A 66-year-old Chinese woman was referred to our hospital in June 2021 due to olfactory hallucination. In 2004 the patient had been admitted to our hospital due to insomnia and nightmares. She had difficulty in initiating sleep and frequently awaked almost every night. The sleep disturbance caused her distress in daily life. She was diagnosed with insomnia disorder. Administration of 12.5 mg doxepin per night improved her sleep, and the patient reported stable mood and good social function during follow-up. However, in May 2017 she gradually manifested olfactory hallucinations, claiming that she could smell some Chinese medicines, even in wide open spaces on mountains. She did well in her job as a storekeeper and took good care of her grandson. At first, she went to the otorhinolaryngologic department, but the nasal endoscopy revealed normal structural nasal cavity or nasopharynx, axial and coronal computed tomography of the nose did not show abnormalities, so she did not get any treatment but psychiatric consultation was recommended. She was diagnosed with brief psychotic disorder after 20 days of olfactory hallucination onset in a local hospital, and she denied manic, depressive or anxious mood, denied unexpected panic attacks, denied psychotic symptoms except olfactory hallucination. The psychological tests administered by clinicians indicated a Hamilton Depression Scale (HAMD) score of 5, Hamilton Anxiety Scale (HAMA) score of 3. She received olanzapine (10 mg/night) for 2 months, followed by aripiprazole (20 mg/day) for 1 month, but her symptoms continued.
When the patient was admitted to our hospital in June 2021, she reported that 6 months before, her olfactory hallucinations had worsened and that the phantom smells had changed to something like a mixture of scallion, ginger, and garlic. At the same time, she reported being unable to smell normal scents, being unable to fall asleep at night, feeling restless and fatigued, having difficulty concentrating on daily activities, and often feeling limb muscle tension and sweating. She worried a lot about her daughter's marriage, feared that some accidents would happen to her family members. She can still take care of her grandson. She denied depressed mood, unexpected panic attacks, and phobic avoidance.
The patient had completed primary school and had worked as a storekeeper until her retirement. She reported having grown up in a strict family environment and having a bad relationship with her ex-husband. She brought up her daughter alone and she lives alone since her daughter got married.
She had a history of tuberculosis and cholecystectomy. In 2011 she had been diagnosed with hyperlipidemia and since then she had been taking 5 mg atorvastatin every night. The patient and her family members denied any drug abuse, smoking or drinking. She had no family history of mental disorders.
In light of the patient's long history of olfactory hallucination, the otorhinolaryngology department was asked to examine her, and those clinicians suggested the possibility of phantom olfactory perception. To exclude organic lesions, auxiliary examination and nasal endoscopy were performed. Endoscopy failed to reveal obvious structural auxiliary abnormalities, or abnormalities in the nasal cavity or nasopharynx (see Figure 1). Axial and coronal computed tomography of the nose showed only paranasal sinusitis (see Figure 2). And brain magnetic resonance imaging only showed a few ischemic foci in the brain parenchyma and paranasal sinusitis (see Figure 3). Chest computed tomography showed soft tissue nodules in the anterior basal segment of the lower lobe of the right lung, while both lungs showed multiple, scattered, small inflammatory nodules as well as mild chronic inflammation. Bilateral pleural thickening and adhesion, enlarged mediastinal lymph nodes, and aortic wall calcification were also observed. Thyroid color Doppler ultrasonography revealed bilateral lobular thyroid nodules suggestive of nodular goiter, while conventional color ultrasonography of the abdomen and urinary system indicated the presence of fatty liver, liver cyst, dilated common bile duct, and enlarged spleen. Electrocardiography and electroencephalography were unremarkable.
Neurological examination showed no obvious abnormalities, and her apolipoprotein E genotype was E3/E3, suggesting low risk of Alzheimer's disease. In addition, no obvious abnormalities were found in routine blood or urine indices, liver or kidney function, electrolytes, blood lipids or glucose, coagulation or thyroid function, tumor markers, or glycosylated hemoglobin.
Assessment of symptoms was based on a Chinese version of HAMD and HAMA administered by a psychiatrist. HAMD score of 8, HAMA score of 22. Chinese version of Childhood Trauma Questionnaire score 33 (emotional abuse score 9, physical abuse score 5, sexual abuse score 5, emotional neglect score 9, and physical neglect score 5) which indicated without childhood trauma. Mini-mental State Examination score25, and Montreal Cognitive Assessment score of 24, indicating no obvious abnormalities in cognitive function.
Based on the patient's reported symptoms and the tests, the patient was diagnosed at our hospital with generalized anxiety disorder based on the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition.
After diagnosis, the patient was treated with paroxetine (20 mg/day), tandospirone (10 mg three times a day), and lorazepam (0.5 mg/night) to relieve anxiety and control sleep disorders, as well as atorvastatin calcium (5 mg/night) to control hyperlipidemia. This medication was combined with electroencephalographic biofeedback training and repetitive transcranial magnetic stimulation once a day. After 4 days of this therapy, the patient started to smell strong odor of ammonia in the restroom, especially in the afternoon. Therefore, we adjusted the medication to tandospirone (10 mg three times a day), paroxetine (40 mg/day), and lorazepam (0.25 mg/noon and 0.5 mg/night). After 6 days on the modified drug regime, the patient claimed that the odor became mild, but she still had hyposmia for normal smells, especially in the afternoon. After 10 days on the physiotherapy and modified drug regime, the patient reported feeling relaxed and sleeping well at night, with no olfactory hallucination. After a total of 20 days hospitalization, transcranial magnetic stimulation sessions were stopped. She was discharged on tandospirone at 10 mg three times a day, paroxetine at 40 mg/day, and lorazepam 0.5 mg/night. She scored 7 on the HAMD and 8 on the HAMA. A timeline of treatment is shown in Figure 4.
At 3-month follow-up, she reported no olfactory hallucination, and she slept well. She scored 5 on the HAMD and 4 on the HAMA. She lived with her daughter and took good care of her grandson every day. She denied anxious and her mood was relatively easy to maintain a smooth. She also had good tolerability of the medication.