ABSTRACT
The study investigates the effect of zolpidem (CAS 82626-48-0) on brain injuries and cerebellar diaschisis. Four patients with varied brain injuries, three of them with cerebellar diaschisis, were imaged by 99mTc HMPAO Brain SPECT before and after application of zolpidem. The baseline SPECT before zolpidem showed poor tracer uptake in brain injury areas and cerebellar diaschisis. After zolpidem, cerebral perfusion through brain injury areas improved substantially in three patients and the cerebellar diaschisis was reversed. Observations point to a GABA based phenomenon that occurs in brain injury and diaschisis that is reversible by zolpidem.
Subject(s)
Brain Injuries/drug therapy , Cerebellar Diseases/drug therapy , Hypnotics and Sedatives/therapeutic use , Pyridines/therapeutic use , Radiopharmaceuticals , Technetium Tc 99m Exametazime , Adult , Brain Injuries/diagnostic imaging , Brain Injuries/metabolism , Cerebellar Diseases/diagnostic imaging , Cerebellar Diseases/metabolism , Cerebrovascular Circulation/drug effects , Child, Preschool , Diabetes Mellitus/physiopathology , Humans , Male , Near Drowning/diagnostic imaging , Persistent Vegetative State/diagnostic imaging , Persistent Vegetative State/drug therapy , Spinocerebellar Ataxias/diagnostic imaging , Spinocerebellar Ataxias/drug therapy , Spinocerebellar Ataxias/microbiology , Stroke/diagnostic imaging , Stroke/drug therapy , Stroke/metabolism , Tomography, Emission-Computed, Single-Photon , ZolpidemABSTRACT
Previous studies have shown that zolpidem (CAS 82626-48-0) can lead to improved perfusion in damaged brain tissue. Zolpidem belongs to the imidazopyridine chemical class and it illicits its pharmacological action via the gamma-aminobutyric acid (GABA) receptor system through stimulation of particularly the omega 1 receptors and to a lesser extent omega 2 receptors. Previously it was reported that no cerebral blood flow effects were observed in normal baboons after treatment with zolpidem, whereas an asymmetric regional increase in cerebral blood flow was observed in a neurologically abnormal baboon. In this study, the effect of a combination of the benzodiazepine receptor antagonist flumazenil (CAS 78755-81-4) and zolpidem on brain perfusion was examined by the 99mTc-hexamethyl-propylene amine oxime (99mTc-HMPAO) split dose brain single photon emission computed tomography (SPECT). Four normal baboons and the neurologically abnormal baboon from the previous zolpidem study were examined. In the current study the asymmetric changes observed after zolpidem--only treatment in the abnormal baboon was attenuated by flumazenil intervention. A decreased brain blood flow was observed after combination treatment of zolpidem and flumazenil in the normal baboons. The involvement of the omega receptors is suggested by these results. Up- or down-regulation of omega receptors may also contribute to the observed responses in the abnormal baboon and a brain injured patient.
