imaging of infection of brain and its linings

MODERATOR: DR R.K. GOGOI

Presenter Dr CHARUSMITA CHAUDHARY

infection of brain and its linings 2

There has been a significant decrease in the morbidity and mortality of patients with intracranial infections with the advent of computed tomography (CT) scanning and magnetic resonance imaging (MRI

Recent advances in technology positron emission tomography (PET) single photon emission computed tomography (SPECT) diffusion imaging proton magnetic resonance spectroscopy (MRS). additional imaging modalities to use in the evaluation

of intracranial infection

Source

Risk factors : diabetes mellitus alcoholism malignancy agammaglobulinemia radiation therapy and

chemotherapy steroids HIV

3

Hematogenous spread direct extension

infection of brain and its linings

Forms of Intracranial infections

Cerebritis AbscessEmpyemaGranuloma EncephalitisMeningitisOsteomyelitis

4infection of brain and its linings

Forms of Intracranial infections CEREBRITIS: focal usually pyogenic without capsule or pus formation

ABSCESS: pyogenic encapsulated pus containing cavity

EMPYMA: an abscess forms in an enclosed or potential space epidural or subdural

GRANULOMA: : a focal, more or less encapsulated, inflammatory lesion

usually chronic, without pus formation


Forms of Intracranial infections continue…..Encephalitis:

direct infection of the brain, usually viral and often diffuse Meningitis:

infection of the meninges, may be suppurative or granulomatous


MENINGITIS


LeptomeningitisThe pachymeninges make up the dura

mater, which consists of the periosteum and a meningeal layer.

The leptomeninges consist of the pia and arachnoid


Leptomeningitis inflammation of the leptomeninges and the adjacent

subarachnoid space Characteristic pathogens

Bacterial meningitis or purulent meningitis Non-bacterial meningitis often referred to as aseptic

meningitisCan be divided into acute pyogenic (bacterial),lymphocytic (viral), and

chronic (TB) meningitisThe diagnosis is usually made clinically.

The role of neuroimaging is to exclude complications of meningitis (e.g., abscess, ventriculitis, empyema)


Causative organism


Aseptic MeningitisAll non-bacterial causes of meningitisTypically less ill appearing than bacterial

meningitisMost common cause is viral

HSV type II

Enterovirus (coxsackie, echovirus) Affects all ages Generally self-limited illness

Aseptic Meningitis Other Viral

HIV Lymphocytic

choriomeningitis virus Arbovirus Mumps CMV EBV VZV Adenovirus Measles Rubella Rotavirus Influenza and

parainfluenza

Other infectious Borrelia burgdorferi Mycobacterium tuberculosis Treponema pallidum Mycoplasma pneumoniae Rickettsia, erlichia, brucella

Chlamydia Fungal

Cryptococcus Coccidiodes Histoplasmosis

Parasitic Angiostrongylus

Toxoplamosis Medication

NSAID’s Bactrim Pyridium

Malignancy Lymphoma and leukemia Metastatic carcinoma

Autoimmune Sarcoid Behcet’s SLE

Pathogens- Special Situations

VP shunts/penetrating head trauma- Staph epiNeural tube defects- Staph aureus, enteric

organismsT-cell defects (HIV)- cryptococcus, listeriaSinus fracture- Strep pneumoAsplenia (HgB SS)- Neisseria, H. flu, S.

pneumoTerminal compliment deficiency- Neisseria


Clinical Presentation Clinical manifestations are due to local

immune response to bacteria Ensuing inflammatory response increases

blood-brain permeability Cerebral edema Increased ICP Local thrombosis and infarction


Clinical Presentation Con’t…


Pathological responses INITIALLY: vascular congestion, edema, and minute

hemorrhages CT and MRI findings may be normal early in the disease

process ONCE INFECTION PROGRESSESNECT :obliteration of the basal cisterns. results from a

combination of hypervascularity in the acutely inflamed leptomeninges and exudate in the subarachnoid space.

Diffuse cerebral swelling may be seen. Contrast-enhanced CT scan : show enhancement in the

basal cisterns and sylvian fissure, regardless of the causative organism


Imaging continue…Routine MRI scans :obliteration of the basal

cisterns on T1-weighted images. Fluid-attenuated inversion recovery (FLAIR)

sequence may show hyperintensity of the cerebrospinal fluid (CSF) within the subarachnoid space in contrast to the hypointense CSF in the ventricles. Abnormal cortical hyperintensity may be seen on T2-weighted images.

