pathological calcification
Introduction
Introduction In addition to bone and teeth, calcium deposits occur in other tissues of the body, called pathological calcification. The calming calcium salt is mainly calcium phosphate, followed by calcium carbonate. The presence or absence of symptoms and signs depends on the presence of underlying disease and the nature of the lesion, the location and extent of calcification. Physiological intracranial calcification is usually asymptomatic and is inadvertently found during imaging studies. The clinical manifestations of pathological intracranial calcification depend on the nature of the primary disease (brain tumors, vascular abnormalities, inflammatory lesions, and metabolic abnormalities, etc.). Calcification of the basal ganglia (idiopathic or secondary) is usually asymptomatic, but some patients may have abnormal movements (chore, hand and foot dyskinesia, dystonia, etc.) and Parkinson's-like symptoms (muscle stiffness, reduced movement) Etc.); cerebellar signs can occur in patients with cerebellar calcification; cognitive dysfunction can also occur in some patients. Treatment of the primary disease sometimes reduces or eliminates intracranial calcification.
Cause
Cause
The causes of pathological calcification are as follows:
1. Neoplasia:
1 craniopharyngioma; 2 glioma; 3 meningioma; 4 ependymoma; 5 choroid plexus papilloma; 6 chordoma; 7 dermoid cyst; 8 epidermoid cyst; 9 teratoma; Tumor; 9 lipoma; 10 pituitary adenomas (rare); 10 metastases (rare).
2. Vascularity:
1 atherosclerotic plaque; 2 aneurysm; 3 hemangioma; 4 subdural hematoma; 5 intracranial hematoma; 6 cerebral infarction.
3. Infectivity:
1 tuberculosis; 2 congenital intracranial infection; 3 cysticercosis; 4 hydatid cysts; 5 trichinosis; 6 cryptococcosis; 7 sporozoites.
4. Congenital and hereditary:
1 tuberous sclerosis; 2Stureg-Weber syndrome; 3 neurofibromatosis; 4 no cerebral malformation; 5 Fahr disease; 6 Cockayne syndrome; 7 Gor1in-Goltz syndrome.
5. Metabolic and other reasons:
1 hypoparathyroidism; 2 pseudohypoparathyroidism; 3 X-ray radiation; 4 methotrexate; 5 hemodialysis; 6 hyperparathyroidism; 7 vitamin D poisoning; 8 carbon monoxide poisoning; Poisoning; 10 systemic lupus erythematosus.
Examine
an examination
Related inspection
Brain MRI examination of brain CT examination
Intracranial calcification can be detected by CT scan, MRI imaging and cranial plain film, and can also be displayed by intracranial ultrasound in neonates. Among them, CT is the most sensitive method for finding intracranial calcification, showing that intracranial calcification is the best, and it shows high density (like bone density) on CT.
MRI is not as sensitive to CT as it shows calcification. The signal of calcification on MRI varies with the local composition of the lesion: if the calcification component is greater than 30%, calcification tends to be low due to the mainly low proton signal effect; when the calcification component is less than 30%, due to T1 Shortened, calcifications may also behave as high signals on the T1 phase. Since calcifications usually show low or no signal on MRI, the signal reduction is more pronounced in the T1 and T2 weighted phases and on the gradient echo sequence, and the signal loss is more pronounced on the gradient echo sequence.
Diagnosis
Differential diagnosis
Pathological calcification can be divided into two types: malnutrition calcification and metastatic calcification. The former mainly occurs on the basis of local tissue degeneration and necrosis. The deposition of calcium and phosphorus ions in the blood is promoted due to changes in the physical and chemical environment of the local tissue. The latter occurs on the basis of high blood calcium. When the concentration of calcium ions in the blood increases, the calcium salt can settle in many healthy organs and tissues. The morphological manifestations of the two calcifications are basically the same, but their mechanisms and effects on the body are different.
