dysregulation encountered in delirium. The fluctuating alertness and apparent confusion in Ganser syndrome resemble delirium’s altered arousal and cognitive features. As its name suggests, delirious mania presents as a mixture of hyperactive delirium and mania; additional features may include psychosis, autonomic activation, and catatonia. Both delirium and catatonia have hypokinetic and hyperkinetic variants, and the two syndromes can also co-occur.
Conclusions:
The clinical presentations of several psychiatric conditions can blend with the phenotype of delirium, at times even co-occurring with it. Detailed evaluation is often required to differentiate such instances of pseudodelirium from delirium proper.
Case Study
A 52-year-old woman with unknown medical history was brought to the emergency department for “acting bizarrely.” A neighbor had called 911 after finding her wandering agitatedly in their apartment complex, picking at invisible objects, disheveled, and confused. No prior records for the patient were available at the hospital. Her vital signs on arrival were remarkable for tachycardia and hypertension. Initial workup in the emergency department—including complete blood count, comprehensive metabolic panel, liver function tests, urine toxicology screen, thyroid-stimulating hormone, vitamin B12, chest X-ray, and head computerized tomography—was remarkable only for prerenal azotemia. Her creatine phosphokinase level was 2,152 units/L. Urinalysis results were equivocal and revealed many squamous cells. She received 1 mg of intravenous haloperidol twice in the emergency department without appreciable effect. She was admitted to the general medical service for “altered mental status.”
The patient screened positive on the Confusion Assessment Method (CAM) administered by nursing staff on initial assessment, as she was hyperactive with grossly altered mentation and unable to attend to conversation. Shortly after admission, collateral revealed that her medication regimen included divalproex sodium delayed release (500 mg qAM and 750 mg qhs), zolpidem (5 mg qhs), and hydrochlorothiazide (25 mg daily). Her valproic acid level was found to be undetectable, and liver function tests and ammonia were unremarkable. Her outpatient medications were held out of concern that they may have contributed to delirium. CAM results continued to be positive. Despite rehydration and normalization of renal status, the patient continued to exhibit confusion, spoke in a shrill staccato voice, and was occasionally found to be shirtless. Further 1-mg doses of intravenous haloperidol were ineffective.
Psychiatry was consulted to assist with delirium management. On psychiatric evaluation, the patient was unable to engage in cognitive testing or provide a meaningful narrative. The psychiatrist noted the shrill voice as manneristic speech and identified verbigeration when the patient repeated the phrase “Is it 10 o’clock?” several times, prompting consideration of catatonia (1). Her Bush-Francis Catatonia Rating Scale score was 13 for excitement, stereotypy, mannerism, verbigeration, rigidity, and autonomic abnormality. Lorazepam (2 mg) was given intravenously, and assessment 30 minutes later revealed moderate improvement in speech fluency, reduction in mannerisms and verbigeration, and improvement in abnormal tone. The patient was able to explain that she had bipolar disorder and had not taken valproic acid for the past week due to an upset stomach, diarrhea, and feeling “under the weather.” Lorazepam (2 mg three times a day) was recommended to treat catatonia secondary to bipolar disorder type I until valproic acid was again therapeutic.
Introduction
Delirium presents as an acute change in mental status characterized by a disturbance in attention, awareness, cognition, and arousal (2), and its clinical phenotype is often readily identifiable on bedside tests, including ultra-brief screening instruments (3). As opposed to most primary psychiatric conditions, in which only a subset of neuropsychiatric domains are affected (e.g., mood or discrete psychotic symptoms), delirium represents a global disturbance in mentation, cognitive clarity, and psychomotor activity. Differentiating between primary psychiatric conditions and delirium—which requires the presence of an underlying encephalopathy (4, 5)—is important for several reasons. Diagnostically, DSM-5 disallows the diagnosis of primary psychiatric disorders during delirium, but, most importantly, differentiation is essential for timely and appropriate clinical management.
Although the phenotypic differences between primary psychiatric conditions and delirium are generally unambiguous on clinical evaluation, this is not always the case. In fact, occasionally the clinical phenotypes of certain psychiatric conditions are practically indistinguishable from delirium, even to seasoned clinicians. Some psychiatric conditions can resemble the clinical phenotype of delirium so closely that they lead to positive screens on common delirium instruments (e.g., CAM [6]), as in the opening case study. It is also noteworthy that no delirium instrument has been formally validated in cohorts of patients with serious mental illness.
