12 b. ct brain

CT BRAIN / MR – An introduction CT BRAIN / MR – An introduction to Normal Anatomy, to Normal Anatomy,

Interpretation and Some Interpretation and Some Common PathologiesCommon Pathologies

Anupama ChandrasekharanAnupama ChandrasekharanAssociate Professor & Consultant RadiologistAssociate Professor & Consultant Radiologist

Dept of Radiology and Imaging SciencesDept of Radiology and Imaging SciencesSri Ramachandra Medical College & Research Sri Ramachandra Medical College & Research

InstituteInstituteChennaiChennai

Indications for CT / MR ……..Indications for CT / MR ……..

StrokeStroke TraumaTrauma Altered sensoriumAltered sensorium Neurological deficitNeurological deficit SeizuresSeizures Headache Headache

How the CT study is usually How the CT study is usually planned…planned…

15-20 degree angulation to canthomeatal line to decrease radiation to the lens.

Plain CT Contrast CT

Indications for a contrast Indications for a contrast CT….CT….

SeizuresSeizures InfectionsInfections Venous thrombosisVenous thrombosis TumorsTumors Atypical stroke findings on plain CTAtypical stroke findings on plain CT Atypical hemorrhage on plain CTAtypical hemorrhage on plain CT Focal edema on plain CTFocal edema on plain CT

Brain Window Bone Window

Descriptive Terms …….Descriptive Terms …….

Hypodense / HypointenseHypodense / Hypointense

Isodense / IsointenseIsodense / Isointense

Hyperdense / HyperintenseHyperdense / Hyperintense

Lesions appearing Lesions appearing Hypodense on Plain CTHypodense on Plain CT

InfarctInfarct (non (non hemorrhagic)hemorrhagic)

EdemaEdema

Lesions appearing Lesions appearing Hyperdense on Plain CTHyperdense on Plain CT

HemorrhageHemorrhage

CalcificationsCalcifications

Normal Intracranial CalcificationsNormal Intracranial Calcifications

NINDS trial

Thrombolysis

CT criteria

No hemorrhage

CT criteria

No hemorrhage

Parenchymal hypodensity

in 1/3 MCA

ECASS

  Purpose of imaging in strokePurpose of imaging in stroke

Definite diagnosis of stroke.Definite diagnosis of stroke. To document the presence or absence To document the presence or absence

of hemorrhageof hemorrhage This information is critical since This information is critical since

anticoagulation is a standard therapy anticoagulation is a standard therapy for ischemic strokefor ischemic stroke

Identify ischemic penumbraIdentify ischemic penumbra Assess location & extent of brain Assess location & extent of brain

damage (e.g. impending herniation)damage (e.g. impending herniation) To exclude stroke mimics.To exclude stroke mimics.

Ischemic Penumbra

Stroke Frequency Based on Aetiology : Stroke Frequency Based on Aetiology : Harvard Stroke SeriesHarvard Stroke Series

Ischaemic Ischaemic (82%)(82%)Atherosclerotic Thrombosis – 22%

Embolism – 30 %

Lacunar – 18 %

Indeterminate

Cerebral Venous

Dissection Haemorrhagic (18%)

Primary Intracerebral Hematoma – 12%

AVM + Aneurysm – 4%

Others: Cavernoma, AVF, bleeding disorders -2 %

Stroke Based on TerritoryStroke Based on Territory

Anterior circulation strokeAnterior circulation strokeEmbolus : 70%

Thrombosis : 30%

Posterior circulation stroke

Thrombosis : 70%

Embolus : 30%

Normal in 50% of ischemic strokes < 6 hrs

2 hrs 24 hrs

CT in Hyperacute Stroke ( 0-6 hrs )CT in Hyperacute Stroke ( 0-6 hrs )

Not v.sensitive for infarctionNot v.sensitive for infarction

Sensitive for a/c hemorrhage & gross Sensitive for a/c hemorrhage & gross lesions precluding thrombolytic lesions precluding thrombolytic therapytherapy

20 % within 2 hrs

82 % within 6 hrs

Neuroradiology.1996

Jan;38(1):31-33

Hyperacute Stroke On CT

EARLY ISCHEMIC CHANGES

Hyperdense vessel sign

Attenuation of lentiform nucleus

Loss of insular ribbon

Effacement of sulci

Loss of corticomedullary differentiation

Significance of Early Ischemic Signs

No contraindication to thrombolysisPatel et al JAMA 2001;286:2830–2838

Indicate more extensive ischemiaAJNR 2004;25:933-938

Hyperdense vessel signObscuration of basal gangliaLoss of grey-white matter interfaceEffacement of sulci

Strong association with later hemorrhagic transformation AJNR 1991;12:1115-1121

Subacute infarct (1-7 days )Subacute infarct (1-7 days )

Hemorrhagic transformation in 5-40 % of Hemorrhagic transformation in 5-40 % of all ischemic strokeall ischemic stroke Neurology 2001; 57:1603-1610

Stroke 1999;30:761-764

Lacunar InfarctsLacunar Infarcts

Diffusion Weighted ImagingDiffusion Weighted Imaging

Radiology 2000;217:331-345

Detects Infarct As Early As 15-30 minutes

AJNR 2003 ;24:878-885

• 46 patients with acute stroke

• CT and DWI within 6 hours

• Mean delay 24.5 min. (R 10–41 min.)

