Combination of High-Density Lipoprotein Cholesterol and Lipoprotein(a) as a Predictor of Collateral Circulation in Patients With Severe Unilateral Internal Carotid Artery Stenosis or Occlusion

Background@#and Purpose Collateral circulation is considered an important factor affecting the risk of stroke, but the factors that affect collateral circulation remain unclear. This study was performed to identify the factors associated with collateral circulation, especially blood lipids. @*Methods@#The study involved patients who had undergone digital subtraction angiography and were confirmed as having severe unilateral stenosis or occlusion of the internal carotid artery (ICA). We classified the collateral circulation status of each patient as good (Grade 3 or 4) or poor (Grade 0, 1, or 2) according to the grading system of the American Society of Interventional and Therapeutic Neuroradiology/American Society of Interventional Radiology. We collected data on patients’ characteristics and identified the factors that affect collateral circulation. @*Results@#This study included 212 patients. The multivariate logistic regression analysis showed that the high-density lipoprotein cholesterol (HDL-C) concentration and a complete anterior half of the circle of Willis were independent protective factors for good collateral circulation, whereas elevated lipoprotein(a) [Lp(a)] and serum creatinine concentrations were independent risk factors for good collateral circulation. The area under the receiver operating characteristics curve (AUC) was 0.68 (95% confidence interval [CI], 0.61–0.76) for HDL-C and 0.69 (95% CI, 0.62–0.76) for Lp(a). A binary logistic regression model analysis of the joint factor of HDL-C and Lp(a) yielded an AUC of 0.77 (95% CI, 0.71–0.84). @*Conclusions@#In patients with severe unilateral ICA stenosis or occlusion, the combination of HDL-C and Lp(a) is a useful predictor of collateral circulation.

Progress in the diagnosis and treatment of rapid eye movement sleep behavior disorder / 中国临床药理学与治疗学

Rapid eye movement sleep behavior disorder (RBD) is characterized by dream enactment and rapid eye movement (REM) sleep without atonia. RBD is closely related to α-synucleinopathy disease, including Parkinson's disease (PD), Lewy body dementia (DLB) and multiple system atrophy (MSA). Many studies have discussed the markers, heredity, cognition, autonomic nervous function of RBD, and the predictive value for neurodegenerative diseases. This article reviews the research progress of early markers and treatments in recent years, and discusses future research directions.

The P2X7 receptor in activated microglia promotes depression- and anxiety-like behaviors in lithium -pilocarpine induced epileptic rats.

Depressive and anxious behaviors are the most common psychiatric symptoms of epilepsy, and may aggravate the epileptic condition and affect the patient's quality of life. Accumulating data obtained from both experimental animal models and patients have convincingly shown a critical role of P2X7 receptor (P2X7R) during depression and anxiety. Our study showed for the first time that the P2X7R is involved in promoting depression- and anxiety-like behaviors in lithium pilocarpine-induced epileptic rats. More importantly, direct anti-depressive and anti-anxiety effects were produced by the P2X7R antagonist Brilliant Blue G (BBG) is in this study, and the effect was similar to that of the classic anti-depressant and anti-anxiety drug fluoxetine. We also found that BBG did not affect the development of spontaneous recurrent seizures (SRS) and had a neuroprotective effect via inhibition of microglial activation after status epilepticus (SE). Thus, our data provide evidence that the P2X7R in activated microglia promotes depression- and anxiety-like behaviors in lithium-pilocarpine induced epileptic rats. Since previous studies have indicated that some anti-depression and anti-anxiety drugs may exacerbate seizures, our data support that the P2X7R is a promising therapeutic target for epilepsy associated with depression and anxiety.

Losartan inhibits development of spontaneous recurrent seizures by preventing astrocyte activation and attenuating blood-brain barrier permeability following pilocarpine-induced status epilepticus.

Blood-brain barrier (BBB) damage and astrocyte activation are important cause of recurrent epilepsy. There is experimental evidence for increased angiotensin receptor type 1 (AT1) expression during BBB breakdown and brain injury, and that blocking the AT1 receptor (e.g., with losartan) can improve microcirculation, attenuate inflammation and oxidative stress, and exhibit neuroprotective effects. Thus, in the present study, we examined the effects of losartan on status epilepticus-induced astrocyte activation and BBB damage in the lithium-pilocarpine model of epilepsy in rats. We found that losartan treatment reduced astrocyte activation and BBB damage. However, under physiological condition, losartan have not effect on BBB permeability and astrocyte activation. Further, losartan exhibited a direct antiepileptic effect, which was mediated, at least in part by normalizing AQP4 expression after SE. As the changes of AQP4 expression were closely related to astrocyte activation and BBB permeability, the antiepileptic action of losartan likely relates to its effects on astrocyte activation and BBB permeability. Overall, these data suggest that losartan may be a useful antiepileptic agent in the clinic, either alone or in combination with other antiepileptic drugs.