Contrast-enhanced MRI studies may show basal cisternal and sylvian enhancement as well as enhancement deep within the cortical sulci


Meningitis


complicationsEarly complications abscess, subdural empyema, ventriculitis,

and infarction. Late complications subdural effusion, encephalomalacia,

hydrocephalus, and atrophy


20

Contrast-enhanced MRI more sensitive than contrast-enhanced CT in detection of meningitis and its complications

The MRI differential diagnosis includes only meningeal carcinomatosis


Grp b streptococcal meningitisLeading cause of newborn meningitis in developed countriesBest diagnostic clue: Meningoencephalitis in anewborn


PACHYMENINGEAL ENHANCEMENT

may be seen as a normal finding -- the dura mater does not produce a blood-brain

barrier.dural reflections of the falx and tentorium. intracranial hypotension, meningiomas, metastatic disease,

lymphoma, and granulomatous disease]

Postoperative meningeal enhancement may be pachymeningeal or leptomeningeal in appearance.


Subdural Effusion irritation of the dura by the infectious agents or its by-

products or by inflammation of subdural veins with loss of fluid and albumin into the subdural space.

H. influenzae is a common pathogen On neuroimaging, effusions look similar to CSF and are

frequently seen in the frontal region. On contrast study , no evidence of abnormal

enhancement

The subdural effusion usually resolves spontaneously



INTRACRANIAL EMPYEMA

Subdural empyema collection of pus between dura and leptomeninges as a complication of meningitis, paranasal sinusitis, otitis

media, osteomyelitis, or a penetrating wound of the skull Frontal sinusitis is the most common cause Route: retrograde fashion through a dural sinus or through

bridging veins even when small, usually cause focal neurologic deficits considered a neuro-surgical emergency because of its

progressive clinical course. Despite recent improvement in surgical technique and

antibiotics, mortality remains high (25% to 40%). Complications :venous thrombosis and infarction


CT scan -hypodense or isodense crescentic or lenticular area adjacent to the inner table of the skullCECT-enhancement of the medial rim may be seen Enhancement of the margin of the empyema is characteristicbetter visualized with MRI than with CT.


Epidural Empyemacollection of pus between the dura and calvaria, complication of otitis media, mastoiditis, sinusitis, or

osteomyelitis of the skull. not as toxic as that with subdural empyema.Displacement of the falx and dural sinuses away from the

inner table of the skull, an important and useful sign indicating the epidural location of a collection


Epidural Empyema


Epidural Empyema

T2-weighted MR images , A hypointense rim, representing inflamed dura, in an epidural, but not a subdural, empyema

, epidural empyema may extend into the subgaleal space through emissary veins or adjacent

31

Epidural empyema, like epidural hematoma, can across the midline but is limited by the sutures. In contrast, a subdural collection of any kind cannot cross the midline but is not limited by the sutures


Encephalitis refers to diffuse inflammation of the brain

with a parenchymal infiltration of inflammatory cells, usually caused by virus.

The brain damage is due to a combination of intracellular viral growth and the host's inflammatory response

Common herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2


INTRODUCTION

unusual manifestation of human viral infection as most viruses do not attack the human CNS.

Viruses vary in their potential to cause CNS infections. some cause relatively benign infections, others cause prominent neurologic symptoms

Overall, viruses are the most common cause of meningoencephalitis (3.5-7.4 per 100000 persons per year in USA).


INTRODUCTIONViral encephalitides can be divided into 4 typesacute viral encephalitispostinfectious encephalomyelitisslow viral infections of the CNSchronic degenerative CNS disease of viral

origin


VIRUSES THAT CAUSE MENINGOENCEPHALITIS Herpes simplex virus (HSV-1, HSV-2) Other herpes viruses: varicella zoster virus (VZV), cytomegalovirus

(CMV), Epstein-Barr virus (EBV), human herpes virus 6 (HHV6) Adenoviruses Influenza A Enteroviruses, poliovirus Measles, mumps and rubella viruses Rabies Arboviruses—for example, Japanese B encephalitis, St Louis

encephalitis virus, West Nile encephalitis virus, Eastern, Western, and Venezuelan equine encephalitis virus, tick borne encephalitis viruses, Chandipura virus, Dengue virus, chikungunya, KFD.

Bunyaviruses—for example, La Crosse strain of California virus Reoviruses—for example, Colorado tick fever virus Arenaviruses—for example, lymphocytic choriomeningitis virus Paramyxovirus – Nipah virus, hendra virus

Modified from Chaudhury and Kennedy Postgrad Med J. 2002;78:575


VIRUSES THAT CAUSE MENINGOENCEPHALITIS cont.Sporadic ;

HSV1 and 2, Mumps, EB, adenovirus, rabies etc

Epidemic;Arboviruses, influenza, enteroviruses, emerging viruses (Nipah).


VIRUSES THAT CAUSE MENINGOENCEPHALITIS

Indian scenario In India, most common cause for epidemic

encephalitis JE Other viruses cause sporadic

meningoencephalitis include herpes, mumps, measles and polio

In children enterovirus 71, mumps, measles, and JE are major causes. Others include herpes, varicella ,rubella and dengue

Emerging viruses with threat potential – Nipah, chandipura, chikungunya .