• EIC on CT - 33/46 (Sn 73%)

• DWI 42/45 - (Sn 93%)

CT vs DWI

Hyperacute hemorrhage

2.5 hr 18 hr

GRE T2* WI

MRI as sensitive as CT for acute hemorrhage

More sensitive than CT for chronic hemorrhage(JAMA 2004;292:1823-30)

CT sensitivity for SAHCT sensitivity for SAH

Day of SAH – 98 %Day of SAH – 98 % After Day 1 – 90 %After Day 1 – 90 % After Day 5 – 80 %After Day 5 – 80 % After 1 wk – 50 %After 1 wk – 50 %

Neuroradiology 1982:23:153-156

Acute SAH - 100 %

Chronic SAH – 63 %

Chronic SAH ( CT ) – 46 %

Radiology .1995;196(3):773-777

Radiology.1997;203(1):257-262

Acute hemorrhageAcute hemorrhage MRI – 96% sens. 99% accuracyMRI – 96% sens. 99% accuracy CT - 89% sens. 98% accuracyCT - 89% sens. 98% accuracy

Chronic hemorrhage•MRI – 96% sens. 99% accuracy•CT - 40% sens. 78 accuracy

HEME study

CT AngiographyCT Angiography

Site of occlusionSite of occlusion Length of occluded Length of occluded

segmentsegment Arteries beyond Arteries beyond

occluded segment – occluded segment – collateral flowcollateral flow

Detection & exclusion of Detection & exclusion of large vessel intracranial large vessel intracranial occlusion – sens – occlusion – sens – 98.4% and spec.-98.1%98.4% and spec.-98.1%

JCAT 2001; 25(4):520-8

CT PerfusionCT Perfusion

If no penumbra…..increased risk of bleed with If no penumbra…..increased risk of bleed with thrombolysisthrombolysis

RCNA 44(2006)41-62

MTT rCBVrCBF

DWI ADC

Can MR replace CT as first imaging Can MR replace CT as first imaging modality in hyperacute stroke?modality in hyperacute stroke?

YesYes

MR immediately availableMR immediately available Protocol is optimizedProtocol is optimized Skilled personnelSkilled personnel

Unlikely to replace CT .......

• Cost

• Limited availability

• Time

• Lack of evidence that MR has a positive influence on prognosis

Delta SignDelta Sign

Extradural Extradural haematomahaematoma

Subdural Subdural haematoma haematoma

Subarachnoid Subarachnoid haemorrhagehaemorrhage

IntraventricularIntraventricular haemorrhagehaemorrhage

Cerebral Cerebral contusions contusions

Intracerebral Intracerebral haemorrhagehaemorrhage

Diffuse cerebral Diffuse cerebral edemaedema

EXTRA-AXIAL LESIONS INTRA-AXIAL LESIONS

Imaging in Craniocerebral TraumaImaging in Craniocerebral Trauma

Extradural Extradural HematomaHematoma

Acute Subdural Hematoma

Diffuse Axonal Injury Diffuse Axonal Injury

23 yr old male c/o fever and intense headache23 yr old male c/o fever and intense headache

Ring enhancing lesions – Ring enhancing lesions – granuloma / abscessgranuloma / abscess

CalcificationsCalcifications CerebritisCerebritis Meningeal abnormalities Meningeal abnormalities ComplicationsComplications

Differential Diagnosis of Ring Differential Diagnosis of Ring Enhancing LesionsEnhancing Lesions

GranulomasGranulomas Brain abscessBrain abscess Tumors – metastasis, Tumors – metastasis,

gliomaglioma Resolving hematomaResolving hematoma

EncephalitisEncephalitis

MRI – within 48 hrs MRI – within 48 hrs CT - at least 3-5 daysCT - at least 3-5 days

Widely availableWidely available CostCost QuickQuick HemorrhageHemorrhage TraumaTrauma

Hyperacute infarctsHyperacute infarcts Posterior fossaPosterior fossa Diffuse axonal Diffuse axonal

injuriesinjuries White matter White matter

diseasesdiseases Subtle Subtle

abnormalities of abnormalities of neuroparenchymaneuroparenchyma

Contraindications for MRIContraindications for MRI

Metallic implants Metallic implants PacemakersPacemakers Prosthetic valvesProsthetic valves Aneurysm clipsAneurysm clips ClaustrophobiaClaustrophobia

Thank UThank U

Epidural Abscess Subdural Epidural Abscess Subdural Empyema Empyema

Notice the rim Notice the rim

enhancing epdural enhancing epdural fluid collection fluid collection (arrowheads)(arrowheads)

).

EncephalitisEncephalitis Diffuse nonfocal brain parenchymal Diffuse nonfocal brain parenchymal

inflammatory processinflammatory process Most common agents - virusesMost common agents - viruses Immunocompetent individuals - Herpes Immunocompetent individuals - Herpes

virusesviruses Immunocompromised individualsImmunocompromised individuals

Human immunodeficency virus (HIV)Human immunodeficency virus (HIV) Cytomegalovirus (CMV)Cytomegalovirus (CMV) PapovavirusPapovavirus

Tuberculous meningitisTuberculous meningitis

Cerebellar AtrophyCerebellar AtrophyCerebral Atrophy

ARTERIOVENOUS MALFORMATION

ARTERIOVENOUS MALFORMATION

SUBACUTE SDH

ACUTE ON CHRONIC SDH

CONTUSION SAH

ComplicationsComplications

EARLYEARLY ABSCESSABSCESS SUBDURAL/SUBDURAL/

EPIDURAL EMPYEMAEPIDURAL EMPYEMA VENTRICULITISVENTRICULITIS INFARCTIONINFARCTION VENOUS VENOUS

THROMBOSISTHROMBOSIS

LATELATE SUBDURAL/ EPIDURAL SUBDURAL/ EPIDURAL

EFFUSIONEFFUSION ENCEPHALOMALACIAENCEPHALOMALACIA HYDROCEPHALUSHYDROCEPHALUS ATROPHYATROPHY

SUBDURAL EMPYEMA

EXTRA-AXIAL INTRA-AXIAL

Hypertensive Hemorrhage Hypertensive Hemorrhage Hypertensive hemorrhage accounts for Hypertensive hemorrhage accounts for

