The American Psychiatric Association (APA) has updated its Privacy Policy and Terms of Use, including with new information specifically addressed to individuals in the European Economic Area. As described in the Privacy Policy and Terms of Use, this website utilizes cookies, including for the purpose of offering an optimal online experience and services tailored to your preferences.

Please read the entire Privacy Policy and Terms of Use. By closing this message, browsing this website, continuing the navigation, or otherwise continuing to use the APA's websites, you confirm that you understand and accept the terms of the Privacy Policy and Terms of Use, including the utilization of cookies.

×
ArticleNo Access

ELECTRIC SHOCK TREATMENT SUCCEEDED BY COMPLETE FLACCID PARALYSIS, HALLUCINATIONS, AND SUDDEN DEATH

Case Report with Anatomical Findings in the Central Nervous System
Published Online:https://doi.org/10.1176/ajp.106.3.206

1. The case of a 44-year-old woman is reported who developed a flaccid paralysis of all four extremities with areflexia after her second electroshock treatment. After her fourth treatment auditory hallucinations were noted and soon thereafter she died.

2. Adopting the principles of jacksonian neurology the postparoxysmic, flaccid paralysis is explained by the "exhaustion" of the nerve cells of the highest centers after their excessive, sudden, and rapid discharge. This sudden cessation (functional destruction) of nervous function produces in its turn the remote, widespread, and usually transient effects of diaschisis. The hallucinations are interpreted as the result of the overactivity or release of the healthy parts of the highest centers.

3. On histologic examination the central nervous system showed fatty products in the nerve cells, disseminated through all levels, cellular changes and glial reactions in the frontal areas, seen in serial sections, scattered areas of disruption and "explosive" destruction, assuming stellate and circular shapes, but also mere rents and slits, associated with displacement of the ganglion cells. The assumption is made that the changes described are not specific in themselves but gain their importance in relation to the clinical history of shock, paralysis, and sudden death in a relatively young individual show ing no detectable pathology responsible for the changes observed.

Access content

To read the fulltext, please use one of the options below to sign in or purchase access.