Which Changes In Brain Biochemical Function Is Most Associated With Suicidal Behavior?
CNS Neurosci Ther. 2018 November; 24(11): 994–1003.
Brain structure alterations in depression: Psychoradiological evidence
Fei‐Fei Zhang
1 Huaxi MR Enquiry Center (HMRRC), Department of Radiology, Due west China Infirmary of Sichuan University, Chengdu, China
Wei Peng
1 Huaxi MR Research Center (HMRRC), Department of Radiology, West Mainland china Hospital of Sichuan University, Chengdu, China
John A. Sweeney
1 Huaxi MR Research Middle (HMRRC), Section of Radiology, West China Hospital of Sichuan University, Chengdu, China
2 Department of Psychiatry and Behavioral Neuroscience, Academy of Cincinnati, Cincinnati, OH, USA
Zhi‐Yun Jia
1 Huaxi MR Inquiry Center (HMRRC), Department of Radiology, West People's republic of china Infirmary of Sichuan University, Chengdu, Communist china
3 Department of Nuclear Medicine, West Communist china Hospital, Sichuan Academy, Chengdu, Cathay
Qi‐Yong Gong
ane Huaxi MR Research Middle (HMRRC), Section of Radiology, West China Hospital of Sichuan University, Chengdu, China
4 Section of Psychology, School of Public Administration, Sichuan University, Chengdu, China
Received 2017 Nov 30; Revised 2018 Feb 7; Accepted 2018 February 8.
Summary
Depression is the leading cause of disability effectually the world, just lilliputian is known most its pathology. Currently, the diagnosis of depression is made based on clinical manifestations, with little objective show. Magnetic resonance imaging (MRI) has been used to investigate the pathological changes in brain anatomy associated with this disorder. MRI can identify structural alterations in depressive patients in vivo, which could make considerable contributions to clinical diagnosis and treatment. Numerous studies that focused on greyness and white thing have found significant encephalon region alterations in major depressive disorder patients, such as in the frontal lobe, hippocampus, temporal lobe, thalamus, striatum, and amygdala. The results are inconsistent and controversial because of the different demographic and clinical characteristics. All the same, some regions overlapped; thus, nosotros think that in that location may be a "hub" in MDD and that an harm in these regions contributes to disease severity. Brain connections incorporate both structural connections and functional connections, which reflect disease from a different view and back up that MDD may be caused by the interaction of multiple brain regions. According to previous reports, significant circuits include the frontal‐subcortical circuit, the suicide circuit, and the reward circuit. As has been recognized, the pathophysiology of major depressive disorder is circuitous and changeable. The electric current review focuses on the significant alterations in the greyness and white matter of patients with the depressive disorder to generate a amend understanding of the circuits. Moreover, identifying the nuances of depressive disorder and finding a biomarker volition make a significant contribution to the guidance of clinical diagnosis and treatment.
Keywords: Psychoradiology, improvidence MRI; magnetic resonance imaging; major depressive disorder; construction MRI
1. INTRODUCTION
Major depressive disorder (MDD) is characterized by persistent low mood, ofttimes accompanied by cognitive dysfunction, physical symptoms, and impaired social function.1 According to the Globe Health System'south statistics, more 300 meg people worldwide suffer from low. More severely, low can cause suicide, and nearly 800 000 people die every twenty-four hours due to suicide. According to statistics from 2015,2 suicide is the 2d leading crusade of expiry amid people 15‐29 years of age, resulting in vast economic and social burdens. Based on epidemiological studies, more than than 30% of patients with depression suffer from ineffective antidepressant treatments, and their lifetime prevalence charge per unit is approximately 16.two%.3 Currently, the diagnosis of MDD relies on patients' reporting and behavioral assessments. Little is known almost its precise neurobiological biomarkers. Neuroimaging studies have the advantage of beingness noninvasive and repeatable and might provide precise evidence to clinics for more successful individualized therapies.
