| Abstrakt: |
Efforts to disclose the mechanisms of transcranial therapeutic electro-magnetic fields (EMF) acting on the brain's cells (Marino, Kibleur) and recently immune cells (Gülöksüz) meet unsolved physiological details of blood vessels, exclusively arterial vasomotion or the non-glial-related former g(lia)-lymphatic flow (Iliff; Liu DX) - now replaced by an astrocytic AQP4-pipeline cooling the brain (Nakada 2014). Here within the convergent dyn4TAM-framework, which had suggested the first mast cell behavioral experiment (Fitzpatrick & Morrow 2017), three intertwined physiological concepts are contributed: A) "autocrinicity" - how flushed, thus absent, autocrine signals integrate external fluidics into cellular computations e.g. on motility: EMFs could increase such absences by targeting e.g. dipole-cytokines; B) a new concept of the arterial wall based on a tangible interpretation of the coronal histology of all arteries as a co-axial pulse-dampening engine (Treviranus 2012). In the brain this engine might provide the quickest cerebral outflow via the Cerebral IntraMUral Reverse Arterial Flow (Treviranus 2018b), while transmitting further forces acting upstream to the paravascular spaces; C) some key roles for mast cells in neuro-psychiatry (Silver & Curley 2013) and their interactive lymphatic and non-luminal vascular routes to the brain dictated by peripheral imprinting as to destiny (Csaba 1987) and destination (Treviranus 2013). Within the skull they might advance against para-arterial upstream currents. Some known causal mediators of the effects of transcranially applied EFMs and puzzling results are then put tentatively in perspective with the above "tangible" models, e.g. by aligning probable induced currents with arterial segments or the new direct meningeal-calvario-myeloid channels. RESULTS: The case for a role of mast cells and diverse flows in transcranial electromagnetic brain therapy seems promising. |
