- Email: [email protected]
The valsalva maneuver in the study of syncope
T H E V A L S A L V A M A N E U V E R I N T H E STUDY O F SYNCOPE~j ROGER C. DUVOISIN, CAPTAIN, U S A F , M C
Neurological Service, Department of Medicine, USAF Hospital, Lackland, USAF Aerospace Medical Center (A TC), Lackland Air Force Base, Texas ( U.S.A. ) (Received for publication: January 17, 1961)
INTRODUCTION Using firm ocular pressure, Gastaut and his coworkers (1956, 1957, 1958) elicited a reflex cardiac asystole of sufficient duration to cause loss of consciousness in many of their subjects. They believed that the convulsive phenomena which frequently complicated these syncopal episodes and the accompanying EEG patterns comprised a distinctive electroclinical entity, convulsive syncope, unrelated to epilepsy, and showed that reproducing syncopal episodes in the EEG laboratory could help differentiate syncope from epilepsy. Other techniques for inducing syncope (Engel 1950, 1959) are also effective and may be more closely related to the physiological mechanisms underlying some types of syncope commonly encountered in clinical practice. The present report records several observations on the use of the Valsalva maneuver to induce syncope in the laboratory. Initially, the response to the Valsalva maneuver was observed in cases of cough syncope and in several patients whose syncopal "spells" seemed to be related to increased intrathoracic pressure during physical exertion. Subsequently, it was found helpful in the routine evaluation of patients who were referred because of loss of consciousness of uncertain etiology. In addition, it was found to be a practical method of inducing syncope in the EEG laboratory for the purpose of inve~tignting the nature of syncope and convulsive syncope. METHOD The test is performed with the patient sitting up, the electrocardiogram being recorded simultaneously with the EEG. The patient is instructed to inhale deeply, to hold his breath and then to strain as vigorously as possible with the glottis closed as if he were making a bowel movement. In the absence of a significant effect, the maneuver is repeated immediately following 1 rain of hyperventilation. The radial pulse is palpated during the maneuver, and the patient is observed for evidence of syncope and convulsive phenomena. In episodes culminating in syncope the radial pulse becomes unobtainable 5-6 sec before the patient loses consciousness. Usually syncope is complicated by convulsive movements varying in severity from a few clonic twitches of the upper
extremities to a generalized seizure. An occasional patient has been incontinent while unconsciouS. In twelve patients the circulatory effects of the maximal Valsalva maneuver were investigated by simultaneously recording brachial artery, intraesophageal and either right atrial or superior vena cava pressures. Observations made in these subjects and published accounts of similar studies (Goldberg et al. 1952; Sharpey-Schafer 1953; Wilkins and Friedland 1944) of the effects of the limited Valsalva maneuver (i.e., the Flack test) have defined in considerable detail the circulatory dynamics of the Valsalva maneuver. The following brief description will suffice for the purposes of this report: During the strain there is a marked elevation of intrathoracic pressure which is transmitted directly to the great vessels, thus producing a simultaneous and equal rise in central venous and intracranial pressure as well as a transient rise in peripheral arterial pressure. The elevated pressure in the great veins hinders venous return to the heart, cardiac output falls and consequently the initial rise in peripheral arterial pressure is followed by a marked fall in pulse pressure and in systolic and diastolic blood pressure. As shown in a record from a representative case (Fig. 1), a severe hypotension can result with arterial blood pressure at "shock" levels for a sufficient period of time to cause loss of consciousness. The period of hypotension is of such brief duration, rarely exceeding 15 sec, that it cannot easily be detected by taking serial blood pressure readings with a sphygmomanometer and a stethoscope. With loss of consciousness or at the voluntary end of the maneuver the glottis is opened, the intrathoracic and central venous pressures abruptly return to resting values, and there may be a concomitant further drop in peripheral arterial pressure. Peripheral blood pressure then returns rapidly to normal levels and may "overshoot" in a brief period of hypertension usually associated with a bradycardia. RESULTS Performed in the simple manner described, the Valsalva maneuver proved to be an effective means of inducing convulsive syncope in susceptible individuals. It is less painful than ocular compression, and it is a safe procedure which subjects the patient, who is largely in control of the test situation, to a minimum of discomfort. To date, a total of 98 patients have been studied. Of these, 24 fainted on performing a Valsalva maneuver. Their syncopal episodes presented clinical and EEG
1 This paper represents the personal viewpoint of the author and is not to be construed as a statement of official Air Force policy. 622
VALSALVA MANEUVER AND SYNCOPE features identical to those described by Gastaut for convulsive syncope due to cardiac asystole. There first occurred an abrupt loss of consciousness, often accompanied by mydriasis, diaphoresis and hypersalivation. The patients slumped down with head falling forward. Occasionally they stared vacantly for a moment at the onset of the syncope. There followed a variable
623
between the convulsive phenomena and the EEG. Gross clonic movements often appeared during the period of electrical silence but usually occurred with delta activity. At times these movements were seen even earlier in the presence of 6-7 c/sec activity. In no instance was spike or spike-and-wave activity noted nor was there a postictal depression of the EEG.
