Fatal osmotic demyelination following urgent start hemodialysis in a patient with normal serum sodium.

End stage kidney disease (ESKD) patients in the developing countries often present late for dialysis initiation with advanced uremia and life-threatening complications. Urgent start dialysis in such emergent situations exposes the patient to risk of uremia related complications as well as iatrogenic insults. We report the case of a middle-aged man with ESKD who presented late with acute pulmonary edema and hyperkalemia and developed osmotic demyelination syndrome following urgent start hemodialysis. Osmotic demyelination syndrome in this patient is noteworthy since there was no accompanying hyponatremia, the most commonly recognized antecedent. We propose that rapid lowering of serum osmolality by aggressive hemodialysis is sufficient to incite osmotic demyelination syndrome in patients who have long-standing uremia and high blood urea level. Malnutrition resulting from uremia might be a compounding factor in this scenario. Our patient had a characteristic initial presentation of osmotic demyelination syndrome with locked-in-state which later progressed to respiratory failure and death.

An Unusual Case of a Central Pontine Myelinolysis Associated with Primary Splenic Diffuse Large B-cell Lymphoma.

A 54-year-old woman with persistent fatigue and a high fever presented with central pontine myelinolysis (CPM) on brain imaging, despite the absence of neurological symptoms. The patient had a slightly low serum sodium concentration. Further investigation led to a diagnosis of primary splenic diffuse large B-cell lymphoma (PS-DLBCL). Brainstem auditory-evoked potentials (BAEP) indicated minor abnormalities. CPM was successfully resolved after splenectomy and immunochemotherapy. This is the first reported case of CPM in a patient with PS-DLBCL confirmed by a pathological diagnosis following splenectomy and BAEP-detected abnormalities that improved with immunochemotherapy.

The pathologies of migrants who travel by boat documented on imaging.

The migration phenomenon is increasingly common worldwide. It is essential for radiologists to be aware of the endemic diseases of the migrant's country as well as the characteristics of the journey to be able to understand and interpret radiological findings when admitted to our centre. This article aims to use imaging from our centre to describe the most common pathologies that migrant patients present with after long journeys by boat.

Consequences of Hyponatremia: Central Pontine and Extrapontine Myelinolysis in a Chronic Alcohol User.

Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are rare neurological disorders associated with rapid correction of hyponatremia, particularly in individuals with chronic alcohol use. We present the case of a 52-year-old male with a history of chronic alcoholism who developed CPM and EPM following correction of severe hyponatremia. The patient presented with dysarthria, hemiparesis, and altered mental status, which progressed rapidly to pseudobulbar features and spastic quadriparesis. Neuroimaging revealed characteristic findings of CPM and EPM. Treatment with intravenous dexamethasone, intravenous immunoglobulin (IVIG), and methylprednisolone led to gradual neurological improvement. The patient showed significant recovery after two months, highlighting the importance of early recognition and cautious management of electrolyte disturbances in high-risk individuals to prevent devastating neurological complications.

Central Pontine Myelinolysis: A Rare and Life-Threatening Adverse Effect of Clobazam and Quetiapine.

Central pontine myelinolysis (CPM) is a rare neurological disorder characterized by demyelination within the central portion of the pons. While hyponatremia is a well-known precipitating factor, other etiologies, including medication use, have been reported. We present a case of a 69-year-old male with a history of obsessive-compulsive disorder, stroke, and type 2 diabetes mellitus who developed confusion, altered sensorium, and weakness in all four limbs. An MRI brain imaging revealed characteristic findings suggestive of CPM. Despite normal serum sodium levels, discontinuation of clobazam and quetiapine, medications taken by the patient, led to clinical improvement. This case underscores the importance of considering medication-induced CPM in the differential diagnosis of patients presenting with neurological symptoms, even in the absence of electrolyte abnormalities.

Unraveling Neurological Shades: Vitamin D Toxication and Central Pontine Myelinolysis Exposed.