The term pseudodelirium was first coined by Goldney and Lander to describe “acute functional psychoses” that mimic delirium (7). In this review, we have extended their use of pseudodelirium as linguistic shorthand to describe the phenomenon of a psychiatric condition that presents with a clinical phenotype that very closely resembles delirium, especially where mistaken for delirium. Prompt differentiation between pseudodelirium and delirium is essential to guide clinical management. Whereas clinicians are often encouraged not to miss underlying medical conditions that may account for psychiatric symptoms, they receive far less guidance on the potential risks of managing primary psychiatric conditions as delirium. Rather, clinicians should bear in mind the risks of erring on either side—that is, the type I and type II errors of inaccurately ruling delirium in or out (Table 1).
| Risks of diagnosing primary psychiatric illness as delirium | Risks of diagnosing delirium as primary psychiatric illness | ||
|---|---|---|---|
| Risk | Example | Risk | Example |
| Psychiatric treatments withheld | Benzodiazepines or ECT is used for catatonia. Mood stabilizers (e.g., lithium) are used for mania. Antidepressants are used for depression. Delayed pursuit of a “medication over objection” hearing for psychotic decompensation occurs. | Reversible conditions overlooked | The list of medical causes of psychiatric symptoms is extremely long (49). |
| Inappropriate medications given | Antipsychotics are effective for psychosis in a formal thought disorder and for psychosis and mania in delirious mania. However, their use in catatonia requires careful consideration; neuroleptic-induced extrapyramidal symptoms may be difficult to differentiate from features of catatonia, and patients with catatonia may be at higher risk of developing neuroleptic malignant syndrome, especially from high-potency agents. | Inappropriate psychiatric admission | Psychiatric settings are not equipped to manage acute medical conditions. For instance, intravenous antibiotics often cannot be given for infection (i.e., lines represent a safety risk) and supplemental oxygen is often unavailable. |
| Unnecessary workup completed | Expanded workup for delirium is costly, time-consuming (e.g., prolonged length of stay), and potentially invasive (e.g., lumbar puncture). | Inappropriate medications given | Benzodiazepines given to a delirious patient may worsen cognition and delay recovery; use of antipsychotic medication may cause extrapyramidal side effects. |
| Psychosocial and family history overlooked | Legal situation is not obtained (e.g., legal charges may be pending, Ganser syndrome). History of similar presentations for schizophrenia or bipolar disorder is present, including common delusional themes. | Medical deterioration | Delayed treatment of autoimmune encephalopathy is associated with cognitive and functional sequelae. |
TABLE 1. Risks of incorrectly diagnosing primary psychiatric illness and delirium as the other
There are many reviews that parse out the “three Ds” of geriatric psychiatry: delirium, dementia, and depression (8). However, we are unaware of similar reviews that explore the phenotypes of other psychiatric conditions relative to delirium. Here, we describe psychiatric conditions that may be especially challenging to differentiate from delirium. Our goal is to bring awareness to these conditions through this educational resource for clinicians.
Methods
Based on our pooled clinical experience, we identified the following four psychiatric conditions as being among the most difficult to differentiate from delirium: disorganized psychosis, Ganser syndrome, delirious mania, and catatonia. We conducted a clinically focused literature review for each condition to provide a conceptual overview, describe its phenotype, differentiate its clinical presentation from delirium, and review its clinical management. This literature review was initially conducted in preparation for a workshop at a large psychiatric conference, and feedback received at the conference was incorporated into this article.
Results
Disorganized Psychosis
Psychotic disorders can present with disorganized thoughts and behavior as well as the dissolution of reality-based thought content and sensory experiences. Several facets of psychotic disorders can make it difficult to differentiate acute episodes of psychotic decompensation from delirium, especially when patients present with prominent thought disorganization (2). In fact, the full spectrum of symptoms encountered in psychotic disorders can be found in delirium as well. Nevertheless, there is minimal overlap between the diagnostic criteria of psychotic disorders and delirium in DSM-5. Specifically, disorganized speech may lead clinicians to conclude that the patient has a disturbance in awareness (second half of criterion A for delirium), and hallucinations (i.e., altered perceptions) would satisfy criterion C (2).
Psychotic disorders are often described as formal thought disorders. This term refers to the disordered nature of thought form (as opposed to thought content) and to various types of thought disorganization, especially those presenting with disruption of coherent narrative capacity. By way of parallel, some diagnostic systems for delirium, including DSM-III-R, ICD-10, and many well-validated delirium screening tools (e.g., the family of CAM instruments) incorporate disorganized thinking or thought process in their assessment criteria (6, 9–11). Additionally, the comment section in ICD-10 indicates that “disturbances of perception (illusions or hallucinations, often visual) and transient delusions are typical but are not specific indications for the diagnosis” (11).
Clinical features.
