A resting state functional magnetic resonance imaging study of patients with benign essential blepharospasm.

BACKGROUND: Benign essential blepharospasm (BEB) is a neurologic disorder characterized by an adult-onset focal dystonia that causes involuntary blinking and eyelid spasms. The pathophysiology of BEB patients remains unclear. This study investigated intrinsic low-frequency fluctuation in BEB patients during resting state functional magnetic resonance imaging (fMRI). METHODS: The study included 9 patients with BEB (mean age, 61.7 years; range, 52-66 years), in whom the average duration of symptoms was 2.7 ± 1.8 years, and another 9 subjects from an age- and sex-matched control group. Resting state fMRI was performed in both the patients with BEB and the normal controls. Voxel-based analysis was used to characterize the alteration of amplitude of low-frequency fluctuation (ALFF) in both patients with BEB and the normal controls. RESULTS: The whole brain analysis indicated that in comparison with the normal control group, there was a significantly increased ALFF in the left putamen, pallidum, insular lobe, and medial prefrontal cortex and a significantly decreased ALFF in the bilateral somatosensory regions, thalami, cerebellum, and medial and posterior cingulate cortex. CONCLUSION: The present study suggests that both an abnormal default mode network and corticostriatopallidothalamic loop may play a role in the pathophysiology of BEB.

Redox factor 1 inhibits the apoptosis process after intracerebral hemorrhage.

OBJECTIVE: To determine the role of redox factor 1 (Ref-1) in the apoptotic process in perihematoma brain tissue from intracerebral hemorrhage (ICH) patients. METHODS: Thirty ICH patients were selected, and normal brain tissue, inevitably lost during surgery, was used as the control group, while the brain tissue from 1 cm around the hematoma was used as the experimental group. Experimental tissues were further divided according to the time from syndrome onset to the time of operation as follows: <6 hours (n = 6); 6-12 hours (n = 7); 12-24 hours (n = 5); 24-72 hours (n = 6); and >72 hours (n = 6). Apoptotic cells were observed by the terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick-end labeling (TUNEL) reaction. Protein and mRNA expression of Ref-1 and Bax were determined by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) respectively. RESULTS: Immunohistochemistry indicated that Ref-1 expression was the maximal in control tissue, while it slowly declined to a nadir between 12 and 72 hours in the experimental tissue. Bax expression was the lowest in the control tissue, and gradually increased from 12 to 72 hours in the experimental tissue. RT-PCR data showed that patterns of Ref-1 and Bax expression similar to the immunohistochemistry results. Correlation analysis demonstrated a negative correlation among Ref-1, apoptosis, and Bax. CONCLUSION: Ref-1 may play an important role in protecting brain cells and may be able to inhibit apoptosis following ICH.

[The relationship between the aquaporin-4 and brain edema, pathologic change, ultrastructure in peri-hematoma tissue in patients with intracerebral hemorrhage].

OBJECTIVE: To observe the expression of aquaporin-4 (AQP-4) mRNA and study the relationship between AQP-4, brain edema, pathological changes and ultrastructure of peri-hematoma tissue in intracerebral hemorrhage (ICH) patients. METHODS: Intracranial operation was performed via nonfunctional area with a funnel-like approach on 30 ICH patients. The brain tissue which must be removed 1 cm away the hematoma was removed within 12 hours for observation as normal brain tissue and taken as the control group (7 patients), and which of the brain tissue within 1 cm around hematoma was taken as the study specimens. The experimental group was subdivided into five groups according to the time interval after ICH: <6 hours (6 cases), 6-12 hours (7 cases), 12-24 hours (5 cases), 24-72 hours (6 cases), and >72 hours ( 6 cases ). Expression of the AQP-4 mRNA, brain edema, pathological and ultrastructural changes were observed with reverse transcription-polymerase chain reaction (RT-PCR), light microscope and electron microscope. RESULTS: The expression of the AQP-4 mRNA was not remarkable, the morphology and construction were basically normal in control group. The expression of AQP-4 mRNA was mild (1.17+/-0.41)and there was edema of neuroglia in the <6 hours group. After 6 hours, besides neuroglial edema, the expression of the AQP-4 mRNA was gradually obvious, capillary endothelial cells began to swell too, and tight junctions gradually began to loosen. In the 12-72 hours group the expression of the AQP-4 mRNA reached its peak (3.50+/-0.55, 3.60+/-0.55, both P<0.01), and brain edema was most prominent, and electron microscopy showed that neurons, neuroglia, and capillary endothelial cells were markedly deformed. After 72 hours, the expression of AQP-4 mRNA gradually recovered, and brain cells showed less damage. On the 5th day the damage began to repair, and on the 8th day, the damage was basically repaired. The correlation analysis showed that there was a remarkable positive correlation between the expression of the AQP-4 mRNA and the degree of brain edema and the size of hematoma (r(1)=0.67, P<0.01; r(2)=0.44, P<0.05) . CONCLUSION: Secondary edema and brain damage may correlate with the expression of the AQP-4 mRNA in the peri-hematoma brain edema area. Removal of hematoma will help decrease the AQP-4 mRNA expression and brain edema damage in the early stage.

[Study of relationship between inflammatory response and apoptosis in perihematoma region in patients with intracerebral hemorrhage].

OBJECTIVE: To investigate the relationship between inflammatory response and cell apoptosis in the perihematoma region in patients with intracerebral hemorrhage (ICH). METHODS: Surgical specimens were obtained from the area 1 cm adjacent to the hematoma. Thirty patients with ICH were divided into five groups: 6, 7, 5, 6, 6 patients in surgery<6 hours, 6-12 hours, 12-24 hours, 24-72 hours and >72 hours groups after the onset, respectively. The control group specimens were obtained from the brain tissues distant to the hematoma in the process of craniotomy in the patients of two former groups. Sections were stained with hematoxylin and eosin (HE) for the examination of pathological changes. Immunohistochemistry, terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) and reverse transcription-polymerase chain reaction (RT-PCR) were applied to determine apoptosis cells, Bax and Bcl-x protein and mRNA. RESULTS: The tissues from perihematoma region were almost normal in control group and <6 hours group. They were slightly damaged in 6-12 hours group, became worse in 12-24 hours group and most severe in 24-48 hours group, and they became better latter and were similar to the control group on 8th day. Infiltration of neutrophils, macrophages and lymphocyte appeared gradually at 6-12 hours, and became much more prominent at 12-24 hours (all P<0.01). The reactive gliosis began to appear at 24-72 hours, and enhanced after 72 hours (all P<0.01). The expression of the apoptosis and Bax protein increased gradually after 6 hours, reaching the peak at 12-24 hours (P<0.05 or P<0.01), and decreased gradually later. The changes in the levels of Bax mRNA were similar to that of the result of immunohistochemistry. Although the expression of Bcl-x protein and mRNA seemed to be increased at 12-72 hours, there was no significant difference between groups (P>0.05). The correlation analysis showed that the infiltration of neutrophils, macrophages and lymphocyte was positively correlated to the TUNEL positive cells and expression of Bax protein and mRNA (P<0.05 or P<0.01), and showed no correlation to Bcl-x protein and mRNA (all >0.05). CONCLUSION: There is a close relationship between inflammatory response and apoptosis and tissue damage in the perihematoma area in ICH.