In recent years, neuroimaging methods, especially magnetic resonance imaging (MRI), have been used in many studies to identify disorder‐related patterns of the encephalon changes associated with MDD. The MRI browse sequences that are commonly used by researchers include high‐resolution structural imaging (3D‐T1), which depicts gray thing thickness in volume and brain morphology; diffusion tensor imaging (DTI), which depicts the microstructure of the white matter; and functional magnetic resonance imaging (fMRI), which depicts the neuronal activity in target brain regions. Previous studies based on MRI institute that several encephalon regions are significantly impaired in MDD patients. Several regional gray matter changes accept been identified in the frontal lobe, parietal lobe, thalamus, caudate, pallidum, putamen, and temporal lobes (eg, the hippocampus and amygdala)4, 5, 6 by anatomical MRI studies. DTI studies have shown white matter alterations, such equally decreased fractional anisotropy (FA) in the cingulum,7 hippocampus, parietal regions,8 inferior temporal gyrus, and superior frontal gyrus. These findings were confirmed by a contempo meta‐assay.9 In addition, abnormal brain activity was found in the prefrontal cortex,10 occipital lobe,11 temporal gray, caudate,12 and putamen.xiii Different brain regions accept connections with each other and ultimately form complex encephalon networks. A hub is a region that is highly connected and highly cardinal that plays a role in global data integration14 (Effigy1). The impairment of hub nodes or their connections may be a leading cause of disease, such equally MDD. Structural connections between cortical and subcortical areas compose several circuits, such every bit the frontal‐subcortical circuit,xv basal ganglic‐thalamic‐cortical excursion,16 prefrontal hippocampus excursion,17 the limbic‐cortical‐striatal‐thalamic‐cortical circuit,18 and the limbic‐cortical‐striatal‐pallidal‐thalamic19 circuit. The almost common functional connection in MDD patients is the cortical‐subcortical excursion.twenty According to previous findings, the frontal lobe, parietal lobe, thalamus, putamen, and hippocampus are considered hubs in these circuits.xiv, 21, 22
Structural network hubs of the human brain. Structural brain hubs were identified by diffusion tensor imaging, and the nodes normalized to an intramodular degree higher than 1 were defined as hubs.14, 21 ACG, inductive cingulate and paracingulate gyri; CAL, calcarine cleft and surrounding cortex; HIP, hippocampus; INS, insula; Fifty, left; MOG, middle occipital gyrus; MTG, eye temporal gyrus; PCUN, precuneus; PUT, putamen; R, correct; SOG, superior occipital gyrus; SPG, superior parietal gyrus; SFGdor, dorsolateral part of the superior frontal gyrus; SFGmed, medial office of the superior frontal gyrus; THA, thalamus
In the present review, significant structural changes in brain regions and circuits involved in MDD are reviewed, and future inquiry directions in this field are outlined. This commodity focuses on the imaging findings of MDD to explore the findings of neuroimaging, which is helpful for differential diagnosis and accurate medicine.
2. Meaning STRUCTURAL Encephalon ALTERATIONS IN MDD
2.1. Frontal lobe
According to previous reports, the modify in the volume of frontal regions has been considered to be the most common region to manifest anatomic abnormalities in MDD. Of import prefrontal lesions include those of Brodmann surface area 24 (a role of the anterior cingulate cortex), orbitofrontal cortex (OFC), center prefrontal cortex, dorsolateral prefrontal cortex (DLPFC), and other areas of the prefrontal cortex.viii, 23, 24, 25, 26 The anterior cingulate cortex (ACC) has an anatomical connectedness with dorsal neocortical and ventral paralimbic regions and plays a role in cognitive processes and mood regulation.27 The right anterior cingulate cortex was reported to have a decreased magnetization transfer ratio in patients with handling‐refractory MDD relative to healthy controls,28 which increased later electroconvulsive therapy.29 Previous studies have also establish that prefrontal areas undergo a significant reduction in thickness,4, xxx, 31, 32 and these changes are thought to be associated with poor clinical outcomes.33 A negative correlation was observed between the Montgomery‐Asberg Depression Rating Calibration score and cortical thickness in the ACC.34 It has been indicated that the thicker correct caudal ACC is associated with greater symptom comeback across follow‐ups. According to an fMRI study, the ACC has increased functional correlations with the DLPFC and the amygdala35 in MDD patients, suggesting that the ACC is more than similar to a bridge between the DLPFC and the amygdala and plays a critical role in attention and emotion. The OFC is involved in inhibiting background‐contained, redundant, or uncomfortable neural activity, feelings, and behaviors and also plays a crucial part in emotional/motivational direction and decision making.36 It has been reported that the thickness of the right medial orbital cortex in MDD patients is thinner than that in healthy controls,37 and during treatment, increased cortical thickness was plant in the OFC in MDD patients. Functional MRI results found reduced brain activeness in the bilateral OFC.38 Structural and functional changes in the OFC may contribute to