What is the diagnosis and management approach for a patient presenting with symptoms suggestive of a space-occupying lesion in the brain, such as headache, nausea, vomiting, seizures, or focal neurological deficits?

Space-Occupying Brain Lesions: Diagnostic and Management Overview

Initial Clinical Assessment

Obtain a rapid focused history and neurological examination to identify the pattern of presentation, as the clinical syndrome often suggests the underlying pathology and guides urgent management decisions. 1

Key Clinical Presentations by Etiology

Ischemic stroke with mass effect presents with sudden onset of severe neurological deficits including contralateral hemiplegia, sensory hemisyndrome, conjugate eye deviation, nausea, vomiting, and homonymous hemianopia, with progressive headache and impaired consciousness developing 12-72 hours after onset 1. Left MCA territory involvement typically causes aphasia, while right-sided lesions produce hemineglect 1.

Space-occupying cerebellar infarction manifests with progressive impairment of consciousness, diplopia, cranial nerve palsies, progressive ataxia, pyramidal signs (from brainstem compression), nausea, vomiting, and headaches 1, 2. Late signs of impending brainstem compression include hypertension, bradycardia, and progressive reduction of consciousness, which appear immediately before herniation and can lead to sudden respiratory arrest 1, 2.

Subarachnoid hemorrhage presents with "the worst headache of my life" in 80% of awake patients, often associated with nausea/vomiting (77%), loss of consciousness (53%), and nuchal rigidity (35%) 1. Warning or sentinel headaches occur in 20% of patients, typically 2-8 weeks before major rupture 1.

Brain tumors and abscesses in adults typically present with headache (74%), nausea/vomiting, and focal neurological deficits 1. In toddlers, vomiting (53%), behavioral changes (40%), motor weakness (47%), and ataxia (33%) are most common, with 92% having abnormal neurological signs on initial examination 3.

CNS parasitic infections causing space-occupying lesions present with seizures, headache, nausea, vomiting, and focal neurological deficits, typically without fever 1. Neurocysticercosis has an average incubation of 3.5 years and may exceed 10 years 1.

Immediate Diagnostic Imaging

Perform non-contrast head CT as the first-line neuroimaging test in all patients with suspected space-occupying lesions, as it can be done rapidly and safely to detect hemorrhage, mass effect, and hydrocephalus. 1

CT Head Without Contrast

• Mandatory for all patients unless the etiology is clear and risk of intracranial pathology is low 1
• Detects acute contributory findings in 2-45% of patients with altered mental status, depending on risk factors 1
• High-risk features requiring CT include: history of trauma/falls, hypertension, anticoagulant use, headache, nausea/vomiting, older age, impaired consciousness, neurological deficit, and history of malignancy 1
• Sensitivity is proportional to clinical grade and time from hemorrhage onset 1

Advanced MRI Imaging

Follow initial CT with MRI brain with and without IV contrast when intracranial infection, tumor, inflammatory lesions, or vascular pathologies are suspected, as MRI provides superior tissue characterization. 1, 4

• Diffusion-weighted imaging (DWI) detects inflammatory processes in necrotic ring-enhancing lesions and helps distinguish metastases from glioblastomas based on peritumoral characteristics 4
• Perfusion-weighted imaging (PWI) and MR spectroscopy (MRS) differentiate low-grade gliomas from malignant tumors (WHO grade III-IV gliomas and lymphomas) 4
• MRS showing reduced NAA/Cr, Cho/Cr, and NAA/Cho ratios suggests gliosis rather than neoplasm 5
• MRI is more sensitive than CT for detecting small brainstem infarcts 6

Risk Stratification for Malignant Cerebral Edema

MCA Territory Infarction Predictors

Clinical predictors:

• NIHSS ≥20 for left MCA territory 1
• NIHSS ≥15 for right MCA territory 1
• Nausea/vomiting 1

Radiological predictors:

• Hypodensity >50% of MCA territory on initial CT 1
• Involvement of additional vascular territories 1
• Early and large abnormalities on DWI 1

Cerebellar Infarction Predictors

Clinical predictors:

• Impairment of consciousness 1, 2

Radiological predictors:

• Hypodensity >2/3 of cerebellar hemisphere 1, 2
• Compression/displacement of 4th ventricle 1, 2
• Obstructive hydrocephalus 1, 2
• Displacement of brainstem 1, 2
• Compression of basal cisternae 1, 2
• Hemorrhagic transformation 1

Urgent Management Algorithm

Immediate Measures on Admission

All patients with at least one risk factor for space-occupying brain edema must be evaluated immediately in a stroke unit by both a neurologist and neurosurgeon, with a precise management plan defined as soon as possible, as delayed intervention causes additional irreversible brain damage. 1, 2

• Involve intensive care specialist in risk assessment of conservative versus surgical management 1
• Close neurological monitoring in intermediate or intensive care stroke unit for up to 5 days, even if initially stable 2
• Monitor level of arousal and pupillary function frequently to detect deterioration from cerebral swelling 6, 7

Medical Management

For increased intracranial pressure:

• Mannitol 2g every 12 hours for 2 days 5, 8
• Dexamethasone 8mg every 12 hours 5
• Osmotic therapy is reasonable for clinical deterioration but not for routine prophylaxis 7

For parasitic CNS infections with space-occupying lesions:

• Neurocysticercosis: Dexamethasone starting one day before praziquantel, with praziquantel dosing per expert consultation 1
• Schistosomiasis with CNS involvement: Corticosteroids (60mg prednisolone daily for 14 days then wean) +/- albendazole 15mg/kg/day for 14 days 1
• Exclude strongyloidiasis before steroid use 1
• Ivermectin has no role in CNS infections due to insufficient CSF concentrations 1

Surgical Intervention

Surgical decompression is necessary when significant mass effect causes brainstem compression or obstructive hydrocephalus. 2

• Advanced brainstem dysfunction (e.g., locked-in syndrome) is the only known predictor of unfavorable outcome in cerebellar infarctions 1, 2
• Delayed intervention >24 hours after symptom onset may predict unfavorable outcome, though this is not independent of GCS <8 or pupillary dilation 1
• Dominant hemisphere involvement requires preoperative discussion about persistent speech disorders 1

Tissue Diagnosis When Etiology Unclear

Stereotactic biopsy under local anesthesia is the reliable method to obtain histopathological diagnosis of deep-seated or functionally located intracranial mass lesions. 9

• Overall positive diagnostic rate of 96.6% 9
• Brain tumor diagnosis rate of 86.4% 9
• Complication rates: intracranial hematoma 2.4%, seizures 1.2%, transient neurological deficits 4.2%, no deaths 9
• Helps select appropriate definitive management 9

Critical Pitfalls to Avoid

• Do not delay imaging in patients with altered mental status and risk factors, as 7.4% of patients without focal deficits have acute changes on CT 1
• Do not miss sentinel hemorrhage from aneurysmal SAH, as diagnosis before catastrophic rupture is lifesaving; misdiagnosis occurs in 12% of cases and increases mortality/disability 4-fold 1
• Do not wait for late signs of brainstem compression in cerebellar infarction (hypertension, bradycardia), as these appear immediately before herniation and respiratory arrest 1, 2
• Do not assume cerebellar lesions cause contralateral weakness; they cause ipsilateral ataxia, with contralateral weakness only occurring from brainstem compression 7
• Do not use contrast-enhanced CT as first-line in acute setting, as it adds no significant value over non-contrast CT 1