• Diquat
• Mechanisms of intoxication
• Nervous system
• Oxidative stress
• Poisoning

• Humans
• Diquat/toxicity
• Animals
• Nervous System/drug effects
• Nervous System/pathology

• 40B 345 Talent Project of Shengjing Hospital
• 1685953391045 China Medical University High-quality Development Special Fund

• FBA
• TBSS
• end-stage renal disease
• white matter

• National Natural Science Foundation of China
• Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support
• Beijing Municipal Administration of Hospital's Mission Plan
• Beijing Scholar 2015
• Beijing Friendship Hospital, Capital Medical University
• Training Fund for Open Projects at Clinical Institutes and Departments of Capital Medical University

• MYORG
• Astrocyte
• Autopsy
• Blood-brain barrier (BBB)
• Idiopathic basal ganglia calcification (IBGC)
• Olivary hypertrophy
• Pathology
• Primary familial brain calcification (PFBC)

• Adult
• Aged
• Female
• Humans
• Male
• Middle Aged
• Astrocytes/pathology
• Astrocytes/metabolism
• Autopsy
• Brain/pathology
• Brain Diseases/genetics
• Brain Diseases/pathology
• Calcinosis/genetics
• Calcinosis/pathology
• Glycoside Hydrolases
• Pedigree

• JP14ek0109065 Japan Agency for Medical Research and Development
• JP20ek0109491 Japan Agency for Medical Research and Development
• JP21wm0425019 Japan Agency for Medical Research and Development
• 201442014A Japan Agency for Medical Research and Development
• 201442071A Japan Agency for Medical Research and Development
• JP18H02742 JSPS KAKENHI
• JP21K15702 JSPS KAKENHI
• JP21H02842 JSPS KAKENHI
• JP22K15713 JSPS KAKENHI
• JP22K07495 JSPS KAKENHI
• JP22K07519 JSPS KAKENHI
• JP23K06931 JSPS KAKENHI
• JP23K06966 JSPS KAKENHI
• JP20K16604 JSPS KAKENHI
• 2016100002B Ministry of Health, Labour and Welfare
• JSPS KAKENHI

• Humans
• Myelinolysis, Central Pontine/diagnostic imaging
• Myelinolysis, Central Pontine/etiology
• Diffusion Tensor Imaging
• Locked-In Syndrome
• Retrospective Studies
• Pyramidal Tracts/diagnostic imaging

• hyponatremia
• myelinolysis
• central pontine
• hiponatremia
• mielinólise central da ponte

• Humans
• Demyelinating Diseases/etiology
• Demyelinating Diseases/therapy
• Diuretics
• Hospitalization
• Hypokalemia
• Hyponatremia/etiology
• Hyponatremia/therapy

• Osmotic demyelination syndrome
• central pontine myelinolysis
• diffuse large B-cell lymphoma
• hyponatremia
• non-Hodgkin lymphoma

Osmotic demyelination syndrome, comprised of central pontine and extrapontine myelinolysis, is an important and potentially fatal complication primarily related to rapid overcorrection of serum sodium leading to devastating neurological symptoms. While traditionally presenting in the pons, we report the case of a 43-year-old female patient who recently underwent a liver transplant and developed extrapontine myelinolysis and subsequently central pontine myelinolysis resulting in irreversible spastic quadriparesis. This rare case highlights the variability of presentation of osmotic demyelination syndrome on imaging.

