Background and PurposeIt has been shown that sleep problems in Alzheimer's disease (AD) are associated with cognitive impairment and behavioral problems. In fact, most of studies have founded that daytime sleepiness is significantly correlated with cognitive decline in AD. However, a few studies have also shown that nighttime sleep problems are associated with cognitive function and behavioral symptoms in AD. Accordingly, the aim of this study was to evaluate the effects of nighttime sleep on cognition and behavioral and psychological symptoms of dementia (BPSD) in AD.MethodsThe study population comprised 117 subjects: 63 AD patients and 54 age- and sex-matched non-demented elderly subjects. Detailed cognitive functions and behavioral symptoms were measured using the Seoul Neuropsychological Screening Battery (SNSB) and the Korean version of the Neuropsychiatric Inventory (NPI-K). Sleep characteristics were evaluated using the Korean version of the Pittsburgh Sleep Quality Index (PSQI-K). The correlations between PSQI-K and SNSB scores and between PSQI-K and NPI-K scores were analyzed.ResultsIn AD patients, sleep latency was found to be negatively correlated with praxis (p=0.041), Rey-Osterrieth Complex Figure Test (RCFT) immediate recall (p=0.041), and RCFT recognition (p=0.008) after controlling for age and education, while sleep duration and sleep efficiency were positively correlated with praxis (p=0.034 and p=0.025, respectively). Although no significant correlation was found between PSQI-K and NPI-K scores, sleep disturbance and total PSQI-K scores were found to be significantly associated with apathy/indifference in AD.ConclusionsSleep problems such as prolonged sleep duration, sleep latency, and poor sleep efficiency in AD patients were correlated with cognitive dysfunction, and especially frontal executive and visuospatial functions, and BPSD. These findings suggest that treatment of nighttime sleep problems might improve cognition and behavioral symptoms in AD patients.

The insula, one of the five cerebral lobes of the brain, is located deep within the brain and lies mainly beneath the temporal lobe. Insular epilepsy can be easily confused and misdiagnosed as temporal lobe epilepsy (TLE) because of the similar clinical symptoms and scalp electroencephalography (EEG) findings due to the insula location and neuronal connections with the temporal lobe. Magnetoencephalography (MEG) has higher sensitivity and spatial resolution than scalp EEG, and thus can often identify epileptic discharges not revealed by scalp EEG. Simultaneous scalp EEG and MEG were performed to detect and localize epileptic discharges in two patients known to have insular epilepsy associated with cavernous angioma in the insula. Epileptic discharges were detected as abnormal spikes in the EEG and MEG findings. In Patient 1, the sources of all MEG spikes detected simultaneously by EEG and MEG (E/ M-spikes) were localized in the anterior temporal lobe, similar to TLE. In contrast, the sources of all MEG spikes detected only by MEG (M-spikes) were adjacent to the insular lesion. In Patient 2, the sources of all MEG spikes detected simultaneously by EEG and MEG (E/M-spikes) were localized in the anterior temporal lobe. These findings indicate that MEG allows us to detect insular activity that is undetectable by scalp EEG. In conclusion, simultaneous EEG and MEG are helpful for detecting spikes and obtaining additional information about the epileptic origin and propagation in patients with insular epilepsy.

Interictal spikes in patients with epilepsy may be detected by either electroencephalography (EEG) (E-spikes) or magnetoencephalography (MEG) (M-spikes), or both MEG and EEG (E/M-spikes). Localization and amplitude were compared between E/M-spikes and M-spikes in 7 adult patients with extratemporal epilepsy to evaluate the clinical significance of MEG spikes. MEG and EEG were simultaneously measured using a helmet-shaped MEG system with planar-type gradiometers and scalp electrodes of the international 10-20 system. Sources of E/M-spikes and M-spikes were estimated by an equivalent current dipole (ECD) model for MEG at peak latency. Each subject showed 9 to 20 (mean 13.4) E/M-spikes and 9 to 31 (mean 16.3) M-spikes. No subjects showed significant differences in the ECD locations between E/M-and M-spikes. ECD moments of the E/M-spikes were significantly larger in 2 patients and not significantly different in the other 5 patients. The similar localizations of E/M-spikes and M-spikes suggest that combination of MEG and EEG is useful to detect more interictal spikes in patients with extratemporal epilepsy. The smaller tendency of ECD amplitude of the M-spikes than E/M-spikes suggests that scalp EEG may overlook small tangential spikes due to background brain noise. Localization value of M-spikes is clinically equivalent to that of E/M-spikes. magnetoencephalography; electroencephalography; epilepsy; interictal spike; equivalent current dipole

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Amyotrophic lateral sclerosis (ALS) can present with heterogeneous symptoms resulting from the involvement of multiple brain systems including extramotor cortical areas. Involvement of other brain areas can cause diverse clinical symptoms including cognitive impairment and extrapyramidal symptoms. We report the case of a 50-year-old woman with bulbar onset ALS and frontotemporal lobar degeneration (FTLD), confirmed as cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). The patient and her first-degree relatives harbored a mutation (R75P) in the NOTCH3 gene, indicative of vascular deficits. The details of this case add plausibility to the idea that ALS, FTLD, and CADASIL are different aspects of a spectrum of disorders with overlapping pathologic mechanisms.