Intracranial calcifications in childhood: Part 2.

This article is the second of a two-part series on intracranial calcification in childhood. In Part 1, the authors discussed the main differences between physiological and pathological intracranial calcification. They also outlined histological intracranial calcification characteristics and how these can be detected across different neuroimaging modalities. Part 1 emphasized the importance of age at presentation and intracranial calcification location and proposed a comprehensive neuroimaging approach toward the differential diagnosis of the causes of intracranial calcification. Pathological intracranial calcification can be divided into infectious, congenital, endocrine/metabolic, vascular, and neoplastic. In Part 2, the chief focus is on discussing endocrine/metabolic, vascular, and neoplastic intracranial calcification etiologies of intracranial calcification. Endocrine/metabolic diseases causing intracranial calcification are mainly from parathyroid and thyroid dysfunction and inborn errors of metabolism, such as mitochondrial disorders (MELAS, or mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes; Kearns-Sayre; and Cockayne syndromes), interferonopathies (Aicardi-Goutières syndrome), and lysosomal disorders (Krabbe disease). Specific noninfectious causes of intracranial calcification that mimic TORCH (toxoplasmosis, other [syphilis, varicella-zoster, parvovirus B19], rubella, cytomegalovirus, and herpes) infections are known as pseudo-TORCH. Cavernous malformations, arteriovenous malformations, arteriovenous fistulas, and chronic venous hypertension are also known causes of intracranial calcification. Other vascular-related causes of intracranial calcification include early atherosclerosis presentation (children with risk factors such as hyperhomocysteinemia, familial hypercholesterolemia, and others), healed hematoma, radiotherapy treatment, old infarct, and disorders of the microvasculature such as COL4A1- and COL4A2-related diseases. Intracranial calcification is also seen in several pediatric brain tumors. Clinical and familial information such as age at presentation, maternal exposure to teratogens including viruses, and association with chromosomal abnormalities, pathogenic genes, and postnatal infections facilitates narrowing the differential diagnosis of the multiple causes of intracranial calcification.

Intracranial calcifications in childhood: Part 1.

This article is the first of a two-part series on intracranial calcification in childhood. Intracranial calcification can be either physiological or pathological. Physiological intracranial calcification is not an expected neuroimaging finding in the neonatal or infantile period but occurs, as children grow older, in the pineal gland, habenula, choroid plexus and occasionally the dura mater. Pathological intracranial calcification can be broadly divided into infectious, congenital, endocrine/metabolic, vascular and neoplastic. The main goals in Part 1 are to discuss the chief differences between physiological and pathological intracranial calcification, to discuss the histological characteristics of intracranial calcification and how intracranial calcification can be detected across neuroimaging modalities, to emphasize the importance of age at presentation and intracranial calcification location, and to propose a comprehensive neuroimaging approach toward the differential diagnosis of the causes of intracranial calcification. Finally, in Part 1 the authors discuss the most common causes of infectious intracranial calcification, especially in the neonatal period, and congenital causes of intracranial calcification. Various neuroimaging modalities have distinct utilities and sensitivities in the depiction of intracranial calcification. Age at presentation, intracranial calcification location, and associated neuroimaging findings are useful information to help narrow the differential diagnosis of intracranial calcification. Intracranial calcification can occur in isolation or in association with other neuroimaging features. Intracranial calcification in congenital infections has been associated with clastic changes, hydrocephalus, chorioretinitis, white matter abnormalities, skull changes and malformations of cortical development. Infections are common causes of intracranial calcification, especially neonatal TORCH (toxoplasmosis, other [syphilis, varicella-zoster, parvovirus B19], rubella, cytomegalovirus and herpes) infections.

High-resolution neurosonographic examination of the lenticulostriate vessels in neonates with hypoxic-ischemic encephalopathy.

OBJECTIVE: To assess the feasibility of visualizing lenticulostriate vessels (LV) using a linear high-resolution ultrasound probe and characterize LV morphology to determine whether morphological alterations in LV are present in neonatal hypoxic-ischemic encephalopathy (HIE) as compared to the unaffected infants. METHODS: We characterized LV by their echogenicity, width, length, tortuosity, and numbers of visualized stems/branches in neurosonographic examinations of 80 neonates. Our population included 45 unaffected (non-HIE) and 35 with clinical and/or imaging diagnosis of HIE. Of the neonates with clinical diagnosis of HIE, 16 had positive MRI findings for HIE (HIE+MRI) and 19 had negative MRI findings (HIE-MRI). Annotations were performed twice with shuffled data sets at a 1-month interval and intrarater reliability was assessed. Focused comparison was conducted between non-HIE, HIE+MRI and HIE-MRI neonates whose images were acquired with a high frequency linear transducer. RESULTS: Studies acquired with the two most frequently utilized transducers significantly differed in number of branches (p = 0.002), vessel thickness (p = 0.007) and echogenicity (p = 0.009). Studies acquired with the two transducers also significantly differed in acquisition frequency (p < 0.001), thermal indices (p < 0.001) and use of harmonic imaging (p < 0.001). Groupwise comparison of vessels imaged with the most frequently utilized transducer found significantly fewer branches in HIE + MRI compared to HIE-MRI negative and non-HIE patients (p = 0.005). CONCLUSION: LV can be visualized in the absence of pathology using modern high-resolution neurosonography. Visualization of LV branches varies between HIE + MRI, HIE-MRI neonates and controls. ADVANCES IN KNOWLEDGE: High-resolution neurosonography is a feasible technique to assess LV morphology in healthy neonates and neonates with HIE.