scholarly journals Diverse Pathophysiological Processes Converge on Network Disruption in Mania

2018 ◽  
Author(s):  
Ivy Lee ◽  
Kathryn Nielsen ◽  
Mei-Hua Hall ◽  
Dost Öngür ◽  
Matcheri Keshavan ◽  
...  

AbstractBackgroundNeuroimaging of psychiatric disease is challenged by the difficulty of establishing the causal role of neuroimaging abnormalities. Lesions that cause mania present a unique opportunity to understand how brain network disruption may cause mania in both lesions and in bipolar disorder.MethodsA literature search revealed 23 case reports with imaged lesions that caused mania in patients without history of bipolar disorder. We traced these lesions and examined resting-state functional Magnetic Resonance Imaging (rsfMRI) connectivity to these lesions and control lesions to find networks that would be disrupted specifically by mania-causing lesions. The results were then used as regions-of-interest to examine rsfMRI connectivity in patients with bipolar disorder (n=16) who underwent imaging longitudinally across states of both mania and euthymia alongside a cohort of healthy participants scanned longitudinally. We then sought to replicate these results in independent cohorts of manic (n=26) and euthymic (n=21) participants with bipolar disorder.ResultsMania-inducing lesions overlap significantly in network connectivity. Mania-causing lesions selectively disrupt networks that include orbitofrontal cortex, dorsolateral prefrontal cortex, and temporal lobes. In bipolar disorder, the manic state was reflected in strong, significant, and specific disruption in network communication between these regions and regions implicated in bipolar pathophysiology: the amygdala and ventro-lateral prefrontal cortex.LimitationsThe was heterogeneity in the clinical characterization of mania causing lesions.ConclusionsLesions causing mania demonstrate shared and specific network disruptions. These disruptions are also observed in bipolar mania and suggest a convergence of multiple disorders on shared circuit dysfunction to cause mania.


2005 ◽  
Vol 86 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Paolo Brambilla ◽  
Jeffrey A. Stanley ◽  
Mark A. Nicoletti ◽  
Roberto B. Sassi ◽  
Alan G. Mallinger ◽  
...  


2019 ◽  
Vol 54 (3) ◽  
pp. 1900362 ◽  
Author(s):  
Ayaka Ando ◽  
Stuart B. Mazzone ◽  
Michael J. Farrell

Cough is important for airway defence, and studies in healthy animals and humans have revealed multiple brain networks intimately involved in the perception of airway irritation, cough induction and cough suppression. Changes in cough sensitivity and/or the ability to suppress cough accompany pulmonary pathologies, suggesting a level of plasticity is possible in these central neural circuits. However, little is known about how persistent inputs from the lung might modify the brain processes regulating cough.In the present study, we used human functional brain imaging to investigate the central neural responses that accompany an altered cough sensitivity in cigarette smokers.In nonsmokers, inhalation of the airway irritant capsaicin induced a transient urge-to-cough associated with the activation of a distributed brain network that included sensory, prefrontal and motor cortical regions. Cigarette smokers demonstrated significantly higher thresholds for capsaicin-induced urge-to-cough, consistent with a reduced sensitivity to airway irritation. Intriguingly, this was accompanied by increased activation in brain regions known to be involved in both cough sensory processing (primary sensorimotor cortex) and cough suppression (dorsolateral prefrontal cortex and the midbrain nucleus cuneiformis). Activations in the prefrontal cortex were highest among participants with the least severe smoking behaviour, whereas those in the midbrain correlated with more severe smoking behaviour.These outcomes suggest that smoking-induced sensitisation of central cough neural circuits is offset by concurrently enhanced central suppression. Furthermore, central suppression mechanisms may evolve with the severity of smoke exposure, changing from initial prefrontal inhibition to more primitive midbrain processes as exposure increases.



2020 ◽  
Vol 87 (9) ◽  
pp. S434-S435
Author(s):  
Man Choi Ho ◽  
Alejandra Cabello Arreola ◽  
Aysegul Ozerdem ◽  
Craig A. Stockmeier ◽  
Grazyna Rajkowska ◽  
...  


2015 ◽  
Vol 206 (2) ◽  
pp. 136-144 ◽  
Author(s):  
Edith Pomarol-Clotet ◽  
Silvia Alonso-Lana ◽  
Noemi Moro ◽  
Salvador Sarró ◽  
Mar C. Bonnin ◽  
...  

BackgroundLittle is known about how functional imaging changes in bipolar disorder relate to different phases of the illness.AimsTo compare cognitive task activation in participants with bipolar disorder examined in different phases of illness.MethodParticipants with bipolar disorder in mania (n = 38), depression (n = 38) and euthymia (n = 38), as well as healthy controls (n = 38), underwent functional magnetic resonance imaging during performance of the n-back working memory task. Activations and de-activations were compared between the bipolar subgroups and the controls, and among the bipolar subgroups. All participants were also entered into a linear mixed-effects model.ResultsCompared with the controls, the mania and depression subgroups, but not the euthymia subgroup, showed reduced activation in the dorsolateral prefrontal cortex, the parietal cortex and other areas. Compared with the euthymia subgroup, the mania and depression subgroups showed hypoactivation in the parietal cortex. All three bipolar subgroups showed failure of de-activation in the ventromedial frontal cortex. Linear mixed-effects modelling revealed a further cluster of reduced activation in the left dorsolateral prefrontal cortex in the patients; this was significantly more marked in the mania than in the euthymia subgroup.ConclusionsBipolar disorder is characterised by mood state-dependent hypoactivation in the parietal cortex. Reduced dorsolateral prefrontal activation is a further feature of mania and depression, which may improve partially in euthymia. Failure of de-activation in the medial frontal cortex shows trait-like characteristics.



