scholarly journals Topiramate-induced severe electrolyte abnormalities and hypernatremia leading to central pontine myelinolysis

2021 ◽  
Vol 14 (11) ◽  
pp. e245870
Author(s):  
Luba Muaddi ◽  
Omar Osman ◽  
Barbara Clark
Keyword(s):  
Multiple Sclerosis ◽  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Motor Deficits ◽  
Baseline Serum ◽  
Pontine Myelinolysis ◽  
History Of ◽  
Renal Tubular ◽  
Central Pontine ◽  
Electrolyte Abnormalities

Central pontine myelinolysis (CPM) develops due to acute hypernatremia from a normal baseline serum sodium in the setting of electrolyte abnormalities induced by topiramate use. Topiramate is a commonly used medication with several indications including migraines, myoclonic jerks and seizures. It has been reported to cause renal tubular acidosis and severe electrolyte abnormalities, which in turn predispose patients to neuropathology via renal concentration defects and osmotic shifts. Our patient is a 55-year-old woman with a history of multiple sclerosis and myoclonus on topiramate for several years who presented with weakness and was found to be profoundly hypokalemic. She went on to develop changes in mental status, motor deficits and evidence of CPM on MRI during her hospitalisation. Surprisingly, the patient never had hyponatremia; however, she had an acute rise in serum sodium from a normal baseline after fluid resuscitation with normal saline for hypotension during her admission.

scholarly journals A Case of Central Pontine Myelinolysis Caused by Hypophosphatemia Secondary to Refeeding Syndrome

2015 ◽  
Vol 7 (3) ◽  
pp. 196-203 ◽  
Author(s):  
Chikara Yamashita ◽  
Hiroshi Shigeto ◽  
Norihisa Maeda ◽  
Takako Torii ◽  
Yasumasa Ohyagi ◽  
...  
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Rapid Change ◽  
Serum Biochemistry ◽  
Refeeding Syndrome ◽  
Pontine Myelinolysis ◽  
History Of ◽  
Biochemistry Test ◽  
Magnetic Resonance Imaging Mri ◽  
Central Pontine

Central pontine myelinolysis (CPM), which was originally considered to be the result of rapid correction of chronic hyponatremia, is not necessarily accompanied by hyponatremia or drastic changes in serum sodium level. Here, we report a case of an anorexic 55-year-old male with a history of pharyngo-laryngo-esophagogastrectomy, initially hospitalized with status epilepticus. Although his consciousness gradually recovered as we were controlling his convulsion, it deteriorated again with new onset of anisocoria, and magnetic resonance imaging (MRI) at this point revealed CPM. Rapid change of serum sodium or osmolarity, which is often associated with CPM, had not been apparent throughout his hospitalization. Instead, a review of the serum biochemistry test results showed that serum phosphate had drastically declined the day before the MRI first detected CPM. In this case, we suspect that hypophosphatemia induced by refeeding syndrome greatly contributed to the occurrence of CPM.

scholarly journals Atypical presentation of central pontine myelinolysis in hyperglycemia

2017 ◽  
Vol 2017 ◽  
Author(s):  
Swapna Talluri ◽  
Raghu Charumathi ◽  
Muhammad Khan ◽  
Kerri Kissell
Keyword(s):  
Case Report ◽  
Blood Glucose ◽  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Blood Glucose Control ◽  
Clinical Suspicion ◽  
Serum Osmolality ◽  
Pontine Myelinolysis ◽  
History Of ◽  
Central Pontine

