Tumefactive multiple sclerosis: an uncommon diagnostic challenge

Abstract

Objective: This case report describes a rare presentation of multiple sclerosis (MS) that was initially diagnosed as a peripheral nerve lesion in the emergency department.

Clinical features: A 30-year-old woman presented to a chiropractic teaching clinic with a complaint of a sudden right foot drop. Magnetic resonance imaging of the brain revealed a large mass in the left parietal lobe with additional white matter lesions. The mass and smaller lesions were consistent with a rare presentation of demyelinating disease, tumefactive MS.

Intervention and outcome: The patient was referred to a neurologist for further evaluation and treatment. Her short-term clinical course was punctuated by recurrent myospasms and neurologic deficits.

Conclusion: Tumefactive MS may mimic the clinical and magnetic resonance imaging characteristics of glioma or a cerebral abscess. The clinical presentation, pathophysiology, differential diagnosis, role of diagnostic imaging, and treatment options of MS are described. This case report illustrates that the timely diagnosis and optimal treatment of MS require recognition of its varied, sometimes atypical, and often nonspecific clinical and imaging manifestations.

Fig 1

Contrast T1-weighted axial MRI examination of the brain demonstrated a 3.0-cm intraaxial mass in the left parietal lobe with an open-ring enhancement pattern directed toward the cortical surface. This pattern is frequently encountered with tumefactive MS. There was minimal mass effect.

Fig 2

T2-weighted fluid-attenuated inversion recovery coronal MRI examination of the brain revealed a heterogeneous high-signal intraaxial lesion in the superior aspect of the left parietal lobe resulting in sulcal effacement.

Fig 3

The H-MRS of the left parietal lobe lesion. It demonstrated elevation in the choline (arrow) and creatine (crossed arrow) peaks with a decrease in the NAA peak (arrowhead). An increased choline peak indicated elevated cell membrane destruction consistent with demyelination and inflammation. The reduction of the NAA concentration indicated neuronal and axonal damage.