approximately 70-90% of non-traumatic primary approximately 70-90% of non-traumatic primary intracerebral hemorrhages. It is commonly due to intracerebral hemorrhages. It is commonly due to vasculopathy involving deep penetrating arteries of vasculopathy involving deep penetrating arteries of the brain. Hypertensive hemorrhage has a the brain. Hypertensive hemorrhage has a predilection for deep structures including the predilection for deep structures including the thalamus, pons, cerebellum, and basal ganglia, thalamus, pons, cerebellum, and basal ganglia, particularly the putamen and external capsule. Thus, particularly the putamen and external capsule. Thus, it often appears as a high-density hemorrhage in the it often appears as a high-density hemorrhage in the region of the basal ganglia. Blood may extend into region of the basal ganglia. Blood may extend into the ventricular system. Intraventricular extension of the ventricular system. Intraventricular extension of the hematoma is associated with a poor prognosis.the hematoma is associated with a poor prognosis.

Haemorrhagic StrokeHaemorrhagic StrokeEtiologyEtiology HypertensionHypertension Vascular malformationVascular malformation AneurysmAneurysm TraumaTrauma Amyloid angiopathyAmyloid angiopathy TumorTumor CoagulopathyCoagulopathy Hemorrhages can occur in the Hemorrhages can occur in the

intraparenchymal, subarachnoid, intraparenchymal, subarachnoid, intraventricular, subdural and extradural spaces.intraventricular, subdural and extradural spaces.

Location of hypertensive hemorrhage: Location of hypertensive hemorrhage: Putamen, external capsule, thalamus, pons, Putamen, external capsule, thalamus, pons, cerebellum, subcortical white mattercerebellum, subcortical white matter

Subarachnoid hemorrhageSubarachnoid hemorrhage In the absence of trauma, the most common cause of In the absence of trauma, the most common cause of

subarachnoid hemorrhage is a ruptured cerebral subarachnoid hemorrhage is a ruptured cerebral aneurysm. Cerebral aneurysms tend to occur at branch aneurysm. Cerebral aneurysms tend to occur at branch points of intracranial vessels and thus are frequently points of intracranial vessels and thus are frequently located around the Circle of Willis. Common aneurysm located around the Circle of Willis. Common aneurysm locations include the anterior and posterior locations include the anterior and posterior communicating arteries, the middle cerebral artery communicating arteries, the middle cerebral artery bifurcation and the tip of the basilar artery. bifurcation and the tip of the basilar artery. Subarachnoid hemorrhage typically presents as the Subarachnoid hemorrhage typically presents as the "worst headache of life" for the patient. Detection of a "worst headache of life" for the patient. Detection of a subarachnoid hemorrhage is crucial because the subarachnoid hemorrhage is crucial because the rehemorrhage rate of ruptured aneurysms is high and rehemorrhage rate of ruptured aneurysms is high and rehemorrhage is often fatal.rehemorrhage is often fatal.

Subarachnoid hemorrhageSubarachnoid hemorrhage CT is currently the imaging modality of choice because of its high CT is currently the imaging modality of choice because of its high

sensitivity for the detection of subarachnoid hemorrhage. CT is sensitivity for the detection of subarachnoid hemorrhage. CT is most sensitive for acute subarachnoid hemorrhage. After a period most sensitive for acute subarachnoid hemorrhage. After a period of days to weeks CT becomes much less sensitive as blood is of days to weeks CT becomes much less sensitive as blood is resorbed from the CSF. If there is a strong clinical indication, LP resorbed from the CSF. If there is a strong clinical indication, LP may be warranted despite a negative CT since small bleeds can may be warranted despite a negative CT since small bleeds can be unapparent on imaging.be unapparent on imaging.On CT, a subarachnoid hemorrhage appears as high density On CT, a subarachnoid hemorrhage appears as high density within sulci and cisterns. The insular regions and basilar cisterns within sulci and cisterns. The insular regions and basilar cisterns should be carefully scrutinized for subtle signs of subarachnoid should be carefully scrutinized for subtle signs of subarachnoid hemorrhage. Subarachnoid hemorrhage may have associated hemorrhage. Subarachnoid hemorrhage may have associated intraventricular hemorrhage and hydrocephalus.intraventricular hemorrhage and hydrocephalus.

MR SpectroscopyMR Spectroscopy

Normal Infarct

  Venous Sinus Thrombosis with Venous Sinus Thrombosis with

Venous InfarctVenous Infarct Clinical symptoms – head ache, seizuresClinical symptoms – head ache, seizures Pathology is due to decrease in perfusion pressure Pathology is due to decrease in perfusion pressure

as the venous pressures elevate due to occlusion. as the venous pressures elevate due to occlusion. Predisposing conditions are dehydration, infection, Predisposing conditions are dehydration, infection,

polycythemia, sickle cell disease, hypercoagulable polycythemia, sickle cell disease, hypercoagulable states, peripartum, OCP poisoning.states, peripartum, OCP poisoning.

Imaging findingsImaging findings Unilateral / bilateral parenchymal hypodensitiesUnilateral / bilateral parenchymal hypodensities Not limited to an arterial territoryNot limited to an arterial territory May be associated with hemorrhageMay be associated with hemorrhage Signs: Delta sign, Enhancement of walls of sinus Signs: Delta sign, Enhancement of walls of sinus

than their contents.than their contents.

MR SpectroscopyMR Spectroscopy Dynamic study depicting Dynamic study depicting

intracellular metabolism of intracellular metabolism of cerebral ischemia.cerebral ischemia.

