J Pain (2003) 4:125–131 DOI 10.1007/s10194-003-0046-5 REVIEW

Juan A. Pareja Nummular headache, trochleitis, supraorbital Julia Pareja Julio Yangüela neuralgia, and other epicranial and neuralgias: the epicranias

Received: 7 April 2003 Abstract Nummular headache is char- accompaniments, tenderness on the Accepted in revised form: 28 August 2003 acterized by mild to moderate, pres- emergence or course of a pericranial sure-like head pain exclusively in a nerve or on the tissues where pain orig- small, rounded or oval area without inates, and possible presence of symp- underlying structural lesions. Either toms and signs (including effective during symptomatic periods or interic- treatment with locally injected anes- tally, the affected area shows a variable thetics or ) of nerve dys- combination of hypoesthesia, dysesthe- function. These observations led to the sia, paresthesia, tenderness or discom- emergence of a conceptual model of fort. The particular topography and head pain with an epicranial origin that signs of sensory dysfunction suggest we propose to group under the appella- that nummular headache is an extracra- tion of epicranias (headaches and peri- nial headache probably stemming from cranial neuralgias stemming from epi- J.A. Pareja () epicranial tissues such as the terminal cranial tissues). Nummular headache is Department of Neurology, branches of sensory nerves. Apart from the paradigm of epicranias. Epicranias Alcorcón Hospital Foundation, nummular headache, other headaches essentially differ from other primary Budapest 1, 28922 Alcorcón, Madrid, Spain and neuralgias such as idiopathic stab- headaches with an intracranial origin e-mail: [email protected] bing headache, trochleitis, supraorbital and features of visceral pain, i.e. Tel.: +34-91-6219513 neuralgia, external compression splanchnocranias that are characterized Fax: +34-91-6219975 headache, nasociliary neuralgia, occipi- by a painful area wider than that of J. Pareja tal neuralgias, and auriculotemporal epicranias, no clear borders, presence Department of Pediatrics, neuralgia have temporal or spatial fea- of autonomic features, regional muscle Santa Bárbara Hospital, tures that suggest a peripheral tension, and driving of the process Puertollano, Ciudad Real, Spain (extracranial) origin, i.e. stemming from the brain and brainstem. J. Yangüela from the bone, , or pericranial Department of Ophthalmology, nerves. Common to these disorders is a Key words Nummular headache • Alcorcón Hospital Foundation, focal localization or a multidirectional Trochleitis • Supraorbital neuralgia • Alcorcón, Madrid, Spain sequence of paroxysms, paucity of Epicranias • Splanchnocranias

Introduction there are a few phenotypes a headache can express [1]. These are , tension-type headache, cluster headache, increased and decreased intracranial pressure, local lesion type, In the secondary headaches section of the 1988 classification vasodilator type and stabbing type. Theoretically, all such types of the International Headache Society (IHS), it was stated that of headache may have a primary and a symptomatic form. 126

