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Definition

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ETIOLOGY

1.Infection :

•Infection spread by either direct or through veins

(thrombophlibitis of diploic vein)

•Characterized by solitary and located superficially

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PREDISPOSING CONDITION & LOCATION OF PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESSBRAIN ABSCESS

Otitis/mastoiditis Temporal lobe, Cerebellum

Frontal/ethmoid sinusitis Frontal lobe

Sphenoidal sinusitis Frontal lobe,

Sella turcica

Dental infection Frontal > temporal lobe.

Remote source Middle cerebral artery distribution (often multiple)

PATHOGENESISPATHOGENESIS

• Direct spread from contiguous foci (40-50%)

• Hematogenous (25-35%)

• Penetrating trauma/surgery (10%)

• Cryptogenic (15-20%)

Predisposing Conditions & Microbiology of Predisposing Conditions & Microbiology of Brain AbscessBrain Abscess

Predisposing Condition Usual Microbial Isolates

Otitis media or mastoiditis Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., Enterobacteriaceae

Sinusitis (frontoethmoid or sphenoid) Streptococci, Bacteroides spp., Enterobacteriaceae, Staph. aureus, Haemophilus spp.

Dental sepsis Fusobacterium, Prevotella and Bacteroides spp., streptococci

Penetrating trauma or postneurosurgical S. aureus, streptococci, Enterobacteriaceae, Clostridium spp.

PPID,2000

PREDISPOSING CONDITION USUAL MICROBIAL ISOLATES

Lung abscess, empyema, bronchiectasis Fusobacterium, Actinomyces, Bacteroides Prevotellaspp., streptococci, Nocardia

Bacterial endocarditis S. aureus, streptococci

Congenital heart disease Streptococci, Haemophilus spp.

Neutropenia Aerobic gram-negative bacilli, Aspergillus Mucorales, Candidaspp.

Transplantation Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp., Toxoplasma gondii

HIV infection Toxoplasma gondii, Nocardia spp., Mycobacterium spp., Listeria monocytogenes, Cryptococcus

neoformans

PPID, 2000

• Symptoms : 1. Head ache ( 90 %) 2. Change in conscious level ( 60 %) 3. FND ( 60 %)

Parietal lobe : hemiparesis Temporal lobe : dysphasia Cerebellar : ataxia and nystagmus

4.Fever (more than 50 %) 5. Nausea and vomiting ( 50 %) 6. Seizure ( 50 %) 7.Papilledema and meningismus

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LOCATION & CLINICAL FEATURESLOCATION & CLINICAL FEATURES • FRONTAL LOBE: H/A, drowsiness, inattention,

hemiparesis, motor speech disorder, AMS

• TEMPORAL LOBE: Ipsilateral H/A, aphasia, visual field defect

• PARIETAL LOBE: H/A, visual field defects, endocrine disturbances

• CEREBELLUM: Nystagmus, ataxia, vomiting, dysmetria

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSIS

• Malignancy– Abscess has hypo-dense center, with surrounding smooth, thin-walled

capsule, & areas of peripheral enhancement. – Tumor has diffuse enhancement & irregular borders.– SPECT (PET scan) may differentiate. CRP too?

• CVA• Hemorrhage• Aneurysm• Subdural empyema/ICEpidural abscess

DIAGNOSISDIAGNOSIS

• High index of suspicion• Contrast CT or MRI• Drainage/biopsy, if ring enhancing

lesion(s) are seen

PATHOGENESIS AND HISTOPATHOLOGY OF BRAIN ABSCESS

• Preceding antibody formation there is an area of necrosis which is seeded by bacteria

• Brain abscess formation are 4 stages 1.stage I:early cerebritis (day 1 to day 3) : Necrotic tissue ,local inflammatory response, marked edema This stage there is no demarcation between the lesion and surrounding brain

2.stage two (late cerebritis)(day 4-10):

pus , maximum edema

3.stage three (early encapsulation)(day10—13) :

Capsule limits spread of infection

Capsule develops slowly in medial wall of abscess?

4.Stage four: late capsule stage ( >day 14)

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Radiological characteristic1. Brain CTS with contrast

• ring enhancement • Multi loculation • Multiplicity• Finding of gas

2. MRI : • T1 :

• necrotic center ( hypointence) • Capsule ( hyperintence)• Edema ( hypointence)

• T2 :• necrotic center ( hyperintence) • Capsule ( hypointence)• Edema ( hyperintence

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Brain abscess. Axial fluid-attenuated inversion recovery (FLAIR) MRI of a left occipital-parietal brain abscess. The edema pattern (white arrows)

surrounds the central abscess (A). A secondary (daughter) abscess is

noted anterior to the primary abscess cavity.

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Brain abscess. Sagittal T1-weighted spin-echo

gadolinium-enhanced MRI demonstrates an enhanced mass within the right medial cerebellum (yellow arrow).

The thick-walled cystic mass was opened. Nocardia

organisms were cultured from within the abscess.

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Brain abscess. Axial T2-weighted MRI in a patient with a right

frontal abscess. Note the mass effect and surrounding edema.

The wall of the abscess is relatively thin (black

arrows).

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Brain abscess. Gadolinium-enhanced coronal T1-weighted MRI in a patient who presented

with headache, fever, and diplopia. The right frontal lobe

of the brain is shifted across the midline (double arrow) by an

intracranial abscess (single black arrow) that has extended upward from the medial right orbit and medial ethmoid air cells (curved dotted arrow). Aspergillus organisms were

recovered from the sinuses and brain tissue.

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Follow up •CT weekly during antibiotic therapy•And then monthly CT •2-3 week decrease size of abscess •3-4 months complete resolution of abscess• 6-9 months no residual contrast enhancement

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Before Rx

After completion of Rx

Armstrong ID,Mosby inc 1999

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