2015年 · 第31卷第04期

intracranial arachnoid cyst (IAC) is mostly a congenital disease. It is a common benign intracranial lesion in children, accounting for about 1% of intracranial lesions^[1]。 Intracranial hypertension caused by cyst compression of surrounding tissues mostly causes headache, epilepsy, skull deformation and protrusion, or secondary hydrocephalus, developmental delay, etc. See a doctor, and find it during head trauma examination. At present, the most commonly used surgical method is arachnoid cyst-peritoneal shunt. However, some complications of shunt surgery cannot be avoided, such as excessive shunt, insufficient shunt, shunt infection, blockage, rupture, shedding, displacement and even entanglement and knotting^[2,3,4,5]。 A case of benign intracranial hypertension caused by subcutaneous tension cyst in the chest wall caused by shunt displacement and entanglement in a child admitted to the Department of Neurosurgery of Beijing Tiantan Hospital affiliated to Capital Medical University is reported as follows.

Female, age 35 years. Admitted to hospital due to head trauma caused by car accident for 2 h. The consciousness was basically clear, the GCS score was 13, the bilateral pupil diameter was 2.5 mm, the light response was sensitive, the neck was resistant, the muscle strength and tension of the limbs were normal, the physiological reflex was normal, and the pathological reflex was not drawn out. Scalp contusion in the right temporo-occipital region. The first CT showed a small amount of subdural hematoma on the left side with left frontal brain contusion, with midline centered and coronal suture open. After 4 hours of admission, the patient's consciousness decreased to GCS score of 10. After CT reexamination, the left frontal lobe brain contusion and intracerebral hematoma were significantly enlarged, and the space-occupying effect was obvious, but no epidural hematoma was found (Figure 1)。 Under general anesthesia, left craniotomy was performed to explore hematoma evacuation. The left frontotemporal "?" incision was taken during the operation, and about 50 ml of left frontal lobe brain contusion and intracerebral hematoma were removed during the operation. When the operation was performed for about 1.5 h, encephalocele suddenly appeared, the brain tissue was pushed out of the bone margin about 2 cm, and a large amount of epidural venous blood gushed out. Immediately, bedside CT examination showed a delayed epidural hematoma of the upper riding trans-sagittal sinus, with a hematoma volume of about 150 ml (Figure 2)。 Immediately re-operate, make a transverse incision parallel to the coronal suture in the original incision, open the flap up and down, and drill holes on both sides of the sagittal sinus to form a bone flap. During the operation, the coronal suture was opened, and the bleeding was extensive sagittal sinus bleeding, and the bleeding was fierce. During the operation, the bleeding spot was covered with gelatin sponge, and then an occipital autologous fascia was taken. The fascia size was selected according to the bleeding range, and the autologous fascia was covered with gelatin sponge. Then, it was sutured on the dura mater and maintained a certain tension. Bone flap reduction. Return to the left side again to remove the hematoma, stop the hemorrhage and close the skull, and postoperative CT reexamination showed that the hematoma was cleared (Figure 3，4)。 He was discharged from hospital after 2 months of treatment, and his discharge GCS was 15 points.

Intracranial aneurysm is one of the common types of stroke. subarachnoid hemorrhage (SAH) caused by aneurysm rupture is a neurosurgical emergency, with an overall mortality rate of 50%, which seriously threatens human health and life. Early brain injury after subarachnoid hemorrhage is closely related to delayed brain injury and the prognosis of patients^[1]。 blood-brain barrier (BBB) disruption is an important pathophysiological basis of early brain injury after SAH. Blood-brain barrier In addition to its barrier role, the blood-brain barrier maintains internal environmental stability by strictly controlling the circulation of ions and molecules, providing oxygen and nutrients according to nervous system needs and protecting the brain from toxic substances and pathogens^[2]。 However, the changes and specific mechanisms of blood-brain barrier in early and middle brain injury after SAH are still unclear.

