Neurally mediated (reflex; vasovagal) syncope is the final pathway of a complex central and peripheral nervous system reflex arc. There is a transient change in autonomic efferent activity with increased parasympathetic outflow, plus sympathoinhibition, resulting in brady cardia, vasodilation, and/or reduced vasoconstrictor tone (the vasodepressor response) and reduced cardiac output. The resulting fall in systemic blood pressure can then reduce cerebral blood flow to below the compensatory limits of autoregulation (Fig. 1). In order to develop neurally mediated syncope, a functioning autonomic nervous system is necessary, in contrast to syncope resulting from autonomic failure (discussed below).

Fig1. The paroxysmal hypotensive-bradycardic response that is characteristic of neurally mediated syncope. Noninvasive beat-to-beat blood pressure and heart rate are shown >5 min (from 60 to 360 s) of an upright tilt on a tilt table. B. The same tracing expanded to show 80 s of the episode (from 80 to 200 s). BP, blood pressure; bpm, beats per minute; HR, heart rate.

Multiple triggers of the afferent limb of the reflex arc can result in neurally mediated syncope. In some situations, these can be clearly defined, e.g., orthostatic stress, and stimulation of the carotid sinus, the gastrointestinal tract, or the bladder. Often, however, the trigger is less easily recognized and the cause is multifactorial. Under these circumstances, it is likely that different afferent pathways converge on the central autonomic network within the medulla that integrates the neural impulses and mediates the vasodepressor-bradycardic response.

Classification of Neurally Mediated Syncope

 Neurally mediated syncope may be subdivided based on the afferent pathway and pro vocative trigger. Vasovagal syncope (the common faint) is provoked by intense emotion, pain, and/or orthostatic stress, whereas the situational reflex syncopes have specific localized stimuli that provoke the reflex vasodilation and bradycardia that leads to syncope. The underlying mechanisms have been identified and pathophysiology delineated for most of these situational reflex syncopes. The afferent trigger may originate in the pulmonary system, gastrointestinal system, urogenital system, heart, and carotid sinus in the carotid artery (Table 1).

Table1. Causes of Syncope

Hyperventilation, leading to hypocarbia and cerebral vasoconstriction, and raised intrathoracic pressure that impairs venous return to the heart play a central role in many of the situational reflex syncopes. The afferent pathway of the reflex arc differs among these disorders, but the efferent response via the vagus and sympathetic pathways is similar.

Alternately, neurally mediated syncope may be subdivided based on the predominant efferent pathway. Vasodepressor syncope describes syncope predominantly due to efferent, sympathetic, vasoconstrictor failure; cardioinhibitory syncope describes syncope predominantly associated with bradycardia or asystole due to increased vagal outflow; and mixed response syncope describes syncope in which there are both vagal and sympathetic reflex changes.

Features of Neurally Mediated Syncope In addition to symptoms of orthostatic intolerance such as dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present in patients with neurally mediated syncope. These include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning. During the syncopal event, proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of a seizure. The eyes typically remain open and usually deviate upward. Pupils are usually dilated. Roving eye movements may occur. Grunting, moaning, snorting, and stertorous breathing may be present. Urinary incontinence may occur. Fecal incontinence is very rare, however. Postictal confusion is also rare, although visual and auditory hallucinations and near death and out-of-body experiences are sometimes reported.

Although some predisposing factors and provocative stimuli are well established (for example, motionless upright posture, warm ambient temperature, intravascular volume depletion, alcohol ingestion, hypoxemia, anemia, pain, the sight of blood, venipuncture, and intense emotion), the underlying basis for the widely different thresholds for syncope among individuals exposed to the same provocative stimulus is not known. A genetic basis for neurally mediated syncope may exist. Several studies have reported an increased incidence of syncope in first-degree relatives of fainters, and some candidate genes have been identified with sex-specific associations. These have not been reproduced in other large cohorts. It is likely that environmental, social, and cultural factors play a large role.

TREATMENT

Neurally Mediated Syncope Reassurance, education, avoidance of provocative stimuli, and plasma volume expansion with fluid and salt are the cornerstones of the management of neurally mediated syncope. Isometric counterpressure maneuvers of the limbs (tensing of the abdominal and leg muscles, handgrip and arm tensing, and leg crossing) may raise blood pressure by increasing central blood volume and cardiac output. Of these, abdominal and leg muscle tensing is the most effective. By maintaining pressure in the autoregulatory zone, these maneuvers, which may be particularly helpful in patients with a long prodrome, avoid or delay the onset of syncope. A randomized controlled trial supports this intervention.

Fludrocortisone, vasoconstricting agents, and β-adrenoreceptor antagonists are widely used by experts to treat refractory patients. Of these, only midodrine has been shown to be effective in international, multicenter randomized controlled trials. Because vasodilation, decreased central blood volume, decreased stroke volume, and cardiac output are the dominant pathophysiologic syncopal mechanisms in most patients, use of a cardiac pacemaker is rarely beneficial. In patients with a cardioinhibitory syncope response during tilt-table testing, however, recent sham-controlled randomized clinical trial data have shown that a dual-chamber pacemaker with a closed-loop stimulation algorithm can decrease syncope recurrence. These studies restricted enrollment to older patients (>40 years) with frequent recurrence of syncope and a cardioinhibitory response on tilt-table test. In these patients, dual-chamber pacing may be helpful, although this continues to be an area of uncertainty.

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معتمدة على منظومة عدّ إلكتروني دقيقة العتبة العباسية المقدسة تعلن أعداد الزائرين المشاركين في إحياء زيارة الأربعين

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المزيد

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المزيد

مواضيع ذات صلة

Special Characteristics of Signal Transmission in Nerve Trunks

Peripheral nerves

خواص الإيعاز العصبي

العوامل التي تؤدي إلى تكون جهد الراحة

Astrocytes

المستقبلات الكولنيرجية والأدرينرجية

الجهاز العصبي الذاتي

الأعصاب الدماغية

الأعصاب الشوكية

الجهاز العصبي الطرفي Perioheral

الدماغ الأوسط

الدماغ الخلفي