Granuloma

A granuloma is an organised collection of macrophages (often epithelioid and multinucleated giant cells) that forms around a persistent antigen. Intracranial granulomas arise from infection (tuberculosis, fungi such as Aspergillus and Cryptococcus, parasites), from systemic inflammatory disease (sarcoidosis, granulomatosis with polyangiitis, IgG4-related disease) or as a reaction to foreign material. They may involve the dura and skull base (pachymeningitis), the leptomeninges, the pituitary stalk and hypothalamus, cranial nerves or the brain parenchyma, and they closely mimic meningioma, lymphoma, metastasis and glioma.

Cholesterol granuloma of the petrous apex is a separate entity: an expansile cyst caused by repeated haemorrhage into obstructed, pneumatised petrous air cells, with a foreign-body reaction to cholesterol crystals^[1].

Symptoms depend on location: headache and cranial neuropathies with pachymeningitis, seizures or focal deficits with parenchymal lesions, and diabetes insipidus or hypopituitarism with hypothalamic–pituitary involvement. Systemic features (fever, weight loss, pulmonary or sinonasal disease, uveitis, renal involvement) point toward the cause. Petrous-apex cholesterol granulomas cause headache, hearing loss, tinnitus, and abducens or facial palsy.

Tuberculomas are typically ring- or nodular-enhancing lesions, often multiple, with a T2-hypointense centre; basal meningeal enhancement and hydrocephalus suggest tuberculous meningitis. Neurosarcoidosis shows leptomeningeal or dural enhancement, often along the basal meninges and the hypothalamic–pituitary axis. Cholesterol granulomas are expansile petrous-apex lesions that are bright on both T1 and T2 MRI and do not suppress with fat saturation, distinguishing them from trapped fluid, mucocoeles and cholesteatoma.

Work-up includes chest imaging, serum markers (ACE, ANCA), interferon-gamma release assays, CSF analysis and a search for an accessible extracranial site to biopsy. The consensus criteria for neurosarcoidosis grade diagnostic certainty as definite (nervous-system histology), probable (extraneural histology) or possible, which helps decide whether intracranial biopsy is needed^[2].

• Diagnostic biopsy (stereotactic, endoscopic or open) when the diagnosis cannot be made from an extraneural site or from CSF; send tissue for histology, mycobacterial and fungal culture, and molecular testing.
• Resection or decompression for lesions causing significant mass effect, raised pressure or failure of medical therapy.
• CSF diversion for hydrocephalus.
• Drainage of petrous-apex cholesterol granulomas, by an endoscopic endonasal route when the lesion abuts the sphenoid sinus, or by an infracochlear or infralabyrinthine transtemporal route, with a stent or wide marsupialisation to keep the cavity aerated^[1].

Infectious granulomas are treated with targeted antimicrobial therapy, often for many months; tuberculomas may paradoxically enlarge early in treatment. Inflammatory disease is treated with corticosteroids and steroid-sparing immunosuppression or biological agents. Outcome depends on the cause and the extent of irreversible neurological injury at diagnosis. Cholesterol granulomas can recur if the drainage pathway closes.