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Neuroanatomie (Subject) / Alles (Lesson)

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• Subgaleal hematoma Soft tissue swelling of the scalp located beneath subcutaneous fibrofatty tissue and above temporalis muscle.
• Intracranial air, pneumocephalus, may be seen with what fractures Compound skull fractures. Fractures involving paranasal sinuses.
• Epidural hematoma generalities Usually arterial in origin. Often result from skull fracture disrupting middle meningeal artery.Strips dura from inner table of the skull. Forms an ovoid mass. Generally does not cross suture lines.
• Venous epidural hematomas Less common than arterial epidurals. Tend to occur at the vertex, posterior fossa, or anterior aspect of middle cranial fossa. Usually result from disrupted dural venous sinuses. Vertex epidurals can cross sagittal suture.
• Subdural hematomas Typically result from tearing of cortical veins that traverse the subdural space. Will not cross falx cerebri or tentorium. Can cross sutural margins. Frequently layer along hemispheric convexity from anterior falx to posterior falx. Crescent-shaped in axial plane. Biconvex in coronal plane.
• Subarachnoid hemorrhage Result from disruption of small subarachnoid vessels, aneurysm, or direct extension by a contusion or hematoma. Hyperdense linear areas within cisterns and sulci. May lead to subsequent hydrocephalus by impaired CSF resorption at the arachnoid villi.
• Intraventricular hemorrhage May result from tearing of subependymal veins, direct extension of parenchymal hematoma, retrograde flow of subarachnoid hemorrhage. Risk of hydrocephalus by obstruction of the aqueduct or arachnoid villi. Hyperdense material layering within ventricular system.
• Diffuse axonal injury (DAI) Widespread disruption of axons due to acceleration or deceleration injury. Small, petechial hemorrhages at gray-white junction of cerebral hemispheres and or corpus callosum.
• T2 shinethrough T2 and DW bright and ADC dark.
• Cortical contusions Focal brain injury involving superficial gray matter. Occur near bony protuberances_ Temporal lobes above petrous bone or posterior to greater sphenoid wing. Frontal lobes above cribriform plate, planum sphenoidale, and lesser sphenoid wing.
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• Traumatic Intracerebral Hematoma Rupture of small intraparenchymal blood vessels. Tend to have less surrounding edema than cortical contusions. Most are located in the frontotemporal white matter.
• Traumatic subcortical gray matter injury Uncommon manifestation of primary intra-axial injury. Multiple petechial hemorrhages primarily affecting basal ganglia and thalamus.
• Von Hippel-Lindau syndrome imaging manifestations Visceral_ Renal cell carcinomas. Pheochromocytomas. Pancreatic islet cell tumors. Pancreatic, hepatic, renal, and splenic cysts. CNS_ Retinal capillary hemangiomas. Spinal cord and posterior fossa hemangioblastomas. Endolymphatic sac adenocarcinomas.
• Distinguishing epidermoids from arachnoid cysts on MR imaging. Both follow CSF T1 and T2 signal. Epidermoids restrict diffusion, are bright at DWI. Arachnoid cysts do not restrict diffusion. Epidermoids are composed of epithelial cells that grow in layers. Arachnoid cysts contains CSF.
• Pachymeningeal versus leptomeningeal enhancement findings unfinished. Pachymeningeal enhancement is characteristically thick, smooth, and uninterrupted.
• Rare cystic lesion classically located at the anterior roof of the third ventricle at the foramen of Monro. Colloid cyst. Generally are hyperdense to brain parenchyma. Do not enhance.
• Carotid cavernous fistula (CCF) Communication between cavernous portion of internal carotid artery and surrounding venous plexus. Typically follows a full-thickness arterial injury. Results in venous engorgement of cavernous sinus, ipsilateral superior ophthalmic vein, inferior petrosal sinus.
• Diffuse cerebral edema CT imaging findings Decreased cerebral density. Loss of gray-white differentiation. Usually spares cerebellum and brainstem, which appear relatively hyperdense.. Falx and cerebral vessels may appear dense, mimicking acute subarachnoid hemorrhage.
• Subfalcial herniation Most common form of brain herniation. Cingulate gyrus is displaced across midline under the falx. May compress adjacent lateral ventricle. May enlarge contralateral ventricle (obstruction of the foramen of Monro). Both anterior cerebral arteries may be displaced to contralateral side.
• Uncal herniation Medially displaced medial temporal lobe over free margin of tentorium. Focal effacement of ambient cistern and lateral suprasellar cistern. Rarely compresses contralateral cerebral peduncle (Kernohans notch) against tentorial margin.
