Study of brainstem auditory evoked potentials and its correlation with pontine volume in olivopontocerebellar atrophy / 中国应用生理学杂志

<p><b>AIM</b>To investigate the change of latency and interpeak latency of each component of BAEP (brainstem auditory evoked potential, BAEP) and its correlation with PV/PFV (pontine volume/posterior fossa volume, PV/PFV) ratio in OPCA (olivopontocerebellar atrophy, OPCA).</p><p><b>METHODS</b>We used Keypoint EMG/EP to determine waves I PL (peak latency, PL), III PL, V PL and I - III IPL (interpeak latency, IPL), III - V IPL, I - V IPL and used 1.5TMR 3D volume rendering software to determine PV (pontine volume, PV), CV(cerebellar volume, CV) and PFV (posterior fossa volume,PFV). Then calculated PV/PFV ratio, CV/PFV ratio and PV/ CV ratio in OPCA group and control group.</p><p><b>RESULTS</b>Compared with control group, in OPCA group wave IIII PL, I - III IPL were significantly elongated (P < 0.05), III - V IPL was significantly shorten (P < 0.05), PV/PFV ratio was significantly decreased (P < 0.01); there was a positive correlation between III-V IPL and PV/PFV ratio (r = 0.83, P < 0.01).</p><p><b>CONCLUSION</b>In patients with OPCA, III PL, I - III IPL of BAEP were elongated and III - V IPL of BAEP was shorten. III - V IPL became shorter when the volume of pontine decreased.</p>

Lance-Adams syndrome: a report of two cases / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Chronic post-hypoxic myoclonus, also known as Lance-Adams syndrome (LAS), is a rare complication of successful cardiopulmanry resuscitation often accompanied by action myoclonus and cerebellar ataxia. It is seen in patients who have undergone a cardiorespiratory arrest, regained consciousness afterwards, and then developed myoclonus days or weeks after the event. Worldwide, 122 cases have been reported in the literature so far, including 1 case of Chinese. Here we report 2 Chinese LAS patients with detailed neuroimagings. Cranial single photon emission computed tomography (SPECT) of patient 1, a 52-year-old woman, showed a mild hypoperfusion in her left temporal lobe, whereas patient 2, a 54-year-old woman, manifested a mild bilateral decrease of glucose metabolism in the frontal lobes and a mild to moderate decrease of the N-acetyl aspartate (NAA) peak in the bilateral hippocampi by cranial [(18)F]-fluorodeoxyglucose positron emission tomographic (PET) scan and cranial magnetic resonance spectroscopy (MRS), respectively. We also review the literature on the neuroimaging, pathogenesis, and treatment of LAS.

GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo/reperfusion rat / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

<p><b>OBJECTIVE</b>To determine the protective effect of monosialoganglionside (GM1) and evaluate the influence of GM1 on expression of N-methyl-D-aspartate receptor subunit 1 (NMDAR1) in Sprague-Dawley (SD) rats with focal cerebral ischemia-reperfusion (I/R).</p><p><b>METHODS</b>Left middle cerebral artery (MCA) was occluded by an intraluminal suture for 1 h and the brain was reperfused for 72 h in SD rats when infarct volume was measured, GM1 (10 mg/kg) was given ip (intraperitoneally) at 5 min (group A), 1 h (group B) and 2 h (group C) after MCA occlusion (MCAo). Expression of NMDAR1 was detected by Western blot at various time after reperfusion (4 h, 6 h, 24 h, 48 h and 72 h) in ischemic hemispheres of the rats with or without GM1 administered.</p><p><b>RESULTS</b>(1) Adjusted relative infarct volumes of groups A and B were significantly smaller than that of group C and the control group (P<0.01 and P<0.05, respectively). (2) Expression level of NMDAR1 was temporally high at 6 h after reperfusion, and dipped below the normal level at 72 h after reperfusion. GM1 at 5 min after MCAo significantly suppressed the expression of NMDAR1 at 6 h after reperfusion (P<0.05 vs the control). At 72 h after reperfusion, the NMDAR1 expression level of rats treated with GM1 administered (at 5 min or 2 h after MCAo) was significantly higher than that of the control (P<0.05).</p><p><b>CONCLUSION</b>GM1 can time-dependently reduce infarct volume in rats with focal cerebral I/R partly through stabilizing the expression of NMDAR1.</p>

