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