Reward Circuitry and Drug Addiction

Author(s):  
Vaughn R. Steele ◽  
Vani Pariyadath ◽  
Rita Z. Goldstein ◽  
Elliot A. Stein

Addiction is a complex neuropsychiatric syndrome related to dysregulation of brain systems including the mesocorticolimbic dopamine reward circuit. Dysregulation of reward circuitry is related to each of the three cyclical stages in the disease model of addiction: maintenance, abstinence, and relapse. Parsing reward circuitry is confounded due to the anatomical complexity of cortico-basal ganglia-thalamocortical loops, forward and backward projections within the circuit, and interactions between neurotransmitter systems. We begin by introducing the neurobiology of the reward system, specifically highlighting nodes of the circuit beyond the basal ganglia, followed by a review of the current literature on reward circuitry dysregulation in addiction. Finally, we discuss biomarkers of addiction identified with neuroimaging that could help guide neuroprediction models and development of targets for effective new interventions, such as noninvasive brain stimulation. The neurocircuitry of reward, especially non-prototypical nodes, may hold essential keys to understanding and treating addiction.

Author(s):  
Henrik Hogh-Olesen

Chapter 7 takes the investigation of the aesthetic impulse into the human brain to understand, first, why only we—and not our closest relatives among the primates—express ourselves aesthetically; and second, how the brain reacts when presented with aesthetic material. Brain scans are less useful when you are interested in the Why of aesthetic behavior rather than the How. Nevertheless, some brain studies have been ground-breaking, and neuroaesthetics offers a pivotal argument for the key function of the aesthetic impulse in human lives; it shows us that the brain’s reward circuit is activated when we are presented with aesthetic objects and stimuli. For why reward a perception or an activity that is evolutionarily useless and worthless in relation to human existence?


2020 ◽  
Vol 20 (4) ◽  
pp. 401-412
Author(s):  
Alejandra Cardenas-Rojas ◽  
Kevin Pacheco-Barrios ◽  
Stefano Giannoni-Luza ◽  
Oscar Rivera-Torrejon ◽  
Felipe Fregni

2020 ◽  
Vol 31 (8) ◽  
pp. 905-914 ◽  
Author(s):  
Yali Feng ◽  
Jiaqi Zhang ◽  
Yi Zhou ◽  
Zhongfei Bai ◽  
Ying Yin

AbstractNoninvasive brain stimulation (NIBS) techniques have been used to facilitate the recovery from prolonged unconsciousness as a result of brain injury. The aim of this study is to systematically assess the effects of NIBS in patients with a disorder of consciousness (DOC). We searched four databases for any randomized controlled trials on the effect of NIBS in patients with a DOC, which used the JFK Coma Recovery Scale-Revised (CRS-R) as the primary outcome measure. A random-effects meta-analysis was conducted to pool effect sizes. Fourteen studies with 273 participants were included in this review, of which 12 studies with sufficient data were included in the meta-analysis. Our meta-analysis showed a significant effect on increasing CRS-R scores in favor of real stimulation as compared to sham (Hedges’ g = 0.522; 95% confidence interval [CI], 0.318–0.726; P < 0.0001, I2 = 0.00%). Subgroup analysis demonstrated that only anodal transcranial direct current stimulation (tDCS) of the left dorsolateral prefrontal cortex (DLPFC) significantly enhances the CRS-R scores in patients with a DOC, as compared to sham (Hedges’ g = 0.703; 95% CI, 0.419–0.986; P < 0.001), and this effect was predominant in patients in a minimally conscious state (MCS) (Hedges’ g = 0.815; 95% CI, 0.429–1.200; P < 0.001). Anodal tDCS of the left DLPFC appears to be an effective approach for patients with MCS.


2014 ◽  
Vol 111 (10) ◽  
pp. 1949-1959 ◽  
Author(s):  
Alan D. Dorval ◽  
Warren M. Grill

Pathophysiological activity of basal ganglia neurons accompanies the motor symptoms of Parkinson's disease. High-frequency (>90 Hz) deep brain stimulation (DBS) reduces parkinsonian symptoms, but the mechanisms remain unclear. We hypothesize that parkinsonism-associated electrophysiological changes constitute an increase in neuronal firing pattern disorder and a concomitant decrease in information transmission through the ventral basal ganglia, and that effective DBS alleviates symptoms by decreasing neuronal disorder while simultaneously increasing information transfer through the same regions. We tested these hypotheses in the freely behaving, 6-hydroxydopamine-lesioned rat model of hemiparkinsonism. Following the onset of parkinsonism, mean neuronal firing rates were unchanged, despite a significant increase in firing pattern disorder (i.e., neuronal entropy), in both the globus pallidus and substantia nigra pars reticulata. This increase in neuronal entropy was reversed by symptom-alleviating DBS. Whereas increases in signal entropy are most commonly indicative of similar increases in information transmission, directed information through both regions was substantially reduced (>70%) following the onset of parkinsonism. Again, this decrease in information transmission was partially reversed by DBS. Together, these results suggest that the parkinsonian basal ganglia are rife with entropic activity and incapable of functional information transmission. Furthermore, they indicate that symptom-alleviating DBS works by lowering the entropic noise floor, enabling more information-rich signal propagation. In this view, the symptoms of parkinsonism may be more a default mode, normally overridden by healthy basal ganglia information. When that information is abolished by parkinsonian pathophysiology, hypokinetic symptoms emerge.


Basal Ganglia ◽  
2011 ◽  
Vol 1 (2) ◽  
pp. 65-77 ◽  
Author(s):  
Thomas Wichmann ◽  
Mahlon R. DeLong

2007 ◽  
Vol 4 (5) ◽  
pp. 605-614 ◽  
Author(s):  
Sara Marceglia ◽  
Lorenzo Rossi ◽  
Guglielmo Foffani ◽  
AnnaMaria Bianchi ◽  
Sergio Cerutti ◽  
...  

2018 ◽  
Vol 8 (7) ◽  
pp. 135 ◽  
Author(s):  
Terence D. Sanger ◽  
Mark Liker ◽  
Enrique Arguelles ◽  
Ruta Deshpande ◽  
Arash Maskooki ◽  
...  

Deep brain stimulation (DBS) for secondary (acquired, combined) dystonia does not reach the high degree of efficacy achieved in primary (genetic, isolated) dystonia. We hypothesize that this may be due to variability in the underlying injury, so that different children may require placement of electrodes in different regions of basal ganglia and thalamus. We describe a new targeting procedure in which temporary depth electrodes are placed at multiple possible targets in basal ganglia and thalamus, and probing for efficacy is performed using test stimulation and recording while children remain for one week in an inpatient Neuromodulation Monitoring Unit (NMU). Nine Children with severe secondary dystonia underwent the NMU targeting procedure. In all cases, 4 electrodes were implanted. We compared the results to 6 children who had previously had 4 electrodes implanted using standard intraoperative microelectrode targeting techniques. Results showed a significant benefit, with 80% of children with NMU targeting achieving greater than 5-point improvement on the Burke–Fahn–Marsden Dystonia Rating Scale (BFMDRS), compared with 50% of children using intraoperative targeting. NMU targeting improved BFMDRS by an average of 17.1 whereas intraoperative targeting improved by an average of 10.3. These preliminary results support the use of test stimulation and recording in a Neuromodulation Monitoring Unit (NMU) as a new technique with the potential to improve outcomes following DBS in children with secondary (acquired) dystonia. A larger sample size will be needed to confirm these results.


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