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Spine (Phila Pa 1976). 2009 Mar 1;34(5):501-11. doi: 10.1097/BRS.0b013e31819712f5.

Hyponatremia in the acute stage after traumatic cervical spinal cord injury: clinical and neuroanatomic evidence for autonomic dysfunction.

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Division of Genetics and Development, Toronto Western Research Institute, Canada.



Retrospective cohort study supplemented by analysis of postmortem spinal cord tissue.


This study examines the frequency of hyponatremia in early stage (2 weeks) after cervical spinal cord injury (SCI), and the relationship between integrity of key autonomic pathways and hyponatremia.


Interruption of key circuits in the spinal cord can induce autonomic dysfunction with disordered metabolic and physiologic homeostasis. Given that hyponatremia may be a common electrolyte disorder during the acute stage post-SCI, we hypothesized that disconnection of descending sympathetic renal spinal cord tracts may be associated with hyponatremia after SCI.


Consecutive individuals with cervical spine trauma were included in our cohort of patients, which was divided into a SCI group and a control group (patients with spine trauma without SCI). Also, postmortem spinal cord sections from individuals with cervical, motor complete SCI, and control cases without CNS trauma were evaluated regarding the extent of axonal preservation within the descending vasomotor pathways, the descending renal sympathetic pathways (DRSPs), the corticospinal tracts, and the dorsal columns.


There were 21 SCI individuals (6 women, 15 men; ages, 17-83 years; mean, 57.1) and 12 patients in the control spine trauma group who did not have SCI (4 women, 8 men; ages 18-90 years; mean, 45.9). Patients had either motor complete (7/21) or motor incomplete (14/21) tetraplegia. Hyponatremia occurred in 85.7% after SCI, which was significantly more frequent than the control group. Postmortem analysis included 5 control cases and 6 SCI individuals of whom 3 developed hyponatremia. The number of preserved axons within the DRSPs from normonatremic SCI patients was significantly lower than the number of axons within DRSPs from hyponatremic SCI patients, but development of hyponatremia was not associated with the integrity of the descending vasomotor pathways. Hyponatremic SCI individuals also showed greater evidence of neurogenic hypotension than normonatremic SCI individuals.


Hyponatremia is common in the early stage post-SCI. Our results also suggest that hyponatremia is associated with the integrity of descending renal sympathetic circuits which mediate the renin-angiotensin response to neural injury, in the setting of neurogenic hypotension with cardiovascular dysfunction.

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