Abstract
Limbic encephalitis may occur as an infectious, paraneoplastic, or autoimmune phenomenon. One such cause of limbic encephalitis is voltage gated potassium channel antibodies (VKGC). Hyponatremia with new cognitive decline may be one of the presenting symptoms. The exact mechanism of hyponatremia is unknown though findings consistent with syndrome of inappropriate antidiuretic hormone (SIADH) are observed. We retrospectively reviewed all cases admitted to an academic medical center with a diagnosis of limbic encephalitis (848 adults between 2004 to 2010) and found six cases of VGKC antibody associated limbic encephalitis. Three of the six cases had SIADH that completely or partially resolved with a combination of water restriction and immunotherapy. The reversibility of hyponatremia and limbic encephalitis with immunomodulation suggests an antibody-mediated cause. We further review available literature for association of hyponatremia and VGKC limbic encephalitis and propose mechanisms of for the hyponatremia in autoimmune encephalitis
Highlights
Limbic encephalitis (LE) may occur as a paraneoplastic or autoimmune phenomenon and may be associated with syndrome of inappropriate anti-diuretic hormone secretion (SIADH)
Only voltage gated potassium channel antibody (VGKC)-LE has been found associated with hyponatremia with an incidence between 30-100% [3,4,5]
We present here a retrospective review of our cases of limbic encephalitis with a case series of VGKC-LE and its association of syndrome of inappropriate antidiuretic hormone (SIADH) and review of literature discussing the possible mechanism
Summary
Limbic encephalitis (LE) may occur as a paraneoplastic or autoimmune phenomenon and may be associated with syndrome of inappropriate anti-diuretic hormone secretion (SIADH). Ectopicantibody production can explain SIADH in paraneoplastic cases but the exact mechanism of hyponatremia in antibody-mediated LE, such as voltage gated potassium channel (VGKC), is unknown. VGKC antibodies have been reported in association with several clinical syndromes involving the central and peripheral nervous systems [1,2]. Only VGKC-LE has been found associated with hyponatremia with an incidence between 30-100% [3,4,5]. We present here a retrospective review of our cases of limbic encephalitis with a case series of VGKC-LE and its association of SIADH and review of literature discussing the possible mechanism
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