[Carotid artery dissection with Horner syndrome as main manifestation: a case report].

A 44-year old male patient was admitted to the First Affiliated Hospital, Zhejiang University School of Medicine with left ptosis and pain on the left head and neck for 20 days.Brain MRI showed subacute cerebral infarction on left parietal lobe and intramural hematoma on left internal carotid artery. CT angiography showed stenosis line on the C1 segment of left internal carotid artery. Digital subtraction angiography showed dissection on the C1 segment of left internal carotid artery.The condition of patients was improved after anticoagulant therapy.

Protective action of B1R antagonist against cerebral ischemia-reperfusion injury through suppressing miR-200c expression of Microglia-derived microvesicles.

BACKGROUND AND OBJECTIVE: Cerebral ischemia-reperfusion (I/R) injury is a common side-effect for cerebral ischemic disease and its therapeutic regimen is limited. Kinin is pro-inflammatory peptide that is released and acts at the site of injury and inflammation such as brain and it works through bradykinin 1 receptor (B1R). The present study was to examine the effect of B1R antagonist on cerebral I/R injury and the potential mechanism. METHODS: Cerebral I/R injury was induced in mice by transient middle cerebral artery occlusion (MCAO). Neurological function was assessed by Bederson score. Infarct volumes were measured using planimetry. In vitro cell model was made by oxygen-glucose deprivation-Hypoxia/Reoxygenation (OGD-H/R) treatment to N9 microglia cell; and the cultured medium was collected for microvesicles (MVs) isolation and subsequent co-cultured with HT22 cell for sake of assessing their function on neural cell. Relative expression of miR-200c was determined by real time quantitative PCR. Dual luciferase reporter assay was performed to detect the regulatory function of miR-200c to syntaxin-1A. RESULTS: R715 (B1R antagonist) treatment (500 µg/kg) improves neurologic function after cerebral I/R injury indicated by the decrease of Bederson score and infarct volume. MVs from OGD-H/R treated-N9 cell attenuated neural HT22 cell viability, treatment with LDBK (B1R agonist) accelerated the suppression of HT22 resulted from OGD-H/R; whereas this attenuation was partly weakened by B1R antagonist pretreatment (100 nmol/L). At the same time, B1R antagonist pretreatment caused downregulation of miR-200c in N9 cell and N9-derived MVs, and contributed to syntaxin-1A over expression in HT22 cell. Result of luciferase reporter assay suggested that miR-200c can regulate syntaxin-1A expression. MVs from miR-200c knockdown N9 cells medium had the same effect of B1R antagonist that caused the upregulation of syntaxin-1A and improved OGD-H/R-induced reduction of HT22 cell viability. CONCLUSION: Our data suggested that blockage of B1R by B1R antagonist provides neuroprotection action through suppressing signaling delivery of microglia-MVs-miR-200c to neural cell.

TCD study of hemodynamic changes in PCA response to photic stimulation.

OBJECTIVES: During visual stimulation, the elevated metabolism rate will couple with increase of blood flow velocity(BFV) in posterior cerebral artery(PCA). This study with TCD was aimed to investigate whether the coupling might change according to the different vasoneuronal conditions. METHODS: Ninety-nine volunteers including 24 hypertension(HT) patients and 2 patients suffering from both HT and diabetes mellitus (DM) were enrolled in this trial. BFV and pulse indexes(PI) in P2 segments of PCA on both sides were monitored during visual stimulation. RESULTS: In all subjects, Mean BFV increased and PI went down in response to visual stimulation. The percentages of changes (deltaV and deltaP) of both mean BFV and PI were larger in young group( < 55 years old) than in old one(> or = 55 years old). There was significant positive correlation between deltaV and deltaP. Multivariated regression analysis did not show HT and DM, but age related to deltaV(deltaP). We did not find significant difference of deltaV(deltaP) between left and right sides. CONCLUSIONS: Blood flow velocity in PCA P2 segment increased due to decreased cerebrovascular resistance during visual stimulation and the response weakened with aging of the patient.

MRS study on lentiform nucleus in idiopathic Parkinson's disease with unilateral symptoms.

OBJECTIVE: To investigate changes in magnetic resonance spectroscopy (MRS) of lentiform nucleus during the early stage of Parkinson's disease. METHODS: Twenty-five patients with idiopathic Parkinson disease with unilateral symptoms (IPDUS) and 25 healthy volunteers were enrolled in this study. MRS of the lentiform nucleus in each patient was taken and then concentrations of N-acetylaspartate (NAA), Creatine (Cr) and Choline (Cho) were calculated. RESULTS: Compared to that in the control, NAA/ (Cho+Cr) was significantly lower in the lentiform nucleus contralateral to symptoms and even that in the ipsilateral side in IPDUS patients (all P<0.05); while there was no difference between the two sides in the healthy volunteer (P>0.05). The ratio of NAA/(Cho+Cr) ipsilateral to the sympatomatic side of the patient was also lower than that of the control (P<0.05). CONCLUSIONS: There might be some changes with MRS on the lentiform nucleus during the early stage of idiopathic Parkinson's disease with unilateral symptom. MRS may be one of the reliable methods for early or even sub-clinical diagnosis.

[Dynamical examination of auditory event-related potentials P300 and sympathetic skin response in people with insomia of Sweet Dream Capsule therapy].

OBJECTIVE: To observe the change of auditory event-related potentials (P300) and sympathetic skin response (SSR) in people with insomia of Sweet Dream Capsule therapy. METHODS: 30 patients meeting criteria for primary insomnia and 30 healthy volunteers with age matching controls were selected for the study. P300 and SSR were measured before treatment of Sweet Dream Capsule and at week 4 , 8 of the therapeutic course. That the change of P300 and SSR before and after treatment and their relations with PSQI were studied. RESULT: Compared with those of normal controls, both P300 latency and SSR latency were prolonged while amplitude was decreased in patients with insomnia (P < 0.01). P300 amplitude was increased significantly at central (Cz) electrode sites only at week 8 when compared with amplitude before treatment (P < 0.05). With improvement of symptom and PSQI scores, latency and amplitude of SSR were improved at week 4 and week 8 (P < 0.05 and P < 0.01) . CONCLUSION: P300 has a some improvement in people with insomia of Sweet Dream Capsule therapy while SSR im proves significantly, and PSQI scores are ameliorated too.