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We report a Native American male in his 50s with a complex medical history including alcohol use disorder and seizure disorder who presented with complaints of generalized weakness and multiple falls. The patient was admitted for altered mental status, community acquired pneumonia, sepsis, and bacteremia. On hospital day 23, the patient reported a sudden onset of sensation of food stuck in his upper chest. Brain MRI confirmed osmotic demyelination syndrome (ODS) within the central pons. Further workup revealed this finding was likely due to malnutrition, alcoholism, hypoalbuminemia, and vitamin B6 deficiency. However, the patient presented with normonatremia throughout his entire hospital stay. After acute onset of ODS, the patient was transferred to the ICU where he continued to decline. After 68 days from initial presentation, the patient died in hospice care from myelinolysis complications. This case demonstrates a case of ODS of the central pons in a patient with normonatremia, hypoalbuminemia, and severe vitamin B6 deficiency.

This report aims to present an elderly woman with persistent delirium after hospitalization for lethargy secondary to hyponatremia. The diagnosis of pontine myelinolysis was made and there were no characteristic neurological manifestations such as pupillary changes or spastic tetraparesis. Hallucinations and personality changes were the clues to the diagnosis and should be considered an atypical manifestation of pontine myelinolysis.
O objetivo deste relato é apresentar uma idosa que apresentou, após internação por letargia secundária à hiponatremia, delirium persistente depois da alta hospitalar. O diagnóstico de mielinólise pontina foi feito após a alta hospitalar e não houve manifestações neurológicas características, como alterações pupilares ou tetraparesia espástica. Alucinações e mudança de personalidade foram as pistas para o diagnóstico e devem ser consideradas como uma manifestação atípica de mielinólise pontina.

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BACKGROUND: In clinical practice, sodium correction rates are frequently limited in patients with severe hyponatremia to prevent neurologic complications. The implications of correction rates on overall mortality and length of hospital stay are unclear. METHODS: In this multicenter observational study, we evaluated the association of sodium correction rates with mortality, length of stay, and central pontine myelinolysis (CPM) in patients hospitalized with severe hyponatremia (admission serum sodium level less than 120 mEq/l). RESULTS: The cohort included 3274 patients. A correction rate of less than 6 mEq/l/24 hours was observed in 38%, 6 to 10 mEq/l/24 hours was observed in 29%, and greater than 10 mEq/l/24 hours was observed in 33%. Compared with 6 to 10 mEq/l/24 hours, a correction rate of less than 6 mEq/l/24 hours exhibited higher in-hospital mortality in multivariable-adjusted and propensity score–weighted analyses. Compared with 6 to 10 mEq/l/24 hours, a correction rate of greater than 10 mEq/l/24 hours was associated with lower in-hospital mortality and shorter length of stay in multivariable analyses. Seven patients with CPM were identified, with five of seven developing CPM despite a sodium correction rate of less than or equal to 8 mEq/l/24 hours. Six of seven patients who developed CPM had alcohol use disorder, malnutrition, hypokalemia, or hypophosphatemia. CONCLUSIONS: Limiting the sodium correction rate was associated with higher mortality and longer length of stay. Whether the sodium correction rate influences neurologic complications needs further evaluation.

OBJECTIVE: Central pontine myelinolysis (CPM) is a rare demyelinating disease that affects the pons and which can cause extreme disabilities such as locked-in syndrome (LIS) in the initial phase. The aim of the study was to describe the evolution over a 12-month period of two patients with CPM causing an initial LIS.
METHODS: We retrospectively report the unexpected clinical outcome of these two patients in relation with the anatomical damages documented by brain MRI, associated with diffusion tensor imaging and reconstruction of corticospinal tracts in tractography. The following clinical parameters systematically assessed at 3, 6, 9, and 12 months: muscle testing on 12 key muscles (Medical Research Council), prehension metrics (box and block test and purdue pegboard), and independence for acts of daily living (functional independence measure).
RESULTS: Both patients showed a progressive recovery beginning between 2 and 3 months after the onset of symptoms, leading to almost complete autonomy at 12 months (FIM > 110), with motor strength greater than 4/5 in all joint segments (MRC > 50/60). On brain MRI with tractography, CST appeared partially preserved at pons level.
CONCLUSIONS: The possibility of a near-complete functional recovery at 12 months is important to consider given the ethical issues at stake and the discussions about limiting care that may take place initially. It seems to be the consequence of reversible myelin damage combined with partially preserved neurons. Development of collateral pathways or resolution of conduction block may explain this recovery. MRI comprising DTI and tractography could play a key role in the prognosis of motor recovery.

A patient in her 50s presented with altered mental status and shortness of breath at 4600 m elevation. After descent to the base of the mountain, the patient became comatose. She was found to have bilateral pulmonary infiltrates and a serum sodium of 102 mEq/L. She was rapidly corrected to 131 mEq/L in 1 day. Initial MRI showed intensities in bilateral hippocampi, temporal cortex and insula. A repeat MRI 17 days post injury showed worsened intensities in the bilateral occipital lobes. On admission to acute rehabilitation, the patient presented with blindness, agitation, hallucinations and an inability to follow commands. Midway through her rehabilitation course, antioxidant supplementations were started with significant improvement in function. Rapid correction of hyponatraemia may cause central pontine myelinolysis or extrapontine myelinolysis (EPM). In some cases of hypoxic brain injury, delayed post-hypoxic leucoencephalopathy (DPHL) may occur. Treatment options for both disorders are generally supportive. This report represents the only documented interdisciplinary approach to treatment of a patient with DPHL and EPM. Antioxidant supplementation may be beneficial as a treatment option for both EPM and DPHL.

OBJECTIVE: Myelinolysis is a neurological condition that can display diverse psychiatric symptoms, with electrolyte imbalance, alcoholism and malnutrition being the frequent causes. Rapid correction of hyponatremia may trigger pontine and extra-pontine myelinolysis.
METHODS: This paper examines two cases: one of hyponatremia after antihypertensive use and the other of myelinolysis due to rapid correction of hyponatremia. Since myelinolysis appeared as a manic episode, the patients sought treatment at the psychiatry outpatient clinic. Further tests were conducted to rule out organic causes and the diagnosis was confirmed prior to referring the patients to the neurology clinic.
CONCLUSIONS: Psychiatrists should be meticulous in excluding organic causes in first-episode mania and consider these possibilities in the differential diagnosis for the pertinent patient group.

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A 41-year old woman was treated for cholera at one of the health centers in Blantyre. Two days after discharge from the treatment unit, she developed weakness of all 4 limbs and difficulties with speech. She was referred to the Queen Elizabeth Central Hospital. A CT scan of the brain showed hypodense lesions in the pons. A diagnosis of central pontine myelinolysis was made. She recovered slowly and was discharged from hospital 17 days after admission.