Seven cases of toxic encephalopathy associated with diquat poisoning / 中华急诊医学杂志

Objective:To improve the understanding of the clinical features of toxic encephalopathy associated with diquat poisoning.Methods:This study collected and analyzed the diagnosis and treatment process of 7 patients with acute diquat poisoning combined with central nervous system complications admitted to the First Affiliated Hospital of Zhengzhou University from April 2021 to April 2022. "Diquat" and "Poisoning" were used as keywords to search in CNKI, Wanfang database and PubMed database, and the literature of previous cases was reviewed for summary analysis.Results:Among the 7 patients in our hospital, there were 2 males and 5 females, with an average age of 31 years (range14-57) and an average dose of 23.14 g [(10-40)g]. During the treatment, 3 patients developed irritability and convulsions, 3 patients occurred coma, and one had generalized tonic-clonic seizures. Four patients died and 3 survived, of which 2 patients returned to normal life and study, and one remained abnormal mental behavior (currently in long-term follow-up). All three survivors developed neurological symptoms later than those who died, and were awake about 30 days after taking the drug.Conclusions:Toxic encephalopathy associated with diquat poisoning has rapid progression, poor prognosis and high mortality. This study found that the survival rate of patients with > 48 h of first onset of neurological symptoms is much higher than that of patients with ≤ 48 h of first onset of neurological symptoms, while sex, age, estimated oral dose, and type of presentation of neurological symptoms for the first time have little effect on the survival rate of hospital discharge. The earlier neurological symptoms appear, the greater the likelihood of a poor prognosis.

Desmielinización osmótica pontina y extrapontina durante un puerperio complicado / Osmotic demyelination pontine and extrapontine during complicated puerperium

La mielinolisis pontina central es una rara alteración neurológica de etiología desconocida. La causa más frecuente es el tratamiento de una hiponatremia cuando los niveles de sodio se elevan demasiado rápido. La lesión básica consiste en la destrucción de las vainas de mielina, que afecta parte o toda la base de la protuberancia en forma simétrica (desmielinización pontina). Los pacientes con esta enfermedad suelen presentar tetraparesia progresiva subaguda acompañada de parálisis seudobulbar con disartria e imposibilidad de protruir la lengua. Se presenta un estudio con el objetivo de describir el comportamiento de un caso de desmielinización osmótica en una paciente como parte de un puerperio complicado. Se trata de una paciente femenina, mestiza, de 33 años de edad, con embarazo complicado, secundario a cesárea por óbito fetal, tras la cual lleva ingreso en terapia intensiva. Luego de varias alteraciones hidroelectrolíticas se detecta cuadriplejia fláccida, con síndrome de enclaustramiento, con diagnóstico por neuroimagen de una desmielinización osmótica, con evolución favorable(AU)

Central pontine myelinolysis is a rare neurological disorder of unknown etiology. The most frequent cause is the treatment of hyponatremia when sodium levels rise too fast. The destruction of the myelin sheaths is the basic lesion, which affects part or the entire base of the protuberance symmetrically (pontine demyelination). Patients with this disease usually present subacute progressive tetraparesis accompanied by pseudobulbar paralysis with dysarthria and the inability to protrude their tongue. A study is presented with the objective of describing the behavior of a case of osmotic demyelination in a patient as part of complicated puerperium. This is a 33-year-old female patient, with complicated pregnancy, secondary to cesarean section due to fetal death, after which she is admitted to intensive care. After several hydroelectrolyte alterations, flaccid quadriplegia was detected, with Locked-in Syndrome, with neuroimaging diagnosis of osmotic demyelination, with a favorable evolution(AU)

Central pontine myelinolysis after liver transplantation: case report / Mielinolisis Póntica Central post-trasplante hepático: Reporte de Caso

SUMMARY Central Pontine Myelinolysis (CPM) is a demyelinating disease with central pontine localization which presents in patients with chronic hepatic disease and hydroelectrolytic disturbances. In spite of pathophysiology still unknown, the patient liver transplanted has several risk factors to CPM. Its clinical manifestations are mainly motor and awareness alterations. Diagnosis requires brain images like magnetic resonance and it has a poor prognosis in critical care patients and it is very important to know about the possibility of presentation and to be aware about this pathology. The main objective to present this case report is sensitizing the medical community regarding the CPM in patients with liver transplant. The case report of a 40-year-old female patient who had previous history of biliary cirrhosis secondary to autoimmune hepatitis and liver transplantation was performed; subsequently developed alteration of awareness, hydroelectrolytic disturbances and abnormal findings in brain imaging. CPM is a neurological demyelinating disease with multifactorial origin, its treatment is supportive and prevention is the main goal in patients with risk factors like patient after liver transplantation.