Demyelinated lesions in human pons observed after osmotic shifts in serum have been referred to as central pontine myelinolysis (CPM). Astrocytic damage, which is prominent in neuroinflammatory diseases like neuromyelitis optica (NMO) and multiple sclerosis (MS), is considered the primary event during formation of CPM lesions. Although more data on the effects of astrocyte-derived factors on oligodendrocyte precursor cells (OPCs) and remyelination are emerging, still little is known about remyelination of lesions with primary astrocytic loss. In autopsy tissue from patients with CPM as well as in an experimental model, we were able to characterize OPC activation and differentiation. Injections of the thymidine-analogue BrdU traced the maturation of OPCs activated in early astrocyte-depleted lesions. We observed rapid activation of the parenchymal NG2⁺ OPC reservoir in experimental astrocyte-depleted demyelinated lesions, leading to extensive OPC proliferation. One week after lesion initiation, most parenchyma-derived OPCs expressed breast carcinoma amplified sequence-1 (BCAS1), indicating the transition into a pre-myelinating state. Cells derived from this early parenchymal response often presented a dysfunctional morphology with condensed cytoplasm and few extending processes, and were only sparsely detected among myelin-producing or mature oligodendrocytes. Correspondingly, early stages of human CPM lesions also showed reduced astrocyte numbers and non-myelinating BCAS1⁺ oligodendrocytes with dysfunctional morphology. In the rat model, neural stem cells (NSCs) located in the subventricular zone (SVZ) were activated while the lesion was already partially repopulated with OPCs, giving rise to nestin⁺ progenitors that generated oligodendroglial lineage cells in the lesion, which was successively repopulated with astrocytes and remyelinated. These nestin⁺ stem cell-derived progenitors were absent in human CPM cases, which may have contributed to the inefficient lesion repair. The present study points to the importance of astrocyte-oligodendrocyte interactions for remyelination, highlighting the necessity to further determine the impact of astrocyte dysfunction on remyelination inefficiency in demyelinating disorders including MS.

• Astrocytes
• Multiple sclerosis
• Neural stem cells
• Oligodendrocyte precursor cells
• Remyelination

• efficacy
• hypertonic saline
• intracranial hypertension
• mannitol
• traumatic brain injury

• Adult
• Brain Injuries, Traumatic/complications
• Cerebrovascular Circulation/drug effects
• Diuretics, Osmotic/administration & dosage
• Diuretics, Osmotic/adverse effects
• Diuretics, Osmotic/therapeutic use
• Female
• Humans
• Intracranial Hypertension/drug therapy
• Intracranial Hypertension/etiology
• Intracranial Pressure/drug effects
• Male
• Mannitol/administration & dosage
• Mannitol/adverse effects
• Mannitol/therapeutic use
• Middle Aged
• Saline Solution, Hypertonic/administration & dosage
• Saline Solution, Hypertonic/adverse effects
• Saline Solution, Hypertonic/therapeutic use
• Trauma Severity Indices

Introduction. Central pontine myelinolysis is characterized by the occurrence of acute demyelinating lesions of cells in the pons secondary to abrupt oscillations of serum osmolarity. Its exact incidence is not well defined, but studies show a prevalence of 0.25 to 0.5% in the general population, 2.5% in the intensive care unit, and up to 10% in patients with risk factors, such as chronic liver disease and hepatic transplantation, alcoholism, malnutrition, diuretic therapy, electrolyte imbalance, hypoglycemia, and hyperglycemia. Case Report. A 70-year-old white female with extranodal diffuse large B-cell non-Hodgkin's lymphoma (extensive mass on the left anterior chest wall), stage IVA, developed pontine myelinolysis secondary to hypovolemic acute hypernatremia, which occurred due to diarrhea caused by chemotherapy (rituximab, cyclophosphamide, doxorubicin, and vincristine). Discussion. Pontine myelinolysis occurs most often due to the rapid correction of chronic hyponatremia. But here, we describe a case of the disease secondary to the occurrence of hypovolemic acute hypernatremia in a patient with a hematological malignancy under treatment, who was on chronic treatment with thiazide diuretics and who presented with other electrolyte disturbances as risk factors for the development of pontine myelinolysis.

