Abstract
Dear Sir,
We appreciated the comment by Elliot Shevel (1). Indeed, little is known about the pathophysiology of Airplane Headache (AH).
We agree that the final mechanism that leads to the pain is not simply a sinus barotrauma. In our recent paper (2), we stressed that the intrasinus changes due to pressure modifications during airplane travel cannot explain why only a few subjects suffer from AH, since, on equal terms of external conditions, it could be speculated that all the passengers during a particular flight should experience a headache. Nor can individual theoretical abnormalities of paranasal sinuses ostia completely elucidate AH physiopathology, since in an individual subject AH can start after several normal flight experiences and does not recur consistently in following flights, as confirmed by the very gratifying editorial on the subject by Purdy (3). Therefore, the most likely AH physiopathology seems to be related to a variety of multimodal contributing factors: anatomic factors, such as acquired or congenital abnormalities of sinus outlet, environmental factors (cabin pressure, aircraft speed, angle of ascent/descent, maximum altitude), concurrent factors that act by reducing the sinus ventilation, such as a temporary mucosal edema, possibly worsened, in predisposed individuals, by the above reported alterations. However, the exclusion of other possible diseases underlying AH, in primis sinusitis, is mandatory, given the existence of similar clinical pictures attributable to paranasal sinus disorders.
Indeed, the fact that pain occurs in relation to a change in cabin pressure during ascent or descent of the aircraft is sustained by the similarity between AH and the clearly secondary headache due to barotraumatic sinusitis, which could occur in the aviator with upper respiratory tract inflammation, as it is very well described in the following quotation taken from the Aerospace Medical Association Guidelines, where cruiser phase is not mentioned (4):
For the vast majority of patients acute or chronic sinusitis is problematic only for discomfort. In fact, chronic sinusitis may only be minimally symptomatic at ground level. However, perturbations of atmospheric pressure as seen in the aviator or scuba diver may develop sudden, incapacitating pain. This phenomenon is called barotraumatic sinusitis, sinus “block” or “squeeze.” This event can occur on ascent but usually occurs on descent. Should that event occur immediately prior to or during landing procedures in the aviator, it could lead to an aircraft mishap. This is a flight safety issue and can threaten the life of the pilot and his passengers. The current recommendation is that no aviator fly with a “cold” or viral upper respiratory tract infection, or with the condition of rhinosinusitis. The aviator should be considered grounded until he or she is off medications and has had complete resolution of the condition. Acute barotraumatic sinusitis is preventable by keeping the patient grounded until complete resolution. Should a pilot or aircrew member experience difficulty on descent topical oxymetazoline could be used to decrease symptomatology and get him or her “down.” Primary prevention is quite simple: “No flying with a URI or rhinosinusitis”. (4)
For the above mentioned reasons, we maintain that the pressure change during landing and/or takeoff is the necessary prerequisite, although by no means sufficient by itself, in the pathophysiology of AH.
We wish to take this opportunity to express our appreciation to Irfan Mohamad for his sound comment (5) to our paper, which also adds some information to the considerations we reported above.