PathogenesisCNS access of the virus can be through two

routes Hematogenous (eg. Arboviruses) –most

common Intraneuronal ( eg. HSV, rabies, varicella

zoster) After hematogenous entry → transient viremia

→ seeding of reticuloendothelial system, →replication →secondary viremia→seeding of CNS


Pathology:Gross: variable degree of meningitis, brain

swelling, congestion and hemorrhage.Some viruses preferentially attack certain brain

sites Herpes virus – temporal neocortex, ponsJE- thalamus, basal ganglia, substantia nigra,

hippocampusThis may reflect as fairly characteristic imaging

findings


ImagingCTHypoattenuated

lesions affecting grey matter, deep gray matter and white matter.

Focal or generalized brain swelling

Focal hemorrhage+- enhancement

MRIMore sensitive T2 hyper and

T1 hypo to isointense single or multifocal lesions

+- enhancement

+-hemorrhage


DWMRIoIn acute stage- DW may show ↑ or equal lesions compared to conventional MR. In later stages may show less lesions[1,2]

CONGENITAL CMVTransplacental transmission of human herpes virusBest diagnostic clue o Microcephaly o Cerebral calcification (40-70%) • Periventricular (sub ependymal) o Cortical gyral abnormalities • Agyria ~ pachygyria ~ diffuse polymicrogyria ~ focal cortical dysplasia o Cerebellar hypoplasia o Myelin delay or destructionLocation: Dystrophic periventricular Ca++ has

predilection for germinal matrix zones


IMAGING

CT Findingso Cerebral parenchymal Ca++ (40-70%)• Periventricular (subependymal)o Ventricular dilatation and WM volume

losso Focal regions of WM low attenuationo Cortical gyral abnormalitieso Cerebellar hypoplasia

MR Findings• TIWI o Periventricular subependymal foci of

Tl shortening due to Ca ++ o Ventricular dilatation and

periventricular WM volume loss


CONGENITAL HIVVertical HlV 1 infection early in-utero/latepregnancy, at delivery or, by breast-feedingImaging Findings• Best diagnostic clue: Basal ganglia Ca++,

volume lossMRA: Fusiform vasculopathy Image Interpretation Pearls• Consider HIV if bilateral symmetrical

calcifications in BG are found in a child> than 2 months


CONGENITAL HIV

Scattered Ca++• Hydrocephalus

Periventricular Ca++


Herpes encephalitis


Herpes simplex encephalitismost common endemic encephalitis in the USA (2

per million) and causes 10-20% of all viral encephalitis.

In India exact incidence is not known and it is under diagnosed due to lack of awareness and diagnostic facilities

Early diagnosis is important because AV therapy can decrease mortality and morbidity.

HSV1 causes 95% of HSE. Most commonly occurs due to virus reactivation. HSV2 causes 80-90% of neonatal encephalitis

[1] Panagaria A. Neurol In. 49:360; 2001.


Herpes simplex encephalitis Definitive diagnosis: PCR, intrathecal

antibodies, brain biopsy – take time and may be false negative in early disease [1].

Imaging helps in establishing an early diagnosis.

1) Akyldz BN Paeditr Emerg Care 24;377 :2008.


Herpes simplex encephalitis


Usually bilateralHemorrhage and enhancement seenBasal ganglia tend to be spared or

involved in contiguity with the TL.Pons may be involved [Tien AJR:161,1993]

MR is more sensitive and shows lesions earlier than CT or SPECT




Rare paraneoplastic syndromelimbic system, often bilateral

Active seizures may disrupt BBB, cause signalabnormalities and enhancement


HSV 2Both HSV1 and 2 are commonly prevalent in Indian population.

(Mixed=83%, HSV1=10%, HSV2=1%) [1]HSV2 along with TORCH agents are major causes of neonatal encephalitis.Infections result from maternal birth canal or transplacental spreadUnlike HSV1, HSV2 infection in neonates is diffuse.

1.Shivaswami 2005. IJDVL 71:26


HSV 2Imaging findings are nonspecific.CT scans in early disease may be negative or

show subtle areas of low density. Conventional MR and DWI show lesions

better. Lesions may be multifocal involving almost any

area of brain or limited to temporal lobes brainstem and cerebellum.

