A 68-year-old man with a history of chronic hypertension, dyslipidemia and gastroesophageal reflux under treatment.
One month before admission she had had a generalized tonic-clonic seizure, with no clinical signs suggestive of focal onset, which had been studied with magnetic resonance imaging (MRI) of the brain and phenytoin which started negative (EEG).
Two weeks later, the patient developed repeated episodes of distress, difficulty speaking, visual and/or facial expressions, and tremor of the upper extremities of seconds, which led to hospitalization.
The general physical examination at admission was normal and the neurological examination only investigated one patient with brachypsychic syndrome.
Laboratory tests revealed the presence of hyponatremia (122 meq/1) with normal effective volume, which improved with restricted water supply. For this reason, an undiuretic secretion syndrome was diagnosed (SS antidiuretic hormone).
Complete recovery was normal.
MRI of the brain showed signal hyperintensity in T2 and FLAIR sequences in both hippocampus, with a slight increase in volume of the left hippocampus.
Cerebrospinal fluid showed normal cellularity, discrete elevation of proteins (43 mg/dl), absence of oligoclonal bands, albumin/IgG index and normal flow cytometry and PCR for herpes simplex virus negative.
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Due to recurrent episodes of ictal-onset and term anxiety associated with aphasia or paraphasiaml and the left visual lougosis, an EEG was requested, which documented 3 focal electroconvulsive seizures due to levetiracetam.
The patient maintained his condition so he received intravenous valproic acid at a loading dose (20 mg/kg), with no response.
Phenytoin was discontinued and the patient was added to the dressing (200 mg c/12 h) and clobazam (20 mg/night), which completely controlled epileptiform activity within 48 h.
Successive EEGs showed only diffuse slowness, higher in the left temporal level and, from a clinical point of view, did not present new episodes of distress or disturbance.
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Computed tomography of the chest, abdomen and pelvis and testicular ultrasound were normal.
MRI of the control encephalon showed persistence of bilateral temporal hyperintensity, the diagnosis of LS was proposed.
A study of anti-ckvd antibodies was requested outside the country and steroid therapy was initiated empirically (methylprednisolone 1 g/day for 5 consecutive days), with a partial response observed.
The patient was discharged on the 15th day with a confusional syndrome in resolution and EEG without epileptic activity.
The result of the anti-ckvd antibody test was positive, confirming the diagnosis of LD.
Currently, the patient is asymptomatic, with normal EEG control and completely autonomous.
He was kept on treatment with valproic acid 500 mg c/8 h, levetiracetam 1.5 g c/12 h and prednisone 20 mg daily.
