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Development and Developmental Disorders
Published in Andrei I. Holodny, Functional Neuroimaging, 2019
In the work by Just et al. (2006) (85), fMRI results from a group of high-functioning autistic spectrum individuals were compared with those of age-, gender-, and IQ-matched normal subjects using a Tower of London test modified to fMRI for assessment of executive functioning. Results demonstrated activation of similar brain areas between the two groups, but decreased functional connectivity between frontal and parietal regions. Functional connectivity was assessed by time course of activation in 15 regions of interest (ROIs)—seven paired brain ROIs and the medial frontal gyrus. This study further supports the theory of underconnectivity in autistic spectrum patients and helps to explain piecemeal processing of data (85).
Customized DNA–directed precision nutrition to balance the brain reward circuitry and reduce addictive behaviors
Published in Debmalya Barh, Precision Medicine in Cancers and Non-Communicable Diseases, 2018
Kenneth Blum, Marcelo Febo, Eric R. Braverman, Mona Li, Lyle Fried, Roger Waite, Zsolt Demotrovics, William B. Downs, Debmalya Barh, Bruce Steinberg, Thomas McLaughlin, Rajendra D. Badgaiyan
The integrity of resting state functional connectivity is crucial for normal homeostatic function. Zhang et al. (2015) showed that heroin addicts exhibit reduced connectivity between the dorsal anterior cingulate cortex (dACC) and rostral anterior cingulate cortex (rACC), as well as reduced connectivity between the subcallosal anterior cingulate cortex (sACC) and dACC. The heroin addicts’ variations in functional connectivity of three subregions of the ACC indicate that these three subregions, along with other key brain areas (such as the dorsal striatum, putamen, orbital frontal cortex, dorsal striatum, cerebellum, amygdala) potentially modulate heroin addiction. Blum's laboratory and Zhang's group (Blum et al., 2015b) showed that in abstinent heroin addicts, KB220Z™ (a putative dopamine D2 agonist) increased BOLD activation in caudate-accumbens-dopaminergic pathways, compared to a placebo following one-hour acute administration. In addition, KB220Z™ also induced the reduction of resting state activity in the putamen. In the second phase of this pilot study, all 10 abstinent heroin-dependent subjects had three brain regions of interest (ROIs), which were shown to be significantly activated from the resting state by KB220Z™ compared to the placebo (P < 0.05). Increased functional connectivity was also observed in a system involving the dorsal anterior cingulate, medial frontal gyrus, nucleus accumbens, posterior cingulate, occipital cortical areas, and cerebellum.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Most authors of recent textbooks in basic neuroanatomy describe the superior frontal gyrus as extending from the lateral surface of the cerebral hemisphere over the superomedial margin onto the medial surface, including cortex all the way to the cingulate sulcus (e. g., C&S. p. 33, Nolt, p. 14; a&b. p. so [Fig. 3–6]; w&G, p. 208 [Fig. 5–24]. n&d, p. 7, 484 [Fig. 16–4]). Several other authors, however, describe this area on the medial surface of each hemisphere, extending back to the paracentral sulcus and down to the cingulate sulcus, as a separate gyms, called the “medial frontal gyms” (B&K. p. 217. W&W, p. 986 989; M&M, p. 54; also, “Gyrus frontal is medialis” in IANC, p. A71). Al least two authors are inconsistent in this regard. On p. 130, Romero-Sierra (1986) states that “The cortex anterior to the paracentral sulcus and anterosuperior to the cingulate sulcus is part of the superior frontal gyrus”, however, in Fig. 8–5 (p. 130), he labels this area as “medial frontal gyrus.” Similarly, Snell states that “The cingulate gyrus is separated from the superior frontal gyrus by the cingulate sulcus” (1980, p. 236); but. in Fig. 14–3 (ibid.), he labels that area as the “Medial frontal gyms.”
Postoperative Focal Lower Extremity Supplementary Motor Area Syndrome: Case Report and Review of the Literature
Published in The Neurodiagnostic Journal, 2021
Nicholas B. Dadario, Joanna K. Tabor, Justin Silverstein, Xiaonan R. Sun, Randy S. DAmico
The supplementary motor area (SMA) is found bilaterally within the posterior frontal lobe in the medial frontal gyrus. The SMA is bordered posteriorly by primary motor cortex and inferiorly by the cingulate sulcus and cingulate, and the genu of the corpus callosum. Cortical models suggest that the SMA demonstrates extensive connections within and outside of the motor network and participates in a variety of functions Briggs et al. (2021). Primarily, the SMA is involved in the initiation and coordination of internal and externally cued movements – especially speech and bilateral motor control (Sheets et al. 2021; Vergani et al. 2014). Recent data suggest that the SMA is part of a prefrontal cognitive initiation “axis” in the medial frontal lobe where it coordinates with the default mode network and salience network to execute goal-directed behavior (Poologaindran et al. 2020).
Cortico-limbic connectivity as a possible biomarker for bipolar disorder: where are we now?
Published in Expert Review of Neurotherapeutics, 2019
Benedetta Vai, Carlotta Bertocchi, Francesco Benedetti
Abnormalities within fronto-limbic structures have been proposed as the neurological underpinning of bipolar emotional and mood dysregulation [67,68]. These are functionally characterized by a hyperactivated emotional ventral system, which includes amygdala (Amy), insula, ventral striatum (VS), ACC and PFC, and by a hypoactivated dorsal system, which includes hippocampus, dorsal ACC and dorsolateral PFC (DLPFC), areas usually recruited for planning and explicit regulation of emotional states. The unbalanced homeostasis between these two systems might trigger the unstable cognitive control of emotions and affect in BD [69]. These regions interact in regulating affective states and in defining the emotional significance of stimuli [69]. The PFC plays a key role in regulating the intensity of emotional responses [70,71], especially amygdala response, a critical area for perceiving stimuli with affective salience [72,73]. An erratic amygdala activity might result from a reduced control of cortical regions, contributing to mood lability [74]. Two meta-analyses confirmed a reduced activation in VLPFC in BD compared to HC during cognitive and emotional processing, paralleled by an overactivation of the limbic areas (parahippocampal gyrus, hippocampus, amygdala), thalamus and basal ganglia [75,76]. Differentiating among mood states, VLPFC abnormalities were confirmed only in mania, whereas euthymia was characterized by an increased amygdala activation [75]. Another meta-analysis confirmed a reduced neural response in superior and medial frontal gyrus, and in the insula [77].
Epidemiology, characterization, and diagnosis of neuropsychiatric events in systemic lupus erythematosus
Published in Expert Review of Clinical Immunology, 2019
Jaqueline Cristina de Amorim, Renan Bazuco Frittoli, Danilo Pereira, Mariana Postal, Sergio San Juan Dertkigil, Fabiano Reis, Lilian TL Costallat, Simone Appenzeller
Mood disorders are the second most frequent NP manifestation observed in SLE occurring in up to 20% of SLE patients [14,36]. Mood disorders are of multifactorial etiology. They may occur in isolation or in association with other NP manifestations and influences negatively quality of life [36,37]. Several factors have been associated with mood disorders including anti-ribosomal P antibodies, serum antiendothelial antibodies (AECA), antiphospholipid antibodies (aPL) and TNF alfa [38–42]. Development of mood disorders or worsening of mood disorders may be associated with treatment, such as corticosteroids and hydroxicloroquine use [43]. Neuroimaging studies have shown hypometabolism in the medial frontal gyrus in SLE patients with major depressive disorder [44].