Pontine Myelinolysis Research Articles

Symptomatic and asymptomatic pontine hyperintensities: are they central pontine myelinolysis? Case series.

The diagnosis of central pontine hyperintensities on cranial magnetic resonance imaginghas wide-spectrum clinical entities, and the pro-type diagnosis of these is central pontine myelinolysis. The rapid changes in extracellular environment due to an imbalance of electrolytes or metabolic ortoxic stress to the myelin sheath can cause demyelination of white matter tracts in pons, which is why this situation could have different etiologies than just rapid sodium changes. Central pontine myelinolysiscan be presented with different clinical scenarios from asymptomatic to death. Here, we present eight patients who had central pontine hyperintensities on radiological imaging but showed various clinical symptoms and different etiologies. The etiologies of these cases are hypertriglyceridemia, alcohol consumption, antidepressant usage, immunocompromised situations, uncontrolled diabetes mellitus, liver and kidney failure, electrolyte changes, and adrenal insufficiency. We aimed to take attention with this case series to the fact that not only fast correction of hyponatremia is the cause of central pontine myelinolysis, but also different etiologies could play a role in this situation, and making the central pontine myelinolysis diagnosis considering different diagnosis is very important.

Osmotic Demyelination Syndrome after Correction of Hyponatremia

Osmotic demyelination syndrome is a rare neurological disease resulting in cerebral apoptosis and loss of myelin due to osmotic stress. Based on anatomical localization and pathological attributes, ODS can be categorized as Central Pontine Myelinolysis (CPM) and Extrapontine Myelinolysis (EPM). It has a biphasic course, with first phase reflecting electrolyte imbalance and the second with pontine dysfunction, impaired vigilance and movement disorders. In an autopsy-based study, a prevalence rate of 0.25–0.5% was seen in the general population and 10% in patients undergoing liver transplantation. Being a rare disease with variable, but preventable outcome, the present case was managed with Ayurvedic oral medication and Panchakarma therapy with an aim to improve the quality of life. In Ayurvedic perspective, Vata kshaya lakshanas occur during the phase of hyponatremia and further correction of this leads to disruption of osmolality (Kapha pitta accumulation) resulting in Avarana of Vata. This may be the reason for demyelination and localisation of Vata in Sira and Snayu leading to Sira snayu shoshana on both halves of the body resulting in Sarvangaroga (full body afflicted with Vata). Thus Avaranahara, Srotosodhana and Vatanulomana principles were adopted. An improvement in Barthel index and modified rankin scale were observed after a course of treatment for 30 days.

THU379 A Case Of Hyperglycemia With Severe Anion Gap Metabolic Acidosis: HHS Vs DKA

Abstract Disclosure: M. Shrivastava: None. B.J. Armendariz: None. U. Asija: None. A. Shah: None. M. Levy-kern: None. D. Klamp: None. Background: DKA is more profoundly associated with metabolic acidosis secondary to excessive ketones production in the setting of low insulin. Whereas HHS is associated with hyperglycemia with mild acidemia because ketone production is not as severe, as insulin is high/normal. We present a case of hyperglycemic state which challenged this stereotype. Clinical Case: 57 YO male with no prior history of DM or CKD presented with altered mental status, abdominal pain, 15lbs weight loss. As per wife, patient had URI and his condition had been deteriorating since then. Initial labs revealed leukocytosis, BUN 105, serum creatinine 5.8, Anion gap 37, and blood glucose (BG) 1433mg/dl. Blood Gas significant for pH 7.1, PCO2 20, PO2 138, bicarbonate 7.8, and Lactic acid 1.5. Further testing revealed Urine ketone 15, Serum beta-hydroxybutyrate 0.5 mmol/l, HbA1c 13%, serum Osmolarity 391mOsm/kg. Treatment was initiated with 0.9% NS, electrolyte replacement, and IV insulin infusion. Serum glucose corrected at 50-75mg/dl/hr unmasked underlying hypernatremia. Fluid was switched to 0.45% NS with dextrose 5%. Despite BG correction, patient’s mentation remained altered. Further imaging including MRI brain was negative for osmotic demyelination syndrome. Eventually, BG came below 200mg/dl, and acidemia resolved. Pt was transitioned to subcutaneous insulin. Mentation started improving. Clinical Lesson: T1DM and T2DM are Insulin deficient vs insulin resistant states respectively[1]. Insulin deficiency causes decreased intracellular consumption of glucose, triggering intracellular starvation, promoting lipolysis in presence of stress hormones like glucagon, Norepinephrine, and cortisol[2]. Free fatty acids, produced from lipolysis undergo beta-hydroxylation forming ketones. Hence, metabolic acidosis in DKA is secondary to ketoacidosis. HHS is seen in insulin-resistant states, with normal/high serum insulin. Insulin promotes lipogenesis, hence HHS has minimal ketoacidosis, and is rarely associated with AGMA. Both DKA and HHS are hyperosmolar states most commonly triggered by infections[3], but in HHS, osmolarity generally exceeds 320mmol/l, free water deficit is more profound. This reflects severe dehydration, decreased intravascular volume, tissue hypoperfusion, possibly end organ damage including AKI[4], and in severe cases present as Acute renal failure(ARF)[4][5][6]. Hyperosmolarity can itself induce rhabdomyolysis and thus AKI[5][6]. In our case, ARF caused elevated BUN, decreased acid secretion from renal tubule, worsened acidosis, and presented as AGMA, mimicking DKA. In such situations measuring serum beta-hydroxybutyrate and C-Peptide can differentiate the two conditions. Hypernatremia and dysregulated osmolarity pose risk of osmotic demyelination syndrome. It is pertinent to correct AGMA, osmolarity, and hyperglycemia concurrently. Presentation: Thursday, June 15, 2023

