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Neuroscience and Biobehavioral Reviews May 2020Akinetic mutism (AM) is a rare neurological disorder characterized by the presence of an intact level of consciousness and sensorimotor capacity, but with a simultaneous... (Review)
Review
Akinetic mutism (AM) is a rare neurological disorder characterized by the presence of an intact level of consciousness and sensorimotor capacity, but with a simultaneous decrease in goal-directed behavior and emotions. Patients are in a wakeful state of profound apathy, seemingly indifferent to pain, thirst, or hunger. It represents the far end within the spectrum of disorders of diminished motivation. In recent years, more has become known about the functional roles of neurocircuits and neurotransmitters associated with human motivational behavior. More specific, there is an increasing body of behavioral evidence that links specific damage of functional frontal-subcortical organization to the occurrence of distinct neurological deficits. In this review, we combine evidence from lesion studies and neurophysiological evidence in animals, imaging studies in humans, and clinical investigations in patients with AM to form an integrative theory of its pathophysiology. Moreover, the specific pharmacological interventions that have been used to treat AM and their rationales are reviewed, providing a comprehensive overview for use in clinical practice.
Topics: Adrenergic Uptake Inhibitors; Akinetic Mutism; Animals; Dopamine Agonists; Dopamine Uptake Inhibitors; Dopaminergic Neurons; GABA-A Receptor Agonists; Gray Matter; Humans; Motivation; Zolpidem
PubMed: 32044373
DOI: 10.1016/j.neubiorev.2020.02.006 -
BMC Psychiatry Apr 2023Previous studies discovered the presence of abnormal structures and functions in the brain regions of patients with obsessive-compulsive disorder (OCD). Nevertheless,...
BACKGROUND
Previous studies discovered the presence of abnormal structures and functions in the brain regions of patients with obsessive-compulsive disorder (OCD). Nevertheless, whether structural changes in brain regions are coupled with alterations in dynamic functional connectivity (dFC) at rest in medicine-free patients with OCD remains vague.
METHODS
Three-dimensional T-weighed magnetic resonance imaging (MRI) and resting-state functional MRI were performed on 50 medicine-free OCD and 50 healthy controls (HCs). Firstly, the differences in gray matter volume (GMV) between OCD and HCs were compared. Then, brain regions with aberrant GMV were used as seeds for dFC analysis. The relationship of altered GMV and dFC with clinical parameters in OCD was explored using partial correlation analysis. Finally, support vector machine was applied to examine whether altered multimodal imaging data might be adopted to distinguish OCD from HCs.
RESULTS
Our findings indicated that GMV in the left superior temporal gyrus (STG) and right supplementary motor area (SMA) was reduced in OCD, and the dFC between the left STG and the left cerebellum Crus I and left thalamus, and between the right SMA and right dorsolateral prefrontal cortex (DLPFC) and left precuneus was decreased at rest in OCD. The brain regions both with altered GMV and dFC values could discriminate OCD from HCs with the accuracy of 0.85, sensitivity of 0.90 and specificity of 0.80.
CONCLUSION
The decreased gray matter structure coupling with dynamic function in the left STG and right SMA at rest may be crucial in the pathophysiology of OCD.
TRIAL REGISTRATION
Study on the mechanism of brain network in obsessive-compulsive disorder with multi-model magnetic resonance imaging (registration date: 08/11/2017; registration number: ChiCTR-COC-17,013,301).
Topics: Humans; Gray Matter; Cerebral Cortex; Brain; Parietal Lobe; Magnetic Resonance Imaging; Obsessive-Compulsive Disorder
PubMed: 37098479
DOI: 10.1186/s12888-023-04740-w -
Journal of Alzheimer's Disease : JAD 2024The potential neuroprotective effects of regular physical activity on brain structure are unclear, despite links between activity and reduced dementia risk.
BACKGROUND
The potential neuroprotective effects of regular physical activity on brain structure are unclear, despite links between activity and reduced dementia risk.
OBJECTIVE
To investigate the relationships between regular moderate to vigorous physical activity and quantified brain volumes on magnetic resonance neuroimaging.
METHODS
A total of 10,125 healthy participants underwent whole-body MRI scans, with brain sequences including isotropic MP-RAGE. Three deep learning models analyzed axial, sagittal, and coronal views from the scans. Moderate to vigorous physical activity, defined by activities increasing respiration and pulse rate for at least 10 continuous minutes, was modeled with brain volumes via partial correlations. Analyses adjusted for age, sex, and total intracranial volume, and a 5% Benjamini-Hochberg False Discovery Rate addressed multiple comparisons.
