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Neuroradiology Teaching Files

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1 Neuroradiology Teaching Files
Department of radiology Faculty of Medicine Chiang Mai University

2 Case 1 20-year-old woman with motorcycle accident

3 Findings: 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 patient The 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.

4 Frontal EDH EDH 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.

5 Extra-axial collections

6 Case 2 25-year-old man with motorcycle accident

7 Findings: 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.

8 Brain herniation 1.Subfalcine herniation 2.Transtentorial herniation - Descending (Uncal herniation) - Ascending 3. Tonsillar herniation 4. External herniation Brain herniation causes compression of brain, brain stem, nerves, and blood vessels againts the rigid bony and dural margins

9 First CT: Left SDH with left- to-right subfalcine and left descending transtentorial herniation FU CT 4 days later: left PCA infarction secondary to ipsilateral descending transtentorial herniation.

10 Each 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 SDH CT of a head-injured patient whose clinical was not improved after craniotomy to remove the left EDH.

11 Case 3 A young man with motorcycle accident

12 Findings: axial NECT shows multifocal, droplet-shaped, very low density foci of air within the basal cisterns and right cerebellar fissures (subarachnoid space) Diagnosis: Traumatic Pneumocephalus Discussion: 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.

13 MR Cisternography shows CSF Fistula (arrow) in 2 cases with posttraumatic CSF rhinorrhea

14 Case 4 63-year-old patient with hypertension and left hemiparesis

15 Findings: 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.

16 Hypertensive hemorrhage
Criteria for Dx of hypertensive hemorrhage: 1. HT 2. Age > 45 y 3. Common location: BG(60%), thalamus, pons, cerebellum Basal ganglia Thalamus Pons

17 Case 5 A patient with sudden onset of headache and alteration of consciousness

18 Findings: 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.

19 Clinically suspected SAH
Investigation guideline for patient with suspected rupture intracranial aneurysm Clinically suspected SAH Plain CT brain (-) (+) CTA and/or DSA or MRA (+) (+) LP Treatment (-) (+) Repeat DSA 2 weeks

20 SAH (Ruptured ACoA Aneurysm)
NECT DSA Focal 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.

21 CTA:sagittal MPR DSA: 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 VR DSA: frontal view Aneurysm 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.

22 A man presented with right hemiparesis 6 hours PTA
Case 6 A man presented with right hemiparesis 6 hours PTA

23 Findings: 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 infarction Discussion: 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).

24 Early sign of MCA Infarct
Hyperdense MCA sign Insular ribbon sign and obscuration of the lentiform nucleus

25 Etiology of stroke 80-85% Ischemic infarct :
Focal: large arterial infarction Cardioembolic Small vessel occlusion (lacunar infarction) global hypoxia (respiratory arrest) watershed infarction (systemic hypotension, stenosis or occlusion of large artery in the neck) Venous infarction 15-20% Hemorrhage (ICH, SAH )

26 Threshold of ischemia CBF 50-60 ml/100 gm/min normal
” Neurological dysfunction < ” infarction Ischemic penumbra In the complete absence of cerebral blood flow, the available energy can maintain neuronal viability for approximately 2-3 minutes.

27 CBF in ml/g/min Regions of decreased CBF can be quantified to three zones: central core with irreversible damage salvageable penumbra (tissue at risk) oligemic penumbra (low flow without risk of cell death)

28 Early detection of ischemia 3 hrs
Stroke onset Early detection of ischemia 3 hrs Thrombolytic Rx (iv rtPA) Recombinant tissue plasminogen activator (rt PA). Salvage ischemic brain risk of hemorrhage (5.2%)

29 Goals 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 thrombus Perfusion: Assess CBV, CBF, MTT(TTP) Penumbra: Assess tissue at risk of dying if ischemia continues without recanalization of intravascular thrombus Ref: Rowley. AJNR 2001;22: ประเมิน

30 Acute stroke imaging “4P”
Parenchyma: NECT: to exclude hemorrhage, other lesions large area of infarct(>1/3 of MCA territory) DWI: detect hyperacute infarction Pipes: CTA, MRA Perfusion: CTP, MR-PWI Penumbra: Perfusion CT (CBV/CBF mismatch) Perfusion MR (Diffusion/perfusion mismatch)

31 Patients with ischemic stroke who could be treated with rtPA
Onset of symptoms < 3 hours before Rx No head trauma or prior stroke in previous 3 months No myocardial infarction in previous 3 months No GI or urinary tract hemorrhage in previous 21 days No major surgery in the previous 14 days No history of previous intracranial hemorrhage BP: systolic <185, diastolic < 110 No seizure with postictal residual neurological impairment…. Ref: AHA/ASA Scientific statement.

32 Acute stroke imaging protocol

33 Plain CT brain within 3 hours
Stroke fast track Plain CT brain within 3 hours Indication for thrombolytic Rx (IV rt-PA) Normal CT or early sign infarction Contraindication to thrombolytic Rx: hemorrhage large 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.

34 Acute MCA infarction 78 –year-old woman with sudden left hemiparesis 1 day PTA NECT shows a hypodense area of large infarction involving the right middle cerebral artery vascular territory.

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