ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Cluster headache: Epidemiology, clinical features, and diagnosis

Cluster headache: Epidemiology, clinical features, and diagnosis
Literature review current through: Jan 2024.
This topic last updated: Jun 06, 2023.

INTRODUCTION — Cluster headache belongs to the trigeminal autonomic cephalalgias (TACs), a group of idiopathic headache disorders characterized by unilateral headache accompanied by ipsilateral cranial autonomic symptoms.

The TACs include cluster headache, paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks, and hemicrania continua. Cluster headache is the most common form.

The epidemiology, clinical features, and diagnosis of cluster headache are discussed here. The treatment and prognosis of cluster headache are discussed separately. (See "Cluster headache: Treatment and prognosis".)

Other TACs are discussed elsewhere.

(See "Paroxysmal hemicrania: Clinical features and diagnosis" and "Paroxysmal hemicrania: Treatment and prognosis".)

(See "Short-lasting unilateral neuralgiform headache attacks: Clinical features and diagnosis" and "Short-lasting unilateral neuralgiform headache attacks: Treatment and prognosis".)

(See "Hemicrania continua".)

PATHOPHYSIOLOGY — The pathogenesis of cluster headache is complex and remains incompletely understood. The most widely accepted theory is that primary cluster headache is characterized by hypothalamic activation with secondary activation of the trigeminal-autonomic reflex, probably via a trigeminal-hypothalamic pathway (figure 1) [1]. The vascular theory is an alternate construct described by neurogenic inflammation within the walls of the cavernous sinus due to obliteration of venous outflow that injures the traversing trigeminal c-fibers and sympathetic fibers along the intracranial internal carotid artery [2].

The pathophysiology of trigeminal autonomic cephalalgias is presented in greater detail separately. (See "Pathophysiology of the trigeminal autonomic cephalalgias".)

EPIDEMIOLOGY AND RISK FACTORS — The prevalence of cluster headache is <1 percent and mostly affects males [3-6]. The typical onset of cluster headache is between 20 and 40 years of age but has also been reported in school-aged children and adults over age 80 years [7-9].

In a meta-analysis of 16 population-based epidemiologic studies, the lifetime prevalence of cluster headache for adults of all ages was 124 per 100,000 (95% CI 101-154), or approximately 0.1 percent [6]. The overall male-to-female ratio was 4.3:1 [3-6].

The male preponderance in cluster headache may be decreasing with increased awareness of the diagnosis [10-13]. In a review of 482 patients with cluster headache from Italy, the male-to-female ratio dropped from more than 6:1 for patients diagnosed in the 1960s to nearly 2:1 for those diagnosed in the 1990s. The probable explanation is improved understanding of the pathophysiology of this syndrome leading to more frequent diagnosis. Changes over time in the male preponderance of risk factors such as tobacco use may also contribute to this observation [11]. However, a decreasing male preponderance has not been confirmed in other studies [4,6].

Case reports and epidemiologic studies have identified factors associated with an elevated risk of cluster headache compared with the general population.

Family history – Cluster headache appears to have a genetic component, at least in some families [3,14,15]. Epidemiologic studies have reported a family history of cluster headache in 5 to 20 percent of patients with cluster headache [4,14,16-18]. Compared with the general population, the risk of cluster headache for first-degree relatives was increased by 14- to 39-fold and for second-degree relatives by 2- to 8-fold [16-18]. Genome-wide association studies have identified multiple loci associated with cluster headache [19,20].

Tobacco use – In observational reports and surveys of patients with cluster headache, up to 88 percent are also chronic cigarette smokers [21,22]. In addition, secondary exposure to tobacco smoke may be a risk factor for the development of cluster headache, possibly on the basis of a genetic predisposition [22,23]. A study of clinically detected cluster headache showed a marked decline in the incidence of the diagnosis between 1979 to 1981 and 1990 to 1991 in Olmsted County, Minnesota, when the incidence of smoking also declined in the population [24].

