The Effect of Sneezing on the Reduction of Infarct Volume and the Improvement of Neurological Deficits in Male Rats

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Stroke is defined as acute focal damage to the central nervous system, divided into three categories of cerebral infarction, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage. Stroke is one of the remarkable causes of disability and death in the world. The WHO definition of stroke in the 1970s has been globally accepted. The clinical symptoms are rapidly developing signs of focal or universal disturbances in the function of the brain that last longer than 24 h or even lead to death, and do not have other apparent causes other than that of vascular origin. Cerebral infarction is known to occur as focal ischemia within the perfusion territory of specified arteries due to a clot or stenosis. On the other hand, ICH can be defined as the blood accumulation in the cerebral parenchyma or the ventricles that is not caused by traumatic accidents. The ICH has a lower prevalence of embolism but higher morbidity and mortality.[1]

The mechanism involved in sneezing reflex is similar to the Valsalva maneuver, in which venous return to the heart is reduced, and the autonomic system is involved by changing the tone of the vessels.[2,3,4]

The response of the cardiovascular system to Valsalva maneuver is divided into several phases. The first phase is the start of the strain, and during this phase, we could see the increased intrathoracic pressure, compressed significant vessels and subsequently increased the pressure of the aorta. Changes in cardiac output in this phase are insignificant. In the second phase, an increase in intrathoracic pressure causes compression of the veins at the thoracic inlet and disrupts the venous return. The blood volume of the heart decreases by 25%–30%, resulting in a decrease in the preload of the heart and ultimately lowers the stroke volume. Then, arterial pressure and subsequently, pulse pressure are reduced. These changes cause sympathetic stimulation and vasoconstriction. As mean aorta pressure and pulse pressure are reduced, the carotid sinus baroreceptors are stimulated and this stimulation results in the sympathetic activation, heart rate elevation, and increased resistance of the arteries and veins outside the thorax. As a result, cardiac output and blood pressure (BP) are raised, and the sudden and the short-term occurrence of these processes cause the excessive increase in arterial pressure.[3,5]

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Stroke is a significant cause of long-term disability due to neurological impairment,[6] and there are no broadly effective therapies to rescue neurological deficits. Sneezing increases intrathoracic and intraabdominal pressure, resulting in acute hypertension and transiently elevated cerebral blood flow.[7] Induced sneezing in the early period, following the stroke, may be a feasible method to restore cerebral blood flow because it can be evoked reliably even in unconscious subjects.

Induced sneezing and concomitant acute hypertension during the 1st h of recovery after ischemic stroke can improve recovery, presumably because the cerebral BP elevation causes recanalization of blocked vessels[8] and early vascular reperfusion is strongly related to clinical outcomes.[9] Furthermore, the rise in BP increases blood flow to ischemic regions.[10] Some studies have stated that Valsalva maneuver may increase the risk of ICH, and a few case report studies demonstrated that some individuals had blown O-ring in their heads while lifting weights, presumably under Valsalva maneuver. It is stated that sneezing could result in increased intrathoracic pressure and BP and intracranial pressure (ICP) and therefore, sneezing may predispose ICH. Hence, sneezing could be useful in the embolic stroke but is a risk factor for hemorrhagic stroke.[11,12,13,14]

Of the numerous animal stroke models, the embolic stroke model induced by natural clots is most relevant to the pathophysiological situation in patients with ischemic stroke.[15] Thus, we tested whether induced sneezing in rats could decrease infarct volume and improve neurological deficits, following clot occlusion of the middle cerebral artery (MCA).


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About the Author: Tung Chi