Convulsive syncope

Thomas Lempert MD (Dr. Lempert of Charité University Hospital has no relevant financial relationships to disclose.)
Matthew Lorincz MD PhD, editor. (Dr. Lorincz of the University of Michigan receives salary support from Wilson Therapeutics AB for performing UWDRS examinations in a clinical trial.)
Originally released May 22, 2000; last updated January 23, 2017; expires January 23, 2020

This article includes discussion of convulsive syncope, anoxic seizure, hypoxic convulsion, and reflex anoxic seizure. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

In this article, the author provides an overview of convulsive syncope. Syncope is commonly accompanied by tonic or myoclonic muscle activity, eye deviations, automatisms, vocalizations, and hallucinations, which may all complicate the distinction from epileptic seizures. Differential diagnosis is based on the specific features and not the mere presence or absence of these phenomena. Recognition of syncope depends also on accurate information about premonitory symptoms and postictal events. Investigations such as tilt testing or creatine kinase levels may be helpful but are never diagnostic in isolation. EEG should not be ordered routinely. An increasingly recognized and treatable cause of syncope is ictal asystole or bradycardia during temporal lobe seizures.

Key points

 

• Syncope is often accompanied by tonic or myoclonic muscle activity.

 

Myoclonus is usually brief, arrhythmic, and multifocal.

 

• Specific provocation and rapid reorientation helps to distinguish syncope from generalized tonic clonic seizures.

Historical note and terminology

Syncope is defined as a brief loss of consciousness and upright posture due to global cerebral hypoxia. The term “convulsive syncope” specifies a common variant of syncope that is accompanied by tonic or myoclonic activity.

Animal experiments on convulsive syncope date back to the middle of the 19th century, when Kussmaul and Tenner showed that anoxic convulsions occur after ablation of the telencephalon but not after destruction of the brainstem (Dell et al 1961). A century later, Dell and colleagues demonstrated that motor activation in the early stages of cerebral hypoxia resulted from the combined effects of direct hypoxic activation of the brainstem reticular formation and cortical suppression with subsequent reticular disinhibition (Dell et al 1961). Gastaut and colleagues were the first to conduct studies on the clinical and electroencephalographic features of experimentally induced syncope in human subjects (Gastaut and Fischer-Williams 1957). They observed tonic and myoclonic phenomena during syncope in the absence of epileptic EEG activity and coined the term “convulsive syncope."

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