Brain abscess (cerebral hemispheres, cerebellum)

Causes of Brain and Cerebellar Abscesses

Brain abscesses arise from the introduction of infectious organisms into the brain parenchyma. Key causes and risk factors include:

• Contiguous Spread (most common [3]):
  • Otogenic infections: Chronic or acute suppurative otitis media, mastoiditis, especially if complicated by cholesteatoma, are frequent sources for temporal lobe and cerebellar abscesses.
  • Sinusitis: Infections of the paranasal sinuses (frontal, ethmoid, sphenoid) can spread directly or via venous pathways (thrombophlebitis) to cause frontal lobe abscesses.
  • Dental infections: Apical abscesses or infections following dental procedures can occasionally spread to the brain, typically the frontal or temporal lobes.
• Hematogenous Spread (Bloodborne): Infections from distant sites seed the brain via the bloodstream, often causing multiple abscesses, commonly at the gray-white matter junction. Sources include:
  • Lung infections (pneumonia, lung abscess, empyema, bronchiectasis).
  • Infective endocarditis.
  • Skin infections.
  • Abdominal or pelvic infections (e.g., diverticulitis).
  • Intravenous drug use.
  • Congenital heart disease with right-to-left shunting (e.g., Tetralogy of Fallot), which bypasses pulmonary capillary filtering.
  • Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) with pulmonary arteriovenous malformations.
• Direct Inoculation:
  • Head trauma: Penetrating injuries or compound/depressed skull fractures introduce organisms directly.
  • Neurosurgical Procedures: Postoperative infection (e.g., after craniotomy, shunt placement, deep brain stimulation), though rare with modern techniques and prophylaxis.
• Immunocompromised State: Individuals with weakened immune systems (due to HIV/AIDS, chemotherapy, organ transplantation, chronic steroid use, diabetes mellitus) are susceptible to opportunistic pathogens (e.g., fungi like Aspergillus, Candida; parasites like Toxoplasma gondii; bacteria like Nocardia) causing abscesses.
• Cryptogenic: In some cases (around 15-20 percent [4]), the source of infection cannot be identified despite thorough investigation.

Regarding otogenic sources, brain abscesses occur more frequently as a complication of chronic suppurative otitis media compared to acute otitis media [5]. Intriguingly, in acute otitis media, an abscess can sometimes develop even without tympanic membrane perforation or after the acute ear infection appears clinically resolved with a normal otoscopic exam.

In chronic suppurative otitis media, the risk is highest with cholesteatoma involving the epitympanum or mastoid, although chronic mucosal disease (mesotympanitis) alone can also be a source.

The microbiology of brain abscesses is often polymicrobial, particularly those from contiguous sources [6]. Common bacterial isolates include aerobic and anaerobic streptococci (especially Streptococcus intermedius group, viridans streptococci), Staphylococcus aureus (common after trauma/surgery or with endocarditis), Bacteroides species, Prevotella species, Enterobacteriaceae (like E. coli, Klebsiella, Proteus), and less commonly, fungi (Aspergillus, Candida, Mucorales) or parasites (Toxoplasma gondii, neurocysticercosis) particularly in immunocompromised hosts. The specific organisms often depend on the primary source of infection (e.g., anaerobes common in dental/sinus/otogenic; S. aureus in trauma/post-op; specific pathogens in immunocompromised). Notably, cultures from the abscess pus may not perfectly match organisms found in ear discharge, suggesting involvement of additional pathogens or selection within the abscess environment.

Factors predisposing to abscess development include reduced host resistance (systemic illness, immunosuppression, malnutrition) and specific anatomical features, such as extensive temporal bone pneumatization or variations in venous sinus anatomy (e.g., prominent sigmoid sinus, low-lying middle cranial fossa floor), which might facilitate infectious spread.

Infection spreads from the temporal bone or sinuses via several routes [7]: Direct extension occurs through erosion of the bone separating the middle ear/mastoid/sinus from the cranial cavity (e.g., the tegmen tympani for temporal lobe abscesses, posterior fossa plate for cerebellar abscesses, posterior frontal sinus wall for frontal lobe abscesses). Hematogenous spread can occur via thrombophlebitis (inflammation and clotting) of small emissary veins draining the infected area or major dural sinuses (sigmoid, transverse, superior petrosal, cavernous). Less commonly, spread occurs along preformed pathways like congenital bone defects, prior fractures, or cranial sutures.

