3Findings: axial NECT shows biconvex hyperdense extraaxial mass at left temporal convexity with non-displaced linear fracture of the overlying temporal bone. The left temporal lobe is displaced medially with effacement of the ipsilateral suparsellar cistern. The midbrain is shifted away from the herniating temporal lobe.Diagnosis: Skull fracture with left temporal epidural hematoma (EDH) and left descending transtentorial herniation.Discussion:Acute hematoma is high density or high attenuation on CT. Overlying skull fractures can often be visualized on bone windows.Classic finding of EDH: well-defined biconvex or lentiform-shaped hyperdense extraaxial mass.Associated fracture in 85-95% (with lacerated meningeal artery or dural sinus)95% supratentorial (most common in the temporal parietal region)Classic lucid interval develops in 50% of patientThe classic EDH has been associated with a brief initial period of unconsciousness followed by a lucid interval during which the patient’s neurological status is normal. Subsequently, as EDH increases in size, rapid deterioration of consciousness occurs.
4Frontal EDHEDH exists in the potential space between the dura and the inner table of the skull. EDH can cross the midline but cannot cross cranial sutures where the dura is more firmly attached.
7Findings: axial NECT shows crescentic mixed hyper/hypodense extraaxial mass at the left frontoparietal convexity. The left cerebral gray-white matter interface is displaced medially. The lateral ventricles are shifted to the right with mild dilatation of the right lateral ventricle secondary to foramen of Monro obstruction.Diagnosis: Left frontoparietal subdural hematoma (SDH) and subfalcine herniation.Discussion:SDH exists between the dura and arachnoid due to stretching and tearing of bridging cortical veins. SDH can cross sutures but cannot cross dural attachment.Low density areas within the SDH could represent fresh unclotted blood, serum extruded from the clot, or CSF from arachnoid tear.A definite history of trauma may be lacking, particularly in elderly patients.
8Brain herniation1.Subfalcine herniation2.Transtentorial herniation- Descending (Uncal herniation)- Ascending3. Tonsillar herniation4. External herniationBrain herniation causes compression of brain, brain stem, nerves, and blood vessels againts the rigid bony and dural margins
9First CT:Left SDH with left- to-right subfalcine and left descending transtentorial herniationFU CT 4 days later: left PCA infarction secondary to ipsilateral descending transtentorial herniation.
10Each examination demonstrates the brain at the time of the study Each examination demonstrates the brain at the time of the study. No any imaging modality can substitute good clinical history and physical examination.Isodense acute EDH Post-op delayed SDHCT of a head-injured patient whose clinical was not improved after craniotomy to remove the left EDH.
12Findings: axial NECT shows multifocal, droplet-shaped, very low density foci of air within the basal cisterns and right cerebellar fissures (subarachnoid space)Diagnosis: Traumatic PneumocephalusDiscussion:skull base fracture with dural tear and direct communication with air-containing paranasal sinus or mastoid air cells may cause pneumocephalus.Pneumocephalus can occur in epidural, subdural, subarachnoid space, ventricles or brain parenchyma.Most cases of pneumocephalus resolve spontaneously within days.CSF fistulae may occur in the patients presenting with headache, rhinorrhea and recurrent meningitis. High resolution coronal CT, CT cisternography, Isotope tracers and MR cisternography have been used to localize the fistula site.
13MR Cisternography shows CSF Fistula (arrow) in 2 cases with posttraumatic CSF rhinorrhea
14Case 463-year-old patient with hypertension and left hemiparesis
15Findings: axial NECT shows a hyperdense mass at right thalamus and deep white matter with extension into the right lateral ventricle.Diagnosis: Acute hypertensive intraparenchymal hemorrhage with accompanying intraventricular hemorrhage (IVH).Discussion:Hypertension is the most common cause of nontraumatic intraparenchymal hemorrhage in elderly patients. They commonly occur in the basal ganglia, thalamus, and pons.Hemorrhage into the posterior fossa with mass effect or extension into the ventricular system is associated with poor prognosis.Vascular malformations (AVM, cavernous angioma) are more common causes of hemorrhage in the younger patients.Hemorrhagic brain tumors are more complex, heterogenous with associated edema. They usually has nonhemorrhagic areas that enhance after contrast administration.Other causes of nontraumatic intraparenchymal hemorrhage include amyloid angiopathy, hemorrhagic transformation of infarction, coagulopathy, venous infarction etc.
16Hypertensive hemorrhage Criteria for Dx of hypertensive hemorrhage:1. HT2. Age > 45 y3. Common location: BG(60%), thalamus, pons, cerebellumBasal ganglia Thalamus Pons
17Case 5A patient with sudden onset of headache and alteration of consciousness
18Findings: axial NECT shows diffuse high attenuation or high density within the basal cisterns, Sylvain fissures and cortical sulci. Small focal hyperdense hematoma is seen at the left inferior frontal lobe. Small amount of hyperdense IVH is also present in occipital horns with dilatation of temporal horns from hydrocephalus.Diagnosis: Diffuse subarachnoid hemorrhage (SAH) with small intraparenchymal hematoma, small amount of IVH and hydrocephalus.Discussion:SAH exists in CSF space between the arachnoid and pia. SAH extends into the cisterns and sulci, while SDH does not extend into the sulci.The most common cause of nontraumatic SAH is rupture of intracranial aneurysm. Focal SAH or ICH are helpful in localizing the bleeding source.90 % of SAH is cleared from the CSF within 1 week. It is difficult to detect SAH on CT if it is a low hematocrit and a delay in scanning. A lumbar puncture revealing red blood cells or xanthochromia may confirm a suspected SAH.