Head trauma – Some reports have noted an apparently high incidence of head trauma in patients with cluster headache [25]. As an example, one study of 374 patients found a history of head injury prior to cluster headache onset in 15 percent [21]. However, such an association does not establish a causal relationship and may reflect other shared features. As an example, in one retrospective study of 200 patients with cluster headache, patients with a history of head trauma were more likely to be heavy tobacco users than those without head trauma [26]. In addition, the long interval between head injury and onset of cluster headache (average of 10 years) casts doubt on a causative role of head injury.

Some patients with headaches that follow head trauma may instead be classified as having post-traumatic headache [27]. (See "Post-traumatic headache".)

CLINICAL FEATURES — Cluster headache is a condition characterized by attacks of severe unilateral pain, accompanied by ipsilateral cranial autonomic symptoms and/or restlessness or agitation [28].

Headache — Cluster headaches are severe and sharp or stabbing in quality. Patients are typically restless and often prefer to pace about or sit and rock back and forth during a cluster headache attack. Some patients may report cutaneous allodynia [29]. Symptoms most commonly occur in periorbital or temporal regions. Cluster headache attacks are strictly unilateral, and the symptoms almost always remain on the same side of the head during a single attack. However, the symptoms can switch to the other side during a different cluster attack (so-called side shift) in approximately 15 percent of cases [30].

A typical attack persists for 15 minutes up to three hours in duration and may strike from once every other day to up to eight times a day. These frequently recurring attacks occur in a cluster or bout and are separated by periods of remission, often for months, when patients are asymptomatic. (See 'Patterns of symptom recurrence' below.)

Cluster headache can be debilitating and associated with psychiatric comorbidity [31,32]. The lifetime risk of depression is common in cluster headache, reported in up to 44 percent of patients [33]. In one case series of 175 patients with cluster headache, suicidal ideation was reported by 64 percent [34].

Autonomic symptoms — The autonomic symptoms associated with cluster headache typically occur only during the acute attack. They are ipsilateral to the headache and may include ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and/or nasal congestion. Sweating and increased cutaneous blood flow may also occur during the attack, particularly in areas of sympathetic deficit [35,36].

Some patients with cluster have chronic signs of sympathetic paralysis such as miosis and ptosis that transiently intensify during acute attacks [37]. In rare cases, sympathetic disturbances persist on the previously affected side of the face in patients whose cluster headache has switched sides [38].

Autonomic symptoms are absent in approximately 3 percent of patients with cluster headache [39].

Patterns of symptom recurrence — A core clinical feature of the cluster headache syndrome is the rhythmicity of the relatively short-lived (15 to 180 minutes) painful attacks. In the episodic form of cluster headache, recurring daily attacks persist for several weeks in a single bout and are followed by a period of remission. Typically, a cluster bout lasts 6 to 12 weeks, while remissions can last up to 12 months or longer. In the chronic form, attacks occur without significant periods of remission.

The frequency of daily attacks during active bouts varies in individual patients, but a mean of two attacks per day was reported in one study, and variability appeared to decrease with increasing attack frequency [40]. Some studies have reported a circadian and seasonal variability with higher frequency of attacks at nighttime and during both spring and autumn [40-42].

Episodic cluster bouts – The episodic form affects 80 to 90 percent of patients with cluster headache. It is characterized by alternating periods of attacks and remission. Bouts may last from 7 days to 12 months if untreated [31]. Periods of remission last at least three months, during which time patients are usually asymptomatic.

Chronic cluster bouts – Patients with the chronic form of cluster headache report either continual attacks (persisting bout) or report brief remissions of less than three months. Chronic cluster headache may arise de novo or evolve both from and to the episodic type. Cluster headache is considered chronic once a bout persists for a year without remission [28].

DIAGNOSIS AND EVALUATION — Cluster headache should be considered in patients with unilateral headaches and ipsilateral cranial autonomic symptoms. Cluster headache, in its typical form, is unmistakable. The clinical diagnosis is made in patients with a compatible history and based on diagnostic criteria (table 1) [28].

We suggest neuroimaging with magnetic resonance imaging (MRI) of the brain with gadolinium contrast to exclude an underlying cause for all patients with suspected cluster headache. A clinical evaluation with history and physical examination is insufficient to differentiate accurately among primary and secondary cluster headache syndromes [43-45]. Symptoms compatible with the clinical diagnosis of cluster headache may be due to an underlying cause. (See 'Secondary headache syndromes' below.)