Watershed infarcts may be seen [1] In-utero infections can result in microcephaly,

encephalomalacia or calcification.1)Vossough.2008. Neuroradiol 50:355


Axial T2WI MR shows areas of high signal in frontal lobes WMdue to acute H5V-2

Axial T1WI MR shows diffuse cystic encephalomalaciaand prominent CSF-containing spaces

Scattered Ca++, hydrocephalusPeriventricular Ca++,55infection of brain and its linings

HIV Encephalitis

Syndrome of cognitive, behavioral, and motor abnormalities attributed to direct HIV effect on brain, in the absence of opportunistic brain infections

Location: Bilateral periventricular and centrum semiovale WM, basal ganglia, cerebellum, brainstem

56

Best diagnostic clue: Combination of atrophy andsymmetric, periventricular or diffuse white matter(WM) disease suggests HIVE


Introductionmosquito borne Flaviviral encephalitis. Pigs and heron like birds are main amplifiers.leading cause of acute meningoencephalitis

affecting children and adults in the world. JE is endemic to Indian subcontinent, particularly

in the NE state of AssamEpidemics occur in the summer rainy season

which favor breeding of mosquitoes.First recognized in India in 1955, Epidemics

occur every year in several Indian states since the first in WB(1973).


Pathology

1)Tiroumourougane. Postgrad. Med. J. 2002; 78: 20560infection of brain and its linings

Some neurons have specific receptors with strong affinity for JEV [1

Lesions of JE are most commonly seen in the thalami and substantia nigra,

Basal ganglia, cerebral cortex, hippocampi, midbrain, pons, medulla and cerebellum lesions are also seen.

Lesions hyperintense on T2 and FL and iso to hypo on T1 with local or generalized brain swelling.

No enhancement. Hemorrhagic change has been reported from India [1]. MRI is the investigation of choice with reported

sensitivity of 89-100% compared to CT (38-55%) [1,2]. DWI has been reported to help in early diagnosis and in

assessing temporal evolution of lesions[1] Was helpful in making an early diagnosis in JE showing

additional lesions

1)Kalita. J Neurol Sci 2000; 174: 361infection of brain and its linings

Imaging

Evolution of lesions in JE


Temporal lobe involvement in JE

Fairly characteristic pattern of TL involvement with posterior hippocampal involvement and sparing of anterior temporal lobe and neocortex. Insula occasionally involved

Associated lesions characteristic of JE usually seen in thalamus, SN, BG etc. Can help differentiate from HSE [1]

1)Handique AJNR 2006 27:1027



T2 DWI

PATTERN 1 DWI>T2 [1]

Neurocysticercosis and JE

More than a casual relationship between NCC and JE has been suggested by many studies in China and India [1,2,3]

Co-infections have been advocated as prognosticator of poor outcome[1]

1.Desai Epidemiol Infect 1997;118:1652. Shankar. Ind J Med Res 1983; 78:4313. Liu. Chinese Med J 1957;75:1010


Neurocysticercosis and JE

asymmetric with lateralization to the side of the brain having maximum NCC or a cyst with edema.

were more florid with significantly higher amount of abnormal CT scans and more abnormal MR imaging

more common in children.Altered immune status in co-infections were

suggested by significantly lowered levels of JE IgM.



co-infection

Mumps, measles and varicella Mumps, measles and varicella viruses may

occasionally cause acute encephalitis besides its primary infectious manifestations.

Acute measles encephalitis is much more common than the more well known (amongst radiologists) SSPE

In a study of VE in children from India, 10% was caused by mumps, 7% by measles and 1.8% by varicella [1]

(1) Karmarkar. Ind JPaediatr.2008;75:801


Mumps, measles and varicellaVery few large scale imaging studies exist for

these encephalitis as the findings are non specific.

Mumps encephalitis shows white matter and brainstem lesions[1].

Measles shows lesions in the basal ganglia with multifocal lesions in the gray and white matter, thalamus (rare) with gyriform enhancement of gray matter lesions [2].

Varicella shows multifocal cortical lesions[3] (1)Koyama Int Med 2000 ;39:499 (2) Lee. Neuroradiol 2003; 45:100

(3) Tien AJR 19937; 161:16


Enterovirus 71MRI revealed lesions in the brainstem and

cerebellum in 71% patients with rhombencephalitis. Anterior horn cells showed lesions in patients with flaccid paralysis [1]

In study from India lesions were also described in the thalamus, basal ganglia, parieto occipital, frontal, temporal lobes, substantia nigra besides brainstem and cerebellar involvement [2]

1) Huang. New Eng J Med. 1999;341:936 (2) Karmarkar. Ind JPaediatr.2008;75:801


DengueDengue is caused by a mosquito borne

flavivirus like JE. Neurologic manifestations in dengue fever, hemorrhagic fever and Shock syndrome have been thought to be due to encephalopathy

Recent reports have shown that dengue virus can cause neuroinvasion and encephalitis [1,2]

(1) Lum. Am J Trop Med Hyg. 1996;54:256 (2) Muzaffar. Sing Med J 2006;47:975


Dengue


From. Muzaffar. Sing Med J 2006;47:975

Imaging studies have shown cerebral edema, lesions in the hippocampus and temporal lobes

Rabies encephalitisTransmitted by bites of infected animals or

by transplants. 100% fatal. In India rabies occurs in all parts of the

country except in Lakshadweep, Andaman and Nicobar islands.