RESULTS
Participant average age was 52.98±13.04 years (range 18-97) and 52.3% were biologically male. Of these, 7,606 (75.1%) reported engaging in moderate or vigorous physical activity approximately 4.05±3.43 days per week. Those with vigorous activity were slightly younger (p < 0.00001), and fewer women compared to men engaged in such activities (p = 3.76e-15). Adjusting for age, sex, body mass index, and multiple comparisons, increased days of moderate to vigorous activity correlated with larger normalized brain volumes in multiple regions including: total gray matter (Partial R = 0.05, p = 1.22e-7), white matter (Partial R = 0.06, p = 9.34e-11), hippocampus (Partial R = 0.05, p = 5.96e-7), and frontal, parietal, and occipital lobes (Partial R = 0.04, p≤1.06e-5).
CONCLUSIONS
Exercise-related physical activity is associated with increased brain volumes, indicating potential neuroprotective effects.
Topics: Humans; Male; Female; Aged; Aged, 80 and over; Neuroprotective Agents; Brain; Gray Matter; Magnetic Resonance Imaging; Exercise
PubMed: 38073389
DOI: 10.3233/JAD-230740 -
Seminars in Perinatology Aug 2022While intraventricular hemorrhage (IVH) predominantly damages the periventricular white matter, it induces substantial injury to the cerebral gray matter. IVH destroys... (Review)
Review
While intraventricular hemorrhage (IVH) predominantly damages the periventricular white matter, it induces substantial injury to the cerebral gray matter. IVH destroys the germinal matrix, suppresses neurogenesis, and disrupts corticogenesis, thereby reducing the number of neurons in the upper cortical layer and volume of the cerebral gray matter. The pathogenesis of gray matter injury is attributed to IVH-induced oxidative stress, inflammation, and mass effect damaging the germinal matrix as well as to post-hemorrhagic ventricular dilation (PHVD). The IVH-induced cerebral gray matter injury and PHVD contribute to cognitive deficits and neurobehavioral disorders. Neuroimaging has enhanced our understanding of cerebral gray matter injury and is a valuable predictor of neurodevelopmental outcomes. Evidence from therapies tested in preclinical models and clinical trials suggests that strategies to promote neurogenesis, reduce cerebral inflammation and oxidative stress, and remove blood clots from the ventricles might enhance the outcome of these infants. This review offers an integrated view of new insights into the mechanisms underlying gray matter injury in premature infants with IVH and highlights the imminent therapies to restore neurodevelopmental dysfunction in IVH survivors.
Topics: Cerebral Hemorrhage; Cerebral Ventricles; Gray Matter; Humans; Infant; Infant, Newborn; Infant, Premature, Diseases; Inflammation
PubMed: 35418320
DOI: 10.1016/j.semperi.2022.151595 -
Frontiers in Endocrinology 2021Subclinical hypothyroidism (SCH) brain structure and resting state of functional activity have remained unexplored.
BACKGROUND
Subclinical hypothyroidism (SCH) brain structure and resting state of functional activity have remained unexplored.
PURPOSE
To investigate gray matter volume (GMV) and regional brain activity with the fractional amplitude of low-frequency fluctuations (fALFF) in subclinical hypothyroidism (SCH) patients before and after treatment.
MATERIAL AND METHODS
We enrolled 54 SCH and 41 age-, sex-, and education-matched controls. GMV and fALFF of SCH were compared with controls and between pre- and post-treatment within SCH group. Correlations of GMV and fALFF in SCH with thyroid function status and mood scales were assessed by multiple linear regression analysis.
RESULTS
Compared to controls, GMV in SCH was significantly decreased in Orbital part of inferior frontal, superior frontal, pre-/postcentral, inferior occipital, and temporal pole gyrus. FALFF values in SCH were significantly increased in right angular, left middle frontal, and left superior frontal gyrus. After treatment, there were no significant changes in GMV and the local brain function compared to pre-treatment, however the GMV and fALFF of the defective brain areas were improved. Additionally, decreased values of fALFF in left middle frontal gyrus were correlated with increased mood scales.
CONCLUSION
In this study we found that patients with SCH, the gray matter volume in some brain areas were significantly reduced, and regional brain activity was significantly increased. After treatment, the corresponding structural and functional deficiencies had a tendency for improvement. These changes may reveal the neurological mechanisms of mood disorder in SCH patients.
Topics: Adult; Asymptomatic Diseases; Brain; Brain Mapping; Case-Control Studies; China; Female; Gray Matter; Humans; Hypothyroidism; Magnetic Resonance Imaging; Male; Middle Aged; Neuroimaging; Organ Size; Thyroid Function Tests; Young Adult
PubMed: 33716959
DOI: 10.3389/fendo.2021.582519 -
Proceedings of the National Academy of... Oct 2023Recent studies have revealed the production of time-locked blood oxygenation level-dependent (BOLD) functional MRI (fMRI) signals throughout the entire brain in response...