Fig. 1 EEG, right brachial artery pressure, intraesophageal pressure and E K G recorded synchronously during an episode of convulsive syncope in case 3. The Valsalva maneuver began at A, loss of consciousness occurred at B, and the patient had recovered at C. Note the pronounced arterial hypotension preceding the loss of consciousness. number of clonic jerks of the upper extremities and bobbing of the head. In the more severe episodes there was a generalized clonic seizure with extensor thrusts of the legs. After a b r i e f moment of inactivity the patients promptly regained consciousness. A transient confusion was frequently observed but recovery was always complete within several seconds. Neither the initial tonic phase nor the tonic-clonic sequence characteristic of the grand real seizures of idiopathic epilepsy was observed. There was no postictal stupor, headache or other symptomatology suggestive of epilepsy. The EEG showed a characteristic sequence of events. There was at first a minimal slow activity, which increased rapidly and progressively to culminate in high amplitude delta waves. In the more severe episodes, the delta activity ended abruptly in a period of electrical silence lasting 4-5 sec. A burst of high voltage slow waves followed, obscured largely by the movement artefact produced by a generalized clonic seizure. Recovery was marked by a progressive diminution of slow activity resulting in a return to the resting pattern in 5-10 sec. Loss of consciousness occurred concurrently with or immediately after the earliest alteration of the resting pattern. However, there was no constant relationship
ILLUSTRATIVE CASES Case 1. A 23-year old heavy equipment operator was referred because of recurrent episodes of syncope. He was a well developed young male adult of stocky build. A complete physical examination was performed with normal findings. A number of syncopal episodes induced by the Valsalva maneuver were studied with simultaneous recording of the EEG, E K G and left brachial artery pressure. It was found that a severe hypotension of 6 or more sec duration consistently preceded loss of consciousness. The EEG consisted of irregular slow activity during a convulsion (Fig. 2) and returned promptly to the resting pattern on recovery. A pentylenetetrazol activation test using 750 mg given by intravenous injection at 50 mg/min elicited minimal aspecific changes. The patient was also subjected to cerebral congestion induced by inflating a blood pressure cuff around the neck to 60 mm Hg for 1 min. Hypoxia was produced by having the patient breathe a mixture consisting of 7 per cent oxygen and 93 per cent inert gas. These procedures failed to reproduce his episodes. Diphenylhydantoin, 400 mg by mouth daily for over 6 months neither reduced the frequency of spontaneous episodes nor rendered it more
624
Rc
~
R . C . DUVOISIN
, ~ECaND
~o~1
A
~T ~ L0 o
'
~
~
Fig. 2 EEG record of an episode of convulsive syncope in case 1. The vertex lead is used for reference. The arrow marks the movement artefact produced when the patient's head fell forward as he lost consciousness 11 sec after the onset of the Valsalva maneuver. Clonic jerking of the arms began at A.
difficult for the subject to reproduce an episode of convulsive syncope at will by holding his breath and straining. Comment: During the period of observation the patient had several spontaneous "spells" which could usually be related to some activity in which it seemed likely that he had inadvertently performed a Valsalva maneuver. On one occasion, for example, he had been wrestling. Case 2. This 18-year old male youth was seen in consultation because of numerous "spells" in which he appeared frightened and then had a momentary vacant expression followed by blinking of the eyes and several rhythmic myoclonic jerks of the upper extremities. On examination he was found to be a tall thin youth with no significant physical abnormalities. A complete neurological examination was unremarkable. On performing a Valsalva maneuver the patient abrubtly lost consciousness and had a generalized clonic seizure from which he rapidly recovered. The EEG during this event consisted of irregular slow waves in a pattern similar to that shown in Fig. 2. However, on routine EEG examinations there were infrequent brief bilaterally synchronous bursts of spike and wave activity. These were occasionally accompanied by one or two myoclonic jerks of the arms and a transient lapse of consciousness. A similar seizure was reproduced by the intravenous administration of 300 mg of pentylenetetrazol. The patient stated that the pentylenetetrazol seizure was identical to his "spells", whereas the episodes induced by breath-holding were to him an entirely new experience. Methsuximide, 900 mg daily, provided dramatic and complete relief of the seizures during a one-month period of observation. A study of the circulatory effects of the Valsalva maneuver in this patient with simultaneous recording of brachial artery, right atrial and intraesophageal pressures showed that a severe hypotension always preceded episodes of convulsive syncope.