Cerebellar abscesses often arise from infection spreading from the labyrinth (inner ear) in chronic otitis or via a thrombosed lateral (sigmoid) sinus. From labyrinthitis, infection can erode bone (e.g., posterior semicircular canal) or travel along the vestibular/cochlear aqueducts or internal auditory canal.

Abscesses located distant from the primary otogenic or sinus focus often result from septic emboli originating from dural sinus thrombosis (e.g., transverse sinus thrombosis) or distant sources via hematogenous spread. Retrograde spread through cerebral veins or metastatic seeding can lead to abscesses in the frontal, parietal, or occipital lobes, multiple abscesses, or contralateral abscesses.

The dura mater, particularly its dense outer layer with a rich blood supply, provides a relative barrier against infection spreading from adjacent bone. Often, the infection is contained extradurally, forming an epidural abscess, or causes meningitis. An epidural abscess rarely progresses directly to an intraparenchymal brain abscess but can be an intermediate stage or co-exist.

While tight junctions between dural layers and the leptomeninges (pia-arachnoid) can limit spread into the subarachnoid space (preventing diffuse meningitis), these same vascularized meningeal layers can facilitate entry of infection into the brain parenchyma, particularly via perivascular spaces (Virchow-Robin spaces).

The most frequent pathways for parenchymal infection are thought to be venous thrombophlebitis with retrograde spread or extension along perivascular spaces. Direct arterial seeding via infected emboli causing thrombosis and infarction, followed by abscess formation in the white matter, is considered less common but occurs with hematogenous spread.

Importantly, the introduction of bacteria into the brain does not automatically lead to abscess formation. Host immune responses play a critical role, and abscesses are more likely to develop in individuals with compromised immunity or underlying brain tissue damage (e.g., previous stroke, trauma).

Types based on location:

• Cerebral Hemisphere Abscess:
  • Located within the cerebrum (frontal, temporal, parietal, occipital lobes).
  • Temporal lobe abscesses are commonly linked to middle ear infections.
  • Frontal lobe abscesses often stem from sinus infections or dental sources.
• Cerebellar Abscess:
  • Located in the cerebellum (posterior fossa).
  • Frequently associated with otogenic infections spreading posteriorly.
  • Can cause symptoms related to balance, coordination, and potentially hydrocephalus due to fourth ventricle compression.

 

Symptoms and Clinical Course of Brain and Cerebellar Abscesses

The clinical presentation of brain abscesses is highly variable, influenced by factors such as abscess location and size, the virulence of the infecting organism, the stage of abscess development (cerebritis vs. encapsulated), the presence of surrounding edema and mass effect, intracranial pressure (ICP) levels, and the patient's overall health and immune status. Symptoms generally fall into three categories: those related to infection/inflammation, those due to increased ICP and mass effect, and focal neurological deficits specific to the abscess location.

The classic triad of headache, fever, and focal neurological deficit occurs in less than 50% of patients [9]. Common signs and symptoms include:

