Government and Espionage Delusions in Major Neurocognitive Disorders and Delirium

Terminology: The DSM-5-TR classifies what was formerly called “dementia” as major neurocognitive disorder (MND), with specifiers for etiologies (Alzheimer’s, Lewy body, vascular, etc.). MND is defined by a significant decline from prior cognitive function in ≥1 domain (memory, executive, language, etc) that impairs daily activities, not occurring only during delirium. ICD-11 similarly groups these under “neurocognitive disorders,” distinguishing delirium (acute) from mild versus major neurocognitive disorders (chronic). In ICD-11, delirium is coded under acute neurocognitive disorder (6D70) and dementia under codes 6D80–6D8Z.

Etiologies of Major NCD: Alzheimer disease is the most common cause of MND, accounting for ~60–70% of cases. Other etiologies include:

• Dementia with Lewy bodies (DLB): Often presents with well-formed visual hallucinations, marked fluctuations in attention/alertness, REM sleep behavior disorder, and Parkinsonian features. Lewy body dementia and Parkinson’s disease dementia (PDD) share pathology (α-synuclein) and both commonly cause hallucinations and paranoid delusions in later stages.
• Vascular cognitive impairment: Results from multiple infarcts or small-vessel ischemia, leading to stepwise declines in cognition (especially executive function and processing speed). Neuropsychiatric symptoms may occur but usually follow the evolving brain injury (e.g. “multi-infarct” dementia).
• Frontotemporal degeneration (FTD): Characterized by early behavioral changes (disinhibition, apathy, compulsiveness) and speech/language deficits. Memory may be relatively spared early on. Psychotic symptoms (hallucinations, delusions) are less common in FTD than in Alzheimer or Lewy dementias. When present, delusions in FTD often involve theft, infidelity, or misidentification (e.g. “phantom boarder,” Capgras/Fregoli).
• Parkinson’s disease dementia (PDD): Develops in advanced Parkinson’s disease (usually ≥1 year after motor symptoms). Like DLB, PDD features parkinsonism (tremor, rigidity, bradykinesia) and can include visual hallucinations and persecutory delusions, especially in late stages.
• Other causes: Less common etiologies include prion disease (rapid decline with myoclonus), Huntington’s disease (chorea, personality change), normal-pressure hydrocephalus (“wet, wacky, wobbly”), traumatic brain injury, toxic/metabolic encephalopathies, and mixed etiologies. Creutzfeldt–Jakob (prion) causes myoclonus and rapid dementia. Mixed Alzheimer/vascular dementia is frequent in the elderly.

Cognitive and Perceptual Features: Memory impairment is the hallmark of Alzheimer’s MND. In contrast, FTD and vascular dementia often show early deficits in executive function (planning, judgment, abstract reasoning) and behavior, with memory impairment developing later. Confabulation (fabricating memories without intent to deceive) is most pronounced in disorders of severe anterograde amnesia (e.g. Wernicke–Korsakoff syndrome); it is uncommon as a primary feature in typical dementias. Patients with any NCD may have impaired recognition (agnosia) of people or places, contributing to misidentification delusions.

Importantly, visual hallucinations are especially common in Lewy body and Parkinsonian dementias. About 60–70% of patients with DLB experience complex visual hallucinations (animals, people, shapes) as an early symptom. Auditory/olfactory hallucinations occur but are less frequent. By contrast, hallucinations can occur in advanced Alzheimer’s but are less prominent. The Parkinson’s Foundation notes that 20–40% of PD patients report hallucinations or delusions over the disease course; delirium or medication changes often contribute to acute psychosis in PD.

Patients with dementia often misinterpret missing items and may form persecutory delusions (beliefs others have stolen or are conspiring). For example, an Alzheimer’s patient might believe a caregiver is stealing money or that someone is following them by police. These false beliefs are firmly held (delusions) and fit the context of memory loss: inability to recall where something was placed may become a narrative of theft. Practical Neurology notes that theft, infidelity, and phantom boarder delusions are characteristic of neurodegenerative dementia. In FTD and Lewy dementia, misidentification syndromes (Capgras: “my spouse is an impostor”; Fregoli: “my persecutor disguises as others”) can occur.