Changes in CD40 expression in the pallium and hippocampus in epileptic rats / 中南大学学报(医学版)

OBJECTIVE@#To investigate the expression of inflammatory molecule CD40 in the pallium and hippocampus of rats after status epilepticus (SE).
@*METHODS@#The expression of CD40 in the pallium, the different areas of hippocampus and the different cells from the lithium-pilocarpine epileptic rats at different time points were examined by immunohistochemistry and double-immunofluorescent labeling.
@*RESULTS@#After SE, CD40 expression was obviously inhibited, especially in hippocampus. CD40 was mainly expressed in the activated microglia. CD40 positive cells reached a peak at the 3rd day and returned to a slightly higher level at the 7th day after SE compared with the level before SE.
@*CONCLUSION@#Elevation of CD40 expression in the activated microglia can promote inflammatory injury of rat's hippocampus, suggesting that CD40 induced-signal pathway is involved in inflammatory injury in the hippocampus after SE.

The PPARγ agonist rosiglitazone prevents neuronal loss and attenuates development of spontaneous recurrent seizures through BDNF/TrkB signaling following pilocarpine-induced status epilepticus.

Hippocampal neuronal loss plays an important role in epileptogenesis, and it is considered a trigger of repeated spontaneous recurrent seizures (SRS). The BDNF/TrkB signaling pathway regulates neuronal plasticity in the CNS, and promotes epileptogenesis. Previous studies have shown that Peroxisome proliferator-activated receptor gamma (PPARγ) agonists exert neuroprotective effects by inhibiting oxidative stress and inflammation in epilepsy. In the present study, the PPARγ agonist rosiglitazone inhibited increases in BDNF and TrkB after status epilepticus (SE), and also prevented hippocampal neuronal loss. More importantly, our study showed that rosiglitazone suppressed SRS. However, the effects of rosiglitazone were significantly reversed by cotreatment with K252a, an antagonist of TrkB. Additionally, rosiglitazone did not affect the development and severity of SE. Thus, our data provide evidence that rosiglitazone exerts neuroprotective and antiepileptic effects involve BDNF/TrkB signaling. Our study also offers new perspectives for the treatment of epilepsy.

The PPARγ agonist rosiglitazone prevents cognitive impairment by inhibiting astrocyte activation and oxidative stress following pilocarpine-induced status epilepticus.

Epilepsy is commonly associated with cognitive impairment. Astrocyte activation and oxidative stress occur following seizures, and play a role in the pathological injury of epilepsy with cognitive impairment. The peroxisome proliferator-activated receptor gamma (PPARγ) has been shown to exhibit neuroprotective and antioxidative effects in CNS diseases. Thus, we hypothesized that rosiglitazone, a PPARγ agonist, would prevent cognitive impairment by inhibiting astrocyte activation and regulating glutathione (GSH) homeostasis after status epilepticus (SE). Using a lithium pilocarpine-induced SE model, we found that rosiglitazone significantly prevented cognitive impairment induced by SE, and potently inhibited astrocyte activation with maintenance of GSH homeostasis in the hippocampus after SE. These protective effects were significantly reversed by co-treatment with the PPARγ antagonist T0070907. These data suggest that rosiglitazone can improve cognitive impairment, and inhibit astrocyte activation and oxidative damage following SE. Rosiglitazone may be a promising agent for treatment of epilepsy involving SE-induced cognitive impairment.