• Headache: The most frequent symptom (present in over 70 percent of cases [3]), often described as persistent, dull, and initially localized near the abscess but becoming generalized and severe as ICP rises. May be worse in the morning or with Valsalva maneuvers.
• Fever: Present in only about 50 percent of patients [3], often low-grade or absent, especially once the abscess is encapsulated. High fever may suggest associated meningitis, ventriculitis, or systemic sepsis.
• Nausea and Vomiting: Common symptoms associated with increased ICP or direct irritation of brainstem centers. Vomiting can be projectile, especially with posterior fossa (cerebellar) abscesses causing hydrocephalus.
• Changes in Mental Status: Lethargy, drowsiness, confusion, irritability, or decreased level of consciousness are frequent (occurring in over 50% [7]), reflecting increased ICP, generalized inflammation, or direct involvement of specific brain regions. Progression to stupor or coma indicates severe disease and impending herniation.
• Focal Neurological Deficits: Develop in about 50-65% of patients and depend on the abscess location:
  • Temporal lobe: Seizures (common), contralateral upper quadrantanopia (visual field defect affecting Meyer's loop), aphasia (if dominant hemisphere - Wernicke's or receptive), memory impairment.
  • Frontal lobe: Hemiparesis, personality changes (apathy, disinhibition, poor judgment), executive dysfunction, expressive aphasia (if dominant hemisphere - Broca's).
  • Parietal lobe: Contralateral sensory loss, hemiparesis, visual field defects (contralateral lower quadrantanopia or hemianopia), spatial neglect (if non-dominant), apraxia, agnosia.
  • Occipital lobe: Contralateral homonymous hemianopia.
  • Cerebellum: Ipsilateral limb ataxia (difficulty with coordination, dysmetria, intention tremor), gait ataxia (wide-based, unsteady), nystagmus (involuntary eye movements, often gaze-evoked), dysarthria (slurred, scanning speech), truncal ataxia.
  • Brainstem: Cranial nerve palsies (multiple), hemiparesis/quadriparesis, altered consciousness, respiratory changes. Often rapidly progressive and high mortality.
• Seizures: Occur in 25-50 percent of cases [10], can be focal (simple or complex partial) or secondarily generalized tonic-clonic. New-onset seizure is a common presenting symptom.
• Papilledema: Swelling of the optic disc due to increased ICP, seen in about 25 percent of patients on funduscopic examination [3]. Usually a later sign.
• Meningismus: Neck stiffness and signs of meningeal irritation (Kernig's, Brudzinski's signs) may occur if the abscess is near the meninges or if there is associated meningitis or rupture into the subarachnoid space.

The clinical course of an otogenic or sinusogenic brain abscess is often described in stages, though these may overlap or be indistinct [11]:

1. Initial Stage (Early Cerebritis): Localized brain inflammation. Symptoms often subtle or non-specific: low-grade fever, malaise, headache, possibly related to the primary infection (e.g., otalgia, sinus pain). This stage frequently goes unrecognized or is masked by treatment of the primary infection.
2. Latent Stage: Abscess begins to organize and encapsulate. Symptoms may be minimal or absent, perhaps only intermittent, vague headaches. This stage can last weeks to months, leading to delayed diagnosis.
3. Manifest Stage (Late Cerebritis/Capsule Formation): Abscess enlarges, surrounding vasogenic edema increases, leading to significant mass effect and raised ICP. Symptoms become more pronounced: severe, persistent headache, nausea/vomiting, altered mental status (lethargy, confusion), and focal neurological deficits emerge corresponding to the abscess location.
4. Terminal Stage (Late Capsule/Impending Rupture/Herniation): If untreated, progressive neurological deterioration occurs due to severe ICP elevation leading to brain herniation syndromes (e.g., uncal, central, tonsillar) causing brainstem compression (leading to Cushing's triad - hypertension, bradycardia, irregular respirations; pupillary changes; coma; respiratory arrest). Alternatively, abscess rupture into the ventricles or subarachnoid space causes catastrophic ventriculitis or meningitis with rapid decline and high mortality.

General toxic symptoms like a cachectic appearance, weight loss, constipation, dry coated tongue, and poor appetite can be seen, particularly in later stages or with underlying chronic illness.

Laboratory findings in uncomplicated brain abscess often show an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), indicating inflammation but non-specifically. Leukocytosis (elevated white blood cell count) with a neutrophilic predominance (left shift) may be present but is not universal (found in ~60%). Body temperature is often normal or only slightly elevated once the abscess is well-encapsulated.

Headache, the most constant symptom, can be localized initially (e.g., temporal pain with temporal abscess, occipital/neck pain with cerebellar abscess) but often becomes diffuse and progressive as ICP increases.

Vomiting, especially projectile vomiting without preceding nausea, is particularly suggestive of increased ICP, common with posterior fossa lesions like cerebellar abscesses causing hydrocephalus.

Significant bradycardia (slow heart rate) can occur in the manifest stage as part of Cushing's response due to raised ICP affecting the brainstem.

