Rapid Sodium Correction Research Articles

Síndrome de secreción inadecuada de hormona antidiurética

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is defined as a disorder in renal free water excretion control due to the inability to suppress the secretion of antidiuretic hormone (ADH) or vasopressin. The most frequent causes are usually acquired, notable among which are central nervous system involvement, malignancy, pulmonary diseases, or drugs. Up to 35% of admitted patients have hyponatremia, of which up to 40% can be attributed to SIADH. It is considered acute when it occurs in less than 48hours. It can trigger vomiting, convulsions, coma, and death due to cerebral herniation resulting from increased intracranial pressure. Chronic forms are more common and entail symptoms such as nausea, confusion, weakness, or agitation. In order to diagnose it, it is necessary to identify the presence of a true hypoosmolar euvolemic hyponatremia, ruling out other hormonal abnormalities or drug use. Treatment of the acute form is based on the emergency use of hypertonic saline solution, avoiding excessively rapid sodium correction that would trigger an osmotic demyelination syndrome. In the case of chronic hyponatremia, water restriction, increased osmole intake, and tolvaptan can be used in addition to acting on the triggering causes.

Rate of Sodium Correction and Osmotic Demyelination Syndrome in Severe Hyponatremia: A Meta-Analysis.

Current guidelines recommend limiting the rate of correction in patients with severe hyponatremia to avoid severe neurologic complications such as osmotic demyelination syndrome (ODS). However, published data have been conflicting. We aimed to evaluate the association between rapid sodium correction and ODS in patients with severe hyponatremia. We searched PubMed, Embase, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials from inception to November 2023. The primary outcome was ODS and the secondary outcomes were in-hospital mortality and length of hospital stay. We identified 7 cohort studies involving 6,032 adult patients with severe hyponatremia. Twenty-nine patients developed ODS, resulting in an incidence rate of 0.48%. Seventeen patients (61%) had a rapid correction of serum sodium in the first or any 24-hour period of admission. Compared with a limited rate of sodium correction, a rapid rate of sodium correction was associated with an increased risk of ODS (RR, 3.91 [95% CI, 1.17 to 13.04]; I2 = 44.47%; p = 0.03). However, a rapid rate of sodium correction reduced the risk of in-hospital mortality by approximately 50% (RR, 0.51 [95% CI, 0.39 to 0.66]; I2 = 0.11%; p < 0.001) and the length of stay by 1.3 days (Mean difference, -1.32 [95% CI, -2.54 to -0.10]; I2 = 71.47%; p = 0.03). Rapid correction of serum sodium may increase the risk of ODS among patients hospitalized with severe hyponatremia. However, ODS may occur in patients regardless of the rate of serum sodium correction.

Syndrome of Inappropriate Antidiuretic Hormone Release Secondary to Ectopic Olfactory Neuroblastoma: Case Report and Review of Literature.

Ectopic olfactory neuroblastoma (ONB) is a rare neuroendocrine sinonasal malignancy which arises from sinonasal regions where olfactory neuroepithelium does not exist. Presentation of syndrome of inappropriate antidiuretic hormone release (SIADH) in patients with ectopic ONB is extremely rare. We report a case of a 22-year-old patient with ectopic ONB and paraneoplastic SIADH that was managed at our center. The ONB was arising from the left lamina papyracea and extending into the maxillary and ethmoid sinuses and filling the nasal cavity. Correction of sodium levels occurred within 24 hours of endoscopic resection via a combined trans-nasal transorbital approach. To avoid negative sequela secondary to rapid sodium correction, the patient was managed by desmopressin to obtain gradual sodium correction, which was achieved on the fourth postoperative day. Ectopic presentation of ONB with paraneoplastic SIADH is extremely rare with only 7 cases reported in the literature to date. Management via surgical resection and/or radiotherapy for these patients requires the managing clinician to be vigilant of serum sodium levels. A multidisciplinary approach is essential for optimal outcomes.

Correcting Hypernatremia in Children.

