GAMMA-HYDROXYBUTYRATE IN THE TREATMENT OF INCREASED INTRACRANIAL-PRESSURE AND VASOSPASM

Citation
U. Diedrich et al., GAMMA-HYDROXYBUTYRATE IN THE TREATMENT OF INCREASED INTRACRANIAL-PRESSURE AND VASOSPASM, Aktuelle Neurologie, 23(2), 1996, pp. 63-67
Citations number
12
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
ISSN journal
03024350
Volume
23
Issue
2
Year of publication
1996
Pages
63 - 67
Database
ISI
SICI code
0302-4350(1996)23:2<63:GITTOI>2.0.ZU;2-Q
Abstract
Gamma-hydroxybutyrate (GHB), a suspected neurotransmitter, has sedativ e properties, reducing brain metabolism and body temperature and thus inducing effects resembling hibernation. Introduced as a narcotic 25 y ea rs ago, it has been employed in recent years for basic sedation of intensive-care patients in need of long-term respiratory support. In t his study we analysed the effects of continuous GHB application in 19 patients suffering from increased intracranial pressure (ICP) subarach noid haemorrhage (SAH), or both. GHB, which is only available as a sod ium salt, frequently causes hypernatremia and metabolic alcalosis when given continually in dosages higher than 12 mg/kg body weight per hou r. GHB is, therefore, often limited to preserve the potential usefulne ss of controlled hyperventilation or osmotherapy, respectively, when I CP increases. In 7 out of 8 patients with total infarctions in the ter ritory of the middle cerebral artery GHB could not prevent the develop ment of a malignant brain edema. The survivors with territorial infarc tions or SAH in whom ICP was monitored showed no critical decreases in cerebral perfusion pressure during GHB application. Early GHB adminis tration seemed beneficial in the prevention of vasospasm subsequent to severe SAH. The intracranial blood flow velocities did not exceed 99 cm/s in all three cases treated with GHB within the first three days a fter SAH, whereas three out of four cases without GHB showed marked ac celeration with values over 90 cm/s. In two patients, the administrati on of GHB after the development of severe vasospasm was followed by a continuous decrease of flow velocities in the cerebral arteries.