the reduced inhibition of negative stimuli in depressive patients. The book of grey matter in the left middle frontal gyrus was found to be decreased in untreated depressive patientsii and to increase after drug treatment.39 These changes are associated with emotional bias, aloofness, and loss of motivation.v The fibers in the medial frontal cortex are part of the default‐manner network40 and play an essential role in the execution of long‐term mental plans from immediate environmental or internal demands.41 A study constitute a reduction in both the middle frontal cortex and the connection of the corpus callosum in treatment‐refractory MDD.42 Fibers extending through the bilateral medial frontal lobe to the anterior corpus callosum and passing fibers connecting the medial frontal lobe to the amygdala via the uncinate fasciculus during stimulation of the "best" contacts accept been deemed to be the switch in MDD.43 The DLPFC plays an essential role in emotional, motivational, attentional, and executive functions.44 Gray affair book reductions have besides been plant in the DLPFC in MDD patients compared to good for you controls.2 Brain activity in the DLPFC was also found to be decreasedxiii and could be increased to the average level afterwards antidepressant treatment.2 Transcranial magnetic stimulation of the left DLPFC induces morphological increases in the left ACC and the heart frontal OFC,45 indicating that the DLPFC has connections with the ACC and the OFC.
2.2. Thalamus
The thalamus is considered a complicated sensory information node that controls emotion, memory, and arousal.46 Dysfunction and structural disruptions in the thalamus can lead to an amnestic syndrome due to impairments in recall and recognition.47 The thalamus is structured as several anatomical parts. The subthalamic nuclei accept fibers from the pallidum and motor cortex and send out fibers to the substantia nigra. The lateral dorsal thalamic nucleus sends out fibers to the parietal lobe, and the ventral lateral thalamic nucleus has connections with the cerebellum and the brainstem. Significant book reductions and changes in shape take been observed in the left thalamus48 of patients with MDD. Based on a shape assay of the vertex, the dorsal attribute of the left thalamus was found to exist negatively correlated with the severity of depression (Hamilton Depression Rating Calibration).48 A probabilistic tractography study reported that the areas with shape deformities in the bilateral putamen and left thalamus had connections with the frontal and temporal lobes.48 The gray affair volume of the right thalamus was likewise found to be reduced in MDD patients,42, 49 and this finding was confirmed by a recent meta‐analysis.fifty As some studies have shown, drugs and acute attacks can impact the book of the thalamus, which may suggest a land‐dependent manner of low.v As the anterior thalamic nuclei grade a key region involved in emotional regulation,48, 51 the decreased FA in these regions in MDD might contribute to emotional deregulation and could exist a target for diagnostic assessments and therapies.52, 53
2.iii. Striatum
The striatum is an of import office of basal ganglia.54 A big number of neuroimaging studies have reported significant changes in the striatum of MDD patients. Decreased greyness thing intensity in the ventral striatum55 was besides reported in MDD patients who committed suicide. Disruptions in striatal output may lead to impulsive and suicidal behavior.56 Functional magnetic resonance imaging has shown that striatal action was reduced in reward system defects,57 and decreased reward network connections were constitute to be associated with low severity.58 These findings suggest that abnormal striatal activity plays an essential part in disease progression. The striatum contains the putamen, the caudate, and the ventral striatum.47 The results of previous studies have shown that compared with a control group, the volume of the bilateral putamen decreased significantly in MDD patients.48 In add-on, structural alterations in the putamen may exist related to the consequence of drugs59 and the historic period of onset in MDD. According to previous results, the putamen plays a key role in mood, cerebral processes, motivation, and regulation of movement.lx The putamen is a component of the hate circuit61 and has connections with the OFC and the ACC.62 Increased functional activity in the putamen has been reported,13 which may lead to a weakening of the ability to control emotions and a low threshold of provoking feelings of hatred toward oneself or others. The caudate nucleus is a critical component of the reward system in the brain and is often associated with the treatment of reward stimuli.63 Information technology has been reported that the book of the caudate is reduced in MDD patients64 and that it has a negative correlation with disease severity. Reduced action was also reported in the caudate57 in patients with MDD. Dysfunction of the caudate nucleus may lead to a disruption in dopaminergic signaling, as this region receives inputs from the ventral tegmental dopaminergic neurons.65 Therefore, the decrease in the gray matter density in the right caudate nucleus66 of MDD patients can explain the core features of depression or even the lack of responsiveness to positive stimuli or reward constituents in patients with MDD.
