2016年 · 第32卷第09期

At present, the commonly used surgical methods for hydrocephalus are divided into catheter shunt surgery and neuroendoscopic surgery, both of which play an important role in the treatment of hydrocephalus. However, catheterization shunt brings many disadvantages due to implants, such as shunt obstruction and improper location, infection, excessive shunt and shunt dependence, etc. Although the manufacturing process of the shunt pipe has been greatly improved at present, and the adjustable pressure shunt pipe and the anti-infection shunt pipe have appeared, the above problems still cannot be completely solved. endoscopic third ventriculostomy (ETV) can avoid shunt implantation and related complications. The surgical method conforms to the physiological characteristics of human cerebrospinal fluid circulation, and the incidence of postoperative complications is relatively low. At present, it is gradually replacing catheter shunt surgery and becoming the first choice for the treatment of obstructive hydrocephalus^[1,2,3,4]。

moyamoya syndrome (MMS), also known as moyamoya-like disease, refers to cerebrovascular disease caused by more than one underlying disease, in which the terminal end of bilateral or unilateral internal carotid artery (ICA) or the initial segment of middle cerebral artery (MCA) or anterior cerebral artery (ACA) is narrowed or occluded, accompanied by abnormal vascular network formation. Its underlying diseases include: Graves disease, atherosclerosis, systemic lupus erythematosus, etc^[1,2]。 MMS combined with Graves' disease is rare in clinical practice. Since the first case of hyperthyroidism (hyperthyroidism) MMS was reported in 1991, people have gradually discovered that there are potential common pathophysiological mechanisms between the two. This article retrospectively analyzed the clinical data of five patients with MMS complicated with Graves' disease admitted to the Department of Neurosurgery of Aviation General Hospital of China Medical University from January 2011 to July 2015, and now reported as follows.

A 34-year-old male was found to have a progressive enlarged mass in front of the right ear for more than 2 months. Physical examination: There is a 2cm ×3cm subcutaneous texture in front of the right ear, and there is no redness, swelling and tenderness in the skin. CT examination of the head showed subcutaneous lesions in the right temporal region and space-occupying lesions in the right middle fossa (Figure 1)。 During the operation, the tumor appeared fleshy brown, hard in texture, with calcified tissue inside, adhered to the maxillary joint, invaded and destroyed the bone in the anterior wall of the external auditory canal, the anterior wall of the Eustachian tube, and the inner side of the zygomatic arch, destroyed the temporal bone and protruded into the cranium, invaded the dura mater, and destroyed the bone in the skull base and protruded into the cranium. The boundary between tumor and normal bone is clear, and it is easy to scrape out with a curette. Skull base reconstruction was performed after tumor resection. Pathological examination: The submitted object was dark red tissue with a total volume of about 3cm ×5cm ×7cm, hard in texture and scattered calcification. Microscopically, the tumor was composed of chondroblasts, multinucleated giant cells and chondroid matrix (Figure 1)。 Immunohistochemical results: AE1 (−), AE3 (−), Vim (+), EMA (−), CD163 (+), KP1 (+), 514H12 (+), S-100m (−), NSE (−), CD57 (−), CEA (−), Desmin (−), CD34 (vascular +), Ki-67 (less +), CD45 (−), HMB45 (−), Me1A (−), CAM5.2 (−), CK19 (−), S-100p (+), SMA (+), NF (+), GFAP (−). The diagnosis suggested chondroblastoma. No tumor recurrence was observed after 2 years of follow-up.

Male, 6 years old. He was admitted to hospital in March 2015 due to pain in his right shoulder for 2 months, pain in his right upper limb for 1 month, pain in his neck and head for 20 days, and pain in his left upper limb for 10 days. Physical examination: consciousness was clear, limbs moved freely, muscle strength and muscle tone were normal, and pathological reflexes were not drawn out. There were no abnormalities in the past history, and no similar diseases were found in the family. MRI of the neck showed that the lesion was located at C_4～7Horizontal, extramedullary subdural, ventral side of the spinal cord, compressing the spinal cord backwards, with obvious tumor enhancement and meningeal rat tail sign (Figure 1), considered a benign meningioma. During the operation, it was found that the lesion was located on the ventral side of the spinal cord, firmly attached between the dura mater and the vertebral dissection, and had no boundary with the dura mater. The tumor was gray-white in color, tough and brittle in texture, and the blood supply was abundant. The tumor was totally resected under a microscope (Figure 1)。 Postoperative pathological diagnosis: consistent with rhabdoid meningioma (Figure 2)。 Follow-up by telephone after discharge, loss of contact after 2 months.