Recent studies have revealed the production of time-locked blood oxygenation level-dependent (BOLD) functional MRI (fMRI) signals throughout the entire brain in response to tasks, challenging the existence of sparse and localized brain functions and highlighting the pervasiveness of potential false negative fMRI findings. "Whole-brain" actually refers to gray matter, the only tissue traditionally studied with fMRI. However, several reports have demonstrated reliable detection of BOLD signals in white matter, which have previously been largely ignored. Using simple tasks and analyses, we demonstrate BOLD signal changes across the whole brain, in both white and gray matters, in similar manner to previous reports of whole brain studies. We investigated whether white matter displays time-locked BOLD signals across multiple structural pathways in response to a stimulus in a similar manner to the cortex. We find that both white and gray matter show time-locked activations across the whole brain, with a majority of both tissue types showing statistically significant signal changes for all task stimuli investigated. We observed a wide range of signal responses to tasks, with different regions showing different BOLD signal changes to the same task. Moreover, we find that each region may display different BOLD responses to different stimuli. Overall, we present compelling evidence that, just like all gray matter, essentially all white matter in the brain shows time-locked BOLD signal changes in response to multiple stimuli, challenging the idea of sparse functional localization and the prevailing wisdom of treating white matter BOLD signals as artifacts to be removed.
Topics: White Matter; Brain Mapping; Brain; Gray Matter; Magnetic Resonance Imaging
PubMed: 37824529
DOI: 10.1073/pnas.2219666120 -
Aging Aug 2021To investigate the interplay between gray matter (GM) and white matter (WM) neurodegeneration in subjective cognitive decline (SCD), including thickness across the whole...
AIMS
To investigate the interplay between gray matter (GM) and white matter (WM) neurodegeneration in subjective cognitive decline (SCD), including thickness across the whole cortical mantle, hippocampal volume, and integrity across the whole WM.
METHODS
We included 225 cognitively unimpaired individuals from a community-based cohort. Subjective cognitive complaints were assessed through 9 questions covering amnestic and non-amnestic cognitive domains. In our cohort, 123 individuals endorsed from one to six subjective cognitive complaints (i.e. they fulfilled the diagnostic criteria for SCD), while 102 individuals reported zero complaints. GM neurodegeneration was assessed through measures of cortical thickness across the whole mantle and hippocampal volume. WM neurodegeneration was assessed through measures of mean diffusivity (MD) across the whole WM skeleton. Mediation analysis and multiple linear regression were conducted to investigate the interplay between the measures of GM and WM neurodegeneration.
RESULTS
A higher number of complaints was associated with reduced hippocampal volume, cortical thinning in several frontal and temporal areas and the insula, and higher MD across the WM skeleton, with a tendency to spare the occipital lobe. SCD-related cortical thinning and increased MD were associated with each other and jointly contributed to complaints, but the contribution of cortical thinning to the number of complaints was stronger.
CONCLUSIONS
Neurodegeneration processes affecting the GM and WM seem to be associated with each other in SCD and include brain areas other than those typically targeted by Alzheimer's disease. Our findings suggest that SCD may be a sensitive behavioral marker of heterogeneous brain pathologies in individuals recruited from the community.
Topics: Adult; Aged; Cognition; Cognitive Dysfunction; Cohort Studies; Female; Gray Matter; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Neuropsychological Tests; Spain; White Matter
PubMed: 34433132
DOI: 10.18632/aging.203467 -
Human Brain Mapping Dec 2017Inter-hemispheric asymmetries are a common phenomenon of the human brain. Some evidence suggests that neurodegeneration related to aging and disease may preferentially... (Meta-Analysis)
Meta-Analysis Review
Inter-hemispheric asymmetries are a common phenomenon of the human brain. Some evidence suggests that neurodegeneration related to aging and disease may preferentially affect the left-usually language- and motor-dominant-hemisphere. Here, we used activation likelihood estimation meta-analysis to assess gray matter (GM) loss and its lateralization in healthy aging and in neurodegeneration, namely, mild cognitive impairment (MCI), Alzheimer's dementia (AD), Parkinson's disease (PD), and Huntington's disease (HD). This meta-analysis, comprising 159 voxel-based morphometry publications (enrolling 4,469 patients and 4,307 controls), revealed that GM decline appeared to be asymmetric at trend levels but provided no evidence for increased left-hemisphere vulnerability. Regions with asymmetric GM decline were located in areas primarily affected by neurodegeneration. In HD, the left putamen showed converging evidence for more pronounced atrophy, while no consistent pattern was found in PD. In MCI, the right hippocampus was more atrophic than its left counterpart, a pattern that reversed in AD. The stability of these findings was confirmed using permutation tests. However, due to the lenient threshold used in the asymmetry analysis, further work is needed to confirm our results and to provide a better understanding of the functional role of GM asymmetries, for instance in the context of cognitive reserve and compensation. Hum Brain Mapp 38:5890-5904, 2017. © 2017 Wiley Periodicals, Inc.
