This study assessed the cognitive impact of ECT using: a paired words and short story test, a spatial and pattern recognition memory subtest, a pattern-location associated learning subtest, a delayed matching to sample subtest, a modified version of Kopelman’s Autobiographical Memory Interview (AMI), and a subjective memory test was also included. Tests were conducted on ECT patients, before treatment (baseline), after four treatments, after the final ECT and one month following the final ECT treatment, to measure short and long-term memory loss. Baseline data was collected from 26 patients, thereafter patient numbers varied (details are reported in the results section). This study found that paired word and a short story tasks were insensitive at detecting cognitive deficits during or after ECT; however a delay of one hour increased the sensitivity of these tests. The visual memory battery detected deficits in visual and visuospatial memory during and immediately following a course of ECT but only spatial recognition memory deficits remained one month post-ECT. The modified AMI appeared to be a sensitive measure of retrograde memory loss. Deficits were observed in both semantic and episodic memory. Memory for recent events displayed the greatest losses. Subjective memory complaints were significantly reduced during, after, and at one month following ECT; however these were highly correlated with depression scores. In conclusion, the battery of neuropsychological memory tests adopted for this study appear to be sensitive to the adverse effect of ECT on aspects of anterograde and retrograde memory loss generally. However, the sensitivity of the subjective test is questionable as outcome on this test appears to be influenced by mood.

Thesis (M.Sc. (Clinical Psychology)) --University of the North, 1981 / Refer to the document

Treatments such as electroconvulsive shock (ECS) impair later performance of learned responses if presented shortly after learning, but not if delayed for a sufficient time. These gradients are frequently termed retrograde amnesia and interpreted as reflecting a memory consolidation process. The present investigation was concerned with the relationship of the length of the gradient produced by a single ECS to the duration of the memory consolidation process. In the first experiment, rats were trained on a one-trial passive avoidance task and then presented with one of three ECS treatments. The treatments were five ECSs of 0.5 seconds duration spaced either 1 minute apart, 5 seconds apart, or in one continuous 2.5 second duration burst. The five ECSs spaced 1 minute apart were found to impair performance when presented immediately, 1 hour, 24 hours, and 48 hours but not 9 days after passive avoidance training. Five ECSs spaced 5 seconds apart impaired performance when presented immediately or 1 hour but not 24 hours after training. In contrast, the single 2.5 second duration ECS impaired performance when presented immediately but not 1 hour or longer after training. The impairments produced by the five ECSs spaced 1 minute apart at 1 hour and 24 hours were found to be permanent over 11 days. The second experiment examined whether the long gradient produced by five ECSs spaced 1 minute apart was qualitatively different from single ECS gradients. Five ECSs spaced 1 minute apart were presented following passive avoidance training to rats anesthetized with ether or sodium pentobarbital. In both cases, the series of ECSs still impaired performance when presented 1 or 24 hours but not 9 days following passive avoidance training. This finding does not provide support for a distinction between the gradients produced by a single ECS and a series of ECSs. These results were therefore interpreted as showing that the length of the gradient produced by a single ECS in a passive avoidance task is not a good estimate of the duration of time required for memory consolidation. In this passive avoidance task, consolidation appears to continue for a period of at least several days, while the gradient produced by a single ECS was less than 1 hour. In the third experiment, rats were trained on a one - trial appetitive taste and then presented with either five ECSs spaced 1 minute apart, or a single ECS of 0.5 seconds or 2.5 seconds duration. In contrast to the results in the passive avoidance task, the five ECSs paced 1 minute apart did not produce a longer gradient than a single ECS of either 0.5 or 2.5 seconds duration. All three treatments impaired performance when presented 15 seconds but not 1 hour after training. Several possible explanations for the different effects of the series of ECSs in the two tasks are considered, and it is concluded that this difference probably reflects differences between the memory consolidation processes in the two tasks. / Arts, Faculty of / Psychology, Department of / Graduate

Recent experimental evidence indicates that the effectiveness of posttraining electroconvulsive shock in disturbing retention is not constant but highly variable. One factor which appears to contribute to this variation is the strength of the electroshock current. Currents of higher intensity or of longer duration have generally been found to be more effective in disturbing retention. Indirectly, this evidence suggests that an electroshock treatment does not invariably stop memory consolidation. It appears that following a weak electroshock treatment, the interference with consolidation is not complete and that consolidation may continue afterwards. This possibility was directly examined in the present experiment with a one-trial passive avoidance task. The results showed that rats given one electroconvulsive shock 5 min after the passive avoidance training suffered only a slight loss of retention. However, when a second electroconvulsive shock was given at 1 hr after training, there was a significantly greater retention loss than that following one electroconvulsive shock at 5 min or at 1 hr. Additional results indicate that the disruptiveness of the second electroconvulsive shock is time-dependent and that the retention deficit does not appear to be due to punishing or disinhibitory effects of the electroconvulsive shocks. These findings are interpreted as indicating that memory consolidation can continue after electroconvulsive shock. / Arts, Faculty of / Psychology, Department of / Graduate

When periodic electroconvulsive shocks (ECSs) were administered, a progressive intensification of the motor seizure (MS) pattern occurred. This effect was observed when ECSs at either 15 or 75 mA were administered at 3-day, but not 1-hr intervals. The magnitude of the increase in severity of the MS pattern was a function of the number of ECSs which approached asymptote, in these experiments, at approximately ten ECSs. Periodic ECSs were also found to potentiate the alcohol withdrawal syndrome. In general, those conditions which were found to facilitate the kindling of MSs were the same as those which produced the potentiation of the alcohol withdrawal syndrome. Furthermore, this potentiation was found to persist up to 3 weeks after the last ECS under the conditions used in these experiments. Finally, the potentiation of the alcohol withdrawal syndrome occurred even after the MSs had been pharmacologically blocked. The results of these experiments were discussed in light of their implications to both basic and clinical research. / Arts, Faculty of / Psychology, Department of / Graduate

No description available.

