OBJECTIVE:To investigate the changes of subcortical gray matter volume and cortical thickness,andexplorethe correlations between regional abnormalities of cortical thickness and cognitive impairment and the effect of ...OBJECTIVE:To investigate the changes of subcortical gray matter volume and cortical thickness,andexplorethe correlations between regional abnormalities of cortical thickness and cognitive impairment and the effect of modified Bushenyisui decoction(补肾益髓汤,BSYSD)on the cognitive function of multiple sclerosis(MS).METHODS:This prospective study was approved by the institutional review board.92 subjects were recruited,including 46 relapsing-remitting multiple sclerosis(RRMS)patients and 46 healthy controls(HC).Of the 46 patients,22 patients experienced the treatment of BSYSD for half a year.A conventional three-dimensional T1-weighted sequence were acquired for all participants on a 3.0 tesla magnetic resonance system.Basic information,detailed cognitive scales Montreal Cognitive Assessment(MoCA),symbol digit modalities test(SDMT),immediate memory,delayed recall,and long-term recognition were evaluated.Subcortical gray matter volume and cortical thickness weremeasured by FreeSurfer.The correlations between cortical thickness which MS patients showed reduced with respect to HC and cognitive scales wereanalyzed by Pearson correlation in RRMS patients.The influence of modified BSYSD on MS patients'cognition was analyzed by paired T Test.RESULTS:MoCA,immediate memory,delayed recall,and long-term delayed recognition in RRMS were significantly decreased than those of HC.Gray matter atrophy measured by FreeSurfer showed mainly in thalamus and hippocampus of RRMS patients.Compared with HC,the cortical thickness of several regions in frontal lobe,parietal lobe,temporal lobe,hippocampal,cingulate gyrus,and fusiform gyrus of RRMS patients were decreased with significant difference.The regions of cortical thickness thinning related to MoCA,immediate memory,delayed recall,and long-term delayed recognition were temporal lobe and fusiform gyrus.Modified BSYSD could improve MoCA,SDMT,immediate memory,delayed recall,and long-term delayed recognition of MS patients,and it could promote the recovery of cognitive function in MS patients.CONCLUSIONS:Gray matter atrophy and cortical thickness thinning were validated in RRMS.Cortical thickness thinning of temporal lobe and fusiform gyrus strongly related to cognitive deficits in RRMS.The modified BSYSD could promote the recovery of cognitive function in MS.展开更多
In multiple sclerosis, gray matter atrophy is extensive, and cognitive deficits and mood disorders are frequently encountered. It has been conjectured that focal atrophy is associated with emotional decline. However, ...In multiple sclerosis, gray matter atrophy is extensive, and cognitive deficits and mood disorders are frequently encountered. It has been conjectured that focal atrophy is associated with emotional decline. However, conventional MRI has revealed that the pathological characteristics cannot fully account for the mood disorders. Moreover, there is no correlation between cognitive disorders and MRI results in clinically isolated syndromes or in cases of definite multiple sclerosis. In this casecontrol study, voxel-based morphometric analysis was performed on 11 subjects with relapsing-remitting multiple sclerosis, and the results show that these patients exhibit gray matter atrophy. Moreover, the gray matter atrophy in the superior and middle gyri of the right frontal lobe in patients with multiple sclerosis was correlated with scores from the Hamilton Anxiety Rating Scale. The scores obtained with the Repeatable Battery for the Assessment of Neuropsychological Status were associated with gray matter atrophy in the middle gyrus of the left frontal lobe, the superior and middle gyrus of the right frontal lobe, the middle gyrus of the left cingulate, the superior and middle gyri of the left frontal lobe, and the triangular area of the left frontal lobe. However, there was no statistical significance. These findings suggest that the cingulate and frontal cortices of the dominant hemisphere are the most severely atrophic regions of the brain, and this atrophy is correlated with cognitive decline and emotional abnormalities.展开更多
BACKGROUND This study describes the efficacy of a tacrolimus treatment regimen used to treat two patients with relapsing-remitting chronic inflammatory demyelinating polyradiculoneuropathy(CIDP).CASE SUMMARY Two patie...BACKGROUND This study describes the efficacy of a tacrolimus treatment regimen used to treat two patients with relapsing-remitting chronic inflammatory demyelinating polyradiculoneuropathy(CIDP).CASE SUMMARY Two patients(17-year-old female and 27-year-old male)were enrolled in the current study and were followed up for 12 mo.The first patient was administered tacrolimus(2 mg/d)for 12 mo and prednisolone(40 mg/d)for six months.The second patient was administered tacrolimus(3 mg/d)for six months.Both patients were followed up for 12 mo and the degree of recurrent weakness or normalized motor function was monitored.In addition,nerve conduction studies and tacrolimus levels were recorded.Following tacrolimus treatment,both patients showed marked improvement in clinical outcomes.In the first patient,prednisolone treatment was successfully withdrawn after six months.Sensory as well as motor nerve conduction velocities showed evident recovery following treatment.However,conduction velocities did not completely return to normal,suggesting that electrophysiological recovery can be slower than clinical recovery.CONCLUSION Neither patient exhibited any adverse effects due to the tacrolimus therapy.Therefore,tacrolimus can be effective for the treatment of patients with steroidresistant CIDP.展开更多