Diagnostic criteria — Diagnostic criteria for cluster headache, according to the International Classification of Headache Disorders, 3rd edition (ICHD-3), require all of the following [28]:

At least five attacks

Attacks characterized by severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting 15 to 180 minutes when untreated; during part (but less than half) of the time-course of cluster headache, attacks may be less severe and/or of shorter or longer duration

Either or both of the following:

At least one of the following symptoms or signs ipsilateral to the headache:

-Conjunctival injection and/or lacrimation

-Nasal congestion and/or rhinorrhea

-Eyelid edema

-Forehead and facial sweating

-Miosis and/or ptosis

A sense of restlessness or agitation

Attacks have a frequency between one every other day and eight per day; during part (but less than half) of the active time-course of cluster headache, attacks may be less frequent

Not better accounted for by another ICHD-3 diagnosis

Diagnostic criteria for episodic cluster headache require the following [28]:

Attacks fulfilling criteria for cluster headache and occurring in bouts (cluster periods)

At least two cluster periods lasting from seven days to one year (when untreated) and separated by pain-free remission periods of three months or more

Diagnostic criteria for chronic cluster headache require the following [28]:

Attacks fulfilling criteria for cluster headache

Attacks occurring without a remission period, or with remissions lasting less than three months, for at least one year

Patients whose symptoms meet all but one of these diagnostic criteria (eg, <5 attacks, >8 attacks per day) may be considered to have probable cluster headache once secondary causes are excluded. (See 'Differential diagnosis' below.)

Neuroimaging — We suggest MRI of the brain with gadolinium contrast for the initial evaluation of all patients with suspected cluster headache, including those with typical features and a normal neurologic examination. Some patients with typical clinical features of cluster headache and a normal neurologic examination may be found to have a potential secondary cause for headache, such as a structural brain lesion [44]. In addition, neuroimaging is essential for all patients with an abnormal neurologic examination and those with a clinical suspicion for a pituitary abnormality. (See 'Secondary headache syndromes' below.)

We obtain MRI of the brain, if possible, and use computed tomography (CT) of the head with contrast as an alternative. Additional imaging of the face, sinuses, or vascular structures is usually reserved for patients with atypical symptoms to identify other entities. (See 'Secondary headache syndromes' below.)

Other diagnostic testing — Routine laboratory testing, electrophysiologic tests (eg, evoked potential, electroencephalography), and lumbar puncture for cerebrospinal fluid analysis are typically not helpful in the routine evaluation of patients with cluster headache. Additional diagnostic tests are reserved for patients with atypical symptoms to evaluate for secondary causes. (See 'Secondary headache syndromes' below.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of cluster headache includes syndromes that present with recurrent, brief attacks of unilateral headaches. Such conditions include both primary headaches, including other trigeminal autonomic cephalalgias (TACs), as well as secondary headache syndromes due to an underlying cause.

Multiple types of headache may coexist in an individual. Patients with cluster headache may also have symptoms from other primary or secondary headache syndromes [46-48]. Headache types are distinguished by distinctions in clinical features, diagnostic criteria, or responsiveness to treatments.

Primary headache syndromes

Other trigeminal autonomic cephalalgias — The headache syndromes that comprise the TACs are characterized by unilateral headache accompanied by ipsilateral cranial autonomic symptoms [28]. The TACs include paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks, and hemicrania continua, in addition to cluster headache. They may be distinguished by the duration, frequency, and rhythmicity of attacks as well as by the intensity of pain and autonomic symptoms (table 2) [49]. They also may respond to different pharmacologic treatments.

Paroxysmal hemicrania – Paroxysmal hemicrania is a TAC with similar clinical features to cluster headache. Both syndromes are characterized by paroxysmal headache attacks, with severe and unilateral temporal/orbital pain along with cranial autonomic symptoms such as conjunctival injection or nasal congestion (table 2).

