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Published on: August 28, 2018
Intracranial calcification in paediatric computed tomography
Insights
Intracranial calcification in children is rare, with physiological types increasing by age 15. Pathological calcification, often linked to neoplasms, neuroectodermal syndromes, or infections, requires further investigation.
Area of Science:
- Pediatric Radiology
- Neuroradiology
- Medical Imaging
Background:
- Intracranial calcification in children can be physiological or pathological.
- Understanding its incidence and causes is crucial for diagnosis.
Purpose of the Study:
- To assess the diagnostic significance of intracranial calcification in children.
- To determine the incidence and common causes of pathological intracranial calcification.
Main Methods:
- Analysis of computed tomograms from 18,000 consecutively examined children.
- Correlation of calcification findings with clinical symptomatology and biochemical studies.
Main Results:
- Physiological calcification incidence is low (approx. 2% up to age 8), increasing by age 15.
- Pathological calcification occurred in 1.6% of cases, most commonly due to neoplasms (43%), neuroectodermal syndromes (20%), and infections (12%).
- Diffuse basal ganglia calcification showed limited correlation with clinical symptoms; metabolic disorders were found in only 6 cases.
Conclusions:
- Confirms low incidence of physiological intracranial calcification in children.
- Identifies neoplasms, neuroectodermal syndromes, and infections as primary causes of pathological calcification.
- Highlights the limited clinical correlation of basal ganglia calcification and the low yield of routine biochemical studies for metabolic disorders in these cases.
Abstract:
An analysis of the computed tomograms of 18000 children examined consecutively form the basis of an assessment of the diagnostic significance of intracranial calcification. The low incidence of physiological calcification in the pineal and choroid of about 2% up to the age of 8 years, but increasing 5-fold by the age of 15 years, is confirmed. Pathological calcification occurred in 1.6%, the commonest causes being neoplasms (43%), neuroectodermal syndromes (20%) and infections (12%). Diffuse basal ganglia calcification (15%) bore little relation to the diverse clinical symptomatology, and routine biochemical studies showed a disorder of metabolism to be present in only 6 cases. Calcification has not been previously noted in acute haemorrhagic leukoencephalitis, Pertussis or Cocksackie encephalitis, infantile neuraxonal dystrophy, Marinesco-Sjögren syndrome or in the basal ganglia in neurofibromatosis.
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