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Vasovagal syncope interrupting sleep: Difference between revisions
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(Created page with "''CT Paul Krediet, David L Jardine‡, Pietro Cortelli§, AGR Visman || and Wouter Wieling*; * Department of Internal Medicine, Academic Medical Center, University of Amsterd...") |
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''CT Paul Krediet, David L Jardine‡, Pietro Cortelli§, AGR Visman || and Wouter Wieling*; | ''CT Paul Krediet, David L Jardine‡, Pietro Cortelli§, AGR Visman || and Wouter Wieling*; \* Department of Internal Medicine, Academic Medical Center, University of Amsterdam (The Netherlands); ‡ Department of General Medicine, Christchurch Hospital, Christchurch (New Zealand); § Neurological Section, University of Modena and Reggio Emilia, Bologna (Italy); ||Department of Cardiology, Beatrix Ziekenhuis, Gorinchem (The Netherlands)''<br /><br /> | ||
* Department of Internal Medicine, Academic Medical Center, University of Amsterdam (The Netherlands); ‡ Department of General Medicine, Christchurch Hospital, Christchurch (New Zealand); § Neurological Section, University of Modena and Reggio Emilia, Bologna (Italy); ||Department of Cardiology, Beatrix Ziekenhuis, Gorinchem (The Netherlands) | |||
''<br /><br /> | |||
{{case_present| | {{case_present| | ||
[[File:NocturnalSyncope_Fig1.png | thumb | | [[File:NocturnalSyncope_Fig1.png | thumb | 500px | left ]] | ||
A female patient had her first nocturnal syncopal episode at the age of 40. She woke up at night after sleeping for some hours, aware of nausea, abdominal discomfort and an urge to defecate. She lost consciousness while supine. She sweated profusely but did not bite her tongue. Her husband observed transient myoclonic jerking. After this, similar episodes occurred regularly (at least one per month) and only at night. The syncopal episodes never exceeded one minute and were atraumatic. She was incontinent of urine and faeces once. A tilt test provoked a vasovagal reaction followed by 7 seconds of asystole and reproduced her nocturnal symptoms. Because of ongoing symptoms she underwent neurological investigations and a typical nocturnal episode was recorded during permanent EEG and ECG monitoring.}} | A female patient had her first nocturnal syncopal episode at the age of 40. She woke up at night after sleeping for some hours, aware of nausea, abdominal discomfort and an urge to defecate. She lost consciousness while supine. She sweated profusely but did not bite her tongue. Her husband observed transient myoclonic jerking. After this, similar episodes occurred regularly (at least one per month) and only at night. The syncopal episodes never exceeded one minute and were atraumatic. She was incontinent of urine and faeces once. A tilt test provoked a vasovagal reaction followed by 7 seconds of asystole and reproduced her nocturnal symptoms. Because of ongoing symptoms she underwent neurological investigations and a typical nocturnal episode was recorded during permanent EEG and ECG monitoring.}} | ||
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Panel C: time 5:52 AM (after calling for nurse), patient lying supine in bed unable to move, EEG unchanged, heart rate 36 bpm. Patient is pale and sweating profusely. | Panel C: time 5:52 AM (after calling for nurse), patient lying supine in bed unable to move, EEG unchanged, heart rate 36 bpm. Patient is pale and sweating profusely. | ||
The EEG was judged normal by two independent neurologists. The ECG however showed a pronounced bradycardia (36 bpm) during the episode, with an atrioventricular node escape rhythm. At the age of 44 a permanent dual chamber pacemaker was implanted and the patient reported less syncope but ongoing episodes of nocturnal pre-syncope with abdominal discomfort | The EEG was judged normal by two independent neurologists. The ECG however showed a pronounced bradycardia (36 bpm) during the episode, with an atrioventricular node escape rhythm. At the age of 44 a permanent dual chamber pacemaker was implanted and the patient reported less syncope but ongoing episodes of nocturnal pre-syncope with abdominal discomfort <cite>Krediet</cite>. | ||
== Editor's comments == | == Editor's comments == | ||