However, typical attacks of paroxysmal hemicrania are shorter (2 to 30 minutes) and more frequent (often more than 10 attacks per day) than cluster attacks. In addition, the autonomic symptoms are often less severe than in cluster headache, and predictable periodicity is less prominent.

Paroxysmal hemicrania is a rare condition. About 80 percent of patients with paroxysmal hemicrania have the chronic form, while the remaining 20 percent have the episodic form. Paroxysmal hemicrania usually starts between the ages of 20 and 40. (See "Paroxysmal hemicrania: Clinical features and diagnosis".)

The most important criterion for the diagnosis of paroxysmal hemicrania is the complete response to indomethacin (table 3). Within one week (often within three days) after the initiation of indomethacin at an adequate dose, the attacks should disappear, and this effect should be sustained. (See "Paroxysmal hemicrania: Clinical features and diagnosis" and "Paroxysmal hemicrania: Treatment and prognosis".)

Short-lasting unilateral neuralgiform headache attacks – The rare syndrome of short-lasting unilateral neuralgiform headache attacks is a TAC characterized by moderate or severe, strictly unilateral head pain lasting seconds to minutes, occurring at least once a day and usually associated with prominent lacrimation and redness of the ipsilateral eye (table 2).

There are two subtypes: short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) and short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA) (table 4). They may present as an episodic form when remissions between attacks last at least three months or as a chronic form when remissions are shorter.

SUNCT and SUNA attacks are usually much briefer than cluster attacks and may recur in a single bout much more frequently, up to 200 times in a day. (See "Short-lasting unilateral neuralgiform headache attacks: Clinical features and diagnosis".)

Hemicrania continua – Hemicrania continua is an uncommon TAC that presents with unilateral headache with superimposed recurrent attacks of more severe pain and cranial autonomic symptoms (table 5).

It is typically distinguished from cluster headache and other TACs by the continuous nature of baseline head pain (table 2). However, some patients may have pain-free intervals. The pain intensity is less severe in hemicrania continua than cluster. (See "Hemicrania continua".)

Symptoms in patients with hemicrania continua improve with indomethacin, as do patients with paroxysmal hemicrania and unlike patients with cluster headache (table 2).

Trigeminal neuralgia — Trigeminal neuralgia is one of the most common forms of cranial neuralgia characterized by paroxysmal attacks of lancinating facial pain, typically in the lower divisions of the trigeminal nerve. It is most commonly unilateral and may be associated with autonomic symptoms in some cases. Attacks in trigeminal neuralgia may be triggered by a tactile stimulus or facial movement, last for several seconds to minutes, and may be followed by a refractory period, unlike the spontaneous attacks of several-minute duration in cluster headache. (See "Trigeminal neuralgia".)

Some patients have cluster headache with coexistent trigeminal neuralgia, a condition known as cluster-tic syndrome. Patients with cluster-tic syndrome require treatment directed at both cluster headache and trigeminal neuralgia to achieve remission. (See "Overview of craniofacial pain", section on 'Cluster-tic syndrome'.)

Primary stabbing headache — Primary stabbing headache is characterized by transient, sharp jabbing pains that occur within a small, localized area of the scalp, exclusively or predominantly at variable locations within the first division of the trigeminal nerve. The stabs last from 1 to 10 seconds and occur at irregular intervals from one to many times each day. Unlike cluster headache, patients with primary stabbing headache have no associated cranial autonomic symptoms. (See "Primary stabbing headache".)

Secondary headache syndromes — Structural cranial lesions may present with clinical attacks that resemble cluster headache, although a causal relationship is often uncertain. One report identified 31 patients with symptoms typical for one of the TACs and an associated structural lesion, including 21 thought to have cluster headache [50]. Features suggestive of a secondary cause were present in several cases, including abnormalities on examination such as chronic ophthalmoplegia or hyperreflexia, a sudden increase in the frequency or intensity of attacks, or poor response to preventive medications. However, features typical for cluster headache were reported in other cases. In each case, headaches improved or resolved after treatment of the lesion, suggesting but not proving a causal role for the lesion.