In children with hypernatremia, current clinical guidelines recommend a reduction in serum sodium of 0.5 mmol/L per hour or less to avoid complications of cerebral edema. However, no large-scale studies have been conducted in the pediatric setting to inform this recommendation. Therefore, this study aimed to report the association between the rate of correction of hypernatremia, neurological outcomes, and all-cause mortality in children. A retrospective cohort study was conducted from 2016 to 2019 at a quaternary pediatric center in Melbourne, Victoria, Australia. All children with at least one serum sodium level ≥150 mmol/L were identified through interrogation of the hospital's electronic medical record. Medical notes, neuroimaging reports, and electroencephalogram results were reviewed for evidence of seizures and/or cerebral edema. The peak serum sodium level was identified and correction rates over the first 24 hours and overall were calculated. Unadjusted and multivariable analyses were used to examine the association between the rate of sodium correction and neurological complications, the requirement for neurological investigation, and death. There were 402 episodes of hypernatremia among 358 children over the 3-year study period. Of these, 179 were community-acquired and 223 developed during admission. A total of 28 patients (7%) died during admission. Mortality was higher in children with hospital-acquired hypernatremia, as was the frequency of intensive care unit admission and hospital length of stay. Rapid correction (>0.5 mmol/L per hour) occurred in 200 children and was not associated with greater neurological investigation or mortality. Length of stay was longer in children who received slow correction (<0.5 mmol/L per hour). Our study did not find any evidence that rapid sodium correction was associated with greater neurological investigation, cerebral edema, seizures, or mortality; however, slow correction was associated with a longer hospital length of stay.

Effective treatment of osmotic demyelination syndrome with corticosteroid therapy: A case report

Background: Osmotic demyelination syndrome (ODS) is characterized by widespread degeneration of myelin within the central nervous system (CNS) and has no established treatment. A limited number of cases have reported positive outcomes with corticosteroid in the treatment of ODS. We report the case of complete recovery of ODS with corticosteroid. Case presentation: A 48-year-old man presented with a stupor condition and exhausted. He was hospitalized at the Endocrinology Department with hyponatraemia, which was rapidly corrected with hypertonic saline from 103 to 116mmol/L. He was transferred to the Stroke Department because of worsening consciousness, arising rigidity and bradykinesia of the extremyties, worsening dysarthria and bradyphrenia. A brain magnetic resonance imaging (MRI) scan revealed later on pontine myelinolysis. He was commenced on corticoid 11 days after rapid correction of sodium. His status began to improve gradually after 10 days from starting of corticosteroid therapy and at 44 day-follow-up had no neurological deficit. Conclusion: Corticosteroid therapy can be considered as an effective treatment modality in osmotic demyelination syndrome.

Tolvaptan for the treatment of the syndrome of inappropriate antidiuresis (SIAD).

The syndrome of inappropriate antidiuresis (SIAD), the commonest cause of hyponatraemia, is associated with significant morbidity and mortality. Tolvaptan, an oral vasopressin V2-receptor antagonist, leads through aquaresis to an increase in serum sodium concentration and is the only medication licenced in Europe for the treatment of euvolaemic hyponatraemia. Randomised controlled trials have shown that tolvaptan is highly efficacious in correcting SIAD-related hyponatraemia. Real-world data have confirmed the marked efficacy of tolvaptan, but they have also reported a high risk of overly rapid sodium increase in patients with a very low baseline serum sodium. The lower the baseline serum sodium, the higher the tolvaptan-induced correction rate occurs. Therefore, a lower starting tolvaptan dose of 7.5 mg has been evaluated in small cohort studies, demonstrating its efficacy, but it still remains unclear as to whether it can reduce the risk of overcorrection. Most international guidelines, except for the European ones, recommend tolvaptan as second-line treatment for SIAD after fluid restriction. However, the risk of unduly rapid sodium correction in combination with its high cost have limited its routine use. Prospective controlled studies are warranted to evaluate whether tolvaptan-related sodium increase can improve patient-related clinical outcomes, such as mortality and length of hospital stay in the acute setting or neurocognitive symptoms and quality of life in the chronic setting. In addition, the potential role of a low tolvaptan starting dose needs to be further explored. Until then, tolvaptan should mainly be used as second-line treatment for SIAD, especially when there is a clinical need for prompt restoration of normonatraemia. Tolvaptan should be used with specialist input according to a structured clinical pathway, including rigorous monitoring of electrolyte and fluid balance and, if needed, implementation of appropriate measures to prevent, or when necessary reverse, overly rapid hyponatraemia correction.