RESUMEN La Mielinólisis Pontica Central es una enfermedad desmielinizante con localización pontina central que se presenta especialmente en pacientes con enfermedad hepática crónica y alteraciones hidroelectrolíticas. A pesar de la fisiopatología aún desconocida, el paciente con trasplante hepático tiene varios factores de riesgo para su desarrollo. Sus manifestaciones clínicas son principalmente alteraciones motoras y de conciencia. El diagnóstico requiere imágenes cerebrales como la resonancia magnética y se asocia a mal pronóstico. En los pacientes de cuidados críticos y es muy importante conocer la posibilidad de presentación y tener conciencia de esta patología. El objetivo principal de este reporte de caso es sensibilizar a la comunidad médica respecto en pacientes posterior a trasplante hepático. Se realizó el reporte de una paciente de 40 años de edad con antecedente de cirrosis biliar secundaria a hepatitis autoinmune y trasplante de hígado; posteriormente desarrolló alteración de la conciencia, alteraciones hidroelectrolíticas y hallazgos anormales en la imagen cerebral. La Mielinolísis Póntica es una enfermedad desmielinizante neurológica de origen multifactorial, su tratamiento es de apoyo y la prevención es el objetivo principal en pacientes con factores de riesgo como el paciente tras trasplante hepático.

Central Pontine Myelinolysis Induced by Alcohol Withdrawal: A Case Report

Central pontine myelinolysis (CPM) is a demyelinating disorder characterized by the loss of myelin in the center of the basis pons, and is mainly caused by the rapid correction of hyponatremia. We report the case of a young woman who presented with gait disturbance and alcohol withdrawal, and who was eventually diagnosed with CPM. Generally, the cause and pathogenesis of CPM in chronic alcoholics remain unclear. In this cases, the CPM may be unrelated to hyponatremia or its correction. However, it is possible that the osmotic pressure changes due to refeeding syndrome after alcohol withdrawal was the likely cause in this case. This case illustrates the need for avoiding hasty, and possibly incomplete diagnoses, and performing more intensive test procedures to ensure a correct diagnosis.

Ataxic Form of Central Pontine Myelinolysis Developed during Alcohol Withdrawal in a Chronic Alcoholic

Central pontine myelinolysis (CPM) is well-recognized osmotic demyelination syndrome that is related to various conditions such as rapid correction of hyponatremia and chronic alcoholism. Acute ataxia as a sole clinical sign in CPM is rare. We report a case of a 59-year-old man with dysarthria, intention tremor, and a significant gait ataxia starting after alcohol withdrawal, with radiological evidence of CPM. CPM should be included in the differential diagnosis of alcoholic patients who develop a sudden ataxia. Chronic alcohol abuse is one of the most commonly encountered predisposing factors. Alcohol withdrawal represents an additional vulnerability factor, being responsible for electrolyte imbalances which are not always demonstrable but are certainly involved in the development of CPM.

Primary Sjogrens Syndrome with Renal Tubular Acidosis with Central Pontine Myelinolysis – A rare case report

A middle aged female patient, a case of Primary Sjogren’s Syndrome with renal tubular acidosis as revealed by severe hypokalemia along with normal anion gap, metabolic acidosis and acidic urinary pH had brain stem lesion which presented as quadriplegia, dysphagia and dysarthria. Laboratory tests revealed that anti-nuclear antibodies (ANA) and anti Ro/SSA antibodies were positive. MRI showed hyper intense lesion in T2W images in middle pons, typical characteristic of central pontine myelenolysis. So, patient was diagnosed as Primary Sjogren’s Syndrome with renal tubular acidosis with central pontine myelinolysis. She recovered with correction of hypokalemia, intravenous methyl prednisolone and cyclophosphamide.

Mielinólise pontina em paciente etilista / Pontine myelinolysis in an alcoholic patient

A Mielinólise Pontina (MP) define-se como uma lesão desmielinizante, associada a quadro de tetraparesia e incapacidade na fala, frequentemente relacionada a distúrbios eletrolíticos e observada em pacientes etilistas. Relatamos o caso de um paciente com diagnóstico de MP firmado por ressonância magnética (AU)

Pontine myelinolysis (MP) is defined as a demyelinating lesion associated with tetraparesis and disability in speech, often related to electrolyte disturbances and observed in alcoholic patients. Here we report the case of a patient diagnosed with MP through MRI (AU)

Osmotic Demyelination Syndrome: Why Should Hypernatremia be Corrected Slowly : A Case Report.