Comment: It seems significant that in this patient with a centrencephalic seizure disorder no relationship could be demonstrated between the epileptic phenomena and the episodes of convulsive syncope. The latter apparently were not epileptic seizures triggered by anoxia. Case 3. A 23-year old male in good health was referred because of a single episode of syncope. He had experienced severe rectal discomfort and a desire to move his bowels. On arising he felt dizzy and then fainted. He regained consciousness promptly and in several minutes felt well again. Physical examination uncovered no abnormal findings. Routine laboratory studies including a chest X-ray, an EKG and a hemogram were within normal limits. A routine awake resting EEG presented normal patterns. During a Valsalva maneuver he experienced a typical episode of convulsive syncope. This was repeated with simultaneous recording of intraesophageal and right brachial artery pressures (Fig. I). Comment: This case is presented to show the precise temporal relationship of the blood pressure changes to syncope and the EEG changes when they are recorded synchronously. The patient was thought to have had an episode of vasovagal syncope. Case 4. A 33-year old male had experienced an occasional "blackout spell" over a period of several years. Jerking movements of the head and arms had been observed and the patient was thought to have epileptic seizures. He recalled that several episodes had been preceded by a bout of coughing. The patient was an obese adult who presented no abnormal findings on examination. A complete neurological examination was within normal limits. The awake resting EEG was normal but a Valsalva maneuver produced an episode which the patient stated was identical to the "spells" he had experienced following coughing. It began with the patient looking vacantly up to the left and making a loud blubbering sound as he released his breath. At this time the EEG (Fig. 3) showed some irreg-
! ! ! i ~,3,, Y C --~ ~ r , ~ - - . / - - - - - ~ . . . . . . . . . . A
~cvbS~co D
B
-
/~, - -
"
[
Fig. 3 EEG record of a severe episode of convulsive syncope in case 4 showing period of electrical silence. At A, 10 sec after the onset of the Valsalva maneuver, the patient became unresponsive, released his breath, and stared upwards and to the left. A generalized seizure began at B with clonic jerking of the arms.
625
VALSALVA MANEUVER AND SYNCOPE ular slowing which progressively increased in amplitude. There followed a period of electrical silence toward the end of which the patient developed a clonic jerking of the upper extremities. The seizure rapidly became generalized with irregular thrashing movements of the arms, extensor thrusts of the legs and violent vertical bobbing of the head. Simultaneous recording of the EKG, the left brachial artery pressure and the superior vena cava pressures during several similar episodes showed that a severe period of hypotension preceded the loss of consciousness. It was concluded that the patient's "spells" represented episodes of cough syncope rather than epileptic seizures.
occurring, for example, during physical exertion, defecation or micturition. Patients with postural hypotension or some deficiency in peripheral vascular reflexes (Sharpey-Schafer and Taylor 1960) are particularly prone to faint on forced expiration. Consequently, properly standardized, the Valsalva maneuver might serve as a test of syncopal predisposition. Finally, it is a useful means of studying syncope which may shed additional light on the relationship, if any, between syncope and epilepsy and on the character of the convulsive phenomena which may complicate cardiovascular syncope.
DISCUSSION
The Valsalva maneuver can, in susceptible individuals, produce episodes with clinical and EEG features identical to those described by Gastaut in convulsive syncope induced by a reflex asystole. A severe hypotension of 6 sec or longer invariably precedes the onset of syncope. The addition of a Valsalva maneuver to the EEG examination may be useful in the study of patients having certain types of syncope, can help to distinguish convulsive syncope from epilepsy, and provides an effective method of studying convulsive syncope in the EEG laboratory.
