Key points

Rhinogenic headache is a term that has been used in a variety of ways in the medical literature. Traditionally, it was used interchangeably with “sinus headache” until a wealth of literature showed that sinus headache complaints are likely to represent migraine and seldom represent a sinus infection. The most recent (2013) International Classification of Headache Disorders by the International Headache Society (IHS) includes a category of secondary headaches, which, in turn, includes headache attributed to acute rhinosinusitis ( Box 1 ), with the stipulation that other signs and symptoms of acute sinusitis are present. Chronic rhinosinusitis (CRS) is also supported as a cause of headache ( Box 2 ) although some controversy still exists in this regard. Headache attributed to disorder of the nasal mucosa, turbinates, or septum ( Box 3 ) is described in the appendix of the Classification , although the questionable validity of this entity is noted. This category replaced the term mucosal contact point headache, which was included in the appendix of the second edition Classification in 2004 and which has now been abandoned. This term is still used extensively in the surgical literature and is discussed in detail later.

Reviewing the literature on nonneoplastic rhinogenic headache is complicated by many factors: crossover symptoms with primary headache syndromes (especially migraine), published literature of surgical series lacking controls or precise inclusion or diagnostic criteria, and comorbidity between primary headaches and nasal diseases such as allergic rhinitis and CRS. Radiographic studies similarly have been less than reliable for inclusion or exclusion of rhinogenic headache. All of these factors make a review of this topic worthy of inclusion in this issue. Please note that neoplastic causes of nasal pain (eg, sinonasal carcinoma) are excluded in this discussion.

Relevant nasal anatomy

The maxillary (V-2) and ophthalmic (V-1) divisions of the trigeminal nerve provide sensation to the nose and paranasal sinuses. These afferents project via the trigeminal ganglion to the trigeminal brainstem sensory nuclear complex (VBSNC). Autonomic innervation of the nose is provided by sympathetic nerve fibers (originating at the superior cervical ganglion, to the deep petrosal nerve, to the vidian nerve, then through the sphenopalatine ganglion) and parasympathetic fibers (from the superior salivatory nucleus of VII, then to the greater superficial petrosal nerve, vidian nerve, and synapsing then in the sphenopalatine ganglion). The trigeminal fibers in the nose terminate as bare nerve terminal endings, along with the parasympathetic nerves near the basal cells of the nasal epithelium. Unlike the skin or tendons, no specialized sensory organs are present.

Relevant nasal anatomy

The maxillary (V-2) and ophthalmic (V-1) divisions of the trigeminal nerve provide sensation to the nose and paranasal sinuses. These afferents project via the trigeminal ganglion to the trigeminal brainstem sensory nuclear complex (VBSNC). Autonomic innervation of the nose is provided by sympathetic nerve fibers (originating at the superior cervical ganglion, to the deep petrosal nerve, to the vidian nerve, then through the sphenopalatine ganglion) and parasympathetic fibers (from the superior salivatory nucleus of VII, then to the greater superficial petrosal nerve, vidian nerve, and synapsing then in the sphenopalatine ganglion). The trigeminal fibers in the nose terminate as bare nerve terminal endings, along with the parasympathetic nerves near the basal cells of the nasal epithelium. Unlike the skin or tendons, no specialized sensory organs are present.

Relevant neurophysiology

Nasal pain is mediated by Aδ fibers (fast responding, primarily mechanoreceptive pain fibers) and C fibers (slower, unmyelinated fibers associated with a more dull pain from mechanothermal and chemosensory stimulation). Activation of the pain fibers is typified by the release of tachykinins (substance P, neurokinin A, neuropeptide K) and neuropeptides like calcitonin gene-related peptide. Sympathetic neurons are associated with neuropeptide Y, in addition to norepinephrine, and the parasympathetic fibers release acetylcholine and vasoactive intestinal peptide. These neurotransmitters and neurochemicals are nonspecific markers of nerve activation and are associated with primary headache phenomena like migraine and seemingly unrelated disease such as allergic rhinitis, as well as rhinogenic pain. Thus, earlier reports citing the presence of these chemicals (eg, substance P) as evidence for contact point headache validity were poorly founded.

Neuroplasticity is also a phenomenon of unclear cause, in which acute pain may become chronic or more easily triggered (hyperalgesia) or is temporarily reduced, with a temporary reduction of headache pain mediated by the VBSNC after induction of surgical pain in the same distribution. This area of the brainstem (including the trigeminal nucleus caudalis) is critically important in the pathophysiology of migraine, as is covered elsewhere in this issue.

Relevant psychobiology

Researchers have documented the importance of cognitive dissonance as a factor in a possible placebo effect in surgical studies for headache. This effect stems from the fact that a patient reports a psychological benefit from a surgical procedure (which required pain or expense, initiated by the patients’ willingness to participate) regardless if the surgery had no benefit (hence the dissonance between reality and psychological benefit). This finding may thus confound studies evaluating surgical interventions for mucosal contact point or migraine surgeries.

Primary headaches and rhinogenic headache

Most patients complaining of “sinus headache” have migraine as an underlying cause. The pathophysiology of migraine has relevance to the topic of rhinogenic headache. Although the central nervous system is likely the initiator of the migraine process, this is followed by sensitization of the peripheral neurons of the trigeminal nerve. This situation can then lead to central sensitization at the level of the trigeminal nucleus caudalis in the brainstem, and pain in the distribution of the first (ophthalmic, V-1) or second (maxillary, V-2) divisions of the trigeminal nerve. This early sensitization phase is commonly accompanied by cutaneous allodynia (pain associated with ordinarily minor stimuli) in most patients (80%). The causation of pain by stimulation that is normally nonpainful often occurs in the distribution of V-1 and V-2. This situation may include stimuli to the nose, such as breathing cold air. To make matters more complex, the migraine attack itself may include secondary nasal symptoms (possibly mediated from stimulation of the parasympathetic nervous system, via the superior salivatory nucleus of the seventh cranial nerve [VII]). Nasal engorgement could then lead to mucosal contact in areas of nasal narrowing with or without allodynia-related pain. This factor has been suggested as supporting a potentially beneficial role for contact point surgery, even in patients with underlying migraine. Conversely, this situation may theoretically create a false-positive contact point test, in which application of an anesthetic or induction of pain (injection) in the nose may downregulate a migraine headache by interrupting a source of allodynia.

The problem of comorbidity

Migraine is a common phenomenon, and does not exist in a vacuum. Jackson and Dial reported that 49 of 100 patients referred to an ear, nose, and throat (ENT) office for sinus headache had migraine, but only 13% had migraine alone; 19 (of the migraineurs) had allergic rhinitis as well, 11 had sinusitis, and 6 had both allergic rhinitis and sinusitis. A second study found extensive radiographic abnormalities on sinus computed tomography (CT) studies in patients with sinus headache with migraine. The mean CT scan Lund-Mackay (L-M) score in this study did not differ significantly between the migraine (2.1) and nonmigraine cohort (2.7). Five of the migraine group had substantial sinus disease radiographically (with L-M scores ≥5), as did 2 of the nonmigraineurs. A more recent study found a history of headache in general to be more common in patients with CRS than in non-CRS controls, although a second series found that facial pain (not facial pressure), headache, and photophobia were negatively predictive of the presence of radiographic evidence of CRS. CRS has been reported to be a factor in the worsening of the course of migraine, potentially making it more refractory or chronic. Thus, the association of CRS and migraine remains unclear.

Allergic rhinitis and migraine have been found to be comorbid as well, with some evidence suggesting that allergy management may have some headache benefits in patients with both disorders. Whether this situation stems from shared pathophysiology, reduction of mucosal contact, or perhaps from secondary benefits such as stress reduction in the migraineur remains to be seen.