Intracranial Pathology: Brain Tumors, ICP, and Abscess Management
Increased Intracranial Pressure (ICP)
The skull is a rigid compartment. Any added volume (tumor, blood, edema, or CSF) raises the Intracranial Pressure (ICP). ICP is considered elevated when it is greater than 20 mmHg (normal is typically less than 15 mmHg).
The relationship between ICP and Cerebral Perfusion Pressure (CPP) is critical: CPP = MAP − ICP. A rising ICP reduces CPP, leading to cerebral ischemia.
Causes of Elevated ICP
- Intracranial mass (tumor, hematoma, large infarct)
- Cerebral edema
- Hydrocephalus or CSF obstruction
- Venous sinus thrombosis
- Infection or trauma
- Toxic or idiopathic intracranial hypertension
Pathogenesis of ICP Rise
Early compensation occurs via displacement of venous blood and CSF (approximately 40 mL in young adults, up to 80 mL in the elderly). Decompensation leads to:
- Increased ICP (↑ ICP)
- Decreased CPP (↓ CPP)
- Ischemia
- Herniation
Clinical Features of Raised ICP
General Symptoms:
- Morning headache
- Nausea and vomiting
- Hiccups
- Progressive decrease in consciousness
- Chronic apathy
Ocular Signs:
- Papilledema
- Enlarged blind spot
- Transient visual loss
- Cranial Nerve (CN) VI palsy (sometimes CN III palsy)
Impending Herniation (Severe Signs):
- Coma
- Abnormal respiration
- Cushing Triad (hypertension, bradycardia, irregular respiration)
- Dilated pupils
- Extensor posturing
Types of Brain Herniation
- Subfalcine: Compression of the Anterior Cerebral Artery (ACA) leading to leg weakness.
- Uncal: Cranial Nerve III palsy and dilated pupil.
- Central: Decreased consciousness and posturing.
- Tonsillar: Medullary compression, resulting in respiratory and cardiac failure.
Diagnosis and Management of ICP
Diagnosis:
CT or MRI should be performed first. Lumbar Puncture (LP) is contraindicated if increased ICP is suspected. Ventricular ICP monitoring is considered the gold standard.
Treatment Strategies:
- Head elevation and optimization of oxygenation.
- Maintenance of normoglycemia and normothermia.
- Osmotic therapy: Mannitol or hypertonic saline.
- Sedation and short-term hyperventilation.
- Steroids for vasogenic edema.
- External Ventricular Drain (EVD) for hydrocephalus.
- Decompressive craniectomy in selected cases.
Brain Tumors: Classification and Management
Brain tumors are classified as either primary (originating in the CNS) or secondary (metastatic, which are most common).
WHO Classification of Primary Brain Tumors
Neuroepithelial tumors are the most common type.
Astrocytomas (Graded I–IV):
- Grade I: Pilocytic Astrocytoma
- Benign, common in children.
- Location: Cerebellum/posterior fossa.
- Often curable by resection.
- Grade II: Diffuse Astrocytoma
- Young adults, infiltrative.
- Location: Frontal/temporal lobes.
- Risk of malignant transformation.
- Grade III: Anaplastic Astrocytoma
- Malignant, significant mass effect.
- Grade IV: Glioblastoma (GBM)
- Most malignant form (age 50–70).
- Characterized by necrosis and microvascular proliferation.
- Typically presents as a ring-enhancing lesion on imaging.
Other Neuroepithelial Tumors:
- Oligodendroglioma: Occurs in adults (40–50), often in the frontal lobes. Seizures are common, and calcifications are frequent.
- Ependymoma: Arises from the ventricular lining in children. Causes obstructive hydrocephalus, often located in the posterior fossa.
- Medulloblastoma (PNET): Affects children, highly malignant (Grade IV). Located in the roof of the 4th ventricle, characterized by rapid growth and early raised ICP.
Non-Neuroepithelial Tumors
- Meningioma: Benign, dural-based tumor, common in middle age. Associated with seizures and late rise in ICP.
- Schwannoma (Acoustic Neuroma): Involves Cranial Nerve VIII, causing hearing loss, tinnitus, and vertigo (located in the posterior fossa/Cerebellopontine Angle – CPA).
