Skull hyperplasia

Introduction Skull hyperplasia is often characterized by increased skull and/or thickness, divided into diffuse and localized. Diffuse cranial hyperplasia is common in systemic diseases such as deformity 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, bone fiber abnormal proliferation, chronic osteomyelitis and old fractures.

Cause

Diffuse cranial hyperplasia is common in systemic diseases such as deformity 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, bone fiber abnormal proliferation, chronic osteomyelitis and old fractures.

Most people think that osteofibrous dysplasia is a genetic disorder, but some people think that it is related to inflammation or dysfunction of blood vessels, nutritional nerves, endocrine, etc., and some people think that it is related to abnormal growth of bone interstitial. The relationship between craniocerebral trauma and abnormal fibrosis of the skull has yet to be further explored in the future.

an examination

Related inspection

Brain CT examination brain MRI examination EEG examination brain function imaging brain nerve examination

According to the clinical manifestations of age, location, etc., especially in combination with the characteristics of the skull X-ray, diagnosis can be made.

Other auxiliary inspections:

X-ray examination: Diagnostic value for the diagnosis of sham fibrosis. The flat film of the skull is mainly characterized by a circular or round-shaped translucent area in the cranial sulcus, and the skull base lesion is characterized by dense and thick bone. Since normal bone is replaced by fibrous tissue and has bone hyperplasia and cartilage residue, its performance can be varied. There are roughly three types:

1. Cyst type: more common in the early stage of the disease or lesions in the calvarial area, cystic bone density reduction areas of varying sizes can be seen between the skull barriers, and some are multi-atrial, widened, and outer plates The ridges are thinner and the inner panels are often unaffected.

2. Sclerosing type: more common in the late stage of the disease or in the bottom of the skull, the lesions are more extensive, often causing changes in the skull deformity, thickening of the bone, increased shadow density is "ivory" hardening changes, more common in the frontal bone The winglet of the plate and sphenoid bone.

3. Hybrid: Both cystic and sclerotic types exist at the same time, more common in the skull, and the smaller one needs to be differentiated from the skull changes caused by meningiomas. If it is multiple, the above-mentioned similar performance can be seen in the bones of other parts of the body. When there is cartilage tissue, it is cloud-like or cotton-like shadow. When there is more bone tissue, it can be ground glass.

Differential diagnosis

Differential diagnosis of skull hyperplasia:

1, head deformation: pointed and short head deformity more common in narrow cranial disease; scaphoid head seen in narrow cranial head and mucopolysaccharidosis; partial deformity seen in narrow cranial disease and one side of brain hypoplasia.

2, the skull enlargement: often combined with thinning of the cranial wall, cranial suture widening or deepening of the cerebral gyrus, more common in infants with hydrocephalus; if accompanied by thickening of the cranial wall, it is more common in deformed osteitis, bone Fibrous dysplasia and acromegaly.

3, the skull becomes smaller: if the cranial suture is not closed or the cranial suture is closed but there is no sign of increased intracranial pressure, mostly small brain malformation or brain development disorder; if the cranial suture is closed and accompanied by signs of increased intracranial pressure, it is narrow Cranial disease.

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