Nipah virus encephalitisparamyxovirus spread to man from fruit-bats

or pigs infected by fruit-bats. Subsequent spread from man to man occurs. First identified in Malaysia and Singapore in

1988-89, outbreaks have occurred in Bangladesh (2001-4,5)and Siliguri (2001). Case fatality in India and Bangladesh was 75%[1]

(1) Halder. Ann Ind Acad Neurol 2006;9:137


Nipah virus encephalitisMR shows fairly

characteristic findings with small T2 hyperintense white or gray matter lesions with transient T1 hyperintense punctate cortical lesions in subacute phase [1]

(1) Lim. Radiol 2002;222:219


Other emerging virusesChandipura virus is transmitted to humans

possibly by sandflies and primarily causes encephalitis in children. Major outbreaks have occurred in Gujarat, Andhra Pradesh, Madhya Pradesh and Maharashtra with fatality rates of 50-80%.

Brainstem encephalitis has been reported. CT and MRI scans have showed no abnormality in

few (CT=5,MR=1)reported patients from India [1,2]. No large scale imaging studies available.

Other emerging viruses that ocassionally cause encephalitis include Chikungunya and KFD.


ADEM acute Disseminated Encephalomyelitis an immune response to a preceding viral infection or

vaccinationneurologic signs and symptoms 5 days to 2 weeks later. Both humoral and cell-mediated immunity A hypersensitivity reaction to a myelin .Perivenous demyelination is the hallmark of the diseaseThe disease primarily involves white matter, but change

may also be apparent in gray matter and brain stemThe differential diagnosis includes multiple sclerosis,

vasculitis, and embolic infarction. In later stages of the disease, encephalomalacia,

ventriculomegaly, and atrophy may be seen.


Other EncephalitidesCreutzfeldt-Jakob Disease human spongiform encephalopathy that results from an

infection by a priontransmission has been traced to inoculations by injections of

human growth hormone, transplantation of corneas, and implantation of cerebral electrodes

butchers and meat handlers are at greater risk of contracting the disease

variant ;bovine spongiform encephalopathy (so-called mad cow disease).

The infective prion is a proteinaceous particle that contains little or no nucleic acid.

The disease occurs in adults in their late 50s



Cortical gray matter involvement without cerebral atrophy may represent an early phase of the disease.

[In contrast to Creutzfeldt-Jakob disease, wherein bilateral involvement of the corpus striata and thalami is seen on the imaging studies, the bovine spongiform encephalopathy is characteristically demonstrated by bilateral thalamic pulvinar hyperintensity on T2-weighted and FLAIR images

. A, FLAIR image demonstrates hyperintensity in both thalami, in the periatrial white matter, and in the anterior cingulated gyri. B, Diffusion-weighted image shows restricted diffusion in both thalami and cingulated gyri

Subacute Sclerosing Panencephalitismeasles virusseen in children and young adults with

previous measles infection 3 to 9 years earlierCT scans low-density changes in subcortical white matter

as well as in basal ganglia. MRI studies show hyperintensity in the periventricular

white matter, subcortical white matter, basal ganglia, cerebellum, and pons on T2-weighted and FLAIR images.[

Abnormal signal intensity on T2-weighted and FLAIR images involving the splenium of corpus callosum can occur.

Atrophy is a late-stage finding.81infection of brain and its linings

Reye's Syndromedisease of unknown etiology in children. It usually follows a viral infection such as

type A or B influenza and varicella. Exogenous toxins, such as salicylates, and

intrinsic metabolic defects have been implicated as other factors

CT scans show diffuse low density of the supratentorial structures, a finding consistent with diffuse cerebral edema.[124]


Encephalitis in Immunocompromised Patients

Human Immunodeficiency Virus Encephalitis

neurotropic viruscauses a subacute form

of encephalitisCT scans low density in

the periventricular white matter.

MRI hyperintensity in the periventricular white matter on T2-weighted and FLAIR images Normal neuroimaging studies do not exclude HIV

encephalitis.


Encephalitis in Immunocompromised Patients

Progressive Multifocal Leukoencephalopathy

a JC virus infecting the oligodendrocyte

seen in immunocompromised patients.

affects all parts of the brain, including the cerebellum, and does not have the propensity to involve the parieto-occipital region, as previously describe


Progressive Multifocal Leukoencephalopathy

CT scans low-density lesions in white matter.

Early involvement -asymmetrical pattern,

later disease -symmetrical and diffusely confluent.

Contrast enhancement is usually absent but may occur.[155.

MRI shows a focal region of hypointensity in the white matter on T1-weighted images and hyperintensity on T2-weighted images

. Involvement of the subcortical U-fiber is characteristic for PML, as opposed to other HIV- related encephalopathy.

. MRI is more sensitive than CT in detecting abnormalities

T2-weighted image shows high signal intensity in the parieto-

occipital white matter bilaterally.


