Abstract
BackgroundOnly one case of syndrome of inappropriate secretion of antidiuretic hormone with lateral medullary syndrome has been reported so far. We report a case of lateral medullary syndrome showing syndrome of inappropriate secretion of antidiuretic hormone and analyze the pathomechanism underlying its clinical features.Case presentationA 67-year-old man was admitted to our hospital for dizziness, dysarthria, and dysphagia. He was diagnosed with lateral medullary syndrome based on the neurological examination and brain magnetic resonance imaging. Horner syndrome was absent. Asymptomatic hyponatremia appeared 9 days after admission and the patient was diagnosed with syndrome of inappropriate secretion of antidiuretic hormone. Fluid restriction and intravenous furosemide injection improved the hyponatremia.ConclusionLateral medullary syndrome could be associated with syndrome of inappropriate secretion of antidiuretic hormone.
Highlights
One case of syndrome of inappropriate secretion of antidiuretic hormone with lateral medullary syndrome has been reported so far
Lateral medullary syndrome could be associated with syndrome of inappropriate secretion of antidiuretic hormone
It has been reported that secretion of antidiuretic hormone (SIADH) is difficult to distinguish from cerebral salt wasting syndrome, another cause of hyponatremia characterized by renal loss of sodium and decreases in extracellular fluid volume during intracranial disorders [6]; the abnormal antidiuretic hormone (ADH) secretion and lack of clinical symptoms of dehydration in our patient were consistent with the characteristics of SIADH [7], precise evaluation of the volemic state has been considered difficult [8]
Summary
Our patient with lateral medullary syndrome showed asymptomatic hyponatremia 13 days after the onset of lateral medullary syndrome. SIADH in our patient would be related to the exaggerated ADH response to ischemic damage as discussed in the previously reported [12], we speculated that the ischemic damage of the ascending neural pathway from the NTS to the PVH could be related to the pathogenesis of SIADH in lateral medullary syndrome. The absence of Horner syndrome in our patient indicated that the sympathetic descending tract was spared from severe ischemic damages, and the sympathetic descending tract would be anatomically separated from the ascending neural pathway from the NTS to PVH Both patients presented no sign of dysgeusia, suggesting that the NTS was spared from severe ischemic damages, the MRI findings in both patients were similar to those of typical lateral medullary syndrome [14]. Abbreviations ADC, apparent diffusion coefficient; ADH, antidiuretic hormone; DWI, diffusion weighted imaging; NTS, the nucleus of the solitary tract; PVH, the paraventricular nucleus in the hypothalamus; SIADH, syndrome of inappropriate secretion of antidiuretic hormone
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