FRI357 A Rare Case Of Paraneoplastic Syndrome Of Inappropriate Secretion Of Antidiuretic Hormone In Oropharyngeal Squamous Cell Carcinoma

Abstract Disclosure: N. Torres: None. H. Rios: None. G. Rios: None. Y. Medina: None. L. Valerio: None. S. Rosa: None. A. Ortiz: None. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by hyponatremia that results from water retention attributable to persistent arginine vasopressin release. SIADH is considered the most common cause of euvolemic hyponatremia. Head and neck cancers are linked with 1.5% of SIADH cases. Cases reported in the literature about this association with oropharyngeal squamous cell carcinoma (SCC) were few, and no incidence data is currently available. We present a rare case of a patient with SIADH secondary to well-differentiated oropharyngeal squamous cell carcinoma. A case of 63 y/o male with Oropharyngeal SCC, previous gastrostomy, and tracheostomy due to malignancy. The patient initially presented with general malaise and weakness. Maxillofacial and neck CT scans were remarkable for a mass at the left lateral floor of the mouth, measuring approximately 5.7 cm AP x 2.5 cm transverse x 3.7 cm CC. Physical examination was remarkable for cachexia, but normal skin turgor and moist oral mucosa. An incidental finding of severe hyponatremia of 114 mEq was found. Confirmation of hypotonic euvolemic hyponatremia was performed with a urine osmolality of >100 mOsm per kg and high urine sodium (>40 mEq). These findings presented a strong case for our differential diagnosis of SIADH. Other differential diagnoses were hypothyroidism or adrenal insufficiency. The patient’s thyroid stimulating hormone was within normal levels, and adrenal insufficiency workup was negative, making paraneoplastic SIADH the more likely diagnosis due to SCC. Initial treatment was started with a 3% hypertonic solution drip running at 15 ml/hr. The chemistry panel was monitored every six hours to achieve a 6 mEq change, at a slow rate to avoid osmotic demyelination syndrome, a goal of 122 mEq. Sodium was corrected in 24 hours; 3% saline solution drip was discontinued. Once this level was reached, we continued the fluid restriction (<1L daily), and salt packets with meals. After consultation, Nephrology and Endocrinology services agreed with our diagnosis of hypotonic euvolemic hyponatremia due to ectopic production of paraneoplastic SIADH due to the oropharyngeal SCC. The patient’s hypotonic euvolemic hyponatremia was corrected, symptoms improved, and he was discharged with close follow-up with Hematology/Oncology, Nephrology, and Endocrinology services. Paraneoplastic SIADH due to squamous cell carcinoma is rarely observed in the hospital setting. It is important to consider paraneoplastic SIADH from SCC in the differential diagnosis of hypotonic euvolemic hyponatremia since early diagnosis and treatment can decrease long-term complications. We could have also considered pharmacological therapy for SIADH including the use of demeclocycline, vaptans, and furosemide if the patient had not responded to our interventions. We followed guideline therapy with intravenous hypertonic saline at the start, then transitioned to only using oral salt tablets and fluid restrictions. The patient's hyponatremia steadily improved with our interventions and was able to be discharged with close outpatient follow-up. Presentation: Friday, June 16, 2023

