2015年 · 第95卷第07期

Due to the continuous emergence of dopaminergic drugs, most of the motor symptoms of Parkinson's disease (PD) can be well controlled, but there are still many problems that plague us and directly affect the quality of life and working ability of patients. Recently Deane et al.^[1]Surveys of PD patients, doctors, and nursing staff show that among the top ten studies to be carried out while waiting for a radical cure or effective treatment, the first is to solve balance problems, followed by reducing anxiety and depression in patients, and reducing exercise complications only ranks third. Even though this is a survey based on Western populations, these questions are equally what we should be focusing on. Among the 26 issues of concern screened, only 30% are related to motor symptoms, and more are non-motor symptoms, including cognition, sleep disorders, autonomic dysfunction, gastrointestinal symptoms, pain, etc. These non-motor symptoms not only have a high incidence rate, but also can appear in the early stage of the disease, accompanied by the whole process of PD progression, and even before the appearance of PD motor symptoms, and sometimes can become the main reason affecting the quality of life of patients. Among them, combined pain is not paid attention to in clinic, and it is often an important reason for diagnosis delay in the early stage.

Skin and soft tissue injuries in the posterior calcaneal area are more common in children. Because of children's poor self-protection awareness, such injuries are increasing day by day. The peroneal artery perforator pedicled sural neurovascular flap is a common method for clinical repair of soft tissue defects in the heel of foot because of its reliable blood supply and stable survival. However, when the cutting area of the flap is large, the donor area cannot be directly sutured, and skin grafting is often used to repair the postoperative depression and scar hyperplasia, which seriously affects the appearance of the calf. Based on the shortcomings of the above surgical methods, this study proposed a method of repairing the skin and soft tissues of the posterior calcaneal region by peroneal artery perforator pedicled sural neurovascular flap on the basis of anatomy, and repairing the wound of the donor site of the sural nerve island flap by proximal tibial artery perforator pedicled V-Y advancing flap. The goal of direct suture of the donor site wound was achieved by proximal perforator pedicled V-Y advancing flap.

The patient, a 50-year-old man, developed dull pain in the upper abdomen without obvious trigger 1 week ago, which was interstitial, radiated to the lower back, and did not relieve with the change of body position. He had no fear of cold and fever at the time of attack, and no skin and sclera yellowing. He was admitted to the Second Affiliated Hospital of Nanjing Medical University for hospitalization in April 2014. Physical health in the past, no special physical examination. Laboratory tests: high sensitivity C-reactive protein 12 mg/L (elevated), blood glucose 7.36 mmol/L (slightly elevated), globulin 36.5 g/L (slightly elevated), neurospecific enolase 27.09 μ g/L (slightly elevated), CA19-9 30.06 U/ml (normal), and other blood tumor indexes were normal. Using Philips Brilliance 64-slice CT, total abdominal plain scan + enhanced examination showed that the body and tail of the pancreas were obviously enlarged, and 6.8 cm ×4.4 cm low-density soft tissue masses were seen, with uniform density. The CT value was 24-28 HU (normal pancreas CT value 35-40 HU). After enhancement, the lesions in the arterial phase were less enhanced than those in the normal pancreas, and the enhancement was less uniform. The CT value was 34-50 HU (normal pancreas 60-65 HU). The lesions in the portal vein phase and the delayed phase continued to delay the enhancement, and the enhancement tends to be uniform. The CT values were 45-55 HU (normal pancreas 55-60 HU) and 52-58 HU (normal pancreas 45-50 HU), respectively. CT diagnosis: mass in the body and tail of the pancreas, pancreatic cancer possible; Multiple small lymph nodes in splenic hilum and retroperitoneum (Figure 1)。 Surgery considers surgical treatment of pancreatic tumors. During the operation, tumors in the body and tail of the pancreas were seen, invading the kidney fat sac, and multiple enlarged lymph nodes were seen next to the splenic artery. Pancreatectomy and splenectomy were performed. Postoperative pathology showed that the size of the pancreas was 9.0 cm ×7.0 cm ×5.0 cm, and a gray mass was seen on the section, the size was 6.0 cm ×7.0 cm ×4.5 cm. The mass adhered to the spleen, and the boundary with the surrounding tissues was unclear. Pathological diagnosis: Chronic inflammation of the body and tail of the pancreas with lymphoid tissue hyperplasia, considering that IgG4-related immune disease may be large.

