Cerebral paragonimiasis: A retrospective analysis of 89 cases

Purpose

We reviewed the clinical and follow-up data of 89 cases with cerebral paragonimiasis and summarized the disease characteristics, diagnostic strategies and treatment experience, with an expectation of establishing standard diagnosis and treatment for cerebral paragonimiasis.

Methods

A total of 89 cases (age: 2–64 years) of cerebral paragonimiasis admitted and treated in our hospital in the past 10 years were included in this study. The clinical symptoms were manifested by headache, epilepsy, paralysis, etc. In order to confirm the diagnosis, we performed imaging examinations (e.g., CT and MRI) and laboratory tests (ELISA and eosinophil counting). Seventy-two patients received oral administration of praziquantel only, 16 cases received surgical resection of the lesions and 33 cases received appropriate anti-epileptic therapies. The diagnostic, treatment and follow-up data were statistically analyzed.

Results

Follow-up was performed for 73 cases for a period of 6–48 months and the original symptoms were markedly improved without recurrence. 15 patients were lost to follow-up after discharge. One patient died of epilepticus insult, high fever and convulsions. Although 4 patients still had seizures within 6 months of treatment, seizure frequency was significantly reduced. Histopathological evaluation demonstrated inflammatory changes with esoinophilic infiltration in all 16 patients who underwent surgical resection.

Conclusions

Young patients (age: <18 years) are more likely to have cerebral hemorrhage. SWI imaging contributes to the diagnosis of hemorrhagic lesions. Cerebral paragonimiasis can cause epilepsy, especially grand mal seizures.     

脑淀粉样血管病变与脑微出血

脑淀粉样血管病（CAA）是造成血压正常的老年人自发性皮质．皮质下脑内出血的重要原因。由于很多病例无症状,对共诊断及预防受到很大限制。研究显示,脑微出血（CMB）和CAA的发生与预后密切相关,本研究仅对CAA与CMB的相关性做一综述。     

脑血管支架成形术后脑高灌注综合征

目的 探讨脑动脉支架成形术后高灌注综合征（cerebral hyperperfusion syndrome,CHS）的发病机制及 临床表现。 方法 回顾性分析中国人民解放军第306医院4例脑动脉狭窄支架成形术后发生CHS患者的临床资料。 结果 本组4例CHS中男性3例,女性1例,年龄43～77岁。2例行颈动脉狭窄支架成形术（carotid artery stenting,CAS）,1例行CAS及椎动脉支架置入术,1例行基底动脉狭窄支架成形术。发生CHS症状时间 在术后1 h～3 d。症状为头痛3例,右侧肢体偏瘫1例,视物不清1例,意识障碍1例,头计算机断层扫描 （computed tomography,CT）提示脑实质出血2例,蛛网膜下腔出血1例,脑水肿1例。经降压、脱水等治 疗后,3例均恢复良好,1例死亡。 结论 脑动脉支架成形术后CHS是一种少见及严重的疾病,需提高认识,尽早诊断,尽早治疗。     

无症状性脑梗塞患者脑血流灌注的相关研究

目的:探讨无症状性脑梗塞(Slient Cerebral lnfarction,SCl)患者的脑血流灌注状况,确定监测病情变化的有效手段。方法:采用Diamox药物负荷,99mTc-ECD SPECT核素显像技术,对20例SCI患者及15例正常对照组进行静态时及负荷后脑血流定量测定。结果:1、静态显像时,SCI组大脑平均脑血流量、额、颞、顶叶皮质及基底节区局部脑血流较对照组轻度降低(P<0.05),负荷后与对照组相比血流降低更加明显(P<0.01);2、危险因素种类个数与SCI患者平均脑血流变化呈有意义的负相关(r=-0.5648,P<0.05)。结论:SCI患者脑血流灌注处于低下状态,脑血管代偿能力降低;2、危险因素的累积作用进一步降低SCI患者的血流灌注;负荷脑血流定量检测技术能客观地反映SCI的脑循环动态情况,可作为有效的病情监测手段。     

Cerebral malaria

Cerebral malaria may be the most common non-traumatic encephalopathy in the world. The pathogenesis is heterogeneous and the neurological complications are often part of a multisystem dysfunction. The clinical presentation and pathophysiology differs between adults and children. Recent studies have elucidated the molecular mechanisms of pathogenesis and raised possible interventions. Antimalarial drugs, however, remain the only intervention that unequivocally affects outcome, although increasing resistance to the established antimalarial drugs is of grave concern. Artemisinin derivatives have made an impact on treatment, but other drugs may be required. With appropriate antimalarial drugs, the prognosis of cerebral malaria often depends on the management of other complications-for example, renal failure and acidosis. Neurological sequelae are increasingly recognised, but further research on the pathogenesis of coma and neurological damage is required to develop other ancillary treatments.     

Cerebral vasospasm

The cellular mechanisms responsible for cerebral vasospasm (CVS) occurring after subarachnoid hemorrhage (SAH) have been of major interest over the past 50 years. The present review describes how each of the discrete anatomic components that comprise the cerebral artery may contribute to the pathology of CVS. The blood extravasated after SAH is hemolyzed and undergoes degradation with resultant production of free radicals, known to be powerful initiators of vascular damage. An inflammatory response is generated activating both leukocytes and platelets with subsequent release of inflammatory agents. The cerebral artery affected by CVS undergoes phenotypic change involving both the endothelial and smooth muscle cells. In the endothelium the production of nitric oxide and prostacyclin is affected. In the smooth muscle cells signal transduction pathways that enhance the function of the contractile proteins and induce the upregulation of contractile receptors are activated. In parallel, there is evidence that nervous reflex pathways involving the trigeminal ganglion and the hypothalamus are activated. However, the relative contributions of each of the systems are speculative. Therapy may be directed at disrupting the cascade leading from the SAH insult to CVS or at overcoming the dysfunction incurred by CVS; possible therapeutical interventions are considered.     

Cerebral gangliocytoma

Summary We report a case of cerebral gangliocytoma (GC) with a variety of unusual structures in the tumor cells. Light microscopically, the tumor consisted of typical ganglion cells, atypical cells which has argyrophilic granules in the cytoplasm, and a few astrocytes. Electron microscopically, the tumor cells showed typical gangliocytic features, which had abundant rough endoplasmic reticula, ribosomes and cored vesicles of 90–150 nm diameter, a few 50-nm-diametered non-cored vesicles, and other common organelles in their cytoplasm. Furthermore, neoplastic ganglion cells contained a variety of abnormal structures, including membranous cytoplasmic bodies (MCB), Zebra bodies (ZB), tubular structures, branched tubular structures (BTS), concentrical laminated bodies and curvilinear bodies (CB). The MCB, ZB and CB resembled those in GM2 gangliosidosis (GMG), and the BTS that in infantile neuroaxonal dystrophy (INAD). Although the significance of these inclusions is still unknown, it is considered that some common mechanism might play a role in the metabolism of both neoplastic neuronal cells and degenerating neurons (GMG and INAD). Synapses could not be observed anywhere despite complete neuronal differentiation of many tumor cells.