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Lung Cancer with Brain Metastasis After Late-Onset Bipolar Disorder: A Case Report
Bipolar disorder is a multifactorial illness with uncertain etiology and geriatric new-onset manic episodes are highly associated with secondary organic causes. The presented case demonstrates the importance of excluding secondary causes during the entire disease course.
Bipolar disorder is a chronic mental illness characterized by extreme shifts in mood ranging from manic to a depressive state. The peak age of onset of bipolar disorder is 20-40 years. About 90% of cases are reported to have onset ≥ age 50 years; up to 5-10% will present with onset after 50 years and are defined as late-onset bipolar disorder.
Although symptoms are similar to those of the early age of onset groups, growing evidence suggests that geriatric-onset bipolar disorder or late-onset bipolar disorder is often attributable to a variety of organic etiologies. Studies also reported that about 10% of late-onset bipolar disorder patients develop new-onset mania later in life. This is often associated with neurovascular factors, epilepsy, central nervous system infections, head injuries, brain tumors, endocrine disorders, vitamin deficiencies, dementia, and drug side effects (e.g., steroids and stimulants). Therefore, a thorough work-up along with a detailed review of the patient’s history is imperative.
Mr. F, a 65-year-old man, presented to the Psychiatric outpatient clinic of Chang Gung Memorial Hospital, Taiwan with manic episodes. The patient was in a healthy state until 3 weeks before presenting to the clinic when he started to become hyperactive, grandiose, overly talkative and had decreased need of sleep. The patient was also reported to have auditory and visual hallucinations. He became aggressive both verbally and physically; there were instances of self-harm, too. A trigger event occurred 1 month previously when the family discovered his affairs. Mr. F initially became depressed and anxious and then developed mania, a week later late-onset bipolar disorder I was diagnosed.
The initial laboratory investigation results were as follows: balanced electrolytes, normal thyroid function, and negative syphilis rapid plasma reagin (RPR). However, electroencephalography (EEG) showed mild diffuse cortical dysfunction. The patient was started on combined therapy with valproic acid 500 mg/day and olanzapine 10 mg/day. The manic symptoms gradually improved within a week. Unfortunately, agitation, paranoia, auditory hallucinations, and persecutory delusions aggravated. Neither valproic acid 1000 mg/day nor the switch from olanzapine to paliperidone 9 mg/day improved these symptoms. Therefore, he was admitted in the acute psychiatric ward.
In the first 2 weeks of hospitalization, he remained agitated and paranoid, and was placed in a seclusion and protection room (SPR) for safety concerns and to maintain his sleep schedule. With the medication adjustment, the symptoms improved gradually. After 6 weeks of hospitalization, he was discharged on valproic acid 500 mg/day, aripiprazole 20mg/day, and quetiapine 150 mg/day. On the day of discharge, his Cognitive Abilities Screening Instrument (CASI) score and clinical dementia rating scale (CDR) score were 82.5 and 0.5 respectively.
In the following 8 months, the patient remained free of psychosis and mood swings. Therefore, valproic acid was tapered to 500 mg/day and quetiapine 50 mg/day. Subsequent MRI showed only atrophy. However, after remaining stable for another year, he developed acute cognitive function decline and an unsteady gait for 2 months. The cerebral positron emission tomography (PET) revealed a decrease in [18F]2-fluoro-2-deoxy-D’Glucose (FDG) uptake in the cortex, compatible with typical Alzheimer’s disease. Antidementia drug rivastigmine (9 mg) was prescribed since the psychological tests revealed a CASI-2.0 score of 73.4 and a CDR score of 0.5. The patient’s response to anti-dementia drugs was poor and he experienced a visual hallucination, irritability, negative thoughts, insecure feelings, inappropriate behaviors, paranoia, and delusions involving theft and jealousy – the symptoms attributed to behavioral and psychological symptoms of dementia or BPSD.
One month later, the patient presented a severe clinical dementia, with a CDR score of 2. Hence, a neuropsychological assessment was done. At that point, even though the patient’s cognitive function was declining rapidly, there were no significant neurologic deficits or physiological abnormalities. Three months later, he had presented progressive left side extremity weakness and frequent choking for a week and was hospitalized. A chest X-ray showed a mass in the right upper lobe of the lung; CT and MRI scans revealed a mass lesion of 8:4×4:4×6:0cm size in the left occiput parietotemporal lobe with a midline shift to the right. Metastatic adenocarcinoma of pulmonary origin was confirmed and he underwent excisional surgery. FDG PET-CT confirmed right upper lung cancer with lung-to-lung and distant brain metastasis. Mr. F was then referred to a pulmonary oncologist for chemotherapy.
The patient did not take any psychiatric medication post-surgery; however, he was on valproic acid 1000 mg/day for post brain surgery seizure prophylaxis.
Numerous cases of cancer patients presenting prodromal or neuropsychiatric symptoms have been previously reported in the literature. The psychological symptoms may occur either concurrently or a group of symptoms predominates over another. In some cases, the psychiatric symptoms precede neurological symptoms. In patients presenting with mood-related or psychotic symptoms alone, psychiatrists must order for neuro-imaging tests in tumor suspicion. This is especially critical in patients with new-onset symptoms or atypical behavioral and psychiatric symptoms.
In the present case, Mr. F had new-onset mania and was diagnosed with bipolar disorder in his later life at the age of 65 years. This was in agreement with the case presented by Van Gerpen et al., whereas in contrast with Kessler et al who reported that bipolar disorder is always present between late adolescence to early adulthood. The patient underwent initial surveys including serum chemistries, complete blood count, thyroid function test, and rapid plasma reagin (RPR) for syphilis. All results were within normal limits. Brain MRI performed 10 months later revealed only atrophy without any solid lesions. However, a year later, Mr. F suddenly developed neurologic symptoms and brain metastasis of pulmonary origin was confirmed.
Warren et al and S. El Hayek and J. El-Khoury reported cases of new late-onset bipolar disorder associated with lung cancer with or without brain metastasis; in both studies, the patients had underlying lung cancer and developed subsequent acute-onset and late-onset manic symptoms. In this case, there was neither a lung lesion nor a brain lesion. Therefore it was difficult to determine whether the manic episodes of Mr. F were a consequence of cancer or an independent condition.
Various studies have described that signs and symptoms of lung cancer might appear if cancer has spread to other organs including the brain. Therefore, it is possible that Mr. F had underlying lung lesions that went undetected on the chest X-ray taken at the onset of the symptoms of bipolar disorder.
This case report shows that a patient with bipolar disorder, despite the absence of neurological symptoms at the beginning of the episode, had a large brain tumor. The present case demonstrates that in geriatric patients excluding secondary causes of late-onset bipolar disorder is important at the beginning, during, and throughout the course of disease.
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