Parkinson's disease (PD) is a common neurodegenerative disease in middle-aged and elderly patients. In addition to motor symptoms such as tremor, myotonia, slow movement and postural disorders as its main clinical manifestations, non-motor symptoms (NMS) such as anosmia, constipation, sleep disorders and depression are also its significant features^[1]。 There is a high incidence of NMS in PD patients, which occurs earlier than motor symptoms, and exists at any time of PD^[2]。 deep brain stimulation (DBS) was first used in China in 1998, and it has been more than ten years since now. It has significantly improved the motor symptoms and improved the quality of life of patients^[3]。 It has been widely used in the treatment of intermediate and advanced PD, and the surgical targets are mainly subthalamic nucleus (STN), globus pallidus (GPi) and ventralis intermedius nucleus (VIM). STN-DBS significantly improved the motor symptoms such as tremor, rigidity, bradykinesia and dyskinesia^[4]。 The effect of DBS on NMS in PD patients is still unclear, but NMS also seriously affects the quality of life of PD patients. In recent years, it has gradually attracted clinicians' attention. NMS is mainly divided into four parts: neurological disorders, autonomic dysfunction, sleep disorders and sensory disorders. This article will make a summary of recent literature as follows.

As a novel tumor suppressor gene, leucine zipper tumor suppressor 2 (LZTS2) is widely involved in the occurrence, proliferation, migration and maintenance of tumor stem cell function of various tumors including glioma. It is an important candidate tumor suppressor gene and can be used as a novel therapeutic target for glioma.

intracranial aneurysm (IA) refers to tumor-like protrusion caused by local cerebral vascular wall abnormalities, including sac aneurysm with neck and fusiform aneurysm without neck^[1]。 Vlak et al.^[2]According to statistics from 1998 to 2011, the incidence of unruptured intracranial aneurysms in healthy people in 21 countries was about 3.2%, among which women were about 1.6 times higher than men; From 2007 to 2011, another researcher selected 4,813 people aged 35-75 in two areas of Shanghai (one in the urban area and one in the suburbs) for a census. The results showed that the prevalence of unruptured intracranial aneurysms was 7%, of which 5.5% were men and 8.4% were women. Most aneurysms are less than 5 mm in diameter^[3]。 Fujinaka et al.^[4]It is reported that the annual incidence of ruptured intracranial aneurysms in Japan is about 20/100,000, and 40% of them have a poor prognosis. 10% to 15% of patients with ruptured intracranial aneurysms have died before receiving effective medical assistance^[5]。 The mortality rate was close to 5% within 24 hours and up to 50% within 30 days after the onset of the disease^[5,6]。 25% to 30% of survivors will be at risk of bleeding again at any time within 4 weeks of onset^[7]。 In view of the high incidence, high disability and mortality of IA, it has always attracted much attention^[2]。 Although the European Stroke Organization has issued the latest guidelines for the diagnosis and treatment of IA and subarachnoid hemorrhage (SAH)^[8]However, the diagnosis and treatment according to the guidelines did not greatly improve the treatment results. This article reviews the risk factors for the formation and rupture of IA.

Craniocerebral injury is the main cause of death and disability in adolescents, and its accurate assessment and effective intervention have always been a concern in the field of neurosurgery. However, the traditional evaluation methods, such as Glasgow coma scale (GCS) and CT examination, are not high in specificity and sensitivity, which can no longer meet the needs of modern medicine. In recent years, the rapid development of neuroimaging, neuroelectrophysiology and detection of craniocerebral injury markers provides more objective and accurate methods for the diagnosis and prognosis of craniocerebral injury, and is also conducive to the study of pathological mechanism of craniocerebral injury and the exploration of new treatment methods. The progress in clinical application of modern evaluation techniques for craniocerebral injury is reviewed.

neurofibromatosis (NF) is a class of autosomal dominant hereditary diseases, which mainly include three subtypes: type 1 NF, type 2 NF and Schwann cell tumorosis. Such diseases have great phenotypic differences, mainly nervous system tumors, skin lesions and peripheral nervous system lesions, causing multiple and progressive damage, which brings great difficulties to treatment. Current reasonable measures include screening of at-risk populations, early diagnosis, close follow-up, and the establishment of a framework for multidisciplinary treatment based on the characteristics of the development of the natural course of NF. In this paper, the latest research on the pathogenesis, genetics, clinical manifestations and treatment of NF is reviewed.