Related Research Articles
The putamen is a round structure located at the base of the forebrain (telencephalon). The putamen and caudate nucleus together form the dorsal striatum. It is also one of the structures that compose the basal nuclei. Through various pathways, the putamen is connected to the substantia nigra, the globus pallidus, the claustrum, and the thalamus, in addition to many regions of the cerebral cortex. A primary function of the putamen is to regulate movements at various stages and influence various types of learning. It employs GABA, acetylcholine, and enkephalin to perform its functions. The putamen also plays a role in degenerative neurological disorders, such as Parkinson's disease.
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterised by executive dysfunction occasioning symptoms of inattention, hyperactivity, impulsivity and emotional dysregulation that are excessive and pervasive, impairing in multiple contexts, and otherwise age-inappropriate.
Methylphenidate, sold under the brand names Ritalin and Concerta among others, is a central nervous system (CNS) stimulant used medically to treat attention deficit hyperactivity disorder (ADHD) and, to a lesser extent, narcolepsy. It is a primary medication for ADHD ; it may be taken by mouth or applied to the skin, and different formulations have varying durations of effect, commonly ranging from 2–4 hours.
In the human brain, the anterior cingulate cortex (ACC) is the frontal part of the cingulate cortex that resembles a "collar" surrounding the frontal part of the corpus callosum. It consists of Brodmann areas 24, 32, and 33.
The caudate nucleus is one of the structures that make up the corpus striatum, which is a component of the basal ganglia in the human brain. While the caudate nucleus has long been associated with motor processes due to its role in Parkinson's disease, it plays important roles in various other nonmotor functions as well, including procedural learning, associative learning and inhibitory control of action, among other functions. The caudate is also one of the brain structures which compose the reward system and functions as part of the cortico–basal ganglia–thalamic loop.
Dextroamphetamine is a potent central nervous system (CNS) stimulant and enantiomer of amphetamine that is prescribed for the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It is also used as an athletic performance and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.
Adderall and Mydayis are trade names for a combination drug called mixed amphetamine salts containing four salts of amphetamine. The mixture is composed of equal parts racemic amphetamine and dextroamphetamine, which produces a (3:1) ratio between dextroamphetamine and levoamphetamine, the two enantiomers of amphetamine. Both enantiomers are stimulants, but differ enough to give Adderall an effects profile distinct from those of racemic amphetamine or dextroamphetamine, which are marketed as Evekeo and Dexedrine/Zenzedi, respectively. Adderall is used in the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy. It is also used illicitly as an athletic performance enhancer, cognitive enhancer, appetite suppressant, and recreationally as a euphoriant. It is a central nervous system (CNS) stimulant of the phenethylamine class.
Adult attention deficit hyperactivity disorder is the neurological condition of attention deficit hyperactivity disorder (ADHD) in adults. About one-third to two-thirds of children with symptoms from early childhood continue to demonstrate ADHD symptoms throughout life.
The posterior cingulate cortex (PCC) is the caudal part of the cingulate cortex, located posterior to the anterior cingulate cortex. This is the upper part of the "limbic lobe". The cingulate cortex is made up of an area around the midline of the brain. Surrounding areas include the retrosplenial cortex and the precuneus.
Despite the scientifically well-established nature of attention deficit hyperactivity disorder (ADHD), its diagnosis, and its treatment, each of these has been controversial since the 1970s. The controversies involve clinicians, teachers, policymakers, parents, and the media. Positions range from the view that ADHD is within the normal range of behavior to the hypothesis that ADHD is a genetic condition. Other areas of controversy include the use of stimulant medications in children, the method of diagnosis, and the possibility of overdiagnosis. In 2009, the National Institute for Health and Care Excellence, while acknowledging the controversy, states that the current treatments and methods of diagnosis are based on the dominant view of the academic literature.
Lisdexamfetamine, most commonly sold under the brand name Vyvanse and Elvanse among others, is a stimulant medication that is used to treat attention deficit hyperactivity disorder (ADHD) in children and adults, and for moderate-to-severe binge eating disorder in adults. Lisdexamfetamine is taken by mouth. Its effects generally begin within two hours and last for up to 14 hours. In the United Kingdom, it is usually less preferred than methylphenidate for the treatment of children.