Cytomegalovirus Encephalitisaffect the immunocompetent as well as immunocompromised

patientscause meningoencephalitis or subacute encephalitis. CMV can produce demyelination and necrosis within the

white matter.CMV is the most frequent cause of fetal and neonatal viral

infection. calcifications are usually in the subependymal region, whereas in

infants with toxoplasmosis, calcifications are seen everywhere, including the periventricular region.


CT scans show low density in the white matter, which may or may not enhance with contrast agents

. MRI shows high signal intensity in the white matter on T2-weighted and FLAIR images and is more sensitive than CT in detecting leukoencephalitis

Nonenhanced CT scans in a newborn show periventricular calcification and ventricular dilatation


Cytomegalovirus Encephalitis

Cerebritis and Abscess


most brain abscesses are bacterial streptococci accounting for the majorityhaematogenous dissemination, penetrating

trauma or direct spread Blood-borne infection can occur anywhere

in the brain, but has a predilection for the territory of the middle cerebral arteries

fever ,headache and focal neurological deficits. Brain abscesses are multiple in 10–50 per


stages in the evolution of cerebral abscessthere are four stages 1. Acute cerebritis (the

first 4 to 5 days). In early cerebritis, mild

central nodular enhancement may be seen on contrast-enhanced CT or MRI scans



2. Late cerebritis (at 7 to 10 days). In the late cerebritis stage brain

enhancement on CT scans

Late cerebritis. A, Gadolinium-enhanced MRI study shows thick, smooth, ringlike enhancement with surrounding edema. B, Gadolinium-enhanced MRI study (coronal view) shows a second small, adjacent ringlike enhancement

stages in the evolution of cerebral abscess3. Early abscess (at 10 to

14 days). Formation of a collagenous capsule by fibroblasts is seen. The central necrotic area is liquefied. Surrounding edema persists.4. Mature abscess (after 14 days). A decrease in surrounding edema

gliotic reaction at outer margin of the abscess capsule.


Usually, more than 2 weeks is required to form a firm capsule

The wall of the mature abscess consists of three layers: (1) an inner inflammatory layer of granulation tissue containing macrophages, (2) a middle collagenous layer, and (3) an outer gliotic layer


Abscess treated conservatively with antibiotics.


Abscess caused by gas-forming organism.

The most distinctive feature of abscess on imaging is the presence of a smooth, thin capsule with a moderate amount of cerebral edema.[57]

It is located at the corticomedullary junction and usually extends into the white matter.

Nonenhanced CT scans show a low-density area with mass effect and compression of the ventricular system.

rupture of the abscess into an adjacent ventricle {medially into the ventricular system because the medial wall is thinner than the lateral wall

Differential diagnosis necrotic primary brain tumor, cystic metastatic tumor,

infarction, resolving hematoma, cysticercosis, and thrombosed aneurysm

Thick, nodular enhancing wall typical

History of trauma or vascular lesion• Blood products present

Enhancement often incomplete ring

• Thick, nodular enhancing wall typical


Infarcts often show gyral enhancement, occasionally mimicking ring enhancementThe MRI differential diagnosis of abscess is similar to the CT diagnosis except for hematomas, which can be recognized by their characteristic MRI signal intensity patterns, depending on the age of the hematomas

Ependymitis Ventriculitis, or ependymitis, is an

inflammation of the ependymal lining of the ventricular system

\rupture of periventricular abscess or from retrograde spread of infection from the basal cisterns by way of the fourth ventricle

Hydrocephalus may result from intraventricular adhesions and septation caused by organization of intraventricular exudate and debris, resulting in blockage of the interventricular foramina.

A trapped fourth ventricle may result from obstruction of its outlets and the aqueduct because of ependymitis



NECT scan -normal or may show only slightly increased density in region of affected ependyma

MRI -marginal ventricular abnormality or only slightly increased signal intensity in the region of affected ependyma

proton-density-weighted images. The fluid within the ventricles may show slightly increased intensity,.

Contrast-enhanced CT or MRI studies show uniform, thin ependymal enhancement

Gadolinium-enhanced MRI studies show thin, smooth ependymal enhancement in an AIDS patient with

cytomegalovirus ependymitis.

The differential diagnosis on CT and MRI studies includes ependymal seeding of intracranial neoplasm. The ependymal enhancement may be irregular or nodular if it is secondary to seeding of neoplasm, the clinical history may be helpful in arriving at the correct diagnosis

typically nodular• Parenchymal disease usually present Ventricles typically not

enlarged


Granulomatous Infection

99

Tuberculosis


TuberculosisMycobacterium tuberculosis very young and very old persons are affected, with the

highest incidence in the first 3 years of life Increased in incidence in immunocompromised patients,

drug abusers, and patients with AIDSTuberculous meningitis is the most frequent

manifestation and tends to involve the basal leptomeninges.

