Atypical onset of obsessive‐compulsive disorder at age 50 following post‐SARS‐COV‐2 syndrome: A case report

Abstract

Background

The coronavirus disease 2019 (SARS‐COV‐2) pandemic has been associated with an increased risk of developing or exacerbating obsessive‐compulsive disorder (OCD). This report presents a case of OCD onset in a 50‐year‐old male following recovery from acute SARS‐COV‐2 infection, highlighting the potential neuroinflammatory and neuroimmune mechanisms involved.

Case Presentation

Mr. A, a 50‐year‐old cook with no prior psychiatric history, developed a loss of smell and taste by SARS‐COV‐2. This sensory impairment triggered severe anxiety, leading to compulsive checking behaviors and reassurance‐seeking after recovering from SARS‐COV‐2. Initial treatment with fluvoxamine at 50 mg/day was insufficient, and his symptoms necessitated inpatient care. His compulsive behaviors continued during hospitalization, and escalation of fluvoxamine to 150 mg/day, alongside adjunctive risperidone at 3 mg/day was needed. Along with cognitive‐behavioral therapy (CBT) advises, this resulted in symptom stabilization and eventual discharge. Postdischarge, Mr. A's OCD symptoms remained stable with ongoing medication, despite continued sensory disturbances.

Conclusion

This case illustrates the atypical onset of OCD in an older adult following SARS‐COV‐2 infection, potentially driven by neuroinflammation and altered neural pathways. The partial response to fluvoxamine and the need for risperidone suggest that SARS‐COV‐2‐related OCD may involve complex neuroimmune changes beyond serotonin dysregulation. This case emphasizes the importance of recognizing neuropsychiatric complications in SARS‐COV‐2 survivors and underscores the need for further research into the mechanisms and management of SARS‐COV‐2‐related neuropsychiatric symptoms, including OCD.

INTRODUCTION

The coronavirus disease 2019 (SARS‐COV‐2) pandemic has been associated with a heightened risk of developing or exacerbating obsessive‐compulsive disorder (OCD) symptoms. Several studies have documented new‐onset OCD cases following SARS‐COV‐2 infection, as well as a general worsening of symptoms among both diagnosed individuals and the general population during the pandemic. ¹ Research indicates a notable increase in the prevalence and severity of OCD symptoms during this time. ² Specifically, individuals demonstrated higher scores across all symptom dimensions of OCD, including contamination fears, responsibility for harm, intrusive unacceptable thoughts, and concerns related to symmetry. ³ , ⁴ Predisposing factors for this worsening included younger age, lower resilience, insufficient social support, and excessive exposure to SARS‐COV‐2‐related news. ⁴ These findings highlight the extensive impact of the pandemic on OCD symptomatology, extending beyond just contamination fears.

Additionally, many SARS‐COV‐2 survivors experience lingering symptoms following their recovery from the acute phase of infection, commonly referred to as post‐SARS‐COV‐2 syndrome. These symptoms, which can endure for weeks or months after the acute infection phase, encompass physical, cognitive, and mental health impairments across multiple organ systems. Reported symptoms include fatigue, shortness of breath, headaches, memory problems, anxiety, and depression. ⁵ A few studies suggest that the severity of the acute phase of SARS‐COV‐2 is not necessarily related to the severity or persistence of Post‐SARS‐COV‐2, ⁶ , ⁷ while other studies have reported some associations. ⁸ , ⁹ However, Post‐SARS‐COV‐2 syndrome is not easily categorized into purely physical or psychological symptoms because it often presents a complex interaction of pathophysiological processes.

In this report, we present the case of a patient who experienced the onset of OCD after losing his sense of smell and taste after recovering from acute SARS‐COV‐2 infection.

The patient's clinical course was atypical for OCD, not only due to the late onset at age 50 but also because of the abrupt symptom emergence following SARS‐COV‐2 infection.

CASE PRESENTATION

Mr. A is a 50‐year‐old married man with no significant medical history who worked as a cook and manager at a restaurant in Tokyo. His pre‐illness personality had some inflexible traits, but generally he was optimistic and had many friends. He had been in good health until 1 month before his admission to our hospital, when he developed fever, body aches, fatigue, and a dry cough. Following public health guidance, he underwent a PCR test for SARS‐COV‐2, which returned positive. He was isolated in a hotel for 14 days and treated with acetaminophen and common antitussive medications to manage his symptoms. Within 2 weeks, most symptoms resolved, except for a persistent loss of smell and taste. By the third week, as he resumed his daily routine, he began to experience increasing anxiety related to these sensory impairments, which led to compulsive checking behaviors.

In July 2021, accompanied by his wife, Mr. A sought care at our hospital due to intrusive thoughts and compulsive behaviors centered on the fear that his sensory loss might be permanent. Despite prior treatment with zinc supplements and herbal medicine at another facility, there was no improvement. There were no signs of thought suppression or decreased motivation, or hallucinations, but the sleep disorder was evident. Physical examinations and laboratory tests, including CT scans and thyroid function tests, showed no abnormalities. Although he was aware of the irrationality of his compulsive behaviors, he repeatedly expressed, “Will my taste and smell come back? It's troubling since I run a restaurant.” he persistently sought reassurance from family members, making it difficult for him to carry out daily activities.