Attention deficit hyperactivity disorder management options are evidence-based practices with established treatment efficacy for ADHD.
Obsessive–compulsive disorder (OCD) is a mental and behavioral disorder in which an individual has intrusive thoughts and feels the need to perform certain routines (compulsions) repeatedly to relieve the distress caused by the obsession, to the extent where it impairs general function.
Seed-based d mapping or SDM is a statistical technique created by Joaquim Radua for meta-analyzing studies on differences in brain activity or structure which used neuroimaging techniques such as fMRI, VBM, DTI or PET. It may also refer to a specific piece of software created by the SDM Project to carry out such meta-analyses.
The biology of obsessive–compulsive disorder (OCD) refers biologically based theories about the mechanism of OCD. Cognitive models generally fall into the category of executive dysfunction or modulatory control. Neuroanatomically, functional and structural neuroimaging studies implicate the prefrontal cortex (PFC), basal ganglia (BG), insula, and posterior cingulate cortex (PCC). Genetic and neurochemical studies implicate glutamate and monoamine neurotransmitters, especially serotonin and dopamine.
The cause of obsessive–compulsive disorder is understood mainly through identifying biological risk factors that lead to obsessive–compulsive disorder (OCD) symptomology. The leading hypotheses propose the involvement of the orbitofrontal cortex, basal ganglia, and/or the limbic system, with discoveries being made in the fields of neuroanatomy, neurochemistry, neuroimmunology, neurogenetics, and neuroethology.
William "Bill" Gehring is a psychologist, and in 2014 is the Arthur F. Thurnau Professor of Psychology at the University of Michigan in Ann Arbor, Michigan. He researches Event Related Potentials and is one of the discoverers of the Error Related Negativity. He has made contributions to the field of cognitive neuroscience through his studies on the electrophysiological markers of obsessive-compulsive disorder.
The delayed-maturation theory of obsessive–compulsive disorder suggests that obsessive–compulsive disorder (OCD) can be caused by delayed maturation of the frontal striatal circuitry or parts of the brain that make up the frontal cortex, striatum, or integrating circuits. Some researchers suspect that variations in the volume of specific brain structures can be observed in children that have OCD. It has not been determined if delayed-maturation of this frontal circuitry contributes to the development of OCD or if OCD is the ailment that inhibits normal growth of structures in the frontal striatal, frontal cortex, or striatum. However, the use of neuroimaging has equipped researchers with evidence of some brain structures that are consistently less adequate and less matured in patients diagnosed with OCD in comparison to brains without OCD. More specifically, structures such as the caudate nucleus, volumes of gray matter, white matter, and the cingulate have been identified as being less developed in people with OCD in comparison to individuals that do not have OCD. However, the cortex volume of the operculum (brain) is larger and OCD patients are also reported to have larger temporal lobe volumes; which has been identified in some women patients with OCD. Further research is needed to determine the effect of these structural size differences on the onset and degree of OCD and the maturation of specific brain structures.
Katya Rubia is a Professor of Cognitive Neuroscience at the MRC Social, Genetic and Developmental Psychiatry Centre and Department of Child and Adolescent Psychiatry, both part of the Institute of Psychiatry, King's College London.
Bipolar disorder is an affective disorder characterized by periods of elevated and depressed mood. The cause and mechanism of bipolar disorder is not yet known, and the study of its biological origins is ongoing. Although no single gene causes the disorder, a number of genes are linked to increase risk of the disorder, and various gene environment interactions may play a role in predisposing individuals to developing bipolar disorder. Neuroimaging and postmortem studies have found abnormalities in a variety of brain regions, and most commonly implicated regions include the ventral prefrontal cortex and amygdala. Dysfunction in emotional circuits located in these regions have been hypothesized as a mechanism for bipolar disorder. A number of lines of evidence suggests abnormalities in neurotransmission, intracellular signalling, and cellular functioning as possibly playing a role in bipolar disorder.