A discussion of the physiological basis of the convulsive phenomena observed in these patients is beyond the scope of this report, lt seems, however, difficult to view them merely as epileptic seizures triggered by cerebral anoxia. The EEG showed no evidence of massive neuronal discharge nor activity typical of epilepsy but displayed patterns characteristic of anoxia varying in degree with the severity of the syncopal episode. The convulsive phenomena failed to show any constant relationship to this EEG pattern. Thus, it may be said that they had, per se, no EEG expression and were probably subcortical in origin. These considerations and theillustrative cases presented above appear to support Gastaut's view that convulsive syncope is entirely unrelated to epilepsy. Wilkins and Friedland (1944) recorded intra-arterial pressure in a patient with cough syncope who was able to reproduce his "blackouts" by performing a Valsalva maneuver and concluded that the circulatory effects of an acute increase in intrathoracic pressure constituted the basic mechanism of cough syncope or "laryngeal epilepsy". Sharpey-Schafer has recently presented further evidence supporting this view (1953). Although only six patients having cough syncope were encountered during the course of the present study, it seems significant that each one was able to reproduce syncopal episodes by straining against a closed glottis after a deep inspiration. In each instance, the characteristic EEG pattern of convulsive syncope was recorded and the patients thought that the episodes reproduced in the laboratory were identical to their spontaneous "spells". These observations would seem to refute the view that cough syncope represents a special form of reflex epilepsy. On the clinical level the differential diagnosis of "faint" versus "fit" may sometimes prove embarrassingly difficult. It may be helpful in such cases to observe a syncopal episode during the EEG examination. Ocular compression, carotid sinus massage, compression of the carotid artery and other procedures may succeed in producing an episode. The Valsalva is another and particularly useful maneuver which can also be performed during the EEG examination. It provides a mechanism probably identical to that responsible for cough syncope and may be of value when the history suggests that syncope was related to an acute increase of intrathoracic pressure
SUMMARY
The author acknowledges the assistance of Dr. Donald Saunders, formerly of the Cardiology Service, USAF Hospital, Lackland and presently Honorary Assistant Registrar, Institute of Cardiology, London, England, who recorded the circulatory effects of the Valsalva maneuver during cardiac catheterization. REFERENCES ENGEL, G. L. Fainting: physiological and psychological considerations. C. C. Thomas, Springfield, II1., 1950, 141 pp. ENGEL, G. L. On the existence of the cerebral form of the carotid sinus reflex. Neurology (Minneap.), 1959, 9: 565-568. GASTAU'r, H. Sur la grande fr6quence des anoxies c6r6brales aigu6s et leur confusion avec l'6pilepsie. Essai de r6habilitation de la syncope. Bull. Acad. nat. Med. (Paris), 1958, 142:723 726. GASTAUT, H. Syncope and seizure with reference to clinical note presented by Dr. Lloyd-Smith and W. F. Tatlow. Electroenceph. c/in. Neurophysiol., 1958, 10: 571-572. GASTAUT, H. and FISCHER-WILLIAMS,E . M . Electroencephalographic study of syncope; its differentiation from epilepsy. Lancet, 1957, 2: 1018-1025. GASTAUT, H., FISCHER-WILLIAMS,E. M., BIRMINGHAM E., et LUGARESI,E. Etude 61ectroenc6phalographique des syncopes. II. Corr61ations 61ectrocliniques cbez 25 sujets enregistr6s pendant leur syncope. Rev. neurol., 1956, 95: 542-547. GASTAUT, H., NAVARRANNE,P., PITOT, M. et SALAMON, G. Etude 61ectroenc6phalographique des syncopes. I. Corr61ations 61ectrocliniques chez 150 sujets pr6sentant des syncopes vasovagales. Rev. neurol., 1956, 95:541 542.
626
R . C . DUVOISIN
GOLDBERG, H., ELISBERG,E. I. and KATZ, L. N. The effect of the Valsalva-like maneuver upon the circulation in normal individuals and patients with mitral stenosis. Circulation, 1952, 5: 38-47. SHARPEY-SCHAFER,E. P. Effects of coughing on intrathoracic pressure, arterial pressure and peripheral blood flow. J. Physiol. (Lond.), 1953, 122: 351-357.
SHARPEY-SCHAFER,E.P. The mechanism of syncope after coughing. Brit. reed. J., 1953, 2: 860-863. SHARPEY-SCHAFER, E. P. and TAYLOR, P. J. Absent circulatory reflexes in diabetic neuritis. Lancet, 1960, 1 : 559-562. WILrdNS, R. W. and FRIEDLAND, C. K. Laryngeal epilepsy due to increased intrathoracic pressure. J. clin. Invest., 1944, 23: 939.