- Primary CNS Lymphoma: Often EBV-associated and periventricular.
Metastatic Brain Tumors
Metastases account for approximately 15% of brain tumors. Primary sources, in order of frequency, include:
- Lung cancer (most common)
- Breast cancer
- Melanoma
- Renal Cell Carcinoma (RCC)
Metastatic lesions often present with marked surrounding edema.
Clinical Patterns and Presentation
- Malignant Tumors: Cause early raised ICP, focal neurological deficits, severe edema, and a higher risk of herniation.
- Benign Tumors: Typically cause a late rise in ICP with mild edema.
Posterior Fossa Tumors (e.g., medulloblastoma, meningioma, pilocytic astrocytoma, ependymoma) often present with cerebellar signs:
- Truncal ataxia and dysmetria
- Visual blurring
- Cranial Nerve III, IV, VI, or VIII dysfunction
- Tinnitus, hearing loss, and imbalance
Diagnosis and Treatment of Brain Tumors
Diagnosis:
- MRI with contrast is the gold standard.
- CT is useful for detecting calcifications, bone involvement, and in emergency settings.
- Histology is mandatory (obtained via surgical resection or stereotactic biopsy).
- CSF analysis is usually not helpful, except in cases of leptomeningeal spread or selected lymphomas.
Treatment:
- Maximal safe surgical resection.
- Radiotherapy for malignant or residual disease.
- Chemotherapy (tumor-dependent).
- Dexamethasone for managing edema.
- Antiepileptics for seizure control.
Brain Abscess: Etiology and Treatment
A brain abscess is a focal intracerebral infection characterized by tissue necrosis and pus formation within the brain parenchyma. Abscesses may be solitary or multiple.
Etiology and Risk Factors
The most common causative organisms are Streptococci and Staphylococci. The risk is significantly increased in immunocompromised patients.
Routes of Infection:
- Contiguous Spread: From adjacent infections (e.g., otitis media, mastoiditis, sinusitis).
- Hematogenous Spread: Via the bloodstream (e.g., lung infections, endocarditis, sepsis).
- Direct Inoculation: Following open head injury or neurosurgery.
Pathogenesis (Abscess Development Timeline)
- Early Cerebritis (Days 1–3): Localized inflammation, edema, vascular congestion, and neutrophil infiltration. No capsule formation yet.
- Late Cerebritis (Days 4–9): Tissue necrosis, pus accumulation, central liquefaction, and increasing perifocal edema.
- Capsule Formation (Days 10–14): Development of a fibroblastic collagen capsule with surrounding gliosis, leading to significant mass effect.
- Mature Abscess (>2 Weeks): Well-formed capsule, necrotic purulent center, and marked edema, resulting in raised ICP and focal deficits.
A special form, focal encephalitis (cerebritis), represents the early stage of an abscess and may be multifocal due to septic or embolic spread.
Clinical Features and Diagnosis
Clinical Presentation:
Symptoms often include signs of raised ICP (headache, vomiting, papilledema, impaired consciousness), focal neurological deficits, and seizures. Fever and leukocytosis may or may not be present. Marked perifocal edema contributes significantly to the mass effect.
Diagnosis:
- Laboratory tests may show elevated CRP and ESR.
- CSF analysis is usually avoided due to the risk associated with raised ICP.
- CT/MRI: Typically shows a ring-enhancing lesion with a hypodense center and surrounding edema. Early cerebritis may show diffuse enhancement.
Complications and Treatment
Complications:
Potential complications include subdural empyema, epidural abscess, and rapid, life-threatening progression.
Treatment:
- Neurosurgical Drainage: Preferred method, combined with prolonged antibiotic therapy.
- Antibiotics Alone: Used if the abscess is small (less than 3 cm) or if the condition is still in the early cerebritis stage.
- Antibiotic Regimen: Typically prolonged (≥6 weeks) and includes a 3rd-generation cephalosporin, metronidazole, and an anti-staphylococcal agent.
- Adjunctive Therapy: Corticosteroids are used for managing significant edema.
- It is crucial to always identify and treat the primary source of infection.