Osmotic demyelination as a complication of hyponatremia correction: a systematic review / Desmielinização osmótica como complicação da correção de hiponatremia: uma revisão sistemática

ABSTRACT Background: Rapid correction of hyponatremia, especially when severe and chronic, can result in osmotic demyelination. The latest guideline for diagnosis and treatment of hyponatremia (2014) recommends a correction limit of 10 mEq/L/day. Our aim was to summarize published cases of osmotic demyelination to assess the adequacy of this recommendation. Method: Systematic review of case reports of osmotic demyelination. We included cases confirmed by imaging or pathology exam, in people over 18 years of age, published between 1997 and 2019, in English or Portuguese. Results: We evaluated 96 cases of osmotic demyelination, 58.3% female, with a mean age of 48.2 ± 12.9 years. Median admission serum sodium was 105 mEq/L and > 90% of patients had severe hyponatremia (<120 mEq/L). Reports of gastrointestinal tract disorders (38.5%), alcoholism (31.3%) and use of diuretics (27%) were common. Correction of hyponatremia was performed mainly with isotonic (46.9%) or hypertonic (33.7%) saline solution. Correction of associated hypokalemia occurred in 18.8%. In 66.6% of cases there was correction of natremia above 10 mEq/L on the first day of hospitalization; the rate was not reported in 22.9% and in only 10.4% was it less than 10 mEq/L/day. Conclusion: The development of osmotic demyelination was predominant in women under 50 years of age, with severe hyponatremia and rapid correction. In 10.4% of cases, there was demyelination even with correction <10 mEq/L/day. These data reinforce the need for conservative targets for high-risk patients, such as 4-6 mEq/L/day, not exceeding the limit of 8 mEq/L/day.

RESUMO Antecedentes: A correção rápida da hiponatremia, principalmente quando grave e crônica, pode resultar em desmielinização osmótica. A última diretriz para diagnóstico e tratamento da hiponatremia (2014) recomenda um limite de correção de 10 mEq/L/dia. Nosso objetivo foi sumarizar os casos publicados de desmielinização osmótica para avaliar a adequação dessa recomendação. Método: Revisão sistemática de relatos de caso de desmielinização osmótica. Incluímos casos confirmados por imagem ou anatomia patológica, em maiores de 18 anos, publicados entre 1997 e 2019, nas línguas inglesa ou portuguesa. Resultados: Avaliamos 96 casos de desmielinização osmótica, sendo 58,3% do sexo feminino e com média de idade de 48,2 ± 12,9 anos. A mediana de sódio sérico admissional foi 105 mEq/L e > 90% dos pacientes apresentavam hiponatremia grave (<120 mEq/L). Foram comuns os relatos de distúrbios do trato gastrointestinal (38,5%), etilismo (31,3%) e uso de diuréticos (27%). A correção da hiponatremia foi feita principalmente com solução salina isotônica (46,9%) ou hipertônica (33,7%). Correção de hipocalemia associada ocorreu em 18,8%. Em 66,6% dos casos houve correção da natremia acima de 10 mEq/L no primeiro dia de internamento; a velocidade não foi relatada em 22,9% e em apenas 10,4% foi menor que 10 mEq/L/dia. Conclusão: O desenvolvimento da desmielinização osmótica foi predominante em mulheres, abaixo de 50 anos, com hiponatremia grave e correção rápida. Em 10,4% dos casos, houve desmielinização mesmo com correção <10 mEq/L/dia. Esses dados reforçam a necessidade de alvos conservadores para pacientes de alto risco, como 4-6 mEq/L/dia, não ultrapassando o limite de 8 mEq/L/dia.

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.

Probable first report of a motor deafferentation syndrome in the Paraguayan War / Provável primeiro relato de uma síndrome de desaferentação motora na Guerra do Paraguai

ABSTRACT The Paraguayan War ended 150 years ago. Back then, there were outbreaks of combatants' limb weakness and tingling related to "palustrian cachexia", not clearly funded at the time on nutritional deficiency, the use of native flora to feed troops, and alcoholism. We report a case of a soldier with ascending paralysis, mental confusion and finally tetraplegia with preserved oculomotricity. This would probably be a case of locked-in syndrome (LIS) due to Gayet-Wernicke's encephalopathy consequent to thiamine deficiency. The role of thiamine in the peripheral or central nervous system expression was shown decades later to be related to poor diet, or use of foods containing thiaminase or thiamine antagonists, worsened by the fact that the bodily stores of thiamine are restricted, and deficits may grow fast.

