A 42 year-old man with a past medical history of schizoaffective disorder, hyperlipidemia, and gastrointestinal reflux disease was admitted to an adult psychiatric unit secondary to intrusive thoughts that were sexual, homicidal, and suicidal in nature. Similar thoughts with tics were first reported 2 decades prior to the current hospital admission; however symptoms of depression were most prominent then and he was initially diagnosed with only major depressive disorder. During the following years there were documented reports of “paranoia and delusions related to contamination” as well as continued reports of intrusive violent thoughts also believed to be delusions. This led to a diagnosis of schizoaffective disorder; and antipsychotics became the primary modality of treatment over the next decade. Documented antipsychotics trials included aripiprazole, olanzapine, lurasidone, and quetiapine, all of which were associated with a lack of adequate improvement or adverse events. Records indicated that haloperidol combined with fluvoxamine did result in partial improvement. Antidepressants were also utilized intermittently over this 20-year period to target mood symptoms. Historically, the antidepressant trial with the highest documented relative dose was paroxetine 60 mg. It was during this time period with paroxetine that there was documented improvement of the patient's intrusive thoughts. Side effects limited use of the paroxetine 60 mg, and after it was decreased the violent intrusive thoughts worsened.\nInevitably the patient's outpatient provider after years of suboptimal response to antipsychotics initiated clozapine to target what was continued to be described as psychotic symptoms in the medical record. However, as the clozapine was gradually increased to 400 mg the patient noted a severe worsening of intrusive thoughts causing secondary depressed mood, anxiety, and suicidal ideation leading to hospitalization at our facility. It was during this admission that there was exploration of the patient's intrusive thoughts, which were clearly obsessions in that they were persistent, unwanted, egodystonic thoughts. Efforts by the patient to suppress or ignore these thoughts were futile, resulting in significant anxiety and distress. Yet while these obsessions occupied a significant amount of time during the day, impacting his social and work functioning, he denied any ritualistic behaviors or compulsions. Family history was found to be positive for an aunt and mother with hoarding disorder and a cousin with OCD. As the obsession were not attributable to the use of substances, a medication condition, or other mental disorders, the diagnosis of OCD was given for the first time based on criteria from the Diagnostic and Statistical Manual of Mental Disorders, 5th edition []. With the patient now diagnosed with OCD, he was appropriately treated; and there was a plan to initiate fluoxetine with a goal dose of 80 mg. Given the historical nature of the schizoaffective diagnosis, clozapine was continued taking into account there had been improvement during the hospitalization and that it would need to be slowly tapered as an outpatient to avoid adverse effects. The patient was safely discharged with minimal intrusive thoughts and it was recommended to the patient's outpatient provider that clozapine be discontinued after a slow taper. However, in the following months, the patient's outpatient provider had increased clozapine to 700 mg. This was associated again with a subsequent worsening and exacerbation of distressing intrusive thoughts leading to another hospitalization. Serum clozapine and norclozapine levels upon admission were found to be 453 ng/mL and 464 ng/mL, respectively. Clozapine was rapidly discontinued due to the association with OCS, as well as the patient's clinical presentation after each clozapine escalation. Clozapine was tapered over approximately 2 weeks without complications such as cholinergic rebound, catatonia, serotonin syndrome, or withdrawal dyskinesias [–]. More importantly there was no emergence of psychotic symptoms, strengthening the likelihood that the patient did not have schizoaffective disorder based on DSM-5 criteria.\nIn review of records and after discussion with the patient, it was determined that the past fluvoxamine trial did not reach an adequate dose for the treatment of OCD. Fluvoxamine was started and increased to 200 mg after clozapine had been allowed to wash out. Low-dose aripiprazole was also initiated to augment the fluvoxamine given the severity of the presentation, the benefits of this antipsychotic in treatment resistant OCD, and the low risk of inducing OCS []. The patient was discharged with resolution of intrusive thoughts and improvement in mood and still without emergence of psychotic symptoms. Following this hospitalization the patient began to see a therapist who specialized in exposure and response prevention therapy to address his OCD. Longitudinally, the patient struggled with depression and anxiety associated with residual obsessions resulting in fluvoxamine being changed to clomipramine. The last known dose of clomipramine was 150 mg and reported as having reasonable control of OCS as an outpatient. Up to a year following the second reported hospitalization at our facility there were no patient reports or documentation noted of criteria sufficient for a diagnosis of schizoaffective disorder or other psychotic disorders.