two.iv. Parietal lobe
The parietal lobe is involved in the organization, decision making, and predictions of rewards during workout that evaluates outcomes for hereafter response choices that are uncertain.67 This region is also related to emotional processing and cognitive changes and is part of the default‐fashion network. Increased cortical thickness has been noted in the left inferior parietal gyrus68 in MDD patients compared to good for you controls, and morphometric correlation analysis found a positive caudate‐cortical connexion in the bilateral superior parietal lobe.68 The superior parietal lobe is office of the default‐way network. The default‐fashion network has a functional connection with the caudate via dopaminergic projections. Striatal dopaminergic circuits may regulate knowledge and emotion by modulating the DMN in MDD.68 Recently, our group observed a lower magnetization transfer ratio in the left superior parietal lobule in MDD patients than that in healthy controls and increased grayness affair volume in the right postcentral gyrus in MDD patients compared to healthy controls.69 Increased thickness and correlations may signal compensatory mechanisms associated with inflammation or other aspects of the pathophysiology of low. The regional homogeneity value was found to be increased in the right inferior parietal lobule70 and in the right frontoparietal region11 in depressive patients. The calculation of the regional homogeneity value depends on the regional cerebral blood flow. A chore positron emission tomography report constitute that the blood flow in the parietal lobe would increase along with information complexity and subtract when the subjects adopted the data.71 This finding indicated that an increased regional homogeneity value of the parietal lobe may lead to impairments in information reception and in learning.
2.5. Hippocampus
The hippocampus is associated with retention call up and the rules of advantage.72 Previous studies have shown that the hippocampus is smaller in depressed patients than in healthy controls,73 and this finding has been confirmed by meta‐analyses.74, 75 There is evidence that stress via the hypothalamic‐pituitary‐adrenal axis can consequence in elevated glucocorticoid levels in patients with MDD and tin can act on the glucocorticoid receptors in the hippocampus.76 Thus, hippocampal atrophy occurs every bit a result.77 Antidepressant treatment research78 and a longitudinal study of electroconvulsive therapy institute an increased gray thing volume in the hippocampus in MDD patients subsequently handling,29, 79 suggesting that the increased hippocampal volume was associated with clinical improvement. A study reported that people with low who are over 40 years of historic period, or those with astringent or multiple episodes, were more probable to have a pocket-size hippocampus.eighty Additionally, other studies have found that a small hippocampus may be associated with illness duration in MDD.81 According to an fMRI written report, decreased encephalon activity in the hippocampus was reported82 in depressive patients. Reduced greyness matter volume and reduced functional activity in the hippocampus would lead to negative emotion and the inability of cerebral processing in depressive patients.