Topics: Aging; Brain; Functional Laterality; Gray Matter; Humans; Neurodegenerative Diseases
PubMed: 28856766
DOI: 10.1002/hbm.23772 -
AJNR. American Journal of Neuroradiology Jul 2021Modifications of magnetic susceptibility have been consistently demonstrated in the subcortical gray matter of MS patients, but some uncertainties remain concerning the...
BACKGROUND AND PURPOSE
Modifications of magnetic susceptibility have been consistently demonstrated in the subcortical gray matter of MS patients, but some uncertainties remain concerning the underlying neurobiological processes and their clinical relevance. We applied quantitative susceptibility mapping and longitudinal relaxation rate relaxometry to clarify the relative contribution of atrophy and iron and myelin changes to deep gray matter damage and disability in MS.
MATERIALS AND METHODS
Quantitative susceptibility mapping and longitudinal relaxation rate maps were computed for 91 patients and 55 healthy controls from MR images acquired at 3T. Applying an external model, we estimated iron and myelin concentration maps for all subjects. Subsequently, changes of deep gray matter iron and myelin concentration (atrophy-dependent) and content (atrophy-independent) were investigated globally (bulk analysis) and regionally (voxel-based and atlas-based thalamic subnuclei analyses). The clinical impact of the observed MRI modifications was evaluated via regression models.
RESULTS
We identified reduced thalamic (< .001) and increased pallidal (< .001) mean iron concentrations in patients with MS versus controls. Global myelin and iron content in the basal ganglia did not differ between the two groups, while actual iron depletion was present in the thalamus (< .001). Regionally, patients showed increased iron concentration in the basal ganglia (≤ .001) and reduced iron and myelin content in thalamic posterior-medial regions (≤ .004), particularly in the pulvinar (≤ .001). Disability was predicted by thalamic volume (B = -0.341, = .02), iron concentration (B = -0.379, = .005) and content (B = -0.406, = .009), as well as pulvinar iron (B = -0.415, = .003) and myelin (B = -0.415, = .02) content, independent of atrophy.
CONCLUSIONS
Quantitative MRI suggests an atrophy-related iron increase within the basal ganglia of patients with MS, along with an atrophy-independent reduction of thalamic iron and myelin correlating with disability. Absolute depletions of thalamic iron and myelin may represent sensitive markers of subcortical GM damage, which add to the clinical impact of thalamic atrophy in MS.
Topics: Atrophy; Brain; Brain Chemistry; Gray Matter; Humans; Iron; Magnetic Resonance Imaging; Multiple Sclerosis; Myelin Sheath
PubMed: 33888456
DOI: 10.3174/ajnr.A7093 -
Asian Journal of Psychiatry Aug 2022Gray matter abnormalities have been widely reported in individuals with and at familial risk for bipolar disorder (BD). However, inconsistent findings were reported, and... (Meta-Analysis)
Meta-Analysis Review
Gray matter abnormalities and associated familial risk endophenotype in individuals with first-episode bipolar disorder: Evidence from whole-brain voxel-wise meta-analysis.
Gray matter abnormalities have been widely reported in individuals with and at familial risk for bipolar disorder (BD). However, inconsistent findings were reported, and whether shared abnormalities exist between at-risk individuals and patients which can represent an endophenotype remained unclear. This meta-analysis aimed at identifying robust patterns of gray matter changes in patients with first-episode BD (FEBD) and associated risk endophenotype of BD. A systematic literature search was performed to identify eligible voxel-based morphometry studies comparing FEBD patients and healthy controls. Findings of included studies were integrated using the Seed-based d Mapping toolbox. Common and distinct patterns of gray matter abnormalities between FEBD patients and unaffected at-risk individuals were explored. A total of 16 VBM studies comparing 411 FEBD patients and 521 controls were included. FEBD patients showed increased gray matter volume in the cerebellum, posterior cingulate cortex and striatum, and decreased gray matter volume in the medial superior frontal gyrus and gyrus rectus. No common abnormalities were identified between FEBD patients and unaffected at-risk individuals. More gray matter loss in the medial superior frontal gyrus and insula were found in FEBD patients relative to unaffected at-risk individuals. These findings revealed robust gray matter abnormalities in the cortico-striato-cerebellar and default mode network regions in FEBD, and implicated that gray matter deficits may not represent a familial risk endophenotype of BD.
Topics: Bipolar Disorder; Brain; Endophenotypes; Genetic Predisposition to Disease; Gray Matter; Humans; Magnetic Resonance Imaging
PubMed: 35691059
DOI: 10.1016/j.ajp.2022.103179