Mr. F, a 65-year-old male, was brought to the psychiatric outpatient clinic by his family who reported labile mood, impulsivity, decreased need for sleep, grandiosity, talkativeness, and increased goal-directed behaviors for 3 weeks. Several instances of physical aggression toward family members and self-harm were also reported. He also reported auditory hallucinations without visual hallucinations. A trigger event occurred one month previously, when his affairs were discovered by his family. He initially became depressed and anxious and then experienced mania, as mentioned above, a week later. The patient was oriented and communicable at the clinic despite his irritability. Late-onset bipolar I disorder was diagnosed, and a combination of valproic acid 500 mg/day and olanzapine 10 mg/day was prescribed for acute mania. The subsequent laboratory examination revealed balanced electrolytes, normal thyroid function, and negative syphilis rapid plasma reagin (RPR). Electroencephalography (EEG) showed mild diffuse cortical dysfunction.
The patient's condition improved gradually within the first week of psychiatric treatment. However, he became more agitated and paranoid thereafter, with aggravated auditory hallucinations and persecutory delusions. These symptoms did not improve despite titrating valproic acid to 1000 mg/day and switching from olanzapine to paliperidone 9 mg/day. He was hospitalized in the acute psychiatric ward, and his blood tests and chest X-ray were unremarkable.
In the first 2 weeks of hospitalization, the patient remained agitated and paranoid, and he was frequently placed in a seclusion and protection room (SPR) due to concerns about safety and maintaining his sleep schedule. With the medication adjustment, the patient's clinical condition improved gradually. He was discharged after 6 weeks of hospitalization; the discharge regimen was valproic acid 500 mg/day, aripiprazole 20 mg/day, and quetiapine 150 mg/day. Psychological tests before discharge were performed; the cognitive abilities screening instrument-2.0 (CASI-2.0) score was 82.5/100, and the clinical dementia rating scale (CDR) score was 0.5.
In the following 8 months, his mood remained stable and no psychosis was observed; therefore, the medication was gradually tapered to valproic acid 500 mg/day and quetiapine 50 mg/day. We performed brain magnetic resonance imaging (MRI) to exclude other physiological causes of late-onset bipolar disorder; the findings showed only old, small insults and atrophy. However, after remaining stable for another year, the patient developed acute cognitive function decline and an unsteady gait for 2 months. Laboratory blood tests were unremarkable, while cerebral positron emission tomography (PET) showed decreased [18F]2-fluoro-2-deoxy-D-glucose (FDG) uptake in the cortex regions, compatible with typical Alzheimer's disease. Psychological tests revealed a CASI-2.0 score of 73.4/100 and a CDR score of 0.5, so rivastigmine 9 mg was given. Despite the prescription of antidementia drugs, the patient experienced exacerbations of disorientation, paranoia, delusions involving theft, delusions involving jealousy, visual hallucination, irritability, negative thoughts, insecure feelings, and inappropriate behaviors. These symptoms were considered to be attributed to behavioral and psychological symptoms of dementia (BPSD).
One month later, a neuropsychological assessment was performed because of the presentation of severe clinical dementia, with a CDR score of 2 (Table 1). His rapidly declining cognitive function was alarming, but there were no remarkable neurologic deficits or physiological abnormalities at that time. Three months later, his family reported progressive left side extremity weakness and frequent choking for a week, so he was referred to the emergency room (ER) by the outpatient clinic. Laboratory blood tests were still unremarkable, but a chest X-ray showed a mass in the right upper lobe of the lung (Figure 1). Brain computed tomography (CT) and MRI revealed a mass lesion in the left occipito-parietotemporal lobe, sized 8.4 cm x 4.4 cm x 6.0 cm, with a midline shift to the right (Figure 2). Malignant origin was favored, and neurosurgery specialists were consulted for evaluation.
Given the concern about the effect of this large tumor and the rapid progression of neurologic deficits, the patient underwent emergency tumor removal surgery. The pathological report showed metastatic adenocarcinoma of pulmonary origin. Whole-body CT with a contrast agent revealed a necrotic lung mass in the right upper lobe and a solid lung nodule in the left upper lobe. FDG PET-CT confirmed right upper lung cancer with lung-to-lung and distant brain metastasis. The patient was then transferred to a pulmonary oncologist for chemotherapy.
The patient did not take any psychiatric medication after surgery; however, valproic acid 1000 mg/day was prescribed by the neurosurgery specialist for postbrain surgery seizure prophylaxis.