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.