• Transtentorial Herniation Descending transtentorial herniation_ Effacement of suprasellar and perimesencephalic cisterns. Pineal calcification is displaced inferiorly. Ascending transtentorial herniation_ May involve vermis and parts of cerebellar hemispheres. Large posterior fossa hematomas
• Leptomeningeal cyst Known as a growing fracture. Caused by traumatic tear of the dura. Outpouching of arachnoid at site of suture or skull fracture.
• Duret hemorrhage Midline hematoma within tegmentum of rostral pons and midbrai. Associated with descending transtentorial herniation. Due to stretching or tearing of penetrating arteries.
• Nonaccidental trauma head findings Skull fractures. Subdural hematomas. Diffuse brain swelling.
• Moya moya disease Rare leptomeningeal vascular collaterals that form due to stenosis or occlusion of Circle of Willis arteries. Puff of smoke appearance at angiography. Associations_ Sickle cell disease. Neurofibromatosis type I. Downs syndrome. Fibromuscular dysplasia.
• Differential diagnosis of supratentorial partially cystic, partially solid mass in a child_ Pilocytic astrocytoma. PNET (primitive neuroectodermal tumor). Hemorrhage.
• Le Fort I Floating palate. Horizontal fracture through maxillary sinuses, nasal septum, and inferior ptyergoid plates.
• Le Fort II Pyramidal fracture through bridge of nose, medial orbits, lateral and posterior maxillary walls, nasal septum, inferior orbital rim (infraorbital nerve injury), and midportion of ptyergoid plates.
• Le Fort III Craniofacial dysjunction. Horizontal fracture through orbits. Begins near nasofrontal suture and extends posteriorly through nasal septum, medial and lateral orbit walls, zygomatic arch, and base (superior aspect) of pterygoid plates.
• CT scans done within 6 hours of MCA occlusion will commonly exhibit Insular ribbon sign_ Subtle blurring of gray-white layers of insula. Caused by early edema. Lentiform nucleus edema sign_ Hypodense putamen.
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• Ischemic penumbra ischemic but not infarcted (salvageable) tissue. Peri-infarct tissue.
• Diffusion-Weighted MR in Acute Ischemia Brain water diffusion rates fall rapidly during acute ischemia. Bright signal on DWIs.
• Apparent diffusion coefficient (ADC). Reflects pure diffusion behavior. Free of underlying T2 contributions (shine through or dark through).
• Fluid-Attenuated Inversion Recovery (FLAIR) in Ischemia Suppresses free water CSF signal but allows T2 weighting of parenchyma. Increases conspicuity of T2 changes in ischemia. May help detect small cortical lesions and acute subarachnoid hemorrhage.
• Fogging effect CT finding occuring during 2nd week after infarction. Cerebral edema and mass effect subside while proteins accumulate from cell lysis. Injurred brain morphology and density appear normal at CT.
• Hemorrhagic Transformation of Infarction Seen 1 to 2 weeks postinfarction. Hemorrhage of reperfused capillaries. Serpiginous line of petechial blood following gyral contours of infarcted cortex.
• Time course of CT-detected enhancement of infarcted brain Begins at about 1 week. Peaks at 7 to 14 days. Often assumes a gyral pattern. As gliosis ensues and blood-brain barrier is repaired, enhancement fades and resolves by 3 months.
• Intravascular MR enhancement of infarcted brain Commonly seen in infarct during the first week. May be due to slow flow or vasodilation in arteries and veins. May be detected within minutes of vessel occlusion. Seen in a majority of cortical infarcts at 1 to 3 days. Resolves by 10 days.
• Maximal brain swelling post brain infarction occurs at what days 3 to 7 days postinfarction.
• Encephalomalacia post brain infarction occurs when 30 to 90 days (1 to 3 months) postinfarction.
• ACA (anterior cerebral artery) three subgroups_ Medial lenticulostriate branches_ Rostral portions of basal ganglia. Pericallosal branches_ Corpus callosum. Hemispheric branches_ Medial frontal and parietal lobes.
• Two main branch groups of MCA (middle cerebral artery) Lateral lenticulostriate branches_ Supply most of basal ganglia. Hemispheric branches_ Lateral cerebral surface.
• Major branches of PCA (posterior cerebral artery) Midbrain and thalamic perforating branches. Posterior choroidal arteries. Cortical branches to medial temporal and occipital lobes.
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Leg weakness _ ACA/Hemispheric branch/either side
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Incontinence, akinetic mutism _ ACA/Hemispheric branch/both sides
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Facial weakness _ ACA/Medial lenticulostriates/either side
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Dysarthria with or without motor aphasia _ ACA/Medial lenticulostriates/Left
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Face and arm weakness > leg weakness _ MCA/Hemispheric branch/either side
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Motor aphasia (anterior lesion) _ MCA/Hemispheric branch/Left
• (Deficit/Syndrome _ Cerebral artery/branch/side affected), Receptive aphasia (posterior lesion) _ MCA/Hemispheric branch/Left

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