Aim: Our aim is to present a case of hypernatremia which has led on to a flaccid quadriparesis due to brain stem demyelination. Rapid correction of hypernatremia as a cause for pyramidal tract demyelination is not documented in the literature. Presentation of Case: A 53 year old male was brought to the emergency services with suspected stroke. He was treated with intravenous mannitol and oral glycerine from the primary health centre. We detected hypoglycemia (blood sugarwas 50mg/dl-Ref range: ≤70mg%) and dextrose was given intravenously. Subsequently the patient went into a hypernatremic state with serum sodium 170milli equivalents /liter which was corrected rapidly. This was corrected over 48 hours to 140milli equalents/litre. The rate of correction exceeded 0.62millimols/liter/hour (Ideal: 0.5 mmol/L/h). On the 6th day the patient developed acute quadriparesis. Magnetic resonance imaging (MRI) of brain revealed bilateral symmetric demyelination of the corticospinal tracts. Over six months the neurological deficit improved with complete resolution of the changes in previous Discussion: Osmotic Demyelination Syndrome (ODS) has been a recognized complication of rapid correction of hyponatremia. Experiments in animals and clinical experience suggest that correction of chronic hyponatremia should be kept at a slow rate to combat this complication. The characteristic sites include pons and basal ganglia. Such a complication has not been described due to rapid correction of hypernatremia.This is probably the first case report in the literature where acute onset of quadriparesis resulted from demyelination of the pyramidal tract consequent to a rapid correction of hypernatremia. We had to wait about 6 months for the patient to obtain a complete functional recovery and the neuro imaging was repeated after 6 months to confirm the disappearance of the initial findings thus implicating rapid correction of hypernatremia as the cause of his morbidity. Conclusion: This is the first time extrapontine reversible myelinolysis due to rapid correction of hypernatremia has been documented. To prevent this potentially fatal complication it will be prudent if hypernatremia is corrected slowly.

Alcoholism with central pontine demyelination: a case report.

Central pontine myelinolysis is a non-inflammatory demyelinating disease characterized by loss of myelin with relative neuron sparing, associated with rapid correction of hyponatremia and sometimes hypernatremia or chronic alcoholism. We are reporting a case of 52 year old male patient who was chronic alcoholic from past 20 years, presented to us with complaints of altered sensorium and dysarthria of 5 days duration .He was investigated and diagnosed as case of central pontine myelinosis associated with chronic alcoholism.

Locked-in Syndrome due to Central Pontine Myelinolysis: Case Report

Central pontine myelinolysis (CPM) classically occurs in alcoholics, malnourished individuals, chronic liver diseases, and rapid correction of hyponatremia. This report presents locked-in syndrome due to CPM following rapid correction of hyponatremia. A 44-year-old male came to the hospital due to a short period of loss of consciousness. He was alert and had no focal neurological abnormalities at admission. The serum sodium concentration was 118 mEq/L and was corrected to 134 mEq/L in the first 18 hours. One week later, progressive weakness in limbs developed and he progressed to a complete quadriplegic state and bulbar palsy, with only eye blinking preserved. Brain magnetic resonance imaging revealed a characteristic hyperintense signal abnormality in both pons, so he was diagnosed to locked-in syndrome caused by CPM. The patient gradually improved following continuous intensive rehabilitation for more than 2 years. He was able to move all joint muscles against gravity in generally and he could gait under supervision.

Central Pontine and Extrapontine Myelinolysis in a Patient with Traumatic Brain Injury Following Not Rapid Correction of Hyponatremia: A Case Report / 대한신경손상학회지

Central pontine myelinolysis occurs inconsistently as a complication of severe and prolonged hyponatremia, particularly when corrected too rapidly. This condition is a concentrated, frequently symmetric, noninflammatory demyelination within the central basis pontis. We describe a head injury patient who developed central pontine and extrapontine myelinolysis following a gradual correction of hyponatremia. More attention should be paid to correcting hyponatremia combined with hypokalemia in patients who have a history of alcoholism.