This case report is about a middle-aged female who presented with complaints of pain in the abdomen with intractable vomiting for three months, pain and weakness in bilateral lower limbs for two months, and irritability for three days. She was previously treated for lumbar disc bulge and severe narrowing of the spinal cord whose treatment also included vitamin D supplements. After taking high doses of a vitamin D supplement daily for approximately four months, it resulted in vitamin D toxicity. The sodium level of the patient was in the normal range throughout the treatment. Her magnetic resonance imaging brain revealed features of central pontine myelinolysis. The development of central pontine myelinolysis due to vitamin D toxicity, with normal sodium levels, makes this a rare case for discussion.

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

The diagnosis of central pontine hyperintensities on cranial magnetic resonance imaging has 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 or toxic 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 myelinolysis can 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.

Experience of Rehabilitation Treatment for Osmotic Demyelination Syndrome with Locked-in Syndrome / The Japanese Journal of Rehabilitation Medicine

Osmotic demyelination syndrome is a pathological condition that leads to electrolyte imbalances and rapid correction, resulting in pseudobulbar palsy, quadriplegia, and altered consciousness. Approximately 33-55％ of affected patients experience residual functional impairment. Herein, we describe a case of a patient with osmotic demyelination syndrome who developed locked-in syndrome during the disease course, underwent rehabilitation treatment, and achieved complete remission without sequelae.The patient was a 47-year-old man who was admitted to hospital A owing to weakness in the lower extremities and dysarthria. He had severe hyponatremia and received sodium correction. However, on hospital day 9, dysarthria redeveloped and involuntary finger movements were noted. Osmotic demyelination syndrome was suspected based on the findings of magnetic resonance imaging of the head and clinical course, leading to his transfer to hospital B. Steroid pulse and rehabilitation therapies were initiated at hospital B. By the 19th day of symptom onset, his limb and facial muscle paralysis progressed, leading to locked-in syndrome. Thereafter, the patient was transferred to hospital C, where he received physiotherapy, occupational therapy, and eating training, markedly improving his physical functions. He was discharged from hospital C, 4 months after the symptom onset, with limited range of motion of the fingers and weakness of the extremities and continued to receive outpatient rehabilitation treatment. His symptoms improved further, and 1 year after the onset of symptoms, he returned to work without any sequelae.

Rhabdomyolysis Complicated with Hyponatremia Due to Water Intoxication and Severe Aspiration Pneumonia: Description of a Patient with Chronic Schizophrenia and Literature Review.

Hyponatremia due to water intoxication is frequently observed in patients with chronic schizophrenia. We herein present a 49-year-old man who developed schizophrenia at the age of 23 and had been admitted to the closed ward of our hospital for 7 years. He was found by a round nurse standing at the bedside, covering both ears with his hands and making groaning noises. He was disoriented and immediately after being returned to bed, a general tonic-clonic seizure occurred. Severe hyponatremia (Na 104 mEq/L) was noted and intravenous sodium correction was started. A few hours later, due to glossoptosis and massive vomiting, ventilation got worse to the point where he had to be put on a ventilator. On the following day, he developed aspiration pneumonia and antimicrobial treatment was started. In addition, a blood sample taken 36 hours later revealed an extensive elevation of creatine kinase (41,286 U/L), pointing to a possibility of rhabdomyolysis as a complication. Subsequently, the general condition gradually improved with antimicrobial therapy and sodium correction. He eventually recovered without any complications including central pontine myelinolysis. He had no history of polydipsia before this event but it was later found that esophageal stricture triggered complusive fluid intake, resulting in acute hyponatremia, seizure, aspiration pneumonia and rhabdomyolysis. A brief discussion will be provided on the issues surrounding hyponatremia, rhabdomyolysis and schizophrenia.

Central pontine myelinolysis: a rare finding in hyperosmolar hyperglycemia.

Central pontine myelinolysis (CPM) is a heterogeneous nervous system disease of pontine demyelination, usually caused by rapid correction of hyponatremia. In the present study, we report a unique case of a 46-year-old man with a hyperglycemic state complicated with CPM. MRI demonstrated a high signal on T2 and symmetric restricted diffusion in the pontine. In conclusion, the clinical case described confirmed that the hyperosmolar state inherent in hyperglycemia was a likely cause of CPM.