Reference: DUVOlSIN, R. C. The Valsalva maneuver in the study of syncope. Electroenceph. clin. Neurophysiol., 1961, 13: 622-626.
Neurological Service, Department of Medicine, USAF Hospital, Lackland, USAF Aerospace Medical Center (A TC), Lackland Air Force Base, Texas ( U.S.A. ) (Received for publication: January 17, 1961)
INTRODUCTION Using firm ocular pressure, Gastaut and his coworkers (1956, 1957, 1958) elicited a reflex cardiac asystole of sufficient duration to cause loss of consciousness in many of their subjects. They believed that the convulsive phenomena which frequently complicated these syncopal episodes and the accompanying EEG patterns comprised a distinctive electroclinical entity, convulsive syncope, unrelated to epilepsy, and showed that reproducing syncopal episodes in the EEG laboratory could help differentiate syncope from epilepsy. Other techniques for inducing syncope (Engel 1950, 1959) are also effective and may be more closely related to the physiological mechanisms underlying some types of syncope commonly encountered in clinical practice. The present report records several observations on the use of the Valsalva maneuver to induce syncope in the laboratory. Initially, the response to the Valsalva maneuver was observed in cases of cough syncope and in several patients whose syncopal "spells" seemed to be related to increased intrathoracic pressure during physical exertion. Subsequently, it was found helpful in the routine evaluation of patients who were referred because of loss of consciousness of uncertain etiology. In addition, it was found to be a practical method of inducing syncope in the EEG laboratory for the purpose of inve~tignting the nature of syncope and convulsive syncope. METHOD The test is performed with the patient sitting up, the electrocardiogram being recorded simultaneously with the EEG. The patient is instructed to inhale deeply, to hold his breath and then to strain as vigorously as possible with the glottis closed as if he were making a bowel movement. In the absence of a significant effect, the maneuver is repeated immediately following 1 rain of hyperventilation. The radial pulse is palpated during the maneuver, and the patient is observed for evidence of syncope and convulsive phenomena. In episodes culminating in syncope the radial pulse becomes unobtainable 5-6 sec before the patient loses consciousness. Usually syncope is complicated by convulsive movements varying in severity from a few clonic twitches of the upper
extremities to a generalized seizure. An occasional patient has been incontinent while unconsciouS. In twelve patients the circulatory effects of the maximal Valsalva maneuver were investigated by simultaneously recording brachial artery, intraesophageal and either right atrial or superior vena cava pressures. Observations made in these subjects and published accounts of similar studies (Goldberg et al. 1952; Sharpey-Schafer 1953; Wilkins and Friedland 1944) of the effects of the limited Valsalva maneuver (i.e., the Flack test) have defined in considerable detail the circulatory dynamics of the Valsalva maneuver. The following brief description will suffice for the purposes of this report: During the strain there is a marked elevation of intrathoracic pressure which is transmitted directly to the great vessels, thus producing a simultaneous and equal rise in central venous and intracranial pressure as well as a transient rise in peripheral arterial pressure. The elevated pressure in the great veins hinders venous return to the heart, cardiac output falls and consequently the initial rise in peripheral arterial pressure is followed by a marked fall in pulse pressure and in systolic and diastolic blood pressure. As shown in a record from a representative case (Fig. 1), a severe hypotension can result with arterial blood pressure at "shock" levels for a sufficient period of time to cause loss of consciousness. The period of hypotension is of such brief duration, rarely exceeding 15 sec, that it cannot easily be detected by taking serial blood pressure readings with a sphygmomanometer and a stethoscope. With loss of consciousness or at the voluntary end of the maneuver the glottis is opened, the intrathoracic and central venous pressures abruptly return to resting values, and there may be a concomitant further drop in peripheral arterial pressure. Peripheral blood pressure then returns rapidly to normal levels and may "overshoot" in a brief period of hypertension usually associated with a bradycardia. RESULTS Performed in the simple manner described, the Valsalva maneuver proved to be an effective means of inducing convulsive syncope in susceptible individuals. It is less painful than ocular compression, and it is a safe procedure which subjects the patient, who is largely in control of the test situation, to a minimum of discomfort. To date, a total of 98 patients have been studied. Of these, 24 fainted on performing a Valsalva maneuver. Their syncopal episodes presented clinical and EEG
1 This paper represents the personal viewpoint of the author and is not to be construed as a statement of official Air Force policy. 622
VALSALVA MANEUVER AND SYNCOPE features identical to those described by Gastaut for convulsive syncope due to cardiac asystole. There first occurred an abrupt loss of consciousness, often accompanied by mydriasis, diaphoresis and hypersalivation. The patients slumped down with head falling forward. Occasionally they stared vacantly for a moment at the onset of the syncope. There followed a variable
623
between the convulsive phenomena and the EEG. Gross clonic movements often appeared during the period of electrical silence but usually occurred with delta activity. At times these movements were seen even earlier in the presence of 6-7 c/sec activity. In no instance was spike or spike-and-wave activity noted nor was there a postictal depression of the EEG.