RESUMO A Guerra do Paraguai terminou há 150 anos. Houve surtos de fraqueza dos membros dos combatentes e parestesias relacionadas à "caquexia palustre", não claramente fundamentados na época sobre deficiência nutricional, o uso da flora nativa para alimentar as tropas e o alcoolismo. Referimo-nos a um caso de um militar com paralisia ascendente, confusão mental e finalmente tetraplegia com oculomotricidade preservada. Esse relato seria provavelmente devido a um caso de "síndrome do encarceramento" secundário à encefalopatia de Gayet-Wernicke consequente à deficiência de tiamina. O papel da tiamina na expressão periférica ou do SNC foi previsto décadas mais tarde em relação a uma dieta pobre, ou ao uso de alimentos contendo tiamina ou antagonistas da tiamina, agravado pelo fato de que as reservas corporais de tiamina são restritas, e os déficits podem se manifestar rapidamente.

Status Epilepticus in a Patient with Extrapontine Myelinolysis

Extrapontine myelinolysis is a demyelinating disorder usually caused by rapid correction of chronic hyponatremia. We present an 82-year-old female patient with general weakness, and severe hyponatremia (103 mEq/L) which was corrected 14 mEq/L during 21 hours. She was stuporous and presented status epilepticus. Brain T2-weighted image showed high signal intensities of bilateral thalami and electroencephalogram monitoring indicated right hemisphere lateralized periodic discharges, maximal in the right frontal region. This case shows that status epilepticus can occur in a patient of extrapontine myelinolysis involved bilateral thalami without pontine lesions.

Osmotic Demyelination Syndrome Presenting with Emotional Incontinence

No abstract available.

Síndrome neuroléptico maligno con mielinolisis central pontina / Neuroleptic malignant syndrome with central pontine myelinolysis

RESUMEN El síndrome neuroléptico maligno (SNM) es una complicación severa de los antipsicóticos, en especial los de primera generación como el haloperidol, que fue el primero en el que se describió esta patología, caracterizada por fiebre, rigidez, alteración del estado de conciencia y disautonomías. Por otro lado, la mielinólisis central pontina (ahora llamada síndrome de desmielinización osmótica) resulta de las alteraciones agudas séricas del sodio, como las que ocurren en las reposiciones de hiponatremia, y podría poner en riesgo la vida al igual que el SNM. La asociación de estas dos patologías es inusual y hasta el momento no se conoce con claridad su relación causal, producto de los pocos casos reportados. Aunque se conoce la mortalidad del síndrome neuroléptico maligno, la compañía de la mielinolisis central pontina podría aumentar la morbimortalidad de esta entidad, por lo cual es necesario reconocerla rápidamente para prevenir la aparición de complicaciones, ya que no cuenta con un tratamiento específico. Presentamos el caso de un paciente joven que cursó con estas dos patologías, y consideramos que la causa de la mielinolisis central pontina fue el haloperidol, así como del SNM. A pesar de ello, este medicamento continúa siendo muy seguro en la práctica clínica ya que la aparición de estas complicaciones es una reacción idiosincrática por algún tipo de susceptibilidad genética desconocida.

SUMMARY Neuroleptic malignant syndrome (NMS) is a severe complication of antipsychotics, especially those of first generation such as haloperidol, which was the first in which this pathology was described, characterized by: fever, rigidity, alteration of the state of consciousness and dysautonomies. On the other side, central pontine myelinolysis (Now Called Osmotic Demyelination Syndrome), search results of acute sodium alterations of sodium, as those occurring in hyponatremia replenings and could put life at risk just like the NMS. The association of these two pathologies is unusual and until now, their causal relationship, the result of the few cases reported, is not clearly known. Although the relationship of the neurological syndrome may be limited, the company of central myelolysis could increase the morbidity of this entity, so it is necessary to be required quickly to prevent the onset of complications, which does not have a specific treatment. We present the case of a young patient who has these pathologies and we consider that the cause of centralized myelinolysis is haloperidol as well as NMS, despite this, this medication continues to be very safe in clinical practice since the appearance of These complications is an idiosyncratic reaction due to some type of unknown genetic susceptibility.

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.

