2014年 · 第94卷第35期

Dural damage during spinal surgery can cause postoperative cerebrospinal fluid to flow out of the body, including cerebrospinal fluid flow out of the incision or the appearance of cerebrospinal fluid in the drainage. Patients will have low cranial pressure headache, which is aggravated when standing, reduced when lying, nausea, vomiting, dizziness, electrolyte disorder, and even some neurological symptoms. Cerebrospinal fluid leakage not only affects incision healing, but also causes pseudodural cyst, retrograde central nervous system infection, etc. The rate of intracranial infection after spinal surgery was 0.4%^[1]。 The incidence of dural injury in spinal surgery is 1% ~17%^[2]The incidence of cerebrospinal fluid leakage after spinal surgery was 2.31% ~9.37%^[3], the associated incidence of revision surgery was higher. Therefore, cerebrospinal fluid leakage after spinal surgery is one of the common complications of spinal surgery, which needs to be actively treated. Except for a few cases caused by trauma, most of them were caused by iatrogenic injuries. Risk factors for dural injury and cerebrospinal fluid leakage include advanced age, revision surgery, ossification of ligaments, spinal deformity, and unskilled operation techniques. In the elderly patients, the dura thinning, wrinkling and peridural adhesion are prone to dura damage and tear during intraoperative operation. Spinal revision surgery has a higher risk of dural damage due to unclear normal anatomical landmarks and scar adhesion than initial surgery. The main risk factor in cervical spine surgery was ossification of the posterior longitudinal ligament. The dural damage in patients with ossification of the posterior longitudinal ligament was 13.7 times that in patients without ossification of the posterior longitudinal ligament^[4]The incidence of postoperative CSF leakage in patients with thoracic ligamentum flavum ossification is as high as 32%^[5]。 Patients with severe spinal deformity are more prone to dura injury and cerebrospinal fluid leakage due to uneven dura tension distribution and inability to operate according to normal anatomical structure during operation. In addition, due to the operator's unskilled operation technique, insufficient experience, and too rough in separating dural adhesions, it is also easy to lead to dural injury and postoperative cerebrospinal fluid leakage.

In recent years, the academic conferences of lumbar spine at home and abroad have systematically studied and discussed the indications, methods and curative effects of lumbar spinal stenosis surgery, and formed some preliminary clinical guidance. Among them, the guidelines for the diagnosis and treatment of lumbar spinal stenosis formulated by the North American Spine Association in 2011 have been widely recognized. In China, the Annual Academic Meeting (COA) of the Orthopedic Branch of the Chinese Medical Association, the Beijing Annual Academic Meeting (BOA) of the Orthopedic Branch of the Chinese Medical Association and other meetings have also reached some expert consensus on the surgical treatment of lumbar spinal stenosis, but there is a lack of systematic elaboration. Now, through the cooperation of a number of large tertiary hospitals, an expert consensus on the diagnosis and treatment standards of lumbar spinal stenosis has been formed, which I would like to share with my colleagues here.

Insomnia is a common physiological and psychological disorder, which usually refers to the subjective experience of patients' insatisfaction of sleep time and/or quality and affecting their social function during the day^[1]。 Outpatient patients with insomnia often complain of varying degrees of cognitive decline. Previous studies have also proved that primary insomnia can affect cognitive function, among which learning and memory difficulties are the most common^[2,3,4]。 In recent years, many studies have proved that patients with primary insomnia have extensive memory impairment. A foreign meta-analysis combined with a large number of data showed that episodic memory and working memory were mildly to moderately impaired in patients with primary insomnia^[5]。 Domestic Ge Yijun et al^[6]It was found that both procedural and declarative memory were impaired in patients with primary insomnia. Previous studies of our research group also confirmed impaired prospective memory in patients with chronic primary insomnia^[7]。 Although outpatient insomnia generally reflects different degrees of improvement in memory function after treatment. However, there are few studies at home and abroad on whether the impaired memory function of chronic insomnia can be recovered after treatment. This study adopted a prospective study to observe the episodic memory changes of patients with chronic primary insomnia before and after treatment, and to understand the influence of chronic primary insomnia on episodic memory and prognostic outcome.

panic disorder (PD) is an acute anxiety disorder with recurrent panic attacks as the main clinical manifestation. Clark^[1]The theory of catastrophic cognition holds that panic attacks stem from an unrealistic misjudgment of some somatic sensations by the individual. Our research team used event-related potential (ERP) studies to find^[2]The information gating ability of patients with panic disorder decreases, and some "pseudo-dangerous information" is mistaken for threat information for processing, resulting in inappropriate defense and fear response, and even panic attacks. Therefore, we speculate that the inability of patients with panic disorder to effectively detect, recognize and correct their own false cognition may be an important mechanism for the recurrent occurrence of panic attacks and the difficulty of self-control. error-related negativity (ERN) and error positivity (Pe) are two defined ERP components related to error processing, which can reflect the processing of misinformation in the brain. This study adopts flanker paradigm and ERP technique to discuss the above theoretical assumptions.

