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Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with lateral medullary syndrome: case report and literature review
© The Author(s). 2016
- Received: 10 April 2016
- Accepted: 20 July 2016
- Published: 27 July 2016
The Erratum to this article has been published in BMC Neurology 2016 16:192
Only 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.
A 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.
Lateral medullary syndrome could be associated with syndrome of inappropriate secretion of antidiuretic hormone.
- Syndrome of inappropriate secretion of antidiuretic hormone
- Lateral medullary syndrome
- Antidiuretic hormone
- The nucleus of the solitary tract
- The paraventricular nucleus in the hypothalamus
Hyponatremia, defined as condition in which serum sodium is <135 mEq/L, is the most common electrolyte abnormality encountered worldwide . One of the major causes of hyponatremia is syndrome of inappropriate secretion of antidiuretic hormone (SIADH), which is caused by various conditions such as malignancies, pulmonary disorders, medications, and acute central nervous system diseases . A previous study reported hyponatremia in nearly 13.8 % of more than 8,500 cases of stroke patients . However, only one case of SIADH with lateral medullary syndrome has been reported so far . In this report, we present SIADH in a patient with lateral medullary syndrome and discuss the pathomechanism of SIADH.
Hematological examination showed normal serum sodium levels of 139 mEq/L on admission, however, the serum sodium levels decreased gradually, and 9 days after admission (13 days after onset), he developed asymptomatic hyponatremia (109 mEq/L) with a decreased serum osmolarity of 223 mOsm/L (normal range, 275 – 295 mOsm/L). The turgor in all four limbs was normal, and he did not present with obvious thirst. Thyroid, renal, and adrenal functions were normal, but increased serum levels of antidiuretic hormone (ADH) (6.9 pg/mL; normal range, 0.3 – 4.2 pg/mL) were observed. Urine osmolarity was 668 mOsm/kgH2O (normal range, 100 – 1,300 mOsm/kgH2O), and urine sodium was 121 mOsm/L (normal range, 40 – 90 mOsm/L). Thoracoabdominal CT images showed no abnormalities, such as mass lesions or lymphadenopathy. He was diagnosed as having SIADH based on the diagnostic criteria of Bartter and Schwartz . He was treated with fluid restriction and intravenous furosemide injections.
Laboratory examination on the 23rd day after admission showed almost normal serum sodium levels (136 mEq/L) with normal serum ADH levels (1.2 pg/mL). His neurological symptoms, such as dizziness and dysarthria, also gradually resolved, and thereafter, hyponatremia was not observed.
Our patient with lateral medullary syndrome showed asymptomatic hyponatremia 13 days after the onset of lateral medullary syndrome. With the exclusion of other causes of hyponatremia, we diagnosed the hyponatremia as SIADH. It has been reported that 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 ; nonetheless, the abnormal ADH secretion and lack of clinical symptoms of dehydration in our patient were consistent with the characteristics of SIADH , although precise evaluation of the volemic state has been considered difficult . Thoracoabdominal CT images indicated no evidence of ectopic ADH producing tumors. Nine days after admission, the serum sodium levels gradually improved. After the primary treatment for SIADH, our patient presented almost normal serum sodium levels with resolution of his neurological symptoms, and thereafter, he showed no relapse of hyponatremia, indicating that SIADH could be closely related to ischemic damage in the dorsolateral medulla. As edaravone was administered for 9 days after admission, the possibility that edaravone contributed to the pathophysiology of SIADH cannot be ruled out, although no case of SIADH associated with edaravone has been reported so far.
In retrograde tracing studies, two major neural pathways were identified between the dorsolateral medullary area and the hypothalamus [9, 10]. These include (1) the sympathetic descending tract and (2) the interacting neural pathway between the paraventricular nucleus in the hypothalamus (PVH) and the nucleus of the solitary tract (NTS), although the neurological function of the later pathway is not understood yet. The NTS could be involved in the mechanism of SIADH in lateral medullary syndrome, as discussed in the previously reported case . However, as the NTS is occasionally involved in lateral medullary syndrome , the ischemic damage of the NTS cannot simply explain the pathogenesis of SIADH in lateral medullary syndrome. Although SIADH in our patient would be related to the exaggerated ADH response to ischemic damage as discussed in the previously reported , 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.
Previous case 
mean age: 57 ± 11.9
Male: Female = 2.25:1
dizziness, dysarthria, dysphagia
headache, dysphagia, hiccups,
dizziness, vertigo, gait ataxia, dysarthria, dysphagia
crossed sensory disturbance, cerebellar ataxia, nystagmus
crossed sensory disturbance, cerebellar ataxia
crossed sensory disturbance, cerebellar ataxia
hypertension, diabetes mellitus, cigarette smoking
Treatment for cerebral infarction
edaravone oral clopidogrel argatroban
varies depend on the causes
Interval days between the onset of Wallenberg syndrome and hyponatremia
Symptom of hyponatremia
Treatment for hyponetremia
restriction of fluid intake, intravenous furosemide
restriction of fluid intake
We described SIADH in a patient with lateral medullary syndrome. Taken together with the previously reported case, we suggest that lateral medullary syndrome could be associated with hyponatremia.
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
We receive no funding support.
Availability of data and materials
The datasets supporting the conclusions of this article are included within the article.
Study concept and design: HN, DY. Analysis and interpretation of data: HN, DY, MY. Drafting of the manuscript: HN, DY. Critical revision of the manuscript for important intellectual content: HN, DY, MY. All authors have read and approved the final manuscript.
The authors declare that they have no competing interests.
Consent for publication
We obtained written informed consent from the patient for publication of this case report, and any accompanying images. A copy of the written consent is available for review by the Editor of this journal.
Ethics approval and consent to participate
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