Summary Central pontine myelinolysis (CPM) usually occurs with rapid correction of severe chronic hyponatremia. Despite the pronounced fluctuations in serum osmolality, CPM is rarely seen in diabetics. This is a case report of CPM associated with hyperglycemia. A 45-year-old non-smoking and non-alcoholic African American male with past medical history of type 2 diabetes, hypertension, stage V chronic kidney disease and hypothyroidism presented with a two-week history of intermittent episodes of gait imbalance, slurred speech and inappropriate laughter. Physical examination including complete neurological assessment and fundoscopic examination were unremarkable. Laboratory evaluation was significant for serum sodium: 140 mmol/L, potassium: 3.9 mmol/L, serum glucose: 178 mg/dL and serum osmolality: 317 mosmol/kg. His ambulatory blood sugars fluctuated between 100 and 600 mg/dL in the six weeks prior to presentation, without any significant or rapid changes in his corrected serum sodium or other electrolyte levels. MRI brain demonstrated a symmetric lesion in the central pons with increased signal intensity on T2- and diffusion-weighted images. After neurological consultation and MRI confirmation, the patient was diagnosed with CPM secondary to hyperosmolar hyperglycemia. Eight-week follow-up with neurology was notable for near-complete resolution of symptoms. This case report highlights the importance of adequate blood glucose control in diabetics. Physicians should be aware of complications like CPM, which can present atypically in diabetics and is only diagnosed in the presence of a high index of clinical suspicion. Learning points: Despite the pronounced fluctuations in serum osmolality, central pontine myelinolysis (CPM) is rarely seen in diabetics. This case report of CPM associated with hyperglycemia highlights the importance of adequate blood glucose control in diabetics. Physicians should be aware of complications like CPM in diabetics. CPM can present atypically in diabetics and is only diagnosed in the presence of a high index of clinical suspicion.

scholarly journals Pontine and extrapontine myelinolysis secondary to alcoholism: A case report.

2021 ◽  
Author(s):  
Carolina Ferreira Colaço ◽  
André Eduardo de Almeida Franzoi ◽  
Amanda Maieski ◽  
Talita Aparecida Conte ◽  
Luís Eduardo de Macedo Zubko ◽  
...  
Keyword(s):  
Case Report ◽  
Central Pontine Myelinolysis ◽  
Heavy Drinking ◽  
Orotracheal Intubation ◽  
Plasma Sodium ◽  
Level Of Consciousness ◽  
Midbrain Region ◽  
Pontine Myelinolysis ◽  
History Of ◽  
Central Pontine

Context: Osmotic demyelination syndrome (ODS) is rare, acute, severe and non-inflammatory. It is caused by the demyelination of neurons with the preservation of axons. It is called central pontine myelinolysis (CPM) when it affects the central pontine region and extra-pontine myelinolysis (EPM) when it affects other areas. Few cases of ODS due to non-electrolytic causes are reported. Case report: 54-year-old man with a history of heavy drinking. After about 24 hours of alcohol withdrawal, he developed generalized tonic-clonic seizures, associated with a lower level of consciousness. Protective orotracheal intubation was performed and the use of anti-crisis drugs was initiated. After sedation was switched off and mechanical ventilation was set to minimum parameters, the patient remained comatose and with convergence-retraction nystagmus movements. A skull MRI was performed, which showed lesions compatible with CPM and EPM. There was no variation in the patient’s plasma sodium during hospitalization. Conclusion: this is a patient with no evidence of any significant hydro-electrolyte disturbance and who presented a compatible neurological condition and neuroimaging characteristic of CPM / EPM. There is no specific clinical treatment for this pathology. Furthermore, the patient presents with the finding of convergence-retraction nystagmus, possibly explained by atrophy of the dorsal midbrain region.

scholarly journals A Rare Case of Central Pontine Myelinolysis in Overcorrection of Hyponatremia with Total Parenteral Nutrition in Pregnancy

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Kalyana C. Janga ◽  
Tazleem Khan ◽  
Ciril Khorolsky ◽  
Sheldon Greenberg ◽  
Priscilla Persaud
Keyword(s):  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Serum Sodium ◽  
Rare Case ◽  
Central Pontine Myelinolysis ◽  
Graph Representation ◽  
Radiological Findings ◽  
Complicated Case ◽  
Pontine Myelinolysis ◽  
Central Pontine

A 42-year-old high risk pregnant female presented with hyponatremia from multiple causes and was treated with total parenteral nutrition. She developed acute hypernatremia due to the stage of pregnancy and other comorbidities. All the mechanisms of hyponatremia and hypernatremia were summarized here in our case report. This case has picture (graph) representation of parameters that led to changes in serum sodium and radiological findings of central pontine myelinolysis on MRI. In conclusion we present a complicated case serum sodium changes during pregnancy and pathophysiological effects on serum sodium changes during pregnancy.