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Tilt table testing was performed in 11 patients and was positive in 7 with typical prodromal symptoms. A significant (asystole >3s) cardio-inhibitory reaction was recorded in 4 of the 7. The possibility of organic cardiac or cerebral pathology causing as a cause for the episodes was excluded by appropriate additional testing. Interictal EEG performed in 7 patients revealed epileptiform activity in one. | Tilt table testing was performed in 11 patients and was positive in 7 with typical prodromal symptoms. A significant (asystole >3s) cardio-inhibitory reaction was recorded in 4 of the 7. The possibility of organic cardiac or cerebral pathology causing as a cause for the episodes was excluded by appropriate additional testing. Interictal EEG performed in 7 patients revealed epileptiform activity in one. | ||
We concluded that the patient in this report, as all of the patients mentioned above have nocturnal vasovagal syncope as the primary cause of their symptoms. Although the attacks start when the patient is supine, the associated symptoms described are typical of vasovagal syncope. These include: nausea, sweating, light headedness, abdominal discomfort and weakness during the attack, followed by tiredness afterwards. Because the attacks occur at night in bed, epilepsy is often diagnosed especially if muscle jerking is observed. However it should be realized that transient myoclonic jerking is more often a feature of cerebral hypoperfusion than epilepsy (see Case about EEG). Other more reliable features of epilepsy including tongue biting, post ictal confusion and hypersomnolence are absent. Based on an algorithm derived from a recent study on historical criteria that distinguish syncope from seizures | We concluded that the patient in this report, as all of the patients mentioned above have nocturnal vasovagal syncope as the primary cause of their symptoms. Although the attacks start when the patient is supine, the associated symptoms described are typical of vasovagal syncope. These include: nausea, sweating, light headedness, abdominal discomfort and weakness during the attack, followed by tiredness afterwards. Because the attacks occur at night in bed, epilepsy is often diagnosed especially if muscle jerking is observed. However it should be realized that transient myoclonic jerking is more often a feature of cerebral hypoperfusion than epilepsy (see Case about EEG). Other more reliable features of epilepsy including tongue biting, post ictal confusion and hypersomnolence are absent. Based on an algorithm derived from a recent study on historical criteria that distinguish syncope from seizures <cite>Sheldon</cite>, all of our patients fulfilled the diagnostic criteria for vasovagal syncope with very high levels of certainty (>90%). Furthermore, we have demonstrated a normal EEG during a typical nocturnal episode in one patient and normal inter-ictal EEG’s in 46% of the group. | ||
The association with nightmares is suggestive of a central trigger similar to the mechanism proposed for vasovagal syncope associated with phobias. Syncope is occasionally triggered by bowel evacuation or colonoscopy, and has been induced reliably by inflating rectal balloons. Thus the predominance of pronounced gastrointestinal symptoms associated with these attacks would suggest a gastro-intestinal trigger mechanism. Because there was no association with the consumption of spicy food or alcohol, nor were there any symptoms of gastro-enteritis we think that abdominal discomfort is more likely to be an effect of vagal over-activity rather than the cause. The prominent cardio-inhibitory response during tilt table testing suggests a cardiovascular autonomic imbalance which may also occur during sleep. | The association with nightmares is suggestive of a central trigger similar to the mechanism proposed for vasovagal syncope associated with phobias. Syncope is occasionally triggered by bowel evacuation or colonoscopy, and has been induced reliably by inflating rectal balloons. Thus the predominance of pronounced gastrointestinal symptoms associated with these attacks would suggest a gastro-intestinal trigger mechanism. Because there was no association with the consumption of spicy food or alcohol, nor were there any symptoms of gastro-enteritis we think that abdominal discomfort is more likely to be an effect of vagal over-activity rather than the cause. The prominent cardio-inhibitory response during tilt table testing suggests a cardiovascular autonomic imbalance which may also occur during sleep. | ||