Anxiety disorder is prevalent and costly. But its diagnosis is underdeveloped and treatment ad hoc. This could be corrected if the neural mechanisms of anxiety were known. All anxiolytic medications produce a decrease in rodent hippocampal theta rhythm - so hippocampal theta could underlie some types of anxiety. But, a review (Chapter 2) showed that ethanol and other anxiolytics increase FM-theta in the human scalp EEG and have other properties unlike hippocampal theta. The experiments in this thesis, therefore, tested for other potential homologues (Chapter 3) of hippocampal theta in the human EEG.
The phase of hippocampal theta activity is reset in a working memory task and not an equivalent reference memory task in rats. Furthermore, low doses ethanol increases and high dose ethanol (and other anxiolytics) decrease theta activity. So, EEG was recorded from 15 scalp sites while participants performed non-verbal working memory and reference memory tasks before and after ethanol administration and assessed for the presence of phase-reset and ethanol-related changes in 5-7Hz and 8-11Hz spectral power (chapter 4 and 5).
There was little general evidence for stimulus-induced phase-resetting of the ongoing EEG activity (Chapter 6). Increased post-stimulus synchronization in the theta frequency range was accompanied by increases in post-stimulus spectral power - suggesting that the synchronised activity was evoked rather than reset.
Across 3 experiments (Chapter 7), low dose ethanol (54.5-146.6[mu]g/l) increased 5-7Hz theta, while the highest dose (307[mu]g/l) reduced task-related-increases in 5-7Hz activity. These effects were noted across electrode locations including frontal-midline sites and particularly at the beginning of the delay period. The suppression of 5-7Hz activity also coincided with an impairment in working memory performance. The dose-response curve for 5-7Hz theta was as predicted from rat hippocampal work. This particular component, linked to high working memory load or task difficulty, is a potential of homologue hippocampal theta. A clear decrease in theta with high dose ethanol, of this type, has not been reported previously.
Activity in the 8-11Hz range typically increased with all doses of ethanol. It is clearly not a homologue of hippocampal theta. This is consistent with previous reports of increased alpha with high doses of ethanol - although these have been accompanied by increased, not decreased, theta.
There is a potential homologue of hippocampal theta that can be detected in the human EEG (chapter 8); but the observed changes in 5-7Hz activity cannot be localised and may not be related to the hippocampus. It is clear there is more than one type of theta within the human EEG - with opposing sensitivities to ethanol. Critically, these types were detected at a single site and apparently in phase with one another. The current data, together with the previous literature, suggest that theta can be generated concurrently in distinct networks that, under specific task demands, can become coherent and so produce synchonised activity. Future studies need to test higher doses of ethanol and other anxiolytics and use different experimental paradigms to further differentiate the theta systems in the human EEG. Human EEG could be useful for differentiating sub-types of anxiety, and the choice and effectiveness of interventions delivered.
| Identifer | oai:union.ndltd.org:ADTP/222198 |
| Date | January 2009 |
| Creators | Mitchell, Damon John, n/a |
| Publisher | University of Otago. Department of Psychology |
| Source Sets | Australiasian Digital Theses Program |
| Language | English |
| Detected Language | English |
| Rights | http://policy01.otago.ac.nz/policies/FMPro?-db=policies.fm&-format=viewpolicy.html&-lay=viewpolicy&-sortfield=Title&Type=Academic&-recid=33025&-find), Copyright Damon John Mitchell |
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