For Emergency Doctors Dr Suzanne Smallbane November 2011
A: Orbit B: Sphenoid Sinus C: Temporal Lobe D: EAC E: Mastoid air cells F: Cerebellar hemisphere
A: Frontal lobe B: Frontal bone C: Dorsum sellae D: Basilar Artery E: Temporal lobe F: Mastoid Air Cells G: Cerebellar hemisphere
A: Frontal Lobe B Sylvian Fissure C: Temporal Lobe D: Suprasellar cistern E: Midbrain F: 4 th Ventricle G: Cerebellar hemisphere
A: Falx Cerebri B: Frontal Lobe C: Ant Horn Lat ventricle D: 3 rd Ventricle E: Quadrigeminal Plate Cistern F: Cerebellum
A: Ant horn lat ventricle B: Caudate C/E: Internal capsule D: Putamen and GP F: 3 rd Ventricle G: Quadrigeminal Plate Cistern H: Cerebellar vermis I: Occipital Lobe
A:Genu of CC B: Ant horn lat vent C: IC D: Thalamus E: Pineal gland F: Choroid Plexus G: Straight Sinus
A: Falx Cerebri B: Frontal Lobe C: Lat ventricle D: Splenum of CC E: Parietal Lobe F: Occipital Lobe G: SSS
Presence or Absence of haemorrhage Dense Middle Cerebral Artery Dense Basilar Artery Subtle changes of acute ischaemia Obscuration of the lentiform nuclei Loss of the insular ribbon Loss of grey/white distinction Sulcal effacement
At 1-3 days: Wedge shaped low density Haemorrhagic transformation At 4-7 days: Gryal enhancement Mass effect persists At 1-8 weeks: Mass effect resolves Enhancement may persist
70-90% of non-traumatic intracerebral bleeds Usually due to vasculopathy of deep penetrating arteries Most likely to involve: Thalamus Pons Cerebellum Basal Ganglia (putamen and IC) Blood may extend into ventricular system which is associated with a poor prognosis Fluid levels often indicate cause is due to coagulopathy
Trauma Ruptured Cerebral Aneurysm in the absence of trauma Occurs at branch points on Circle of Willis Ant and Post Communicating arteries MCA Bifurcation Basilar Artery Scrutinize the Insular region and Basilar Cistern carefully Complicated by Intraventricular Haemorrhage and Hydrocephalus
Trauma Usually over the cerebral convexity adjacent to the site of injury or cerebral contusion If a large amount of blood is present in the basilar cistern consider a primary SAH with secondary fall and subsequent brain injury
Forms from the tearing of bridging veins Blood collects between the arachnoid and dura mater Crescent shaped Hyperdense when acute (may have hypodense foci secondary to serum, CSF or active bleeding) Does not cross dural reflections Isodense when subacute and Hypodense when chronic
Suspect if there is midline shift without any obvious mass Clues: Compressed lateral ventricle (asymmetry) Effaced Sulci White matter buckling (inward compression) Thick cortical mantle
Located between skull and dura Usually secondary to trauma, # and venous or arterial laceration Biconvex in shape Limited in spread by sutures Usually hyperdense but may have some hypodensity contained within
50% of all primary injuries are DAI Caused by acceleration/deceleration and rotational forces Scan may appear normal May also have illdefined areas of high density haemorrhage in characteristic locations: Subcortical wm Post limb IC CC Dorsolateral brain
Usually occur when brain impacts dural fold or osseous ridge Appear as ill defined hypodense area mixed with acute foci of haemorrhage Often associated with traumatic SAH Common locations: Temporal Lobe (anterior, inferior and sylvian regions) Frontal Lobe (anterior and inferior portions) Dorsolateral midbrain Inferior Cerebellum
Likely Primary Tumors: Lung 48% Breast cancer 15% Genitourinary tract cancers 11% Osteosarcoma 10% Melanoma 9% Head and neck cancer 6% Neuroblastoma 5% Gastrointestinal cancers especially colorectal and pancreatic carcinoma 3% Lymphoma 1%
http://www.neurosurvival.ca/computerassis tedlearning/readingcts/anatomy_guide/alph a.htm