3. IMPAIRED CIRCUITS IN MDD
three.1. Prefrontal‐subcortical circuit
The striatum, thalamus, and prefrontal cortex constitute the prefrontal‐subcortical circuit,47 which is involved in emotional and cognitive processing and is considered to exist a potential pathophysiological target in MDD.83 The structural connectivity of the prefrontal‐subcortical circuit begins at the prefrontal cortex. The striatum receives information from the PFC and outputs the information to the globus pallidus and the substantial nigra. All information is then projected through the thalamus to the prefrontal cortex. The thalamus is the final neuronal link back to the cortex, making the circuit a closed loop. This review mainly introduces three prefrontal circuits (Effigyii), which were originally described by Alexander.84 In each circuit, 2 pathways have mainly been reported (Effigy3): 1 direct pathway goes from the striatum to the pallidum, and the other pathway projects from the striatum to the pallidum, then to the subthalamic nucleus, and back to the pallidum.85 Basic research has found that gamma‐aminobutyric acid (GABA) and glutamate participate in these two pathways.83 Directly, the prefrontal cortex, hippocampus, and thalamus elicit excitement and project to the striatum. The striatum transmits information through GABAergic neurons that project to the globus pallidus. Indirectly, the subthalamic nucleus receives information from the cortex and the globus pallidus via GABAergic neurons and and then outputs through glutamatergic neurons to the globus pallidus. Both the direct and indirect pathways enter the thalamus through gamma fibers, just impairments in these two pathways could pb to differential pathology. Damage to the direct pathway results in abnormal suppression of the thalamus. In contrast, dysfunction in the indirect pathway leads to disinhibition and thalamic hyperactivity.47
Prefrontal excursion. The striatum, thalamus, and prefrontal cortex found the prefrontal‐ subcortical circuit (A). The dorsolateral prefrontal circuit (B) originates in the dorsolateral prefrontal cortex, which projects to the dorsolateral caudate. Then, fibers runway through the direct or indirect pathway to the lateral dorsomedial globus pallidus and the substantia nigra. The globus pallidus and the substantia nigra so project to the ventral anterior and medial dorsal thalamus.86 The thalamus collects all the information and sends information technology back to the dorsolateral prefrontal cortex; the orbitofrontal prefrontal circuit (C) originates in the inferolateral prefrontal cortex. The OFC fibers project to the ventromedial caudate. Then, the caudate outputs fibers through the direct and indirect pathways to the medial dorsomedial globus pallidus and the substantia nigra. The pallidum and the substantia nigra have connections with the ventral anterior and medial dorsal thalamic nuclei. All data will ultimately render to the orbitofrontal cortex; the anterior cingulate‐prefrontal excursion (D) begins in the ACC, and the fibers projection to the ventral striatum and the substantia nigra. The striatum outputs to the medial dorsal thalamus. Finally, the thalamus sends all the information back to the ACC. ACC, anterior cingulate cortex; DLPFC, dorsolateral prefrontal cortex; GPs, globus pallidus; mid, centre; OFC, orbitofrontal prefrontal cortex; SN, substantia nigra; THA, thalamus
Two pathways from the caudate to the thalamus. The prefrontal‐subcortical circuit originates from the prefrontal cortex and outputs fibers projecting to the striatum. Direct, the striatum transmits information through GABAergic neurons and projects to the globus pallidus. Indirectly, the striatum projects to the globus pallidus. The subthalamic nucleus receives information from the cortex via glutamatergic neurons and from the globus pallidus via GABAergic neurons, which and then output through glutamatergic neurons to the globus pallidus. All data ultimately returns to the prefrontal cortex. ACC, anterior cingulate cortex; DLPFC, dorsolateral prefrontal cortex; GABA, gamma‐aminobutyric acid; Glu, glutamatergic; GPs, globus pallidum; OFC, orbitofrontal prefrontal cortex; SN, substantia nigra; THA, thalamus
3.1.1. The dorsolateral prefrontal circuit
The dorsolateral prefrontal circuit originates from the dorsolateral prefrontal cortex (BA seed based ix and BA 10) and connects to the dorsolateral caudate. The caudate outputs to the lateral dorsomedial globus pallidus and the substantia nigra through the direct or indirect pathway. The pallidum and substantia nigra have connections with the ventral anterior and medial dorsal thalamus.86 Finally, all messages are returned through the thalamus to the dorsolateral prefrontal cortex. A functional connectivity assay reported coactivity in the bilateral DLPFC and the dorsal caudate.54 The dorsolateral prefrontal cortex and the caudate nucleus are unable to preserve recognition. According to a previous fMRI study, decreased activity in the caudate and increased activity in Brodmann area 10 were reported during advantage anticipation57 in patients with MDD. These findings suggested that patients with depression accept the intention of inducing pleasurable emotions. Thus, MDD patients with impaired dorsolateral prefrontal circuits may exhibit executive dysfunction.47
