Diagnostic modalities of the Central Nervous System

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NEURORADIOLOGY Kinga Karlinger, MD, PhD Associate Professor Semmelweis University, Budapest Diagnostic modalities of the Central Nervous System X-ray: screening is not used any more, x-ray images instead Pneumoencephalography, ventriculography was too invasive, not in use any more. Myelography (+CT). Ultrasound (acustic window needed) neonatal CT: (x-ray!, c.m.) bone, Ca, air. Soft tissue MDCT, CTA, 3D, dynamic, perfusion examination. MRI focus on hydrogen ion: MRA, MRS, fmr Pros: multiplanar, good tissue contrast, without bone artefact, superior imaging of white matter lesions Cons: bone, Ca, fresh bleeding (stroke differentiation only with advanced sequences) cannot be seen; danger of clips Angiography /DSA : contrast material needed, use of catheter (invasive) mass effect, vascular, vasc. (SAH, AVM) preoperative. not for diagnostics, rather for intervention! Nuclear medicine: SPECT = > PET circulation, metabolism (You should know about MR imaging: What s in focus (H), the medium (magnetic field), and energy (RF). Magnets (stable-, electro-: resistive, superconductive) T1, T2 relaxation, signal localization, flow phenomenon, contrast materials (T1, T2) Artefacts, hazards, contraindications (absolute, relative) future) CNS pathology Cerebrovascular: Parenchyma (infarction) acute neurological deficit: ischemic (80%), hemorrhagic (15%) SAH Hematome: subdural, epidural. Trauma: fracture (impression! CT), hemorrhage, contusion, diff. diagnostics of subdural vs. epidural bleeding. Shaken baby syndrome Tumor: localization: extra-, intraaxial, supra-, infratentorial, (sellar, parasellar) Inflammation: bacterial (meninx, parenchyma), viral, parasite (MRI) 1 / 5

Parenchyma lesion: white matter lesions (demyelinisation) MRI Head trauma patients lesions Primary Extraaxial hemorrhage EDH, SDH, SAH,(IVH) Intraaxial lesions: Cerebral contusion Diffuse axonal damage Deep cerebral and primer brainstem lesion IVH and choroids plexus hemorrhage Secondary Diffuse cerebral oedema Mass effect with cerebral herniation Anoxia or hypoxia Secondary infract with hemorrhage Infection Cerebral infarction: CT Hyperacute infarction (until 12 hours): normal (50-60 %), hyperdense artery Gács sign (25-50 %), the borders of nucleus lentiformis disappear Acute infarction (12-24 h-ig): ganglia bas. hypodense, insular the border of the cortex-medulla disappears, the sulci compress 1-3 day infarction: mass effect, hypodensity (cortex + medulla), possible hemorrhagic transformation (ganglia bas. + cortex) 4-7 day: gyri : enhancement, mass effect, persistent oedema 1-8 weeks: persistent enhancement, mass effect, transient calcification (mainly infant.) Months-years: encephalomalacy (cyst), parenchyma decrease of the volumen, hydrocephalus localis ex vacuo, (calcification possible) Most emphasis ictus /stroke : ischaemic, haemorrhagic (CT,MR) haematoma sub-/epidurale columna vertebralis v.s. myelon (CT, MR) 2 / 5

IMAGES: Os petrosum transv. fractura (laesio n.facialis 50%) (CT): Contusio cerebri (CT): Haematoma subdurale: Haematoma epidurale: 3 / 5

Subacut ISCHAEM. INFARCT chronic Apoplexia cerebri (CT): SAH (CT): Glioblastoma multiforme: Metatases cerebri: 4 / 5

White matter laesion (MR): DSA: MRA: Intraorbital foreign body (3DCT): Hypophysis microadenome (MRI): 5 / 5

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