Within the region of infarct, Within the region of infarct, lactate appears elevated whereas lactate appears elevated whereas NAA and total creatinine are NAA and total creatinine are reduced.reduced.

Radionucleotide studies in acute Radionucleotide studies in acute strokestroke

PET is an accurate method of quantifying PET is an accurate method of quantifying changes in cerebral hemodynamics.changes in cerebral hemodynamics.

As cerebral blood flow (CBF) falls, cerebral As cerebral blood flow (CBF) falls, cerebral blood volume (CBV) and oxygen extraction blood volume (CBV) and oxygen extraction factor (OEF) increase.factor (OEF) increase.

PET measures changes in CBF, CBV and PET measures changes in CBF, CBV and OEF using O15 OEF using O15

Plays a limited role due to limited Plays a limited role due to limited availability .availability .

SPECT with Tc 99m HMPAO or ECD will SPECT with Tc 99m HMPAO or ECD will show a perfusion defect.show a perfusion defect.

RadionucleotideRadionucleotide Studies in Acute Studies in Acute StrokeStroke

SPECT – Tc99m HMPAOSPECT – Tc99m HMPAO PET – O15PET – O15 Adv – Early detectionAdv – Early detection Limitation - Not widely Limitation - Not widely

availableavailable

MRI has been increasingly utilized MRI has been increasingly utilized in early stroke since it is more in early stroke since it is more sensitive than CT in the first sensitive than CT in the first twelve hourstwelve hours

Bright on Diffusion weighted Bright on Diffusion weighted images (detected as early as 15 to images (detected as early as 15 to 30 min after vessel occlusion).30 min after vessel occlusion).

CT / MR Perfusion imagingCT / MR Perfusion imaging Concentrates on the assessment of Concentrates on the assessment of

mean transit time (MTT), relative cerebral mean transit time (MTT), relative cerebral blood volume (RCBV) and derived relative blood volume (RCBV) and derived relative cerebral blood flow. RCBF = MTT / RCBVcerebral blood flow. RCBF = MTT / RCBV

Prolonged MTT is the earliest & most Prolonged MTT is the earliest & most consistent sign of impaired perfusion.consistent sign of impaired perfusion.

In addition to this, there is a simultaneous In addition to this, there is a simultaneous drop in RCBV indicating tissue at risk for drop in RCBV indicating tissue at risk for infarction.infarction.

Stroke in ChildrenStroke in Children Constitutes 3% of cerebral infarcts Constitutes 3% of cerebral infarcts Most common cause is congenital Most common cause is congenital

heart disease. Other causes are heart disease. Other causes are vasospasm & vasculitis, vasospasm & vasculitis,

Echo, CT, MRI & catheter Echo, CT, MRI & catheter angiogram should be performed as angiogram should be performed as and when required.and when required.

There are several There are several advantages to performing a CTadvantages to performing a CT scanscan instead of other imaging modalities. A CT scan: instead of other imaging modalities. A CT scan:- Is readily available- Is readily available- Is rapid- Is rapid- Allows easy exclusion of hemorrhage- Allows easy exclusion of hemorrhage- Allows the assessment of parenchymal damage- Allows the assessment of parenchymal damage

The The disadvantages of CTdisadvantages of CT include the following: include the following:- Old versus new infarcts is not always clear- Old versus new infarcts is not always clear- No functional information (yet)- No functional information (yet)- Relatively limited evaluation of vertebrobasilar - Relatively limited evaluation of vertebrobasilar systemsystem

A CT is 58% sensitive for infarction within the first 24 A CT is 58% sensitive for infarction within the first 24 hours (Bryan et al, 1991). MRI is 82% sensitive. If the hours (Bryan et al, 1991). MRI is 82% sensitive. If the patient is imaged greater than 24 hours after the patient is imaged greater than 24 hours after the event, both CT and MR are greater thanevent, both CT and MR are greater than 90% 90% sensitive.sensitive.

Epidural Hematoma Epidural Hematoma

An epidural hematoma is usually associated with a An epidural hematoma is usually associated with a skull fracture. It often occurs when an impact skull fracture. It often occurs when an impact fractures the calvarium. The fractured bone fractures the calvarium. The fractured bone lacerates a dural artery or a venous sinus. The lacerates a dural artery or a venous sinus. The blood from the ruptured vessel collects between the blood from the ruptured vessel collects between the skull and dura. On CT, the hematoma forms a skull and dura. On CT, the hematoma forms a hyperdense biconvex masshyperdense biconvex mass. It is usually uniformly . It is usually uniformly high density but may contain hypodense foci due to high density but may contain hypodense foci due to active bleeding. Since an epidural hematoma is active bleeding. Since an epidural hematoma is extradural it can cross the dural reflections unlike a extradural it can cross the dural reflections unlike a subdural hematoma. However an epidural subdural hematoma. However an epidural hematoma usually does not cross suture lines hematoma usually does not cross suture lines where the dura tightly adheres to the adjacent skullwhere the dura tightly adheres to the adjacent skull

Cerebral Contusion Cerebral Contusion Cerebral contusions are the most common Cerebral contusions are the most common

primary intra-axial injury. They often occur primary intra-axial injury. They often occur when the brain impacts an osseous ridge when the brain impacts an osseous ridge or a dural fold. The foci of punctate or a dural fold. The foci of punctate hemorrhage or edema are located along hemorrhage or edema are located along gyral crests. The following are common gyral crests. The following are common locations:locations:- Temporal lobe - anterior tip, inferior - Temporal lobe - anterior tip, inferior surface, sylvian regionsurface, sylvian region- Frontal lobe - anterior pole, inferior - Frontal lobe - anterior pole, inferior surfacesurface- Dorsolateral midbrain- Dorsolateral midbrain- Inferior cerebellum- Inferior cerebellum

Cerebral ContusionCerebral Contusion On CT, cerebral On CT, cerebral contusion appears as an contusion appears as an ill-defined hypodense ill-defined hypodense area mixed with foci of area mixed with foci of hemorrhage.hemorrhage. Adjacent Adjacent subarachnoid subarachnoid hemorrhage is common. hemorrhage is common. After 24-48 hours, After 24-48 hours, hemorrhagic hemorrhagic transformation or transformation or coalescence of petechial coalescence of petechial hemorrhages into a hemorrhages into a rounded hematoma is rounded hematoma is common.common.