Funduscopic changes (papilledema) are seen in about 25-50 percent of patients and usually indicate significant, sustained ICP elevation, typically appearing later in the course alongside other cerebral symptoms.

Meningeal signs (neck stiffness, Kernig's/Brudzinski's signs) may be present even without frank meningitis if the abscess irritates the nearby meninges or leaks inflammatory contents.

Lumbar puncture (LP) findings in uncomplicated abscesses might show elevated opening pressure, elevated protein, and sometimes a mild pleocytosis (increased cell count, often lymphocytes or mixed cells), but CSF glucose is typically normal. However, LP carries a significant risk of brain herniation if ICP is elevated (which is common) and is often contraindicated until mass effect is ruled out by imaging [12]. CSF cultures are usually negative unless the abscess has ruptured or there is concomitant meningitis.

Mental status changes like stupor, confusion, somnolence, and apathy are common in the manifest stage. Personality changes, intellectual decline, distractibility, and memory impairment can occur. Frank psychosis or systematized delusions are rare. Unmotivated euphoria or disinhibition might suggest frontal lobe involvement.

Specific focal signs relate to location. Left temporal lobe abscesses (in right-handed individuals) can cause sensory (Wernicke's) or amnestic aphasia (difficulty understanding or recalling words). Hemianopsia (visual field loss), often a contralateral superior quadrantanopia ("pie in the sky"), can result from involvement of optic radiations (Meyer's loop) but may be difficult to test reliably in acutely unwell patients.

Cerebellar abscesses often cause symptoms of cerebellar dysfunction: spontaneous nystagmus (often gaze-evoked, may be horizontal, vertical, or rotary; direction can vary but maybe more prominent beating away from the lesion side initially), ipsilateral limb ataxia (incoordination), dysmetria (past-pointing on finger-nose testing), adiadochokinesis (inability to perform rapid alternating movements), gait ataxia (wide-based, unsteady gait, difficulty with tandem walking), and falling towards the lesion side (especially noted in Romberg test or with gait). Dysarthria (slurred, explosive, scanning speech) may also occur. Muscle hypotonia on the side of the abscess can be present.

These cerebellar signs reflect dysfunction of the cerebellar hemisphere itself or its connections (e.g., cerebellar peduncles) with the brainstem.

Significant limb paresis is uncommon with isolated cerebellar abscesses but, if present, is usually ipsilateral and mild. Cranial nerve palsies (III, V, VI, VII - often peripheral type if involving brainstem nuclei or tracts) are more typical of complicated cerebellar abscesses involving the brainstem or causing significant posterior fossa mass effect.

Focal symptoms can be subtle or detected late, especially with abscesses in neurologically "silent" areas like the right (non-dominant) temporal lobe or non-dominant parietal/occipital lobes.

Symptoms resulting from pressure on distant brain structures (e.g., contralateral pyramidal tract signs causing hemiparesis/paralysis due to brainstem compression, sensory deficits, hyperreflexia) or from widespread edema/encephalitis are common. Jacksonian seizures (focal motor seizures starting in one area and spreading) can occur. Palsies of various cranial nerves (III, VI causing double vision due to raised ICP or direct compression; V causing facial numbness; VII central type causing contralateral lower facial weakness; XII causing tongue deviation) can result from direct compression or raised ICP.

The clinical course often involves an initial stage (early cerebritis) with non-specific symptoms (fever, headache) that is frequently missed or attributed to the primary infection. This may be followed by a latent phase of variable duration with minimal symptoms. The manifest stage typically heralds significant abscess growth or surrounding inflammation, leading to increased ICP and more obvious neurological signs. Unfortunately, progression to the terminal stage (due to herniation or rupture) can sometimes be rapid, with patients presenting in a critical state.

Rupture of the abscess into the ventricles (causing severe ventriculitis with high fever, meningismus, rapid decline in consciousness) or subarachnoid space (causing meningitis) is a catastrophic complication, often leading to rapid deterioration and death within hours if not treated aggressively.

