to 1g daily for 0.5 up to 12 years) with severity depending on the duration of addiction and daily intake of ketamine. Cortical atrophy and holes in superficial white matter are seen early on. After 4 years of addiction lesions spread throughout the brain and damage is evident in the pons and other deeper brain structures. Prevention In medical settings, NMDA receptor antagonists are used as anesthetics, so GABAA receptor positive allosteric modulators are used to effectively prevent any neurotoxicity caused by them. Drugs that work to suppress NAN include anticholinergics, benzodiazepines, barbiturates and Alpha-adrenergic agonists, such as clonidine. Conversely, coadministration of NMDA-antagonists with alpha-2 adrenergic antagonists, like yohimbine, could theoretically potentiate NAN. Controversy In Karl L. R. Jansen's book, Ketamine: Dreams and Realities, unpublished studies are cited on monkey brains. The opinion that DXM caused Olney's Lesions therefore came under fire. Jansen writes: See also NMDA receptor NMDA receptor antagonist Dissociative Neurotoxic drug References External links "Lycaeum" about NAN Neurotrauma Toxicology Lesion de:John W. Olney