Electroencephalographic Studies Following Electric Shock Therapy

Weil, André

doi:10.1001/archneurpsyc.1947.02300290079005

Cited by 41 publications

(2 citation statements)

References 13 publications

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“…Some studies used alternative procedures to obtain the EEG, such as hyperventilation, with questionable relevance (22, 23). In a 1980 review, Weiner considered the duration of EEG slowing based on analysis of 21 studies and summarized (p. 224), “This slowing typically disappears by a few weeks to a few months following completion of the ECT course but in rare cases may persist for longer periods.” Weiner (24) noted that in 11 of the 21 studies, EEG slowing was observed for “a few” or “most” patients at “several weeks,” with only two studies not finding this.…”

Section: Frontotemporal Effectsmentioning

confidence: 99%

Electroconvulsive Treatment: Hypotheses about Mechanisms of Action

Fosse¹,

Read²

2013

Front. Psychiatry

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No consensus has been reached on the mode of action of electroconvulsive treatment (ECT). We suggest that two features may aid in the delineation of the involved mechanisms. First, when effective, ECT would be likely to affect brain functions that are typically altered in its primary recipient group, people with severe depression. Central among these are the frontal and temporal lobes, the hypothalamus-pituitary-adrenal (HPA) stress axis, and the mesocorticolimbic dopamine system. Second, the involved mechanisms should be affected for a time period that matches the average endurance of clinical effects, which is indicated to be several days to a few weeks. To identify effects upon frontal and temporal lobe functioning we reviewed human studies using EEG, PET, SPECT, and fMRI. Effects upon the HPA axis and the dopamine system were assessed by reviewing both human and animal studies. The EEG studies indicate that ECT decelerates neural activity in the frontal and temporal lobes (increased delta and theta wave activity) for weeks to months. Comparable findings are reported from PET and SPECT studies, with reduced cerebral blood flow (functional deactivation) for weeks to months after treatment. The EEG deceleration and functional deactivation following ECT are statistically associated with reduced depression scores. FMRI studies indicate that ECT flattens the pattern of activation and deactivation that is associated with cognitive task performance and alters cortical functional connectivity in the ultra slow frequency range. A common finding from human and animal studies is that ECT acutely activates both the HPA axis and the dopamine system. In considering this evidence, we hypothesize that ECT affects the brain in a similar manner as severe stress or brain trauma which activates the HPA axis and the dopamine system and may compromise frontotemporal functions.

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Section: Frontotemporal Effectsmentioning

confidence: 99%

Electroconvulsive Treatment: Hypotheses about Mechanisms of Action

Fosse¹,

Read²

2013

Front. Psychiatry

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“…This slowing builds up over the course of treatments and then diminishes with time. The persistence of this phenomenon was considered by Weiner (1980b), who reviewed 21 studies in which some comparison between baseline EEG measures and a follow-up period of at least 10 days could be made (Bagchi, Howell & Schamale 1945;Bergman, Gabriel, Impastato & Wortis 1952;Blaurock, Lorimer, Segal & Gibbs 1950;Callaway & Boucher 1950;Chusid & Pacella 1952;Fink, Kahn, Karp, Pollack, Green, Alan & Lefkowits 1961;Fukuda & Matsuda 1969;Honcke & Zahle 1946;Klotz 1955;Levy, Serota & Grinker 1942;Marjerrison, James & Reichert 1975;Moriarity & Siemens 1947;Mosovich & Katzenelbogen 1948;Murillo & Exner 1973;Pacella, Barrera & Kalinowsky 1942;Proctor & Goodwin 1943;Roth 1951;Sutherland, Oliver & Knight 1969;Taylor & Pacella 1948;Weil & Brinegar 1947). The results of this review indicate that while residual slowing at 10 days following a course of ECT is quite common, most EEGs return to normal by a month, and that by 3 months the presence of such slowing is uncommon.…”

Section: What Is the Physiologic Morbidity With Ect?mentioning

confidence: 99%

Does electroconvulsive therapy cause brain damage?

Weiner

1984

Behav Brain Sci

113

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Although the use of ECT has declined dramatically from its inception, this decrease has recently shown signs of leveling out because of ECT's powerful therapeutic effect in severely ill depressed individuals who either do not respond to pharmacologic alternatives or are too ill to tolerate a relatively lengthy drug trial. Notwithstanding its therapeutic benefits, ECT has also remained a controversial treatment modality, particularly in the eye of the public. Given the unsavory qualities associated with the word “electroconvulsive,” claims of possible, probable, or even certain brain damage with ECT have easily found listeners. A careful, nonselective assessment of data covering the areas of pathology, radiology, electrophysiology, biochemistry, and neuropsychology leads both to certain conclusions and to certain unanswered questions. ECT is not the devastating purveyor of wholesale brain damage that some of its detractors claim. For the typical individual receiving ECT, no detectable correlates of irreversible brain damage appear to occur. Still, there remains the possibility that either subtle, objectively undetectable persistent deficits, particularly in the area of autobiographic memory function, occur, or that a rarely occurring syndrome of more pervasive persistent deficits related to ECT use may be present. Clearly, more research directed toward answering these questions needs to be carried out so that the role of ECT can be more rigorously defined. While such research is pending, however, we cannot expect that the conditions that predispose to clinical referrals for ECT will disappear. Given the misery, anguish, and risk of death by suicide, starvation, or debilitation associated with severe depressive illness, for example, it still appears that ECT, at least for the present, must continue to be available.

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Elektrokrampf und EEG

Schuchardt¹,

Will²

1950

Deutsche Zeitschrift f. Nervenheilkunde

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Electroencephalographic Studies Following Electric Shock Therapy

Cited by 41 publications

References 13 publications

Electroconvulsive Treatment: Hypotheses about Mechanisms of Action

Electroconvulsive Treatment: Hypotheses about Mechanisms of Action

Does electroconvulsive therapy cause brain damage?

Elektrokrampf und EEG

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