Endovascular surgery is advantageous in experimentally induced ischemic stroke because it causes fewer cranial traumatic lesions than invasive surgery and can closely mimic the pathophysiol-ogy in stroke patients. However, the outcomes are highly variable, which limits the accuracy of evaluations of ischemic stroke studies. In this study, eight healthy adult rhesus monkeys were randomized into two groups with four monkeys in each group:middle cerebral artery occlusion at origin segment (M1) and middle cerebral artery occlusion at M2 segment. The blood lfow in the middle cerebral artery was blocked completely for 2 hours using the endovascular microcoil placement technique (1 mm × 10 cm) (undetachable), to establish a model of cerebral ischemia. The microcoil was withdrawn and the middle cerebral artery blood lfow was restored. A revers-ible middle cerebral artery occlusion model was identiifed by hematoxylin-eosin staining, digital subtraction angiography, magnetic resonance angiography, magnetic resonance imaging, and neurological evaluation. The results showed that the middle cerebral artery occlusion model was successfully established in eight adult healthy rhesus monkeys, and ischemic lesions were apparent in the brain tissue of rhesus monkeys at 24 hours after occlusion. The rhesus monkeys had symp-toms of neurological deifcits. Compared with the M1 occlusion group, the M2 occlusion group had lower infarction volume and higher neurological scores. These experimental ifndings indicate that reversible middle cerebral artery occlusion can be produced with the endovascular microcoil technique in rhesus monkeys. The M2 occluded model had less infarction and less neurological impairment, which offers the potential for application in the ifeld of brain injury research.

The transcription factor early growth response protein 3 (EGR3) is involved in schizophrenia. We developed a putative rat model of schizophrenia by transfecting lentiviral particles carrying the Egr3 gene into bilateral hippocampal dentate gyrus. We assessed spatial working memory using the Morris water maze test, and neuronal metabolite levels in bilateral hippocampus and thalamus were determined by 3.0 T proton magnetic resonance spectroscopy. Choline content was significantly greater in the hippocampus after transfection, while N-acetylaspartate and the ratio of N-acetylaspartate to creatine/phosphocreatine in the thalamus were lower than in controls. This study is the first to report evaluation of brain metabolites using 3.0 T proton magnetic resonance spectroscopy in rats transfected with Egr3, and reveals metabolic abnormalities in the hippocampus and thalamus in this putative model of schizophrenia.

This study compared the difference in brain structure in 12 mine disaster survivors with chronic post-traumatic stress disorder, 7 cases of improved post-traumatic stress disorder symptoms, and 14 controls who experienced the same mine disaster but did not suffer post-traumatic stress disorder, us-ing the voxel-based morphometry method. The correlation between differences in brain structure and post-traumatic stress disorder symptoms was also investigated. Results showed that the gray matter volume was the highest in the trauma control group, fol owed by the symptoms-improved group, and the lowest in the chronic post-traumatic stress disorder group. Compared with the symptoms-improved group, the gray matter volume in the lingual gyrus of the right occipital lobe was reduced in the chronic post-traumatic stress disorder group. Compared with the trauma control group, the gray matter volume in the right middle occipital gyrus and left middle frontal gyrus was reduced in the symptoms-improved group. Compared with the trauma control group, the gray matter volume in the left superior parietal lobule and right superior frontal gyrus was reduced in the chronic post-traumatic stress disorder group. The gray matter volume in the left superior parietal lobule was significantly positively correlated with the State-Trait Anxiety Inventory subscale score in the symptoms-improved group and chronic post-traumatic stress disorder group (r = 0.477, P = 0.039). Our findings indicate that (1) chronic post-traumatic stress disorder patients have gray matter structural damage in the prefrontal lobe, occip-ital lobe, and parietal lobe, (2) after post-traumatic stress, the disorder symptoms are improved and gray matter structural damage is reduced, but cannot recover to the trauma-control level, and (3) the superior parietal lobule is possibly associated with chronic post-traumatic stress disorder. Post-traumatic stress disorder patients exhibit gray matter abnormalities.

Embodied semantics theory asserts that the meaning of action-related words is neural y represented through networks that overlap with or are identical to networks involved in sory-motor processing. While some studies supporting this theory have focused on Chinese cha-racters, less attention has been paid to their semantic radicals. Indeed, there is stil disagreement about whether these radicals are processed independently. The present study investigated whether radicals are processed separately and, if so, whether this processing occurs in sensory-motor gions. Materials consisted of 72 high-frequency Chinese characters, with 18 in each of four ries:hand-action verbs with and without hand-radicals, and verbs not related to hand actions, with and without hand-radicals. Twenty-eight participants underwent functional MRI scans while reading the characters. Compared to characters without hand-radicals, reading characters with hand-radicals activated the right medial frontal gyrus. Verbs involving hand-action activated the left inferior parietal lobule, possibly reflecting integration of information in the radical with the semantic meaning of the verb. The findings may be consistent with embodied semantics theory and suggest that neural representation of radicals is indispensable in processing Chinese characters.

Alcohol use disorder (AUD), mild traumatic brain injury (mTBI), and posttraumatic stress dis-order (PTSD) commonly co-occur (AUD + mTBI + PTSD). These conditions have overlapping symptoms which are, in part, relfective of overlapping neuropathology. These conditions become problematic because their co-occurrence can exacerbate symptoms. Therefore, treatments must be developed that are inclusive to all three conditions. Repetitive transcranial magnetic stimu-lation (rTMS) is non-invasive and may be an ideal treatment for co-occurring AUD + mTBI +PTSD. There is accumulating evidence on rTMS as a treatment for people with AUD, mTBI, and PTSD each alone. However, there are no published studies to date on rTMS as a treatment for co-occurring AUD + mTBI + PTSD. This review article advances the knowledge base for rTMS as a treatment for AUD + mTBI + PTSD. This review provides background information about these co-occurring conditions as well as rTMS. The existing literature on rTMS as a treatment for people with AUD, TBI, and PTSD each alone is reviewed. Finally, neurobiological ifndings in support of a theoretical model are discussed to inform TMS as a treatment for co-occurring AUD + mTBI + PTSD. The peer-reviewed literature was identiifed by targeted literature searches using PubMed and supplemented by cross-referencing the bibliographies of relevant review arti-cles. The existing evidence on rTMS as a treatment for these conditions in isolation, coupled with the overlapping neuropathology and symptomology of these conditions, suggests that rTMS may be well suited for the treatment of these conditions together.

Reward-based decision-making has been found to activate several brain areas, including the ven-trolateral prefrontal lobe, orbitofrontal cortex, anterior cingulate cortex, ventral striatum, and meso-limbic dopaminergic system. In this study, we observed brain areas activated under three degrees of uncertainty in a reward-based decision-making task (certain, risky, and ambiguous). The tasks were presented using a brain function audiovisual stimulation system. We conducted brain scans of 15 healthy volunteers using a 3.0T magnetic resonance scanner. We used SPM8 to analyze the location and intensity of activation during the reward-based decision-making task, with respect to the three conditions. We found that the orbitofrontal cortex was activated in the certain reward con-dition, while the prefrontal cortex, precentral gyrus, occipital visual cortex, inferior parietal lobe, ce-rebel ar posterior lobe, middle temporal gyrus, inferior temporal gyrus, limbic lobe, and midbrain were activated during the ‘risk’ condition. The prefrontal cortex, temporal pole, inferior temporal gyrus, occipital visual cortex, and cerebel ar posterior lobe were activated during ambiguous deci-sion-making. The ventrolateral prefrontal lobe, frontal pole of the prefrontal lobe, orbitofrontal cortex, precentral gyrus, inferior temporal gyrus, fusiform gyrus, supramarginal gyrus, inferior parietal lo-bule, and cerebel ar posterior lobe exhibited greater activation in the‘risk’ than in the‘certain’ con-dition (P<0.05). The frontal pole and dorsolateral region of the prefrontal lobe, as wel as the ce-rebel ar posterior lobe, showed significantly greater activation in the ‘ambiguous’ condition com-pared to the ‘risk’ condition (P < 0.05). The prefrontal lobe, occipital lobe, parietal lobe, temporal lobe, limbic lobe, midbrain, and posterior lobe of the cerebel um were activated during deci-sion-making about uncertain rewards. Thus, we observed different levels and regions of activation for different types of reward processing during decision-making. Specifical y, when the degree of reward uncertainty increased, the number of activated brain areas increased, including greater ac-tivation of brain areas associated with loss.

Previous neuropathological studies regarding traumatic brain injury have primarily focused on changes in large structures, for example, the clinical prognosis after cerebral contusion, intrace-rebral hematoma, and epidural and subdural hematoma. In fact, many smaller injuries can also lead to severe neurological disorders. For example, cerebral microbleeds result in the dysfunc-tion of adjacent neurons and the disassociation between cortex and subcortical structures. These tiny changes cannot be adequately visualized on CT or conventional MRI. In contrast, gradient echo sequence-based susceptibility-weighted imaging is very sensitive to blood metabolites and microbleeds, and can be used to evaluate traumatic cerebral microbleeds with high sensitivity and accuracy. Cerebral microbleed can be considered as an important imaging marker for dif-fuse axonal injury with potential relevance for prognosis. For this reason, based on experimental and clinical studies, this study reviews the role of imaging data showing traumatic cerebral mi-crobleeds in the evaluation of cerebral neuronal injury and neurofunctional loss.

The brain is highly plastic after stroke or epilepsy;however, there is a paucity of brain plasticity investigation after traumatic brain injury (TBI). This mini review summarizes the most recent evidence of brain plasticity in human TBI patients from the perspective of advanced magnetic resonance imaging. Similar to other forms of acquired brain injury, TBI patients also demonstrat-ed both structural reorganization as well as functional compensation by the recruitment of other brain regions. However, the large scale brain network alterations after TBI are still unknown, and the ifeld is still short of proper means on how to guide the choice of TBI rehabilitation or treat-ment plan to promote brain plasticity. The authors also point out the new direction of brain plas-ticity investigation.

Diffusion-tensor imaging can be used to observe the microstructure of brain tissue. Fractional sotropy reflects the integrity of white matter fibers. Fractional anisotropy of a young adult brain is low in gray matter, high in white matter, and highest in the splenium of the corpus cal osum. Thus, we selected the anterior and posterior limbs of the internal capsule, head of the caudate nucleus, se-mioval center, thalamus, and corpus cal osum (splenium and genu) as regions of interest when using diffusion-tensor imaging to observe fractional anisotropy of major white matter fiber tracts and the deep gray matter of healthy rhesus monkeys aged 4-8 years. Results showed no laterality ferences in fractional anisotropy values. Fractional anisotropy values were low in the head of date nucleus and thalamus in gray matter. Fractional anisotropy values were highest in the sple-nium of corpus cal osum in the white matter, fol owed by genu of the corpus cal osum and the posterior limb of the internal capsule. Fractional anisotropy values were lowest in the semioval center and posterior limb of internal capsule. These results suggest that fractional anisotropy values in major white matter fibers and the deep gray matter of 4-8-year-old rhesus monkeys are similar to those of healthy young people.

Negative motor evoked potentials after cerebral infarction, indicative of poor recovery of limb motor function, tend to be accompanied by changes in fractional anisotropy values and the cerebral pe-duncle area on the affected side, but the characteristics of these changes have not been reported. This study included 57 cases of cerebral infarction whose motor evoked potentials were tested in the 24 hours after the first inspection for diffusion tensor imaging, in which 29 cases were in the negative group and 28 cases in the positive group. Twenty-nine patients with negative motor evoked potentials were divided into two groups according to fractional anisotropy on the affected side of the cerebral peduncle: a fractional anisotropy < 0.36 group and a fractional anisotropy ≥ 0.36 group. Al patients underwent a regular magnetic resonance imaging and a diffusion tensor imaging examina-tion at 1 week, 1, 3, 6 and 12 months after cerebral infarction. The Fugl-Meyer scores of their he-miplegic limbs were tested before the magnetic resonance and diffusion tensor imaging tions. In the negative motor evoked potential group, fractional anisotropy in the affected cerebral peduncle declined progressively, which was most obvious in the first 1-3 months after the onset of cerebral infarction. The areas and area asymmetries of the cerebral peduncle on the affected side were significantly decreased at 6 and 12 months after onset. At 12 months after onset, the area asymmetries of the cerebral peduncle on the affected side were lower than the normal lower limit value of 0.83. Fugl-Meyer scores in the fractional anisotropy ≥ 0.36 group were significantly higher than in the fractional anisotropy < 0.36 group at 3-12 months after onset. The fractional anisotropy of the cerebral peduncle in the positive motor evoked potential group decreased in the first 1 month after onset, and stayed unchanged from 3-12 months; there was no change in the area of the ce-rebral peduncle in the first 1-12 months after cerebral infarction. These findings confirmed that if the fractional anisotropy of the cerebral peduncle on the affected side is < 0.36 and the area asymme-tries < 0.83 in patients with negative motor evoked potential after cerebral infarction, then poor he-miplegic limb motor function recovery may occur.