Natural Product-Derived Carbon Dots in Neurodegenerative Diseases: Advances in Blood-Brain-Barrier-Related Delivery, Neuroprotection, and Theranostics.

Osmotic demyelination syndrome (ODS) is a rare but serious neurological complication that includes central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM). It results from significant changes in serum sodium levels and plasma osmolality, leading to cerebral apoptosis and myelin loss. The most common cause is iatrogenic rapid correction of chronic hyponatremia [, ]. Risk factors for ODS include excessive alcohol use, malnutrition, chronic diuretic use, psychogenic polydipsia, dehydration and eating disorders among others [–]. CPM presents with a range of neurological symptoms, including altered consciousness, spastic tetraparesis, oculomotor dysfunction, and pseudobulbar paresis manifesting as dysarthria and dysphagia. Prompt recognition and appropriate management are essential to mitigate the complications and reduce mortality []. We report a patient who presented at the emergency department (ED) with hypernatremia and is presumed to have developed CPM prior to admission. A 45-year-old man with severe alcohol dependence presented to the ED with abdominal pain, vomiting, generalized weakness and altered consciousness. The patient was not taking any regular medications and had no ongoing medical follow-up. Collateral history revealed significant weight loss and progressive deterioration over the past 4 months, with immobility for approximately 1 week. His speech had become increasingly slurred and difficult to understand. On examination in the ED, he was disoriented, confused, and unable to provide his medical history. He demonstrated generalized weakness with upper motor neuron signs, including brisk tendon reflexes in all extremities and bilateral extensor plantar responses, as well as dysarthria and cerebellar impairment, although he retained the ability to move in bed. Except for sinus tachycardia of 117 bpm his vital signs were normal.