Delayed Presentation of Osmotic Demyelination Syndrome Treated With Plasmapheresis.

We present a unique case of a 42-year-old gentleman with alcohol use disorder who developed osmotic demyelination syndrome (ODS) despite appropriate hyponatremia correction. This patient initially presented with severe hyponatremia (Na 97 mEq/L) due to beer potomania, which was corrected gradually over eight days, resulting in no observed neurological deficits upon discharge. However, he was readmitted with respiratory failure from aspiration pneumonia, leading to endotracheal intubation. Laboratory findings revealed a sodium level of 134 mEq/L and serum osmolality (293 mOsm/kg). The patient had neurological exam findings of spontaneous eye opening with left gaze preference and decreased power ⅕ in all extremities. Following extubation, he experienced a relapse with evolving subacute central pontine myelinolysis and bulbar weakness necessitating reintubation. Subsequently, five sessions of plasmapheresis were conducted, resulting in stable clinical findings. Despite remaining non-verbal, the patient demonstrated gradual neurological motor improvement, progressing from 1/5 power in all extremities to 4/5 on the right side and 3/5 on the left side. He was discharged with ventilator support, tracheostomy, and PEG tube placement to a long-term care facility. This case underscores the importance of vigilant monitoring in high-risk individuals following hyponatremia treatment because ODS presentation can be delayed.

Central Pontine Myelinolysis and Hypokalemic Paralysis as Presenting Manifestations of Sjogren's Syndrome.

Neurological involvement in Sjogren's syndrome can have varied manifestations and can precede the classical sicca symptoms of Sjogren's syndrome. A 32-year-old woman presented with acute quadriparesis and dysarthria. She had severe hypokalemia, and an MRI of the brain showed a lesion in the central pons that was hyperintense on T2 and fluid-attenuated inversion recovery (FLAIR) sequences sparing the periphery, a trident appearance characteristic of central pontine myelinolysis (CPM). On further evaluation, she was found to have distal renal tubular acidosis (dRTA) due to primary Sjogren's syndrome. She was treated with steroids and other supportive measures, and she recovered completely in one month. We describe a mild form of CPM with classical MRI features in a patient with Sjogren's syndrome and hypokalemia due to dRTA.

A case of acute pulmonary complication due to botulinum toxin: Patient with central pontine myelinolysis developed acute respiratory distress syndrome after botulinum neurotoxin type A injection into spastic lower extremity muscles.

Chemodenervation with botulinum neurotoxin type A (BoNTA) is the preferred method for focal spasticity management among various treatment options. While BoNTA injection is considered safe, its widespread use and increasing evidence raise safety concerns. In this paper, we present a patient with central pontine myelinolysis, a rare disease, who developed acute respiratory distress syndrome on the third day after BoNTA application to the spastic gastrocnemius muscle group and required intubation in the intensive care unit due to this complication. To our knowledge, this is the first case reported in the literature to develop an acute pulmonary complication after BoNTA injection into spastic lower extremity muscles.

A Case of Alcohol Withdrawal-Induced Central and Extrapontine Myelinolysis.

A 40-year-old female with a history of chronic alcohol use disorder presented with an acute intractable left-sided headache for three days and progressively worsening unsteady gait requiring a wheelchair to ambulate. The patient had a history of chronic alcoholism since 2019 but reported abstinence since September 2021. One month after quitting alcohol, she experienced a sudden deterioration in bilateral extremity neuropathy, forgetfulness, difficulty writing, and severe mood swings, which continued to worsen until her presentation in July 2022. Laboratory tests, including complete blood count and electrolyte levels, were within normal ranges. A previous MRI performed during the investigation for alcoholic neuropathy a few months before she quit drinking showed no abnormalities. However, a subsequent MRI during work-up for the current acute symptoms revealed significant signal abnormalities involving the central pons, bilateral cerebral peduncles, and medullary pyramids, consistent with chronic central pontine myelinolysis (CPM) with extrapontine myelinolysis (EPM) extending into the peduncles. The patient received treatment with folate and multivitamins and was scheduled for outpatient follow-up with physical therapy for rehabilitation. This case highlights CPM as a consequence of alcohol withdrawal and emphasizes the importance of timely diagnosis and appropriate management in such patients.