Severe Hyponatremia Correction, Mortality, and Central Pontine Myelinolysis

BackgroundIn clinical practice, sodium correction rates are frequently limited in patients with severe hyponatremia to prevent neurologic complications. The implications of correction rates on overall mortality and length of hospital stay are unclear.MethodsIn this multicenter observational study, we evaluated the association of sodium correction rates with mortality, length of stay, and central pontine myelinolysis (CPM) in patients hospitalized with severe hyponatremia (admission serum sodium level less than 120 mEq/l).ResultsThe cohort included 3274 patients. A correction rate of less than 6 mEq/l/24 hours was observed in 38%, 6 to 10 mEq/l/24 hours was observed in 29%, and greater than 10 mEq/l/24 hours was observed in 33%. Compared with 6 to 10 mEq/l/24 hours, a correction rate of less than 6 mEq/l/24 hours exhibited higher in-hospital mortality in multivariable-adjusted and propensity score–weighted analyses. Compared with 6 to 10 mEq/l/24 hours, a correction rate of greater than 10 mEq/l/24 hours was associated with lower in-hospital mortality and shorter length of stay in multivariable analyses. Seven patients with CPM were identified, with five of seven developing CPM despite a sodium correction rate of less than or equal to 8 mEq/l/24 hours. Six of seven patients who developed CPM had alcohol use disorder, malnutrition, hypokalemia, or hypophosphatemia.ConclusionsLimiting the sodium correction rate was associated with higher mortality and longer length of stay. Whether the sodium correction rate influences neurologic complications needs further evaluation.

Safety and Efficacy of Vaptans in the Treatment of Hyponatremia from Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): A Systematic Review and Meta-Analysis.

The utilization of vasopressin receptor antagonists, known as vaptans, in the management of hyponatremia among patients afflicted with the syndrome of inappropriate antidiuretic hormone (SIADH) remains a contentious subject. This meta-analysis aimed to evaluate the safety and efficacy of vaptans for treating chronic hyponatremia in adult SIADH patients. Clinical trials and observational studies were identified by a systematic search using MEDLINE, EMBASE, and Cochrane Database from inception through September 2022. The inclusion criteria were the studies that reported vaptans' safety or efficacy outcomes compared to placebo or standard therapies. The study protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD 42022357307). Five studies were identified, comprising three RCTs and two cohort studies, enrolling a total of 1840 participants. Regarding short-term efficacy on days 4-5, vaptans exhibited a significant increase in serum sodium concentration from the baseline in comparison to the control group, with a weighted mean difference of 4.77 mmol/L (95% CI, 3.57, 5.96; I2 = 34%). In terms of safety outcomes, the pooled incidence rates of overcorrection were 13.1% (95% CI 4.3, 33.6; I2 = 92%) in the vaptans group and 3.3% (95% CI 1.6, 6.6; I2 = 27%) in the control group. Despite the higher correction rate linked to vaptans, with an OR of 5.72 (95% CI 3.38, 9.70; I2 = 0%), no cases of osmotic demyelination syndrome were observed. Our meta-analysis comprehensively summarizes the efficacy and effect size of vaptans in managing SIADH. While vaptans effectively raise the serum sodium concentration compared to placebo/fluid restriction, clinicians should exercise caution regarding the potential for overcorrection.

Delayed Osmotic Demyelination Syndrome Treated Successfully with Therapeutic Plasma Exchange: A Case Report

Delayed Osmotic Demyelination Syndrome Treated Successfully with Therapeutic Plasma Exchange: A Case Report

Osmotic demyelination syndrome with transient diabetes insipidus in postpartum female: a case report.

The authors present a case of 29-year-old female who presented with chief complaint of altered sensorium and quadriparesis. Two days prior to onset of symptoms, she underwent caesarean section, was kept on nil per oral and free fluid restriction, after which she had confusion, altered sensorium, and weakness in all four limbs. Sodium level was 170mEq/l. Urine osmolality and plasma osmolality was 150 and 410mOsm/kg of water, respectively. MRI showed high signal intensity lesion in pons suggestive of demyelination. She was diagnosed ODS with transient DI and quadriparesis, in postpartum period due to further rise in sodium after free fluid restriction and nil per oral. She was treated with desmopressin, 5% dextrose and 0.9% normal saline, her quadriparesis recovered and desmopressin was tapered and stopped over 45 days and discharged at stable state. ODS can rarely be associated with hypernatremia in postpartum female presenting as quadriparesis and altered sensorium. Clinicians should be familiar of ODS with hypernatremia with transient DI in postpartum period, which is reversible and can be managed by desmopressin and fluid replacement.