Recovery from a Complicated Case of Central Pontine and Extrapontine Myelinolysis by Dopaminergic Treatment: One-Year Follow-up: A Case Report

Central pontine and extrapontine myelinolysis are well-recognized osmotic demyelination syndromes related to the rapid correction of hyponatremia, chronic alcoholism, and malnutrition. They are reported to show brain stem signs and various movement disorders. A 58-year-old man with a history of chronic alcoholism was admitted for dysarthria, dysphagia, and gait disturbance that had developed five days after a right forearm cellulitis. Magnetic resonance imaging revealed demyelinating patterns in the central portion of the pons and both thalami. He showed severe extrapyramidal symptoms with truncal swaying and postural instability that resulted in severe gait disturbance. Postural instability showed little improvement after conventional physical therapy, but his symptoms markedly improved after five days of dopamine administration. Cessation of dopamine agents was attempted two times, but postural instability and gait disturbance recurred. Therefore, medication was continued for one year. The patient showed stable gait and no further deterioration of postural instability during dopamine therapy.

Mielinolisis pontina central sin hiponatremia / Central pontine myelinolysis without hyponatremia

Mujer de 31 años con antecedentes de obesidad mórbida a, cirugía bariátrica, desnutrición severa crónica, laparotomía exploratoria por abdomen agudo séptico y trastorno hidroelectrolítico. Presento en su post quirúrgico (3er día) en la unidad de cuidados intensivos, Mielinolisis póntica central. Un hallazgo inusual en este caso, fue la ausencia de hiponatremia y/o su corrección brusca, quien comúnmente se asocia a esta enfermedad y a su pronóstico. Analizando todas sus comorbilidades y factores de riesgo, pensamos que existe evidencia que justifique su enfermedad. Según las fuentes revisadas (PubMed), es el primer caso reportado en América Latina. (AU)

A 31-year-old woman, with a history of morbid obesity, bariatric surgery, chronic severe malnutrition, exploratory laparotomy for acute abdomen and septic electrolyte disorder. In his post-surgical (Third day) at intensive care unit, presented central pontine myelinolysis. An unusual finding in this case was the absence of hyponatremia and I or its sharp correction, which is commonly associated with this disease and its prognosis. Analyzing all comorbidities and risk factors, we suspect, that there is evidence to support your disease. According to the sources reviewed (PubMed), is the first case reported in Latin America. (AU)

Clinical Features and Prognosis of Central Pontine Myelinolysis / 中国康复理论与实践

@#Objective To analyze the clinical features and prognosis of central pontine myelinolysis. Methods 20 cases with CPM diagnosed in last 10 years were reviewed and compared with those patients of foreign studies. Results 10 patients with hemoptysis were treated with hypophysin, which resulted in severe hyponatremia and osmotic myelinolysis. The main syndrom were dysarthria and dysphagia (secondary to corticobulbar fiber involvement), flaccid quadriparesis (as corticospinal tract involved) which later became spastic. The myelinolysis distrubuted symmetrically along the myelin disruption in the center basal, as well as independently in other brain areas (extrapontine myelinolysis or EPM), including the cerebellar and neocortical white/gray junctional areas, thalamus and striatum. Conclusion Supplement of sodium should be slower and more persistent for hyponatremia, the selection of drugs should be based on the patients' specific conditions.

A Case of Central Pontine Myelinolysis in a Type 2 Diabetic Patient without Electrolyte Changes

Central pontine myelinolysis (CPM) by complicating rapid correction of severe hyponatremia has been widely reported. Additionally, CPM was occasionally reported among patients with post-liver transplantation, burns, chronic renal failure with dialysis, or other diseases associated with or not associated with other electrolyte changes or hyperosmolarity. However, there have been a few reports of CPM occurring in diabetic patients without documented electrolyte changes. This report is, to the best of our knowledge, the first report of CPM in type 2 diabetic patients without electrolyte changes in Korea. A 40-year-old man with type 2 diabetes mellitus with abruptly developed dysarthria and ataxia was admitted to our facility. He suffered from poor glucose control and multiple diabetic complications. Brain magnetic resonance imaging (MRI) revealed a well-defined bilateral symmetric hyperintense lesion in the central portion of the pons on T2- and diffusion-weighted images, which was consistent with CPM. After the patient's blood glucose and blood pressure normalized, his dysarthria and ataxia improved. Six months after discharge, follow-up MRI showed a persistent, but greatly reduced symmetric lesion in the central pons. It is certainly possible for CPM to be overlooked clinically in diabetic patients, but more cases could be diagnosed if careful attention was paid to this syndrome.