Local lesion-type headache was described as continu- painful area does not seem to change in either shape or ous pain having a distinct maximum in a circumscribed size with time. area of 5 cm or less, but eventually spreading to the sur- Either during symptomatic periods or interictally, the roundings or referring to more distant areas. Pain from affected area may show a variable combination of hypoes- cranial bone metastasis was noted as the prototype of this thesia, dysesthesia, paresthesia, tenderness or discomfort. symptomatic focal headache. A primary circumscribed The pain is usually continuous with a chronic or remitting headache has recently been described as nummular temporal pattern. Pseudoremissions may be observed when headache (NH) [2]. It is characterized by mild to moder- the pain reaches a very low grade or when only discomfort ate, pressure-like, rather continuous pain, exclusively felt (not pain) in the affected area is reported. At times discom- in a rounded or elliptical area typically 2–6 cm in diame- fort may prevail. Lancinating exacerbations lasting for sev- ter, and neither attributed to local lesion nor systemic dis- eral seconds or gradually increasing from 10 minutes to 2 order [2]. hours may superimpose the baseline pain. Autonomic symp- Head pain is mostly conveyed by the , toms are typically absent. but the clinical manifestations may essentially differ Most patients worried that a serious underlying disease depending on the level of trigeminal lesion or dysfunction. could be the cause of their focal cranial pain. Since the pain Intracranial activation of the trigeminovascular system is a itself is, in most cases, not annoying, only reassurrance is final common pathway for many primary hedaches [3]. generally necessary. However, the extracranial, sensitive branches of the trigeminal nerve could be at either the origin of the pain or the conveyance of local (extracranial) nociceptive head pain. In such cases, the painful area would be restricted to Idiopathic stabbing headache either the cutaneous territory of a dysfunctioning pericra- nial nerve or the involved tissues within a focal area. In Idiopathic stabbing headache (ISH) is characterized by the addition, signs and symptoms of neuropathic pain, such as extreme brevity of the paroxysms, generally lasting 1–2 tenderness along the course of the nerve, hypoesthesia or seconds and rarely up to 10 seconds. The stabs can affect dysesthesia should be found, indicating nerve dysfunction. any area of the head, with erratic changes in the location of Otherwise, there may also be focal discomfort or tender- the pain between one paroxysm and the next, either in the ness on the tissues of the affected area. same or the opposite hemicranium. Stabs may even syn- Herein, we review a number of headaches and neuralgias chronously occur on either side of the hemicranium. The that we postulate share the common characteristics of being paroxysms may appear always in the same region, usually highly localized and supposedly stemming from extracranial the [4–9]. structures. For the head pain with a presumed peripheral ori- The lack of topographic organization of ISH parox- gin, we propose the general term epicranias which includes ysms makes their occurrence unpredictable both tempo- epicranial headaches and epicranial neuralgias. rally and spatially. Such chaotic localization could be the expression of multiple presumed origins, most probably in the terminal sensory fibers of the pericranial nerves [9]. This is why we postulate that ISH may have a “peripher- Epicranial headaches al” origin. ISH is a benign entity, it does not associate with any Nummular headache structural lesion and it often coexists with other primary headaches, usually migraine, tension-type headache, and This recently described headache [2] has an unusual, dis- hemicrania continua. ISH either appears synchronously with tinct feature: it is characterized by mild to moderate, pres- the concurrent headache, or both headaches follow an inde- sure-like pain exclusively felt in a rounded or oval area pendent course. Only in those cases in which the stabs are typically 2–6 cm in diameter, without underlying structur- confined to the same area, it is highly recommended to al lesions. The disorder tends to start from the forth decade exclude an underlying structural process. of life, and it prevails in women. The frequency is highly variable, going from one to sev- Although any region of the head may be affected, the eral paroxysms a day. Rarely, it has been described a “stab- parietal area, particularly its most convex part (tuber pari- bing headache status”. Usually the clinical course is either etale) is the common localization of this circumscribed sporadic or recurrent, and only exceptionally can a chronic headache. The pain remains confined to the same sympto- temporal pattern be recognized. matic area without duplication or multiplication of the The paroxysms are of moderate intensity, but at the symptoms in other parts of the head. Moreover, the same time surprising and alarming to the patients, who 127 ask for a reasonable explanation. Therefore, the patients congenital restrictive ophthalmopathy with shortening must be reassurred and clearly informed of the benignity and fibrosis of the tendon. It of the process. Only on rare occasions, when the parox- causes but no pain. Acquired Brown’s syn- ysms become extremely frequent, treatment with drome (symptomatic trochleitis) [13–17] is produced by indomethacin is recommended. A dose of 75 mg/day has local inflammatory processes, such as rheumatoid arthri- proved to be partially or totally effective in two-thirds of tis, hyperthyroidism, , or enteropathic patients. arthropathy (inflammatory bowel disease: ulcerative coli- tis and Crohn’s disease). Exceptionally, it can be caused by sinusitis, trauma or metastasis. In symptomatic trochleitis there is a severe restriction of vertical eye External compression headache movements with . Blood tests (routine blood work, erythrocyte sedimentation rate, standard biochemi- External compression headache results from continued cal determinations, thyroid function, antinuclear antibod- stimulation of cutaneous nerves of the head by the appli- ies, rheumatoid factor) and urine analysis are essential to cation of pressure, for example by a band around the head, exclude symptomatic trochleitis. Only exceptionally it is a tight hat, oxygen or anesthetic masks, or swimming gog- necessary to perform a biopsy. It is important to remark gles [1, 10]. It is an in crescendo, non-pulsating headache that when biopsies of cases of idiopathic trochleitis have without accompaniments, with maximum pain in the been performed, the only findings were non-specific points of more external compression. Involved nerves in inflammation. such a type of hedache seem to be mostly the supraorbital The efficient treatment of trochleitis consists of corti- and the supratrochlear. coid infiltration in the trochlear region. This procedure The headache is clearly dependent on the local compres- provides a rapid (24–48 hours) and substantial or absolute sion and resolves once the external pressure has been benefit. Only on rare occasions, reappearance of pain removed. Interestingly, external compression may lead to a makes it necessary to repeat corticoid infiltration. The pro- more severe migrainous headache if the stimulus is pro- cedure is simple and safe. Exceptionally, traumatic hemor- longed enough. rhage may be a complication, but it generally disappears spontaneously. Trochleitis may occur with migraine [12]. The striking association of migraine and trochlear pain seems to Trochleitis exceed any expected coexistence just by chance, bringing to mind the concept of a possible comorbidity. Interestin- Trochleitis is a local inflammatory process of the gly, patients with concurrent migraine ipsilateral to the trochlea-oblique muscle complex [11, 12] with pain felt trochlear pain were substantially alleviated upon local in the inner angle of the orbit, frequently extended to the trochlear treatment [12], suggesting that the trochlear ipsilateral forehead. In trochleitis, the pain is of moder- painful process could have contributed to the worsening ate intensity, typically exacerbated upon situations that of the migrainous pain. Seemingly succesful treatment of require vertical eye movements: reading, knitting, com- the trochlear pain may considerably decrease the nocicep- puter work, watching TV, etc. There are no oculofacial tive contingent to the caudalis trigeminal nuclei, thus autonomic accompaniments. Pain in the trochlear region, relieving such neurons from the excessive input and exacerbation in supraduction, and hypersensitivity upon decreasing their firing. palpation of the trochlea strongly suggest the syndrome. Conversely, pain is relieved by injecting lidocaine or cor- ticosteroids on the sore trochlea, but not by placebo injection. Epicranial neuralgias In trochleitis, the typical induration and swelling of the inflammed trochlea is easily assessed by palpation. The term “neuralgia” means pain in the territory supplied by Eye movement restriction is an extremely rare feature of a nerve or a nerve root [18]. The temporal pattern of a neu- idiopathic trochleitis. In the eventual rare case of diplop- ralgia does not have to be necessary abrupt, lancinating, and ia appearing, it will be of minimum intensity and inter- short-lived. In fact, central neuropathic pain may be brief mittently appearing. This remark is important to distin- and abrupt whereas peripheral neuropathic pain may show a guish idiopathic trochleitis from other trochlear syn- continuous pattern. Precisely, pain arising from lesions or dromes that typically present with restriction and diplop- dysfunctions of pericranial nerves (Fig. 1) mostly attains a ia: Brown’s syndrome (oblique superior syndrome) is a chronic-continuous pattern. 128