Diffuse Axonal Injury Diffuse Axonal Injury Diffuse axonal injury is often referred to as "shear injury". It is Diffuse axonal injury is often referred to as "shear injury". It is

the most common cause of significant morbidity in CNS trauma. the most common cause of significant morbidity in CNS trauma. Fifty percent of all primary intra-axial injuries are diffuse axonal Fifty percent of all primary intra-axial injuries are diffuse axonal injuries. Acceleration, deceleration and rotational forces cause injuries. Acceleration, deceleration and rotational forces cause portions of the brain with different densities to move relative to portions of the brain with different densities to move relative to each other resulting in the deformation and tearing of axons. each other resulting in the deformation and tearing of axons. Immediate loss of consciousness is typical of these injuries. Immediate loss of consciousness is typical of these injuries. The The CTCT of a patient with diffuse axonal injury of a patient with diffuse axonal injury may be normalmay be normal despite despite the patient's presentation with a profound neurological deficit.the patient's presentation with a profound neurological deficit. With CT, diffuse axonal injury may appear as ill-defined areas of With CT, diffuse axonal injury may appear as ill-defined areas of high density or hemorrhage in characteristic locations.high density or hemorrhage in characteristic locations. The injury The injury occurs in a sequential pattern of locations based on the severity occurs in a sequential pattern of locations based on the severity of the trauma. The following list of diffuse axonal injury locations of the trauma. The following list of diffuse axonal injury locations is ordered with the most likely location listed first followed by is ordered with the most likely location listed first followed by successively less likely locations:successively less likely locations:- Subcortical white matter - Subcortical white matter - Posterior limb internal capsule- Posterior limb internal capsule- Corpus callosum- Corpus callosum- Dorsolateral midbrain- Dorsolateral midbrain

EncephalitisEncephalitis CT scan is often normal , especially CT scan is often normal , especially early in the disease.early in the disease.

Ill defined hypodense lesions may be Ill defined hypodense lesions may be seen e.g. temporal lobe changes are seen e.g. temporal lobe changes are predominant in Herpes Encephalitis.predominant in Herpes Encephalitis.

MRI is far more sensitive in the MRI is far more sensitive in the evaluation of patients with encephalitisevaluation of patients with encephalitis

Skull FracturesSkull Fractures Skull fractures are categorized as Skull fractures are categorized as linear or linear or

depressed,depressed, depending on whether the fracture depending on whether the fracture fragments are depressed below the surface of fragments are depressed below the surface of the skull. Linear fractures are more common. the skull. Linear fractures are more common. The bone windows must be examined carefully.The bone windows must be examined carefully. A skull fracture is most clinically significant if A skull fracture is most clinically significant if the paranasal sinus or skull base is involved. the paranasal sinus or skull base is involved. Fractures must be distinguished from sutures Fractures must be distinguished from sutures that occur in anatomical locations (sagittal, that occur in anatomical locations (sagittal, coronal, lambdoidal) and venous channels. coronal, lambdoidal) and venous channels. Sutures have undulating margins both sutures Sutures have undulating margins both sutures and venous channels have sclerotic margins. and venous channels have sclerotic margins. Venous channels have undulating sides. Venous channels have undulating sides. Depressed fractures are characterized by Depressed fractures are characterized by inward displacement of fracture fragments.inward displacement of fracture fragments.

Ventriculitis / EpendymitisVentriculitis / Ependymitis

Inflammation and enlargement of the Inflammation and enlargement of the ventricles characterizes ventriculitis. ventricles characterizes ventriculitis. Ependymitis shows hydrocephalus with Ependymitis shows hydrocephalus with damage to the ependymal lining and damage to the ependymal lining and proliferation of subependymal glia. A CT proliferation of subependymal glia. A CT of patients with these conditions reveals of patients with these conditions reveals the presence of periventricular edema the presence of periventricular edema and subependymal enhancement. and subependymal enhancement. Ventriculitis and Ependymitis affect Ventriculitis and Ependymitis affect approximately 30% of the adult patients approximately 30% of the adult patients and 90% of the pediatric patients with and 90% of the pediatric patients with meningitis.meningitis.

Cerebrovascular Complications Cerebrovascular Complications of Meningitisof Meningitis

The development of cerebrovascular The development of cerebrovascular problems is the most common complication problems is the most common complication of meningitis. Arterial infarction can occur of meningitis. Arterial infarction can occur which often affects the basal ganglia due to which often affects the basal ganglia due to the occlusion of small perforating vessels. the occlusion of small perforating vessels. Hemispheric infarction can also occur due Hemispheric infarction can also occur due to major vessel spasm. Venous infarctions to major vessel spasm. Venous infarctions are also common and can include cortical are also common and can include cortical venous occlusion or the involvement of the venous occlusion or the involvement of the superior sagittal sinus.superior sagittal sinus.

