Leucine-rich glioma inactivated-1 (LGI1) antibody encephalitis was first described in 2010, and is the most common antibody found in limbic encephalitis. The clinical presentation include subacute cognitive decline, short-term memory loss, behavioral changes and seizures.

During the course of the disease 60-88% of the patients develop hyponatremia, mainly mild to moderate, but which also may be severe and life threatening. Upon presentation, the occurrence of seizures may be attributed to hyponatremia and thus delay the diagnosis of encephalitis.  The etiology of the sodium disorder is unclear, frequently presumed to be related to the syndrome of inappropriate anti-diuretic hormone secretion (SIADH).

We retrospectively screened the medical records of the Tel-Aviv medical center for patients who were diagnosed with LGI1 antibody encephalitis. We then retrieved blood tests results in order to prove the notion of SIADH as the etiology for Hyponatremia.

Fourteen patients with LGI1 antibody encephalitis were found. Among those, all patients had hyponatremia at some point, 12 exhibited moderate to severe hyponatremia during the course of their disease (86%), with 8 (57%) having hyponatremia on presentation.

8/14 patients had sufficient data collected to check for SIADH. All eight  had blood and urine tests compatible with SIADH. The remaining 6 patients had low BUN and Uric acid that support the diagnosis of SIADH.

All 12 patients with moderate to severe hyponatremia improved after immunotherapy.

Hyponatremia in LGI1 antibody encephalitis is caused by SIADH, resulting probably from inflamatory process in the hypothalamus due to LGI1 presentation.

In patients with hyponatremia and seizures, LGI1 antibody encephalitis should be in the differential diagnosis in order not to delay immunotherapy treatment.

Hyponatremia in LGI1 antibody encephalitis is responsive to immunotherapy rather than electrolyte treatment.