A 19-year-old male was admitted to the hospital for "repeated fever for 2 months with thoracic, lumbar and back pain". Physical examination: Body temperature 37.3℃, no anemia, superficial lymph nodes not swollen, both lungs normal, mild tenderness in chest and back, mild limitation of lumbar spine movement, and normal sensory movement of limbs. Imaging examination: CT showed multiple circular low-density changes in lumbar vertebra, sacral vertebra, left ilium and ischium, thoracic vertebra, ribs and sternum, with smooth boundaries, high central density, partial cortical bone destruction and slight swelling of soft tissue (Figure 1、Figure 2)； Chest enhanced CT showed patchy low-density shadows in the upper lobe of the left lung, with uneven enhancement after enhancement (Figure 3)。 The erythrocyte sedimentation rate was significantly increased in laboratory (75 mmHg, 1 mmHg =0.133 kPa). The patient was admitted for diagnosis: multiple bone destruction. Malignant lymphoma? Bone tuberculosis? There were no abnormalities in other relevant laboratory tests and abdominal B-ultrasound. CT showed circular annular bone destruction of thoracic 7 vertebral bodies and adnexes, local cortical bone rupture, and no obvious soft tissue mass (Figure 4)。 MRI showed multiple circular annular signal shadows in lumbar and sacrococcygeal vertebrae, with smooth boundaries, T₁WI and T₂WI showed low signal in the upper interior, slightly high signal in the periphery, partial bone destruction, accompanied by slight swelling of soft tissue, and ring enhancement and surrounding soft tissue enhancement were observed after enhancement (Figure 5)。 Under the guidance of CT, puncture of thoracic 7 vertebral lesions, left ilium and left lung paramediastinal lesions was performed successively, but the diagnosis could not be confirmed. Therefore, incision biopsy of thoracic 7 lesions was performed. During the operation, fish-like soft tissue was seen under the thoracic 7 vertebral lamina, adhering to surrounding tissues, and local dead bone was formed. Epithelioid cells and many Langhan's giant cells were observed under the postoperative pathological microscope, and dead bone (Figure 6)。 After the pathological diagnosis was confirmed as tuberculosis, anti-tuberculosis treatment was given. The pain basically disappeared after 12 months of treatment. MRI reexamination showed that the abnormal signal range of lower thoracic vertebra, lumbar vertebra and sacral vertebra was reduced, T₁WI signals vary from high to low, T₂WI is dominated by high signal (Figure 7), the erythrocyte sedimentation rate dropped to 35 mm/h, and is currently continuing anti-tuberculosis therapy.

Alzheimer disease (AD) often attacks, mainly manifested as progressive development of memory loss, aphasia, apraxia, agnosia, visual and spatial skill impairment, executive dysfunction, personality and behavior changes, etc. It has become one of the main diseases that seriously threaten the life health and quality of life of the elderly. According to the annual report of the International Academic Organization of Alzheimer's Disease, in 2010, there were 759 million elderly people aged>60 years old in the world, of which 35.56 million (about 4.7%) suffered from AD of different degrees, and it is expected to reach 65.69 million in 2030. China will also become the country with the largest number of dementia, so it is urgent for us to have a clearer understanding of the pathogenesis of AD. However, the etiology and mechanism of AD are not fully understood at present. Researchers are trying to explore it from the aspects of genetics, neurotransmitter disorders, inflammation theory, cytoskeletal changes, immune dysfunction, etc. In recent years, with the rapid development of imaging technology, the relationship between AD and vascular diseases has attracted much attention. More and more studies have found that microvascular diseases are common in the brain of AD patients, such as cerebral amyloid angiopathy, white matter damage, lacunar infarction, blood-cerebrospinal fluid barrier destruction and cerebral microbleeds (CMBs), etc. It was found that these cerebral microvascular lesions may accelerate the production, aggregation and deposition of A β, reduce the clearance of A β, promote the pathological process of AD, and thus aggravate the cognitive impairment^[1]。 At present, the influence of cerebral microhemorrhage on the cognitive function of AD has become a hot research topic. Therefore, this paper reviews the clinical research status of AD and cerebral microhemorrhage.

In 1895, Roentgen reported the first use of X-ray imaging of hand bones, and won the 1st Nobel Prize in Physics in 1901. Since then, medical imaging has developed for 118 years. The development of imaging equipment such as MRI (the discovery of nuclear magnetic resonance phenomenon in 1930 produced three Nobel Prizes; the application of nuclear magnetic resonance imaging produced two Nobel Prizes in 1973), CT (invented in 1970, Nobel Prize in 1979), PET and ultrasound have further provided more accurate information for clinical medicine and matured into the core content of medical imaging.

Most of the time, malignancy death occurs due to metastasis and complications rather than the primary tumor itself. The most common site of metastasis of the tumor is the liver, followed by the lungs and bones. Spinal metastases account for about 70% of bone metastases, and 5% ~20% of patients with spinal metastases eventually lead to spinal cord compression^[1]。 Anticipatory prognostic studies of spinal metastases are significant in guiding treatment decisions. On the one hand, spinal metastases can cause severe bone pain and pathological fractures, and spinal cord compression can often lead to paraplegia, so the treatment of spinal metastases needs to be carried out in a short time. On the other hand, the adverse factors such as bone marrow suppression, severe neurological impairment, urinary incontinence, obesity, malnutrition and corticosteroid use after radiotherapy and chemotherapy in patients with spinal metastases are difficult to control before operation, and the incidence of complications such as incision non-union and infection after operation is high. In addition, although the survival expectancy of patients with metastatic spinal cord compression (MSCC) is relatively short, the treatment of spinal metastases and their complications consumes healthcare resources and costs^[2]。 Prognostic studies of spinal metastases mainly include three categories: (1) studies that predict risk factors affecting overall survival; (2) To determine the risk factors affecting the survival of MSCC and/or spinal compression fractures after surgery and radiotherapy; (3) Studies to assess clinical or imaging risk factors for the progression of spinal metastases to MSCC and/or spinal compression fractures. The purpose of the predictive prognosis study of spinal metastases is to: (1) avoid excessive medical treatment and avoid the risk of surgery; (2) before the patient's health deteriorates, choose the treatment mode reasonably; (3) Define the risk factors and reduce the postoperative complication rate of aggressive surgery; (4) Provide the basis for the choice of interventional treatment.