Best diagnostic clueo Basilar meningitis + extracerebral TB (pulmonary)o Meningitis + parenchymal lesions highly suggestive


TBM pathologyPenetration of meningeal vessel walls by

haematogenous spread• Rupture of subependymal or subpial

granulomata into the CSF


Tuberculous meningitis involve the basal leptomeninges. CT shows - obliteration of the basal cisterns by isodense or

slightly hyperdense exudate, which shows diffuse enhancement with IV contrast medium

The most useful CT criteria of abnormal basal meningeal enhancement are:

(A) linear enhancement of the middle cerebral artery cisterns;

(B) obliteration by contrast of the CSF spaces around normal vascular enhancement;

(C) Y-shaped enhancement at the junction of the suprasellar and middle cerebral artery cisterns and

(D) asymmetry of enhancement



MRI depicts the basal meningeal enhancement, hydrocephalus and basal ganglia infarcts with greater sensitivity than CT

Late sequelae of tuberculous meningitis include hydrocephalus, infarction, syringobulbia, and syringomyelia.

Tuberculous meningitisdifferential diagnosis includes fungal

meningitis, sarcoid and carcinomatous meningitis


tuberculoma found in any portion of the intracranial compartment When tuberculoma and tuberculous meningitis are seen

together, the diagnosis of tuberculosis is easily made.

105

Tuberculoma pathophysiology• Hematogenous spread (GM-WM junction lesions)• Extension of meningitis into parenchyma via cortical veins or small penetrating arteries


106

NECT scans isodense, hyperdense, or of mixed density CECT- ringlike enhancement[152] or, less likely, areas of nodular

enhancement A central nidus of calcification with surrounding ringlike

enhancement, known as the target sign, suggests tuberculoma. Gadolinium-enhanced MRI studies show enhancing patterns

similar to those on contrast-enhanced CT scans


107

T1-weighted image shows isointense to hyperintense capsules with central pus and debris and surrounding edema. B, T2-weighted image shows the abscess capsules with an inner ring of hypointensity and an outer ring of hyperintensity; pus shows hyperintensity, and debris shows hypointensity. C, Gadolinium-enhanced MRI study shows smooth, ringlike enhancement of the abscess capsule


Neurosyphilismeningovascular syphilis

syphilitic gumma

widespread thickening of the meninges, with lymphocytic infiltration involving the meninges and around the small vessels

CT shows multiple low- density areas involving both gray and white matter.

Contrast-enhanced CT scans show linear, nonhomogeneous enhancement.

Contrast-enhanced MRI studies may demonstrate meningeal enhancement in addition to a gyriform pattern of enhancement

consist of masses of granulation tissue and are rare

originate in the meninges and blood vessels and spread into the brain parenchyma.

On CT scans, gummas are well-delineated masses with ringlike or nodular enhancement.

On contrast-enhanced MRI, gumma shows nodular or ringlike enhancement. Cerebral atrophy may develop in patients with neurosyphilis


Fungal infection

involve intracranial blood vessels, leptomeninges, and brain parenchyma. Intracranial infection is frequently secondary to pulmonary disease

HIV, diabetes, pregnancy, and malignancy.CNS fungal infection displays neuroimaging features

similar to those seen with tuberculosis


The fungi of yeast forms tend to spread hematogenously to the meningeal microcirculation, with resultant leptomeningitis attributable to their smaller size; the larger hyphal form more commonly involves the brain parenchyma, with resultant cerebritis or encephalitis

AspergillosisAspergillus fumigatus infection is seen

predominantly in immunocompromised patients

hematogenous spread of pulmonary disease and less commonly caused by direct extension of disease in the nasal cavity and paranasal sinuses

produces meningitis and meningo-encephalitis.


Patho physiology


Imaging CT scans low-density areas with

little or no contrast enhancement and mass effect, representing areas of infarction

Incomplete ringlike contrast enhancement may be seen

MRI studies demonstrate a peripheral ring of low signal intensity

The ring of low signal intensity corresponds to a dense population of Aspergillus hyphal elements and small areas of hemorrhage histologically.


CryptococcosisCryptococcosis is the most

common fungal infection in patients with AIDS

. a yeast with a polysaccharide capsule

CNS infection is usually secondary to pulmonary infectio

nmeningitis, meningoencephalitis, or cryptococcal mass

. Meningitis is the most common presentation.

Ocular symptoms are common in patients with cryptococcal meningitis.


Mucormycosis

infection of brain and its linings114

Candidiasis-most common cause

of human fungal infection and represents 75% of the fungal infections in patients with neoplasm

present as meningitis, granuloma, or microabscess


T1-weighted image reveals a hyperintense area in the left thalamus, consistent with focal hemorrhage. B, FLAIR image demonstrates abnormal hyperintense areas in the corpus striati bilaterally and in the left thalamus. C, Postcontrast image demonstrates patchy abnormal enhancement in the corpus striati bilaterally as well as in the left thalamus

Cysticercosisone of the most common parasitic diseases involving

the brain ingesting the ova of the pork tapeworm (Taenia

solium), usually on unwashed, fecally contaminated vegetables or water

By ingesting poorly cooked pork infected with cysticercosis, the human becomes the definitive host for T. solium

through the anus-finger-mouth route.