Achados de fala, deglutição e qualidade de vida na mielinólise extrapontina: relato de caso de uma adolescente com germinoma do sistema nervoso central / Speech, swallowing and quality of life outcomes in extrapontine myelinolysis: a case report of a teenager with central nervous system germ cell tumor

RESUMO O presente trabalho é um relato de caso que descreve os achados fonoaudiológicos e de qualidade de vida apresentados por uma adolescente com um tumor do sistema nervoso central acometida pela mielinólise extrapontina. A mielinólise extrapontina é uma doença desmielinizante aguda que pode ser causada por variações abruptas na osmolaridade sérica, como o que ocorre na rápida correção da hiponatremia. Os dados foram obtidos a partir da avaliação clínica fonoaudiológica, de questionários pediátricos sobre a qualidade de vida e dados contidos no prontuário médico. A paciente apresentou mutismo, disartria e disfagia decorrentes da mielinólise extrapontina, com impactos significativos na sua comunicação verbal, alimentação e qualidade de vida. Os escores de qualidade de vida após a mielinólise extrapontina apresentaram piora quando comparados aos do período anterior à doença. Recebeu atendimento fonoaudiológico hospitalar e ambulatorial. Foram observadas evoluções nos padrões de fala, deglutição e mobilidade das estruturas orofaciais, com reversão parcial dos déficits neurológicos. A atuação fonoaudiológica, como parte de uma equipe multiprofissional de saúde, é de grande importância na reabilitação funcional dos pacientes acometidos por esta doença.

ABSTRACT This paper is a case report describing the speech-language and quality of life outcomes presented by a teenager with a central nervous system germ cell tumor affected by extrapontine myelinolysis. The extrapontine myelinolysis is an acute demyelinating disease that can be caused by abrupt changes in serum osmolality, as in the rapid correction of hyponatremia. Data were obtained from clinical assessment protocols, pediatric inventory about quality of life and medical records information. The patient presented mutism, dysphagia and dysarthria caused by extrapontine myelinolysis, with significant impacts on their verbal communication, feeding and quality of life. The scores of quality of life after extrapontine myelinolysis decreased compared to the time before the disease. She received speech-language therapy during hospital admission and in the outpatient clinic. We observed changes in patterns of speech, swallowing and mobility of orofacial structures; with partially reverse of neurological deficits. The speech therapists, as part of a multidisciplinary team of health care, are of great importance in the functional rehabilitation of patients affected by this disease.

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.

Central and Extrapontine Myelinolysis after Alcohol Withdrawal and Correction of Hypernatremia in a Chronic Alcoholic: a Case Report

Osmotic demyelination syndrome (ODS) is a demyelinating disorder related to the rapid correction of hyponatremia. It usually affects the pontine area; hence, the name central pontine myelinolysis (CPM). However, it rarely occurs with the correction of hypernatremia and hyperosmolarity and involves extrapontine areas. A 56-year-old chronic alcoholic had been admitted with a history of confusion. He had been in alcohol withdrawal for 4 days. Laboratory examinations showed severe hypernatremia and hyperosmolarity. After serum sodium level was normalized; however, his clinical course did not improve and deteriorated to semicoma progressively. Magnetic resonance imaging (MRI) revealed abnormal signal intensity in the pontine and extrapontine areas, including the basal ganglia, thalamus, and cerebral cortices. This is the first case report of combined central pontine and extrapontine demyelination after alcohol withdrawal and correction of hypernatremia in a chronic alcoholic.

Leucopatía reversible de la protuberancia: en paciente con SIDA y tratamiento retroviral / Pontine reversible leucopathy in an AIDS patient associated with highly active antiretroviral therapy (HAART): report of one case

Posterior reversible encephalopathy (PRES) is a condition characterized by T2 and FLAIR hyperintensities in magnetic resonance imaging (MRI) studies, localized preferentially in the occipital-parietal white matter regions. Pathological MRI images located in midbrain, pons, medulla and spinal cord, that could be asymptomatic, were recently included in this entity. These images are interpreted as vasogenic edema, which is caused by arterial hypertension or eclampsia, neurotoxicity related to immunosuppressive agents or chemotherapy, among other causes. We report a 25 years old asymptomatic male with AIDS, with normal blood pressure who after initiating highly active antiretroviral therapy (HAART) reported vertigo. The MRI showed a central pontine T2 hyperintensity with diffusion restriction, which was interpreted as a central pontine myelinolysis (CPM), but the lack of motor symptoms made improbable a real demyelination of the pons. The follow-up MRI revealed complete regression of the images. To our knowledge, this case could be the second report of a reversible leucopathy of the pons in a patient with AIDS, were the MRI images also simulated a CPM. This report extends the knowledge around the variability of the pathogenic interpretation of CPM images and their association with HAART.

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.

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.

