377

Neuroanatomie (Subject) / Alles (Lesson)

alles

This lesson was created by stefy.

Learn lesson

This lesson is not released for learning.

Advertisement
  • Hypoxic ischemic encephalopathy occuring at term Watershed infarcts. Ulegyria. Variable deep, superficial white matter gliosis and atrophy. Myelination delay. Injury to hippocampus and pons.
  • Periventricular Leukomalacia (PVL) Occurs in term infants, premature infants greater than 26 weeks of gestation. Periventricular gliosis. Ex vacuo ventriculomegaly. Apposition of sulci to ventricular surface.
  • Gliosis in the periatrial region (seen best on proton-density scans) is caused by injury to the developing brain at ______ gestational age or older. 28 weeks .
  • Ex vacuo atrial enlargement without gliosis reflects injury prior to _______ gestational age. 26 weeks.
  • Acute imaging findings of Profound Perinatal Hypoxic Ischemic Injury Deep gray matter: Isodense to white matter. Mottled high T1 and low T1 signal. White matter: Normal. May see blurred gray-white junction on protein density images.
  • Subacute imaging findings of Profound Perinatal Hypoxic Ischemic Injury Deep gray matter: Variable T1 and T2 signal. White matter: High T1 and low T2 perirolandic cortex.
  • Chronic imaging findings of Profound Perinatal Hypoxic Ischemic Injury Deep gray matter: High T2 signal. White matter: High T2 perirolandic cortex. Thinned gyri, atrophy.
  • Imaging of Profound Postnatal Hypoxic Ischemic Injury Deep gray (Damage to corpus striatum: high signal on T2WIs Relative sparing of thalami) Cortex (Majority of cortex injured: high signal on T2WIs Relative sparing of perirolandic cortex Thinned gyri)
  • Septo-optic dysplasia (SOD) Congenital disorder with variable hypoplasia of optic nerves and complete or partial absence of septum pellucidum. Squared-off appearance of frontal horns.
  • Alobar holoprosencephaly Poor prognosis. Anterior rind of brain tissue and monoventricle communicating with dorsal cyst. Fused thalami. Absent septum pellucidum, corpus callosum, and falx. Upside-down U-shaped mantle of brain tissue. Ends of U are hippocampal ridges.
  • Advertisement
  • Semilobar holoprosencephaly Partial fusion of hemispheres. Absent or dysgenic corpus callosum and septum pellucidum. High association with migration anomalies. Posterior portion of interhemispheric fissure and falx are usually formed.
  • Lobar holoprosencephaly Partial absence of frontal interhemispheric fissure. Absent septum pellucidum and relatively normal brain overlap with SOD. Body and splenium of corpus callosum are usually present with genu and rostrum absent (dysgenic corpus callosum).
  • Lipomas of corpus callosum Congenital abnormalities. High T1 signal with fat supression. No mass effect. Vessels course through these lesions. Occur because of persistence of meninx primitiva.
  • Lissencephaly and pachygria/agyria complex Synonyms meaning absence of gyri. Smooth hourglass brain. Thick, multilayered cortex. Classic pattern: Arrested neuronal migration with only four cortical layers. Premature infants brain can be a mimic.
  • Hemimegalencephaly Asymmetric hemispheric enlarged with polymicrogyric and pachygyric changes. May be associated with neurofibromatosis.
  • Polymicrogyria and pachygria Pachygyria is a incomplete lissencephaly. Broad, thick gyri with shallow sulci. Normal interdigitating fingers of subcortical white matter are absent. Polymicrogyria is a cortical dysplasia. Thick mantle of gray matter with multiple small gyri. Normal interdigitating fingers of subcortical white matter are absent. Underlying white matter gliosis in polymicrogyria can sometimes help differentiate it from pachygyria.
  • Heterotopic Gray Matter Islands of gray matter anywhere between ependymal surface and subcortical white matter. May cause seizures.
  • Schizencephaly Abnormal neuronal migration resulting in gray matter-lined clefts that invaginate brain. Extend from ventricular ependymal surface to pial cortical surface. Polymicrogyric clefts do not extend to ventricle. Open lip or closed lip (apposed walls) forms.
  • Distinguishing porencephaly from open lipped schizencephaly Porencephaly: encephalomalacia that communicates with ventricle. Schizencephalic clefts are lined by gray matter. Porencephalic cysts are lined by a thin layer of white matter.
  • Chiari II malformations Small posterior fossa: Cerebellum is squeezed up against tentorium, down through foramen magnum (tonsillar herniation), and forward around brainstem. Pons and medulla are squeezed inferiorly with cervicomedullary kink. Cord syrinx is present. Nearly all have hydrocephalus. Most have partial or complete agenesis of corpus callosum. Most present with myelomeningocele.
  • Chiari I malformations Cerebellar tonsillar ectopia (tonsils extend > 5 mm below foramen magnum). Patients may be asymptomatic. May give rise to cervical spinal cord syrinx.
  • Dandy-Walker Malformations Large posterior fossa with high tentorial insertion. Dilated cystic 4th ventricle fills posterior fossa. Cerebellar vermis and hemispheres may be hypoplastic or absent.
  • Neurofibromatosis type 1 imaging findings (chromosome 17) Altered signal in white matter and basal ganglia. Dural ectasia. Optic and other gliomas. Sphenoid dysplasia. Thinning long bone cortex (ribbon ribs). Plexiform neurofibromas. Café au lait spots. Iris hamartomas (Lisch nodules). Vascular stenoses.
  • Neurofibromatosis type 2 imaging findings (chromosome 22) Vestibular schwannomas. Meningiomas. Spinal glial tumors. Optic and other gliomas.
  • Tuberous sclerosis Skin lesions: Adenoma sebaceum. Ash-leaf spots. Brain lesions: Subependymal hamartomas. Cortical tubers. Subependymal giant cell astrocytomas located at foramina of Monro (May lead to hydrocephalus)
  • Sturge-Weber Syndrome Skin and meningeal angiomatous lesions. Port-wine nevus: skin angioma in ophthalmic division of trigeminal nerve. Pial angiomas may result in chronic ischemia, gliosis, and gyral cortical calcifications. Enlargement of deep and subependymal veins may mimic arteriovenous malformations.
  • Von Hippel-Lindau Syndrome Inherited disorder consisting of retinal angiomas and cerebellar and spinal hemangioblastomas. Cerebellar hemangioblastomas: well-circumscribed cystic lesion with enhancing mural nodule. Prone to sudden spontaneous hemorrhage. Other associations: renal cell carcinoma, liver and kidney angiomas.