# Acute Disseminated Encephalomyelitis > Acute disseminated encephalomyelitis for NEET-PG Medicine covering monophasic post-infectious demyelination, MRI features and differences from MS. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/acute-disseminated-encephalomyelitis - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-14 - Last updated: 2026-10-14 - Reference basis: Adams and Victor's Principles of Neurology; Harrison's Principles of Internal Medicine - How to cite: "Acute Disseminated Encephalomyelitis", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/acute-disseminated-encephalomyelitis ## Direct answer Acute disseminated encephalomyelitis is an immune-mediated, monophasic demyelinating illness of the brain and spinal cord, usually following a viral infection or vaccination by one to three weeks. Its presentation is polysymptomatic, often with encephalopathy, and MRI shows large, poorly demarcated lesions rather than the ovoid periventricular plaques of multiple sclerosis. Treatment is high-dose intravenous methylprednisolone, with immunoglobulin or plasma exchange reserved for steroid-refractory disease. ## What you must remember - **Trigger:** typically a viral infection such as measles or varicella, or rarely vaccination, occurring one to three weeks before onset; the illness is immune-mediated rather than direct infection. - **Presentation:** polysymptomatic, with encephalopathy, seizures, optic neuritis or myelitis, and children are commonly affected. - **MRI:** large, diffuse, poorly demarcated lesions, often larger than 1 cm, involving grey matter and deep grey nuclei. - **Monophasic course:** a single episode; a new event more than three months after onset argues against ADEM and favours MS or MOG-associated disease. - **Fulminant variant:** acute haemorrhagic leukoencephalitis, with haemorrhage within lesions and high mortality, is a severe variant of ADEM. - **MOG antibodies:** increasingly tested in ADEM-like presentations, and a positive result reclassifies some cases as MOG antibody-associated disease. - **Treatment:** high-dose intravenous methylprednisolone for several days, often followed by an oral taper; immunoglobulin or plasma exchange if steroid-refractory. ## A diagnostic pathway for a first demyelinating event Distinguishing ADEM from multiple sclerosis drives treatment, prognosis and the decision on long-term disease-modifying therapy. The differences rest on course, clinical picture, imaging and cerebrospinal fluid rather than on any single test. 1. **Confirm the acute picture:** Establish a rapid onset over days, often with fever, headache, drowsiness or seizures, typically one to three weeks after an infection or vaccination. 2. **Map the lesions:** MRI of brain and spine showing multifocal, large, diffuse lesions with grey matter and deep nuclear involvement favours ADEM over the smaller periventricular plaques of MS. 3. **Examine the CSF:** Mild pleocytosis or raised protein can occur, and oligoclonal bands are usually absent in ADEM, so their presence points towards MS. 4. **Exclude mimics:** Look for infection such as herpes simplex encephalitis, vasculitis, metabolic disease and neoplasm, and send MOG and aquaporin-4 antibody tests where the picture is atypical. 5. **Treat early:** Start high-dose intravenous methylprednisolone promptly once infection is reasonably excluded, and reserve plasma exchange or immunoglobulin for patients who fail to respond. 6. **Follow up over months:** Watch for new events beyond three months, which would revise the diagnosis towards MS or MOG-associated disease. ## Where the exam tries to catch you Most traps here come from forcing the first episode into the label of multiple sclerosis or of a simple infection. - **Trap:** Labelling every first demyelinating event as multiple sclerosis — **Correct:** ADEM is polysymptomatic with encephalopathy, large diffuse lesions and a monophasic course, so the picture is distinct. - **Trap:** Accepting ADEM when a second episode appears months later — **Correct:** a new event beyond three months argues for MS or MOG-associated disease, so the diagnosis must be revised. - **Trap:** Treating ADEM as a simple viral encephalitis without excluding it — **Correct:** herpes simplex encephalitis must be excluded first, after which steroids are the mainstay of immune-mediated treatment. - **Trap:** Ignoring CSF oligoclonal bands — **Correct:** their presence favours MS and their absence supports ADEM, though neither result is decisive alone. ## Frequently asked questions ### How does ADEM differ from multiple sclerosis on MRI? ADEM typically shows large, diffuse, poorly demarcated lesions involving grey and white matter, sometimes including the thalamus and basal ganglia. Multiple sclerosis shows smaller, ovoid periventricular and juxtacortical lesions in a pattern that evolves over time. Lesion appearance supports the diagnosis but is interpreted with the clinical course. ### Which infections commonly precede acute disseminated encephalomyelitis? Viral infections such as measles and varicella are classic triggers of acute disseminated encephalomyelitis, and influenza and other respiratory viruses are also reported. Occasional cases follow vaccination. The illness typically begins one to three weeks after the trigger, reflecting an immune response rather than direct infection. ### What is the first-line treatment for acute disseminated encephalomyelitis? High-dose intravenous methylprednisolone is the first-line treatment for acute disseminated encephalomyelitis, given for several days and often followed by an oral taper. Patients who do not respond may receive plasma exchange or intravenous immunoglobulin. Infection must be reasonably excluded before immunosuppression is started. ### Why is acute haemorrhagic leukoencephalitis considered a severe variant of ADEM? Acute haemorrhagic leukoencephalitis is a fulminant form of acute demyelination with haemorrhage within the lesions and high mortality. It is regarded as a severe variant of acute disseminated encephalomyelitis rather than a separate condition. Early aggressive immunotherapy is used, though outcomes remain poor in many reported cases. ### What is the role of MOG antibody testing in ADEM? MOG antibody testing identifies MOG antibody-associated disease, which overlaps clinically and radiologically with ADEM and can present as a single episode. A positive result changes the expected course and relapse risk, so it guides follow-up. Testing is most useful when the presentation is atypical or the disease relapses.