A 52-year-old woman with a 9-year history of schizophrenia presented with a persistent headache and depression after she was mauled by five people 2 months ago, with the left side of the top of her head hit by a crabstick and no disturbance of consciousness after the attack. She had two head MRI scans after the hit, but all of them showed negative results. The woman presented argumentative hallucinations and paranoid delusions 9 years ago. She was diagnosed with schizophrenia and was then treated with 600 mg quetiapine daily. The treatment was effective, and quetiapine was maintained at a dosage of 200 mg daily. During these 9 years, she sometimes heard some people talking about her, but even if she heard this, she thought these voices had nothing to do with her. She worked as a cleaner during these years. She has been hard-working and self-disciplined. The hallucinations increased in both frequency and intensity 6 months ago, and she could constantly hear her neighbours and people from nearby villages commenting on her. Two months ago, a white dog and a yellow dog were fighting in front of her house, and then her neighbour shouted at these dogs. At that time, the patient was dressed in yellow, and she thought her neighbour was shouting at her, so she went to fight her neighbour; then, the neighbour's family came out and mauled her. As an outpatient, she had taken 15 mg olanzapine daily, 10 mg aripiprazole daily, and 100 mg sertraline daily during the following two months, but her headache had worsened.\nWhen the patient came to the inpatient ward, she was kempt but made passive contact, talked little, and avoided eye contact with psychiatrists; her only complaint was a severe and unbearable headache. Her thoughts were consistent and logical, but her reaction was slow. She could hear several different kinds of auditory hallucinations. The first was a kind of functional auditory hallucination triggered by whispering, barking, or car noises, and these whispers could present as argumentative swearing. The second was a kind of primary auditory hallucination, which could occur without any sign, and it could be combined with a persecutory delusion in which she thought there were people nearby talking about her. The third kind of functional hallucination was that when she talked with psychiatrists, she could hear psychiatrists swearing at her at the same time as the real psychiatrists' voice. The fourth kind of hallucination was a psycho-hallucination that stemmed from her brain. These voices often commented on her or presented themselves as the fifth form and broadcasted her thoughts, which coincided with the dilution of the diffusion of her thoughts. When she heard the commenting and criticizing voice, thoughts of guilt came to her mind. When thoughts of guilt emerged, she denied them and swore against them in her mind, but she could not avoid these thoughts. Every time she swore against these people, she felt shameful and repentant because she believed that speaking ill of others was immoral; she then was angry with herself, and her headache then appeared. When she lived in the hospital, she often wandered around the garden, which she said could relieve her headache because she could verify that nobody was talking about her in the garden. She had insomnia because the auditory hallucinations were too loud to allow her to sleep, and in the early morning, the auditory hallucinations interrupted her sleep.\nShe did not smoke, did not drink alcohol, and denied the use of illicit drugs. No parental relative was reported to have a diagnosis of mental disorder. There was no comorbid physical illness. The patient only completed 3 years of elementary education. She quit her studies because her family could not afford her tuition fee, and she was required to work to support her family; however, she could read and write. She had been obedient and forbearing since she was a child. She was married at 24 years of age in an arranged marriage. Her first child was a daughter, so she gave birth to a son one year later because of patriarchal culture. However, owing to the one-child policy, she had to pay a large amount of forfeit, and it took her 10 years to repay the debt. Unfortunately, her son accidentally drowned at 7 years old. After her son died, she had an episode of depression. At that time, she had feelings of sorrow and self-condemnation. She laid on the bed every day and quit her job because she heard many colleagues talking about her. She was diagnosed with major depressive disorder, but she did not take medicine, and her depression subsided 6 months later. During these 14 years, she had not shown any sign of mood or psychotic symptoms, and her symptoms during these 9 years was not closely related to the context of her son. She did not avoid to talk about her son, and her son's death no longer bothers her. There was no obvious manic episode in her life.\nOn examination, her head MRI scan was normal. Her blood count, liver function, kidney function, thyroid function, and infectious disease portfolio were normal. Her Hamilton Anxiety Scale (HAMA) was 23, and her 17 items of Hamilton Depression Rating Scale (HAMD-17) was 24. We conducted drug-gene testing, which showed that her CYP2D was ∗10/∗41 and her FKBP genes were GG (rs4713916) and CC (rs1360780), which implied that venlafaxine might not be effective.