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Arch Neurol. 2004;61:1794-1795.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A 51-year-old woman suffering from 20 years of rheumatoid arthritis (RA) had noticed difficulties in walking 2 months earlier. Neurological examinations of the patient disclosed hyperactive deep-tendon reflexes, abnormal bilateral reflexes, and motor weakness of her left upper and lower extremities. Blood analysis demonstrated a highly elevated rheumatoid factor (241 IU/mL), and anticardiolipin antibody was not found. Examination of the cerebrospinal fluid (CSF) demonstrated pleocytosis (205cells/mm³), and the CSF proteinlevel was markedly elevated to 316 mg/dL. The patient’s cranial T2-weighted (Figure 1A) and flair magnetic resonance imaging (MRI) (Figure 1B) investigations revealed high-signal lesions. These abnormalities were revealed as slight T1 hypointensity signals similar to those of the gray matter without any gadolinium-diethylenetriaminepentaacetic acid enhancement. Magnetic resonance angiography did not demonstrate any vascular changes. Cervical MRI showed high-signal lesions in the T2-weighted images (Figure 1C). Based on these findings, we diagnosed the patient . . . [Full Text of this Article]

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AUTHOR INFORMATION
Yasutaka Tajima, MD, PhD; Ri-ichiro Kishimoto, MD; Kazumasa Sudoh, MD, PhD; Akihisa Matsumoto, MD, PhD

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