Patients with thought or behavior disorganization tend to think and act in an aimless, nonconstructive manner. As the severity of thought disorder increases, patients tend to become increasingly psychotic as the reality-basis of thoughts fades. Often a patient may be disheveled, use poor judgment, lack impulse control, and provide inappropriate responses (12). When thoughts are disorganized, a patient will have difficulty formulating ideas and language, which hinders effective communication. Patients may also exhibit loosening of associations, incoherence, thought blocking, flight of ideas, perseveration, reduced concentration, circumstantiality, tangentially, poverty of thought content, concreteness, neologisms, echolalia, verbigeration, world salad, and mutism (12).
Differentiation from delirium.
Detailed clinical evaluation for evidence of systemic illness, polypharmacy, and illicit drug use is indicated. The acuity of onset and course of psychotic symptoms, the patient’s age, and the patient’s medical and psychiatric history (e.g., where a series of similar presentations might suggest recurrence of a primary psychotic illness) often guide diagnostic impressions (13). EEG can help differentiate between primary psychotic illness and delirium: Delirium classically presents with diffuse slowing and increased theta and delta activity, whereas these findings would be rare in primary psychotic disorders (14, 15) (Table 2). Despite its potential usefulness in disentangling delirium from a primary psychiatric disorder, the debate about the utility of EEG in detecting and diagnosing delirium persists. Some have argued that the characteristic background slowing of an EEG in delirium is nonspecific and therefore an unnecessary clinical study, whereas others have reported findings suggesting that generalized slowing on EEG strongly correlates with delirium and may be a marker of delirium severity (15).
| Variable | Delirium | Disorganized psychosis | Ganser syndrome | Delirious mania | Primary catatonia |
|---|---|---|---|---|---|
| EEG | Diffuse slowing | No specific pattern | Typically normal | Unknown | Typically normal |
| Clinical status | Sick, often frail | Medically stable | Medically stable | Variable; often with autonomic activation | Medically stable |
| Arousal | Rarely appropriately alert | Alert | Fluctuates; may be alert for extended periods | Can alternate between hyperkinetic and stuporous | Usually stuporous, occasionally hyperkinetic |
| Interpersonal | Inattentive | Variable; often difficult to rule out inattention | Often engaged | Fluctuates; often inattentive | Disengaged, negativistic; occasionally automatically obedient |
| Verbal responses | Muddled thinking | Speech disorganized | Approximate answers common | Initially hyperverbal; may devolve to mutism | Mute, whispered, verbigeration, or echolalia |
| Sensorium | Clouded | Usually clear | Verbal content suggests clouding | Clouded in mid- to late stages | Often clear but difficult to assess |
| Emotional state | Consistent with motor subtype | Often paranoid | Effortful engagement | Manic, may devolve to blunted state | Fearful, occasionally manic |
| Psychosocial | Reduced engagement | Difficult to engage | Bizarre; psychosocial stressor present | May be initially intrusive, then disengaged | Variable, related to underlying condition |
TABLE 2. Differentiating features of delirium from pseudodelirium
Careful characterization of the clinical phenotype can also provide diagnostic clues. Nonauditory hallucinations are uncommon in primary psychotic disorders. Additionally, when visual hallucinations occur in primary psychotic illness, these tend to be vague or shadowy. In delirium, visual hallucinations may be of any character: vivid, colorful, fragmentary, vague, or even multimodal (e.g., audiovisual). Patients with primary psychotic illness are typically alert with stability of symptoms over the course of the day, whereas delirium commonly presents with altered arousal and circadian fluctuation of symptoms. Clinicians should also be aware of the possibility of apparent disorientation due to “double bookkeeping” in some psychotic conditions, as when a patient has a factual understanding of their autobiographical information but maintains on direct questioning that they live somewhere else (e.g., a person who believes they are the president saying their home address is the White House).
Management.
The mainstay of treatment for disorganized psychosis includes antipsychotics, mood stabilizers for comorbid mania, benzodiazepines for behavioral activation, and occasionally ECT for severe symptoms. Although antipsychotics are still widely used to manage psychotic symptoms or agitation associated with delirium, their efficacy in preventing and treating delirium is unproven (16, 17). Delirium management, on the other hand, involves treating its precipitants, addressing underlying neurophysiological disruption where known (e.g., hyperadrenergic state in alcohol withdrawal delirium), reversing elements of cognitive vulnerability (e.g., malnutrition, inanition), and managing dangerous or distressing symptoms of the delirium phenotype (e.g., agitation, paranoid delusions).