Protective effects and mechanisms of serial TCM "Huoxuehuayu" prescriptions on cerebral ischemia-reperfusion injury in rats / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To determine effects and mechanisms of traditional Chinese medicine serial "Huoxuehuayu" (activating blood flow and removing blood stasis) prescriptions on cerebral ischemia-reperfusion injury in rats.</p><p><b>METHODS</b>Focal cerebral ischemia was induced by 60 min of middle cerebral artery occlusion (MCAO) and followed by 3 d reperfusion. Drugs were orally administered 1 h before MCAO and 4 h after reperfusion and the following 2 d. The neurological scores were evaluated 3 d after reperfusion. Then the animals were sacrificed, the infarct volumes, right and left areas of brain section, the pathologic changes and the normal neurons in hippocampal CA1 and cortex were determined by using an image analyzer. Nitric oxide synthase (NOS), superoxide dismutase (SOD) activities and malondialdehyde (MDA) content in brain tissue were evaluated by spectrophotography. The expression of NMDA R1 subunit (NR1) and endothelial NOS (eNOS) was determined by immunoblotting technique.</p><p><b>RESULT</b>Serial "Huoxuehuayu" prescriptions and nimodipine improved neuronal dysfunction, and reduced infarct size and brain edema. Serial Huoxuehuayu prescriptions and nimodipine reduced MDA content and NOS activity, and increased SOD activity. Western blotting analysis demonstrated induction of NR1.</p><p><b>CONCLUSION</b>Serial Huoxuehuayu prescriptions have a protective effect on cerebral ischemia-reperfusion injury by reducing NOS activity, MDA content, expression of NR1 and increasing SOD activity.</p>

Serum levels of soluble intercellular adhesion molecule-1 in patients with cerebral infarct / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To observe the changes of the levels of soluble intercellular adhesion molecule-1(sICAM-1) in serum of patients with cerebral infarct and to explore the effect of sICAM-1 on cerebral infarct.</p><p><b>METHODS</b>The serum levels of sICAM-1 in 55 patients with cerebral infarct both in acute stage(within 2 days) and convalescence(2 weeks after attack) were detected by using ELISA. At the same time, we compare the results with those of 32 patients having other neurologic diseases(20 patients with sciatica, 12 with trigeminal neuralgia) and 30 healthy subjects.</p><p><b>RESULTS</b>(1) The serum levels of sICAM-1 of patients with cerebral infarct (acute stage: 766+/-179 microgram/L, convalescence: 602+/-155 microgram/L, respectively) were significantly higher than those of the control groups(530+/-77 microgram/L and 521+/-116 microgram/L, respectively, P<0.01). (2)There was a positive correlation of SICAM levels with the amount of leukocytes in acute stage(r=0.285,P<0.05), but negative correlation to clinical severity of cerebral infarct(r= 0.333,P<0.05). And there was no significant correlation between the level of sICAM-1 and the levels of cholesterol and triglyceride in serum(r= 0.042 and r=0.061, respectively, P>0.05). (3)There was no significant difference between sICAM levels of patients of cerebral cortex infarct and those of patients with basal ganglia infarct(773+/-178 microgram/L and 758+/-183 microgram/L, respectively, P>0.05). (4)The levels of sICAM-1 between patients of cerebral infarct with or without hypertension were no significant difference(774+/-189 microgram/L and 754+/-165 microgram/L, respectively, P>0.05).</p><p><b>CONCLUSION</b>The levels of sICAM-1 increase significantly in patients with cerebral infarct. sICAM-1 may participate in the pathophysiologic process through inflammatory mechanism.</p>