Abstract

Benign enlargement of subarachnoid spaces (BESS) constitutes is one of the most frequent neurosonographic findings in infancy and is considered to regress spontaneously by the age of 2 years. Although the majority of children with BESS demonstrate normal developmental milestones, some patients may experience a transient psychomotor delay under the age of 2 year. Besides clinical andneuroimaging findings, the long-term impact of BESS is of great interest (learning difficulties at school, language delay, impairmentsin social-cognitive abilities, reduced quality of life, decreased attention skills and poor visual-motor performance, increased risk ofautism spectrum disorders as well as a higher incidence of epilepsy). It is considered that the risk of long-term consequences may be associated with pathogenetic features of dilation of extra-axial cerebrospinal fluid spaces. In this review, we describe potentialpathogenetic mechanisms of dilatation of the subarachnoid space and its pathological sequelae in children. Generally, numerous pathogenetic hypotheses about developing BESS have been proposed as follows: remarkable physiological imbalance between the skull and brain growth in infants aged from three months to one year; manifestation of cerebral trophy; communicating hydrocephalus due to a distal block with a valve mechanism; a delay in maturation of arachnoid villi/granulations until two years of age; the result of abusive head trauma in infants. However, the hypothesis about pathological consequences of BESS in the long run due to abnormalvenous hemodynamics has emerged in recent years. Impaired venous outflow is the main driving factor of subarachnomegaly and the more severe pathological changes the more significant symptoms of subarachnomegaly. We also highlight the role of impaired cerebralvenous circulation in the development of subarachnomegaly. Further studies are needed to investigate the clinical relevance of chronic increased intracranial pressure due to venous outflow disturbance in infants with enlarged subarachnoid spaces.Тhe subject for future research should be to determine a diagnostic algorithm to help distinguish patients with BESS from those who are at risk of impairedneurological development and require additional diagnostic and therapeutic interventions.

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