2016年 · 第96卷第39期

Although the diagnosis and treatment of craniocerebral trauma and the understanding of pathophysiological mechanisms have made great progress in the past 30 years, the overall incidence of craniocerebral trauma and the mortality and disability rate of severe craniocerebral trauma have not decreased further. For example, the mortality rate of severe craniocerebral trauma patients maintained at 36% ~42%, and the poor prognosis rate was 52% ~60%^[1]。 Multiple large-scale multicenter randomized controlled clinical studies (RCTs) and clinical translation of preclinical research results ended in failure. The guidelines for craniocerebral trauma have not been updated for 10 years, and there are signs that clinical research on craniocerebral trauma is stuck in a puzzle and lacks bright spots, forcing insightful people to reflect in order to seek new theoretical and technical breakthroughs.

A 43-year-old female was admitted to the hospital in July 2015 due to low back pain accompanied by pain and numbness in the right lower limb for 1 year. Physical examination showed L4 and L5 paravertebral percussion pain and hypoesthesia in the right lower limb. Lumbar magnetic resonance imaging (MRI) showed L4/5 mild disc herniation with right nerve root compression, and subsequent discography showed no significant abnormalities. Laboratory tests showed prolonged prothrombin time (16.9 s), prolonged activated partial thromboplastin time (55.0 s), and increased international normalized ratio (INR) (1.41). The patient had a history of obesity (weight 75 kg; height 155 cm; BMI 31.22 kg/m²) and a 10-year smoking history of 5 cigarettes/d. Two months ago, the patient went to the doctor due to numbness in both hands and weakness in both lower limbs. Cervical MRI showed C5/6 disc herniation with nerve compression, and then underwent C5/6 decompression, bone grafting, fusion and internal fixation under general anesthesia. Postoperative numbness in both hands and weakness in both lower limbs were improved compared with those before operation, and there was no obvious abnormality in reexamination and follow-up. The patient underwent L5 right vertebral fenestration nerve root exploration under general anesthesia lying prone, and the operation time was 20 min. During the operation, no obvious abnormalities of nerve roots were found after careful and repeated exploration, and the nerve roots and surrounding tissues were washed with dexamethasone injection. A negative pressure drainage tube was placed in the surgical field, and the incision was sutured layer by layer. No cerebrospinal fluid leakage occurred during operation. Circulation was stable during surgery. The results of intraoperative blood gas analysis showed no abnormalities such as hypoxia, hypercapnia or pH, electrolyte and blood glucose disorders. Intraoperative bleeding 80 ml. After recovery from anesthesia, the patient was conscious, cough sound was clear, and limb movement was normal. The patient experienced speech difficulties, accompanied by depressed mood and slight vomiting at 14 hours after operation. Neurological examination showed good hearing, understanding the meaning of words but difficulty pronouncing them. The muscle strength and activity of the limbs were normal, and there were no abnormalities such as facial skew. Ask a neurologist for consultation, first consider the patient with postoperative neurosis, but the patient's symptoms have not improved significantly after antidepressant treatment. On the 5th day after operation, MRI of the brain showed patchy abnormal signal shadows in part of the left frontoparietotemporal lobe, and other patchy abnormal signal shadows in the left hemioval area, lateral ventricular area, basal ganglia area and bilateral frontal lobes. Carotid CT angiography (CTA) showed stenosis of the right carotid artery. After another consultation by the neurology department, the patient was diagnosed with cerebral infarction complicated with motor aphasia. Subsequently, the patient received active therapies such as anticoagulation (aspirin oral 100 mg, once/d), lipid lowering (atorvastatin oral 10 mg, once/d), improvement of microcirculation, bed rest, etc. The patient's neurological symptoms were not further aggravated. On the 11th postoperative day, the patient was able to make monosyllabic voices, but it was still difficult to make polysyllabic voices. The patient was then transferred to a rehabilitation hospital for hyperbaric oxygen therapy. After 3 months of follow-up, the speech pronunciation was basically normal, but the speech speed was slow (Figure 1，Figure 2，Figure 3)。

A 48-year-old male from Tunchang County, Hainan Province, had a fever of 39.6℃ without obvious trigger 11 days ago, accompanied by headache, exacerbated by paroxysmal aggravation, touch pain in the right occipital region, especially when he had fever, and a 0.5 cm ×1.0 cm skin ulcer was seen on the lateral side of the left waist. He had type 2 diabetes for 5 years and had poor blood sugar control. He was admitted to the hospital on November 7, 2014. After admission, he selected broad-spectrum antibiotics meropenem every 8 h combined with ganciclovir every 12 h, and hydrocortisone for anti-inflammation. CT examination: On November 7, 2014, CT found a stripe-shaped, triangular-like low-density shadow in the superior sagittal sinus, and the density of some layers was slightly uneven (Figure 1A); On November 11, 2014, CT found that compared with the anterior film, the hypodensity of the superior sagittal sinus triangle became uniform and increased, showing a typical "Δ" sign, and a thin crescent-shaped hypodensity shadow was seen under the inner plate of the right occipital skull (FIG. 1B), a crescent-shaped low-density shadow was seen on the left side of the superior sagittal sinus, and a flaky low-density shadow was seen in the left parietal lobe (Figure 1C)。 Chemical examination: admission blood routine, white blood cells 18.95×10⁹/L, the percentage of blood neutrophils is 92%; Alanine aminotransferase 191 U/L and aspartate aminotransferase 67 U/L. Cerebrospinal fluid routine: microscopic examination of white blood cells 0~1/HP, white blood cell count 2×10⁶/L. Blood biochemistry: glucose 11.33 mmol/L, trace protein 1 129 ng/L, chlorine 111 mmol/L. Diagnosis and results: Blood culture and drug susceptibility on November 12, 2014 indicated Burkholderia pseudomallei and imipenem sensitivity, and cerebrospinal fluid culture on November 13, 2014 indicated Burkholderia pseudomallei. At 21: 00 on November 14, 2014, blood pressure and blood oxygen saturation decreased repeatedly, and the family gave up treatment after many rescues failed.