Rhabdomyolysis due to rapid correction of sodium in a patient with hyponatremia secondary to water intoxication

Rhabdomyolysis due to rapid correction of sodium in a patient with hyponatremia secondary to water intoxication

P.035 Impressive MRI findings in the case of iatrogenic osmotic demyelination syndrome: case report

Background: Osmotic demyelination syndrome (ODS) is a known complication of rapid sodium correction. While the pons is classically the most vulnerable region to osmotic shifts, other structures may also be affected. Prognosis varies from death to full recovery, yet we cannot accurately predict a patient’s outcome in the acute phase. Methods: Patient chart, medical imaging, and laboratory findings were reviewed. Results: Here we present the case of a 57-year-old woman seen at our center, who was transferred from a community hospital in the context of ODS after having her serum sodium corrected from 106 mmol/L to 122 mmol/L within 24 hours. She showed depressed mental status, bulbar symptoms, ataxia and respiratory compromise, eventually requiring transfer to the intensive care unit for intubation. MRI of the brain showed striking demyelinating injury at the level of the pons. The patient was discharged to a rehabilitation facility, eventually achieving independence in activities of daily living. Conclusions: This case illustrates canonical neuroimaging findings associated with ODS. Despite extensive initial damage, long-term disability can be mitigated with appropriate care. Future studies seeking to identify specific markers imaging and clinical markers would be of interest to predict functional outcome.

Managing Rapid Sodium Correction: A Case of Osmotic Demyelination (P1-1.Virtual)

Managing Rapid Sodium Correction: A Case of Osmotic Demyelination (P1-1.Virtual)

Hyperosmolar Therapy in the Management of Intracranial Hypertension.

Hyperosmolar Therapy in the Management of Intracranial Hypertension.

Clinical analysis for osmotic demyelination syndrome in patients with chronic hyponatremia

Background: Although osmotic demyelination syndrome (ODS) has been well known to be associated with a rapid correction of sodium (Na+) in patients with chronic hyponatremia, its risk factors and clinical outcomes have not been examined in Taiwan. Aim: The aim of the study was to analyze the underlying causes and overlooked risk factors in patients with ODS. Methods: We retrospectively collected chronic hyponatremic patients developing ODS and analyzed their clinical characteristics. Results: Fourteen patients (7 males and 7 females) with a mean age of 62.7 ± 17.9 years old were enrolled. Their underlying causes included gastrointestinal illness with poor intake (n = 7), chronic use of diuretics (n = 2), syndrome of inappropriate antidiuretic hormone (n = 2), pneumonia (n = 2), and hypopituitarism (n = 1). Their serum Na+ was 107.2 ± 1.2 mmol/L with mild hypokalemia (potassium 3.1 ± 7 mmol/L), hypoalbuminemia (albumin, 3.4 ± 0.6 g/dL), and hypophosphatemia (phosphorus, 2.3 ± 1.0 mg/dL). Their mean Na+ correction rate was 8.4 ± 9 mmol/L/day and most patients (60%) developed ODS in first 3 days. Their manifestations included delirium, seizures, unstable gait, aphasia, and drowsy consciousness. Brain magnetic resonance imaging demonstrated that 42.8% had isolated central pontine myelinolysis. Totally, 43% of ODS patients had unfavorable outcome with death and disability. In addition, patients with rapid Na+ correction rate (>12 mmol/L/day, n = 4) usually exhibited significant hypokalemia (2.5 ± 0.4 vs. 3.5 ± 0.7 mmol/L, P < 0.05) as compared with those without. Conclusion: Nutritional status and concurrent electrolyte deficiencies such as hypokalemia are major risk factors in patients with ODS. Clinicians should timely recognize these potential risks of ODS and reduce Na+ correction rate to avoid catastrophic outcomes.