117

Best diagnostic clue: Cyst with "dot" inside


intracranial compartment is involved in 60% to 90% of patients with cysticercosismeningobasal, parenchymal, intraventricular, or a combination of these sitesConvexity subarachnoid spaces most common( cisterns> parenchyma> ventricles)

STAGES: Escobar, has identified four stages that the parasite undergoes within the brain parenchyma

Vesicular stage (viable larva)Colloidal vesicular stage (degenerating

larva):Granular nodular (healing) stageNodular calcified (healed) stage


119

STAGES ..

VESICULAR STAGE the tiny (4- to 5-mm) live spherical larva Smooth, thin-walled CYST , isodense to CSF, no edema • Hyperdense "dot" within cyst = proto scolex No (or mild) wall enhancement

COLLOIDAL VESICULAR STAGE. Hyperdense cyst fluid with surrounding edema The cyst wall may show enhancement The cyst fluid may show increased density with CT and intensity with MRI. The

scolex begins to degenerate and shrink


GRANULAR NODULAR STAGE

Mild edema calcification may be identified within the scolex and along the cyst wall on CT scan

NODULAR CALCIFIED STAGE,

granular material appears completely mineralized, with the lesion having shrunk to one half or one fourth of the size of the original

Calcification is much better demonstrated on CT than on MRI


Intraventricular cysticercosis potentially lethalThe cysts can be identified by CSF density or

signal intensityA thick, ring like enhancement associated with

intraventricular cysticercosis


EchinococcosisCNS involvement is rareHydatid disease, or echinococcosis, is the larval stage of

Echinococcus granulosusdefinitive host of E. granulosus is the dog, intermediate

hosts are sheep, cattle, and camels.Seizure, focal neurologic signs, and increased intracranial

pressure are the usual clinical presentations . Extradural cysts have been reported



NECT or MRI appear as large intraparenchymal cystic lesions with sharp margins

Cyst fluid is of CSF density or signal intensity. The lack of surrounding edema is an important feature

differentiate this lesion from cerebral abscess. Contrast enhancement may be seen partially or completely

involving the wall. Calcification MAY SEEN

Toxoplasmosis Toxoplasma gondii, a protozoan immunocompromised patients

or in patients with AIDS meningoencephalitis or as

granulomas Granuloma site

corticomedullary junction, in the deep gray matter, or in the periventricular areas

NECT- show multiple low-density areas.

MRI studies are more sensitive in detecting the Toxoplasma lesions than contrast-enhanced CT scans


Rasmussen's Encephalitischildhood disease. severe epilepsy and progressive neurologic deficitsCharacterized by hemispheric volume loss and difficult to

control focal seizure activity partial motor seizure type and tend to be intractableEarly in the disease process, CT and MRI findings may be

normal. MRI may reveal hyperintensity in the white matter and

putamen on T2-weighted images.[143]

PET imaging using 18FDG may show decreased hemispheric activity.


(parieto-occipital most commonHemispheric infarction


Acute Necrotizing Encephalitis infants and children between 6 and 18 months of agehistory of mild antecedent illnesselevated liver enzymesno focal neurologic or meningeal signs. Etiology is unknown; it may be postinfectious (HSV-6 or influenza A and B),

immune mediated, or metabolic. Prognosis is usually poor; less than 10% of patients

recover completely. Focal neurologic deficits are common sequelae


Acute Necrotizing Encephalitis

Thalamic lesions almost always become hemorrhagic

Enhancement in the margin of the thalami may be seen.

MRS may show elevated lipids, glutamate/glutamine complex, and lactate A, T1-weighted image reveals bilateral

thalamic hemorrhage. B, FLAIR image demonstrates hyperintensity in both thalami with adjacent edema.


Intracranial infections take the following formsCerebritis AbscessEmpyemaGranuloma EncephalitisMeningitisOsteomyelitis


132

Even with appropriate antibiotics, mortality rate for bacterial meningitis is significant

imaging can help in establishing a working diagnosis of viral encephalitis, and differentiate from other conditions such as ADEM and TBM.

Keeping in mind the age, geographical location, climate and host immune status, imaging findings can help arrive at an etiological diagnosis of viral encephalitis.

HSV encephalitis can be identified early for early AV therapy

In epidemic situations the alert radiologist can point to the possible etiological agent eg. in JE, NVE and EV71E

Can help in prognostication and identification of associated disease such as NCC with JE


imaging of infection of brain and its linings

Health & Medicine