A Case Report of Olfactory Reference Disorder with Childhood Trauma: Aetiological and neurobiological insights

Summary

We report a 22-year-old male, who presented in 2020 to a clinic in Kahramanmaraş, Turkey, with a 5-year history of a fixed preoccupation with the belief of emitting a ‘plastic smell’ from his anal region. This case illustrates a clinically significant link with a history of childhood sexual abuse. The patient was diagnosed with olfactory reference disorder (ORD) with poor insight and comorbid depressive disorder, based on ICD-11 and DSM-5-TR criteria. Extensive medical workups ruled out organic causes. He responded well to a combination therapy of sertraline and aripiprazole, showing significant symptom reduction. This case supports a diathesis-stress model where ORD can manifest as a somatic metaphor for trauma, mediated by experiential avoidance. It highlights the importance of trauma assessment and a neurobiologically informed psychopharmacological approach in managing ORD.

1. Introduction

Olfactory reference disorder (ORD), formerly known as olfactory reference syndrome, is a severe psychiatric condition defined by a persistent preoccupation with the belief that one emits a foul or offensive body odour, which is not perceptible or is only slightly perceptible to others.1 This core preoccupation is often accompanied by ideas of reference, where individuals misinterpret others' innocuous behaviours as a reaction to their supposed malodor.1 In response, patients engage in repetitive, time-consuming behaviours (e.g., excessive washing, checking) that causes profound social and occupational impairment.2 The distress and functional impairment associated with ORD are severe, with studies indicating a high risk for suicidal ideation and attempts.3

The nosological placement of ORD has evolved. Previously considered a delusional disorder, it is now officially classified in the International Classification of Diseases, 11th Edition under the “Obsessive-Compulsive or Related Disorders” chapter.4 The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision includes it under “Other Specified Obsessive-Compulsive and Related Disorder”.5 This reclassification emphasises its core features of obsessional preoccupations and compulsive behaviours over a primary psychotic process.3,6,7

While precipitating events are noted in many ORD cases, they are often non-specific stressors.8 A direct, thematically congruent link between a specific childhood trauma and the content of ORD symptoms is a significant gap in the literature. This report details the case of a young man with a history of childhood anal sexual abuse who developed a fixed preoccupation with emitting a ‘plastic smell’ from his anal region, offering an opportunity to explore this aetiological connection within a diathesis-stress framework.

2. Case report

A 22-year-old single male presented to a clinic in Kahramanmaraş, Turkey, in 2020. He reported a 5-year history of a persistent ‘burning plastic odour’ he believed was dispersing from his anal region. The symptoms began at age 17, shortly after he moved to a new city to attend university. Following the onset of the preoccupation, he experienced progressive social withdrawal, which subsequently led to a decline in his academic performance. His developmental history was unremarkable aside from the trauma detailed below and he had no prior psychiatric history.

Although no one else could detect the odour, he was convinced that others would react to it by rubbing their noses or opening windows. This belief led him to quit his job and avoid social interactions. He engaged in compulsive behaviours, including changing clothes twice daily and frequent deodorant use. Over the preceding 5 years, the patient had undergone numerous gastroenterology consultations, including colonoscopies and anal manometry, as well as neurological and ear, nose and throat evaluations, all of which yielded no organic pathology. The patient presented before the widespread impact of the COVID-19 pandemic and reported no history of related infection that could account for phantosmia.

During psychiatric assessment, he disclosed a history of anal sexual abuse by a friend at age 9, an event he had never previously revealed. His mental status examination revealed a coherent, goal-directed thought process. His belief about the body odour was a fixed preoccupation with poor insight; he was mostly convinced of its reality and could not be easily reassured otherwise. While formal structured assessment tools such as the Brown Assessment of Beliefs Scale or the Yale-Brown Obsessive-Compulsive Scale were not utilised, clinical evaluation confirmed his conviction was strong and resistant to challenge. His mood was depressive (Hamilton Depression Scale [HDS] score = 16). Extensive medical workups were performed to rule out organic causes, with all results, including neuroimaging, electrophysiological and laboratory findings, being within normal limits [Table 1 and Fig. 1, Fig. 1, Fig. 2 and Fig. 3].

Table 1.

Summary of neuroimaging, neurological examination and comprehensive laboratory investigations of the current patient.