Effective treatment of osmotic demyelination syndrome with plasmapheresis: a case report and review of the literature

BackgroundTreatment options for chronic osmotic demyelination syndrome are limited to case reports and only a very few show complete recovery. We report a case of complete recovery of chronic osmotic demyelination syndrome with plasmapheresis.Case presentationA 43-year-old Sri Lankan man presented with fever, repeated vomiting, unsteady gait, increased tonicity of his right upper limb and paucity of speech for three days. He was treated in the local hospital with antibiotics and antivirals as per central nervous system infection. He had hyponatraemia, which was rapidly corrected with hypertonic saline from 97 to 119 mmol/L. He was transferred to our hospital because of progressive reduction of consciousness, rapidly worsening rigidity and bradykinesia of all four limbs and worsening dysarthria and bradyphrenia. Magnetic resonance imaging of the brain was compatible with osmotic demyelination syndrome. He was commenced on plasmapheresis twenty-two days after rapid correction of sodium. He regained independent mobility with complete resolution of rigidity, bradykinesia and speech dysfunction after five cycles of alternate day plasmapheresis.ConclusionPlasmapheresis can be considered as an effective treatment modality in chronic osmotic demyelination syndrome.

Association Between ICU-Acquired Hypernatremia and In-Hospital Mortality: Data From the Medical Information Mart for Intensive Care III and the Electronic ICU Collaborative Research Database.

Describe the relationship between ICU-acquired hypernatremia and in-hospital mortality and investigate the optimal hypernatremia correction rate. Observational study including two individual ICU cohorts. We used the Medical Information Mart for Intensive Care III v. 1.4 database consists of all ICU patients admitted to the Beth Israel Deaconess Medical Center in Boston from 2001 to 2012 (n = 46,476). The electronic ICU v. 2.0 database consists of all ICU patients admitted to 208 distinct hospitals across the United States from 2014 to 2015 (n = 200,859). We included all adult patients admitted to an ICU with two consecutive sodium samples within normal range (135-145 mmol/L) and without two consecutive hyponatremic samples (< 135 mmol/L) during the ICU stay. Of 23,445 patients identified in Medical Information Mart for Intensive Care III, 9% (n = 2,172) developed hypernatremia during their ICU stay. In electronic ICU, 88,160 patients were identified and 7% (n = 5,790) developed hypernatremia. In both cohorts, patients with hypernatremia had a higher mortality (Medical Information Mart for Intensive Care III: 20% vs 42%; p < 0.01 and electronic ICU: 6% vs 22%; p < 0.01), with hypernatremia increasing the risk of in-hospital mortality (Medical Information Mart for Intensive Care III: odds ratio, 1.15; 95% CI, 1.13-1.17 and electronic ICU: odds ratio, 1.11; 95% CI, 1.10-1.12) and over time using a Cox regression. Rapid sodium correction rate (> 0.5 mmol/L/hr) was associated with an increased in-hospital mortality in both cohorts (Medical Information Mart for Intensive Care III: odds ratio, 1.08; 95% CI, 1.03-1.13 and electronic ICU: odds ratio, 1.10; 95% CI, 1.06-1.13). In the electronic ICU cohort, rapid correction rates were associated with a significant difference in in-hospital mortality, but there was no statistically significant association in the Medical Information Mart for Intensive Care III cohort. ICU-acquired hypernatremia is associated with increased in-hospital mortality. Furthermore, a rapid sodium correction rates may be harmful. This suggests it is important to both prevent ICU-acquired hypernatremia and to avoid rapid correction rates if a patient becomes hypernatremic.

