2 | CASE PRESENTATION
The wife of a 64-year-old right-handed Japanese man complained that her husband’s cognitive function had begun to deteriorate; for example, he had difficulty in performing simple calculations and could not recognize his old friends. His medical history showed no illnesses, and he had no previous history of psychiatric disorders. His educational level was graduation from high school. His wife considered that these impairments could be due to problems at his job. The patient had begun to talk about being eager to quit his job and complain about not feeling well. His wife suspected memory impairment in her husband’s daily life. When he visited our clinic accompanied by his wife, the patient calmly stated that he was not well accustomed to his new job. Although his mental condition showed nothing particular, his episodic memory appeared to be slightly impaired based on medical interviews by a certified psychiatrist. Neurocognitive tests, MR imaging, and IMP-SPECT were therefore performed (Table 1, Figures 1a, 2a, 2b). The results of the neurocognitive tests showed that the patient’s cognitive ability was normal (Table 1) ; however, his structural and functional brain images suggested an AD pattern (Figures 1a, 2a, 2b). It was because bilateral superior parietal lobes showed slight atrophy for his age on MR images, and because hypoperfusion was observed in the bilateral parietal-temporal association areas, posterior cingulate gyrus and precuneus, and frontal association areas, predominantly in the right cerebral hemisphere, based on IMP-SPECT (Figures 1a, 2a, 2b).
Three months after the first visit, the attending psychiatrist suspected that the patient might have SAS, based on the medical interviews. The psychiatrist referred the patient to a medical sleep center, where the patient was diagnosed with moderate to almost severe SAS based on the results of a sleep polysomnography test, which were as follows: apnea-hypopnea index, 29.3; oxygen desaturation index, 17.3; minimum oxygen saturation, 93%; and arousal index, 38.0. CPAP was therefore introduced, which improved his SAS.
The patient underwent neurocognitive tests at one year and at 18 months after the baseline visit (Table 1), which showed, during the 6 months, gradually worsening scores on the mini-mental state examination (MMSE). The patient was diagnosed with non-amnestic MCI or early-stage AD. Eighteen months after the baseline visit, the patient also underwent PiB-PET and THK5351-PET, which revealed positive pathological amyloid β and tau protein accumulation (Figures 3a, 4a), thereby indicating an AD neurological disease.5,6 At that point, the results of MR imaging were almost identical to those of the baseline visit (Figure 1a, 1B).
Nineteen months after the baseline visit, lung cancer (right, S2, T3N0M0) was detected in the patient, but his only clinical feature was a dry cough, which his wife stated appeared occasionally. No metastasis was found, the tumor was surgically removed, and the pathology indicated adenosquamous carcinoma. Per the surgeon’s instructions, the patient ceased the CPAP therapy for 2 months after the surgery.
Two years after the baseline visit, the patient’s MMSE score showed that his general cognitive ability had improved after the resection surgery for his lung cancer (Table 1). However, his neurocognitive test scores were slightly lower 3 years after the baseline visit compared with those 2 years after the baseline visit (Table 1). The MR, PiB-PET, and THK5351-PET images are shown in Figures 1c, 3b, and 4b, respectively. The results of MR imaging were almost identical to those performed at baseline visit and at 18 months after the baseline visit (Figure 1a, 1b, 1c). However, the deposition of pathologic tau protein had slightly increased.