Skull lesions

Introduction Bone lesions are found in almost all patients with Langerhans cell histiocytosis. Individual bone lesions have more bone lesions, mainly manifested as osteolytic lesions. Skull lesions are most common, followed by lower extremity bones, ribs, pelvis and spine, and jaw lesions are also quite common.

Cause

The skull lesions caused by various factors, including: 1. proliferative bone lesions; 2. atrophic bone lesions; 3. ulcerative bone lesions.

an examination

Related inspection

Brain ultrasound examination of brain CT

On the X-ray film, the bone disintegration is characterized by irregular edge. The skull damage changes from the worm-like shape to the large defect or the chisel-like change. The shape is irregular, round or elliptical, and the edge is jagged. The boundary of the initial or progressive lesion is blurred, and the common intracranial pressure is increased, the fracture of the bone is broken or the hydrocephalus of the communication may be accompanied by headache. However, during the recovery period, the bone is gradually clear at the edge, the hardening zone appears, the bone density is uneven, the bone defect gradually becomes smaller, and finally the whole repair does not leave any trace.

Differential diagnosis

Skull fractures: The importance of skull fractures is not in the skull fracture itself, but in the concurrent damage of the cranial cavity. According to the shape of the fracture, it is classified into: linear fracture, depressed fracture, comminuted fracture, and child growth fracture. A fractured piece of a depressed or comminuted fracture can damage the meninges and brain and damage the cerebral blood vessels and cranial nerves. Skull fractures account for about 15-20% of craniocerebral injury, which can occur in any part of the skull, with the largest amount of parietal bone, followed by the frontal bone, followed by the humerus and occipital bone. Generally, the fracture line does not cross the cranial suture. If the violence is too large, it can also affect the adjacent bone. The positive lateral position of the skull can be diagnosed. Because of the different fracture morphology, the treatment and prognosis are also different.

Skull hyperplasia: more manifested as increased skull and / or thickness, divided into diffuse and localized. Diffuse cranial hyperplasia is common in systemic diseases such as malformation osteitis, stony osteopathy, renal rickets, acromegaly, and thalassemia. Localized skull hyperplasia is caused by local bone lesions or secondary to adjacent lesions such as meningioma, osteoma, osteosarcoma, osteomyeloma, chronic osteomyelitis and old fractures.

Wearing a chisel to change the skull destruction: multiple myeloma bone X-ray examination showed multiple osteolytic osteoid-like bone defect areas or osteoporosis, pathological fractures.

Huge skull defects: skull defects, mostly due to open craniocerebral injury or firearm penetrating injury, some patients are residual bone defects due to surgical decompression or diseased skull resection. In recent years, due to the high brain pressure of severe craniocerebral injury, the decompressive method of decompressive craniectomy is prevalent, so there are many artificial large skull defects. In fact, a considerable number of patients do not need large cranial decompression. Most of them are decisions made during the surgery, and there are no defects.

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