Posterior longitudinal ligament ossification (OPLL) is a disease in which heterotopic ossification in the posterior longitudinal ligament of the spine compresses the spinal cord and nerve roots, resulting in impaired function^[1]The concept of cervical posterior longitudinal ligament ossification was established after autopsy of patients with severe spinal symptoms caused by posterior longitudinal ligament ossification^[2]Then it is clear that ossification of spinal ligaments can cause symptoms of spinal cord and nerve roots in patients. Great progress has been made in the epidemiology, natural course, etiology, diagnosis and treatment of this disease. The research progress of natural course of cervical posterior longitudinal ligament ossification is summarized below.

Cervical insufficiency (CIC) refers to the inability of the cervix to maintain pregnancy until full term due to anatomical or functional defects. It is one of the main causes of repeated late abortion and premature delivery caused by painless dilatation of the cervix in the middle and third trimester of pregnancy. It generally occurs in 18~22 weeks of pregnancy, and accounts for about 15% of habitual abortion in 16~28 weeks of pregnancy^[1]。 The rate of premature birth in patients with cervical insufficiency is 3.3 times that of non-cervical insufficiency, accounting for 8% ~9% of all premature births, 40% ~50% of natural premature births, and 20% ~30% of premature water rupture^[2]。 The main functional tissues of the cervix in patients with CIC and the latest progress of cervical cerclage in the treatment of CIC are summarized as follows.

A 34-year-old female was admitted to the hospital on May 2, 2012 due to "limb weakness, dysphagia for 12 days, aggravation with dyspnea for 2 days". The physical examination showed that the body temperature was 36.5 ℃, the heart rate was 76 beats/min, the breathing was 22 beats/min, and the blood pressure was 114/66 mmHg (1 mmHg =0.133 kPa). The fatigue test of both upper eyelids was positive, the abduction of both eyes was 2 mm white, the closing force of both eyelids and lips was significantly weakened, the soft palate was poorly elevated on both sides, the pharyngeal reflex was weakened, the neck turning and shrugging force on both sides was weak, the abdominal bulging force was weak, the muscle strength of the proximal extremities was decreased, and no positive signs were seen in the rest of the nervous system. On admission, neostigmine test was positive, and blood acetylcholine receptor antibody was suspected positive. Repeated electrical stimulation showed 40% attenuation of visible amplitude of orbicularis muscle and deltoid muscle of right eye stimulated at 3 Hz. Single-fiber electromyography showed a significant increase in tremor of right common extensor muscle (mean continuous wave value difference of 69 μ s). Thymus CT enhancement showed space-occupying lesions of anterior superior mediastinum and normal thyroid function. The diagnosis was myasthenia gravis (MG) Osserman classification type III, and the absolute clinical score of MG was 26. An indwelling nasogastric tube was administered with intravenous immunoglobulin needle (IVIg, 0.4 g·kg^–1• d^–1×5 d), supplemented with pyridostigmine bromide tablets 60 mg, 4 times/d. A myasthenic crisis occurred on the 8th day of admission, and ventilation assisted by tracheal intubation and thoracoscopic enlarged thymectomy under general anesthesia was performed. Thymic tissue hyperplasia and tumor-like tissue were observed during the operation. Some external invasion involved pericardium and left mediastinal pleura, and a small amount of adipose tissue could be reached by anterior mediastinum and pericardial fat pad. Pathological examination revealed B3 thymoma with anaplasia. After operation, corticosteroids (methylprednisolone, prednisone) combined with pyridostigmine bromide tablets were always treated. On the 9th postoperative day, tracheotomy was performed due to difficulty in disconnection, and later transferred to the general ward. On May 31, 2012, he had a second myasthenia crisis with cough and fever. In addition to ventilator-assisted ventilation, he was given double filtration plasma exchange therapy (DFPP), 3 times every other day, and his condition improved rapidly and he went offline. However, the absolute clinical score of MG of the patient kept fluctuating between 18 and 25 points. The myasthenic crisis was repeated three times in the next 3 months, and the crisis was quickly relieved after each treatment with DFPP. During this period, on the basis of corticosteroids combined with pyridostigmine bromide, azathioprine tablets 100 mg/d were added to the treatment, but the symptoms did not improve significantly, and then Cyclosporine A (CsA 4 mg · kg^–1• d^–1) After 2 weeks of treatment, the patient was discharged in stable condition, and the blood concentration of CsA at discharge was 55.1 μ g/L. Absolute MG clinical score was 0 at 3 months of discharge follow-up and chest radiotherapy (chest conformal field 10MV – X SAD 100 DT 5000cGy/25F/36d) was performed. After continued follow-up for 18 months, the patient's absolute clinical score of MG remained 0.