Fig. 1a,b Cranial and facial sensory a b nerves. a Emergence and course. b Territory. Ophthalmic division of the trigeminal nerve (V-I): 1, ; 2, supratrochlear nerve; 3, ; 4, (external nasal branch); 5, . Maxillary division of the trigemi- nal nerve (V-II): 6, ; 7, zygomaticofacialis nerve; 8, zygomati- cotemporalis nerve. Mandibular division of the trigeminal nerve (V-III): 9, men- tonian nerve; 10, buccalis nerve; 11, auricu- lotemporal nerve. Second cervical root (C2): 12, greater occipital nerve. Second and third cervical roots (C2,C3): 13, less- er occipital nerve; 14, greater auricular nerve; 15, third occipital nerve

Supraorbital neuralgia bands or bone excrecences. This procedure has been remarkably successful in the group of patients reported by Supraorbital neuralgia is well defined by the triad: pain in Sjaastad et al. [19]. Identification of the causes of chronic the territory (forehead) innervated by the supraorbital nerve compression inside the orbit is more complicated, although (SON), tenderness on the emergence (supraorbital notch) or it should be looked for carefully, in order to clarify the on the course of the nerve, and absolute relief upon anes- mechanisms of such painful syndrome. This is part of an thetic blockade of the nerve [19, 20]. ongoing research effort in our institute. The pain is usually chronic, continous and, less fre- Gabapentin proved to be of avail in some patients [20]. quently, remitting. Primary supraorbital neuralgia rarely Capsaicin topically applied on the symptomatic forehead associates typical features of neuropathic pain, such as has also rendered substantial benefits (JA Pareja, unpub- hypoesthesia, paresthesia, allodynia or lightning exacerba- lished observations). tions [20]. However, we have observed such signs in all patients suffering from post-traumatic supraorbital neural- gia. We postulate that traumatic supraorbital neuralgia pro- duced by strong external forces (delivered suddenly once Supratrochlear neuralgia and for all) is clinically different from primary supraorbital neuralgia (probably caused by subtle chronic trauma to the The term supraorbital neuralgia is preferable to neuralgia of orbit or supraorbital notch). In the orbit, the SON may run the SON in view of the possible anatomic variations that close to both the orbit wall and nearby arteries. This partic- make difficult determining the origin of the pain, in one ular anatomic trajectory would permit a subtle intermittent (SON) or the other (supratrochlear nerve) nerves supplying nerve trauma during ocular movements, which would pro- the forehead [21]. Nevertheless, we have observed several duce stretching, angulation, traction or friction of the SON. patients with pain confined to the medial part of the fore- The nerve and a small artery can be close, and even share the head innerved by the supratrochlear nerve (STN). According adventitia [21]. Therefore, an adjacent artery might produce to these observations, we believe that, at least in some a microvascular compression of the nerve. Since the supra- patients, it may be possible to distinguish between SON and orbital artery accompanies the SON passing through the STN neuralgias. The possibility of trauma, or any other eti- supraorbital notch, an impingement of the nerve by vascular ologic agent, affecting both nerves, has to be considered, engorgement should also be taken into account; this may since anatomic variations make both nerves equally suscep- explain the unexpected effect of triptans in relieving some tible to trauma. cases of supraorbital neuralgia [19, 20]. Otherwise, SON Our experience is solely based on two patients - so with may be subject to compression in the supraorbital notch by due reservations - we postulate that STN neuralgia is bony excrecences or tissue bands [19]. defined as the presence of pain in the medial region of the Treatment includes surgical exploration of the supraor- forehead, with absolute response to anesthetic blockade of bital notch and eventual liberation of the nerve from tissue the STN. 129

