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Brain damages in ketamine addicts as revealed by magnetic resonance imaging

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#1 Claviceps

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Posted 02 January 2014 - 09:33 AM

Abstract

Ketamine, a known antagonist of N-methyl-D-aspartic (NMDA) glutamate receptors, had been used as an anesthetic particularly for pediatric or for cardiac patients. Unfortunately, ketamine has become an abusive drug in many parts of the world while chronic and prolonged usage led to damages of many organs including the brain. However, no studies on possible damages in the brains induced by chronic ketamine abuse have been documented in the human via neuroimaging. This paper described for the first time via employing magnetic resonance imaging (MRI) the changes in ketamine addicts of 0.5–12 years and illustrated the possible brain regions susceptible to ketamine abuse. Twenty-one ketamine addicts were recruited and the results showed that the lesions in the brains of ketamine addicts were located in many regions which appeared 2–4 years after ketamine addiction. Cortical atrophy was usually evident in the frontal, parietal or occipital cortices of addicts. Such study confirmed that many brain regions in the human were susceptible to chronic ketamine injury and presented a diffuse effect of ketamine on the brain which might differ from other central nervous system (CNS) drugs, such as cocaine, heroin, and methamphetamine.

 

Results

The results of lesions observed in all the 21 ketamine addicts were depicted in Table ​Table2.2. Those who had two or less regions in the brain with lesions were classified as light damage. Those that had three to four regions in the brain with lesions were classified as moderate damage, and those with five or more regions with lesions were classified as severe damage. The MRI lesions initially were observed as hyperintense spots (holes or patches) of degeneration in the superficial white matter of the cortex which appeared as early as 1 year after ketamine addiction (Figure ​(Figure1A),1A), while each lesions spread to the internal capsule by 3 years of addiction (Figure ​(Figure1B).1B). Slightly after, patches of hyperintense degeneration spots appeared in the basal forebrain (Figure ​(Figure2A),2A), cerebellum, and pons (Figure ​(Figure2B),2B), and diencephalon at 4 years of addiction (Figure ​(Figure2C).2C). Likewise, diffusion blockage was illustrated by FLAIR image in the parahippocampal gyrus and insula, also by 4 years of addiction (Figure ​(Figure3A),3A), while atrophy of the parahippocampal gyrus was observed a bit later by 5 years of addiction (Figure ​(Figure3B).3B). Atrophy of the other parts of cortex was first noted after 4 years of addiction, usually with atrophy on only a small region of the cortex (Figure ​(Figure4)4) and extended to two or three regions (usually frontal, parietal, and occipital) of the cortex by 7 years of addiction (Figure ​(Figure5).5). Hyperintense lesions were also observed in the corpus striatum by 6 years (Figure ​(Figure6).6). In this patient cohort, one patient had a combination of drugs and was taking ketamine together with amphetamine and ecstasy. He demonstrated early atrophy of cortex after taking the three drugs together in 0.5 years, in which the basal prefrontal gyrus rectus already exhibited significant atrophy (Figure ​(Figure7A)7A) when compared with control (Figure​(Figure7B).7B). Similarly, cortical atrophy also occurred early in another patient who had used a high dose of ketamine, in this case 3 g per day for 3 years (Figure ​(Figure8).8). After 7 years of addiction, in all other patients, lesions then appeared in the midbrain (Figure ​(Figure9).9). From 10 to 12 years of addiction, all lesion sites were as those described above.

 

http://www.ncbi.nlm....les/PMC3713393/


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#2 continuum

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Posted 02 January 2014 - 12:02 PM

Na de discussie wordt vermeld dat het om financieel onafhankelijk onderzoek gaat. Vervolgens blijkt het onderzoek gesubsidieerd door een instituut van drugsverslaving (Grant of Wai Yai Association Drug Abuse Research Fund). Googlen op die naam geeft weinig resultaat; vreemd. National institute of drug abuse (NIDA) komt gevoelsmatig nog het meest overeen. Gesubsidieerd door farmaceutische kolom, tabak en alcohol lobby? Zo nee, geen probleem; zo ja, welk doel dient het onderzoek?

 

 

 

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

This study was funded by the Grant of Wai Yai Association Drug Abuse Research Fund.



#3 Lµserg Diethel

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Posted 02 January 2014 - 12:41 PM

Hmm, eng.. Zou zoiets ook gebeuren bij sporadisch gebruik? Ik heb nooit een verslaving gehad, of dagelijks gebruik.. Heb echter wel eens 2-4 gram in een dag weggesnoven.



#4 Claviceps

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Posted 03 January 2014 - 05:20 AM

Hmm, eng.. Zou zoiets ook gebeuren bij sporadisch gebruik? Ik heb nooit een verslaving gehad, of dagelijks gebruik.. Heb echter wel eens 2-4 gram in een dag weggesnoven.

 

Helaas is daar nog geen antwoord op, maar ik vind het ook verontrustende bevindingen. Zover als ik heb gezien zijn de paar studies die er zijn vooral gericht op het dagelijks gebruik. 