Delirium features: Delirium is an acute confusional state with rapid onset (hours–days) and fluctuating consciousness/attention. By definition, delirium involves reduced orientation to the environment and marked difficulty focusing or sustaining attention. Other features include disorganized thinking, perceptual disturbances (illusions, hallucinations) and paranoia. Symptoms often wax and wane over hours; nights are commonly worse (“sun-downing”). A key point is that attention is disproportionately impaired in delirium, unlike early dementia where attention is relatively preserved. In delirium, patients may be lethargic or hyperactive; they may speak incoherently or have illogical, fleeting suspicions. Importantly, delirium arises in the context of an identifiable medical cause (infection, metabolic imbalance, toxin, etc.).

Differentiating delirium vs dementia delusions: A systematized delusion (as in primary psychosis or chronic dementia) is a consistent, complex false belief held with conviction (e.g. “the CIA has planted a camera in my lamp”). By contrast, a fleeting misinterpretation in delirium is often poorly organized and self-corrects (e.g. briefly hearing an unfamiliar noise and thinking “there’s a moving wire on the bed,” but soon forgetting). Delirium’s perceptual errors tend to dissolve with reorientation; dementia patients’ delusions persist across days. Moreover, delirium onset is abrupt and fluctuating, whereas dementia yields a slow decline. As the StatPearls review notes, delirium’s course is abrupt with fluctuating deficits compared to the steady decline of dementia. Caregivers should note whether suspicious beliefs are new and accompanied by clouded consciousness – these favor delirium.

Workup for Delirium: Any adult with new confusion or delusions should be evaluated for reversible causes. Key screens include:

• Infections: chest (pneumonia), urine, sepsis (often without fever in elderly).
• Drugs/toxins: Review medications for anticholinergics, opiates, benzodiazepines, sedatives, antihistamines, steroids, etc., which can precipitate delirium. Also consider alcohol or drug withdrawal.
• Metabolic: Electrolyte imbalances (hyponatremia, hypercalcemia, hypoglycemia), organ failure (renal, hepatic encephalopathy), hypoxia, hypo/hyperglycemia.
• Others: Pain or acute illness, dehydration, vitamin deficiencies (B12, thiamine), fever or hypothermia.
• Sensory and environment: Assess for sensory deprivation or overload (e.g. poor vision/hearing), sleep disruption, ICU stay or change of environment – all can trigger delirium. Ensure hearing aids and glasses are used.

A cognitive screening (e.g. Confusion Assessment Method) is used to confirm inattention and fluctuation. Importantly, even if a patient with dementia has new paranoia, clinicians must rule out delirium (treatable cause) before attributing symptoms to dementia.

Differential diagnoses: When an older adult reports governmental surveillance or theft, clinicians must consider other possibilities besides dementia/delirium:

• Late-onset psychotic disorders: Primary psychoses (schizophrenia-spectrum) with onset after age 60 are uncommon. Such patients tend to have chronic, negative symptoms and lack the cognitive decline of dementia. However, very late-onset paranoia can herald emerging dementia.
• Mood disorders: Major depression with psychotic features can produce persecutory delusions, but these usually include mood symptoms (helplessness, guilt) and lack the disorientation of delirium.
• Sensory deprivations: Charles Bonnet syndrome (visual hallucinations in the sight-impaired) or auditory illusions (from hearing loss) can mimic hallucinations. The Practical Neurology article notes that impaired vision/hearing can exacerbate psychotic-like symptoms in dementia. Always check sensory status.
• Actual abuse/neglect or theft: Crucially, some accusations by cognitively impaired elders reflect true events. A history or evidence of abuse, exploitation or burglary must be explored. One should gently verify whether possessions might indeed have been stolen or family members neglected the patient. Social worker or adult protective services input may be needed. In other words, do not dismiss all claims as delusional – rule out real mistreatment first.

Management: Nonpharmacologic interventions are first-line for perceptual disturbances and agitation in both dementia and delirium. Strategies include reorientation (clocks, calendars, windows), reassurance and calm communication, presence of familiar caregivers, adequate lighting (reduce shadows), and maintaining sleep–wake cues (noise reduction at night). A structured daily routine, mobility and cognitive stimulation help reestablish normal cognition. Treat contributing factors (e.g. correct dehydration, infection, pain) promptly. Review and discontinue deliriogenic medications if possible. Providing glasses/hearing aids, normalizing the environment, and offering simple activities can reduce confusion. Caregiver education is critical: explain that accusations arise from disease-related misinterpretations, not malice, and teach ways to respond calmly (validate feelings, redirect attention).