Fig. 1 EEG, right brachial artery pressure, intraesophageal pressure and E K G recorded synchronously during an episode of convulsive syncope in case 3. The Valsalva maneuver began at A, loss of consciousness occurred at B, and the patient had recovered at C. Note the pronounced arterial hypotension preceding the loss of consciousness. number of clonic jerks of the upper extremities and bobbing of the head. In the more severe episodes there was a generalized clonic seizure with extensor thrusts of the legs. After a b r i e f moment of inactivity the patients promptly regained consciousness. A transient confusion was frequently observed but recovery was always complete within several seconds. Neither the initial tonic phase nor the tonic-clonic sequence characteristic of the grand real seizures of idiopathic epilepsy was observed. There was no postictal stupor, headache or other symptomatology suggestive of epilepsy. The EEG showed a characteristic sequence of events. There was at first a minimal slow activity, which increased rapidly and progressively to culminate in high amplitude delta waves. In the more severe episodes, the delta activity ended abruptly in a period of electrical silence lasting 4-5 sec. A burst of high voltage slow waves followed, obscured largely by the movement artefact produced by a generalized clonic seizure. Recovery was marked by a progressive diminution of slow activity resulting in a return to the resting pattern in 5-10 sec. Loss of consciousness occurred concurrently with or immediately after the earliest alteration of the resting pattern. However, there was no constant relationship
ILLUSTRATIVE CASES Case 1. A 23-year old heavy equipment operator was referred because of recurrent episodes of syncope. He was a well developed young male adult of stocky build. A complete physical examination was performed with normal findings. A number of syncopal episodes induced by the Valsalva maneuver were studied with simultaneous recording of the EEG, E K G and left brachial artery pressure. It was found that a severe hypotension of 6 or more sec duration consistently preceded loss of consciousness. The EEG consisted of irregular slow activity during a convulsion (Fig. 2) and returned promptly to the resting pattern on recovery. A pentylenetetrazol activation test using 750 mg given by intravenous injection at 50 mg/min elicited minimal aspecific changes. The patient was also subjected to cerebral congestion induced by inflating a blood pressure cuff around the neck to 60 mm Hg for 1 min. Hypoxia was produced by having the patient breathe a mixture consisting of 7 per cent oxygen and 93 per cent inert gas. These procedures failed to reproduce his episodes. Diphenylhydantoin, 400 mg by mouth daily for over 6 months neither reduced the frequency of spontaneous episodes nor rendered it more
624
Rc
~
R . C . DUVOISIN
, ~ECaND
~o~1
A
~T ~ L0 o
'
~
~
Fig. 2 EEG record of an episode of convulsive syncope in case 1. The vertex lead is used for reference. The arrow marks the movement artefact produced when the patient's head fell forward as he lost consciousness 11 sec after the onset of the Valsalva maneuver. Clonic jerking of the arms began at A.
difficult for the subject to reproduce an episode of convulsive syncope at will by holding his breath and straining. Comment: During the period of observation the patient had several spontaneous "spells" which could usually be related to some activity in which it seemed likely that he had inadvertently performed a Valsalva maneuver. On one occasion, for example, he had been wrestling. Case 2. This 18-year old male youth was seen in consultation because of numerous "spells" in which he appeared frightened and then had a momentary vacant expression followed by blinking of the eyes and several rhythmic myoclonic jerks of the upper extremities. On examination he was found to be a tall thin youth with no significant physical abnormalities. A complete neurological examination was unremarkable. On performing a Valsalva maneuver the patient abrubtly lost consciousness and had a generalized clonic seizure from which he rapidly recovered. The EEG during this event consisted of irregular slow waves in a pattern similar to that shown in Fig. 2. However, on routine EEG examinations there were infrequent brief bilaterally synchronous bursts of spike and wave activity. These were occasionally accompanied by one or two myoclonic jerks of the arms and a transient lapse of consciousness. A similar seizure was reproduced by the intravenous administration of 300 mg of pentylenetetrazol. The patient stated that the pentylenetetrazol seizure was identical to his "spells", whereas the episodes induced by breath-holding were to him an entirely new experience. Methsuximide, 900 mg daily, provided dramatic and complete relief of the seizures during a one-month period of observation. A study of the circulatory effects of the Valsalva maneuver in this patient with simultaneous recording of brachial artery, right atrial and intraesophageal pressures showed that a severe hypotension always preceded episodes of convulsive syncope.