Ganser Syndrome
The German psychiatrist Sigbert Ganser first described this condition in 1897 among prisoners awaiting trial as a “peculiar hysterical twilight state,” but Ganser syndrome has garnered several terms since, including prison psychosis, the foolish or buffoonery syndrome (German faxensyndrom), pseudodementia, and—especially relevant here—psychogenic delirium (7, 18, 19). Uncertainty over how best to formulate this condition is reflected in its historical traipse through the DSM: It was an adjustment disorder in DSM-II, a factitious disorder in DSM-III, and a dissociative disorder from DSM-III-R to the present. The modern prevailing view is that it represents a psychological need to escape from an intolerable situation or psychosocial reality. Perhaps the simplest way to describe it is that it evinces “what ordinary people … think … madness looks like or should look like” (20). Because of this, malingering should be on the differential when evaluating someone with symptoms of Ganser syndrome.
Clinical features.
The central feature of Ganser syndrome is approximate answers (German vorbeigehen, “to pass over,” or vorbeireden, “to talk at cross-purposes”). When asked even simple questions, patients with Ganser syndrome routinely provide answers that are obviously incorrect but also indicate that they grasp the nature of the question and the kind of response called for (18). In response to the question “What’s the largest number on the face of that clock?” the patient might say “Ten.” Other cardinal symptoms of this condition include clouding of consciousness, audiovisual hallucinations (either reported or inferred based on the patient’s responses to internal stimuli), and conversion symptoms.
Additional clinical features may include disorientation, loss of identity, a fugue state, and regression (puerilism) (20). Patients can experience rapid, astonishing recovery and report amnesia for the episode. Nearly half of patients have a prior psychiatric diagnosis; 10% have a history of dissociation, 10% have prior unexplained physical symptoms, and 10% have a criminal history (21). Although this condition is thought to be generated psychologically, a third of patients have a neurological condition such as previously unrecognized brain pathology discovered as part of the workup; accordingly, some authors have suggested certain brain conditions may confer vulnerability to this syndrome (21, 22).
Differentiation from delirium.
Approximate answers are specific for Ganser syndrome because a patient must have intact cognition and sufficient awareness of the questions to generate such responses consistently and, as in most cases of Ganser syndrome, fluently. Verbal responses tend to offer conceptual clarity even if they are bizarre. The patient in this state may also exhibit unusually effortful engagement. In addition, a psychosocial history typically reveals a situation from which the patient would reasonably want to escape (e.g., emotional trauma due to a recent sexual assault, legal charges). EEG is generally normal as opposed to the generalized slowing seen in delirium (23).
Management.
Accurate diagnosis is key to preventing unnecessary workup. Although the condition is rare enough that a consensus on management has yet to emerge, patient interactions should honor the principles of trauma-informed care and emphasize safety, trust, and clarity of communication because dissociation is a response to perceived threat (24). In addition, person-focused psychological first aid that restores a sense of normalcy and establishes a daily routine should be implemented (25). Other considerations for treatment derive from approaches to conversion disorder and include acknowledgment of the symptoms as real; reassurance that the condition is not dangerous, life-threatening, or progressive; an affirmation of clinical expertise for this condition; and the suggestion that full recovery is anticipated.
Delirious Mania
First described by Calmeil (1832) (26) and Bell (1849) (27), this potentially fatal syndrome is characterized by psychomotor agitation, emotional lability, acute psychosis (delusions and hallucinations), and disorientation. Max Fink later described delirious mania as, “a syndrome of the acute onset of the excitement, grandiosity, emotional lability, delusions, and insomnia characteristic of mania, and the disorientation and altered consciousness [characteristic of delirium]….not associated with prior mental or systemic disorder” (28). In Fink’s description, catatonia was a consistent finding (28). The phenomenology of delirious mania remains unclear and has evolved over the decades, in large part owing to the lack of diagnostic criteria and, as a result, sporadic and discrepant reports.
Clinical features.
In one review, 15%–36% of psychiatrically hospitalized patients with mania had co-occurring delirium (29). The typical course of delirious mania may vary, but patients often exhibit a prodrome of worsening symptoms of mania over days to weeks, followed by frank psychosis. This typically devolves further into an overt delirium-like phenotype, including inattention, disorientation, altered and fluctuating arousal, psychomotor abnormalities, poor recall of events, perceptual abnormalities, and distorted thought process. At times, the patient enters an excited or stuporous catatonia. Symptoms may also fluctuate in severity much like the waxing and waning of delirium. The condition can resolve spontaneously or require intensive treatment to remit. In many cases, patients who experience delirious mania either have a personal history of or a first-degree relative with bipolar disorder.
Differentiation from delirium.