Central pontine myelinolysis after liver transplant: A case report and an updated review.

Based on brain magnetic resonance imaging results, the second and third most frequent causes of central pontine myelinolysis (CPM) were liver transplant (LT) and cirrhosis, which together accounted for 13.7% and 12.5% of all diagnoses of CPM. Medical diseases including cirrhosis, LT, malnutrition, and alcoholism are well-known conditions associated with CPM in addition to hyponatremia. The prognosis is poor and depends on early diagnosis and treatment to achieve better outcomes. This is a case report of CPM occurring after a deceased donor LT in a patient presenting many risk factors such as chronic hyponatremia, previous episodes of encephalopathy, and tacrolimus immunosuppression. We briefly discuss the pathophysiology, risk factors, diagnosis, and treatment, highlighting the role and challenges of the anesthesiologist in managing this kind of patient and preventing the syndrome in the context of major surgery.

Rapid Correction of Hyponatremia With Isotonic Saline Leading to Central Pontine Myelinolysis.

Central pontine myelinolysis (CPM) is a part of the spectrum of osmotic demyelination syndrome (ODS), which is a rare demyelinating disorder due to the rapid correction of low serum sodium. It affects the neurons of the pons but may also involve other extra-pontine sites. The disease is characterized by a wide variety of clinical features ranging from dysarthria, dysphagia, bulbar palsy, quadriplegia, and behavioral and psychiatric disturbances. We present a case of a young female who developed CPM due to rapid sodium correction after vomiting. She presented with quadriplegia and locked-in syndrome. The diagnosis is on the basis of clinical and radiographic features. Magnetic resonance imaging (MRI) of the brain is superior to computed tomography (CT) in detecting changes. It shows hyperintensities on T2-weighted images that are classically known as the trident sign in the region of the pons. The patient was managed supportively, and the family was counseled regarding the poor prognosis of the disease. Unfortunately, she met a fatal fate due to a complication of CPM that is aspiration pneumonia. It is, therefore, imperative to create more awareness regarding the disease, and measures should be taken for its prevention that includes correction of low sodium levels not greater than 10 mmol/L/day.

Primary Sjögren's syndrome with renal tubular acidosis and central pontine myelinolysis: An unusual triad.

Primary Sjögren's syndrome (pSS) is a complex, multisystem autoimmune disorder. It is characterized by lymphocytic infiltration of the exocrine glands. In the setting of pSS, the presence of systemic disease is an important prognostic determinant, but involvement of the kidney is uncommon. The triad of pSS, distal renal tubular acidosis (dRTA), and central pontine myelinolysis (CPM) is rare and potentially fatal. A 42-year-old woman presented with dRTA, profound hypokalemia, and CPM characterized by progressive global quadriparesis, ophthalmoplegia, and encephalopathy. Sjögren's syndrome was diagnosed based on sicca symptoms, clinical features, and strongly positive anti-SSA/Ro and anti-SSB/La autoantibodies. The patient responded well to electrolyte replacement, acid-base correction, corticosteroids, and subsequent cyclophosphamide therapy. Early recognition and appropriate treatment resulted in good kidney and neurological outcomes in this case. This report highlights the need to consider the diagnosis of pSS in unexplained dRTA and CPM, as it has a favorable prognosis if recognized and managed timeously.

A rare presentation of central pontine myelinolysis secondary to hyperglycaemia.

BACKGROUND: Central 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 PRESENTATION: A 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. CONCLUSION: CPM is a potentially fatal neurological condition and can occur in uncontrolled diabetes mellitus. Early diagnosis and timely treatment are crucial for improving the prognosis.