Electroconvulsive shock (ECS) produces a loss of memory for the immediately preceding period, but also produces non-amnesic effects which seriously complicate the interpretation of behavioral results following convulsions. The results of the present investigation indicated that the retrograde amnesia produced by ECS is probably slight, but appears enhanced in passive-avoidance tasks and diminished in aversively-motivated tasks requiring movement, because of a concomitant impairment of movement-inhibiting mechanisms. If this interpretation is valid, it is extremely difficult to make quantitative estimates of the degree or temporal extent of the retrograde amnesia induced by ECS in animals. It may be possible, however, to separate memory mechanisms from movement-inhibiting mechanisms with procedures involving more localized effects upon the brain. / Thesis / Doctor of Philosophy (PhD)

Electroconvulsive therapy (ECT) is used worldwide to treat severe mental disorders. The most common mental disorder, and the third leading cause of disease burden in the world is depression. The clinical efficacy of ECT for severe depression is well-established. However, both the pathophysiology of depression and the mechanism of action of ECT remain elusive. The main aims of this thesis are to address the following issues: 1) the use and practice of ECT in Sweden has not been systematically evaluated since 1975, 2) cognitive side-effects (memory disturbances) are a major concern with ECT and 3) the mechanism of action of ECT remain elusive. The neurobiological aspects of ECT focus on two hypotheses. First, the recent years´ preclinical studies that have provided evidence that ECT induces hippocampal cell proliferation, including neurogenesis. Second, that enhanced functional inhibition of neuronal activity is a key feature. Current use and practice of ECT in Sweden (paper I) is based on data from the national quality register for ECT, the mandatory patient register of the National Board of Health and Welfare and a survey. Treated person rate (TPR) in Sweden 2013 was found to be 41 individuals / 100 000, and thus unchanged since the latest systematic investigation in Sweden 1975. In more than 70% of treatment series the indication was a depressive episode. The selection of patients for ECT and treatment technique in Sweden was similar to that in other western countries, but the consent procedure and the involvement of nurses and nursing assistants in the delivery of ECT differ. Data also shows that there is room for improvement in both the specificity of use and availability of ECT. The second study in this thesis is a longitudinal observational trial where 12 (paper II and III) and 14 (paper IV) patients with depression referred for ECT were investigated. Patients underwent a 3 T MRI structural scanning and DSC-MRI perfusion, a neuropsychological test battery and clinical ratings before ECT, within one to two weeks after ECT and after 6 and 12 months.  In line with preclinical findings and the plasticity hypothesis of mechanism of action of ECT, the hippocampal volume increased after ECT in patients with depression. However, this increase was transient and returned to baseline levels within 6 months. No correlation was found between volumetric changes and clinical effect or cognitive outcome. Instead our results suggested an association to the number of treatments, without relation to the side of stimulation. A right-sided decrease in frontal blood flow distinguished remission from non-remission after ECT. There were significant impairments in verbal episodic memory and verbal fluency within one week after ending the ECT course, but these impairments were transient and no persistent cognitive impairments were seen during the follow-up. In summary, this thesis present the first update on the use and practice of ECT in Sweden in the last 40 years as well as a pioneering MRI-study on the hippocampal volume increase in the treatment of depression with ECT. Supportive to earlier findings we also found the cognitive side-effects that are measurable after ECT to be transient. Furthermore, we found that a decreased frontal blood flow is of importance for the anti-depressive response to ECT.

Conventional treatments for depression, such as pharmacological interventions, are often ineffective. Up to half of patients do not respond, resulting in a poor prognosis for depression. Therefore, treatment options can be invaluable for increasing rates of remission. It is generally assumed that aerobic exercise benefits affective state. However, exercise remains a controversial treatment, possibly due to inconsistent evidence and unknown mechanisms. It is hypothesised variable results (literature is conflicting) are due to/because of heterogeneity in exercise interventions and subjective reports of exercise and mood state. If a biomarker for depression can be identified, the effects of exercise on depression could be objectively assessed. Neuroimaging research has elucidated numerous biomarkers, but has had little benefit on the diagnosis, prognosis or treatment of depression. However, if research can identify which biomarkers respond to treatments, can stratify patients and which can predict response outcome, targets for new interventions can be developed. Therefore, this thesis first establishes the effect of ECT treatment on emotionally salient brain regions in MDD, establishing the basis of a treatment responsive biomarker and potential targets for other interventions. The same functional connectivity methods are then used to analyse the effects of a single bout of aerobic exercise in a healthy population. Similar reductions in functional connectivity were observed in brain structures relevant to depression, suggesting exercise might target relevant brain structures. Finally, using the same functional connectivity methods, a long-term aerobic exercise intervention is shown to reduce functional hyperconnectivity in mildly depressed participants compared to healthy controls. This supports two primary hypotheses: that hyperconnectivity may underlie depressive disorders, constituting a biomarker for depression; and that aerobic exercise is an effective treatment for milder forms of depression.

No description available.