Comment: It seems significant that in this patient with a centrencephalic seizure disorder no relationship could be demonstrated between the epileptic phenomena and the episodes of convulsive syncope. The latter apparently were not epileptic seizures triggered by anoxia. Case 3. A 23-year old male in good health was referred because of a single episode of syncope. He had experienced severe rectal discomfort and a desire to move his bowels. On arising he felt dizzy and then fainted. He regained consciousness promptly and in several minutes felt well again. Physical examination uncovered no abnormal findings. Routine laboratory studies including a chest X-ray, an EKG and a hemogram were within normal limits. A routine awake resting EEG presented normal patterns. During a Valsalva maneuver he experienced a typical episode of convulsive syncope. This was repeated with simultaneous recording of intraesophageal and right brachial artery pressures (Fig. I). Comment: This case is presented to show the precise temporal relationship of the blood pressure changes to syncope and the EEG changes when they are recorded synchronously. The patient was thought to have had an episode of vasovagal syncope. Case 4. A 33-year old male had experienced an occasional "blackout spell" over a period of several years. Jerking movements of the head and arms had been observed and the patient was thought to have epileptic seizures. He recalled that several episodes had been preceded by a bout of coughing. The patient was an obese adult who presented no abnormal findings on examination. A complete neurological examination was within normal limits. The awake resting EEG was normal but a Valsalva maneuver produced an episode which the patient stated was identical to the "spells" he had experienced following coughing. It began with the patient looking vacantly up to the left and making a loud blubbering sound as he released his breath. At this time the EEG (Fig. 3) showed some irreg-
! ! ! i ~,3,, Y C --~ ~ r , ~ - - . / - - - - - ~ . . . . . . . . . . A
~cvbS~co D
B
-
/~, - -
"
[
Fig. 3 EEG record of a severe episode of convulsive syncope in case 4 showing period of electrical silence. At A, 10 sec after the onset of the Valsalva maneuver, the patient became unresponsive, released his breath, and stared upwards and to the left. A generalized seizure began at B with clonic jerking of the arms.
625
VALSALVA MANEUVER AND SYNCOPE ular slowing which progressively increased in amplitude. There followed a period of electrical silence toward the end of which the patient developed a clonic jerking of the upper extremities. The seizure rapidly became generalized with irregular thrashing movements of the arms, extensor thrusts of the legs and violent vertical bobbing of the head. Simultaneous recording of the EKG, the left brachial artery pressure and the superior vena cava pressures during several similar episodes showed that a severe period of hypotension preceded the loss of consciousness. It was concluded that the patient's "spells" represented episodes of cough syncope rather than epileptic seizures.
occurring, for example, during physical exertion, defecation or micturition. Patients with postural hypotension or some deficiency in peripheral vascular reflexes (Sharpey-Schafer and Taylor 1960) are particularly prone to faint on forced expiration. Consequently, properly standardized, the Valsalva maneuver might serve as a test of syncopal predisposition. Finally, it is a useful means of studying syncope which may shed additional light on the relationship, if any, between syncope and epilepsy and on the character of the convulsive phenomena which may complicate cardiovascular syncope.
DISCUSSION
The Valsalva maneuver can, in susceptible individuals, produce episodes with clinical and EEG features identical to those described by Gastaut in convulsive syncope induced by a reflex asystole. A severe hypotension of 6 sec or longer invariably precedes the onset of syncope. The addition of a Valsalva maneuver to the EEG examination may be useful in the study of patients having certain types of syncope, can help to distinguish convulsive syncope from epilepsy, and provides an effective method of studying convulsive syncope in the EEG laboratory.