Subdural Empyema Subdural Empyema Subdural empyema is usually due to Subdural empyema is usually due to

meningitis, sinusitis, trauma or prior surgery. meningitis, sinusitis, trauma or prior surgery. It is a neurosurgical emergency. Subdural It is a neurosurgical emergency. Subdural empyema leads to rapid clinical deterioration, empyema leads to rapid clinical deterioration, especially if it is due to sinusitis. especially if it is due to sinusitis. On CT it On CT it appears as an isodense or hypodense extra-appears as an isodense or hypodense extra-axial mass. It has a lentiform or crescentic axial mass. It has a lentiform or crescentic shape.shape.The margin of collection often enhances with The margin of collection often enhances with contrast material administrationcontrast material administration due to the due to the presence of granulation tissue or subjacent presence of granulation tissue or subjacent cortical inflammation.cortical inflammation.

Extra-axial CNS Infection Extra-axial CNS Infection

Extra-axial CNS infections can cause epidural Extra-axial CNS infections can cause epidural abscess or subdural empyema. Extra-axial CNS abscess or subdural empyema. Extra-axial CNS infections account for 20-30% of CNS infections account for 20-30% of CNS infections. Fifty percent of extra-axial infections infections. Fifty percent of extra-axial infections are associated with sinusitis, usually frontal are associated with sinusitis, usually frontal sinusitis. The infection occurs by direct sinusitis. The infection occurs by direct extension or septic thrombophlebitis. Thirty extension or septic thrombophlebitis. Thirty percent of extra-axial infections occur post-percent of extra-axial infections occur post-craniotomy. Finally, 10-15% of extra-axial CNS craniotomy. Finally, 10-15% of extra-axial CNS infections are related to meningitis. infections are related to meningitis. CT findings CT findings include a focal fluid collection usually with an include a focal fluid collection usually with an enhancing margin in a subdural or epidural enhancing margin in a subdural or epidural location.location.

PathophysiologyPathophysiology

Flow abnormalities - Perfusion

Cellular dysfunction – DWI / CT/ MR

Structural breakdown – CT / MRI

Ischemic StrokeIschemic Stroke

Occurs due to obstruction of cerebral arteries or Occurs due to obstruction of cerebral arteries or cerebral veins. cerebral veins.

The clinical spectrum of ischemia includesThe clinical spectrum of ischemia includes TIA (Transient ischemic attacks) TIA (Transient ischemic attacks) RIND (Reversible ischemic neurological deficit)RIND (Reversible ischemic neurological deficit) PRIND (partially reversible ischemic PRIND (partially reversible ischemic

neurological neurological deficit)deficit)

Evolved strokeEvolved stroke

Pathophysiology:Pathophysiology: Normal cerebral blood flow to the brain cortex is Normal cerebral blood flow to the brain cortex is

approximately 50 to 66 ml/100gm/min. When cerebral approximately 50 to 66 ml/100gm/min. When cerebral perfusion pressure falls below critical levels perfusion pressure falls below critical levels (<15ml/gm/min) ischemia results. Ischemia produces (<15ml/gm/min) ischemia results. Ischemia produces energy depletion in the affected cells. This results in energy depletion in the affected cells. This results in accumulation of Ca++, Na+ and Cl-, along with accumulation of Ca++, Na+ and Cl-, along with osmotically obligated water. This secondary osmotically obligated water. This secondary accumulation of water results in the imaging features of accumulation of water results in the imaging features of stroke such as edema and mass effect.stroke such as edema and mass effect.

Hyperdense vessel signHyperdense vessel sign

Seen in 25% of stroke patients.Seen in 25% of stroke patients. In patients presenting with clinical deficit In patients presenting with clinical deficit

referable to the middle cerebral artery referable to the middle cerebral artery territory, the hyperdense vessel sign is territory, the hyperdense vessel sign is present 35-50% of the time.present 35-50% of the time.

This signThis sign

Lentiform Nucleus ObscurationLentiform Nucleus Obscuration

Due to cytotoxic edema in the basal Due to cytotoxic edema in the basal gangliaganglia

Indicates proximal middle cerebral Indicates proximal middle cerebral artery occlusion, which results in artery occlusion, which results in limited flow to lenticulostriate arterieslimited flow to lenticulostriate arteries

Can be seen as early as one hour post Can be seen as early as one hour post onset of stroke.onset of stroke.

Insular Ribbon SignInsular Ribbon Sign Loss of the gray-white interface at the Loss of the gray-white interface at the

lateral margins of the insula. lateral margins of the insula. Supplied by the insular segment of the Supplied by the insular segment of the

middle cerebral artery middle cerebral artery Particularly susceptible to ischemia Particularly susceptible to ischemia

because it is the most distal region from because it is the most distal region from either anterior or posterior collateralseither anterior or posterior collaterals

May involve only the anterior or the May involve only the anterior or the posterior insulaposterior insula

Diffuse Hypodensity and Sulcal Diffuse Hypodensity and Sulcal EffacementEffacement

Most consistent sign of infarction. Most consistent sign of infarction. Extensive parenchymal hypodensity is Extensive parenchymal hypodensity is

associated with poor outcome.associated with poor outcome. If > 50% of MCA territory If > 50% of MCA territory

involvement ,there is, on average, an 85% involvement ,there is, on average, an 85% mortality rate. Hypodensity in greater than mortality rate. Hypodensity in greater than one-third of the middle cerebral artery one-third of the middle cerebral artery territory is generally considered to be a territory is generally considered to be a contra-indication to thrombolytic therapy.contra-indication to thrombolytic therapy.