3.1.2. The orbitofrontal prefrontal circuit
The orbitofrontal prefrontal excursion starts at the inferolateral prefrontal cortex (BA 10 and BA 11).87 The OFC sends fibers to the ventromedial caudate. And then, the caudate outputs through the direct and indirect pathways to the medial dorsomedial globus pallidus and the substantia nigra. The medial dorsal thalamic nucleus receives input from the pallidum and the substantia nigra and outputs to the OFC. All the information will ultimately be sent to the orbitofrontal cortex. Functional seed‐based studies of the OFC found coactivity with these limbic regions.88 Heavy connections of the orbitofrontal gyrus with other cortical and subcortical regions, such as the parahippocampal gyrus, the ACC, and the posterior cingulate cortex,89 accept been reported. A functional MRI written report showed that a decrease in the OFC circuit connections was associated with unexpected reward receipt tasksninety and pleasant stimuli91 in MDD patients. The causal relationship betwixt the OFC and the ACC is positively correlated with the severity of depression.20 In determination, the orbitofrontal circuit may be negatively related to the severity of depression and the source of negative thinking.92
three.1.three. The inductive cingulate‐prefrontal circuit
The anterior cingulate‐prefrontal excursion begins in the anterior cingulate cortex (BA 24). The ACC outputs letters to the ventral striatum and the substantia nigra. The striatum and the substantia nigra projection to the medial dorsal thalamus.86 Finally, all the information is sent back to the inductive cingulate gray via the thalamus. It is not clear whether there is a straight or indirect connection betwixt the ACC and the striatum. However, there is evidence that the connections between the ventral striatum and thalamic neurons are nowadays.93 The nucleus accumbens is a part of the ventral striatum, which receives excitatory inputs from the ACC and outputs to the thalamus, and has been linked with anhedonia. The relationship between the nucleus accumbens and the thalamus is negatively correlated with the severity of depression94 and is related to emotional regulation and motivational function.95 Functional connectivity studies revealed the coordination betwixt the ventral striatum, the bilateral middle temporal lobe (amygdala and hippocampus), and the ventral midbrain (substantia nigra).54 According to previous findings, the ACC plays an important office in anhedonic symptoms in patients with MDD.xc Therefore, damage to the inductive cingulate circuitry may be negatively correlated with the severity of depressive symptoms.
Different circuits besides take correlations. As mentioned earlier, the functional connectivity of the ACC and the DLPFC is increased. This indicates an increase in the sensitivity to effective conflict.35 A correlation between the OFC and the ACC has too been mentioned. The causal interaction between the OFC and the ACC is positively related to the severity of low.20 The ACC receives input from the PFC and outputs to other brain regions.96 A powerless DLPFC and OFC in MDD effect in a failure to activate the ACC, ultimately leading to circuit impairment.
3.2. Prefrontal‐hippocampal circuit
In the early stage of MDD, a DTI study reported that the prefrontal‐hippocampal circuits,13 which originate from the fornix and output fibers to the hippocampus, project to the mammillary bodies, the anterior nuclei of the thalamus, and finally back to the prefrontal cortex. A lower FA value was observed in the fornix and the hippocampal cingulum17 of depressive patients. The fornix comprises the major fibers that track through the hippocampus, and it is related to the reduction in the hippocampal volume.97 Disruptions in the fornix would result in barriers to the transmission of data between the PFC and the hippocampus. Resting‐state functional research found decreased functional connectivity amidst the bilateral hippocampus, the DLPFC, and the ventral PFC17 in MDD patients, which might betoken emotional and cerebral dysfunction in MDD. There was a meaning correlation between the white matter integrity of the fornix and the functional connectivity of the PFC‐hippocampal circuit in healthy controls, but this was establish to be impaired in the MDD patients.17 In conclusion, prefrontal hippocampal structural damage tin can explain the deficits in attention, information processing, and autobiographical memory in depressive patients.17
3.three. Frontothalamic circuit