• Central pontine myelinolysis
• Diffuse intrinsic pontine glioma
• Normonatremia
• Osmotic demyelination syndrome

• MYORG gene
• autosomal recessive inheritance
• cerebellar atrophy
• pons calcification
• primary familial brain calcification

Hypokalaemia at presentation of diabetic ketoacidosis is uncommon as insulin deficiency and metabolic acidosis shifts potassium extracellularly. However, hypokalaemia is a recognised complication of the management of diabetic ketoacidosis as insulin administration and correction of metabolic acidosis shifts potassium intracellularly. We describe the case of a 9-year-old girl with newly diagnosed type 1 diabetes mellitus presenting in diabetic ketoacidosis, with severe hypokalaemia at presentation due to severe and prolonged emesis. After commencing management for her diabetic ketoacidosis, her serum sodium and osmolality increased rapidly. However, despite maximal potassium concentrations running through peripheral access, and multiple intravenous potassium ‘corrections’, her hypokalaemia persisted. Seventy two hours after presentation, she became drowsy and confused, with imaging demonstrating central pontine myelinolysis – a rare entity seldom seen in diabetic ketoacidosis management in children despite rapid shifts in serum sodium and osmolality. We review the literature associating central pontine myelinolysis with hypokalaemia and hypothesise as to how the hypokalaemia may have contributed to the development of central pontine myelinolysis. We also recommend an approach to the management of a child in diabetic ketoacidosis with hypokalaemia at presentation.

• extrapontine myelinolysis
• parkinsonism
• pituitary adenoma

• Adenoma/surgery
• Adult
• Carbidopa/therapeutic use
• Drug Combinations
• Female
• Humans
• Hyponatremia/complications
• Levodopa/therapeutic use
• Magnetic Resonance Imaging
• Myelinolysis, Central Pontine/etiology
• Parkinsonian Disorders/drug therapy
• Parkinsonian Disorders/etiology
• Pituitary Neoplasms/surgery

• Algorithm
• Algoritmo
• Clasificación
• Classification
• Critical care patients
• Diagnóstico diferencial
• Differential diagnosis
• Etiology
• Etiología
• Hiponatremia
• Hyponatremia
• Pacientes críticos
• Prognosis
• Pronóstico
• Tratamiento
• Treatment
• Vaptanes
• Vaptans

• osmotic demyelination syndrome
• sodium correction

• Osmotic demyelination
• case report
• central pontine myelinolysis
• chronic kidney disease (CKD)
• electrolyte shifts
• extrapontine myelinolysis
• hypernatremia
• hyponatremia
• literature review
• osmolality
• osmolytes
• serum sodium concentration

• Overcorrection
• blood urea nitrogen (BUN)
• congestive heart failure (CHF)
• hyponatremia
• hypouremia
• kidney function
• osmolality
• serum sodium
• syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
• tolvaptan

• Ataxia
• Central pontine myelinolysis
• Hyponatremia
• Osmotic demyelination syndrome
• Piglet sign
• Trident sign

• Central pontine myelinolysis
• EEG
• Electroencephalography
• Intensive care units
• Myoclonus
• Myélinolyse centro-pontique
• Osmotic demyelination syndrome
• Réanimation
• Status epilepticus
• Syndrome de démyélinisation osmotique
• État de mal épileptique

Central pontine myelinolysis (CPM), a potentially fatal and debilitating neurological condition, was first described in 1959 in a study on alcoholic and malnourished patients. It is a condition most frequently related to rapid correction of hyponatremia. Chronic alcoholism associated CPM tends to be benign with a favorable prognosis compared to CPM secondary to rapid correction of hyponatremia. We describe a normonatremic, alcoholic patient who presented with CPM after a rapid rise in his sodium levels. Our case illustrates the fact that CPM can manifest even in patients who are normonatremic at baseline. Rapid rises in sodium levels should be promptly reversed before clinical symptoms manifest in patient with risk factors for CPM irrespective of their baseline sodium levels. Furthermore, clinical evolution of CPM can be difficult to discern from the natural course of alcohol withdrawal delirium, requiring astuteness and maintenance of a high degree of clinical suspicion on the part of the physician.

