EditorialKetamine was developed in 1962 as an anaesthetic agent [1] for use in pediatrics, oncology, and veterinary practice [2]. Ketamine primarily and non-competitively antagonizes NMDA (N-methyl-D-aspartate) receptors, thereby interfering with the excitatory amino acid transmission, which underlines its analgesic and dissociative effects [2]. Ketamine also has weak effects on opioid, muscarinic and monoamine receptors [1], enhances the neurotransmission of noradrenaline, serotonin and dopamine in a dose-dependent fashion, which, together with its effects on glutaminergic system, accounts for its psychotomimetic and sympathomimetic effects [2] and addiction potential [3].During the past decade, ketamine has been proven efficacious in treatment-resistant depression [4]. Due to its unique neurochemical profile, ketamine, and its analogue phencyclidine, has also been tried as a new treatments for psychosis [5] and addiction [6,7]. In contrast to increasing research efforts to understand ketamine's potential as a therapeutic agent, only a few studies focused on understanding ketamine addiction.Ketamine misuse started in the United States in the 1970s, soon after its development and wider availability [2]. Ketamine is still a commonly abused drug around the world [8], particularly in East Asia [9]. Ketamine is the second and third most commonly abused drug in Hong Kong [10] and in mainland China and Taiwan [9], respectively. Ketamine is predominantly consumed by young people [10,11], gay clubbers [12,13] and poly-substance users [8].Heavy ketamine users suffer from both physical and mental problems. Serious lower urinary tracts symptoms (increased urinary frequency, urgency, incontinence, hematuria, and dysuria) [14][15][16], gastritis and liver and kidney dysfunction [16,17] are also common in this population. Psychiatric disorders are often comorbid by ketamine include depression, which is remarkably prevalent among chronic ketamine users [18,19] [29]. However, it is still not clear if chronic ketamine intake is the cause or consequence of these brain alterations due to the cross-sectional design of these studies [28].Further, white matter microstructural abnormalities were found predominantly in left prefrontal region in ketamine chronic users when [27], restricted to the right hemisphere white matter regions when compared with poly-drug users [26]. While a significant correlation between the subgenual ACCdorsal medial prefrontal cortex connectivity and depression score was found in female ketamine users but not in female controls, it is hard to draw a conclusion whether it was ketamine use or depression that accounted for the discrepancy between ketamine users and controls [30].To date, there has been no established treatment for ketamine addiction. Abstinence seems to be the essential step for treating physical symptoms induced by ketamine [31] and probably depressive symptoms as well as cognitive impairments [20]. Lamotrigine, a glutamate release inhibitor showed promising effect in reducing ketamine craving ...