 

Diagnosis of Brain and Cerebellar Abscesses

Diagnosing a brain abscess requires a high index of suspicion, especially in patients with known risk factors (e.g., chronic otitis/sinusitis, recent neurosurgery/trauma, endocarditis, congenital heart disease, immunocompromise) presenting with relevant symptoms (headache, fever, altered mental status, focal neurological deficit, seizure). The classic triad of headache, fever, and focal neurological deficit is present in less than 50 percent of patients. Diagnosis relies on a combination of clinical evaluation, laboratory tests, and crucially, neuroimaging.

Differential Diagnosis of Intracranial Ring-Enhancing Lesions

 

Neuroimaging, particularly Magnetic Resonance Imaging (MRI) with contrast and Diffusion-Weighted Imaging (DWI), is essential when a brain abscess is suspected based on clinical presentation, playing a key role in diagnosis and differentiation from other pathologies.

Key diagnostic steps include:

• Clinical History and Neurological Examination: Detailed history focusing on potential sources of infection (otitis, sinusitis, dental work, lung infection, endocarditis risk factors, trauma, surgery, IV drug use, immune status), symptom onset and progression. Comprehensive neurological exam to identify focal deficits, signs of increased ICP (papilledema), and meningismus.
• Neuroimaging:
  • MRI with Gadolinium Contrast: The imaging modality of choice [2]. MRI offers superior detail of the abscess structure, capsule, central contents, and surrounding brain tissue. Typical findings of a mature bacterial abscess include:
    • Central necrotic core: Appears hypointense (dark) on T1-weighted images, hyperintense (bright) on T2-weighted and FLAIR images.
    • Capsule: A distinct, typically smooth, thin rim that enhances brightly and uniformly after gadolinium administration on T1-weighted images (ring enhancement). The capsule is often notably hypointense (dark) on T2-weighted images, especially the inner layer.
    • Surrounding Edema: Extensive vasogenic edema appearing hyperintense (bright) on T2-weighted and FLAIR images in the adjacent white matter.
    • Diffusion-Weighted Imaging (DWI): Shows markedly restricted diffusion (bright signal) within the abscess cavity (due to viscous pus), with corresponding low signal on Apparent Diffusion Coefficient (ADC) maps. This is a key feature helping differentiate pyogenic abscess from most cystic or necrotic tumors [13].
    • Magnetic Resonance Spectroscopy (MRS): May show elevated peaks for lactate, lipids, and amino acids (succinate, acetate, alanine) within the cavity, with reduced N-acetylaspartate (NAA) and creatine (Cr) [14].
  • CT Scan with Contrast: Often the initial imaging study in emergency settings due to speed and availability. Can detect abscesses > 1cm, especially encapsulated ones, showing a hypodense (dark) center, a ring of contrast enhancement (often thinner medially), and surrounding hypodense edema. CT is excellent for detecting associated bone erosion (from otitis/sinusitis), calcification, gas within the abscess (rare), or skull fractures but is less sensitive than MRI for early cerebritis, smaller lesions, and satellite lesions.
• Laboratory Tests:
  • Blood Tests: Complete blood count (CBC) may show leukocytosis (~60%) or be normal. Inflammatory markers like Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP) are usually elevated but non-specific. Blood cultures should be drawn (ideally before antibiotics), especially if fever is present, to identify potential hematogenous sources (positive in about 10-35 percent of cases [3]). Specific tests based on suspected source (e.g., HIV test, tests for endocarditis).
  • Lumbar Puncture (LP): Generally contraindicated if an abscess (a mass lesion) is strongly suspected or confirmed on imaging, or if there are clinical/imaging signs of significantly increased ICP (papilledema, altered consciousness, midline shift, effaced cisterns), due to the high risk of precipitating fatal brain herniation [15]. If performed cautiously (e.g., to rule out primary meningitis when imaging is non-diagnostic and ICP deemed safe), CSF may show elevated opening pressure, elevated protein, pleocytosis (variable cell type, often neutrophils early or lymphocytes later), and normal or slightly low glucose. CSF cultures are usually negative unless the abscess has ruptured or there is concomitant meningitis.
• Microbiological Diagnosis: Definitive etiological diagnosis requires identifying the causative organism(s). This is typically achieved by:
  • Stereotactic Aspiration or Surgical Excision/Drainage: Obtaining pus or capsule tissue samples from the abscess under sterile conditions for Gram stain, aerobic and anaerobic bacterial cultures (crucial), fungal stains (GMS, PAS) and cultures, AFB stains and cultures (if TB suspected), and potentially specific stains (e.g., for Nocardia) or PCR for organisms like Toxoplasma or bacteria if cultures are negative.
• Source Identification: Investigation for the primary source is crucial for guiding antimicrobial therapy and preventing recurrence. This may involve CT of sinuses/temporal bones, dental evaluation/imaging, echocardiogram (TTE/TEE) for endocarditis, chest X-ray/CT for pulmonary sources.

