Objectively measured short sleep duration increased the odds of reporting hypertension more than threefold after adjusting for potential confounders; this relationship was not significant for subjectively measured sleep duration. This research supports emerging evidence that insomnia with objective short sleep duration is associated with an increased risk of comorbid hypertension.

Given the recent evidence on the association between hyperarousal in insomnia disorder and neurocognitive deficits, we aimed to examine the effect of short sleep duration on neurocognitive reaction time tests in insomnia disorder sufferers. We recruited subjects with insomnia disorder (n = 35, mean age = 40.6 years) who scored ≥29 on a Hyperarousal Scale, and a group of controls (n = 54, mean age = 31.5 years) who had no sleep disorders and scored <26 on the Hyperarousal Scale. Participants completed two in-home polysomnograms and four daytime trials of neurocognitive tests, including simple reaction time, choice reaction time, big circle-little circle, rapid visual information processing, attention switching task, and spatial working memory tests. Total sleep time divided study cohorts into subgroups of short (total sleep time <6 hr) and normal (total sleep time ≥6 hr) sleepers. ANCOVA showed a significant interaction between participant type (insomnia disorder versus controls) and sleep duration (short versus normal) for spatial working memory-latency (p = 0.020) and spatial working memory-errors (p = 0.025). The short-sleeping insomnia disorder group had longer spatial working memory-latencies and more spatial working memory-errors than did normal-sleeping controls. Regardless of sleep duration, those with insomnia disorder had more attentional deficits with longer attention switching task-latency (p = 0.011) and more attention switching task-incorrect trials (p = 0.015) than the control group. Normal-sleepers only had longer attention switching task-latency than short-sleepers (p = 0.004). A phenotype of insomnia disorder with hyperarousal and short sleep duration is associated with daytime cognitive deficits in complex attentional and spatial working memory tasks.

Evidence indicates that the association between insomnia and elevated blood pressure (BP) or stage 1 and 2 hypertension is stronger in those with chronic insomnia, as compared to those with isolated insomnia symptoms, and primarily found in those with the insomnia with objective short sleep duration phenotype. There is a key gap in ambulatory BP monitoring across the sleep-wake cycle as well as in randomized clinical trials testing the effectiveness of pharmacological or cognitive-behavioral insomnia therapies in lowering BP. Insomnia is a strong candidate to join the list of risk factors for hypertension along with obstructive sleep apnea. In the meantime, chronic insomnia should become part of the routine assessment of patients with elevated BP and should be a source for referral, diagnostic evaluation, and treatment, rather than regarded as a symptom of the underlying medical disorder.

Findings suggest that individuals with insomnia and objective short sleep duration <6 h are significantly less responsive to CBT-I than those with insomnia and normal sleep duration ≥6 h. Using an actigraphy TST cutoff of 6 hours to classify sleep duration groups was highly accurate and provided good discriminant value for determining insomnia remission.

MST may be an important component within cognitive remediation programmes for first-episode psychosis.

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