The MITD1 is an largely uncharacterized MIT domain–containing protein. This protein localizes to the midbody, with its recruitment dependent on selective interactions with a number of ESCRT-III proteins. These interactions are required for proper abscission.

A 63-year-old man with a past medical history of nonalcoholic steatohepatitis cirrhosis complicated by hepatic encephalopathy and non-bleeding esophageal varices presented for orthotopic liver transplantation. The patient had no acute complications in the immediate post-operative period, and was extubated on post-operative day (POD) 1. At that time, he was neurologically intact, alert and oriented and with no focal neurological deficits. On POD 3, he became lethargic and quadriplegic (Medical Research Council Scale Grade 0), and developed right-sided focal seizures with secondary generalization. His serum sodium was 128 mmol/L. He was re-intubated, and treated for his seizures with lorazepam 4 mg and levetiracetam 2 g, and then continued on levetiracetam 1 g two times a day. The following day, he was unresponsive and had no motor response to painful stimuli. His serum sodium had corrected without additional exogenous intervention to 135 mmol/L. On post symptom onset day (PSOD) 3, an MRI brain without contrast showed chronic small vessel ischemic changes but no other abnormality (Fig. 1a). The EEG did not show any seizure or epileptiform discharges. Serum chemistry and cerebrospinal fluid analysis did not show any significant abnormalities. On PSOD 13, his presentation remained the same. An MRI brain was repeated showing DWI restriction and high T2 signal in the central pons, suggestive of ODS (Fig. 1b). On PSOD 19, he was started on both IVIG and PP for a total of 5 days. Approximately 3 weeks after treatment with IVIG and Plasmapheresis, a repeat MRI showed similar prominence of T2 hyperintensity in the central pons with sparing of the periphery as compared to prior, findings consistent with central pontine myelinolysis/osmotic demyelination syndrome (Fig. 1c). Over the next 90 days the patient improved, becoming fully alert, regaining spontaneous muscle flicker in all four extremities (Medical Research Council Scale Grade 1), full eye movements and the ability to swallow.Osmotic demyelination syndrome (ODS) is a disorder characterized by the destruction of neuronal myelin sheaths in either the central area of the pons as in central pontine myelinolysis (CPM), or in other susceptible areas such as the basal ganglia, hippocampi or cerebellum known as external pontine myelinolysis (EPM). CPM can present with T2 hyperintensities on MRI in a classic trident-shape pattern. ODS usually presents as a complication of rapid correction of hyponatremia. Although no specific treatment has been described, plasmapheresis (PP) and intravenous immunoglobulin (IVIG) have been suggested as possible options for the management of ODS [1]. A clear association has been established between rapid correction of hyponatremia and the development of ODS. Although not completely understood, the pathophysiology of ODS classically described is the reduced extracellular osmolality causing brain cells to release osmotically-active substances in an attempt to achieve osmotic equilibrium. These osmotic substances cannot be reabsorbed rapidly, an...

While familial MS was associated with more severe T1-lesion volume and its MTR characteristics, there were no clinical status differences between familial and sporadic MS patients. Therefore, a better understanding of the genetic and/or epigenetic influences causing these differences can advance the understanding and management of MS.