Rabdomiólise recorrente secundária à hiponatremia em doente com polidipsia psicogênica primária / Recurrent rhabdomyolysis secondary to hyponatremia in a patient with primary psychogenic polydipsia

A rabdomiólise é caracterizada por destruição de tecido muscular esquelético, sendo as suas principais causas o trauma, os tóxicos e os distúrbios hidroeletrolíticos. Entre esses últimos, inclui-se a rabdomiólise induzida por hiponatremia, uma situação rara, que ocorre principalmente em doentes com polidipsia psicogênica. Esta acomete maioritariamente doentes com esquizofrenia, cursando com hiponatremia em quase 25% dos casos. É também nesse contexto que a rabdomiólise secundária a hiponatremia ocorre mais frequentemente. Neste artigo, descreveu-se o caso de um homem de 49 anos, com antecedentes de esquizofrenia, medicado com clozapina, trazido ao serviço de urgência por quadro de coma e convulsões. Foi objetivada hiponatremia hiposmolar grave, com edema cerebral em tomografia computorizada, sendo feito posteriormente o diagnóstico de hiponatremia secundária à polidipsia psicogênica. Foi iniciada terapêutica de correção de hiponatremia e internado em unidade de terapia intensiva. Feita correção de hiponatremia, contudo apresentou analiticamente marcada rabdomiólise, de agravamento crescente, com creatinofosfoquinase de 44.058UI/L no 3º dia de internação. Houve posterior redução progressiva com a terapêutica, sem ocorrência de lesão renal. Este caso alerta para a necessidade de monitorização dos marcadores de rabdomiólise na hiponatremia grave, ilustrando um quadro de rabdomiólise secundária à hiponatremia induzida por polidipsia psicogênica, situação a considerar em doentes sob terapêutica com neurolépticos.

Rhabdomyolysis is characterized by the destruction of skeletal muscle tissue, and its main causes are trauma, toxic substances and electrolyte disturbances. Among the latter is hyponatremia-induced rhabdomyolysis, a rare condition that occurs mainly in patients with psychogenic polydipsia. Psycogenic polydipsia mostly affects patients with schizophrenia, coursing with hyponatremia in almost 25% of the cases. It is also in this context that rhabdomyolysis secondary to hyponatremia occurs most often. In this article, the case of a 49-year-old male with a history of schizophrenia, medicated with clozapine, and brought to the emergency room in a state of coma and seizures is described. Severe hypoosmolar hyponatremia with cerebral edema was found on a computed tomography examination, and a subsequent diagnosis of hyponatremia secondary to psychogenic polydipsia was made. Hyponatremia correction therapy was started, and the patient was admitted to the intensive care unit. After the hyponatremia correction, the patient presented with analytical worsening, showing marked rhabdomyolysis with a creatine phosphokinase level of 44.058UI/L on day 3 of hospitalization. The condition showed a subsequent progressive improvement with therapy, with no occurrence of kidney damage. This case stresses the need for monitoring rhabdomyolysis markers in severe hyponatremia, illustrating the condition of rhabdomyolysis secondary to hyponatremia induced by psychogenic polydipsia, which should be considered in patients undergoing treatment with neuroleptics.

Analysis of relationship between demyelinating lesions and myelin basic protein in pancreatic encephalopathy / 临床肝胆病杂志

Pancreatic encephalopathy (PE)is one of the severe complications of severe acute pancreatitis (SAP).Early diagnosis mostly depends on the history of disease as well as clinical symptoms and signs.PE progresses rapidly and is often complicated by multiple organ dysfunction,and it may finally develop into multiple organ failure with a high fatality rate if not treated in time.It is currently known that de-myelination is one of the important pathological features of this disease,with fat -soluble demyelination of cerebral gray matter and white matter,as well as inflammatory changes such as hemorrhage and edema.The target antigen of demyelinating lesions,however,is myelin basic protein (MBP).This paper reviews the changes in MBP levels in the demyelinating lesions of the central nervous system among PE pa-tients,with the purpose of providing clues for the early diagnosis and prognostic study of demyelinating lesions in PE.

Reversible Cerebellar Ataxia Related to Extrapontine Myelinolysis without Hyponatremia after Cisplatin-Based Chemotherapy for Cholangiocarcinoma / Journal of the Korean Cancer Association, 대한암학회지

A 60-year-old woman presented with cerebellar signs including dysarthria and ataxia, after intravenous infusion of cisplatin-based chemotherapy. Several blood tests showed mild neutropenia, normocytic normochromic anemia, but no evidence of a marked hyponatremia. Brain magnetic resonance imaging with diffusion-weighted sequences showed hyper-intense signal abnormalities in the extrapontine region, sparing the basis pontis. Here, we report on the case of a patient with reversible cerebellar ataxia related to extrapontine myelinolysis without hyponatremia after treatment with cisplatin-based chemotherapy for cholangiocarcinoma and discuss the literature on cerebellar ataxia in patients who underwent recent chemotherapy for malignancy.

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.