Abstract
Dr Grönbaek raises two questions specifically related to my article on acute and chronic hypertensive headache and hypertensive encephalopathy. The first question inquires about the time the blood pressure of 180/100 was recorded in the patient with hypertensive encephalopathy. The blood pressure was obtained after the seizure, which the patient developed immediately upon arrival in the emergency room. The second question asks whether the patients described in the article were subjected to an angiogram to look for ‘resistance … located in the major supplying vessels to the vertebrobasilar territory’. The patients were only subjected to the examinations described in the article; a cerebral angiogram was not considered indicated in any of them, including the patient with the encephalopathy.
With regard to Dr Grönbaek's comments, nothing of what was written in the article relates specifically to histamine-headache experiments conducted in the 1940s. With regard to the pathogenesis of the hypertensive encephalopathy, Dr Grönbaek apparently favours cerebral vasospasm over the explanation I presented, that is, disruption of the blood–brain barrier. I think that neither of them has been proven; in my opinion, both are possible and they are not mutually exclusive. In fact, I saw a patient with global, as opposed to focal, hypertensive encephalopathy, in whom the cerebral angiogram showed diffuse vasospasm. In this patient, taking a decongestant precipitated the hypertensive crisis; it resulted in severe, generalized headache, palpitations, sweating, blurred vision, nausea, and confusion.