Case Presentation: A 35 year-old female with a past medical history significant for type 2 diabetes mellitus, polycystic ovarian syndrome and migraine headache presented with alteration of mental status for 2 weeks. Patient endorsed progressive, generalized fatigue with intermittent episodes of confusion, behavioral disturbance, hypersomnia and short-term memory loss. Vital signs on admission were significant for tachycardia to 111. Physical examination was significant for confusion and short-term memory loss. Neurologic examination was otherwise unremarkable.  Laboratory studies revealed leukocytosis (19.5) and thrombocytosis (506). Basic metabolic panel was initially within normal limits though patient developed hyponatremia throughout the course of hospitalization. Urine and blood cultures were negative. Toxicology screen was negative. Acyclovir was initiated given concern for herpes encephalitis. Lumbar puncture was performed – studies were significant for mild glucose elevation. An extensive infectious evaluation of cerebrospinal fluid (CSF) was unremarkable. Acyclovir was discontinued. MRI brain revealed abnormal signal of the bilateral medial temporal lobes.  Findings were suggestive of limbic encephalitis.  Patient was found to have voltage-gated potassium channel (VGKC) antibody (Ab), leucine-rich glioma inactivated 1 (LG1) Ab and glutamic acid decarboxylase (GAD) Ab positivity.  Remaining autoimmune and paraneoplastic markers were negative. CT chest, abdomen and pelvis was negative for primary malignancy. EEG revealed rhythmic delta activity concerning for electrographic seizure.  Patient was without clinical seizure activity.  Levetiracetam and IVIG therapy was initiated.  Patient completed 5 days of IVIG followed by 5 days of solumedrol.  Repeat MRI revealed mild improvement in temporal lobe enhancement.  Gradual improvement in short-term memory was noted.  Patient was discharged to home with plan for outpatient neurology follow up and continued IVIG infusions.

Discussion: Limbic encephalitis is broad diagnosis that comprises infectious, autoimmune and malignant pathologies.  VGKC is a rare subset of non-paraneoplastic limbic encephalitis characterized by cognitive decline and seizure. Patients may additionally develop hyponatremia secondary to SIADH. Treatment involves immunotherapeutic modalities including steroids, plasma exchange and IVIG.  GAD positivity may be associated with treatment-resistant epilepsy.  

Conclusions: Here we report a case of VGKC complex antibody-associated limbic encephalitis in a patient presenting with memory loss with subsequent development of hyponatremia. VGKC encephalitis is often overlooked due to the rarity of this condition and its clinical similarity to other infectious, autoimmune and malignant encephalitides.  SIADH is associated with VGKC encephalitis and hyponatremia may be an important diagnostic element.  A high index of suspicion is required in the diagnosis of VGKC encephalitis; prompt diagnosis is required in order to prevent seizure and amnesia.