Newer Imaging Techniques In Acute Newer Imaging Techniques In Acute StrokeStroke

MR Diffusion imaging: MR Diffusion imaging: CT / MR Perfusion imagingCT / MR Perfusion imaging Combined MR perfusion & Diffusion Combined MR perfusion & Diffusion

imagingimaging MR SpectroscopyMR Spectroscopy Radionucleotide studiesRadionucleotide studies

Ventriculitis / Ventriculitis / Ependymitis Ependymitis

Cerebral Blood flow for Cerebral Blood flow for SurvivalSurvival

Average blood flow Average blood flow :: 55ml/ 100gm/ mt55ml/ 100gm/ mt

Ischemic threshold Ischemic threshold :: 20 ml/ 100gm/ mt20 ml/ 100gm/ mt

Tissue deathTissue death : : <10 ml/ 100gm/ mt <10 ml/ 100gm/ mt

Functional failure without cell death: Functional failure without cell death: 10-20ml/ 100gm/ mt.10-20ml/ 100gm/ mt.

Concept of Ischemic PenumbraIschemic Insult

Focal core area of infarct (irreversible)

Surrounded by viable neuronal cell on

the brink of cell death

“Ischemic Penumbra”

Geographic area of tissue surrounding a profoundly ischemic core. Identified on DWI / per MRI

Saving this potential salvageable area leads to significant chance of improvement

Ischemic strokeIschemic stroke

Thrombotic strokeThrombotic stroke Embolic strokeEmbolic stroke Lacunar infarctLacunar infarct Global cerebral hypoperfusionGlobal cerebral hypoperfusion

• Ischemic Stroke (83-85%)

• Hemorrhagic Stroke (15-17%)

MRI in Hyperacute StrokeMRI in Hyperacute Stroke DWI – Infarct coreDWI – Infarct core FLAIR - SAH , Parenchymal changesFLAIR - SAH , Parenchymal changes T2* GRE – Intracranial hemorrhageT2* GRE – Intracranial hemorrhage PWI – Perfusion deficitPWI – Perfusion deficit MRA – Vessel occlusionMRA – Vessel occlusion

Diffusion Weighted ImagingDiffusion Weighted Imaging Sensitivity : 88 – 100 %Sensitivity : 88 – 100 % Specificity : 95 – 100 %Specificity : 95 – 100 % Initial diffusion lesion volume Initial diffusion lesion volume

correlates well with final infarct correlates well with final infarct volume & neurologic and volume & neurologic and functional outcomefunctional outcome

Multiple a/c lesions in diff.vasc Multiple a/c lesions in diff.vasc territories in pts. with 1 territories in pts. with 1 symptomatic insult …. embolicsymptomatic insult …. embolic

Neurology.1999 Jun 10;52(9):1784-

1792

Ann Neurol.1997 Aug;42(2):164-170

False Negative DWI

Brainstem infarct

Deep GM nucleus infarct

Neuroradiology2000;42:444–447 Stroke2000;31:1965–1972 AJNR 1999;20:1871–1875

Neurology 1999;52:1784-52

4 h 24 h

Dept. Neurosciences Univ. of Rome La SapienzaDept. Neurosciences Univ. of Rome La Sapienza

Reversibility of Ischemic lesions on DWI

Occlusion of MCA 1 hour - DWI lesion or resolution

Occlusion of MCA 2 hour - Lesion size same or

Radiology 2000;217:331-345

Successful thrombolysis may revert DWI changes

Diffusion changes in TIAs

• 29% to 67% will show restricted diffusion

• May reverse or persist

• Perfusion deficits

Stroke vs TIADWI lesions of TIA are less intense

Stroke 2004;35:1095

AJNR 2004;25:1645-52

Hyperacute Hemorrhage

Wiesmann M, et al. Eur Radiol. 2001;11:849-53.

Stroke 2004;35:502-506

Nederkoorn PJ et al. Stroke 2003;34:1324-32

MR Spectroscopy in acute stroke Stroke 2003;34:e82-876 pts within 7 hrs of stroke onset

Lactate alone – metabolic injury - Reversible

Lactate + NAA- more severe – Irreversible

Lac/Cho ratio from acute lesions improves the prediction of stroke outcome

Neurology 2000;55:498

CT VenographyCT Venography

25 yr old lady c/o fever and altered sensorium 25 yr old lady c/o fever and altered sensorium x 1 wk. Had 1 episode of GTC seizures. x 1 wk. Had 1 episode of GTC seizures. Admitted elsewhere , LP done showed Admitted elsewhere , LP done showed

proteins-55 mg % and sugar –105 mg % ..proteins-55 mg % and sugar –105 mg % ..ABG- pH – 7.55ABG- pH – 7.55

HCO3 – 28.3 , PCO2-32.9, PO2 –322.9,SPO2-HCO3 – 28.3 , PCO2-32.9, PO2 –322.9,SPO2-99.899.8

CT – Normal CT – Normal Discharged at request.Discharged at request.

H/o fever,headache and vomitting on and off H/o fever,headache and vomitting on and off x 5 mths -x 5 mths -

O/E – GCS – E1V1M5O/E – GCS – E1V1M5BP – 140/100 , PR – 116BP – 140/100 , PR – 116Pupils – 4mm dilated , sluggish light Pupils – 4mm dilated , sluggish light reactionreactionNeck Rigidity +Neck Rigidity +Kernig’s & Brudeski’s - veKernig’s & Brudeski’s - ve Hb-13.5 Hb-13.5 TC- 12,200TC- 12,200 Platelets-4.2Platelets-4.2 MP/MF – negativeMP/MF – negative BUN, creatinine – normalBUN, creatinine – normal Urine R/E – proteins +++, pus cells 5-8Urine R/E – proteins +++, pus cells 5-8 Coagulation Profile - WNLCoagulation Profile - WNL 134/3.4/26/102134/3.4/26/102

QQ qqqq

HIV EncephalopathyHIV Encephalopathy

Thank YouThank You

Hyperdense artery

•SPECIFICTY 100%

•SENSITIVITY 10% TO 50%

Seen as early as 90 minutes AJNR 1996; 17:79-85

Hyperdense MCA / Vessel SignHyperdense MCA / Vessel Sign

Persistent large vessel occlusion Persistent large vessel occlusion Large clot burdenLarge clot burden Not a contraindication for i.v. Not a contraindication for i.v.

