Acupuncture Treatment of Depressive Syndromes after Cerebral Vascular Accidents

Depressive syndrome is a common complication in cerebral vascular accidents (CVA), which accounts for 70% of the complications. A mild case of the syndrome is marked by grief, sleeping disturbance, weakened mental activities, worry, loss of interest, and irritability. A severe case may have worse symptoms and signs, except the above mentioned ones, such as anxiety, reduced appetite, hallucination, delusion, desperation, etc. The author has adopted acupuncture to treat depressive syndromes after CVA with good therapeutic result as reported in the following.

Risk factors of postoperative cerebral hyperperfusion syndrome and its relationship with clinical prognosis in adult patients with moyamoya disease

Background To investigate the incidence,risk factors,and clinical prognosis of cerebral hyperperfusion syndrome(CHS)after superficial temporal artery-middle cerebral artery anastomosis combined with encephalo-duro-arterio-synangiosis(STA-MCA/EDAS)in adult patients with moyamoya disease(MMD).Methods The clinical data of 160 adult patients with MMD treated by STA-MCA/EDAS from January 2016 to January 2017 were retrospectively analyzed.According to CHS diagnosis,MMD patients were divided into CHS and non-CHS group.Univariate and multivariate analysis of risk factors and Kaplan-Meier curve of stroke-free survival for CHS were performed.Results A total of 12 patients(7.5%)developed postoperative CHS,of which 4 patients(2.5%)presented with cerebral hemorrhage.Univariate and multivariate analysis showed moyamoya vessel on the surgical hemisphere(OR=3.04,95%CI=1.02-9.03,P=0.046)and left operated hemisphere(OR=5.16,95%CI=1.09-21.34,P=0.041)were independent risk factors for CHS.The other variables,such as age,gender,presentation,hypertension,diabetes,smoking,mean mRS score on admission,modified Suzuki stage and pre-infarction stage on surgical hemisphere,and bypass patency,had no association with postoperative CHS(P>0.05).At final follow-up with average 38 months,there were 18 out of 133 patients(13.5%,4.91%per person year)presented with newly developed complications.There was no significant difference between newly developed complications,mean mRS scores,and Kaplan-Meier curve of stroke-free survival in patients with and without CHS(P>0.05).Conclusion The concentration of moyamoya vessels and left operated hemisphere was independent risk factors for CHS,which could not affect the clinical prognosis if treated timely and properly.The current study offers a new perspective of moyamoya vessels and supporting data for choosing MMD candidates on cerebral revascularization.

Prediction of Cerebral Hyperperfusion Syndrome with Velocity Blood Pressure Index

Background：Cerebral hyperperfusion syndrome is an important complication of carotid endarterectomy （CEA）.An 〉 100% increase in middle cerebral artery velocity （MCAV） after CEA is used to predict the cerebral hyperperfusion syndrome （CHS） development,but the accuracy is limited.The increase in blood pressure （BP） after surgery is a risk factor of CHS,but no study uses it to predict CHS.This study was to create a more precise parameter for prediction of CHS by combined the increase of MCAV and BP after CEA.Methods：Systolic MCAV measured by transcranial Doppler and systematic BP were recorded preoperatively;30 min postoperatively.The new parameter velocity BP index （VBI） was calculated from the postoperative increase ratios of MCAV and BE The prediction powers of VBI and the increase ratio of MCAV （velocity ratio [VR]） were compared for predicting CHS occurrence.Results：Totally,6/185 cases suffered CHS.The best-fit cut-off point of 2.0 for VBI was identified,which had 83.3% sensitivity,98.3% specificity,62.5% positive predictive value and 99.4% negative predictive value for CHS development.This result is significantly better than VR （33.3%,97.2%,28.6% and 97.8%）.The area under the curve （AUC） of receiver operating characteristic：AUCvBI =0.981,95% confidence interval [CI] 0.949-0.995;AUCvR =0.935,95% CI 0.890-0.966,P =0.02.Conclusions：The new parameter VBI can more accurately predict patients at risk of CHS after CEA.This observation needs to be validated by larger studies.

