A 28-year-old man, with insidious and progressive onset of semantic and phonemic aphasia, associated with evolving numbness and loss of sensation over weeks. Magnetic resonance imaging (MRI) revealed T2-hyperintense expansive lesions, heterogeneous contrast enhancement, and no diffusion restriction in subcortical regions on the left parietal and temporal lobes, right superior parietal lobe, post-central gyrus and splenium of corpus callosum, with perilesional edema and hemorrhagic foci. Steroid and cyclophosphamide pulses were introduced and stabilized the clinical symptoms.One month later, a new MRI (Fig 1) showed improvement of the expansive effect, edema and enhancement of the lesions. Magnetic resonance angiography (MRA) and digital subtraction angiography (DSA) presented only a subtle enhancement in the capillary-venous phase in the left frontal and parietal lobes. The brain biopsy was performed and revealed postischemic necrosis associated with nonspecific perivascular lymphomonocytic infiltrate with predominance of T lymphocytes without atypias. Immunohistochemistry showed small numbers of mature perivascular lymphocytes, CD20+, CD3+ and CD68+ cells, which are compatible with lymphocytic vasculitis. Clinical and pathological picture was compatible with primary lymphocytic angiitis of the central nervous system (PLACNS).Corticosteroid (1 g/day) and cyclophosphamide (1 g/day) pulse therapy was introduced for three days and repeated monthly during three months. Prednisone (20 mg/day) was introduced as maintenance therapy, and resulting in improved clinical outcomes and MRI imaging. In the fifth month, the patient presented worsening of the sensitive symptoms and developed new MRI lesions (Fig 2).New corticosteroid and cyclophosphamide pulse therapy was introduced for three months, resulting in almost complete resolution of the symptoms and improvement of MRI findings. Prednisone 40 mg/day was introduced, but no improvement in the MRI was observed. Later, azatioprine (50 mg/day) was associated with the therapy. A oneyear follow-up MRI showed significant improvement of the lesions (Fig 3).
A MRI of a 59-year-old male with right hemifacial hypoesthesia showed a low signal T2-weighted expansive mass in the right Meckel's cave. After failure of initial conservative treatment (Figure 1), surgery was done with partial lesion resection (Figure 2). The pathology and chest CT were consistent with granulomatous disease: neurosarcoidosis. On follow-up the lesion increased in size but after corticosteroids it reversed (Figure 3). The involvement of the trigeminal nerve is very rare with only few cases described in literature. Although rare, sarcoid infiltration of the Gasserian ganglion must be considered in the differential diagnosis of an isolated mass at Meckel's cave, especially if it has T2 hypointensity signal.
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