A Case of Recurrent Cardiac Asystole and Severe Vasopressor Syncope Presenting as Seizure Mimics
Abstract number :
3.193
Submission category :
4. Clinical Epilepsy / 4B. Clinical Diagnosis
Year :
2023
Submission ID :
1208
Source :
www.aesnet.org
Presentation date :
12/4/2023 12:00:00 AM
Published date :
Authors :
Presenting Author: Adriana Graciela Grau Chaves, MD – Cleveland Clinic Foundation
Ludmila Aragao Feitosa, M.D – POS-GRADUATION - Master, Neurology, STATE UNIVERSITY OF CAMPINAS; Adriana Rodriguez, M.D – Epileptologist, Neurology, Cleveland Clinic Florida; Maria Vera Silva, MD – PGY4, Neurology, Cleveland Clinic Florida
Rationale: This case depicts the clinical challenge of the diagnosis of seizure mimics with a convulsive presentation. First, it is estimated that approximately 20% of epileptic patients remained misdiagnosed. Secondly, the most common causes of misdiagnoses are syncope and psychogenic nonepileptic seizures. We present the case of a 46-year-old man with cardiac arrest and severe vasopressor syncopal episodes misdiagnosed and treated as epileptic convulsions.
Methods: The patient underwent two prolonged video EEG monitorings to elucidate further episodes of seizure-like activity as well as autonomic testing.
Results: A 46-year-old, right-handed male with a past medical history of atrial fibrillation and seizures who presented with 20-year history of seizure-like episodes. Patient had two types of episodes described as generalized tonic-clonic convulsions with postictal fatigue and sleepiness, along with staring off spells. Seizure risk factors include a history of head trauma at 14 years old from playing football. He also had episodes where he was found to have loss of consciousness. Patient was referred to EMU for further characterization of these new episodes. This video EEG evaluation was complicated by a 1 minute and 30 second event of cardiac asystole. The patient reported that while voiding, he felt a headache and lightheaded. He lost consciousness and fell backward. EEG did not show epileptiform activity, but diffuse slowing and attenuation were noted during asystole and was followed by a whole body non epileptic convulsion lasting for approximately 30 seconds. The patient was evaluated by cardiology and was felt to be a malignant vasovagal syncope and underwent dual chamber pacemaker insertion. The patient was discharged but continued to experience episodes despite pacemaker insertion. Patient underwent another four-day diagnostic video EEG that was inconclusive. The EEG was continuous, symmetric, and synchronous with a posterior dominant rhythm of 8-9hz. Sleep was present with normal sleep structure patterns. Sleep deprivation and photic stimulation activations were completed during his stay. Intermittent generalized slowing was present maximum in the right hemisphere which is of unclear significance. No events, epileptiform discharges, or seizures were recorded during this evaluation despite withholding medications. The patient also had a brain MRI which was unremarkable. Upon release, medications were increased with recurrent episodes. The patient underwent tilt table testing that showed a reproduction of symptoms of loss of consciousness and tonic-clonic activity with a marked drop in systolic blood pressure to 64/47 mmHg suggestive of severe vasopressor syncope.
Conclusions: There are a number of possible explanations that can be overlooked after a diagnosis of epilepsy is made. Despite having a comprehensive evaluation in the epilepsy monitoring unit, it is still essential to search for alternative causes even once mimics are diagnosed and addressed with an implantable pacemaker.
Funding: None
Clinical Epilepsy