Mast cells are present in high numbers in the border-zones of the multiple sclerosis-plaques. They are located in small clusters along capillaries and venules, and they are more abundant in females than in men. Mast c...Mast cells are present in high numbers in the border-zones of the multiple sclerosis-plaques. They are located in small clusters along capillaries and venules, and they are more abundant in females than in men. Mast cells can be stimulated to release specific mediators such as histamine, resulting in oedema formation, as well as proteases that may cause demyelination, by several different activation mechanisms. We hypothesize that a putative mast cell activation may be induced by diet factor(s) as well as long lasting mental stress that may lead to the release of catestatin, as well as ACTH released from the pituitary gland. Given a natural flux of mast cell recovery and activation, a putative phenomenon of massive release of mediators and “silent” reload periods may explain the relapsing-remitting phases of multiple sclerosis.展开更多
This paper reviews evidence that the presence of mast cells in specific sites of central nervous system, suggesting inflammatory processes, may explain all the symptoms observed in multiple sclerosis. This hypothesis ...This paper reviews evidence that the presence of mast cells in specific sites of central nervous system, suggesting inflammatory processes, may explain all the symptoms observed in multiple sclerosis. This hypothesis would be relatively easy to test.展开更多
基金Supported by the Fund for BeijingScience&Technology Development of TCM:the Study on the Curative Effect and Mechanism of Modification of Bushenyisui Capsules against Multiple Sclerosis with Depression Based on Magnetic Resonance Multimodal Analysis(No.JJ2018-49)the Effect of Bushenyisui Capsules on Cognitive Impairment in Patients with Relapsing and Multiple Sclerosis(No.QN2014-17)+4 种基金To Explore the Mechanism of Bushenyisui Capsule in Reconstituting NMOSD Immune Balance Based on the Regulation of p38 MAPK Pathway by TAK1(No.QN2018-30)Capital Medical University Scientific Research Cultivation Fund:Rl Promotes the Recovery of Neurological Function in Rats with Cerebral Hemorrhage through the Pathway of Microglial Cells Polarizing Different Neurons to Mediate the Neuroinflammatory Reaction after Cerebral Hemorrhage(No.PYZ2018142)to Explore the Mechanism of Bushenyisui Capsule Promoting Myelin Sheath Regeneration in EAE Mice by Regulating Proliferation,Differentiation and Migration of OPC by Treg Derived Nov(No.PYZ2018141)National Natural Science Foundation of China:to Explore the Mechanism of Catalpol Mediated Proliferation,Migration and Axonal Remyelination of OPC by CCN3 through the Synergetic Regulation of Cdc42 Signaling Pathway by GEFs and mir-148b-3p(No.81973599)the Study on the Mechanism of Regulating the Axon Myelination through NF and NRG1(No.81473640)。
文摘OBJECTIVE:To investigate the changes of subcortical gray matter volume and cortical thickness,andexplorethe correlations between regional abnormalities of cortical thickness and cognitive impairment and the effect of modified Bushenyisui decoction(补肾益髓汤,BSYSD)on the cognitive function of multiple sclerosis(MS).METHODS:This prospective study was approved by the institutional review board.92 subjects were recruited,including 46 relapsing-remitting multiple sclerosis(RRMS)patients and 46 healthy controls(HC).Of the 46 patients,22 patients experienced the treatment of BSYSD for half a year.A conventional three-dimensional T1-weighted sequence were acquired for all participants on a 3.0 tesla magnetic resonance system.Basic information,detailed cognitive scales Montreal Cognitive Assessment(MoCA),symbol digit modalities test(SDMT),immediate memory,delayed recall,and long-term recognition were evaluated.Subcortical gray matter volume and cortical thickness weremeasured by FreeSurfer.The correlations between cortical thickness which MS patients showed reduced with respect to HC and cognitive scales wereanalyzed by Pearson correlation in RRMS patients.The influence of modified BSYSD on MS patients'cognition was analyzed by paired T Test.RESULTS:MoCA,immediate memory,delayed recall,and long-term delayed recognition in RRMS were significantly decreased than those of HC.Gray matter atrophy measured by FreeSurfer showed mainly in thalamus and hippocampus of RRMS patients.Compared with HC,the cortical thickness of several regions in frontal lobe,parietal lobe,temporal lobe,hippocampal,cingulate gyrus,and fusiform gyrus of RRMS patients were decreased with significant difference.The regions of cortical thickness thinning related to MoCA,immediate memory,delayed recall,and long-term delayed recognition were temporal lobe and fusiform gyrus.Modified BSYSD could improve MoCA,SDMT,immediate memory,delayed recall,and long-term delayed recognition of MS patients,and it could promote the recovery of cognitive function in MS patients.CONCLUSIONS:Gray matter atrophy and cortical thickness thinning were validated in RRMS.Cortical thickness thinning of temporal lobe and fusiform gyrus strongly related to cognitive deficits in RRMS.The modified BSYSD could promote the recovery of cognitive function in MS.
文摘In multiple sclerosis, gray matter atrophy is extensive, and cognitive deficits and mood disorders are frequently encountered. It has been conjectured that focal atrophy is associated with emotional decline. However, conventional MRI has revealed that the pathological characteristics cannot fully account for the mood disorders. Moreover, there is no correlation between cognitive disorders and MRI results in clinically isolated syndromes or in cases of definite multiple sclerosis. In this casecontrol study, voxel-based morphometric analysis was performed on 11 subjects with relapsing-remitting multiple sclerosis, and the results show that these patients exhibit gray matter atrophy. Moreover, the gray matter atrophy in the superior and middle gyri of the right frontal lobe in patients with multiple sclerosis was correlated with scores from the Hamilton Anxiety Rating Scale. The scores obtained with the Repeatable Battery for the Assessment of Neuropsychological Status were associated with gray matter atrophy in the middle gyrus of the left frontal lobe, the superior and middle gyrus of the right frontal lobe, the middle gyrus of the left cingulate, the superior and middle gyri of the left frontal lobe, and the triangular area of the left frontal lobe. However, there was no statistical significance. These findings suggest that the cingulate and frontal cortices of the dominant hemisphere are the most severely atrophic regions of the brain, and this atrophy is correlated with cognitive decline and emotional abnormalities.
文摘BACKGROUND This study describes the efficacy of a tacrolimus treatment regimen used to treat two patients with relapsing-remitting chronic inflammatory demyelinating polyradiculoneuropathy(CIDP).CASE SUMMARY Two patients(17-year-old female and 27-year-old male)were enrolled in the current study and were followed up for 12 mo.The first patient was administered tacrolimus(2 mg/d)for 12 mo and prednisolone(40 mg/d)for six months.The second patient was administered tacrolimus(3 mg/d)for six months.Both patients were followed up for 12 mo and the degree of recurrent weakness or normalized motor function was monitored.In addition,nerve conduction studies and tacrolimus levels were recorded.Following tacrolimus treatment,both patients showed marked improvement in clinical outcomes.In the first patient,prednisolone treatment was successfully withdrawn after six months.Sensory as well as motor nerve conduction velocities showed evident recovery following treatment.However,conduction velocities did not completely return to normal,suggesting that electrophysiological recovery can be slower than clinical recovery.CONCLUSION Neither patient exhibited any adverse effects due to the tacrolimus therapy.Therefore,tacrolimus can be effective for the treatment of patients with steroidresistant CIDP.
文摘Mast cells are present in high numbers in the border-zones of the multiple sclerosis-plaques. They are located in small clusters along capillaries and venules, and they are more abundant in females than in men. Mast cells can be stimulated to release specific mediators such as histamine, resulting in oedema formation, as well as proteases that may cause demyelination, by several different activation mechanisms. We hypothesize that a putative mast cell activation may be induced by diet factor(s) as well as long lasting mental stress that may lead to the release of catestatin, as well as ACTH released from the pituitary gland. Given a natural flux of mast cell recovery and activation, a putative phenomenon of massive release of mediators and “silent” reload periods may explain the relapsing-remitting phases of multiple sclerosis.
文摘This paper reviews evidence that the presence of mast cells in specific sites of central nervous system, suggesting inflammatory processes, may explain all the symptoms observed in multiple sclerosis. This hypothesis would be relatively easy to test.