A discussion of the physiological basis of the convulsive phenomena observed in these patients is beyond the scope of this report, lt seems, however, difficult to view them merely as epileptic seizures triggered by cerebral anoxia. The EEG showed no evidence of massive neuronal discharge nor activity typical of epilepsy but displayed patterns characteristic of anoxia varying in degree with the severity of the syncopal episode. The convulsive phenomena failed to show any constant relationship to this EEG pattern. Thus, it may be said that they had, per se, no EEG expression and were probably subcortical in origin. These considerations and theillustrative cases presented above appear to support Gastaut's view that convulsive syncope is entirely unrelated to epilepsy. Wilkins and Friedland (1944) recorded intra-arterial pressure in a patient with cough syncope who was able to reproduce his "blackouts" by performing a Valsalva maneuver and concluded that the circulatory effects of an acute increase in intrathoracic pressure constituted the basic mechanism of cough syncope or "laryngeal epilepsy". Sharpey-Schafer has recently presented further evidence supporting this view (1953). Although only six patients having cough syncope were encountered during the course of the present study, it seems significant that each one was able to reproduce syncopal episodes by straining against a closed glottis after a deep inspiration. In each instance, the characteristic EEG pattern of convulsive syncope was recorded and the patients thought that the episodes reproduced in the laboratory were identical to their spontaneous "spells". These observations would seem to refute the view that cough syncope represents a special form of reflex epilepsy. On the clinical level the differential diagnosis of "faint" versus "fit" may sometimes prove embarrassingly difficult. It may be helpful in such cases to observe a syncopal episode during the EEG examination. Ocular compression, carotid sinus massage, compression of the carotid artery and other procedures may succeed in producing an episode. The Valsalva is another and particularly useful maneuver which can also be performed during the EEG examination. It provides a mechanism probably identical to that responsible for cough syncope and may be of value when the history suggests that syncope was related to an acute increase of intrathoracic pressure
SUMMARY
The author acknowledges the assistance of Dr. Donald Saunders, formerly of the Cardiology Service, USAF Hospital, Lackland and presently Honorary Assistant Registrar, Institute of Cardiology, London, England, who recorded the circulatory effects of the Valsalva maneuver during cardiac catheterization. REFERENCES ENGEL, G. L. Fainting: physiological and psychological considerations. C. C. Thomas, Springfield, II1., 1950, 141 pp. ENGEL, G. L. On the existence of the cerebral form of the carotid sinus reflex. Neurology (Minneap.), 1959, 9: 565-568. GASTAU'r, H. Sur la grande fr6quence des anoxies c6r6brales aigu6s et leur confusion avec l'6pilepsie. Essai de r6habilitation de la syncope. Bull. Acad. nat. Med. (Paris), 1958, 142:723 726. GASTAUT, H. Syncope and seizure with reference to clinical note presented by Dr. Lloyd-Smith and W. F. Tatlow. Electroenceph. c/in. Neurophysiol., 1958, 10: 571-572. GASTAUT, H. and FISCHER-WILLIAMS,E . M . Electroencephalographic study of syncope; its differentiation from epilepsy. Lancet, 1957, 2: 1018-1025. GASTAUT, H., FISCHER-WILLIAMS,E. M., BIRMINGHAM E., et LUGARESI,E. Etude 61ectroenc6phalographique des syncopes. II. Corr61ations 61ectrocliniques cbez 25 sujets enregistr6s pendant leur syncope. Rev. neurol., 1956, 95: 542-547. GASTAUT, H., NAVARRANNE,P., PITOT, M. et SALAMON, G. Etude 61ectroenc6phalographique des syncopes. I. Corr61ations 61ectrocliniques chez 150 sujets pr6sentant des syncopes vasovagales. Rev. neurol., 1956, 95:541 542.
626
R . C . DUVOISIN
GOLDBERG, H., ELISBERG,E. I. and KATZ, L. N. The effect of the Valsalva-like maneuver upon the circulation in normal individuals and patients with mitral stenosis. Circulation, 1952, 5: 38-47. SHARPEY-SCHAFER,E. P. Effects of coughing on intrathoracic pressure, arterial pressure and peripheral blood flow. J. Physiol. (Lond.), 1953, 122: 351-357.
SHARPEY-SCHAFER,E.P. The mechanism of syncope after coughing. Brit. reed. J., 1953, 2: 860-863. SHARPEY-SCHAFER, E. P. and TAYLOR, P. J. Absent circulatory reflexes in diabetic neuritis. Lancet, 1960, 1 : 559-562. WILrdNS, R. W. and FRIEDLAND, C. K. Laryngeal epilepsy due to increased intrathoracic pressure. J. clin. Invest., 1944, 23: 939.
Reference: DUVOlSIN, R. C. The Valsalva maneuver in the study of syncope. Electroenceph. clin. Neurophysiol., 1961, 13: 622-626.