Homozygous Mutation in the MTHFS Gene May Contribute to the Development of Cerebral Folate Deficiency Syndrome

Objective:The purpose of this study was to examine the role of rare variants in the one-carbon metabolic pathway in the etiology of the cerebral folate deficiency(CFD)syndrome.The CFD syndrome is a neurometabolic syndrome identified by low concentrations of 5-methyltetrahydrofolate(5-MTHF)in the cerebrospinal fluid(CSF)in spite of near-normal peripheral folate levels resulting in neurodevelopmental disorders.Methods:The localized folate metabolism impairments in CFD are thought to be either the result of mutations in genes responsible for folate transport or folate turnover through degradation.Genes that have been previously implicated in the etiology of CFD include folate receptor alpha-1(FOLR1),dihydrofolate reductase,proton-coupled folate transporter,and capicua.We performed whole-exome sequencing(WES)analysis of a CFD patient that revealed 99 novel missense mutations,of which 21 were classified as damaging mutations through the Poly-Phen2 prediction algorithm.In vitro functional studies were conducted by transient transfection of wild-type and mutant MTHFS into HEK293T cells to determine the impact of the variants on enzyme activity.Results:Of the damaging variants identified in the WES studies,we focused on the gene coding for the enzyme 5,10-methenyl-tetrahydrofolate synthetase(MTHFS).This enzyme catalyzes the production of methenyl THF which is subsequently converted to 5-MTHF.The CFD patient described within was found to carry a homozygous mutation,c.101G>T(p.R34L,rs200058464)in MTHFS,while the parents of the proband are heterozygotes for the MTHFS gene,and the healthy sibling is not a carrier.Conclusion:The mutant allele displayed a 50%reduction in luciferase activity(P<0.05),suggesting that homozygous loss of the MTHFS gene may play a significant role in the development of CFD.

Risk factors and causes of hyponatremia in patients after radiotherapy for head and neck cancer:A retrospective study

Background:Hyponatremia is the most frequently encountered electrolyte abnormality which is caused by kinds of reasons including kidney,metabolic and central nervous system diseases.The adverse effects of hyponatremia include but not limit to cerebral edema and seizures,which often aggravate neurological damage.Therefore,early diagnosis and intervention would reduce the risk of adverse effects of hyponatremia.Objective:To investigate the differences between patients with or without hyponatremia after radiotherapy for head and neck cancer,and to explore the risk factors and causes of hyponatremia.Methods:Patients who aged over 18 years old and underwent radiotherapy for head and neck cancer were collected from Department of Neurology,Sun Yat-Sen Memorial Hospital from January 2012 to July 2018.The comorbidities of patients and demographic and serological data were retrospectively collected to investigate the causes and risk factors of hyponatremia in these patients.Differences of the length of hospital stay and the cognitive function between patients with and without hyponatremia were analyzed.Results:In this study,798 patients were reviewed.The incidence of hyponatremia was 17.9%.Risk factors of hyponatremia included age(OR 1.05,95%CI 1.03–1.07,P<0.001),gender(OR 0.62,95%CI 0.39–0.99,P=0.046),medical history of hypothyroidism(OR 2.42,95%CI 1.26–4.09,P紏0.006),adrenal insufficiency(OR 15.61,95%CI 2.73–89.07,P=0.002)or dysphagia(OR 1.81,95%CI 1.24–2.65,P=0.002).The most common cause of hyponatremia was cerebral salt-wasting syndrome(CSWS)(32.9%).The insufficient intake due to dysphagia(29.4%),and hypothyroidism(13.3%)were also common in these patients.Clinically,hyponatremia resulted in the prolonged hospitalization time.Conclusion:Hyponatremia would be common in patients who underwent radiotherapy for head and neck cancer.The importance of distinguishing the etiology of hyponatremia is addressed.