 

Acute and chronic effects of ketamine upon human memory: a review. (2006)

Ketamine induces apoptosis via the mitochondrial pathway in human lymphocytes and neuronal cells (2010)

Effects of chronic ketamine use on frontal and medial temporal cognition (2013)

 

EDIT: Op een ander forum werd deze studie uit 2011 gepost die soortgelijke bevindingen heeft.
Reduced Dorsal Prefrontal Gray Matter After Chronic Ketamine Use (2011)

 

Deze studie lijkt een verdere bevestiging voor de bevindingen uit de eerste studie. Er word namelijk een reductie van grey matter vastgesteld in de prefrontale cortex.

 

Duration of ketamine use was negatively correlated with gray matter volume in bilateral frontal cortex, whereas the estimated total lifetime ketamine consumption was negatively correlated with gray matter volume in left superior frontal gyrus.

 

Conclusion: We have demonstrated a reduction in frontal gray matter volume in patients after chronic ketamine use. The link between frontal gray matter attenuation and the duration of ketamine use and cumulative doses of ketamine perhaps suggests a dose-dependent effect of long-term use of the drug.


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#5 Claviceps

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Posted 21 October 2014 - 12:05 PM

Abnormalities in White Matter Microstructure Associated with Chronic Ketamine Use, Neuropsychopharmacology (2014) 39, 329338; doi:10.1038/npp.2013.195;

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist that has been found to induce schizophrenia-type symptoms in humans and is a potent and fast-acting antidepressant. It is also a relatively widespread drug of abuse, particularly in China and the UK. Acute administration has been well characterized, but the effect of extended periods of ketamine useon brain structure in humansremains poorly understood.

We measured indices of white matter microstructural integrity and connectivity in the brain of 16 ketamine users and 16 poly-drug-using controls, and we used probabilistic tractography to quantify changes in corticosubcortical connectivity associated with ketamine use. We found a reduction in the axial diffusivity profile of white matter in a right hemisphere network of white matter regions in ketamine users compared with controls. Within the ketamine-user group, we found a significant positive association between the connectivity profile between the caudate nucleus and the lateral prefrontal cortex and dissociative experiences.

These findings suggest that chronic ketamine use may be associated with widespread disruption of white matter integrity, and white matter pathways between subcortical and prefrontal cortical areas may in part predict individual differences in dissociative experiences due to ketamine use.


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#6 Videlic

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Posted 21 October 2014 - 06:30 PM

Hmm, white matter klinkt als iets waar je niet mee wilt fucken. Sowieso raad ik iedereen chronisch ketamine gebruik af, met name een huisgenote die maar niet onder ogen wil zien dat ze dat beter kan laten, hoeveel wetenschappelijke artiekelen ik ook naar haar hoofd smijt........what to do :wacko: maarja baas in eigen brein right?


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#7 Claviceps

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Posted 21 October 2014 - 09:54 PM

White matter simpel gezegd zorgt dat communicatie tussen de verschillende hersengebieden mogelijk is. Zie het als de netwerkbekabeling van de hersenen.

 

Uiteindelijk kun je zelf weinig aan haar mogelijke verslaving doen. Een persoon die verslaafd is zal het zelf moeten inzien en zelf willen veranderen. Helaas is dat niet iets dat je kunt afdwingen. Uit eigen ervaring kan ik je wel vertellen dat Ketamine mentaal (zeer) verslavend kan zijn. Persoonlijk merkte ik vooral kort na gebruik een enorme craving om opnieuw Ketamine te gebruiken. Als je mentaal niet sterk staat of problemen hebt is het makkelijk om opnieuw hieraan toe te geven. 


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#8 Claviceps

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Posted 30 October 2014 - 07:05 PM

Long-term heavy ketamine use is associated with spatial memory impairment and altered hippocampal activation (Sep, 2014)

Ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, is rising in popularity as a drug of abuse. Preliminary evidence suggests that chronic, heavy ketamine use may have profound effects on spatial memory but the mechanism of these deficits is as yet unclear.

 

This study aimed to examine the neural mechanism by which heavy ketamine use impairs spatial memory processing. In a sample of 11 frequent ketamine users and 15 polydrug controls, matched for IQ, age and years in education. We used fMRI utilising an ROI approach to examine the neural activity of three regions known to support successful navigation; the hippocampus, parahippocampal gyrus and the caudate nucleus during a virtual reality task of spatial memory.

 

Frequent ketamine users displayed spatial memory deficits, accompanied by and related to, reduced activation in both the right hippocampus and left parahippocampal gyrus during navigation from memory, and in the left caudate during memory updating, compared to controls. Ketamine users also exhibited schizotypal and dissociative symptoms that were related to hippocampal activation. Impairments in spatial memory observed in ketamine users are related to changes in medial temporal lobe activation. Disrupted medial temporal lobe function may be a consequence of chronic ketamine abuse and may relate to schizophrenia-like symptomatology observed in ketamine users.


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