Brief Communication Stretch syncope: Reflex vasodepressor faints easily mistaken for epilepsy Ptolemaios Georgios Sarrigiannis a, ⁎, Marc Randall b , Rosalind H. Kandler a , Richard A. Grűnewald b , Kirsty Harkness b , Markus Reuber b a Department of Clinical Neurophysiology, Royal Hallamshire Hospital, Sheffield, UK b Department of Neurology, Royal Hallamshire Hospital, Sheffield, UK abstract article info Article history: Received 6 December 2010 Accepted 9 December 2010 Available online 15 February 2011 Keywords: Stretch syncope Transcranial ultrasound Epilepsy Misdiagnosis Valsalva The pathophysiology of stretch syncope is demonstrated through the clinical, electrophysiological, and hemodynamic findings in three patients. Fifty-seven attacks were captured by video/EEG monitoring. Simultaneous EEG, transcranial (middle cerebral artery) doppler, and continuous arterial pressure measurements were obtained for at least one typical attack of each patient. They all experienced a compulsion to precipitate their attacks. Episodes started with a stereotyped phase of stretching associated with neck torsion and breath holding, followed by a variable degree of loss of consciousness and asymmetric, recurrent facial and upper limb jerks in the more prolonged episodes. Significant sinus tachycardia coincided with the phase of stretching and was followed within 9–16 seconds by rhythmic generalized slow wave abnormalities on the EEG in attacks with impairment of consciousness. Transcranial doppler studies showed a dramatic drop in cerebral perfusion in the middle cerebral arteries during the episodes. The combination of the stereotyped semiology of the attacks, the pseudofocal myoclonic jerking, and the rhythmic generalized slow wave EEG abnormalities with the tachycardia make differential diagnosis from epilepsy challenging. © 2010 Published by Elsevier Inc. 1. Introduction Stretch syncope has only rarely been described in the literature [1–3]. Seven of the eight individuals previously reported were adolescent males; one was a teenage female. Their attacks consisted of stereotyped episodes of stretching actions while performing a valsalva maneuver (VM). Hyperextension of the neck (with or without lateral rotation of the head) was associated with abduction/external rotation of the shoulders during the stretch [1,2,4]. Stretching was followed by a variable degree of loss of consciousness. The pathophysiology of stretch syncope remains obscure although it has been suggested that the cerebral manifestations may be caused by vertebrobasilar insufficiency or occlusion [1–3]. However, it is un- certain whether neck hyperextension or torsion could produce a sufficiently high degree of bilateral vertebral artery stenosis [4]. 2. Methods We describe three male patients with frequent stereotyped attacks. Continuous video/EEG telemetry (Figs. 1–3) was performed in all cases as there was a suspicion that the attacks could be epileptic in nature. All patients underwent further examination with simulta- neous video/EEG recordings, transcranial doppler (TCD) of the middle cerebral artery (MCA), and continuous beat-to-beat (Finometer- Finapres medical systems) arterial pressure measurements during stretch attacks. Case 1 precipitated attacks by playing a computer game. Case 2 had a spontaneous attack. Case 3 experienced a milder version of his usual symptoms by deliberately performing a VM while stretching his trunk and laterally flexing his neck. 2.1. Case 1 This 21-year-old man had a 1-year history of several stereotyped episodes per week, triggered by mental exertion. Attacks were preceded by an overwhelming urge to stretch. Stretching would be followed by a sensation of depersonalization, numbness in body and tongue, a tight sensation in his chest, and (with more severe attacks) loss of consciousness or balance and collapse (Fig. 1). Repetitive asymmetric face and upper limb twitching was reported in some attacks. Attacks would leave the patient feeling washed out and unable to concentrate for several hours. The episodes had failed to respond to carbamazepine, levetiracetam, and topiramate. He had a history of irritable bowel syndrome, obsessive–compulsive disorder, agoraphobia, and mild depression. He took citalopram. Neurological and cardiovascular examinations, interictal EEG, and brain MRI were normal. Epilepsy & Behavior 20 (2011) 450–453 ⁎ Corresponding author. Department of Clinical Neurophysiology, Royal Hallamshire Hospital, Floor N, Glossop Road, Sheffield, South Yorkshire S10 2JF, UK. Fax: +44 114 2713769. E-mail address: p.sarrigiannis@sheffield.ac.uk (P.G. Sarrigiannis). 1525-5050/$ – see front matter © 2010 Published by Elsevier Inc. doi:10.1016/j.yebeh.2010.12.013 Contents lists available at ScienceDirect Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh