Prenatal Origins of Subdural Hemorrhage/Effusions and Related Seizures: Acute, or Crisis in a Chronic Condition?
|Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Du Cane Road, UK|
|Corresponding Author :||Talbert DG
Institute of Reproductive and Developmental Biology
Imperial College School of Medicine
Du Cane Road, London W12 ONN, UK
Tel: +44 20 7589 5111
E-mail: [email protected]
|Received: June 12, 2015 Accepted: July 20, 2015 Published: July 27, 2015|
|Citation:Talbert D (2015) Prenatal Origins of Subdural Hemorrhage/Effusions and Related Seizures: Acute, or Crisis in a Chronic Condition? J Clin Case Rep 5:565. doi:10.4172/2165-7920.1000565|
|Copyright: ©2015 Talbert D. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
|Related article at Pubmed, Scholar Google|
Introduction: Subdural haemorrhages and effusions are collections of blood or tissue fluid that appear in infants between the lining of the skull (Dura Mater) and the brain surface, with an incidence of 21 in 100,000. Method: This study is further analysis of data in a case report of a dichorionic-dizygotic twin pregnancy in which one twin (Twin-A) presented three months postnatally with seizure. The other twin (Twin-B) developed normally and so became a control. The twins showed similar head growth up to 24 weeks but subsequently the rate of head growth of Twin-A exceeded that of Twin-B. Later, from 29 weeks, Twin-A’s femur growth began to lag Twin-B’s, but abdominal growths remained matched. Postnatally Twin-A’s head growth rate continued to exceed that of Twin-B until at 3 months postnatal Twin–A presented with seizure Discussion: This case suggests that a development defect exists in which cerebral venous vessel diameters fail to keep up with the rapidly increasing cerebral blood flow from late pregnancy into infancy. Forcing the increasing cerebral blood flow through inadequate venous vasculature will produce dangerous intracranial venous hypertension, which may lead to subdural and retinal hemorrhages. Venous effusion develops when lumen pressure markedly exceeds intracranial pressure, causing intracranial pressure to follow cerebral venous pressure. An acute crisis can arise at any time if intracranial pressure compresses veins sufficiently to further increase venous resistance. Thus the basic mechanism is not acute, it is chronic, but it has a potential for crisis. Conclusion: There is a condition, caused by inadequate cerebral vein development, where cerebral vein pressure is raised excessively. Starting in late pregnancy and extending into infancy it may remain clinically silent (apart from macrocephaly) or suddenly result in acute bursting in venous vasculature. In this case enduring recovery was produced by fitting a Subdural-Peritonal shunt.