Neuroimaging is performed for patients with symptoms of cluster headache to exclude a structural lesion. Additional diagnostic testing such as vascular imaging or laboratory testing is reserved for patients with atypical signs or symptoms suggestive of an alternative diagnosis and for those with symptoms refractory to treatment. (See 'Neuroimaging' above and 'Other diagnostic testing' above.)

Structural lesions that may present with cluster headache symptoms include:

Vascular pathologies

Carotid artery dissection [51]

Intracranial large artery aneurysms [52,53]

Brain arteriovenous malformations [54,55]

Brain dural arteriovenous fistulas [56]

Cerebral cavernous hemangioma [57]

Cerebral venous thrombosis [57,58]

Neoplasms

Pituitary adenomas [45,59]

Meningiomas [60,61]

Intracranial epidermoid cyst [62]

Carotid paraganglioma [63]

Recurrent nasopharyngeal carcinoma [64]

Inflammatory or infectious pathologies

Temporal arteritis [65]

Sinusitis [66]

Dental pain or abscess [67]

Orbital myositis [68]

Others

Glaucoma [69]

Metallic foreign body in the maxillary sinus [70]

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Migraine and other primary headache disorders".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Headaches in adults (The Basics)")

Beyond the Basics topic (See "Patient education: Headache causes and diagnosis in adults (Beyond the Basics)".)

SUMMARY AND RECOMMENDATIONS

Epidemiology – The lifetime prevalence of cluster headache is approximately 0.1 percent, and the disorder mainly affects males. Cluster headache is associated with tobacco use and head trauma and appears to have a genetic component in some families. (See 'Epidemiology and risk factors' above.)

Clinical features – Cluster headache is a condition characterized by attacks of severe unilateral pain, accompanied by ipsilateral cranial autonomic symptoms and/or restless or agitation. (See 'Clinical features' above.)

Cluster headache attacks are unilateral, severe, and sharp or stabbing in quality. Attacks typically persist for 15 minutes up to 3 hours in duration and may strike from once every other day to up to eight times a day. (See 'Headache' above.)

Autonomic symptoms associated with cluster headache typically occur only during the acute attack. They are ipsilateral to the headache and may include ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and/or nasal congestion. (See 'Autonomic symptoms' above.)

Bouts of recurring daily attacks may persist for several weeks followed by a period of remission. In the episodic form of cluster headache, a bout may last 6 to 12 weeks while remissions last at least 3 months, up to 12 months or longer. In the chronic form, attacks occur without significant periods of remission. (See 'Patterns of symptom recurrence' above.)

Diagnosis – Cluster headache, in its typical form, is unmistakable. The clinical diagnosis is made in patients with a compatible history and based on diagnostic criteria (table 1). (See 'Diagnosis and evaluation' above.)

We suggest neuroimaging with magnetic resonance imaging (MRI) of the brain with gadolinium for the initial evaluation of all patients with suspected cluster headache to exclude a structural abnormality of the brain and pituitary gland. A potential secondary cause may be found in patients with either typical or atypical clinical features of cluster headache and those with either a normal or abnormal neurologic examination. (See 'Neuroimaging' above and 'Secondary headache syndromes' above.)

Differential diagnosis – The differential diagnosis of cluster headache includes syndromes that present with recurrent, brief attacks of unilateral headaches. Such conditions include both primary headaches, including other trigeminal autonomic cephalalgias (TACs) (table 2), as well as secondary headache syndromes due to an underlying cause. (See 'Differential diagnosis' above.)

Multiple types of headache may coexist in an individual. Patients with cluster headache may also have symptoms from other primary or secondary headache syndromes. Headache types are distinguished by clinical features, diagnostic criteria, or responsiveness to treatments.

  1. May A, Schwedt TJ, Magis D, et al. Cluster headache. Nat Rev Dis Primers 2018; 4:18006.
  2. Hardebo JE. Activation of pain fibers to the internal carotid artery intracranially may cause the pain and local signs of reduced sympathetic and enhanced parasympathetic activity in cluster headache. Headache 1991; 31:314.
  3. Russell MB. Epidemiology and genetics of cluster headache. Lancet Neurol 2004; 3:279.
  4. Bahra A, May A, Goadsby PJ. Cluster headache: a prospective clinical study with diagnostic implications. Neurology 2002; 58:354.
  5. Sjaastad O, Bakketeig LS. Cluster headache prevalence. Vågå study of headache epidemiology. Cephalalgia 2003; 23:528.
  6. Fischera M, Marziniak M, Gralow I, Evers S. The incidence and prevalence of cluster headache: a meta-analysis of population-based studies. Cephalalgia 2008; 28:614.
  7. Lampl C. Childhood-onset cluster headache. Pediatr Neurol 2002; 27:138.
  8. Evers S, Frese A, Majewski A, et al. Age of onset in cluster headache: the clinical spectrum (three case reports). Cephalalgia 2002; 22:160.
  9. Burish M. Cluster Headache and Other Trigeminal Autonomic Cephalalgias. Continuum (Minneap Minn) 2018; 24:1137.
  10. Ekbom K, Svensson DA, Träff H, Waldenlind E. Age at onset and sex ratio in cluster headache: observations over three decades. Cephalalgia 2002; 22:94.
  11. Manzoni GC. Gender ratio of cluster headache over the years: a possible role of changes in lifestyle. Cephalalgia 1998; 18:138.
  12. Lin KH, Wang PJ, Fuh JL, et al. Cluster headache in the Taiwanese -- a clinic-based study. Cephalalgia 2004; 24:631.
  13. Lund N, Barloese M, Petersen A, et al. Chronobiology differs between men and women with cluster headache, clinical phenotype does not. Neurology 2017; 88:1069.
  14. Waung MW, Taylor A, Qualmann KJ, Burish MJ. Family History of Cluster Headache: A Systematic Review. JAMA Neurol 2020; 77:887.
  15. Russell MB, Andersson PG, Thomsen LL, Iselius L. Cluster headache is an autosomal dominantly inherited disorder in some families: a complex segregation analysis. J Med Genet 1995; 32:954.
  16. Russell MB, Andersson PG, Thomsen LL. Familial occurrence of cluster headache. J Neurol Neurosurg Psychiatry 1995; 58:341.
  17. El Amrani M, Ducros A, Boulan P, et al. Familial cluster headache: a series of 186 index patients. Headache 2002; 42:974.
  18. Leone M, Russell MB, Rigamonti A, et al. Increased familial risk of cluster headache. Neurology 2001; 56:1233.
  19. Harder AVE, Winsvold BS, Noordam R, et al. Genetic Susceptibility Loci in Genomewide Association Study of Cluster Headache. Ann Neurol 2021; 90:203.
  20. O'Connor E, Fourier C, Ran C, et al. Genome-Wide Association Study Identifies Risk Loci for Cluster Headache. Ann Neurol 2021; 90:193.
  21. Manzoni GC. Cluster headache and lifestyle: remarks on a population of 374 male patients. Cephalalgia 1999; 19:88.
  22. Rozen TD. Cluster Headache Clinical Phenotypes: Tobacco Nonexposed (Never Smoker and No Parental Secondary Smoke Exposure as a Child) versus Tobacco-Exposed: Results from the United States Cluster Headache Survey. Headache 2018; 58:688.
  23. Rozen TD. Childhood exposure to second-hand tobacco smoke and the development of cluster headache. Headache 2005; 45:393.
  24. Black DF, Swanson JW, Stang PE. Decreasing incidence of cluster headache: a population-based study in Olmsted County, Minnesota. Headache 2005; 45:220.
  25. Barloese MCJ, Beske RP, Petersen AS, et al. Episodic and Chronic Cluster Headache: Differences in Family History, Traumatic Head Injury, and Chronorisk. Headache 2020; 60:515.
  26. Lambru G, Castellini P, Manzoni GC, Torelli P. Mode of occurrence of traumatic head injuries in male patients with cluster headache or migraine: Is there a connection with lifestyle? Cephalalgia 2010; 30:1502.