Central pontine myelinolysis and extrapontine myelinolysis: literature review and case report

Central pontine myelinolysis (CPM) is a concentrated, symmetric, non-inflammatory demyelination within the central basis pontis. In 10 % of patients with СРМ, demyelination also occurs in extrapontine regions: the mid brain, thalamus, basal nuclei, and cerebellum. Demyelination occurs in regions of compact interdigitation of white and gray matter as a result of cellular edema, which is caused by fluctuating osmotic forces, results in compression of fiber tracts. The most frequent cause of abrupt change in osmotic pressure is the rapid sodium correction of prolonged hyponatremia. In case that we report, there is a combination of central pontine and extrapontine myelinolysis, which occurs in 71-year-old woman owing to rapid sodium correction of prolonged hyponatremia which by turn developed due to salt-free diet, improper antihypertensive therapy and overheating. The diagnosis was confirmed by magnetic resonance imaging (MRI). The treatment led to significant decrease of neurological deficit.

SUN-436 Severe Hyponatremia as the Presenting Feature of Partially Empty Sella

Introduction: We report a case of severe acute on chronic hyponatremia meeting the laboratory diagnostic criteria of SIADH. Subsequent evaluation showed secondary adrenal insufficiency due to partially empty sella. Hyponatremia completely resolved following hydrocortisone treatment. Clinical Case: A 76-year-old man with history of hypothyroidism and SIADH was admitted with weakness, fatigue, and leg cramps for the past 3 months. He was staying in a cabin with a broken air conditioner during the summer when his symptoms started. Physical exam revealed mild dry mucus membranes, normal skin turgor, capillary refill less than 2 sec., bradycardia, and no skin hyperpigmentation. He was found to have acute-on-chronic hyponatremia with a serum sodium of 115 mEq/L (baseline 124 mEq/L-130 mEq/L), which worsened with initial volume resuscitation. Lasix and salt tablets were not effective treatment. Other labs showed a low serum osmolality (241 mOsm/kg), high urine osmolality (598 mOsm/kg), high urine sodium (121 mmol/L), low serum uric acid (2.7 mg/dL, n 3.3-8.5 mg/dL), normal TSH, and a low normal AM cortisol (5.7 ug/dL, n 4.0-17.0 ug/dL). A subsequent cosyntropin stimulation test confirmed adrenal insufficiency with a 60 min cortisol of 10.3 ug/dL. ACTH was inappropriately normal (23 pg/mL, n 7-69 pg/mL) indicating a central etiology. In addition, he had a mildly elevated prolactin (23 ng/mL, n 4-15 ng/mL), inappropriately normal TSH (2.83 uIU/mL, n 0.30-4.50 uIU/mL), low normal total T4 (5 ug/dL, n 4.9-11.7 ug/dL), and a mildly low total T3 (52.3 ng/dL, n 58.0-159.0 ng/dL) suggesting a possible secondary hypothyroidism. A pituitary MRI revealed partially empty sella without evidence of pituitary adenoma. The patient was started on stress-dose hydrocortisone with subsequent increased urine output (4 L within 8 h of initial treatment) and increased serum sodium as well. To prevent rapid sodium correction, one dose of desmopressin was given with a low rate hypertonic saline to equilibrate the desmopressin effect. Hydrocortisone was tapered to maintenance dose, and the fluid restriction was discontinued to prevent dehydration. His home Levothyroxine dose was increased, and he was discharged with a serum sodium of 133 mEq/L. As an outpatient, his sodium has normalized with continued treatment. Discussion: Secondary adrenal insufficiency is characterized by euvolemic hyponatremia with biochemical features of SIADH without hyperkalemia. ADH increases due to the lack of cortisol negative feedback loop and the reduction in systemic blood pressure and cardiac output from cortisol deficiency. Hyponatremia corrects rapidly with steroid treatment, which turns off ADH and causes free water excretion. Desmopressin and hypertonic saline can be effectively used to prevent or stop rapid sodium correction. An interesting feature about this case is that partially empty sella is the cause for hypopituitarism.

Real-life experience of tolvaptan use in the treatment of severe hyponatraemia due to syndrome of inappropriate antidiuretic hormone secretion.