The inclusion of the term “delirious” in delirious mania chiefly denotes the mental status phenotype; however, delirious mania may at times meet DSM-5 criteria for delirium. The extreme psychomotor dysfunction in this condition often involves muscle rigidity and dehydration, accompanied by lab abnormalities (e.g., elevated creatine phosphokinase, leukocytosis, and creatine) reflecting end-organ dysfunction (acute renal injury or rhabdomyolysis). Additionally, delirious mania is often complicated by autonomic dysfunction (e.g., tachycardia, hypertension, tachypnea, fever), especially in patients with the malignant form (the analogous historical descriptors “lethal” or “pernicious” are now generally discouraged). Further highlighting the ambiguity between mania and delirium, a chart review of 199 patients showed a 14.9% prevalence of delirium in bipolar disorder (29). In short, patients experiencing an episode of delirious mania may simultaneously be manic, psychotic, delirious, and catatonic. Unless conclusive empirical evidence suggests otherwise, the assignment of one diagnostic label (e.g., mania, psychosis or catatonia) should not exclude recognition of another (e.g., delirium).
Management.
The management of delirious mania depends on the clinical presentation. Aside from identifying and treating co-occurring conditions and associated morbidities (e.g., dehydration, rhabdomyolysis, venous thromboembolism, autonomic abnormalities), one of the first steps should be to perform a complete diagnostic interview to elucidate whether there is a contributing bipolar diathesis. If so, that may support the use of mood-stabilizing or antiepileptic medication. Next, a thorough physical exam should be performed with particular attention to the evaluation of catatonic features (e.g., rigidity, mutism, catalepsy, autonomic abnormalities); if present, they should be promptly treated, generally with a trial of a benzodiazepine (typically lorazepam, which can be administered orally, intravenously, or intramuscularly). Depending on the severity of catatonic signs present, patients may require transfer to a medical floor and, in rare circumstances, an intensive care unit. ECT is typically reserved for those whose catatonic signs fail to respond to benzodiazepines or those with prominent mania symptoms not responding to mood stabilization efforts. If catatonic symptoms are present, antipsychotics are generally withheld until malignant features of catatonia have resolved. If antipsychotics are indicated, generally due to prominent positive psychosis symptoms (e.g., hallucinations or delusions), atypical antipsychotics are generally preferred.
Catatonia
Catatonia was first described in 1874 by German psychiatrist Karl Ludwig Kahlbaum (30) as a clinical syndrome of motor, vocal, and behavioral abnormalities. Emil Kraepelin proposed that catatonia was as a motoric presentation of dementia praecox, which was echoed by Eugen Bleuler’s conceptualization of schizophrenia but debated by others (31, 32). Throughout the greater part of the 20th century, catatonia was classified as a subtype of schizophrenia, despite growing evidence that most patients with catatonia have a mood disorder (most commonly bipolar disorder), a psychotic disorder, or a neurological or medical illness (33, 34). DSM-5 classifies catatonia within the chapter on schizophrenia spectrum and other psychotic disorders but no longer as a subtype of schizophrenia. DSM-5 diagnoses include catatonia associated with another mental disorder, catatonic disorder due to another medical illness, or unspecified catatonia (2). The prevailing pathophysiologic hypothesis is that catatonia is caused by dysregulation in GABA-A and glutamate circuitry between the prefrontal cortex, parietal cortex, and basal ganglia (35, 36). Still, a lack of consensus about its nosology and pathophysiology persists.
Clinical features.
The cardinal feature of catatonia is a psychomotor disturbance in which a person’s volition to move or to act is disrupted. The three motoric subtypes of catatonia are hypokinetic, parakinetic, and hyperkinetic; of these, the hypokinetic type is most common (37). Common symptoms of catatonia include staring, immobility, mutism, withdrawal (not eating, drinking, or making eye contact), posturing, catalepsy, and negativism. The Bush-Francis Catatonia Rating Scale is the most widely used of many published catatonia instruments (38). After catatonia resolves, many describe having had an experience of intense anxiety, fear, or the belief that they were dead or dying during the episode (39). A catatonia diagnosis is often confirmed by response to intravenously administered benzodiazepines, with response ranging from partial to full resolution of catatonic symptoms, often within minutes. However, some patients with catatonia—especially those with complex medical disease, neurologic injury, or chronic catatonia due to primary psychotic illness—may experience only partial or no response to benzodiazepines.
Differentiation from delirium.
Both catatonia and delirium have hypoactive and hyperactive variants (40). Perseverative thought process, which may be scored as inattention on the CAM as it represents an inability to shift attention, is also common in catatonia. However, several other features of catatonia are not routinely seen in delirium, including abnormalities in tone (rigidity or waxy flexibility), speech (mutism, manneristic speech, or verbigeration), behavior (posturing, catalepsy, stereotypies, or mannerisms), echophenomena (echolalia or echopraxia), negativism, and severe withdrawal with refusal to eat or drink. Furthermore, the EEG is typically normal in primary catatonia (41), unlike in delirium (42). Recent studies (43, 44) have revealed that delirium and catatonia frequently co-occur in the context of critical illness, so differentiation may not always be feasible.