• Cost-effectiveness
• Cost-utility
• Discrete event simulation
• Hyponatraemia
• SIADH
• Tolvaptan

• Aged
• Antidiuretic Hormone Receptor Antagonists/therapeutic use
• Benzazepines/therapeutic use
• Cost-Benefit Analysis
• Female
• Humans
• Hyponatremia/drug therapy
• Hyponatremia/etiology
• Inappropriate ADH Syndrome/complications
• Inappropriate ADH Syndrome/drug therapy
• Lung Neoplasms/complications
• Male
• Pneumonia/complications
• Quality-Adjusted Life Years
• Sweden
• Tolvaptan

• Central pontine myelinolysis
• Hypokalemia
• Hyponatremia
• Hypophosphatemia
• Refeeding syndrome
• Status epilepticus
• Thiamine deficiency

Hyponatremia is a common electrolyte derangement in the setting of the intensive care unit. Life-threatening neurological complications may arise not only in case of a severe (<120 mmol/L) and acute fall of plasma sodium levels, but may also stem from overly rapid correction of hyponatremia. Additionally, even mild hyponatremia carries a poor short-term and long-term prognosis across a wide range of conditions. Its multifaceted and intricate physiopathology may seem deterring at first glance, yet a careful multi-step diagnostic approach may easily unravel the underlying mechanisms and enable physicians to adopt the adequate measures at the patient’s bedside. Unless hyponatremia is associated with obvious extracellular fluid volume increase such as in heart failure or cirrhosis, hypertonic saline therapy is the cornerstone of the therapeutic of profound or severely symptomatic hyponatremia. When overcorrection of hyponatremia occurs, recent data indicate that re-lowering of plasma sodium levels through the infusion of hypotonic fluids and the cautious use of desmopressin acetate represent a reasonable strategy. New therapeutic options have recently emerged, foremost among these being vaptans, but their use in the setting of the intensive care unit remains to be clarified.

• Arginine vasopressin
• Central pontine myelinolysis
• Extracellular fluid volume
• Hyponatremia
• Hyponatremic encephalopathy
• Osmotic demyelination

• hyponatremia
• osmotic demyelination syndrome
• syndrome of inappropriate antidiuretic hormone
• vasopressin receptor antagonist

• central pontine myelinolysis
• extrapontine myelinolysis
• osmotic demyelination

• acute malnutrition
• ataxia
• diarrhea
• extrapontine myelinolysis
• gluten

• apoptosis
• astrocyte
• central pontine myelinolysis
• hyponatraemia
• schizophrenia
• sodium ion

We report a case of a 50-year-old malnourished African American male with hiccups, nausea and vomiting who was brought to the Emergency Department after repeated seizures at home. Laboratory evaluations revealed sodium (Na⁺) 107 mmol/L, unmeasurably low potassium, chloride < 60 mmol/L, bicarbonate of 38 mmol/L and serum osmolality 217 mOsm/kg. Seizures were controlled with 3% saline IV. Once nausea was controlled with iv antiemetics, he developed large volume free water diuresis with 6 L of dilute urine in 8 h (urine osmolality 40-60 mOsm/kg) and serum sodium rapidly rose to 126 mmol/L in 12 h. Both intravenous desmopressin and 5% dextrose in water was given to achieve a concentrated urine and to temporarily reverse the acute rise of sodium, respectively. Serum Na⁺ was gradually re-corrected in 2-3 mmol/L daily increments from 118 mmol/L until 130 mmol/L. Hypokalemia was slowly corrected with resultant auto-correction of metabolic alkalosis. The patient discharged home with no neurologic sequaele on the 11^th hospital day. In euvolemic hyponatremic patients, controlling nausea may contribute to unpredictable free water diuresis. The addition of an antidiuretic hormone analog, such as desmopressin can limit urine output and prevent an unpredictable rise of the serum sodium.

• Hyponatremia
• Hypokalemia
• Overcorrection
• Polyuria
• Antidiuretic hormone
• Vasopressin
• Desmopressin
• Osmotic demyelination syndrome
• Central pontine myelinolysis

• Central pontine myelinolysis
• Wernicke's encephalopathy
• hyperemesis gravidarum