Neurally Mediated Syncope

In a comment on theCerebellar Fits post, BJR raises the possibility of a relationship between breath holding spells, neurally mediated syncope, vasovagal syncope, reflex anoxic seizure and cerebellar fits. BJR asks an important question, are these “The same thing by another name?”



This post will review neurally mediated syncope. Subsequent posts will consider breath holding spells, reflex anoxic seizures and the possible overlap of these disorders with the Chiari I malformation.



Neurally Mediated Syncope

According toDr. Zaqqa and Dr. Massumiof the Texas Heart Institute in Houston, Texas, neurally mediated syncope (NMS) “is a disorder of the autonomic regulation of postural tone, which results in hypotension, bradycardia, and loss of consciousness.” NMS is also know as neurocardiogenic syncope and vasovagal syncope.



TheNational Dysautonomia Research Foundationdescribes the physiological regulation of blood flow with standing as follows:



“The blood pressure control centers are located in the posterior parts of the brain (the brainstem or medulla). Every time a person stands, gravity pulls blood toward the lower extremities. The brain senses this change and compensates by increasing the heart rate and tightening (constricting) the blood vessels of the legs, forcing blood back upward to the brain. These centers in the brainstem (the autonomic centers), then work as a sort of thermostat to regulate blood pressure. “



If the thermostat is faulty, the blood pressure to falls “too low, causing the brain to lose its blood supply resulting in loss of consciousness (fainting).”



Zaqqa & Massumiexplain it this way:



“The human body has a remarkable ability to maintain a stable blood pressure in the presence of ever-changing forces that constantly shift and redistribute the circulating blood volume. To achieve this steady control, reflex mechanisms continuously adjust the cardiac output and vascular tone. Even a simple change in posture, such as standing up, can result in a relatively “empty” ventricle owing to shifting of blood from the thorax to the abdomen and lower extremities. This shift in blood volume can markedly decrease the cardiac output.



While neurally mediated syncope can occur at any age, it is more frequent in adolescence. Knowing the triggers and warnings of NMS is important as we consider comparing it to CM-I.Zaqqa & Massuminote:



“The triggering factor for NMS varies widely and includes orthostatic stress, emotional stress, urination, coughing, swallowing, physical exercise, and stimulation of the carotid sinus in susceptible persons.”



“Typically, a patient with neurally mediated syncope experiences nausea, lightheadedness, a feeling of warmth, and pallor before abruptly losing consciousness.”



NMS may be prevented “by an increased fluid and salt intake and avoidance of triggering factors such as dehydration, extreme heat, alcohol consumption, and prolonged standing.” Persons with repeated spells are treated with beta blockers. Severe refractory cases may require a pacemaker.



Conclusions

The cause of neurally mediated syncope is dysfunction of the human body’s regulation of blood pressure. While orthostatic stress (assuming the upright position) is the most common trigger, coughing or emotional or physical stress can also trigger syncope.



However,a recently published MRI of a patient with Chiari I malformationshows increased herniation and brain stem compression in the upright position. Could some spells of neurally mediated syncope be due to the Chiari malformation? Cough can trigger syncope in patients with CM-I. Could some NMS patients with cough syncope have CM-I?



Next week, I will consider breath holding spells.



John Oro’, MD



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