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Head phantoms for electroencephalography and transcranial electric stimulation: a skull material study

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 Added by Alexander Hunold
 Publication date 2018
  fields Physics
and research's language is English




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Physical head phantoms allow assessing source reconstruction procedures in electroencephalography and electrical stimulation profiles during transcranial electric stimulation. Volume conduction in the head is strongly influenced by the skull representing the main conductivity barrier. Realistic modeling of its characteristics is thus important for phantom development. In the present study, we proposed plastic clay as a material for modeling the skull in phantoms. We analyzed five clay types varying in granularity and fractions of fireclay, each with firing temperatures from 550 {deg}C to 950 {deg}C. We investigated the conductivity of standardized clay samples when immersed in a 0.9% sodium chloride solution with time-resolved four-point impedance measurements. To test the reusability of the clay model, these measurements were repeated after cleaning the samples by rinsing in deionized water for 5 h. We found time-dependent impedance changes for approximately 5 min after immersion in the solution. Thereafter, the conductivities stabilized between 0.0716 S/m and 0.0224 S/m depending on clay type and firing temperatures. The reproducibility of the measurement results proved the effectiveness of the rinsing procedure. Clay provides formability, is permeable for ions, can be adjusted in conductivity value and is thus suitable for the skull modeling in phantoms.



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Whether transcranial direct current stimulation (tDCS) benefits stroke rehabilitation remains unclear. To investigate how tDCS reorganizes brain circuitry, nineteen post-stroke patients underwent rehabilitation sessions with bi-hemispheric real vs sham tDCS intervention. Resting motor threshold measurements showed tDCS evoked higher excitability in the motor cortex that enhanced the descending conduction from the lesioned primary motor cortex to the target hand muscle. Granger causality analysis further revealed brain circuitry rewiring among the lesioned cerebellum, premotor, and primary motor cortex in the tDCS group compared to the sham owing to the newly formed connections close to the anodal electrode. Rebuilding of these critical pathways was clear via the increase of event related desynchronisation (ERD) and white matter integrity in the same lesioned region. Furthermore, only the tDCS group demonstrated a positive recovery trend in the penumbra regions by the longitudinal functional magnetic resonance imaging (fMRI) analysis. To interpret tDCS mechanism, we introduce a polarized gamma-aminobutyric acid (GABA) theory, where GABAA receptor activity depends on the orientation of dipolar GABA that can be manipulated by tDCS field. Results suggest that tDCS intervention lowers motor excitability via re-orienting GABA, leading to reorganization of the lesioned cortical network, and the motor descending pathway, finally the recovery of motor function.
Purpose: To develop bone material analogues that can be used in construction of phantoms for simultaneous PET/MRI systems. Methods: Plaster was used as the basis for the bone material analogues tested in this study. It was mixed with varying concentrations of an iodinated CT contrast, a gadolinium-based MR contrast agent, and copper sulfate to modulate the attenuation properties and MRI properties (T1 and T2*). Attenuation was measured with CT and 68Ge transmission scans, and MRI properties were measured with quantitative ultrashort echo time pulse sequences. A proof-of-concept skull was created by plaster casting. Results: Undoped plaster has a 511 keV attenuation coefficient (~0.14 cm-1) similar to cortical bone (0.10-0.15 cm-1), but slightly longer T1 (~500 ms) and T2* (~1.2 ms) MR parameters compared to bone (T1 ~ 300 ms, T2* ~ 0.4 ms). Doping with the iodinated agent resulted in increased attenuation with minimal perturbation to the MR parameters. Doping with a gadolinium chelate greatly reduced T1 and T2*, resulting in extremely short T1 values when the target T2* values were reached, while the attenuation coefficient was unchanged. Doping with copper sulfate was more selective for T2* shortening and achieved comparable T1 and T2* values to bone (after 1 week of drying), while the attenuation coefficient was unchanged. Conclusions: Plaster doped with copper sulfate is a promising bone material analogue for a PET/MRI phantom, mimicking the MR properties (T1 and T2*) and 511 keV attenuation coefficient of human cortical bone.
Transcranial static magnetic stimulation is a novel noninvasive method of reduction of the cortical excitability in certain neurological diseases that, unlike ordinary transcranial magnetic stimulation, makes use of static magnetic fields generated by permanent magnets. The physical principle underlying transcranial magnetic stimulation is well known, that is, the Faradays law. By contrast, the physical mechanism that explains the interaction between neurons and static magnetic fields in transcranial static magnetic stimulation remains unclear, which makes it difficult to improve and fine tune the treatment. In the present work it is discussed the possibility that this mechanism might be the Lorentz force exerted on the ions flowing along the membrane channels of neurons. To support this hypothesis, a dimensional analysis it is carried out to compare the Larmor radius of the ions in the presence of a static magnetic field with the dimensions of the cross section of human axons and membrane channels in neurons. This analysis shows that whereas a moderate static magnetic field is not expected to affect the ion flux through axons, nevertheless it can affect the ion flux along membrane channels. The overall effect of the static magnetic field would be to introduce an additional friction between the ions and the walls of the membrane channels, thus reducing its conductance. Calculations performed by using a Hodgkin-Huxley model demonstrate that even a slight reduction of the conductance of the membrane channels can lead to the suppression of the action potential, thus inhibiting neuronal activity.
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