quantitative EEG

Sleep and circadian disturbances in Alzheimer’s disease (AD) affect patients and caregivers, but clinical action depends on the syndrome, measurement, and outcome under consideration. This narrative review links sleep assessment to indication-based care while distinguishing symptomatic benefit, physiological target engagement, and disease modification. A purposive literature search was supplemented by targeted checks of PubMed-indexed and original publisher records through 4 October 2026. Selected studies are described by population, AD ascertainment, comparator, and measured endpoint rather than assigned formal evidence-certainty grades. Actigraphy characterizes behavioral rest–activity patterns; melatonin timing and temperature rhythms address endogenous circadian physiology under controlled conditions. Polysomnography and quantitative electroencephalography characterize respiratory events, sleep architecture, and oscillatory activity. These measurements inform different questions and do not independently assign AD etiology or cognitive-functional stage. Clinical priorities include confirmed obstructive sleep apnea, cognition-adapted insomnia care, irregular sleep timing, medication-related effects, parasomnias, limb symptoms, and excessive daytime sleepiness. Interpretation incorporates hypoxemia, treatment exposure, comorbidity, caregiver support, and competing diagnoses. Randomized sleep benefits remain distinct from observational cognitive associations or exploratory imaging and cerebrospinal fluid changes. Human and animal studies of arousal circuits, protein dynamics, inflammation, and fluid transport provide mechanistic context, with conflicting results interpreted according to the actual experimental endpoint. The review provides a clinically organized account of selected evidence, not a comprehensive treatment ranking. Sleep care and cognitive-etiologic assessment should proceed in parallel, with follow-up matched to patient function, safety, and the specific treatment goal.

Background: Individuals with complex trauma may continue to experience emotional distress, rumination, and maladaptive response patterns despite pharmacological treatment. Integrative interventions addressing affective responses, maladaptive patterns, and adaptive functioning warrant further clinical investigation. Case presentation: This report describes a 23-year-old woman diagnosed with complex trauma who her psychiatrist referred because she was not responding adequately to prescribed antidepressant and anti-anxiety medication. She received an eight-session intervention delivered in three phases: one session of Wiring Affect with ReAttach (W.A.R.A.®) on Day 1; one session of Brain-Switch 2.0® on Day 2 to address maladaptive brain patterns; and six subsequent ReAttach® sessions, emphasizing Cognitive Bias Modification (CBM) 3, followed by CBM 1 and CBM 2. Clinical observations: Following the Day 1 W.A.R.A.® session, the client reported a quieter mind, reduced rumination, greater calmness, and sleeping that night without sleeping medication. Brain-Switch 2.0® was administered on Day 2, which further enhanced her self-agency. Subsequent ReAttach® sessions integrated her sense of identity and improved boundary setting with her parents. At one-month post-therapy follow-up, the client reported improved management of rumination, greater emotional regulation, anxiety within normal ranges, preserved cognitive functioning despite ongoing family difficulties, and greater satisfaction with herself. Pre–post quantitative electroencephalography (qEEG) data showed changes in several recorded measures. The qEEG data indicated the absence of previous mental sluggishness, a clinically significant improvement in the trauma-related marker and emotional regulation within the normative range, and the absence of a depression-related marker.