20SAH (Ruptured ACoA Aneurysm) NECT DSAFocal SAH or ICH are helpful in localizing the bleeding source as in this case, localized SAH in the anterior interhemispheric fissure due to rupture ACoA aneurysm.
21CTA:sagittal MPRDSA: lateral view(A) MPR image in view and(B) 3D color VR image in superior view show a medium- sized saccular aneurysm (arrow) at the right MCA bifurcation with fundus pointing superolaterally.(C, D) Right internal carotid DSA in lateral projection (C) and frontal projection (D) show the same aneurysm (arrows).CTA:3D color VRDSA: frontal viewAneurysm at the right MCA bifurcation in a 46-year-old woman with sudden headache and previous CT showed SAH at the suprasellar cistern and the right sylvian fissure.
22A man presented with right hemiparesis 6 hours PTA Case 6A man presented with right hemiparesis 6 hours PTA
23Findings: axial NECT shows a linear hyperdensity within the left MCA and hypodensity with loss of G-W differentiation of the left insular cortex and left basal ganglia.Diagnosis: hyperacute left MCA infarctionDiscussion:The CT findings in acute cerebral infarction evolve with time.CT scans can detect early signs of MCA infarction within 6 hours in up to 82% of patients.Early signs of MCA infarction include a hyperdense acute intraluminal thrombus in the MCA (hyperdense MCA sign), obscuration of the lentiform nucleus, and loss of gray-white interface of the insular cortex (insular ribbon sign).
24Early sign of MCA Infarct Hyperdense MCA signInsular ribbon sign andobscuration of the lentiform nucleus
25Etiology of stroke 80-85% Ischemic infarct : Focal: large arterial infarctionCardioembolicSmall vessel occlusion (lacunar infarction)global hypoxia (respiratory arrest)watershed infarction (systemic hypotension, stenosis or occlusion of large artery in the neck)Venous infarction15-20% Hemorrhage (ICH, SAH )
26Threshold of ischemia CBF 50-60 ml/100 gm/min normal ” Neurologicaldysfunction< ” infarctionIschemic penumbraIn the complete absence of cerebral blood flow, the available energy can maintain neuronal viability for approximately 2-3 minutes.
27CBF in ml/g/minRegions of decreased CBF can be quantified to three zones:central core with irreversible damagesalvageable penumbra (tissue at risk)oligemic penumbra (low flow without risk of cell death)
28Early detection of ischemia 3 hrs Stroke onsetEarly detection of ischemia3 hrsThrombolytic Rx (iv rtPA)Recombinant tissue plasminogen activator (rt PA).Salvage ischemic brainrisk of hemorrhage(5.2%)
29Goals of acute stroke imaging “4P” Parenchyma: Assess early signs of acute stroke,R/O hemorrhage or other lesions (tumor, infection)Pipes: Assess extra- and intra-cranial circulation for evidence of intravascular thrombusPerfusion: Assess CBV, CBF, MTT(TTP)Penumbra: Assess tissue at risk of dying if ischemia continues without recanalization of intravascular thrombusRef: Rowley. AJNR 2001;22:ประเมิน
30Acute stroke imaging “4P” Parenchyma:NECT: to exclude hemorrhage, other lesionslarge area of infarct(>1/3 of MCA territory)DWI: detect hyperacute infarctionPipes: CTA, MRAPerfusion: CTP, MR-PWIPenumbra: Perfusion CT (CBV/CBF mismatch)Perfusion MR (Diffusion/perfusion mismatch)
31Patients with ischemic stroke who could be treated with rtPA Onset of symptoms < 3 hours before RxNo head trauma or prior stroke in previous 3 monthsNo myocardial infarction in previous 3 monthsNo GI or urinary tract hemorrhage in previous 21 daysNo major surgery in the previous 14 daysNo history of previous intracranial hemorrhageBP: systolic <185, diastolic < 110No seizure with postictal residual neurological impairment….Ref: AHA/ASA Scientific statement.
33Plain CT brain within 3 hours Stroke fast trackPlain CT brain within 3 hoursIndication for thrombolytic Rx (IV rt-PA)Normal CT or early sign infarctionContraindication to thrombolytic Rx:hemorrhagelarge area of infarct (>1/3 of MCA territory)คนไข้ต้องมาถึงรพภายในเวลา 2-2 ½ ชั่วโมงหลังมีอาการ การไม่ทำ perfusion study Tissue change in CT and MRI require hours to fully develop and it is more difficult to clinically differentiate those neurological deficits due to ischemia that they are likely to improve or reverse spontaneously from those that are likely to persist or worsen, and this is a significant value of perfusion imaging.
34Acute MCA infarction78 –year-old woman with sudden left hemiparesis 1 day PTANECT shows a hypodense area of large infarction involving the right middle cerebral artery vascular territory.