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<p> The purpose of this thesis was to design, build and test a prototype artifact suppressing electroencephalogram data acquisition system (AS-EEG-DAQ-S) to collect electroencephalogram (EEG) evoked potential (EP) data during repetitive transcranial magnetic stimulation (rTMS) without the EEG signal being masked by transcranial magnetic stimulation (TMS) artifact. A functional AS-EEG-DAQ-S capable of blocking TMS artifact would provide for the first time a quantitative measurement system to assist in optimal TMS coil positioning during the rTMS treatment of depression, an alternative to electroconvulsive therapy (ECT). This thesis provides the details for an AS-EEGDAQ-S. Preliminary TMS EP results on a human subject were collected. Results showed transcallosal conduction times of 12ms to 31ms, which are consistent with those predicted and collected by other researchers in the TMS field. </p> <p> The first portion of this work provides electrode heating data for modem rTMS Paradigms for the recording ofEEG during rTMS. The concern is that during rTMS EEG electrodes can heat to an unsafe temperature. Seven electrode types were tested: silver/silver chloride, silver cup, gold cup, notched gold cup, notched silver cup, notched gold-plated silver cup, and carbon. All electrodes tested are commercially available, including the carbon electrodes designed for MRI use. The three notched electrodes tested were standard electrodes notched using metal clippers to reduce induced currents. Induced currents are responsible for electrode heating during rTMS and can cause burns to the skin. The results ,of this study show that electrode heating is a concern when collecting BEG during rTMS. However, a number of standard electrodes or slightly modified standard electrodes are suitable for recording BEG during rTMS if certain stimulating parameters are adhered to. </p> <p> The second portion of this work provides the detailed development and design of the AS-EEG-DAQ-S. Four different approaches were tested and their ability to withstand a TMS pulse compared. </p> <p> Short circuiting the input pins of a commercially available EEG amplifier was the first approach tried and yielded only marginal results due to the switches used being designed for digital logic, transistor built, and creating an undesirable offset between input pins. </p> <p> The second approach tested involved continuing to work with a commercially available EEG amplifier and implementing a sample-and-hold circuit between the patient and the EEG machine inputs. This approach had the drawback of requiring that the BEG signal be attenuated back to EEG signal levels, which are near noise amplitude levels. </p> <p> The third approach involved using a high bandwidth amplification circuit to recover quicker from the baseline voltage offset created by the TMS artifact. However, increasing the bandwidth also allows the artifact to saturate the input amplifiers, which then require on the order of 500ms to recover fully. </p> <p> The fourth approach involved combining the second and third approaches to create a high bandwidth amplifier that incorporates a sample-and-hold circuit to prevent amplifier saturation when gain is increased. The fourth approach provide the high bandwidth and artifact blocking behavior desired. </p> / Thesis / Master of Applied Science (MASc)

Thesis (PhD) - Swinburne University of Technology, 2006. / Submitted for the degree of Doctor of Philosophy, Swinburne University of Technology - 2006. Typescript. Bibliography: p. 191-223.

Thesis (M.S.)--University of Michigan, 1985.

Thesis (M.S.)--University of Michigan, 1985.

Thesis (Doctoral)--Ludwig-Maximilians-Universität. / eContent provider-neutral record in process. Description based on print version record.

The mechanisms underlying the generation and spread of seizure activity have remained elusive despite a considerable research effort over the last two decades. Most of this work has concentrated on the characteristics of neuronal excitability and burst discharge at the single cell level. These studies have provided some understanding of the possible abnormalities of neurons within an epileptic focus, but little direct insight into the factors responsible for the striking synchronization of action potentials during interictal discharge or in the spread of synchronous activity across apparently normal brain tissue. Although synaptic activation probably plays a role in the generation of seizure activity, recent evidence indicates that seizure-like discharge can occur during chemical blockade of synaptic transmission (Jefferys and Haas 1982; Taylor and Dudek 1982). This rather surprising result emphasizes the importance of considering non-synaptic mechanisms for both the synchronization and spread of abnormal neuronal activity in the central nervous system. One important non-synaptic mechanism to consider is ephaptic interactions. This term refers to the direct electrical influence of extracellular field potentials on neuronal excitability. It is possible that ephaptic interactions, generated during seizure activity, simultaneously depolarize an entire population of neurons leading to both recruitment and synchronization of action potential discharge. This thesis investigates ephaptic interactions during evoked potentials in the hippocampal formation. The hippocampus is one of the most seizure-prone regions of the brain and its anatomical structure is ideal for the generation of field effects. Evoked potentials were used as "models" of synchronous neuronal discharge since they are more reproducible, easier to control, and better understood than seizure activity. This initial investigation of ephaptic interactions lays the foundation for further studies involving the complexities of epileptic activity. The first phase of this project examined the spatial characteristics of field potentials evoked in the hippocampus and the dentate gyrus. Current source density (CSD) analysis and voltage gradient determinations obtained from these fields were used to characterize the pattern of current flow within the neuropil and to predict the polarity and relative intensity of ephaptic influences on neuronal excitability. The detailed characteristics of extracellular voltage gradients varied between CAl and the dentate gyrus, and also between anti- and orthodromic responses. In general, voltage gradients during the positive components of a somatic population spike predicted ephaptic hyperpolarization of the neuronal population, whereas gradients observed during the negative component predicted depolarization. They were often an order of magnitude greater than the smallest gradient known to influence granule cell activity. An exception to this rule was the minimal gradient observed during the negative component of the dentate response. In the second phase of the study, extracellular voltage gradients were experimentally applied to the dentate gyrus to determine the sensitivity of granule cells to ephaptic interactions. The magnitude of the applied gradients were in the range observed during the evoked potentials studied in the first phase. These experiments demonstrated a remarkable sensitivity of granule cells to the applied fields. The fields could alter the population spike from near minimal to near maximal. Surprisingly, even antidromic potentials were influenced by the gradients. On the other hand, the EPSP phase of the population spike was not influenced. These findings established that extracellular currents can influence the excitability within a neuronal population without altering synaptic drive. The final phase of the project investigated the transmembrane potential (TMP) of pyramidal and granule cells during applied fields and evoked potentials. The TMP was calculated by subtracting the extracellular from the intracellular response. This potential ultimately determines the voltage dependent behavior of a neuron and gives a direct measure of any ephaptic interactions. In order to measure the intracellular influences of applied fields, the TMP was monitored while the impaled cell was exposed to extracellular voltage gradients spanning the same range as used in phase two of the project. The TMP shifted by as much as plus or minus 5 mV, depending on the amplitude and polarity of the gradient. This large shift in TMP accounts for the observed influence of the applied field potentials, and suggests that the voltage gradients associated with evoked potentials should also have a marked effect on the TMP. A depolarizing wave of the TMP occurred during the negative component of anti- and orthodromic CA1 responses. This depolarization was capable of initiating action potentials, and decreased the latency to discharge during orthodromic responses. During epileptiform discharge, a similar depolarizing wave was associated with each negative component of the burst. These depolarizations recruit and synchronize neuronal discharge by simultaneously increasing the excitability within an entire population of cells. These data support the hypothesis that ephaptic interactions in the hippocampal formation influence the pattern of cell discharge during evoked potentials. It is postulated that similar ephaptic interactions may contribute to recruitment and synchronization during seizure activity. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第18180号 / 医博第3900号 / 新制||医||1004(附属図書館) / 31038 / 京都大学大学院医学研究科医学専攻 / (主査)教授 髙橋 良輔, 教授 金子 武嗣, 教授 渡邉 大 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM