The journal of headache and pain
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I suppose that the patient number 14, reported in the article of RJ Lane et al. on "Modified Valsalva test differentiates primary from secondary cough headache "in a recent issue of your esteemed journal, was probably suffering from spontaneous intracranial hypotension syndrome (SIH) caused by cervical manipulation.
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The current definition of cough headache includes provocation of the symptom by Valsalva manoeuvre, and it is generally believed that all cough headache results from a sudden increase in intracranial pressure. We sought to question that presumption and to determine whether the Valsalva test might distinguish primary from secondary cough headache. ⋯ These findings suggest that secondary cough headache results from a transient increase in intracranial CSF pressure during exertion in the presence of obstruction to normal cerebrospinal fluid dynamics. The modified Valsalva test can also determine whether tonsillar herniation found on brain MRI is symptomatic. Primary cough headache appears to be caused by a different mechanism, possibly through congestion of the orbital venous plexus in the presence of jugular venous incompetence and a reduced threshold for trigeminal sensory activation.
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Nitric oxide (NO) is thought to play an important role in the pathophysiology of migraine. Infusion of the nitrovasodilator glyceroltrinitrate (nitroglycerin, GTN), which mobilizes NO in the organism, is an approved migraine model in humans. Calcitonin gene-related peptide (CGRP) is regarded as another key mediator in migraine. Increased plasma levels of CGRP have been found during spontaneous as well as nitrovasodilator-induced migraine attacks. The nociceptive processes and interactions underlying the NO and CGRP mediated headache are poorly known but can be examined in animal experiments. In the present study we examined changes in immunofluorescence of CGRP receptor components (CLR and RAMP1) and soluble guanylyl cyclase (sGC), the intracellular receptor for NO, in rat trigeminal ganglia after pretreatment with GTN. ⋯ Prolonged infusion of GTN caused increased fractions of RAMP1- and decreased fractions of sGC-immunopositive neurons in the trigeminal ganglion. The observed alterations are likely immunophenotypic correlates of the pathophysiological processes underlying nitrovasodilator-induced migraine attacks and indicate that signalling via CGRP receptors but not sGC-mediated mechanisms may be enhanced through endogenous NO production.