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Satu K. Jääskeläinen

Researcher at Turku University Hospital

Publications -  99
Citations -  6810

Satu K. Jääskeläinen is an academic researcher from Turku University Hospital. The author has contributed to research in topics: Burning mouth syndrome & Transcranial magnetic stimulation. The author has an hindex of 35, co-authored 94 publications receiving 5534 citations. Previous affiliations of Satu K. Jääskeläinen include University of Turku.

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Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS)

TL;DR: There is a sufficient body of evidence to accept with level A (definite efficacy) the analgesic effect of high-frequency rTMS of the primary motor cortex (M1) contralateral to the pain and the antidepressant effect of HF-rT MS of the left dorsolateral prefrontal cortex (DLPFC).
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Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS): An update (2014–2018)

TL;DR: These updated recommendations take into account all rTMS publications, including data prior to 2014, as well as currently reviewed literature until the end of 2018, and are based on the differences reached in therapeutic efficacy of real vs. sham rT MS protocols.
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Sensory dysfunction in burning mouth syndrome.

TL;DR: Qualitative sensory tests (QST) in addition to the blink reflex (BR) recordings are used in order to gain further insight into the neural mechanisms of BMS pain.
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Effects of Surgical Levels of Propofol and Sevoflurane Anesthesia on Cerebral Blood Flow in Healthy Subjects Studied with Positron Emission Tomography

TL;DR: Both anesthetic agents caused a global reduction of rCBF (propofol > sevoflurane) at the 1 MAC/EC50 level, and despite the marked global changes, SPM analysis enabled detailed localization of regions with the greatest relative decreases.
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Electroencephalogram spindle activity during dexmedetomidine sedation and physiological sleep

TL;DR: The objective of the present work was to study human electroencephalogram (EEG) sleep spindles during dexmedetomidine sedation and compare them with spindled during normal physiological sleep, to test the hypothesis that dexmedETomidine exerts its effects via normal sleep‐promoting pathways.