Volkow, N. D. et al. Long-term frontal brain metabolic changes in cocaine abusers. Synapse 11, 184-190

Article (PDF Available)inSynapse 11(3):184-90 · July 1992with439 Reads
DOI: 10.1002/syn.890110303 · Source: PubMed
Abstract
Neurological complications from cocaine use are well recognized. We propose that chronic cocaine use can also cause clinically silent brain dysfunction. We investigated brain glucose metabolism with positron emission tomography (PET) and 2-deoxy-2[18F] fluoro-D-glucose (FDG) in 21 neurologically intact chronic cocaine abusers (C) and 18 normal controls (N). The cocaine abusers were tested 1–6 weeks after the last use of cocaine and seven were retested after a 3 month drug-free period. Global cerebral glucose metabolism was not significantly different between controls and cocaine abusers (N = 38.4±3, C = 36.5±5 μmol/100 g of tissue, min). However, cocaine abusers had significantly (P< 0.05) lower metabolic activity in 16 of the 21 left frontal regions and 8 of the 21 right frontal regions. These decreases persisted after 3–4 months of detoxification and were correlated with the dose (P ≤ 0.01) and the years of cocaine use (P ≤ 0.05). This study shows reduced rates of frontal metabolism in neurologically intact cocaine abusers that persist even after 3–4 months of detoxification. © Wiley-Liss, Inc.
    • "In addition, other neurotransmitters, such as glutamate and GABA, are indirectly affected by different drugs, further altering the brain's reward pathway (Parvaz et al. 2011). Importantly, prefrontal cortical (PFC) areas are less active in substance users, a decrease associated with impaired self-control (Goldstein and Volkow 2011; Volkow et al. 1991 Volkow et al. , 1992 Volkow et al. , 1988). Treatments currently available for addiction include both pharmacological interventions as well as behavioral methods. "
    [Show abstract] [Hide abstract] ABSTRACT: Neuroimaging techniques to measure the function and biochemistry of the human brain such as positron emission tomography (PET), proton magnetic resonance spectroscopy (1H MRS), and functional magnetic resonance imaging (fMRI), are powerful tools for assessing neurobiological mechanisms underlying the response to treatments in substance use disorders. Here, we review the neuroimaging literature on pharmacological and behavioral treatment in substance use disorder. We focus on neural effects of medications that reduce craving (e.g., naltrexone, bupropion hydrochloride, baclofen, methadone, varenicline) and that improve cognitive control (e.g., modafinil, N-acetylcysteine), of behavioral treatments for substance use disorders (e.g., cognitive bias modification training, virtual reality, motivational interventions) and neuromodulatory interventions such as neurofeedback and transcranial magnetic stimulation. A consistent finding for the effectiveness of therapeutic interventions identifies the improvement of executive control networks and the dampening of limbic activation, highlighting their values as targets for therapeutic interventions in substance use disorders.
    Full-text · Article · May 2016
    • "In particular, during the resting state of HDIs-OMT, results revealed hypoactivation of the OFC implicated in mediating motivation, a weaker effective connectivity between the OFC and caudate and also a stronger connectivity between the OFC and putamen. Similar results were reported for drug-addicted individuals during withdrawal (Volkow et al. 1992; Adinoff et al. 2001). GCA uncovered a weaker connectivity from the ACC and MPFC, which are involved in mediating inhibitory control, to the caudate, AMY, putamen and insula, and a stronger connectivity between the ACC and OFC, and between the MPFC and putamen. "
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    • "In the pgACC, glucose/tCr ratios were higher in CU compared to HC, which possibly indicating lower metabolic activity or glucose consumption rate. This notion would be in line with PET studies reporting reduced glucose metabolism in the PFC of dependent CU during protracted withdrawal (Volkow et al. 1992). However, changes of glucose metabolism in the ACC of CU measured with 1 H-MRS have not been reported so far warranting further investigation. "
    [Show abstract] [Hide abstract] ABSTRACT: Cocaine addiction is a chronically relapsing disorder that is associated with harmful consequences. Relapses occur frequently and effective pharmacotherapies are currently sparse. Preclinical studies suggest that altered glutamatergic signaling is crucial for the maintenance of cocaine self-administration. However, the translational validity of these models is currently unknown. Therefore, we investigated potential differences of glutamate, glutamine and further metabolite levels in the pregenual anterior cingulate cortex (pgACC) and the right dorsolateral prefrontal cortex (rDLPFC) of chronic cocaine users and controls using the PRior knOwledge FITting 2.0 tool in combination with two-dimensional J-resolved single-voxel 1H-magnetic resonance spectroscopy at 3T and voxel tissue composition and relaxation correction. Glutamate and glutamine levels did not differ between cocaine users and controls, but higher weekly cocaine use and higher cocaine hair concentrations were associated with lower glutamine/creatine ratios in the pgACC. Interestingly, cocaine users exhibited higher glucose/total creatine ratios than controls in the pgACC and higher choline/creatine ratios in the pgACC and rDLPFC. These results imply that cocaine use is associated with altered cortical glucose metabolism and membrane turnover. Finally, cocaine use over the past 6 months appears to decrease cortical glutamine levels indicating changes in glutamate cycling.
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