In a compelling new case report published in BMC Psychiatry, researchers detail an unusual onset of Capgras syndrome following an acute upper respiratory tract infection, shedding light on the potential roles of inflammation and pharmacological exposure in triggering this rare psychiatric condition. Capgras syndrome, characterized fundamentally by the delusional conviction that close relatives have been replaced by impostors, remains poorly understood, with most known cases linked to neurodegenerative or psychotic disorders. However, this recent clinical observation introduces an intriguing intersection between infectious illness, immune response, and neuropsychiatric manifestations.
The case involves a 42-year-old woman who, after enduring a severe upper respiratory tract infection, began exhibiting hallmark symptoms of Capgras syndrome. She developed an unshakeable belief that her husband had been substituted by an identical imposter, a classic delusional misidentification syndrome. This acute psychiatric shift appeared temporally linked to the infection and the treatment regimen prescribed, which included several medications common in managing respiratory symptoms and secondary bacterial infections. The report suggests a multifactorial pathogenesis that warrants further exploration.
Pharmacologically, the patient received a combination of cefuroxime, a beta-lactam antibiotic, along with amoxicillin-clavulanic acid, ibuprofen, pseudoephedrine, and chlorpheniramine. Each of these agents has distinct mechanisms of action ranging from antibacterial effects to anti-inflammatory and sympathomimetic activities. While these drugs are generally considered safe, their possible synergistic or cumulative impact on central nervous system function, particularly in vulnerable patients, should not be overlooked. The authors posit that these medications may have contributed—either directly or indirectly—to the onset of psychotic symptoms.
From a neurobiological standpoint, the underlying inflammatory processes triggered by the infection itself may play a crucial role in the etiopathogenesis of Capgras syndrome in this context. Neuroinflammation is increasingly recognized as a pivotal factor influencing brain function and psychiatric outcomes. Systemic infections can provoke a cascade of cytokine release, disruption of the blood-brain barrier, and microglial activation, possibly precipitating psychotic symptoms in predisposed individuals. The case thereby adds to a growing body of literature hypothesizing immune-mediated mechanisms in psychotic disorders.
The treatment approach for the patient’s psychosis involved initiating paliperidone, an atypical antipsychotic with potent dopaminergic and serotonergic receptor affinity. Dosage was titrated to 6 mg/day, and the intervention yielded partial alleviation of delusional beliefs. However, the patient discontinued follow-up before a comprehensive assessment of long-term outcomes could be made. This partial response underlines the therapeutic challenges faced when dealing with psychoses secondary to acute medical conditions and highlights the need for integrated psychiatric and medical care.
Capgras syndrome remains an enigmatic neuropsychiatric condition without standardized diagnostic biomarkers or a universally accepted treatment protocol. Its rarity and clinical diversity complicate establishing definitive causal mechanisms. This case importantly illustrates that acute infectious processes and pharmacological exposures can act as potential precipitants, expanding the conventional etiological framework beyond neurodegenerative and chronic psychiatric disorders.
Moreover, this report calls attention to the often-overlooked collaboration between somatic and psychiatric medicine. Infectious diseases, frequently regarded as isolated medical events, may carry significant neuropsychiatric sequelae, mediated through immune-neural interplay. Recognition of such links is critical for timely diagnosis and intervention, which may improve patient prognoses and reduce morbidity associated with delusional misidentification syndromes.
The implications of this case reach further into pharmacovigilance, advocating for heightened awareness regarding the neuropsychiatric side effects of common medications when administered in combination or during systemic inflammatory states. It underscores that even widely used antibiotics and anti-inflammatory agents may, in interaction with an active infection, alter central nervous system homeostasis unfavorably, sparking rare but severe psychiatric complications.
In addition to organic and pharmacological factors, psychosocial stressors accompanying acute illness likely contribute to the overall vulnerability to psychosis. The disruption of normal cognitive-emotional integration during illness, compounded by altered sensory perceptions and impaired reality testing, may culminate in manifestations such as Capgras syndrome. The intersection of these diverse pathways reinforces the complexity of such psychiatric presentations.
Future research directions prompted by this case involve elucidating biomarkers for inflammation-related psychoses, determining the exact neuroimmune mechanisms implicated, and assessing the impact of various therapeutic agents on central nervous system function during infections. Longitudinal studies explicitly exploring the temporal relationship between infectious triggers, medication regimens, and neuropsychiatric outcomes could vastly enhance clinical understanding.
In conclusion, the acute onset of Capgras syndrome following an upper respiratory tract infection and concomitant medication exposure represents a significant clinical observation. It suggests a link between transient inflammatory states, pharmacological influences, and complex delusional syndromes previously predominantly associated with chronic neuropsychiatric conditions. This integrative perspective encourages clinicians to consider infectious and drug-related etiologies in patients presenting with sudden-onset delusional misidentification, potentially improving diagnostic precision and patient care.
As research continues into the psychoneuroimmunological interface, this case emphasizes the need to approach psychiatric disorders through a multidisciplinary lens that includes infectious disease and pharmacology expertise. The nuanced understanding of how systemic illness can impinge on mental health may revolutionize treatment paradigms and pave the way for innovative interventions tailored to complex neuropsychiatric syndromes like Capgras syndrome.
Subject of Research: Acute onset Capgras syndrome following upper respiratory tract infection, focusing on the potential roles of inflammation and drug exposure.
Article Title: Acute onset Capgras syndrome after upper respiratory tract infection: a case report on the possible role of inflammation and drug exposure
Article References:
Şimşek, M.H., Korkmaz, U. Acute onset Capgras syndrome after upper respiratory tract infection: a case report on the possible role of inflammation and drug exposure. BMC Psychiatry 25, 795 (2025). https://doi.org/10.1186/s12888-025-07272-7
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