Treatment response to benzodiazepines may prove decisive in differentiating catatonia from delirium. Most presentations of primary catatonia partially or fully respond to lorazepam. Even catatonic features in delirium may show some improvement in response to low-dose benzodiazepines; however, such patients are not expected to show improved cognition with benzodiazepines, especially when the dose is increased. Specifically, lorazepam dose is an independent risk factor for transitioning to delirium in intensive care unit patients (45), so clinicians should use benzodiazepines very cautiously in patients with or at risk for delirium.
Management
Benzodiazepines are the primary treatment of catatonia, beginning with an intravenous dose if possible and, if effective, followed by scheduled around-the-clock dosing (39, 42). Benzodiazepines are hypothesized to restore GABA-A signaling in the prefrontal cortex and hypothalamus. ECT is a highly effective treatment for catatonia, including in patients with inadequate response to benzodiazepines; ECT is first-line treatment for malignant catatonia because of its risk of fatality without assertive treatment (46). Supportive treatments including venous thromboembolism prophylaxis, repositioning, pressure-reducing devices, and physical therapy are pertinent for preventing complications of catatonia such as pulmonary embolism, pressure ulcers, dehydration, malnutrition, and contractures. If catatonia is misdiagnosed as delirium, treatment with benzodiazepines may be withheld due to concerns that they may worsen delirium. Delayed treatment of catatonia is associated with poorer treatment response and prognosis (47), thus highlighting the importance of prompt catatonia diagnosis and treatment.
Discussion
Although the core neurocognitive features of delirium typically allow clinical differentiation from primary psychiatric conditions, the clinical phenotype of delirium is not always unambiguous. Each of its core features may be encountered in primary psychiatric conditions. We consider each of its diagnostic features in turn (Table 3).
| Diagnostic criteriaa | Examples in primary psychiatric conditionsb |
|---|---|
| Criterion A, part 1: “Disturbance in attention” | Catatonia: Mutism and negativism can prevent a patient from demonstrating attention. Mania (especially delirious mania): Flight of ideas and distractibility prevent a patient from engaging consistently on evaluation. ADHD: Inattention and reduced concentration are included as diagnostic features. |
| Criterion A, part 2: “Disturbance …in awareness” | Catatonia: Mutism and negativism can prevent a patient from demonstrating awareness. Disorganized psychosis: Although patients with psychotic illness are typically oriented, acute psychotic decompensation can present with “word salad” or grossly disrupted thought process. Dissociative disorders (including Ganser syndrome): Dissociation is a disruption in the normal integration of consciousness, experience, and actions, often leading to lack of situational awareness. |
| Criterion B: “Develops over a short period …and tends to fluctuate” | Mania: Symptoms typically develop over days. Acute psychosis: Symptoms typically develop over days. Dissociative disorders: Symptoms often occur over hours to days; Ganser syndrome can exhibit fluctuation over the course of the day. |
| Criterion C: “An additional disturbance in cognition,” [including] memory, orientation, language, visuospatial ability, or perception” | Catatonia: Mutism and negativism can prevent a patient from engaging in cognitive evaluation. Acute psychosis: Delusional recall may confound assessment; paranoia may prevent a patient from engaging in assessment. Mania: Profound irritability can prevent a patient from engaging in formal cognitive assessment. Dissociative disorders: Perceptual disturbances may be experienced. |
| Specifier: Hyperactive, hypoactive, and mixed level of activity | Catatonia: Hypokinetic, hyperkinetic, and parakinetic subtypes are exhibited. Mania (especially severe or delirious mania): Marked psychomotor activation is present. |
TABLE 3. Diagnostic criteria of delirium reflected in primary psychiatric conditions
Disturbance in attention (criterion A, part 1) involves a reduced ability to focus, sustain, or shift attention. These factors are assessed by a patient’s ability to engage meaningfully in conversation, to perform a task of concentration (e.g., vigilance A, serial 7s, or months backward), or to change topics appropriately (e.g., perseveration is evidence of impaired ability to shift attention), respectively. Several acute psychiatric syndromes leave patients unable to demonstrate that attention is intact. For instance, patients with mutism in catatonia are unable to engage in conversation, and those with delirious mania may have flight of ideas and distractibility, preventing them from concentrating on a cognitive test.
Disturbance in awareness (criterion A, part 2) describes disorientation to one’s environment and may be thought of as the answer to the question, “Does the patient understand what is going on around them?” Its assessment typically involves narrative content; however, many acute psychiatric conditions present with disturbances in communication (e.g., catatonia) or thought form (e.g., psychotic syndromes), thus making it exceptionally difficult if not impossible at times for a clinician to assess or even intuit a patient’s degree of situational or environmental awareness.