In challenging cases, particularly otogenic abscesses masked by complicated meningitis or sepsis, diagnosis can be difficult. If focal symptoms are present despite treated meningitis, abscess should be suspected. During surgery for the primary otogenic focus (e.g., mastoidectomy), finding specific dural changes (granulations, discoloration, perforation) or a fistula leading towards the brain can strongly suggest an adjacent abscess, prompting diagnostic brain puncture or further imaging/neurosurgical consultation if safe and appropriate.

Occult ('cold') or chronic encapsulated abscesses without significant mass effect may present subtly with seizures or personality change. Advanced MRI sequences (DWI, MRS, perfusion) can be particularly helpful in differentiating abscess from tumor in ambiguous ring-enhancing lesions.

Brain Abscess Stages (Imaging Evolution)

Brain abscess development typically proceeds through distinct pathological and corresponding imaging stages [16]:

Stage (Approx. Timeline)	Pathology Highlights	CT and MRI Findings	Consistency (Aspiration)
I – Early Cerebritis (Days 1-5)	Localized perivascular inflammation, edema, microglial activation, early neutrophil infiltration. Poorly demarcated.	CT: Ill-defined area of low density, minimal or patchy/nodular contrast enhancement. MRI: Poorly defined T1 hypointensity / T2 & FLAIR hyperintensity. Enhancement variable, often faint/patchy. DWI may show early peripheral or central restriction.	Soft/inflamed tissue (not drainable pus)
II – Late Cerebritis (Days 5-14)	Intense inflammation, central necrosis begins due to bacterial toxins/hypoxia, surrounded by inflammatory cells (macros, lymphocytes), edema peaks. Early granulation tissue at periphery.	CT: Central low density, developing peripheral ring enhancement (often thick, irregular). MRI: Central T1 hypo/T2 hyperintensity, marked surrounding T2/FLAIR edema. Ring enhancement becomes more defined. Central DWI shows prominent restriction (bright DWI, dark ADC).	Necrotic/liquefying center (may be partially drainable)
III – Early Capsule (Weeks 2-4)	Central necrotic pus enlarges. Fibroblast proliferation forms a distinct collagen capsule, more developed on cortical side. Neovascularity prominent in capsule. Surrounding inflammation/edema start to decrease.	CT: Well-defined ring enhancement, often thinner and smoother medially (towards ventricle) than laterally. MRI: Ring enhancement prominent, usually smooth and relatively thin. Capsule itself appears iso- to hypointense on T2. Maximal central DWI restriction. Edema starts to recede.	Liquid pus within distinct capsule (drainable)
IV – Late Capsule (Weeks > 4)	Thick, well-formed, dense collagen capsule, surrounding reactive gliosis (scarring). Inflammation and edema significantly reduced. Abscess may shrink.	CT: Ring enhancement may decrease, persist, or become thicker. Central density may increase. MRI: Thick capsule (often markedly hypointense on T2), reduced edema. Ring enhancement persists but may lessen. Central DWI restriction may decrease as inflammation subsides and pus becomes less viscous.	Thick pus, firm capsule (may be harder to aspirate)

 

Treatment and Prevention of Brain and Cerebellar Abscesses

Management of brain abscesses is a neurological emergency requiring a prompt, combined medical and often surgical approach. Goals are to eradicate the infection, reduce mass effect and manage intracranial pressure (ICP), identify and treat the primary source, and prevent neurological sequelae.