Investigation/test name	Result	Interpretation	Reference range
Neuroimaging and neurological
Cranial CT	No pathological signs detected.	-	-
Cranial MRI	No pathological signs detected.	-	-
EEG	No pathological signs detected.	-	-
Neurological Examination	Normal	-	-
Blood Screens	Normal	-	-
Infectious disease markers
Anti-HCV in COI	0.041	Negative	0–1
Anti-HBs in IU/L	9.28	Negative	0–10
HBsAg in COI	0.369	Negative	0–1
Inflammation and autoimmune
Rheumatoid factor in IU/mL	11.3	-	0–16
CRP in mg/L	3	-	0–5
Ferritin in μg/L	80.47	-	30–400
Anti-thyroglobulin antibody in IU/mL	18.80	-	1.4–78
Anti-TPO in IU/mL	24.58	-	0–34
Thyroid function
TSH in mIU/L	2.36	-	0.27–4.2
Free T4 in ng/dL	1.28	-	0.93–1.7
Free T3 in ng/L	3.63	-	2.57–4.43
Metabolic and liver panel
Glucose in mg/dL	103	-	74–105
Creatinine in mg/dL	1.1	-	0.6–1.2
ALT in U/L	27	-	0–41
AST in U/L	30	-	0–40
GGT in U/L	13	-	8–61
Alkaline phosphatase in U/L	58	-	40–130
Total bilirubin in mg/dL	0.38	-	0–1.2
Direct bilirubin in mg/dL	0.15	-	0–0.3
Lipid profile
Triglycerides in mg/dL	45	-	0–200
LDL cholesterol in mg/dL	151	-	50–130
Electrolytes
Sodium in mmol/L	141	-	136–145
Potassium in mmol/L	4.6	-	3.5–5.5
Coagulation profile
Prothrombin time in sec	11.5	-	9–14
Prothrombin time in %	103	-	50–150
INR	0.98	-	0.8–1.3
APTT in sec	33.5	-	24–39.5
Inflammation marker
ESR (1st hour) in mm/hr	9	-	-
Complete blood count
WBC × 103/uL	6.58	-	3.91–10.9
RBC × 106/uL	5.63	-	4.4–5.7
HGB in g/dL	16.0	-	13–17
HCT in %	47.6	-	40–50
PLT × 103/uL	259	-	150–350
MCV in fL	84.5	-	80–97
MCH in pg	28.4	-	27–32.5
MCHC in g/dL	33.6	-	32–36
MPV in fL	11.5	-	9–12.5
LYM × 103/uL	2.45	-	1.2–3.4
LYM in %	37.2	-	19–48
RDW-CV in %	13.2	-	12–14.5
RDW-SD in fL	41.1	-	37–46
BASO × 103/uL	0.05	-	0.01–0.07
BASO in %	0.8	-	0.1–1.2
EOS × 103/uL	0.09	-	0.03–0.6
EOS in %	1.4	-	0.6–8
NEU × 103/uL	3.43	-	1.8–7
NEU in %	52.1	-	40–75
MONO × 103/uL	0.56	-	0.25–1
MONO in %	8.5	-	5–16
PCT in %	0.30	-	0.17–0.4
PDW in fL	14.8	-	10–16
P-LCR in %	37.6	-	17–43

CT = computed tomography; MRI = magnetic resonance imaging; EEG = electroencephalography; Anti-HCV = hepatitis C virus antibody; COI = cutoff index; Anti-HBs = hepatitis B surface antibody; HbsAg = hepatitis B surface antigen; CRP = C-reactive protein; Anti-TPO = anti-thyroid peroxidase antibody; TSH = thyroid-stimulating hormone; T4 = thyroxine; T3 = triiodothyronine; ALT = alanine aminotransferase; AST = aspartate aminotransferase; GGT = gamma-glutamyl transferase; WBC = white blood cell; RBC = red blood cell; HGB = haemoglobin; HCT = haematocrit; PLT = platelet; MCV = mean corpuscular volume; MCH = mean corpuscular hemoglobin; MCHC = mean corpuscular haemoglobin concentration; MPV = mean platelet volume; LYM = lymphocyte; RDW-CV = red cell distribution width-coefficient of variation; RDW-SD = red cell distribution width-standard deviation; BASO = basophil; EOS = eosinophil; NEU = neutrophil; MONO = monocyte; PCT = procalcitonin; PDW = platelet distribution width; P-LCR = platelet-large cell ratio.

Fig. 1.

Axial T2-weighted FLAIR magnetic resonance image at the level of the cerebellum demonstrating normal brainstem and cerebellar structures with no evidence of pathological signal change.

Fig. 2.

Axial T2-weighted FLAIR magnetic resonance image at the level of the lateral ventricles showing normal-appearing cortical and subcortical structures without pathological findings.

Fig. 3.

Axial T2-weighted FLAIR magnetic resonance image at a high cortical level (centrum semiovale) demonstrating normal brain parenchyma.

The patient was diagnosed with ORD (with poor insight) and a comorbid depressive disorder. A treatment regimen of sertraline 50 mg/day and aripiprazole 5 mg/day was initiated simultaneously. This combination was chosen to address both the obsessive-compulsive disorder (OCD) symptoms with the selective serotonin reuptake inhibitor (SSRI) and to target the patient's limited insight and high level of conviction with the atypical antipsychotic. After 1 month, a 40% symptom reduction was observed; after 2 months, there was approximately 60% improvement in both ORD and mood symptoms. His HDS score decreased to 7.

