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Lisa Fox , Physician Assistant
What To Do About MS Fatigue
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7 Dec 2025 | ~04:30 Engagement Time
You are a young adult, just finished college, excited about your career ahead. Then, you start experiencing numbness and tingling in your right arm and leg. At first, you might not think much of it, but a week later the symptoms get stronger, and you are now experiencing headaches, dizziness and weakness in the right arm and leg. A few days later you fall and your concern grows, so you head to the emergency room. They do an MRI of your brain, and the report comes back with possible “tumefactive MS.” You are stunned: Is this a tumor? Is this multiple sclerosis (MS)?
Tumefactive MS is a rare form of multiple sclerosis that affects the central nervous system. It is characterized by large lesions that can mimic brain tumors. The condition is very uncommon, occurring in about 3 people per million each year, and is more common in women.
Due to the large lesions, people with tumefactive MS often experience multiple symptoms at once. Common symptoms include:
A less common symptom of tumefactive MS includes encephalopathy, or a change in how the brain functions that may appear as confusion, memory loss, or personality changes. It is experienced in 19% of patients and is felt to occur secondary to the edema and possible mass effect. Other rare symptoms include intracranial pressure and/or cerebral herniation which are all emergent evaluations requiring aggressive intervention [8].
By comparison, multiple sclerosis (MS) is an inflammatory disease that also affects the central nervous system, including the brain, spinal cord, and optic nerves. MS usually develops over time and in separate areas of the nervous system. It is more common in women, with about three to one ratio to men. MS generally begins between the ages 20 and 40, with a median onset around age 30.
Tumefactive lesions are more commonly located in the cerebral hemispheric white matter, mostly in the focal and supratentorial regions of the frontal and parietal lobes but may be found thought the brain CNS as well [6].
MRI studies in tumefactive MS reveal striking findings. The MRIs demonstrate large (>2cm in diameter) CNS demyelination [2]. Most tumefactive MS lesions present with mass effect, perilesional edema, and enhancement [1,2]. This enhancement on average incompletely surrounds the affected area, with the open portion abutting the gray matter of the cortex or basal ganglia [4,8]. Due to their larger size and enhancing qualities, these tumefactive lesions tend to mimic the appearance of brain tumors or CNS abscesses [6, 8].
In contrast, MS lesions are generally ovoid and smaller in size (less than 2 cm) but may be larger as well and may enhance. MS lesions typically are found in the corpus callosum, periventricular and juxtacortical white matter, as well as in the cerebellum, brainstem, and spinal cord. Further work up is imperative to rule out tumors and abscess due to the completed risk of each. Due to the complexity of lesion characteristics, this work up may include biopsy, magnetic resonance spectroscopy and sometimes spinal taps/lumbar punctures. A lumbar puncture may reveal oligoclonal protein bands and myelin basic protein in up to 74% of patients [9].
Recovery from tumefactive MS in itself is promising, and many people recover quite well with the right treatment. Due to the rarity of Tumefactive MS, there are no clinical trials specifically focused on acute treatments for tumefactive demyelination. The typical first-line treatment for tumefactive MS on average is high-dose intravenous steroids. The majority of patients (80 %) had excellent recovery following IV corticosteroids [7,9]. For those patients who do not respond to steroids, escalation of therapy to plasma exchange has been reported with good clinical response [7]. In those patients who were refractory to corticosteroids and plasmapheresis, literature cited stated Rituxan and Cyclophosphamide as being effective in improving clinical and radiological disease activity [7,8,10].
Tumefactive MS patients may present as a single clinic event but may also develop into clinical definite MS [3,8]. Approximately one-third of patients will not develop a subsequent demyelination attack [9], but of those that do, two-thirds of them will follow the relapsing-remitting course. For those patients that did continue to develop clinically definite MS, it is highly recommended for them to start disease modifying therapies to reduce risk of disability and further neurological symptoms.
Tumefactive multiple sclerosis is a rare variant of multiple sclerosis (MS) with an alarming presentation on MRI striking concern for anyone that may see the lesion or differential diagnosis. Ruling out mimickers and being able to distinguish the lesions from a true demyelinating central nervous system origin to a central nervous system neoplasm or abscess is paramount in improving outcomes in patients diagnosed with tumefactive MS. Swift work up and treatment lends to favorable prognosis. Continued close observation to understand if the tumefactive lesion is a monophasic event or a progression into clinical definite MS or other CNS idiopathic inflammatory demyelinating disease remains imperative to improve quality of life for all patients.
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