PSG recordings included electroencephalogram, chin movements, leg movements, eye movements, electrocardiogram, oxygen saturation, and chest and abdominal wall movement. Patients were required to arrive at the sleep center at 9:00 p.m. The first night’s PSG was performed for patients to become accustomed to the sleep center and only the data from the latter two monitoring sessions were included in the analysis. PSG was recorded three times (twice at baseline and once at posttreatment) at a sleep center (PSG manufacturer: Cadwell Laboratories. We hypothesized that trazodone would improve cognitive function in addition to relieving insomnia. This pilot study was conducted to explore the clinical efficacy and cognitive remediation of trazodone (50 mg dose) treatment for these patients. To the best of our knowledge, few studies have assessed the effects of trazodone on cognitive impairment in individuals with CSVD comorbid with persistent insomnia. The observation periods for the above studies were generally short, and the participants were not patients with cognitive impairment. Roth AJ (2011) used trazodone (50 mg) to treat primary insomnia, and the results showed that trazodone improved sleep quality but caused small impairments in short-term memory after 1 week of treatment ( 13). Sasada K (2013) evaluated the effect of mirtazapine and trazodone (25 mg) on cognitive function in healthy men after 9 days of treatment and reported that trazodone did not affect cognitive function ( 12). Ip EJ (2013) evaluated the cognitive driving ability in healthy adults after a single dose (100 mg) of trazodone and found that the number of individual impairment clues increased 2 h after drug administration ( 11). In the past, studies on the cognitive effects of trazodone focused on the side effects of the drug and the results were inconsistent. This theory is based on the finding that cognitive impairment is related to 5-HT deficiency and the normalization of 5-HT function contributes to the improvement of cognitive function ( 10). Moreover, trazodone may help improve cognitive function by increasing the concentration of 5-HT in the synaptic space. Several studies have demonstrated that trazodone is helpful for improving nocturnal sleep maintenance without a hangover effect due to the relatively short half-value period (3–6 h) ( 9). Because of its dose-dependent pharmacologic actions, low dose trazodone (25–150 mg) is effective in blocking histamine 1 (H 1), 5 hydroxytryptamine 2A (5-HT 2A), and α1-adrenergic receptors and is more often used as a sedative for treating insomnia ( 9). Trazodone, a second-generation triazolopyridine antidepressant, is approved for the treatment of depression. However, cognitive and behavioral therapy is not always an option due to the lack of well-trained therapists and the long treatment sessions required. Medication and psychotherapy are both effective methods for treating chronic insomnia ( 8). Evidence indicates that the effective treatment of insomnia helps to alleviate comorbid disorders ( 7). According to the results of our prophase research, the disruption of sleep continuity caused by insomnia can aggravate the impairment of executive function and memory in CSVD patients ( 4), suggesting that treating insomnia might be a potential target for improving the cognitive function of CSVD patients. Insomnia is frequently associated with cognitive decline and is thought to be partly responsible for the pathological progression of several neurodegenerative diseases ( 6). The sleep patterns of these patients are characterized by increased sleep fragmentation, decreased sleep efficiency, and a reduced slow-wave sleep (SWS) ratio ( 4). An earlier study by our team found that the proportion of individuals with persistent insomnia among CSVD patients (54%) ( 4) was far higher than that among the general elderly population (12–20%) ( 5). CSVD accounts for 50–70% of vascular cognitive impairment cases and 45% of dementia cases and results in a heavy social burden ( 2).Ĭhronic insomnia, the most common sleep disorder in elderly individuals, is often comorbid with physical diseases including cerebral vascular disease ( 3). Cerebral small vessel disease (CSVD) refers to the syndrome of clinical, cognitive, imaging, and pathological manifestations caused by various small vascular diseases ( 1), among which arteriosclerotic CSVD is the most common type ( 1).
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