Home / Barkovich Pediatric Neuroimaging

Barkovich Pediatric Neuroimaging

Author: admin09/09
Barkovich Pediatric Neuroimaging 6,5/10 9527votes

MRI of the Neonatal Brain. Neonatal brain infection. Susan Blaser, Venita Jay, Laurence E Becker and E Lee Ford Jones. Chapter Contents. Neonatal CNS infections, whether acquired in utero congenital, intrapartum or postnatally remain an important cause of acute and long term neurological morbidity. Pathologic features and associated imaging patterns depend upon the stage of development of the CNS, the affinity of a specific infective agent for a specific CNS cell type, and the ability of the host to respond to that insult. With the discovery of cytokines and adhesion molecules, and the demonstration of lymphocyte recruitment across the bloodbrain barrier BBB, the CNS is now known to be able to mount and propagate an inflammatory response to infections. This immune response has been invoked in neonatal brain damage even when the maternal infection, which may have had its onset before pregnancy, does not directly involve the fetal brain. The effects of infection on the rapidly developing brain, which continually evolves in its susceptibility to damage, in association with an evolving immune system lead to complex patterns of pathology and imaging features dissimilar to those seen in an older child ill with a similar infectious agent. Certain factors aid in the diagnosis and differentiation of the congenital and neonatal infections. The etiologic agent may be known if the mother was exposed to an infectious agent or had a symptomatic infection. Conclusive diagnosis is dependent upon comprehensive clinical evaluation, ophthalmologic examination, microbiological testing of the infant and mother, and serial follow up serology of the infant. Additionally, the actual clinical presentations of infection in the neonate are different for viruses, bacteria and parasites. Infants with bacterial infections are likely to present with sepsis, while those with cytomegalovirus CMV or toxoplasmosis infections may be clinically asymptomatic at birth despite their obvious intracranial involvement on imaging or ophthalmologic examination. Neonates with viral infections may present with active hepatitis, skin vesicles or petechiae. The mechanism of infection and damage is also different amongst the infectious agents, leading to more specific imaging and pathologic appearances. Viruses, for example, tend to produce a selective necrosis of specific cell types, whereas bacteria and fungi are less selective. Also, different patterns of calcifications on CT or pathologic specimens are typical for the various STORCH syphilis, toxoplasmosis, rubella, CMV, human immunodeficiency virus HIV and herpes simplex infections, and the timing of insult during fetal life may lead to either teratogenic or encephaloclastic effects. Clinical and imaging differentiation amongst these disorders and amongst their respective infective agents is, therefore, frequently possible. Surface Ligand Controlled Assembly of Functional Nanoparticles for Targeted Imaging and Therapy of Tumors. Malformations dArnold Chiari type 1 et 2 Morel B, Sirinelli D, Cottier JP, Franois P, Carpentier E, Sembly C, MaheutLourmire J CHU Tours. Joubert sendromu anormal solunum dzeni ve gz hareketleri, hipotoni, ataksi, serebellum ve beyin sapnn nropatolojik anomalileri ile birlikte geliimsel. Tuberous sclerosis TS, also known as tuberous sclerosis complex or Bourneville disease, is a neurocutaneous disorder phakomatosis characterised by the development. MRI should include conventional T1 and T2 weighted imaging in at least two planes in any infant with suspected infection. The sagittal plane is useful for detecting thrombosis in the sinuses. Axial images should always include full posterior fossa views to visualize the transverse sinuses. The use of contrast is mandatory for detecting early changes within the meninges or parenchyma and for establishing the full extent of any abnormalities. The role of diffusion weighted imaging in patients with infection is now being recognized. Time allowing, a fluid attenuated inversion recovery FLAIR sequence may give additional postcontrast information. I/51z36ImznrL.jpg' alt='Barkovich Pediatric Neuroimaging' title='Barkovich Pediatric Neuroimaging' />Fig. Tubercular infection with vasculitis. Several vessels are shown in this field with transmural inflammatory infiltrate arrow. Arteritis arrowhead is a common complication in tubercular meningitis. Vasculitis of arteries and veins may lead to thrombosis and hemorrhagic infarction. H E stain, low power view. Predisposing factors for bacterial infections in the newborn include maternal sepsis or chorioamnionitis, maternal cervical colonization of agents such as group B streptococcus, prolonged rupture of membranes prior to delivery, complications of labor and delivery, and deficiencies of cell mediated or humoral immunity in the infant. Microsoft Access Survey Template. Nosocomial and iatrogenic etiologies include exposure to reservoirs of pathogens within the neonatal intensive care unit, and invasive procedures such as endotracheal intubation, central vascular access, or CSF diversion. Group B streptococcus and Escherichia coli E. Infection from enteric organisms is more frequent during the first 2 weeks of life particularly with the use of intrapartum group B streptococcus prophylaxis, while those from streptococcus and staphylococcus species become more prevalent during the second 2 weeks of life. There is a particular propensity for E. S macroglobulin fraction which contains maternal antibodies to coliform bacteria does not cross the placenta, leading to a lack of passively acquired immunity to Gram negative organisms. Other important agents in the neonatal period are Listeria monocytogenes and other members of the Enterobacteriaceae group, Citrobacter sp. Enterobacter sp. Staphylococcus aureus and Epidermidis infections are particularly common in surgical neonates and those with indwelling shunts or central venous lines. By 2 months of age, with loss of passive immunity, there is a rise in CNS infections from Hemophilus, Pneumococcus and Meningococcus. Hematogenous spread of bacteria from omphalitis, urinary tract infection or pneumonia leads to co existence of peritonitis, arthritis, and in some cases, meningitis. Entry into the CNS requires the bacteria to cross an epithelial mucosal barrier, such as upper respiratory tract, intestinal mucosa, or umbilical stump, to reach the blood stream. The actual site and mechanism of egress of bacteria from the blood stream into the CSF is not fully defined in every case. Pathways include extension through structures without intact BBB such as the choroid plexus, factors released by the organism which allow intracellular transport and direct vessel wall invasion, and vascular compromise with direct invasion of adjacent necrotic brain tissue. Non hematogenous pathways leading to CSF infection include direct extension, for example from an overlying scalp infection, or direct inoculation via ventricular shunt or puncture. Neonates with bacterial CNS infections frequently present with apnea, lethargy and other signs of fulminant systemic illness or shock rather than signs of meningeal irritation Fig. Bulging fontanel and seizures are non specific features seen in association with any cause of increased intracranial pressure in this age group, even when there is no intracranial involvement by the infecting agent. Premature infants, due to the deficiencies in neonatal host defense mechanisms and to higher permeability of leptomeninges, are even more susceptible than full term neonates to bacterial infections, including meningitis. They also have a much higher mortality. Mortality rates for infants with group B streptococcus, for example, range from 7. Complications of bacterial meningitis are extremely common in infants under 6 months of age. Follow up imaging is therefore suggested in neonates to exclude the presence of complications requiring surgical intervention or change in therapy. These complications include cerebritis, infarction Fig. The diagnosis of an abnormal fontanel requires an understanding of the wide variation of normal. At birth, an infant has six fontanels. The anterior fontanel is the. Neonatal brain infection Susan Blaser, Venita Jay, Laurence E Becker and E Lee FordJones.

Related Posts