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by the persistence of antiphospholipid antibodies (aPL), with arteriovenous thrombosis and morbid pregnancy as the main clinical manifestations. aPL is a general term for a group of heterogeneous autoantibodies. The 2006 international APS consensus determined that aPL with diagnostic value includes lupus anticoagulants (LA), anticardiolipin antibodies (aCL) and anti-β 2-glycoprotein Ⅰ antibodies (anti-β 2gpⅠ)^[1]。 Thrombosis is the most important pathological feature of APS, but the mechanism of APL-induced thrombosis is still unclear. It has been shown that the occurrence of thrombosis in patients with APS is the result of the interaction of multiple factors. The main factors include: the conformational change of β 2gpⅠ, the activation of cellular components of vascular system (vascular endothelial cells, monocytes, platelets, neutrophils) by antigen-antibody complexes, the disorder of coagulation components (coagulation system, anticoagulation system, fibrinolysis system), and the participation of inflammatory mediators (complement, cytokines). In this paper, the recent research on the mechanism of APS thrombosis is reviewed.

Intervertebral Disc (IVD) is an important structure for maintaining spinal load and motor function. In addition to direct huge medical expenses, Intervertebral Disc degenerative disease also causes indirect economic losses^[1]。 In recent years, artificial intervertebral disc replacement, simple nucleus pulposus replacement and allogeneic intervertebral disc transplantation have emerged^[2,3]But the long-term effect is not satisfactory. Using tissue engineering to construct functionalized intervertebral disc provides new hope for the treatment of intervertebral disc diseases^[4,5,6,7]。 At present, the research on tissue engineering of intervertebral disc mainly focuses on the construction of scaffold materials, seed cells, intervertebral disc tissue, etc. However, compared with bone and cartilage tissue engineering research, the research on intervertebral disc degeneration and regeneration is relatively lagging behind.

In human tissues, hydrogen protons are mainly found in water and adipose tissues, and fat has a short T₁Values and T₂Value, at T₁and T₂The weighted graph showed a high signal, and the higher fat signal reduced the image contrast and T₁Enhancing the scanning effect, fat high signal also makes the motion artifacts such as respiration more obvious, in addition, it will also cause serious chemical shift artifacts on the water-lipid interface, thus reducing the image quality and lesion detection rate. Therefore, in clinical practice, suppression of fat signal is particularly important. By suppressing adipose tissue signal, image contrast can be increased, enhanced scanning effect can be improved, motion artifacts, chemical artifacts and other related artifacts can be reduced, and image quality can be improved^[1]。 At present, fat suppression techniques are mainly based on two mechanisms: (1) the longitudinal relaxation difference between fat and other tissues; (2) Chemical shift effect of fat and water. Traditional methods can be divided into inversion recovery method (STIR) and frequency selection method (SPIR and SPAIR), but these techniques cannot meet the clinical needs in the diagnosis and accurate quantification of diseases containing fat components^[2,3]。 With the development of Dixon technology, the above problems have been solved gradually. The basic principle, development and improvement of Dixon technology and its clinical application progress are reviewed in this paper.

intracranial major artery stenosis/occlusion (ICASO) is one of the most common causes of ischemic stroke worldwide^[1]。 The progress and popularization of non-invasive craniovascular assessment technology has made ICASO become a hot spot in research, especially in the aspects of risk factors and susceptibility genes. Moyamoya disease is a rare and special cerebrovascular disease. Studies have shown that the two are consistent in the distribution of race and vascular involvement. Therefore, there is a hypothesis that Moyamoya disease is a confounding factor with a high incidence of intracranial aortic stenosis/occlusion in Asians. However, it is sometimes difficult for clinicians to accurately identify whether ICASO originates from Moyamoya disease or is related to traditional atherosclerosis risk factors with current examination methods. The ring-finger protein 213 gene was produced by Kamada et al.^[2]Moyamoya disease susceptibility genes discovered by genome-wide association analysis. Recent studies have found that the ring finger protein 213 gene is not only a genetic susceptibility gene for Moyamoya disease in Asians, but also has a clear correlation with intracranial stenosis/occlusion of large arteries in non-diagnostic Moyamoya disease. Some people with positive gene mutations may progress to Moyamoya disease^[3]This suggests that some of the ICASOs that were not previously diagnosed as moyamoya disease may be moyamoya disease. These studies suggest that early identification of intracranial arterial atherosclerotic stenosis and early moyamoya disease by detecting ring finger protein 213 gene may guide the formulation of treatment plan. This paper summarizes and analyzes the recent research progress on the relationship between RF213 gene and Moyamoya disease and ICASO.