In Addition to Marchiavafa-Bignami Disease, many other Diseases are Associated with Bilateral Medial Cerebellar Peduncle Hyperintensity

We read with interest the article by Alshimemeri et al. about a 45-year-old woman who had laparoscopic sleeve surgery complicated by recurrent vomiting since surgery, paraparesis of the lower limbs and slurred speech since 30 days after surgery [1] .Examination revealed double vision, quadruparesis, hypernatremia and a hyperintestinal lesion on both sides of the middle cerebellar peduncle [1] .Marchiavafa-Bignami disease (MBD) was diagnosed and intravenous thiamine treatment was initiated, followed by delayed partial recovery [1] .The study is appealing, but some points should be discussed.The first point is that the diagnosis of MBD is not comprehensible [1] .The patient had normal serum thiamine levels and the MRI findings shown in Figure 1 are not typical of MBD [1] .MBD usually presents with decreased serum thiamine levels, and cerebral MRI shows hyperintensities in the posterior splenium corporis callosum [2] .In addition, there was no immediate response to thiamine infusions and the patient made an incomplete recovery after four months.The second point is that not all differential diagnoses of a lesion of the middle cerebellar peduncle have been sufficiently excluded.Differential diagnoses that should be considered and were adequately ruled out in the index patient include neurodegenerative diseases (multiple systemic atrophy cerebellar type (MSA-C), fragile X-associated tremor/ataxia syndrome (FXTAS), CARASIL involving the pons (Arc sign), CLCN2-associated leukoencephalopathy), metabolic diseases (adrenoleukodystrophy, Wilson's disease, acquired non-Wilsonian hepatocerebral degeneration, hypoglycemic encephalopathy, extrapontine myelinolysis), neoplasms (primary CNS lymphoma, brainstem glioma, leptomeningeal carcinomatosis), cerebrovascular diseases (infarction of the anterior inferior cerebellar artery (AICA)); superior cerebellar artery infarction, Wallerian degeneration secondary to pontine infarction, posterior reversible encephalopathy syndrome (PRES)), inflammatory and demyelinating diseases (myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), Behet disease, Erdheim-Chester disease, neuromyelitis optica spectrum disorder (NMOSD), progressive multifocal leukoencephalopathy (PML)), intoxication (cyclosporin-A encephalopathy, heroin-induced leukoencephalopathy), and infections (HIV encephalopathy, JC virus granule cell neuronopathy and Zika virus encephalitis) [3] .The third point is that a Guillain-Barre syndrome involving the brain stem could not be sufficiently excluded.The patient had dissociation cyto-albuminique and paraparesis [1] .Even if the nerve conduction studies (NCSs) were normal, this does not rule out GBS, as NCSs can be normal at an early stage of the disease.CSF examination and NCS should be repeated at a later stage of the disease.The fourth point is that autoimmune encephalitis (AIE) could not be sufficiently excluded.To rule out AIE, it is essential to perform an MRI of the brain with contrast medium and to determine the antibodies associated with AIE in the serum and cerebrospinal fluid.The exclusion of AIE is of crucial importance as it is usually amenable to treatment.It is also essential to rule out Bickerstaff encephalitis of the brainstem, a subtype of GBS, as the patient had central and peripheral nervous system abnormalities.The fifth point is that the CSF glucose was elevated [1] .Did the patient have diabetes?What was the index patient's HbA1C level?The sixth point is that vomiting can hardly be the cause of the quudruparesis, as the patient had elevated serum sodium levels but no hyponatraemia.Vomiting is usually associated with hypochloremic hyponatraemia.This discrepancy should be clarified.