Treatment strategies include:

• Antimicrobial Therapy:
  • Empirical Therapy: Broad-spectrum intravenous (IV) antibiotics should be started immediately upon suspicion, *after* obtaining blood cultures if possible, but without delaying treatment. The initial regimen depends on the likely source, patient's immune status, and local resistance patterns. Common empirical regimens might include a third-generation cephalosporin (e.g., ceftriaxone or cefotaxime) PLUS metronidazole (excellent anaerobic coverage and CNS penetration). Vancomycin should be added if Staphylococcus aureus (especially MRSA) is suspected (e.g., post-trauma, post-surgery, IV drug use, endocarditis). In severely immunocompromised patients, broader coverage including antifungals or specific agents (e.g., for Nocardia) may be needed.
  • Targeted Therapy: Once causative organisms are identified from abscess aspirate/tissue or blood cultures, antibiotic therapy should be narrowed based on susceptibility testing.
  • Duration: Prolonged IV antibiotic therapy is required, typically for 4-8 weeks, or sometimes longer, guided by clinical response and serial neuroimaging (resolution of enhancement and edema). Transition to oral antibiotics may be possible later in stable patients with susceptible organisms and good oral bioavailability, but total duration remains extended [17].
• Surgical Intervention [18]: Most bacterial brain abscesses, particularly those > 2.0-2.5 cm, significantly symptomatic, causing substantial mass effect, or not responding adequately to antibiotics, require surgical drainage or excision. The choice depends on abscess characteristics, location, and patient condition:
  • Stereotactic Aspiration: Minimally invasive image-guided (CT or MRI) needle aspiration to obtain diagnostic material (culture/stains) and decompress the abscess cavity. May require repeat aspirations if pus reaccumulates. Preferred for deep-seated lesions (e.g., thalamus, basal ganglia), multiple abscesses, surgically risky locations (eloquent cortex), or in patients unfit for open surgery. Can also be used in the late cerebritis stage.
  • Craniotomy with Excision: Open surgical removal ("enucleation") of the abscess, including its capsule. Offers potential for complete removal and definitive histology. Preferred for solitary, superficial, well-encapsulated abscesses, multiloculated abscesses, fungal abscesses, post-traumatic abscesses (may contain foreign bodies), or those failing aspiration. Allows better debridement but is more invasive.
  • Burr Hole Drainage: Simple drainage via a burr hole, similar to aspiration but less precise targeting. May involve placing a drain temporarily. Less common now with stereotaxy available.
  Medical management alone (antibiotics without surgery) may be considered only in very select cases: multiple, small abscesses (< 2.0-2.5 cm), early cerebritis stage without significant mass effect, lesions in surgically inaccessible/high-risk locations, or patients too unstable for surgery, provided a microbiological diagnosis is established (e.g., from blood culture) or strongly suspected and there is rapid clinical/radiological improvement with close monitoring. Failure to improve promptly necessitates surgical intervention.
• Management of Increased Intracranial Pressure (ICP): Standard ICP management techniques may be needed in patients with significant mass effect or hydrocephalus. This includes head elevation (30 degrees), osmotic therapy (mannitol, hypertonic saline), temporary controlled hyperventilation (in emergencies), and potentially sedation.
• Corticosteroids: Dexamethasone may be used short-term (typically only for a few days) to reduce vasogenic edema and mass effect in patients with significant neurological compromise or impending herniation. However, steroid use is controversial as it can reduce antibiotic penetration into the abscess, potentially delay capsule formation (making aspiration harder), mask clinical signs of infection, and increase risk of fungal infection. Steroids should generally be avoided or used judiciously (lowest effective dose, shortest duration) and tapered quickly once neurological status stabilizes [19]. They do not treat the infection itself.
• Seizure Management: Antiepileptic drugs (AEDs) are often administered prophylactically in the acute phase (especially for supratentorial abscesses) due to high seizure risk (up to 70% risk), and continued if seizures occur. The optimal duration of prophylaxis is debated, but AEDs are usually continued long-term if seizures have occurred [20].
• Treatment of Primary Source: Eradicating the initial source of infection (e.g., surgical drainage of sinusitis, mastoidectomy for chronic otitis, dental extraction/treatment, treatment of endocarditis, removal of infected hardware) is essential to prevent recurrence and improve outcomes. This often requires a multidisciplinary approach (e.g., neurosurgery, otolaryngology, infectious disease, cardiology, dental surgery).