Intracranial metastases are the most common intracranial tumors, and the incidence rate is about 10% ~20% of adult cancers^[1]。 Among the primary tumors with brain metastasis, 25% to 30% were lung cancer, 10% to 15% were breast cancer, and 12% to 20% were melanoma^[2]。 Circulating tumor cells of primary tumor can spread through hematogenous, lymphatic tract and direct invasion routes, and metastasize to brain tissue. Most of the metastatic lesions are located in the supratentorial (80%), a few in the cerebellum (15%) and brain stem (5%). The incidence rate corresponds to the volume percentage of each tissue in the brain^[3,4]。 The clinical manifestations of intracranial metastases are not specific, and their diagnosis is mainly based on the symptoms of central nervous system involvement. In the past, due to the insufficient research on intracranial metastases, the treatment was mainly palliative methods, such as the use of glucocorticoids to alleviate peritumoral edema caused by intracranial metastases. In recent years, with the in-depth research on intracranial metastases and the development of imaging medicine, surgery, whole-brain radiotherapy (WBRT), stereotactic radiosurgery (SRS) and chemotherapy have become the standard treatment for intracranial metastases, but the effect is still not satisfactory, and the overall survival (OS) and quality of life of patients have not been significantly improved. Therefore, targeting and immunotherapy based on oncogenesis and molecular typing have gained increasing attention.

tuberous sclerosis complex (TSC) is a systemic disease characterized by multiple organ tissue defects and hamartomas, which is autosomal dominant and has an incidence of 1/6 000 to 1/10 000^[1]。 The disease-causing genes are TSC1 and TSC2, and mutations in either gene encoding them will lead to dysregulation of nervous system development^[2]。

Epilepsy is one of the most common neurological disorders, affecting about 50 million people worldwide^[1]。 Application of neuroexcitatory blockers to prevent the recurrence of epilepsy is a common treatment for epilepsy. However, approximately 1/3 of the clinical population is not satisfactory for this type of treatment^[2]This may be related to the etiological diversity of epilepsy. Existing studies have shown that gene mutations in receptors, channels and neurotransmitters that regulate nerve excitation can cause epilepsy; Factors that can cause brain damage, such as status epilepticus, trauma, infection, and cancer, can also induce epilepsy^[3]。 Epileptic seizures and status epilepticus can be mediated by immunity, and the International League Against Epilepsy (ILAE) has listed immunity as one of the causes of Epilepsy^[4]。 Gene microarray detection showed that the genes related to the activation of immune response were significantly persistently upregulated during epileptogenesis^[5]。 Studies have shown that removal of neutrophils from animal models can inhibit the occurrence and progression of epilepsy^[6]。 In fact, normal, non-epileptic mice do not have white blood cells in the brain tissue^[7]While white blood cells accumulate in the brain during brain injury and subsequent epileptogenesis. In a mouse epilepsy model, blocking the interaction between leukocytes and blood vessels in brain tissue can prevent the aggregation of leukocytes and thus inhibit the induction and occurrence of epilepsy^[6]。 myeloperoxidase (MPO) is a potential regulator of inflammatory response in leukocytes^[8,9]Participate in the occurrence and development of many diseases. This article reviews the related mechanisms of MPO in epileptogenesis, research progress, some challenges and application prospects.

Intracranial arteriovenous malformations (AVM) are vascular malformations caused by abnormal development of intracranial vessels, consisting of dilated malformed arteries and veins. The main purpose of AVM treatment is to completely remove the malformed vascular mass or occlude the blood flow of the malformed vascular mass, so as to avoid serious complications caused by bleeding of the malformed vascular mass. The main treatment methods include surgical resection, endovascular embolization, radiotherapy and combination therapy. According to the different treatment modes of AVM, various evaluation systems have been established to predict the surgical risk and therapeutic effect. This article summarizes the various evaluation systems of AVM as follows.

Endoplasmic reticulum is an organelle with multiple functions in cells, which can modify, fold and secrete newly synthesized proteins and play an important role in maintaining the homeostasis of the internal environment of cells^[1]。 When external stimuli interfere with protein folding and post-translational modification of the endoplasmic reticulum, lipid and steroid synthesis, gene expression and cell metabolism, and calcium channel conduction pathway, unfolded proteins will accumulate in the endoplasmic reticulum cavity, which can induce endoplasmic reticulum stress (ERS)^[2]。 ERS is generally a self-protection behavior of cells, which can help proteins fold correctly to avoid cell death through the repair of endoplasmic reticulum chaperones; However, if persistent ERS response (ERSR) does not restore cell function, apoptosis will be triggered^[3,4]。 Many factors such as oxygen content, pH and nutrient content of tumor parenchyma can cause ERSR, so cancer cells must have the ability to adapt and prevent excessive stress in the endoplasmic reticulum^[5]。 In recent years, researchers dedicated to tumor-targeted drugs have noticed the role of ERS in affecting glioma cell apoptosis, and have tried to develop new targeted antitumor drugs for the treatment of malignant glioma with this goal^[6,7,8]。 The research progress of ERS in malignant glioma is reviewed as follows.

blunt cerebrovascular injury (BCVI) refers to the pathological injury of different tissues of common carotid artery, intracranial and extracranial internal carotid artery, vertebral artery and other blood vessels caused by trauma, which is prone to secondary stroke and can cause serious neurological dysfunction or even death. In 1872, French doctor Verneuil first discovered carotid artery injury through autopsy. In 1967, Yamada et al. reported clinical cases of carotid artery injury. Subsequently, cases were reported in different neurosurgical centers, mostly traumatic aneurysms and arteriovenous fistulas. With the advancement of neuroimaging technology, increased screening of patients at high risk of BCVI and deeper understanding of such diseases, the incidence of BCVI is on the rise^[1,2]。 For trauma patients, BCVI is a kind of occult injury. Although it is uncommon, if it is not diagnosed and treated in time, it has a high disability rate and fatality rate. This paper reviews the current research progress in epidemiology, pathophysiological mechanism, clinical manifestation, screening strategy and treatment of BCVI, so as to strengthen clinicians' understanding of the diagnosis and treatment of this kind of injury.