European guidelines do not recommend tolvaptan for treatment of syndrome of inappropriate antidiuretic hormone secretion (SIADH), principally owing to concerns about risk of overly rapid correction of hyponatraemia. This study evaluated the real-life effectiveness and safety of tolvaptan. Consecutive case series. Inpatients treated with tolvaptan for SIADH in 2 UK hospitals over a 3-year period. The primary outcome measures were serum sodium (sNa) correction at 24 and 48 h after tolvaptan therapy. This case series included 61 patients aged 74·4 ± 15·3 years with (mean ± SD) sNa 119·9 ± 5·5 mmol/l. The mean sNa increase 24 h after tolvaptan initiation was 9 ± 3·9 mmol/l. Excessive correction of hyponatraemia was observed in 23% of patients with all these patients having baseline sNa <125 mmol/l, but no cases of osmotic demyelination syndrome were recorded. At the end of tolvaptan therapy, sNa increase was 13·5 ± 5·9 mmol/l with 96·7% of patients having sNa increase ≥5 mmol/l in 48 h. There was a negative significant correlation (P = 0·012) between baseline sNa and 24-h change; for every 1 mmol/l reduction in baseline value, sNa increased by an additional 0·23 mmol/l (95% CI 0·05-0·41). Tolvaptan is effective in correcting hyponatraemia. Without rigorous electrolyte monitoring, tolvaptan carries a significant risk of overly rapid sodium correction, especially in patients with starting sNa <125 mmol/l. Tolvaptan should be used with great caution under close electrolyte monitoring.

Unpredictable Nature of Tolvaptan in Treatment of Hypervolemic Hyponatremia: Case Review on Role of Vaptans

Hyponatremia is one of the most commonly encountered electrolyte abnormalities occurring in up to 22% of hospitalized patients. Hyponatremia usually reflects excess water retention relative to sodium rather than sodium deficiency. Volume status and serum osmolality are essential to determine etiology. Treatment depends on several factors, including the cause, overall volume status of the patient, severity of hyponatremic symptoms, and duration of hyponatremia at presentation. Vasopressin antagonists like tolvaptan seem promising for the treatment of euvolemic and hypervolemic hyponatremia in heart failure. Low sodium concentrations cause cerebral edema, but the overly rapid sodium correction can also lead to iatrogenic cerebral osmotic demyelination syndrome. Demyelination may occur days after sodium correction or initial neurologic recovery from hyponatremia. The following case report analyzes the role of vasopressin antagonists in the treatment of hyponatremia and the need for daily dosing of tolvaptan and the monitoring of serum sodium levels to avoid rapid overcorrection which can result in osmotic demyelination syndrome (ODS).

Use of Conivaptan for Refractory Syndrome of Inappropriate Secretion of Antidiuretic Hormone in a Pediatric Patient

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is the most common form of hyponatremia in hospitalized patients. The available treatment options for SIADH are limited and not completely effective. A more recent and specific option for treatment of hyponatremia secondary to SIADH are the vasopressin-receptor antagonists. Conivaptan, an intravenous vasopressin-receptor antagonist, is Food and Drug Administration approved for the treatment of euvolemic and hypervolemic hyponatremia in adults; however, data regarding its use in pediatric patients are extremely limited. Conivaptan played an integral role in the treatment of hyponatremia in this situation when conventional treatment modalities were ineffective. This patient did not experience any adverse effects, and his sodium level corrected slowly over a 24-hour period, avoiding complications of rapid sodium correction.