scholarly journals Relowering of Serum Na for Osmotic Demyelinating Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Hideomi Yamada ◽  
Koji Takano ◽  
Nobuhiro Ayuzawa ◽  
George Seki ◽  
Toshiro Fujita
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Supportive Therapy ◽  
Chronic Hyponatremia ◽  
Pontine Myelinolysis ◽  
Extreme Care ◽  
The Brain ◽  
Osmotic Demyelinating Syndrome ◽  
Central Pontine ◽  
Rapid Correction

We report a case in whom slow correction of hyponatremia (5 mmol/day for 3 days) induced central pontine myelinolysis (CPM). After the diagnosis was confirmed by imaging, we started to relower serum Na that completely recovered the sign and symptoms of CPM. Rapid correction of serum sodium is known to be associated with CPM. However, it may occur even after slow correction of hyponatremia. Currently, there is no standard therapy for CPM other than supportive therapy. Other therapy includes sterioid, plasmaphresis and IVIG, but these therapies have not been shown to be particularly effective. The pathophysiology of CPM is related to a relative dehydration of the brain during the correction of hyponatremia, resulting in cell death and demyelination, therefore gentle rehydration with lowering serum sodium may not be an unreasonable therapy. The present case provides supportive evidence that reinduction of hyponatremia is effective in treating CPM if started immediately after the diagnosis is suggested. The present case tells us that severe chronic hyponatremia must be managed with extreme care especially in patients with chronic debilitating illness and that relowering serum Na is a treatment of choice when CPM is suggested.

A Misleading Case of Central Pontine Myelinolysis

1992 ◽  
Vol 160 (4) ◽  
pp. 550-552 ◽  
Author(s):  
Peter McColl ◽  
Christopher Kelly
Keyword(s):  
British Journal ◽  
Schizophrenic Patient ◽  
Serum Sodium ◽  
Psychiatric Patients ◽  
Central Pontine Myelinolysis ◽  
Review Of The Literature ◽  
Psychiatric Referral ◽  
Chronic Schizophrenic Patient ◽  
Pontine Myelinolysis ◽  
Central Pontine

Central pontine myelinolysis (CPM) is an uncommon disorder initially described in alcoholic or malnourished patients. Recent reports suggest an aetiological association with abnormalities of serum sodium. A physically unwell non-alcoholic chronic schizophrenic patient, whose symptoms led to psychiatric referral, died of CPM. A review of the literature reveals that psychiatric patients may indeed be at risk for CPM.British Journal of Psychiatry (1992), 160, 550–552

Association between rise in serum sodium and central pontine myelinolysis

1982 ◽  
Vol 11 (2) ◽  
pp. 128-135 ◽  
Author(s):  
Michael D. Norenberg ◽  
Kevin O. Leslie ◽  
Andrew S. Robertson
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Pontine Myelinolysis ◽  
Central Pontine

scholarly journals Severe hypokalaemia in diabetic ketoacidosis: a contributor to central pontine myelinolysis?

2019 ◽  
Vol 2019 ◽  
Author(s):  
A Chinoy ◽  
N B Wright ◽  
M Bone ◽  
R Padidela
Keyword(s):  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Serum Sodium ◽  
Management Strategies ◽  
Central Pontine Myelinolysis ◽  
Central Line ◽  
List Type ◽  
Pontine Myelinolysis ◽  
Central Pontine

Summary 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. Learning points: Hypokalaemia is a recognised complication of treatment of paediatric diabetic ketoacidosis that should be aggressively managed to prevent acute complications. Central pontine myelinolysis is rare in children, and usually observed in the presence of rapid correction of hyponatraemia. However, there is observational evidence of an association between hypokalaemia and central pontine myelinolysis, potentially by priming the endothelial cell membrane to injury by lesser fluctuations in osmotic pressure. Consider central pontine myelinolysis as a complication of the management of paediatric diabetic ketoacidosis in the presence of relevant symptoms with profound hypokalaemia and/or fluctuations in serum sodium levels. We have suggested an approach to the management strategies of hypokalaemia in paediatric diabetic ketoacidosis which includes oral potassium supplements if tolerated, minimising the duration and the rate of insulin infusion and increasing the concentration of potassium intravenously (via central line if necessary).

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