Long-term low-dose tolvaptan efficacy and safety in SIADH

PurposeTolvaptan, a selective vasopressin V2-receptor antagonist, is approved for the treatment of SIADH-related hyponatremia, but its use is limited. The starting dose is usually 15 mg/day, but recent clinical experience suggests a lower starting dose (<15 mg/day) to reduce the risk of sodium overcorrection. However, long-term low-dose efficacy and safety has not been explored, so far. Aim of our study is to characterize safety and efficacy of long-term SIADH treatment with low-dose Tolvaptan.MethodsWe retrospectively evaluated 11 patients receiving low-dose Tolvaptan (<15 mg/day) for chronic SIADH due to neurological, idiopathic and neoplastic causes. Plasma sodium levels were measured before and 1, 3, 5, 15 and 30 days after starting Tolvaptan and then at 3-month intervals. Anamnestic and clinical data were collected.ResultsMean time spanned 27.3 ± 29.8 months (range 6 months-7 years). Mean plasma sodium levels were within normal range 1, 3 and 6 months after starting Tolvaptan as well as after 1, 2, 3, 5 and 7 years of therapy. Neither osmotic demyelination syndrome nor overcorrection were observed. Plasma sodium levels normalization was associated with beneficial clinical effects. Neurological patients obtained seizures disappearance, improvement in neurological picture and good recovery from rehabilitation. Neoplastic patients were able to start chemotherapy and improved their general condition. Patients did not show hypernatremia during long-term follow-up and reported mild thirst and pollakiuria.ConclusionsThe present study shows that long-term low-dose Tolvaptan is safe and effective in SIADH treatment. No cases of overcorrection were documented and mild side effects were reported.

Loss of Ephaptic Contacts in the Murine Thalamus during Osmotic Demyelination Syndrome

ABSTRACT Background and aim A murine model mimicking osmotic demyelination syndrome (ODS) revealed with histology in the relay posterolateral (VPL) and ventral posteromedial (VPM) thalamic nuclei adjoined nerve cell bodies in chronic hyponatremia, amongst the damaged 12 h and 48 h after reinstatement of osmolality. This report aims to verify and complement with ultrastructure other neurophysiology, immunohistochemistry, and molecular biochemistry data to assess the connexin-36 protein, as part of those hinted close contacts. This ODS investigation included four groups of mice: Sham (NN; n = 13), hyponatremic (HN; n = 11), those sacrificed 12 h after a fast restoration of normal natremia (ODS12h; n = 6) and mice sacrificed 48 h afterward, or ODS48 h (n = 9). Out of these, thalamic zones samples included NN (n = 2), HN (n = 2), ODS12h (n = 3) and ODS48h (n = 3). Results Ultrastructure illustrated junctions between nerve cell bodies that were immunolabeled with connexin36 (Cx36) with light microscopy and Western blots. These cell’s junctions were reminiscent of low resistance junctions characterized in other regions of the CNS with electrophysiology. Contiguous neurons showed neurolemma contacts in intact and damaged tissues according to their location in the ODS zones, at 12 h and 48 h post correction along with other demyelinating alterations. Neurons and ephaptic contact measurements indicated the highest alterations, including nerve cell necrosis in the ODS epicenter and damages decreased toward the outskirts of the demyelinated zone. Conclusion Ephapses contained C × 36between intact or ODS injured neurons in the thalamus appeared to be resilient beyond the core degraded tissue injuries. These could maintain intercellular ionic and metabolite exchanges between these lesser injured regions and, thus, would partake to some brain plasticity repairs.

Osmotic demyelination syndrome: clinical and neuroimaging characteristics in a series of 8 cases.

Osmotic demyelination syndrome: clinical and neuroimaging characteristics in a series of 8 cases.

Isolated bilateral lateral geniculate nuclei T2/FLAIR hyperintensities heralding the development of central pontine myelinolysis in osmotic demyelination syndrome: neuro-images.

Isolated bilateral lateral geniculate nuclei T2/FLAIR hyperintensities heralding the development of central pontine myelinolysis in osmotic demyelination syndrome: neuro-images.

Stroke-like presentation of acute toxic leukoencephalopathy due to capecitabine treatment with extensive intramyelinic edema.

Stroke-like presentation of acute toxic leukoencephalopathy due to capecitabine treatment with extensive intramyelinic edema.

