Abstract
BackgroundOccurrence of basal ganglia involvement in neuromyelitis optica spectrum disorders (NMOSD) has rarely been reported and none documented pathologically.Case presentationA 73-year-old female was clinically diagnosed with a NMOSD based on the clinical and radiological features and positive serum autoantibodies to AQP4. One month before her death, she became acutely ill with disturbed consciousness and right hemiparesis, and was diagnosed and treated as having basal ganglia infarction based on the brain CT. She made a partial recovery but later died from heart failure. At autopsy, the corresponding basal ganglia process revealed a large fresh area of necrosis. Histologically, several pathological signatures of NMOSD could be recognized in the lesion, including inflammatory cell infiltrations by B and T lymphocytes, perivascular complement and fibrinogen deposition, and the appearance of numerous phagocytosed corpora amylacea within the infiltrating macrophages.ConclusionsThe present case illustrates that basal ganglia may be directly involved in the pathological processes of NMOSD, although the possibility of modification of the lesions by superimposed regional ischemia could not be excluded.
Highlights
Occurrence of basal ganglia involvement in neuromyelitis optica spectrum disorders (NMOSD) has rarely been reported and none documented pathologically.Case presentation: A 73-year-old female was clinically diagnosed with a Neuromyelitis optica spectrum disorder (NMOSD) based on the clinical and radiological features and positive serum autoantibodies to AQP4
The present case illustrates that basal ganglia may be directly involved in the pathological processes of NMOSD, the possibility of modification of the lesions by superimposed regional ischemia could not be excluded
We here report a patient with NMOSD who developed a large basal ganglia lesion 1 month prior to her death, which was initially diagnosed as an ischemic infarction
Summary
The present case illustrates that basal ganglia may be directly involved in the pathological processes of NMOSD, the possibility of modification of the lesions by superimposed regional ischemia could not be excluded.
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