Presentation3.pptx, intra cranial infection.

Intra-cranial infection.

Dr/ ABD ALLAH NAZEER. MD.

Intra-cranial infection.. Congenital. . Encephalitis.. Meningitis.. Cerebritis, ependymitis, abscess formation.. Granulomatous infection.. Parasitic and fungal infection.. HIV infection.

Congenital Infections.

TORCH.Toxoplasmosis. Other (syphilis). Rubella.Cytomegalovirus (CMV). Herpes simplex virus (HSV).

Varicella zoster (the chickenpox virus). Entroviruses. Hepatitis B. Parvovirus. HIV (human immune deficiency virus). Chlamydia trachomatis. Mycoplasma. Group B streptococcus. Malaria.

COMMON CLINICAL FEATURES.

Low birth weight for gestational age. Prematurity. Seizures. Chorio-retinitis. Cataracts. Purpura.

Cerebral calcification. Micro-ophthalmia. Jaundice. Anemia. HepatosplenomegalyPneumonitis.

PATHOGENESIS.Neonatal

1.Antenatal (in utero) - 80-96% of cases Primary Maternal Infection Recurrent Maternal Infection

2.Perinatal.3.Postnatal.

Childhood1. Horizontal Transmission

CMV excreted in saliva, urine, stool, tears 2. Organ Transplantation

kidney, marrow, heart, liver, blood (leukocytes)

CLINICAL FEATURES. 90% of infants with congenital CMV infection are clinically silent.

CNS Manifestations 70% - microcephaly. 60% - intellectual impairment. 35% - sensorineural hearing loss seizures. 22% - chorioretinitis.

CONGENITAL TOXOPLASMOSIS.

Caused by the protozoan Toxoplasma gondii ocular, central nervous system (CNS)incidence: 0.3-1/1000 live births.

Routes of Transmission. Neonatal (in utero). Primary Maternal Infection.

acquired by the ingestion of raw or undercooked meat ( cattle), or of infectious oocysts in feces (cats, birds).

1st trimester - 17% - spontaneous abortion. 2nd trimester - 25% - spontaneous abortion or severe disease. 3rd trimester - 65% - subclinical disease.

Congenital toxoplasmosis show the typical multifocalperiventricular and cortical/subcortical punctuate calcifications aswell as a moderate ventriculomegaly as complication of the infection.

Congenital toxoplasmosis shows bilateral microophthalmia and chorionic calcifications as well as deformity of the lenses (white arrows).

Toxoplasmosis of immune compromised patient with multiple ring enhancing lesions.

CONGENITAL RUBELLA(German measles).

Caused by an RNA Togavirus. Vaccine-preventable disease.

Routes of Transmission.

Antenatal (in utero).

1st trimester - 75-90%. 2nd trimester - 35-40%. 3rd trimester - 25-50%.

CLINICAL FEATURES:

Neonatal Manifestations IUGR low birth weight - prematurity. stillbirth - spontaneous abortion.

Early Manifestations cloudy corneas. Cataracts. microcephaly. Hepatomegally. splenomegally .Jaundice. pulmonary valve stenosis. patent ductus arteriosus. thrombocytopenia purpura.

Congenital rubella infection show small calcifications within the basal ganglia, along the intramedullary veins within both frontal lobes and within the deep Layers of the overlying cerebral cortex and adjacent subcortical white matter(white arrows on A). MRI shows ill-defined, multifocal regions of dysmyelination within the periventricular white matter of both cerebral hemisphere.

Rubella. Unenhanced axial CT (a) in a 3-day-old with congenital rubella demonstrates punctate calcifications of the basal ganglia (arrow) and low attenuation of the white matter.

The classic clinicalpicture of cytomegalic inclusion disease (CID) is characterized by involvement of multiple organs, in particular the reticuloendothelial and central nervous system, with or without ocular and auditory damage. Obvious symptoms of CID could be jaundice, Hepatosplenomegaly and petechiae in a growth retarded often prematurely born baby. The neurological involvement includes microcephaly, seizures, hypotonia and lethargy. The most severely affected infants have a mortality rate of about 30%. Deaths are usually due to hepatic dysfunction, bleeding, disseminated intravascular coagulation or secondary bacterial infections. Some 85- 90% of children with a congenital CMV infection are asymptomatic in the neonatal period.

Congenital cytomegalovirus infection.

Congenital CMV-infection show multifocal, predominantly periventricular located calcifications within the supra- and infratentorial brain as well as a thickened, smooth dysplastic cortex, moderate ventriculomegaly, a small cerebellum and a CT-hypodense, T2-hyperintense dysmyelination of the periventricular white matter. In addition, a mild microcephaly is noted.

Axial CT-images (A, D), T2-weighted images (B, E), and SWI images (C, F) of with congenital cytomegalovirus infection presenting with moderate hydrocephalus and white matter volume loss as well as subtle subependymal calcifications are seen on the CT study (white arrow on D). The extent of calcium depositions is however much better appreciated on the SWI images as SWI-hypointense signal abnormalities (C, F). In addition, cerebellar hypoplasia (A, B) and high-grade loss of the hemispheric white matter (E), including a more focal subcortical defect in the right parieto-occipital region are noted.

MENINGITIS & ENCEPHALITIS.

Definitions.Meningitis – inflammation of the meningesEncephalitis – infection of the brain parenchymaMeningoencephalitis – inflammation of brain + meninges.Aseptic meningitis – inflammation of meninges with sterile CSF

Symptoms of encephalitis.

.Many encephalitides are mild and recovery occurs. .In a minority, serious illness develops with high fever, headache, mood change and drowsiness over hours or days. Focal signs, seizures and coma ensue. Death, or brain injury follows.

Herpes simplex encephalitis.

Axial T2-weighted (A), coronal FLAIR (B), axial DWI (C) MR images, and axial ADC map (D) with encephalitis . MRI shows symmetrical, ill defined T2- and FLAIR-hyperintense signal abnormalities in both thalami with matching regions of restricted diffusion (DWI-hyperintense, ADC-hypointense) on diffusion weighted imaging (white arrows on A-D) encephalitis.

Rasmussen's encephalitis with hemispheric volume loss.

Acute disseminated encephalomyelitis.

Symptoms of meningitis. Fever.Altered consciousness, irritability, photophobia vomiting, poor appetite.. Seizures 20 - 30%. Bulging fontanel 30%. Stiff neck or nuchal rigidity. Meningismus (stiff neck + Brudzinski + Kernig signs).

Meningitis:• Infection of the meninges which may be pyogenic, viral or

granulomatous.• Inflammation of the leptomeninges can be divided into acute

pyogenic (bacterial), lymphocytic (viral), and chronic (TB) meningitis. The diagnosis is usually clinical.

• The role of neuroimaging is to exclude complication of meningitis(e. g, abscess, ventriculitis, empyema).

CT and MRI of meningitis with dense basal cistern which is seen enhanced at MRI images.

Acute pyogenic meningitis with basal cistern exudates with enhancement and hydrocephalus.

Meningitis with predominant leptomeningeal enhancement.

Post-meningitis sequale with epidural and subdural empyema.

Cerebritis and abscess formation.

Ventriculitis with wall enhancement.

Tuberculosis meningitis Multiple enhancing tuberculomas.

T.B abscesses with left frontal subdural collection.

Left parietal tuberculous abscess.

Miliary tuberculosis of the brain.

Parasitic infection.

CT and MRI of Cysticercosis

Hydatid cyst with marginal calcification.

Multiple coalescing thin walled hydatid cysts.

HIV Encephalitis with progressive encephalopathy.

HIV Encephalitis