thrombolysisthrombolysis Neurology 2001:57:1603-1610

Infarct Infarct VS VS

TumorTumor

CT Findings in StrokeCT Findings in Stroke

Hyperacute infarct (<12 hrs)Hyperacute infarct (<12 hrs) Normal (50 to 60%)Normal (50 to 60%) Hyperdense MCAHyperdense MCA Obscuration of lentiform nucleusObscuration of lentiform nucleus

Acute infarct (12 – 24hrs)Acute infarct (12 – 24hrs) Loss of grey - white matter interface Loss of grey - white matter interface

(insular ribbon sign)(insular ribbon sign) Low density basal gangliaLow density basal ganglia Sulcal effacement.Sulcal effacement.

Hyperdense vessel signHyperdense vessel sign

• Indicates poor outcome and poor response to iv - TPA therapy.

CT Findings in Stroke (CT Findings in Stroke (ContdContd))……

Subacute infarct (1- 7days)Subacute infarct (1- 7days) Mass effectMass effect Wedge shaped hypodensity involving Wedge shaped hypodensity involving

grey & white mattergrey & white matter Hemorrhagic transformation.Hemorrhagic transformation. Gyral enhancement.Gyral enhancement.

Chronic infarct ( 1 to 8 weeks)Chronic infarct ( 1 to 8 weeks) Encephalomalacic changesEncephalomalacic changes Reduced mass effectReduced mass effect

Global Cerebral HypoperfusionGlobal Cerebral Hypoperfusion

Consequence of global hypoperfusion.Consequence of global hypoperfusion. Common causes are hypotension, cardiac Common causes are hypotension, cardiac

arrest with successful resuscitation, neonatal arrest with successful resuscitation, neonatal asphyxia and CO inhalation.asphyxia and CO inhalation.

Imaging patternsImaging patterns 1)1)            Water shed infarct in the parieto-Water shed infarct in the parieto-

occipital region & basal ganglia infarcts.occipital region & basal ganglia infarcts. 2)2)            Cortical laminar necrosis with Cortical laminar necrosis with

hemorrhagic foci in basal ganglia & cerebral hemorrhagic foci in basal ganglia & cerebral cortical gyri.cortical gyri.

3)3)            In severe cases “reversal sign” is noted. In severe cases “reversal sign” is noted.

Reversal signReversal sign

Infarct With Hemorrhagic Infarct With Hemorrhagic TransformationTransformation

CT CT VSVS MRI in the setting of acute MRI in the setting of acute strokestroke

MRI is more sensitiveMRI is more sensitive Diffusion weighted MR images has the Diffusion weighted MR images has the

highest sensitivity & specificity for acute highest sensitivity & specificity for acute cerebral infarction.cerebral infarction.

CT is more sensitive to detect hemorrhage.CT is more sensitive to detect hemorrhage. CT is more widely available in many CT is more widely available in many

institutions.institutions. CT is less expensiveCT is less expensive CT is more rapidCT is more rapid  

CT AngiographyCT Angiography

Useful in MCA embolic stroke & Useful in MCA embolic stroke & predictive of infarction volume in MCA predictive of infarction volume in MCA territoryterritory

Less useful –deep grey matter & Less useful –deep grey matter & brainstem brainstem

strokestroke(Taipei)1999:62:255-260

Subacute SAHSubacute SAH FLAIR + (GRE) T2*-weighted superior FLAIR + (GRE) T2*-weighted superior

to either aloneto either alone

J Neurol Neurosurg Psychiatry.200170(2):205-211

Hypertensive HemorrhageHypertensive Hemorrhage

Subarachnoid hemorrhageSubarachnoid hemorrhage

Combined MR Perfusion & Combined MR Perfusion & Diffusion ImagingDiffusion Imaging

In hyperacute stage, larger In hyperacute stage, larger abnormality is noted on the perfusion abnormality is noted on the perfusion images than on diffusion weighted images than on diffusion weighted images. This diffusion perfusion images. This diffusion perfusion mismatch is the ischemic penumbra. mismatch is the ischemic penumbra. This is the tissue at risk which would This is the tissue at risk which would benefit from thrombolysis.benefit from thrombolysis.

Stroke Protocol

Normal Infarct Haemorrhage

Diffusion / Perfusion

CT Perfusion Intraparenchymal SAH

HT Atypical site Angiogr

Angiogram

Mismatch Matches

Angiogr

Thrombolysis

To Summarize the Role of CT To Summarize the Role of CT in Strokein Stroke

Haemorrhagic or non-haemorrhagicHaemorrhagic or non-haemorrhagic Arterial or venousArterial or venous Territory involvedTerritory involved Acute,subacute or chronicAcute,subacute or chronic Assess the mass effectAssess the mass effect Exclude Stroke mimics like subdural Exclude Stroke mimics like subdural

hematoma, tumorshematoma, tumors

How the CT study is usually planned…How the CT study is usually planned…

Thinner Thinner sections are sections are studied studied through the through the posterior posterior fossafossa

Hounsfield UnitsHounsfield Units

AIRAIR -- - 1000- 1000

FATFAT -- - 30 to -100- 30 to -100

CSFCSF -- 0 0

GREY MATTERGREY MATTER -- 32 - 41 32 - 41

WHITE MATTERWHITE MATTER -- 23 - 34 23 - 34

ACUTE BLOODACUTE BLOOD -- 56 - 76 56 - 76

CALCIFICATION - 60 - 400CALCIFICATION - 60 - 400

BONEBONE - - 1000 1000