Value of diffusion-weighted imaging in central pontine and extrapontine myelinolysis

Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are rare neurological disorders characterized by demyelination in and/or outside the pons. Whether diffusion-weighted imaging (DWI) might facilitate an earlier diagnosis has not yet been studied systematically. We describe demographics, clinical presentation, and early magnetic resonance imaging (MRI) findings with special emphasis on the relevance for diagnosis of CPM and/or EPM in eight patients. Of the analysed eight patients (aged 37-70 years; two men, six women), CPM was diagnosed in three, EPM in one, and a combination of CPM and EPM in four patients. Aetiology was rapid correction of sodium in two patients; a combination of hyponatremia, alcoholism and alcohol withdrawal in five patients and unclear in one patient. Seven patients suffered from chronic alcoholism and four from malnutrition. Demyelinating lesions were found in the pons, thalamus, caudate nucleus, putamen and midbrain. While the lesions could be clearly delineated on T2- and T1-weighted images, DWI demonstrated a strong signal in only six patients. Furthermore, DWI demonstrated lesions only to some extent in two patients and was completely negative in two patients on initial MRI. In none of the patients did the demonstration of hyperintense lesions on DWI precede detection on conventional MRI sequences. Apparent diffusion coefficient (ADC) values were heterogenous with a decrease in two cases and an increase in the remainder. We conclude that early DWI changes are a common finding in CPM/EPM but do not regularly precede tissue changes detectable on conventional MRI sequences. Heterogenous ADC values possibly represent different stages of disease.

Central pontine myelinolysis associated with pancreatic diabetes

A 60-year-old man presented with subacute progression of difficulty in speaking and walking. The patient had been suffering from chronic pancreatitis due to alcoholism, and glucose level in the serum had been remarkably variable for a few months. Blood pressure was normal under treatment with angiotensin II receptor blocker. Clinical examination showed ocular dysmetria, scanning speech, dysphagia, clumsy hands, and wide-based gait, suggesting cerebellar ataxia. He was alert, and his cognitive function and psychological status were normal. Tendon reflexes were intact in all limbs, and there was no sensory disturbance, muscle weakness, involuntary movement, or autonomic dysfunction. Two weeks after the first symptom emerged, the patient was unable to walk by himself because of the ataxic symptoms. Laboratory tests revealed hyperglycemia (685 mg/dl), which was the highest value for the patient, and HbA1c was 16.9%. Blood urea nitrogen was 36.7 mg/dl and creatinine level was 1.61 mg/dl in the serum, which had been the same level for years, reflecting chronic kidney dysfunction. There were no abnormalities detected in the levels of electrolytes including sodium, and no episodes of correction of hyponatremia. Brain magnetic resonance images (MRI) were normal on admission, but after 3 weeks, symmetrical hyperintensity in the central portion of the pons and middle cerebellar peduncles was evident on T2-weighted and fluid-attenuated inversion recovery images (Fig. 1a, b). The periphery of the pons was not affected, and thus, these MRI findings were considered to be typical of central pontine myelinolysis (CPM). The lesions were not enhanced by an administration of gadolinium, suggesting that tumor and inflammation were unlikely. There was no obvious change in the apparent diffusion coefficient, indicating that infarction and reversible posterior leukoencephalopathy were also unlikely. Abdominal computed tomography demonstrated pancreatic lithiasis (Fig. 1c). There was no malignancy in the chest, abdomen, or pelvis. We diagnosed the patient with CPM caused by a rapid progression of hyperglycemia. After initiating treatment with insulin, his hyperglycemia rapidly improved. The ataxic symptoms gradually recovered with the aid of rehabilitation; ocular dysmetria and dysphagia almost disappeared in 2 months, and the patient was able to walk without help in 3 months. Additionally, his hand clumsiness and speech disturbance improved in 4 months. MRI findings remained the same with minimal improvement at 1 year after the onset. There was no apparent change in the levels of electrolytes in the serum throughout the disease course. CPM is recognized as a complication resulting from a rapid change in serum osmolarity, and a rapid correction of sodium in hyponatremic patients is widely accepted as the most common cause of CPM [1, 2]. A marked shift in the level of serum glucose can rarely be another causative factor, probably because the glucose level also influences the serum osmolarity [3, 4]. However, it is uncertain why CPM is observed in only a limited number of diabetic patients. Our patient developed CPM when his serum glucose levels fluctuated severely over the course of chronic H. Kuwahara (&) Department of Neurology and Neurological Science, Graduate School, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan e-mail: h-kuwahara.nuro@tmd.ac.jp