2010 ◽  
Vol 22 (10) ◽  
pp. 2263-2275 ◽  
Author(s):  
Michal Zaretsky ◽  
Avi Mendelsohn ◽  
Matti Mintz ◽  
Talma Hendler

Interpretation of emotional context is a pivotal aspect of understanding social situations. A critical component of this process is assessment of danger levels in the surrounding, which may have a direct effect on the organism's survival. The limbic system has been implicated in mediating this assessment. In situations of uncertainty, the evaluation process may also call for greater involvement of prefrontal cortex for decision-making and planning of an appropriate behavioral response. In the following study, morphed face images depicting emotional expressions were used to examine brain correlates of subjective uncertainty and perceptual ambiguity regarding danger. Fear and neutral expressions of 20 faces were morphed, and each of the face videos was divided into three sequences of equal length representing three levels of objective certainty regarding the expressions neutral, fear, and ambiguous. Sixteen subjects were scanned in a 1.5-T scanner while viewing 60 × 6-sec video sequences and were asked to report their subjective certainty regarding the level of danger surrounding the face on a four-level scale combining definite/maybe and danger/no-danger values. The individual responses were recorded and used as the basis for a “subjective protocol” versus an “objective protocol.” Significant activations of the amygdala, dorsomedial prefrontal cortex, and dorsolateral prefrontal cortex were observed under the subjective protocol of internally driven uncertainty, but not under objective stimuli-based ambiguity. We suggest that this brain network is involved in generating subjective assessment of social affective cues. This study provides further support to the “relevance detector” theory of the amygdala and implicates its importance to behavior relying heavily on subjective assessment of danger, such as in the security domain context.



2011 ◽  
Vol 42 (2) ◽  
pp. 295-307 ◽  
Author(s):  
E. Bora ◽  
A. Fornito ◽  
M. Yücel ◽  
C. Pantelis

BackgroundRecent evidence from genetic and familial studies revitalized the debate concerning the validity of the distinction between schizophrenia and bipolar disorder. Comparing brain imaging findings is an important avenue to examine similarities and differences and, therefore, the validity of the distinction between these conditions. However, in contrast to bipolar disorder, most patient samples in studies of schizophrenia are predominantly male. This a limiting factor for comparing schizophrenia and bipolar disorder since male gender is associated with more severe neurodevelopmental abnormalities, negative symptoms and cognitive deficits in schizophrenia.MethodWe used a coordinate-based meta-analysis technique to compare grey matter (GM) abnormalities in male-dominated schizophrenia, gender-balanced schizophrenia and bipolar disorder samples based on published voxel-based morphometry (VBM) studies. In total, 72 English-language, peer reviewed articles published prior to January 2011 were included. All reports used VBM for comparing schizophrenia or bipolar disorder with controls and reported whole-brain analyses in standard stereotactic space.ResultsGM reductions were more extensive in male-dominated schizophrenia compared to gender-balanced bipolar disorder and schizophrenia. In gender-balanced samples, GM reductions were less severe. Compared to controls, GM reductions were restricted to dorsal anterior cingulate cortex (ACC) and dorsolateral prefrontal cortex in schizophrenia and ACC and bilateral fronto-insular cortex in bipolar disorder.ConclusionsWhen gender is controlled, GM abnormalities in bipolar disorder and schizophrenia are mostly restricted to regions that have a role in emotional and cognitive aspects of salience respectively. Dorsomedial and dorsolateral prefrontal cortex were the only regions that showed greater GM reductions in schizophrenia compared to bipolar disorder.



Author(s):  
Doğancan Sönmez ◽  
Burak Okumuş ◽  
Çiçek Hocaoğlu

Stressful or traumatic life events can lead to emergence of mood episodes. Events such as migration, relocation, job loss, bankruptcy, economic loss, divorce, natural disasters, accidental injury, or the loss of a loved one can trigger the first episode of bipolar disorder. After such life events, symptoms of depressive episodes often appear. Funeral mania, on the other hand, is defined as the emergence of manic episodes following the death of a close family member. Information on funeral mania, which occurs shortly after the loss of a loved one, is limited with a few case reports. In this study, a 26-year-old female patient who presented with the symptoms of a manic episode for the first time after her father’s death and who had no previous psychiatric disease or treatment history was presented in the light of findings in the literature. It is noteworthy that the patient, who was followed up with the diagnosis of bipolar disorder (mania period) according to DSM-5 diagnostic criteria, had a temporal closeness between her mood symptoms and her father’s death, and had not developed such a reaction to previous traumatic life events. Therefore, the diagnosis was evaluated as funeral mania. It should be kept in mind that, although rare, symptoms of mania can be seen among possible grief reactions



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