Evidence-based hyponatremia management in liver disease.

Hyponatremia is primarily a water balance disorder associated with high morbidity and mortality. The pathophysiological mechanisms behind hyponatremia are multifactorial, and diagnosing and treating this disorder remains challenging. In this review, the classification, pathogenesis, and step-by-step management approaches for hyponatremia in patients with liver disease are described based on recent evidence. We summarize the five sequential steps of the traditional diagnostic approach: 1) confirm true hypotonic hyponatremia, 2) assess the severity of hyponatremia symptoms, 3) measure urine osmolality, 4) classify hyponatremia based on the urine sodium concentration and extracellular fluid status, and 5) rule out any coexisting endocrine disorder and renal failure. Distinct treatment strategies for hyponatremia in liver disease should be applied according to the symptoms, duration, and etiology of disease. Symptomatic hyponatremia requires immediate correction with 3% saline. Asymptomatic chronic hyponatremia in liver disease is prevalent and treatment plans should be individualized based on diagnosis. Treatment options for correcting hyponatremia in advanced liver disease may include water restriction; hypokalemia correction; and administration of vasopressin antagonists, albumin, and 3% saline. Safety concerns for patients with liver disease include a higher risk of osmotic demyelination syndrome.

Management of adverse effects in hyperosmolar therapy of brain edema

Background: Mannitol and hypertonic saline are the most frequently used hyperosmolar agents to treat cerebral edema resulting from acute brain injury. However, there are several issues with using hyperosmolar therapies. Here, we focus on the potential adverse effects of hyperosmolar therapies and practical tips to overcome these issues in the neurointensive care unit.Current Concepts: Among the hyperosmolar agents used, mannitol may decrease intravascular volume and pose a potential risk of acute kidney injury for patients. Complications associated with using hypertonic saline include the risk of central pontine myelinolysis, coagulopathy, electrolyte imbalances, metabolic acidosis, and pulmonary edema. In addition, prolonged use of hypertonic saline increases the risk of hyperchloremic metabolic acidosis, which may be overcome with the concomitant use of sodium acetate.Discussion and Conclusion: Several laboratory variables were monitored in the neurointensive care unit to limit and possibly detect early complications related to hyperosmolar therapies. When using hyperosmolar agents, including mannitol and hypertonic saline, for therapeutic purposes in patients with cerebral edema, determining whether to use peripheral or central lines and determining the appropriate rate and infusion dose can minimize their adverse effects. Clinicians need to be aware of the potential adverse events of administering hyperosmolar agents.

A rare presentation of central pontine myelinolysis secondary to hyperglycaemia

BackgroundCentral pontine myelinolysis (CPM) is a rare demyelinating disorder caused by the loss of myelin in the center of the basis pontis. CPM typically occurs with rapid correction of severe chronic hyponatremia and subsequent disturbances in serum osmolality. Although hyperglycaemia is recognized as a pathogenetic factor in serum osmolality fluctuations, CPM is rarely seen in the context of diabetes.Case presentationA 66-year-old Chinese male presented with a history of gait imbalance, mild slurred speech and dysphagia for two weeks. MRI showed the mass lesions in the brainstem, and laboratory examinations showed high blood glucose and HbA1c, as well as increased serum osmolality. The patient was diagnosed with CPM secondary to hyperosmolar hyperglyceamia and received insulin treatment as well as supportive therapy. After six weeks of followup, the patient had fully recovered to a normal state.ConclusionCPM is a potentially fatal neurological condition and can occur in uncontrolled diabetes mellitus. Early diagnosis and timely treatment are crucial for improving the prognosis.

Fatal central pontine myelinolysis in a patient with uncontrolled HIV and normal sodium levels

Please view the PDF to see the formatted meeting abstract.&#x0D;

Fatal central pontine myelinolysis in a patient with uncontrolled HIV and normal sodium levels

Please view the PDF to see the formatted meeting abstract.&#x0D;

Central Pontine Myelinolysis in a Patient with Hepatosplenic T Cell Lymphoma and Hemophagocytic Lymphohistiocytosis (P6-4.007)