Demyelinative diseases after liver transplantation: The etiology / 第二军医大学学报

Liver transplantation is the only definitive treatment modality of end stage liver diseases. Demyelinative disease is rarely seen in patients after liver transplantation, but a higher incidence has been noticed recently. The disease is liable to be misdiagnosed as immunosuppressant-induced psychiatric disorders at early stage. Central pontine myelinolysis is more disastrous and it will greatly influence the short-term survival and long-term life quality of the patients after liver transplantation. When it is manifested as peripheral nervous system disorder, the disease usually has a subtle onset, making it difficult for diagnosis and treatment. The causes for various demyelinative diseases should be understood to prevent it in patients after liver transplantation. The specific mechanism for demyelinative disease after liver transplantation remains unclear. We introduce the possible causes of common demyelinative diseases, hoping to provide reference for prevention and treatment of such conditions after liver transplantation.

Central Pontine Myelinolysis Presenting With Cerebellar Ataxia

Central pontine myelinolysis (CPM) is a neurologic disorder that is usually related to rapid correction of hyponatremia and chronic alcoholism. CPM involves concentrated, symmetric, noninflammatory demyelination within the central pons; this pathology also occurs in extrapontine regions. Frequently observed clinical manifestations are sudden weakness, dysphagia, dysarthria, loss of consciousness, and locked-in syndrome. We describe herein a case of CPM predominated by cerebellar signs without typical symptoms, but with involvement of the cerebellum or cerebellar peduncle.

Complete Neurological Recovery in Two Cases of Osmotic Demyelination Syndrome Following Rapid Correction of Chronic Hyponatremia / 대한신장학회지

The osmotic demyelination syndrome (ODS) is a distinctive clinical entity with characteristic MR features in the central pons (central pontine myelinolysis, CPM) and other locations (extrapotine myelinolysis, EPM). ODS is mainly seen following rapid correction of the serum sodium level in hyponatremic patients. In the past, ODS used to be considered as fatal. However, some recent reports have described cases of survival from this syndrome, but most survivors seem to suffer irreversible neurological deficits. We report one case of 46-year-old woman who developed stupor at day 7 and the other case of 56-year-old woman with drowsiness, dysarthria and dysphagia at day 3 following the correction of hyponatremia. In both cases, the serum potassium levels were low at the time of presentation with hyponatremia. By means of brain MRI, the first case was diagnosed as CPM with EMP and the second case as isolated EPM. With conservative treatments, complete neurological recovery was achieved at 4-6 weeks after onset of ODS.

Nocturnal Polyuria Developed in Patients with Central Pontine Myelinolysis: A case report

Central pontine myelinolysis is a demyelinating disease of central pons. Nocturnal polyuria is defined as increased urination during nighttime with a nocturnal fraction exceeding from 20% to 33%. We have experienced nocturnal polyuria developed in two patients with central pontine myelinolysis. In these cases, serum antidiuretic hormone and urine osmolality were lower at nighttime than daytime. It suggests that nocturnal polyuria is caused by abnormal diurnal variation of antidiuretic hormone. In the first case, nocturnal polyuria was recovered spontaneously and also follow up brain MRI showed decreased signal intensity in pons. In the second case, nocturnal polyuria was improved after the treatment of intranasal desmopressin. It appeares that central pontine myelinolysis can cause nocturnal polyuria due to the interruption of antidiuretic hormone pathway. The symptom of nocturnal polyuria can be treated by desmopressin.

A Case of Central Pontine Myelinolysis Presenting as Continuous Nausea in the 16th week of Pregnancy

Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated as well with the demyelination of extrapontine areas of the central nervous system. Although the etiology and pathogenesis are unclear, CPM is usually associated with states such as too rapid correction of hyponatremia, alcohol intoxication, malnutrition, liver disease, burn, cancer, addison's disease, dehydrated disease, and electrolyte imbalance. Clinical presentations are nonspecific but are typically characterized by confused mentation, bulbar or pseudobulbar palsy (dysarthria, dysphagia, tetraplegia), rock-in syndrome, and common symptoms such as lethargy and dysarthria. Brain magnetic resonance imaging(MRI) in CPM results in diffuse high signal intensity in the pons on T2-weighted images, and shows slightly decreased signal intensity and no enhancement in the central pons on T1-weighted images. We described a case of a 30-year-old woman presenting with continuous nausea and vomiting in the 16th week of pregnancy. In order to achieve early diagnosis of CPM, We recommend that emergency physicians should consider CPM during differential diagnosis. Prompt diagnosis and management of associated complications are essential for favorable clinical outcomes in CPM.