A multifaceted retrospective analysis of the association between Zolpidem administration and increased brain perfusion and function in neurologically compromised patients

Abstract

This project represents one of the foundation steps to a collaboration between the Department of Human Physiology, University of Pretoria and the Nuclear Medicine Department at Steve Biko Academic hospital. Following the initial discovery of the surprising effect zolpidem has on patients in persistent vegetative states in 1999 by Dr H.W. Nel - namely that zolpidem administration results in a significant qualitative increase in brain function, to the extent that patients were able to once again communicate and respond appropriately to their surroundings - much data has been collected by both Dr Nel as well as the Nuclear Medicine Department of Steve Biko Hospital. Over the course of twelve years SPECT scans have been carried out on patients of various pathologies both before and after a course of zolpidem. To this day, both assessment and follow up of these and new patients is still being done by the Nuclear Medicine Department and Dr Nel. As this vast collection of data grows it has become increasingly daunting for a single research team to consolidate all this information into a usable form and an outside team has been deemed necessary to facilitate this process. The primary goal of this study was to quantify the neurological perfusion changes following zolpidem administration within responder patients. This was achieved through reprocessing and semi-quantification of the existing SPECT scan records held by the Pretoria Academic Hospital. Within the group of responder patients (n = 29), 22 patients (~76%) presented a significant increase in perfusion within at least one lesion with a range of 4.5 - 46.1% (mean = 11.9%). In opposition to this finding non-responsive lesion perfusion decreased with a significant mean change of -14.5%. For both sets the p-value was determined to be <0.01. Of all lesions measured (n = 85) 32% displayed increased perfusion after zolpidem administration, whereas 30.6% presented with a perfusion decrease. It was determined that only one lesion is required to respond to zolpidem in a positive manner to facilitate positive functional improvements with a given patient. In a small minority of patients post-zolpidem functional improvements seems to be connected to wide-spread cortical changes as opposed to singular lesional improvements. This study provides further evidence of zolpidem’s paradoxical action in a subset of brain damaged individuals. Unique quantification of results allows for additional insight and provides further understanding the physiological changes associated with zolpidem administration.