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.
Ms. A, a 40-year-old woman diagnosed with a residual schizophrenia [] was admitted following an exacerbation of psychotic symptoms with a predominance of anxiety despite 700 mg/d of clozapine for two years. The clinical scores and the trough plasma concentrations of clozapine and norclozapine at admission were CGI : 5; total PANSS: 123; positive: 17/49; negative: 18/49; excited component: 12/35; general: 39/112; Hamilton-anxiety: 14/56; clozapine: 896 ng/mL; norclozapine: 551 ng/mL, respectively (clozapine therapeutic range: 350–600 ng/mL [–]). Because of the risks of seizures, the dose was reduced to 500 mg/d, and aripiprazole (10 mg/d) was added. Clozapine and norclozapine plasma concentrations measured after 10 days were decreased according to the reduction of the dose (615 ng/mL and 478 ng/mL, resp.). The aripiprazole plasma concentration after 10 days was 282 ng/mL. Following a clinical reduction of the anxiety, the patient was discharged from the hospital three weeks after the addition of aripiprazole.\nA followup over 6 months did not reveal any change in the CGI and PANSS scores (at 6 months: CGI : 5; total PANSS: 125; positive: 18/49; negative: 23/49; excited component 10/35; general: 38/112). On the other hand, the Hamilton-anxiety score diminished progressively to 12, 7, and 8 after one, three, and 6 months, respectively. Clozapine and norclozapine plasma levels were stable over this period (at the sixth month: 608 ng/mL, 443 ng/mL, and 75 kg, resp.), and the comedications (clorazepate 20 mg/d, valsartane 40 mg/d, zopiclone 7,5 mg/d, and tamsulosine 0.4 mg/d) were not modified. No reports are describing an impact on anxiety by the antihypertensive comedication by valsartane (an angiotensin II receptor antagonist) and tamsulosine (peripheral α1-antagonist). There is no significant pharmacokinetic or pharmacodynamic interactions of that comedication and the antipsychotic/anxiolytic treatments.