Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 7th International Conference on Addictive Disorders and Alcoholism Kuala Lumpur, Malaysia.

Day 2 :

Keynote Forum

Wai Kwong Tang

Professor, The Chinese University of Hong Kong, China

Keynote: Evidence of Brain Damage in Chronic Ketamine Users – a Brain Imaging Study
OMICS International Alcoholism 2017 International Conference Keynote Speaker Wai Kwong Tang photo

WK Tang was appointed to professor in the Department of Psychiatry, the Chinese University of Hong Kong in 2011. His main research areas are Addictions and Neuropsychiatry in Stroke. Professor Tang has published over 100 papers in renowned journals, and has also contributed to the peer review of 40 journals. He has secured over 20 major competitive research grants. He has served the editorial boards of five scientific journals. He was also a recipient of the Young Researcher Award in 2007, awarded by the Chinese University of Hong Kong.


Background and objectives:

The objectives of this study were to ascertain the pattern of grey and white matter volume reduction and regional metabolic and activation abnormalities in chronic ketamine users, and to evaluate the correlations between these brain abnormalities and cognitive impairments in chronic ketamine users in Hong Kong.


Cross-sectional observational study.


Counselling Centre for Psychotropic Substance Abusers in Hong Kong.


One hundred and thirty-six participants were recruited from October 2011 to April 2014. The participants were divided into two groups: ketamine users (79) and healthy controls (57).

Main outcome measures:

Psychiatric assessments included screening with self-rating questionnaires and face-to-face interviews. All of the participants completed a detailed cognitive battery that covered general intelligence, verbal and visual memory, executive functions, motor speed and language. All of the participants underwent magnetic resonance imaging of the brain. 


Many of the participants in the ketamine group also frequently used cocaine and cannabis. Among the ketamine users, 12.6% were diagnosed with a mood disorder and 8.9% with an anxiety disorder. The participants in the ketamine group had worse performance than the healthy controls on tests of general intelligence, verbal, visual and working memory and executive functioning.

In terms of grey matter volumes, the right orbitofrontal cortex, right medial prefrontal cortex, left and right hippocampus and possibly the left orbitofrontal cortex were smaller in the ketamine group. In contrast, the volumes of the left basal ganglia, left putamen and possibly the left caudate were higher in the ketamine group. In terms of white matter volumes, the ketamine group had a lower periventricular white matter volume in the right hemisphere. The grey matter volumes of the left and right orbitofrontal cortex, right medial prefrontal cortex, left basal ganglia and left putamen, and right periventricular white matter volume were negatively correlated with the severity of ketamine dependence. The hippocampal volumes were correlated with performance on the arithmetic, information and digit span tests. The periventricular white matter volume also correlated with the information score.

A functional connectivity examination of the default mode network revealed significantly decreased connectivity in the medial part of the bilateral superior frontal gyrus, left middle frontal gyrus, bilateral gyrus rectus, left superior temporal pole, left inferior temporal gyrus, bilateral angular gyrus and bilateral cerebellum crus II in the ketamine group. This group also displayed increased connectivity in the bilateral precuneus and right inferior occipital gyrus.


The results provide imaging evidence of brain damage in chronic ketamine users. Chronic ketamine use was associated with reduced grey and white matter volumes in certain regions of the brain. Chronic ketamine use was also associated with altered functional connectivity with the default mode network. Abnormal brain structures and altered functional organisation of the brain network may underlie the hypersensitivity towards drug related cues but weakened cognitive control in those with ketamine addiction. Longitudinal or prospective studies would help to strengthen the evidence on the reversibility of the structural and functional brain damage caused by ketamine.

Keynote Forum

Gary Hulse

Professor, The University of Western Australia, Australia

Keynote: Oral and Sustained Release Naltrexone: Improving Clinical Outcomes for Management of Problem Alcohol Use
OMICS International Alcoholism 2017 International Conference Keynote Speaker Gary Hulse photo

Prof. Hulse is based at the School of Psychiatry QE11 Medical Centre University of Western Australia. His research career has been directed at developing evidence based information which will enhance clinical practice, and has in the last several years had a particular focus on assessing the safety and efficacy of sustained release naltrexone as a management tool for substance dependence. He has arguably published more than anyone else globally on sustained release naltrexone for the management of heroin dependence, much of this on the Australian naltrexone implant.


Three oral pharmacotherapies (acamprosate, disulfiram, and naltrexone) are commonly used for the management of alcohol abuse or dependence. Naltrexone is an opioid antagonist which primarily, but not exclusively, targets the μ-opioid receptor. Naltrexone likely exerts its actions by blockade of the high concentration of μ-opioid receptors located in areas of the brain that have been implicated in the reward pathway associated with alcohol. Despite being a relatively effective and safe treatment1, the clinical management of alcohol abuse/dependence by oral naltrexone can be compromised due to the patient’s noncompliance with daily use of this medication2, 3. Over the past decade an increasing body of research has suggested that the use of sustained release depot naltrexone preparations can overcome this issue and deliver improved clinical outcomes4. However, at the same time, research findings from diverse areas of pharmacogenetics, neurobiology and behavioural psychology have also been converging to identify variables including genetic markers, patient psychosocial characteristics and drug use history differences that play a major role in mediating the response of alcohol abuse/dependent persons to treatment by naltrexone4,5. The establishment of clinical procedures to maximise use of oral formula, and characterization of clinical markers to identify those patients who are most likely to benefit from naltrexone will ultimately provide significant benefit to both patients and clinicians by optimizing treatment outcome.