3. Discussion

This case is clinically significant for its illustration of a potential link between the content of a patient's olfactory preoccupation and history of trauma. We propose an integrated model viewing the ORD symptom as a somatic metaphor for trauma, mediated by experiential avoidance and shaped by underlying vulnerabilities.

The patient's specific preoccupation—a ‘plastic smell’ from the anus—can be conceptualised as a striking somatic metaphor for his anal sexual abuse. The concept of trauma manifesting through bodily symptoms is well-established in the literature, where the body is seen as holding memories that cannot be verbally articulated.9 The olfactory system has uniquely potent connections to the brain's primary emotional and memory centres, making it a powerful conduit for traumatic reminders.10 This aligns with neurobiological models of trauma that posit a ‘brain-body disconnect’, where trauma becomes stored somatically, leading to dysregulated interoceptive processing.11 The patient's unshakeable belief can be understood as a phantom sensation arising from a trauma-induced rewiring of sensory pathways, a phenomenon sometimes described as an olfactory hallucination, which is a documented feature of ORD and not necessarily indicative of a primary psychotic disorder.12

The phenomenology of ORD overlaps significantly with both OCD and Social Anxiety Disorder (SAD).7 Hallmark features include referential thinking (misinterpreting others' actions as being related to the smell), compulsive checking and avoidance behaviours. A pivotal study found ORD prevalence to be highest in patients with comorbid SAD/OCD, suggesting an emergent psychopathology.6

However, as a direct causal link between the trauma and the symptoms cannot be definitively established, it is more cautious and scientifically accurate to frame the childhood trauma as a potential non-specific risk factor within a diathesis-stress model. The trauma may have provided the shame-laden content, which was then funnelled through a pre-existing diathesis for obsessive-compulsive processes and social anxiety, possibly triggered by the stress of relocating for university.

This cycle is maintained by experiential avoidance (EA)—the tendency to escape unwanted internal experiences.13 Shame is a core emotion following sexual trauma and EA is known to mediate the relationship between shame and post-traumatic stress disorder symptoms.14 The patient's entire symptom complex functions as an EA strategy: the olfactory preoccupation displaces the traumatic memory, while the compulsive rituals and social withdrawal serve to avoid the internal experience of shame and humiliation.

The patient's positive response to sertraline and aripiprazole is well-supported. SSRIs are a first-line treatment for OCRDs, including ORD.15,16 Augmentation with a low-dose atypical antipsychotic such as aripiprazole is an effective strategy for cases with poor insight or high conviction.17 A proposed mechanism for aripiprazole's efficacy is that its partial D2 agonism restores top-down regulation of the olfactory bulb by the orbitofrontal cortex, correcting faulty olfactory processing.17

While pharmacotherapy was effective in the current case, cognitive behavioural therapy (CBT) tailored for ORD is also a strongly recommended component of care. This therapy typically involves psychoeducation, cognitive restructuring to challenge maladaptive beliefs and exposure with response prevention to reduce avoidance and compulsive behaviours. Although not administered here, its inclusion in a comprehensive treatment plan is considered best practice.18

Furthermore, the shame and avoidance central to ORD often create significant barriers to seeking and engaging in treatment. Novel interventions, such as web-based or mobile chatbot therapies, may offer a promising avenue to reach individuals who are reluctant to engage in face-to-face therapy. Such digital tools have shown effectiveness for anxiety and depression and could be adapted for the self-care and engagement challenges seen in ORD.19,20

4. Conclusion

This case highlights the importance of assessing for trauma in ORD and supports a diathesis-stress model where symptoms may function as a somatic representation of past trauma. The positive response to combination pharmacotherapy demonstrates the value of a neurobiologically informed treatment approach, particularly in cases with poor insight. However, a comprehensive management plan should also integrate evidence-based psychotherapy, such as CBT tailored for ORD, to address maladaptive beliefs and behaviours. Given the high risk of suicidality associated with this condition, this case underscores the clinical urgency for timely recognition and intervention. Finally, for a disorder so marked by shame and avoidance, exploring novel modalities such as digital health interventions may be crucial to improving access to care for this underserved patient population. Future studies are warranted to further explore the integration of pharmacological, psychotherapeutic, and digital approaches in improving outcomes for patients with ORD.

Authors' Contribution

Davut Ocak: Conceptualization, Investigation, Writing- Original Draft, Writing- Review & Editing. Bengü Yücens: Supervision, Writing- Review & Editing.

Acknowledgement

The authors would like to dedicate this work to the memory of their esteemed colleague, Dr. Mustafa Özlü, a fellow psychiatrist in Kahramanmaras, who was tragically lost during the COVID-19 pandemic. His dedication and contributions to the field are remembered with gratitude and respect.

Ethics Statement

Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. The study was conducted in accordance with the Declaration of Helsinki.

Data Availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.