<h3>Objective:</h3> To discuss a rare case of central pontine myelinolysis (CPM) in a patient with hepatosplenic T cell lymphoma (HSTL) and hemophagocytic lymphohistiocytosis (HLH). <h3>Background:</h3> HSTL is a rare disease characterized by infiltration of mature T cells within the sinusoids of the spleen, liver, and bone marrow. Hyponatremia prior to orthotopic liver transplant for liver failure has previously been identified as a risk factor for the development of CPM due to possible disruption of astrocyte metabolism and impaired capacity to regulate osmotic changes leading to secondary dysfunction of the blood brain barrier. CPM has also previously been discovered in EBV positive HLH. <h3>Design/Methods:</h3> We conducted a case report and literature review with PubMed search terms: 1) “central pontine myelinolysis,” “hyponatremia,” and “liver” 2) “central pontine myelinolysis,” “hemophagocytic lymphohistiocytosis,” and “hemophagocytic syndrome” 3) “central pontine myelinolysis” and “hepatosplenic T cell lymphoma.” <h3>Results:</h3> A 20-year-old EBV negative male presented with fever, splenomegaly, and blurry vision with bilateral retinal hemorrhages. Workup was significant for pancytopenia, mild hypovolemic hyponatremia secondary to emesis (initially 132 mmol/L), triglycerides 377, INR 1.2, ALT 55, and ALP 402. HSTL and HLH were confirmed on bone marrow biopsy. He was found to have subclinical CPM on MRI brain without contrast which resolved on 2 month follow-up imaging after 3 rounds of ifosfamide, carboplatin, and etoposide (ICE) intrathecal chemotherapy. We found no prior literature describing HSTL and CPM, 22 articles regarding CPM and liver transplant, and 1 article describing CPM and HLH. <h3>Conclusions:</h3> CPM should be considered as a neurologic complication in patients with HSTL and HLH. We report such a case, despite only mild levels of hyponatremia, the absence of liver failure, and negative EBV status. Future research should explore the connection between these factors to further our understanding of osmotic regulation of the blood brain barrier leading to CPM. <b>Disclosure:</b> Dr. Avila has nothing to disclose. Mr. AW has nothing to disclose. Dr. Danziger has nothing to disclose. Dr. Kim has nothing to disclose. Dr. Tan has nothing to disclose. Dr. Schlick has nothing to disclose.

Osmotic Demyelinating Syndrome Secondary to Breast Cancer Chemotherapy: a Case Report (P10-5.024)

<h3>Objective:</h3> To report a case of osmotic demyelinating syndrome (ODS) secondary to chemotherapy for breast cancer. <h3>Background:</h3> ODS comprises both central pontine demyelination and extrapontine myelinolysis. This condition accounts for 0.4% to 0.56% of neurological admissions to tertiary referral hospitals and 0.06% of medical admissions. Although rapid correction of hyponatremia is the most common cause, other etiologies such as alcohol consumption, chronic renal failure, and organ transplantation are also reported. Chemotherapy can be an infrequent cause of this condition. Here we describe a case of ODS in a normonatremic patient in treatment with trastuzumab, pertuzumab, and docetaxel. <h3>Design/Methods:</h3> Not applicable. <h3>Results:</h3> A 71-year-old female with a history of breast cancer, with lung and brain metastases, is seen in the emergency room due to a decline in her functionality over the past three months, following the initiation of chemotherapy treatment with trastuzumab, pertuzumab and docetaxel. On neurological examination, she exhibited cognitive failures and a non-fluent aphasia without focal neurologic signs. In addition, right-sided focal seizures successfully managed with levetiracetam. On neuroimaging, there were signs of pontine myelinolysis and a reduction in the size of previous brain metastatic lesions. After discontinuing chemotherapy, the patient’s speech and gait significantly improved. <h3>Conclusions:</h3> ODS could be associated with combination chemotherapy treatment in the setting of a normonatremic patient. In 2014, Sungjae Lee and colleagues reported a similar case in a patient with colon cancer who received 5-fluorouracil, oxaliplatin, and leucovorin chemotherapy. In another study published by Cortes and colleagues, the development of osmotic demyelinating syndrome when using a combination of trastuzumab and pertuzumab for breast cancer was reported as a rare finding (one case of twenty-nine patients). To our knowledge, this is one of the first cases describing an ODS following therapy with pertuzumab, trastuzumab, and docetaxel. <b>Disclosure:</b> Dr. Gaitan Alfonso has nothing to disclose. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for Merck. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for Roche. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for BIIB. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Merck. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Novartis. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Biogen. Ms. Rodriguez has nothing to disclose. Dr. Salej has nothing to disclose. Dr. Otero has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for GSK. Dr. Otero has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Janssen . Dr. Otero has received personal compensation in the range of $10,000-$49,999 for serving as an officer or member of the Board of Directors for FICMAC. Dr. Toro has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Watch Neurology .