According to DSM‐5, Mr. A met criteria for OCD. He experienced recurrent intrusive thoughts about permanent sensory loss (obsessions) and engaged in repetitive reassurance‐seeking and checking behaviors (compulsions), which caused significant daily impairment. Physical and neurological examinations revealed no medical cause, and symptoms were not better explained by another psychiatric disorder. Differential diagnosis ruled out generalized anxiety disorder because his anxiety was narrowly focused and involved compulsive rituals, not generalized worry. Adjustment disorder was also excluded due to the chronicity and severity of symptoms.

Due to the severity of his anxiety and initial inability to participate in cognitive behavioral therapy (CBT), fluvoxamine was started at 50 mg/day. His family was also advised to minimize their involvement in his reassurance‐seeking behaviors. Despite these efforts, Mr. A's symptoms worsened, and by September he required inpatient psychiatric care.

At the beginning of hospitalization, he kept saying “not being able to confirm with family is painful,” and communication restrictions were imposed due to his agitation. His compulsive checking behaviors shifted from concerns about his sensory deficits to a preoccupation with being discharged from the hospital. He frequently sought reassurance from doctors and staff, asking repetitive questions, but we provided psychoeducation on OCD, and explained that reducing anxiety through confirmation creates a vicious cycle for the illness. We used CBT theory to aim for controlling anxiety without the need for confirmation (exposure response prevention). As for pharmacotherapy, the dose of fluvoxamine was gradually increased, leading to some symptom improvement. However, his condition fluctuated, with periods of increased agitation when permitted to send mail or leave the facility, necessitating the addition of risperidone to his treatment regimen. Risperidone was selected as the augmenting agent due to its well‐documented efficacy in treatment‐resistant OCD. Among second‐generation antipsychotics, risperidone has the strongest evidence base as an adjunct to SSRIs in OCD management, particularly for patients exhibiting poor response to monotherapy. Carbamazepine was also considered, but we avoided using it due to interactions with other medications. By late September, with fluvoxamine increased to 150 mg and risperidone to 3 mg, his reassurance‐seeking behaviors had significantly decreased, enabling occasional home visits by October.

Despite some temporary setbacks and medication adjustments, Mr. A's condition gradually stabilized. By December, he was able to complete home stays successfully and was discharged voluntarily after demonstrating sustained improvement. After his discharge, he continued to experience disturbances in smell and taste, but his OCD symptoms remained stable with ongoing medication, preventing any significant relapse.

DISCUSSION

In this case report, the patient's clinical course was atypical for OCD, not only due to the late onset at age 50 but also because of the abrupt symptom emergence following a SARS‐COV‐2 infection. While typical OCD often presents in adolescence or early adulthood with a chronic course, ¹⁰ Mr. A exhibited an acute‐onset form. Premorbid personality traits have long been considered relevant in the development of OCD. Individuals with anankastic or obsessive‐compulsive personality features—such as a high need for control, perfectionism, excessive conscientiousness, and heightened sensitivity to uncertainty—may be more vulnerable to developing OCD when exposed to acute stressors. Although Mr. A did not match all these characteristics, his occupation as a restaurant manager required a high level of precision and sensory awareness, suggesting underlying traits such as meticulousness, responsibility, and performance‐oriented mindset. These traits may have heightened his psychological distress when his olfactory and gustatory functions were disrupted, directly threatening his professional identity and competence.

Post‐SARS‐COV‐2 syndrome can lead to various neuropsychiatric symptoms through complex mechanisms. Severe SARS‐CoV‐2 binds to angiotensin‐converting enzyme 2 (ACE2) receptors on neurons and glial cells, potentially exerting direct effects on the nervous system. ¹¹ The subsequent systemic inflammation and hypoxia can weaken the blood–brain barrier, allowing peripheral T cells to penetrate the brain tissue. ¹² This infiltration can trigger neuroinflammation, resulting in microglial and astrocyte dysfunction, akin to changes observed in neurodegenerative diseases. ¹³ , ¹⁴ Disruption of synaptic signaling in upper‐layer excitatory neurons, essential for cognitive functions, has also been reported. ¹² These alterations resemble those seen in chronic neurological conditions and may contribute to persistent cognitive and mental health issues. ¹² , ¹⁴ Sustained microglial activation and astrocyte dysfunction can disrupt homeostasis, potentially driving specific neuropsychiatric symptoms related to SARS‐COV‐2. ¹³ The onset of OCD in the context of post‐SARS‐COV‐2 syndrome may be associated with these mechanisms because neuroinflammation and altered synaptic signaling could impair the neural circuits that govern obsessive thoughts and compulsive behaviors, leading to the development or worsening of OCD symptoms.