References
- 1 2 "2017 Highly Cited Researchers: Radua, Joaquim". clarivate.com/hcr/2017-researchers-list. Retrieved November 17, 2017.
- 1 2 3 "ORCID: Joaquim Radua". orcid.org. Retrieved November 18, 2017.
- 1 2 3 4 "Dr Joaquim Radua MD BStat PhD". www.radua.net. Retrieved November 17, 2017.
- ↑ "Técnicas de Neuroimagen Avanzada: Equipo Docente". www.cursoneuroimagen.es/eqdocent.php. Retrieved November 17, 2017.
- ↑ "BioMed Research International: Editorial Board: Neuroscience". www.hindawi.com/journals/bmri/editors/neuroscience. Retrieved November 18, 2017.
- ↑ "Sociedad Española de Neuroimagen: Current Board of Directors". www.neuroimagen.es/organization/board.php. Retrieved November 17, 2017.
- ↑ "PubMed: Radua J". www.ncbi.nlm.nih.gov. Retrieved November 17, 2017.
- ↑ "Joaquim Radua". scholar.google.com. Retrieved November 17, 2017.
- ↑ Radua, J.; Mataix-Cols, D. (2009). "Voxel-wise meta-analysis of grey matter changes in obsessive-compulsive disorder". British Journal of Psychiatry. 195 (5): 393–402. doi: 10.1192/bjp.bp.108.055046 . PMID 19880927.
- ↑ Radua, J.; van den Heuvel, O.A.; Surguladze, S.; Mataix-Cols, D. (2010). "Meta-analytical comparison of voxel-based morphometry studies in obsessive-compulsive disorder vs other anxiety disorders". Archives of General Psychiatry. 67 (7): 701–711. doi:10.1001/archgenpsychiatry.2010.70. PMID 20603451. S2CID 9501322.
- ↑ Nakao, T.; Radua, J.; Rubia, K.; Mataix-Cols, D. (2011). "Gray matter volume abnormalities in ADHD: voxel-based meta-analysis exploring the effects of age and stimulant medication". American Journal of Psychiatry. 168 (11): 1154–1163. doi:10.1176/appi.ajp.2011.11020281. PMID 21865529.
- ↑ Hart, H.; Radua, J.; Nakao, T.; Mataix-Cols, D.; Rubia, K. (2013). "Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects". JAMA Psychiatry. 70 (2): 185–198. doi:10.1001/jamapsychiatry.2013.277. PMID 23247506.
- ↑ Rubia, K.; Alegria, A.A.; Cubillo, A.I.; Smith, A.B.; Brammer, M.J.; Radua, J. (2014). "Effects of stimulants on brain function in attention-deficit/hyperactivity disorder: a systematic review and meta-analysis". Biological Psychiatry. 76 (8): 616–628. doi:10.1016/j.biopsych.2013.10.016. PMC 4183380 . PMID 24314347.
- ↑ Schurz, M.; Radua, J.; Aichhorn, M.; Richlan, F.; Perner, J. (2014). "Fractionating theory of mind: a meta-analysis of functional brain imaging studies". Neuroscience and Biobehavioral Reviews. 42: 9–34. doi: 10.1016/j.neubiorev.2014.01.009 . PMID 24486722.
- ↑ Radua, J.; Schmidt, A.; Borgwardt, S.; Heinz, A.; Schlagenhauf, F.; McGuire, P.; Fusar-Poli, P. (2015). "Ventral striatal activation during reward processing in psychosis: a neurofunctional meta-analysis". JAMA Psychiatry. 72 (12): 1243–1251. doi: 10.1001/jamapsychiatry.2015.2196 . PMID 26558708.
- ↑ Fullana, M.A.; Harrison, B.J.; Soriano-Mas, C.; Vervliet, B.; Cardoner, N.; Àvila-Parcet, A.; Radua, J. (2016). "Neural signatures of human fear conditioning: an updated and extended meta-analysis of fMRI studies". Molecular Psychiatry. 21 (4): 500–508. doi:10.1038/mp.2015.88. hdl: 10230/26026 . PMID 26122585. S2CID 21966001.
