Rationale: Primary central nervous system (CNS) posttransplant lymphoproliferative disease (PTLD) is a very rare entity. Patients may respond to reduction of immunosuppression or other therapies, but the prognosis is still pessimistic. Patient concerns: Herein, we report a 40-year-old female with a history of renal transplantation developed brain masses 4 years ago. Although brain biopsy was performed, PTLD was underdiagnosed then. No relevant treatment was administered. However, the lesions resolved spontaneously. After 4 years, new lesion appeared in a different brain region. Diagnoses: The history of renal transplantation raised the suspicion of PTLD. Reexamination of previous brain sections confirmed the diagnosis of polymorphic PTLD (P-PTLD). A second biopsy of the new lesion also demonstrated P-PTLD. Interventions: She was referred to hematology department to receive rituximab. Outcomes: After 4 rounds of treatment, the lesion resolved satisfactorily. Lessons: This case demonstrates the natural history of primary CNS P-PTLD. Although self-remission and recurrence is possible, aggressive measures should be taken to this condition.
Background Lymphoplasmacyte-rich meningioma (LPRM) is a rare form of meningioma characterized by prominent lymphoplasmacytic infiltrates into the tumor. Report of flat growth of LPRM mimicking pachymeningitis is rare in the literature. Case presentation A 55-year-old female who suffered from episodes of headache and seizures has been diagnosed with pachymeningitis for 4 years because post contrast brain MRI demonstrated enhanced carpet-like dura lesion in the left frontal lobe. The lesion kept unchanged on yearly follow-ups until a recent brain MRI found the lesion grew significantly into a mass. The lesion was resected and pathology suggested LPRM. Conclusion LPRM may present as carpet-like growth pattern on MRI. Long-term follow-up in patients with pachymeningitis is necessary.
Background Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is a severe autoimmune encephalitis mediated by anti-NMDA receptor antibodies. Brain MRI manifestations vary and are non-specific. If there are any lesions, they tend to be diffusely or multifocally distributed. Solitary lesion is relatively rare. Case presentation We report a 16-year-old girl who initially presented with focal seizures but developed severe psychiatric and extrapyramidal symptoms later on. Brain MRI revealed a solitary juxtacortical demyelinating lesion in the left frontal lobe. No enhancement was noted. Electroencephalogram captured epileptiform discharges in the same region. NMDAR IgGs were tested positive in the serum and cerebrospinal fluid. Corticosteroid and intravenous IgG were administered and the patient completely recovered. Brain MRI revealed a fainter lesion in the left frontal lobe. Conclusion In very rare instances, anti-NMDA receptor encephalitis can present with a solitary brain lesion. A full panel of antibodies for autoimmune encephalitis is the key leading to the diagnosis.
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