To our knowledge, Professor Jia and his squad are the start ones to find and put forward the "suicide loop"6 (Figure4). That particular DTI study institute that the FA value of the left internal capsule was lower in patients who attempted suicide.ane Abnormalities in the fiber connections passing through the left anterior limb of the internal capsule that projects to the left middle frontal cortex and the OFC and finally posteriorly to the left thalamus in MDD patients who committed suicide were found to be more astringent than those who did non commit suicide and controls. The middle frontal cortex and the OFC are related to determination making and problem solving and can affect modulation,49, 98 and the thalamus is involved in the mood‐related neural network.49 These three regions are considered hub nodes of brain connections.21 Changes in the frontal and thalamic circulation may lead to cognitive and emotional changes, thereby increasing the vulnerability to suicidal behavior in patients with depression. The results demonstrating these white thing changes are consistent with those of other studies.99, 100 Abnormal greyness matter in the temporal and parietal lobes was too plant in the patients who committed suicide. Decreased gray affair volume in the limbic cingulate gyrus and the right middle temporal gyrus and increased gray affair book in the right parietal lobe101 were reported, and a negative correlation was observed between the limbic cingulate gyrus and dysfunctional attitude scores. The attitude score reflects the perception of oneself and the world,102 and cognitive distortions often atomic number 82 to negative beliefs and behaviors, such every bit suicide. The reduction in the magnetization transfer ratio in the left inferior parietal lobule and the right superior parietal lobule in patients who attempted suicide was consistent with previous findings.103 Conclusion‐making barriers are associated with suicidal beliefs.68 Thus, the alterations in the parietal lobule may pb to suicidal behaviors. In addition, the hippocampus and the athwart gyrus are the biological markers for MDD, but lilliputian is known about the human relationship between the volume of these regions and suicide attempters. An interesting finding reported that suicide attempters have reduced gray matter book in the hippocampus104 and in the left athwart gyrus,98 particularly in cases of acute suicide. Information technology was too found that the total book of the hippocampal threshold of 5 cmiii had a negative predictive value of 98.2% for acute suicide attempts.104 The angular gyrus is known to be part of the default‐mode network, and impairments in this region in patients are associated with negative thoughts nigh the future or themselves.98 Disruptions in the angular gyrus may lead to suicidal behaviors or may increase the hazard of suicide.
Suicide excursion. MDD patients who committed suicide were found to take aberrant connections amidst the left anterior limb of the internal capsule, the left eye frontal cortex, the orbital prefrontal cortex, and the left thalamus. IC, internal sheathing; L, left; MDD, major depressive disorder; MFC, centre frontal cortex; OFC, orbitofrontal prefrontal cortex; THA, thalamus
4. CONCLUSION AND Future DIRECTION
In vivo MRI scans accept made great achievements in the study of psychiatric disorders, which take resulted in the dawn of the understanding of the pathophysiology of psychosis, especially of MDD. Many brain region alterations have been reported, and some crucial circuits accept as well been revealed via imaging studies. The discovery of brain network put forward new ideas in the understanding of the disease of depression, providing effective stimulation sites and efficacy evaluations for the commonly used transcranial magnetic stimulation or deep brain stimulation techniques. In improver, these findings too advise that MDD is not just due to local lesions but is also a multiloop disorder. However, previous studies even so had limitations, and more inquiry is needed in the future. First, nearly of the studies mentioned small sample sizes, which could have increased the simulated‐positive and (or) false‐negative rates of the results. Therefore, multicenter cooperation not only would solve this problem of sample content but also could result in more in‐depth research. 2nd, the identification of significant lesions relies on long‐term follow‐ups and the comparison of treated and nontreated patients. Future studies need to conduct longitudinal studies with larger samples. Moreover, using fauna experiments to verify the neuroimaging findings and applying the results to humans is very important and will exist a big step in the awarding of neuroimaging to the clinical field.
CONFLICT OF Interest
The authors declare no conflict of involvement.
ACKNOWLEDGMENTS
This study was supported by the National Natural Science Foundation (Grant Nos. 81771812, 81621003, 81571637, and 81271532), and the Program for Changjiang Scholars and Innovative Research Team in University (PCSIRT, Grant No. IRT16R52) of China. Q.G. received the support of Changjiang Scholar Professorship Laurels (Award No. T2014190) of China and the CMB Distinguished Professorship Award (Award No. F510000/G16916411) administered by the Institute of International Education, USA.
Notes
Zhang F‐F, Peng West, Sweeney JA, Jia Z‐Y, Gong Q‐Y. Brain construction alterations in depression: Psychoradiological evidence. CNS Neurosci Ther. 2018;24:994–1003. ten.1111/cns.12835 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
Contributor Data
Zhi‐Yun Jia, E-mail: moc.liamtoh@aijnuyihz.
Qi‐Yong Gong, Email: nc.gro.crrmh@gnoggnoyiq.
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