Many primary psychiatric syndromes such as mania or acute psychosis satisfy Criterion B of delirium as they present over the course of days; however, most primary psychiatric conditions are unlikely to exhibit substantial fluctuation over the course of the day. One notable exception to this is where acute response to specific medications (e.g., an antipsychotic in disorganized psychosis or a benzodiazepine in catatonia) may, at times, be interpreted as evidence of a waxing and waning clinical course.
Criterion C for delirium diagnosis, which requires another cognitive disturbance (i.e., in addition to a disturbance in attention and awareness), identifies several domains: memory, orientation, language, visuospatial ability, or perception. Patients with acute psychosis (especially catatonia, paranoia, or irritable mania) often do not participate in formal cognitive testing, making it very difficult to ascertain cognitive status or evaluate for these findings. Beyond mutism, catatonia can present with a variety of abnormal speech patterns (48). Dissociation not infrequently presents with hallucinations or other perceptual changes, such as time or visual distortions.
Finally, it is important to reflect on the fact that many psychiatric constructs (e.g., delirium, bipolar disorder) as currently defined by the DSM and ICD do not allow for a transdiagnostic relationship between psychiatric entities (e.g., mania, psychosis, catatonia). It is possible that the presence of mania or catatonia, like psychosis, can be driven by or embedded in another psychiatric condition, as in major depressive disorder, severe with psychotic features. Presentations such as delirium “with catatonic features,” “with psychotic features,” and so on, may also be thought of as the behavioral and psychological symptoms of delirium, akin to the behavioral and psychological symptoms of dementia. Further evaluation of the relationships between such entities may prove useful to clinicians and researchers alike.
Conclusions
Several psychiatric conditions can present with a clinical picture that closely resembles delirium or any of its core diagnostic features, a clinical scenario we describe here as pseudodelirium. Specifically, we have reviewed disorganized psychosis, Ganser syndrome, delirious mania, and catatonia as especially challenging to differentiate from delirium, given syndromal overlap. At times, psychiatric syndromes can even co-occur with delirium (e.g., delirious mania or catatonia), introducing further clinical complexity. The risk of false negative and false positive diagnoses of delirium deserve consideration in clinical care. Although difficult at times, differentiation of delirium from pseudodelirium is essential to ensure appropriate clinical care in a timely fashion.
1. : The Bush-Francis Catatonia Rating Scale: Training Manual and Coding Guide. Rochester, NY, University of Rochester
2.
3. : Comparative accuracy and efficiency of four delirium screening protocols. J Am Geriatr Soc 2020; 68:2572–2578Crossref, Medline, Google Scholar
4. : Updated nomenclature of delirium and acute encephalopathy: statement of ten societies. Intensive Care Med 2020; 46:1020–1022Crossref, Medline, Google Scholar
5. : Delirium disorder: integrating delirium and acute encephalopathy. Neurology 2020; 95:173–178Crossref, Medline, Google Scholar
6. : Clarifying confusion: the Confusion Assessment Method: a new method for detection of delirium. Ann Intern Med 1990; 113:941–948Crossref, Medline, Google Scholar
7. : Pseudodelirium. Med J Aust 1979; 1:630Crossref, Medline, Google Scholar
8. : Geriatric psychiatry review: differential diagnosis and treatment of the 3 D’s: delirium, dementia, and depression. Curr Psychiatry Rep 2013; 15:365Crossref, Medline, Google Scholar
9.
10. : Delirium in mechanically ventilated patients: validity and reliability of the confusion assessment method for the intensive care unit (CAM-ICU). JAMA 2001; 286:2703–2710Crossref, Medline, Google Scholar
11.
12. : Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. Philadelphia, Lippincott Williams and Wilkins, 2011Google Scholar
13. : Recognition and differential diagnosis of psychosis in primary care. Am Fam Physician 2015; 91:856–863Medline, Google Scholar
14. : Conventional and quantitative EEG in the diagnosis of delirium among the elderly. J Neurol Neurosurg Psychiatry 1993; 56:153–158Crossref, Medline, Google Scholar
15. : Clinical EEG slowing correlates with delirium severity and predicts poor clinical outcomes. Neurology 2019; 93:e1260–e1271Crossref, Medline, Google Scholar
16. : Antipsychotics for treating delirium in hospitalized adults: a systematic review. Ann Intern Med 2019; 171:485–495Crossref, Medline, Google Scholar
17. : Antipsychotics for preventing delirium in hospitalized adults: a systematic review. Ann Intern Med 2019; 171:474–484Crossref, Medline, Google Scholar
18. : The Ganser syndrome. Br J Criminol 1965; 5:120–126Crossref, Google Scholar
19. : Uncomplicated Gilles de la Tourette syndrome and probable Ganser syndrome: a case report and review of the literature. Eur Child Adolesc Psychiatry 2002; 11:234–239Crossref, Medline, Google Scholar
20. :
21. : Ganser syndrome: examining the aetiological debate through a systematic case report review. Eur J Psychiatry 2012; 26:96–106Crossref, Google Scholar
22. : A case of Ganser syndrome: organic or hysterical? Gen Hosp Psychiatry 2001; 23:230–231Crossref, Medline, Google Scholar
23. : The Ganser syndrome: evidence suggesting its classification as a dissociative disorder. Int J Psychiatry Med 1984; 14:47–56Crossref, Medline, Google Scholar
24. : Trauma informed care in medicine: current knowledge and future research directions. Fam Community Health 2015; 38:216–226Crossref, Medline, Google Scholar
25. : Disaster mental health and community-based psychological first aid: concepts and education/training. J Clin Psychol 2016; 72:1307–1317Crossref, Medline, Google Scholar
26. : Dictionnaire de medicine; ou repertoire general des sciences medicales considerees sous le rapport theorique et pratique, 2nd ed. Paris, Bechet, 1832Google Scholar
27. : On a form of disease resembling some advanced stage of mania and fever. Am J Insanity 1849; 6:97–127Google Scholar
28. : Delirious mania. Bipolar Disord 1999; 1:54–60Crossref, Medline, Google Scholar
29. : Incidence of and risk factors for delirium among psychiatric inpatients. Psychiatr Serv 1996; 47:727–730Crossref, Medline, Google Scholar
30. : Die Katatonie oder das Spannungsirresein. Eine klinische form psychischer Krankheit. Berlin, Hirschwald, 1874Google Scholar
31. : The catatonic syndrome and its relation to manic-depressive insanity. J Nerv Ment Dis 1913; 40:694–704Crossref, Google Scholar
32. : Benign Stupor. New York, Macmillian, 1921Google Scholar
33. : Catatonia in psychiatric classification: a home of its own. Am J Psychiatry 2003; 160:1233–1241Crossref, Medline, Google Scholar
34. : Catatonia: a prospective clinical study. Arch Gen Psychiatry 1976; 33:579–581Crossref, Medline, Google Scholar
35. : Etiopathogenesis of catatonia: generalizations and working hypotheses. J ECT 2010; 26:253–258Crossref, Medline, Google Scholar
36. : What catatonia can tell us about “top-down modulation”: a neuropsychiatric hypothesis. Behav Brain Sci 2002; 25:555–577, discussion 578–604 Crossref, Medline, Google Scholar
37. : The diagnostic criteria and structure of catatonia. Schizophr Res 2015; 164:256–262Crossref, Medline, Google Scholar
38. : Catatonia, I: rating scale and standardized examination. Acta Psychiatr Scand 1996; 93:129–136Crossref, Medline, Google Scholar
39. : Catatonia and its treatment. Schizophr Bull 2010; 36:239–242Crossref, Medline, Google Scholar
40. : Catatonia vis-à-vis delirium: the significance of recognizing catatonia in altered mental status. Gen Hosp Psychiatry 2015; 37:554–559Crossref, Medline, Google Scholar
41. : Clinical electroencephalograms in patients with catatonic disorders. Clin Electroencephalogr 1995; 26:60–64Crossref, Medline, Google Scholar
42. : Catatonia: our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry 2016; 6:391–398Crossref, Medline, Google Scholar
43. : Do patients of delirium have catatonic features? an exploratory study. Psychiatry Clin Neurosci 2014; 68:644–651Crossref, Medline, Google Scholar
44. : Delirium and catatonia in critically ill patients: the delirium and catatonia prospective cohort investigation. Crit Care Med 2017; 45:1837–1844Crossref, Medline, Google Scholar
45. : Lorazepam is an independent risk factor for transitioning to delirium in intensive care unit patients. Anesthesiology 2006; 104:21–26Crossref, Medline, Google Scholar
46. : Electroconvulsive therapy of the lethal catatonia syndrome. Convuls Ther 1990; 6:239–247Medline, Google Scholar
47. : A clinical review of the treatment of catatonia. Front Psychiatry 2014; 5:181Crossref, Medline, Google Scholar
48. : “Narration,” an atypical catatonic speech symptom: a case report. Psychosomatics 2020; 61:385–389Crossref, Medline, Google Scholar
49. : The Diagnosis of Psychosis. Cambridge, England, Cambridge University Press, 2011Crossref, Google Scholar
