Transient lesion of the splenium
Key points
- Reversible, ovoid, non-enhancing lesion centred in the splenium with marked restricted diffusion
- Pathophysiology: intramyelinic oedema (cytotoxic oedema of myelin sheaths, not neuronal injury) - explains reversibility
- Most commonly post-infectious; also AED withdrawal, metabolic, seizures
- Complete resolution on follow-up (days to weeks) is the hallmark - if persistent, reconsider diagnosis
- Two nomenclatures: MERS (mild encephalitis/encephalopathy with reversible splenial lesion) and RESLES (reversible splenial lesion syndrome - broader umbrella)
Epidemiology & risk factors
- More common in children and young adults
- Most frequent trigger: viral infection (influenza, rotavirus, dengue, COVID-19)
- Other causes: AED withdrawal (carbamazepine, phenytoin), hypoglycaemia, hypernatraemia, high-altitude cerebral oedema, seizures, SLE, Kawasaki disease
- Generally self-limiting with excellent prognosis
Pathophysiology
Infection/metabolic insult → inflammatory cytokines → reversible intramyelinic oedema in the tightly packed fibres of the splenium. The splenium is thought to be vulnerable due to its high density of cytokine and glutamate receptors. The oedema is intramyelinic rather than intracellular (neuronal), which accounts for complete reversibility without gliosis or necrosis.
Clinical features
- Mild encephalopathy: confusion, drowsiness, irritability
- Seizures (may be presenting feature or trigger)
- Preceding febrile illness (1-7 days prior) in infectious cases
- Rapid and complete neurological recovery typical
- Type 2 (extrasplenic involvement) may have more prolonged symptoms
Imaging
MRI
- DWI/ADC: Markedly restricted diffusion (bright DWI, low ADC) - most conspicuous sequence
- T2/FLAIR: Hyperintense, well-defined, ovoid, midline lesion in the splenium
- T1: Isointense to mildly hypointense; no cavitation or necrosis
- Post-contrast: No enhancement
- No haemorrhage
- Classification:
- Type 1: splenium only (more common, better prognosis)
- Type 2: extends beyond splenium to involve entire corpus callosum +/- symmetric periventricular white matter
Follow-up
- Complete resolution of signal abnormality and restricted diffusion within days to weeks
- No residual gliosis, atrophy, or cavitation
Differentials
| Differential | Distinguishing feature |
|---|---|
| Marchiafava-Bignami disease | Alcoholism, body > splenium, central layer necrosis ("sandwich sign"), irreversible cavitation |
| Acute infarct | Vascular territory, not midline, clinical stroke syndrome, does not resolve |
| Diffuse axonal injury | Trauma history, haemorrhagic foci, callosal + grey-white junction + brainstem |
| Lymphoma | Enhances, mass effect, may cross midline but irregular morphology |
| Demyelination (MS) | Calloso-septal interface (Dawson fingers), enhancing active plaques, temporal dissemination |
| Posterior reversible encephalopathy | Parieto-occipital predominance, vasogenic oedema (high ADC), hypertension/eclampsia |
Management
- Treat underlying cause (antiviral, AED adjustment, correct metabolic derangement)
- Supportive care
- Follow-up MRI to confirm resolution (typically 1-4 weeks)
- No specific treatment for the lesion itself
Exam pearls
- Post-infectious + splenium + restricted diffusion + complete resolution = MERS/RESLES
- Restricted diffusion mimics infarct, but midline splenial location and reversibility are key
- vs MBD: alcoholism, body predominance, central layer necrosis, irreversible
- Type 1 (splenium only) is more common and has better prognosis than type 2
