Insomnia is the most common form of sleep disorder, and subjective cognitive decline (SCD) in patients with insomnia may be an ultra-early manifestation of AD. Repetitive transcranial magnetic stimulation (rTMS) has emerged as a promising tool for the treatment of insomnia by modulating neural excitability and inducing plasticity. However, there is a lack of studies on rTMS treatment of cognitive impairment associated with insomnia. The efficacy and safety of rTMS for cognitive impairment in insomnia patients with SCD will be assessed by a randomized controlled trial.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
TRIPLE
Enrollment
66
Stimulation coil Cool-B65 A CO, located right lingual gyrus, stimulation frequency 1Hz, stimulation intensity 80% of motor threshold, number of stimuli 3 pulses/train, train interval 1s, 500 trains in total, 1500 total stimulation pulses, total stimulation time 20 min, treatment application once a day, continuous application for two weeks, 5 days a week.
Stimulation coil Cool-B65 P CO, located right lingual gyrus, stimulation frequency 1Hz, stimulation intensity 80% of motor threshold, number of stimuli 3 pulses/train, train interval 1s, 500 trains in total, 1500 total stimulation pulses, total stimulation time 20 min, treatment application once a day, continuous application for two weeks, 5 days a week.
Change from baseline SCD-Q9 to 2 weeks
9-item Subjective Cognitive Decline Questionnaire (SCD-Q9)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline MMSE to 2 weeks
Mini-Mental State Examination (MMSE)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline MoCA scores to 2 weeks
Montreal Cognitive Assessment (MoCA)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline CDR to 2 weeks
Clinical Dementia Rating (CDR)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline RAVLT to 2 weeks
Rey Auditory Verbal Learning Test (RAVLT)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline HAMA to 2 weeks
Human Anti-Murine Antibodies (HAMA)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline HAMD to 2 weeks
Hamilton Rating Scale for Depression (HAMD)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline NPI to 2 weeks
Neuropsychiatric Inventory (NPI)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline CDS to 2 weeks
Coding Digit Symbol subtest (CDS)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline DDS to 2 weeks
Direct Digit Span subtest (DDS)
Time frame: Baseline vs 2 weeks after treatment
Change from baseline inflammatory factors and neuropathological markers to 2 weeks
Aβ, tau, GFAP, α-Synuclein, NFL, VEGF, AQP4, RNA sequencing, pre.Caspase1, cl.Caspase1, pre.IL-1β, cl.IL-1β, IL-18, GSDMD, ASC, NLRP1, Iba-1, GFAP, NeuN, CD86, CD206, iNOS, Arg1, TLR4, TLR2, MyD88, NFκB, tau, p-NFκB, NLRP3, β-actin, ect.
Time frame: Baseline vs 2 weeks after treatment
Change from baseline PAF to 2 weeks
The alpha-peak frequency (PAF) is the frequency with the highest power within the alpha-band.
Time frame: Baseline vs 2 weeks after treatment
Change from baseline structural imaging indicators to 2 weeks
The intra-cellular compartment (Vic) of the Neurite Orientation Dispersion and Density Imaging (NODDI) model represents diffusion within the axons and cells.And NODDI models the dispersion of axonal fibers with the use of an Orientation Dispersion Index (ODI).
Time frame: Baseline vs 2 weeks after treatment
Change from baseline adverse events to 2 weeks
Headache, tinnitus, pure tone hearing disorder, ect.
Time frame: Baseline vs 2 weeks after treatment
Change from baseline TMS-EEG to 2 weeks
Concurrent transcranial magnetic stimulation and electroencephalography (TMS-EEG)
Time frame: Baseline vs 2 weeks after treatment
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