Nasal nerve neuralgia (Charlin’s nasociliary neuralgia) It is important to remark that Charlin considered several ophthalmologic lesions of great importance in this syn- When Charlin described nasociliary neuralgia in 1931 [22], he drome (minor cheratitis, small corneal ulcers, , did not know of cluster headache (described in 1939), chron- iritis, cyclitis, hypopyon). As he was an ophthalmologist, it ic paroxysmal hemicrania (1974) or SUNCT (1989). is understandable that he was impressed by such ocular Therefore, these circumstances were perfect to mix features of lesions. In any case, this syndrome was forgotten shortly different primary orbital syndromes in his observations. This after it was described, although we believe now it is the time is probably the reason why the reported features of nasociliary for nasal nerve neuralgia to be revisited. Hopefully, a thor- neuralgia are so varied. The possible impurity of the original ough study of these patients, excluding those with SUNCT, description could have made it easily forgettable, and in fact cluster headache, CPH, etc., will finally rehabilitate this there have been few reports of nasociliary neuralgia after the interesting syndrome. impetuous emergence of cluster headache in 1939. The nasal (or nasociliary) nerve is a terminal branch of the first division of the trigeminal nerve (V-1); it gives ciliar branches, and divides into infratrochlear nerve and eth- Occipital neuralgias moidal (posterior and anterior) nerves. The infratrochlear nerve supplies the inner part of the , lacrimal ducts Occipital neuralgias should be located in the distribution of the and surrounding skin, including the upper part of the nose. greater and lesser occipital nerves, and third occipital nerve [25, The posterior ethmoidal nerve supplies the sphenoidal and 26]. Some features of occipital neuralgia may be of diagnostic ethmoidal sinuses. The anterior ethmoidal nerve gives four help: hypoesthesia or dysesthesia in the affected area, and nasal branches that supply the internal and external (inferi- superimposed very short-lasting, severe paroxysms, although or) parts of the nose. continuous pain may remain in between. The affected nerve According to Charlin [22, 23], nasociliary neuralgia is may be tender to palpation. Anesthetic block of the nerves usu- characterized by paroxysms of periocular pain with maxi- ally provides transient or relatively long-lasting relief. mum intensity in the region between the inner angle of the orbit and the base of the nose, as well as in the nasal fossae. The pain may last from several minutes to hours. Charlin even admitted the existence of some moderate interictal Auriculotemporal neuralgia pain. The attacks were accompanied by ipsilateral rhinor- rhea or nasal congestion that Charlin believed were due to This rare neuralgia seems to be more prevalent in middle-aged hyperemia and edema of the nasal mucosa. The paroxysms female patients. The symptoms consist in strictly unilateral could also be accompanied by conjunctival injection, attacks of lancinating pain mostly in the temple. The pain may lacrimation, conjunctival hemorrhage, palpebral edema, and also be felt in the mandibular joint, parotid region, and auricle blepharospasm. Apparently, the symptoms appeared in the but spreads upwards into the temple. The symptoms may be form of attacks during symptomatic periods, that lasted from relieved by anesthetic block of the [27]. 3 to 12 weeks [23, 24]. Charlin pointed out the presence of hypersensitivity in the emergence of the infratrochlear nerve and external nasal branch of the anterior ethmoidal nerve, as well as the char- Conclusions acteristic quick alleviation of the pain (considered to be pathognomonic by Charlin) after intranasal instillation of a We propose the term “epicrania” to group all head pain syn- 5% cocaine and adrenaline solution. dromes apparently stemming from the epicranial tissues Charlin attributed the symptoms to nasal nerve neuritis. (Table 1). The objective considering epicranias is to height- He admitted the existence of variants or frustes forms [23], en awareness on the role of the cranium and epicranium in with lack of either the ocular components (ocular pain, con- generating headaches and neuralgias. As in any head pain, junctival injection, lacrimation) or the nasal component (rhi- distinction between primary and symptomatic epicranias is norrhea). Although questioning some signs and symptoms, mandatory, so local structural lesions involving any layer of he postulated the invariable characteristics of nasal nerve the epicranium should be ruled out. neuralgia: hypersensitivity in the area of emergence of the Generally speaking, superficial pain tends to be ultrashort, nasal nerve, triggering of lancinating pain in the medial i.e. jabbing, or localized in a small area, whereas deeper pain frontal region upon touching the lateral aspect of the symp- is less likely localized and may be accompanied by autonom- tomatic nostril, and the prodigious relief after endonasal ic features. Topographically, epicranias are characterized by instillation of a cocaine-adrenaline solution. either a small symptomatic area, even with sharp borders 130

Table 1 Epicranias Table 2 Major categories of splanchnocranias

Epicranial headaches Splanchnocranial headaches Nummular headache Migraine Idiopathic stabbing headache Tension-type headache External compression headache Hemicrania continua Trochleitis Cluster headache Chronic paroxysmal hemicrania Epicranial neuralgias SUNCT Supraorbital neuralgia Supratrochlear neuralgia Splanchnocranial neuralgias Nasal nerve neuralgia (Charlin’s nasociliary neuralgia) Trigeminal neuralgia Greater occipital nerve neuralgia Glosopharyngeal neuralgia Lesser occipital nerve neuralgia Intermediate nerve neuralgia (Hunt’s neuralgia) Auriculotemporal neuralgia area wider than that of epicranias, with no clear borders. The (nummular headache) or according to a pericranial sensory pain is frequently accompanied by a variable combination of nerve territory (epicranial neuralgias). A rather chaotic local- oculofacial or general autonomic symptoms and signs, or ization indicating a multifocal origin of the pain (ISH) also regional (pericranial and cervical) muscle tenderness. Apart fits with the concept, as such a lack of topographic organiza- from migraine, we may also consider tension-type tion may also suggest a “peripheral” origin of the paroxysms, headache, cluster headache, CPH, SUNCT, and hemicrania most likely in the cutaneous nerves of the scalp (Table 1). continua to be splanchnocranias (Table 2). Neuralgias with Epicranial pain is usually chronic but fluctuating. an intracranial origin, i.e. generated in the root or sensory Autonomic accompaniments such as nausea, vomiting, pho- ganglion of a cranial nerve, can also be considered to be tophobia, audiophobia, lacrimation, conjunctival injection, splanchnocranial neuralgias and clinically can be differenti- rhinorrhea or nasal stuffiness are not typical of the epicra- ated from the extracranial (epicranial) neuralgias. For nias. Conversely, there may be local symptoms and signs of unknown reasons, “upstream” and “downstream” trigeminal sensory dysfunction in the symptomatic area. Many times it system pain is clinically different. For instance, first division is possible to find tenderness on the symptomatic area or trigeminal neuralgia behaves clinically different from termi- over the emergence or course of a sensory nerve. This sign nal branch supraorbital nerve neuralgia. is constant in the case of epicranial neuralgias. Interventions A good example of the usefulness of topographic differ- on the apparent origin of the pain by anesthetic blockades or entiation of epicranias and splanchnocranias is the innerva- injection usually provide complete relief, tion of the nuchal area. For anatomical reasons nuchal pain either transitory or relatively long-lasting. with intracranial origin (e.g. migraine) is conveyed by branches of the (V-1) whereas extracra- nially originated nuchal pain is conveyed by occipital nerves stemming from C2 roots. Epicranias vs. splanchnocranias Grouping primary headaches under epicranias (and splanchnocranias) is not intended to be an alternative classi- It is widely acknowledged that primary headaches such as fication but a proposal to take into account the possible migraine are visceral (i.g. splanchnic). Splanchnocranias anatomic source of the pain. This may provide us with inter- originate intracranially and are characterized by a painful esting clues for research purposes.

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