Pharmacologic treatment is used cautiously. Antipsychotics (e.g. low-dose haloperidol or atypicals) may be considered for severe agitation or dangerous delusions only after non‐drug measures fail and underlying causes are addressed. Even then, risks in the elderly are high. Antipsychotics increase stroke, cardiac events, and mortality in dementia, and must be minimized. In delirium, low-dose haloperidol can be used short-term for hallucinations or severe agitation (avoiding benzodiazepines unless delirium is due to withdrawal). In Parkinsonian and Lewy dementias, neuroleptic sensitivity is a major concern: D2-blocking antipsychotics (especially haloperidol, risperidone) can severely worsen motor and cognitive symptoms. If medications are needed in DLB/PDD, quetiapine or the 5-HT2A antagonist pimavanserin are preferred, and cholinesterase inhibitors (e.g. rivastigmine) are first-line for cognitive symptoms. For Alzheimer’s, cholinesterase inhibitors (donepezil, etc.) may modestly improve cognition and even reduce delusions/hallucinations. Treat depression or anxiety with SSRIs as needed. Always aim for the lowest effective dose and re-evaluate continually.

Disorder-specific cautions: - In Lewy body dementia, avoid typical antipsychotics (neuroleptic hypersensitivity). These patients are exquisitely sensitive to dopamine antagonists. - In dementia with significant cerebrovascular disease, avoid centrally acting anticholinergics and be cautious with sedation (risk of stroke). - In all elderly, benzodiazepines should be avoided due to delirium risk. - Cholinesterase inhibitors are relatively safe (though may cause GI upset, bradycardia) and can be particularly helpful in Lewy and Alzheimer’s dementia.

Fictional Vignette (Comparative):

• Patient A: An 80-year-old retired engineer with 5-year history of Parkinson’s disease dementia comes to clinic. His wife reports he has become more confused over weeks, insisting that hospital staff are hiding cameras in his bed to record him and that “spies” swap his shoes at night. He has vivid visual hallucinations of strangers in the room and is sometimes drowsy during the day. Examination shows bradykinesia and mild rigidity (Parkinsonism), fluctuating alertness, and preserved long-term memory but poor attention. No fever or acute illness is found. This presentation (gradual onset, parkinsonism, vivid hallucinations, cognitive fluctuations) is consistent with Lewy body dementia, and his fixed delusional theme of surveillance is a well‐formed persecutory belief. Management focuses on cholinesterase inhibitors (e.g. rivastigmine) and environmental measures. A low dose of quetiapine is trialed only if he becomes dangerously agitated (avoiding haloperidol due to neuroleptic sensitivity).

• Patient B: A 78-year-old woman with no prior cognitive impairment is brought by family from an assisted living facility. Over the past 2 days she became acutely confused after a urinary tract infection. Staff note she is disoriented, inattentive, and intermittently mute; at times she loudly accuses nurses of “tampering” with her IV pump and hiding her dentures. She has a fever and dehydrated appearance. Physical exam shows normal strength and no focal deficit. Mental status testing is impossible due to fluctuating wakefulness. In this case, the rapid onset of confusion, impaired attention, fever and infection indicate delirium (due to UTI). Her accusations are transient and disorganized (not firmly held once she is reoriented). Treatment involves treating the infection, rehydration, and nonpharmacologic reorientation (and a one-time low dose of haloperidol at night for distress if needed). With infection resolution, her surveillance delusions resolve, confirming they were delirium-related rather than a chronic psychotic disorder.

Conclusion: Persecutory delusions of spying or theft can arise in both chronic neurodegenerative dementia and acute delirium, but the context is critical. Dementia‐related delusions tend to be well-defined, persistent beliefs in patients with a known cognitive decline, whereas delirium-related suspicions occur in the setting of acute illness, fluctuate, and often remit with treatment. Clinicians must carefully evaluate older adults for underlying causes (infection, metabolic derangements, drug effects), differentiate delusional misinterpretation from reality, and ensure any actual abuse or neglect is not overlooked. Management emphasizes non-drug approaches (environment, reassurance, treating medical causes) and very cautious use of medications, tailored to the specific dementia type (notably, avoiding neuroleptics in Lewy body disease). This comprehensive approach optimizes patient safety and dignity while addressing both the neuropsychiatric syndrome and any modifiable contributors.

Sources: Authoritative geriatric and neurological references were used, including the DSM-5-TR criteria, professional neurology texts, and clinical reviews on dementia subtypes and delirium, among others listed above. Each statement above is supported by these sources.