Idiopathic intracranial hypertension with obstructive sleep apnea: a case report / 中华神经科杂志

Objective To report a case of continuous positive airway pressure (CPAP) treatment for obstructive sleep apnea (OSA) combined with idiopathic intracranial hypertension (IIH) and review the relationship between the IIH and OSA. Methods A case of increased intracranial pressure in a middle-aged male patient who was diagnosed as IIH after the MRI and angiography ruled out intracranial lesions was reported. This patient presented with drowsiness, obesity and other symptoms. An overnight polysomnography (PSG) confirmed severe OSA. The simple use of intracranial pressure lowering therapy could not achieve sustained effective control of symptoms of high intracranial pressure. The clinical effects of comprehensive treatment for the OSA including CPAP and weight loss were observed. Results After 3 months treatment, the body mass index of this patient dropped from 35.7 to 31.4, apnea hypopnea index dropped from 72.6 to 10. 1, and the minimum SaO2 increased from 67% to 82%. And the symptoms of high intracranial pressure including headache and papillaedema were continuously improved. Conclusion Sleep apnea is a risk factor for IIH, especially for obese male patients. PSG monitoring could help us to find the important but easily overlooked factor of OSA. Taking active measures to treat OSA can effectively relieve the high intracranial pressure symptoms in patients with IIH.

Acute changes of polysomnography in major depressive disorder patients treated with mirtazapine / 中华神经科杂志

Objective To evaluate the acute effects of mirtazapine on sleep polysomnographic variables in patients with major depressive disorder (MDD) using polysomnography (PSG). Methods Twenty-five MDD patients took mirtazapine 15 mg an hour before bedtime during the first three days and then 30 mg during the following four days. Polysomnographic and clinical data were collected at baseline and on the 7th day. Results The scores on the Athens Insomnia Scale (AIS,7.92±3.86,t=10.255,P=0.000), the Hamilton Anxiety Rating Scale (HAMA,6.84±5.57,t=6.137, P=0.000) and the Hamilton Depression Rating Scale (HAMD-17,9.80±4.41,t=12.132,P =0.000) decreased rapidly after a 7-day medication. PSG showed mirtazapine administration significantly increased the total sleep time (402.46±80.75,t=-2.990,P=0.006), the sleep efficiency (76.17%±10.65%,t=-2.750,P=0.011), and the slow wave sleep percentages(19.66%±11.43%,t=3.236, P=0.004) and decreased the wake time after sleep onset (80.38±48.02,t=2.972,P =0.007). However, there was no significant difference in the sleep latency, the number of awakening, the rapid eye movemert (REM) sleep latency, the ratio of REM sleep and the frequency of REM sleep episode. Conclusion Mirtazapine as monotherapy in the treatment of MDD has relieved depressive symptoms rapidly and significantly, increased the total sleep time, the sleep efficiency and the slow wave sleep percentages thus to achieve better sleep quality.

Peripheral neuropathy in multiple sclerosis:an electromyographic and pathological study / 中华神经科杂志

Objective To investgate the electromyographic and pathological features of peripheral nerve involvement in MS,and clarify factors that affect the involvement of PNS Methods Thirty three multiple sclerosis(MS) patients were selected according to Poser's definite diagnosis of MS,without other nervous system disorders and thirty volunteers served as controls All subjects received nerve conduction study:MCV,SCV,F wave and H reflex Sural nerve biopsy and pathological change were observed in light and electronic microscope Results Electromyograph findings:decreased CMAP of the median,tibial and peroneal nerves,and high amplitude of SAP of median and ulnar nerves were observed in MS Our study also showed the prolonged F wave response and H reflex in median and tibial nerves,low F wave rates Electrophysiologic abnormalities in MS showed close relationship to the EDSS,duration and lesion position in spinal cord Sural nerve biopsy revealed myelinated nerve fibers with segmental demyelination by light microscope Inflammatory cellular infiltration and onion bulb formation were not found? Axonal degeneration and laminae dissociation in myelin sheath were demonstrated by electromicroscope Conclusion MS is a demyelinating disease attacking to CNS In some MS patients,both CNS and PNS might be involved at the same time The peripheral demyelinating lesions seem to be common in spinal nerve root But the secondary axonal degeneration in distal segment should be another pathologic feature of MS EMG is a useful test method to evaluate the peripheral nerve damage and prognosis of MS

STUDIES ON THE RELATIONSHIP BETWEEN SUBSTANCE P AND ABNORMAL GASTROINTESTIANL TRANSIT / 药物分析学报

Objective To realize the relationship between substance P(SP) and abnormal gastrointestinal tran- sit. Methods By radioimmunoassay, concentration of SP in sigmoid mucosa was determined in 12 healthy volun- teers, 15 slow and 10 fast transit patients. ResultsThe concentration was (27.68±15.42)μg/g, (24.07+5.76)μg/g and (28.61± 18.34)μg/g,respectively. They had no statistical difference. Conclusion There was no relationship be- tween concentration of SP in sigmoid mucosa and abnormal gastrointestinal transit.