Specific surgical considerations for otogenic abscesses: If suspected, surgery on the temporal bone (e.g., radical or modified radical mastoidectomy) is usually performed first or concurrently to control the source. During this surgery, the dura overlying the temporal lobe (tegmen tympani) or cerebellum (posterior fossa plate) is carefully inspected. If pathology (granulations, defect, pus) is found or clinical suspicion is high, brain puncture/aspiration or direct drainage via the otologic approach may be performed by the otologist or in conjunction with a neurosurgeon. Alternatively, a separate neurosurgical approach (e.g., temporal or suboccipital craniotomy) may be preferred for abscess drainage/excision, particularly if the abscess is large, deep, or requires complete removal. Coordination between otolaryngology and neurosurgery teams is often critical.

Postoperatively, meticulous care includes continued targeted IV antibiotic therapy, management of potential complications (e.g., hydrocephalus, seizures, electrolyte imbalance), nutritional support, DVT prophylaxis, and close monitoring of neurological status. Repeat imaging (MRI or CT) is essential to assess treatment response (decrease in size, enhancement, edema) and guide duration of therapy.

Prevention focuses on:

• Prompt and effective antibiotic treatment of primary bacterial infections like otitis media, sinusitis, dental infections, and pneumonia.
• Surgical management of chronic infections (e.g., chronic sinusitis, chronic otitis media with cholesteatoma).
• Appropriate management of penetrating head trauma (debridement, closure, prophylactic antibiotics).
• Adherence to strict sterile techniques during neurosurgical procedures and appropriate use of perioperative antibiotics.
• Endocarditis prophylaxis in high-risk patients undergoing certain procedures (following current AHA/ESC guidelines).
• Management of underlying conditions, especially immunocompromise and congenital heart disease.

Potential Complications:

• Rupture into ventricles (ventriculitis) or subarachnoid space (meningitis) - often fatal or causing severe disability.
• Persistent seizures / Epilepsy (occurs in 30-60% long-term after supratentorial abscess).
• Hydrocephalus (requiring shunting).
• Permanent neurological deficits (motor weakness, sensory loss, cognitive impairment, visual field defects, aphasia, ataxia).
• Cranial nerve palsies.
• Recurrence of abscess (especially if source not treated or antibiotics inadequate).
• Death (mortality rates are around 5-15 percent with modern treatment in developed countries [3], but significantly higher with delayed diagnosis, abscess rupture, multiple abscesses, fungal etiology, severe neurological deficit on admission, or in immunocompromised patients).

Prognosis:

• Outcome depends heavily on the patient's neurological condition at diagnosis (level of consciousness/GCS score is a major predictor), abscess size and location, causative organism and its susceptibility, presence of complications (like rupture), patient's age and immune status, and the promptness and appropriateness of combined medical and surgical treatment.
• Significant improvements in survival have occurred over decades due to advances in neuroimaging (allowing earlier diagnosis), stereotactic surgical techniques, critical care, and more effective antibiotics.
• However, long-term neurological sequelae, particularly epilepsy and cognitive deficits, remain common challenges for survivors. Rehabilitation (physical, occupational, speech, cognitive) is often necessary.

Attention! Brain abscess is a medical emergency. Symptoms like severe headache, fever, confusion, seizures, or new neurological weakness/numbness, especially in someone with a recent infection, head trauma, or surgery, require immediate evaluation in an emergency department. Prompt diagnosis and treatment are critical to survival and minimizing long-term disability. Never attempt self-diagnosis or delay seeking expert medical care.

References

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2. Osborn AG, Hedlund GL, Salzman KL. Osborn's Brain. 2nd ed. Elsevier; 2018.
3. Brouwer MC, van de Beek D. Brain abscess. N Engl J Med. 2014;371(5):447-56. doi: 10.1056/NEJMra1301635
4. Corsonello A, Settembrini F, Garasto S, et al. Brain Abscess in Elderly Patients. Clin Interv Aging. 2020;15:1303-1309. doi: 10.2147/CIA.S259751
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