In this case, symptom improvement was ultimately achieved through a combination of fluvoxamine and risperidone. Unlike other selective serotonin reuptake inhibitors (SSRIs), fluvoxamine may provide neuroprotective effects by reducing inflammatory cytokine activity. Although fluvoxamine may not significantly lower the risk of hospitalization or clinical deterioration during acute SARS‐COV‐2, ¹⁵ its potential anti‐inflammatory properties could help alleviate the neuroinflammation and immune dysregulation observed in SARS‐COV‐2‐related OCD. The patient did not respond sufficiently to fluvoxamine alone, necessitating the addition of risperidone. This suggests that SARS‐COV‐2‐related OCD may involve not only serotonin dysregulation but also broader neuropsychological changes, such as neuroinflammation and immune system irregularities. ¹² Risperidone, an atypical antipsychotic that acts on dopamine D2 and serotonin 5‐HT2A receptors, is sometimes used as adjunctive therapy for OCD. ¹⁶ It is possible that the neuroimmune changes induced by SARS‐COV‐2 also influenced the dopamine system, resulting in increased dopamine activity. Risperidone may have mitigated this overactivity, thereby enhancing the therapeutic outcome.

Recent findings suggest that even mild cases of SARS‐COV‐2 can result in long‐lasting neuropsychiatric sequelae. Case reports have demonstrated that patients with only minor respiratory symptoms during the acute phase of SARS‐COV‐2 may subsequently develop severe and persistent psychiatric symptoms, including OCD. ¹⁷ On the other hand, some research indicates that the severity of SARS‐COV‐2 may be positively correlated with the likelihood of prolonged physical and neuropsychiatric symptoms. ¹⁸

Although several case studies have reported the onset or exacerbation of OCD following SARS‐COV‐2 infection, a direct association between the severity of the acute illness and the risk of OCD development has not been examined. In the presented case, olfactory and gustatory dysfunctions were central to the patient's obsessive concerns. While no studies to date have established a direct causal relationship between sensory loss and OCD, there is growing evidence that such dysfunctions following SARS‐COV‐2 can lead to significant psychological distress, including depression and suicidal ideation. ¹⁹

Finally, the potential role of dopaminergic dysfunction in COVID‐19‐related OCD should be considered. Although SARS‐CoV‐2 primarily enters the central nervous system via ACE2 receptors, its downstream effects may involve alterations in dopamine regulation. ²⁰ Neuroinflammatory changes, including microglial activation and astrocyte dysfunction, may disrupt dopaminergic pathways implicated in OCD. ²¹ Animal studies have supported the role of dopamine dysregulation in compulsive behaviors, and emerging evidence suggests that compounds such as lactoferrin may offer neuroprotective effects on dopaminergic neurons in the context of SARS‐COV‐2‐induced inflammation. ²⁰ , ²² These findings point to the possibility that SARS‐COV‐2‐associated OCD is not solely a serotonergic disorder but may also involve broader neuroimmune and neurotransmitter system alterations.

In conclusion, this case underscores the possibility of late‐onset OCD as a neuropsychiatric consequence of SARS‐COV‐2, particularly in the context of post‐SARS‐COV‐2 syndrome. The patient's sensory deficits, specifically the loss of smell and taste, combined with his occupational reliance on these abilities, may have heightened his anxiety and contributed to the onset of OCD symptoms. This atypical presentation suggests that the neuroinflammation and immune dysregulation following SARS‐COV‐2 can interfere with the neural pathways that regulate obsessive‐compulsive behaviors. While fluvoxamine offered some symptom relief, the addition of risperidone was required for full stabilization. This indicates that the pathophysiology of SARS‐COV‐2‐related OCD may extend beyond serotonin imbalance, encompassing broader neuroimmune processes. This case emphasizes the need to recognize and address complex neuropsychiatric symptoms in SARS‐COV‐2 survivors as the long‐term effects of the virus continue to emerge. Further research is necessary to elucidate the mechanisms linking SARS‐COV‐2 to neuropsychiatric conditions such as OCD and to refine therapeutic strategies.

AUTHOR CONTRIBUTIONS

All authors made a significant contribution to the work reported, whether that is in the conception, design of the case report, clinical assessment, treatment of the patient, the interpretation of the findings, or all these areas, took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published, agreed on the journal to which the article has been submitted, and agree to be accountable for all aspects of the work.

CONFLICT OF INTEREST STATEMENT

The authors declare no conflicts of interest.

ETHICS APPROVAL STATEMENT

Komakino Hospital has an ethics committee, but it is not involved in case reports. We obtained a consent form from the patient and his family, and this is available on the website of the Japanese Society of Psychiatry and Neurology. This study complies with the Declaration of Helsinki.

PATIENT CONSENT STATEMENT

Written informed consent for presentation of the patient's clinical course was given by the patient.

CLINICAL TRIAL REGISTRATION

N/A.

Sugawara T, Ichiki R. Atypical onset of obsessive‐compulsive disorder at age 50 following post‐SARS‐COV‐2 syndrome: a case report. Psychiatry Clin Neurosci Rep. 2025;4:e70148. 10.1002/pcn5.70148

DATA AVAILABILITY STATEMENT

N/A.