  27. Grangeon L, O'Connor E, Chan CK, et al. New insights in post-traumatic headache with cluster headache phenotype: a cohort study. J Neurol Neurosurg Psychiatry 2020; 91:572.
  28. Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018; 38:1.
  29. Wilbrink LA, Louter MA, Teernstra OPM, et al. Allodynia in cluster headache. Pain 2017; 158:1113.
  30. Manzoni GC, Terzano MG, Bono G, et al. Cluster headache--clinical findings in 180 patients. Cephalalgia 1983; 3:21.
  31. May A. Cluster headache: pathogenesis, diagnosis, and management. Lancet 2005; 366:843.
  32. Rozen TD, Fishman RS. Cluster headache in the United States of America: demographics, clinical characteristics, triggers, suicidality, and personal burden. Headache 2012; 52:99.
  33. Louter MA, Wilbrink LA, Haan J, et al. Cluster headache and depression. Neurology 2016; 87:1899.
  34. Ji Lee M, Cho SJ, Wook Park J, et al. Increased suicidality in patients with cluster headache. Cephalalgia 2019; 39:1249.
  35. Drummond PD. Sweating and vascular responses in the face: normal regulation and dysfunction in migraine, cluster headache and harlequin syndrome. Clin Auton Res 1994; 4:273.
  36. Drummond PD. Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache. Cephalalgia 2006; 26:633.
  37. Drummond PD. Dysfunction of the sympathetic nervous system in cluster headache. Cephalalgia 1988; 8:181.
  38. Cluster Headache Syndrome, Sjaastad O (Ed), W B Saunders Company Ltd, 1992.
  39. Ekbom K. Evaluation of clinical criteria for cluster headache with special reference to the classification of the International Headache Society. Cephalalgia 1990; 10:195.
  40. Brandt RB, Mulleners W, Wilbrink LA, et al. Intra- and interindividual attack frequency variability of chronic cluster headache. Cephalalgia 2023; 43:3331024221139239.
  41. Hagedorn A, Snoer A, Jensen R, et al. The spectrum of cluster headache: A case report of 4600 attacks. Cephalalgia 2019; 39:1134.
  42. Benkli B, Kim SY, Koike N, et al. Circadian Features of Cluster Headache and Migraine: A Systematic Review, Meta-analysis, and Genetic Analysis. Neurology 2023; 100:e2224.
  43. Sandrini G, Friberg L, Jänig W, et al. Neurophysiological tests and neuroimaging procedures in non-acute headache: guidelines and recommendations. Eur J Neurol 2004; 11:217.
  44. Long RJ, Zhu YS, Wang AP. Cluster headache due to structural lesions: A systematic review of published cases. World J Clin Cases 2021; 9:3294.
  45. Grangeon L, O'Connor E, Danno D, et al. Is pituitary MRI screening necessary in cluster headache? Cephalalgia 2021; 41:779.
  46. Pearce SH, Cox JG, Pearce JM. Chronic paroxysmal hemicrania, episodic cluster headache and classic migraine in one patient. J Neurol Neurosurg Psychiatry 1987; 50:1699.
  47. Centonze V, Bassi A, Causarano V, et al. Simultaneous occurrence of ipsilateral cluster headache and chronic paroxysmal hemicrania: a case report. Headache 2000; 40:54.
  48. Alberca R, Ochoa JJ. Cluster tic syndrome. Neurology 1994; 44:996.
  49. Goadsby PJ, Lipton RB. A review of paroxysmal hemicranias, SUNCT syndrome and other short-lasting headaches with autonomic feature, including new cases. Brain 1997; 120 ( Pt 1):193.
  50. Favier I, van Vliet JA, Roon KI, et al. Trigeminal autonomic cephalgias due to structural lesions: a review of 31 cases. Arch Neurol 2007; 64:25.
  51. Elhfnawy AM, Solymosi L, Sommer C. Carotid dissection presenting as a prolonged cluster-like headache in a patient with episodic cluster headache. BMJ Case Rep 2017; 2017.
  52. Gentile S, Fontanella M, Giudice RL, et al. Resolution of cluster headache after closure of an anterior communicating artery aneurysm: the role of pericarotid sympathetic fibres. Clin Neurol Neurosurg 2006; 108:195.
  53. West P, Todman D. Chronic cluster headache associated with a vertebral artery aneurysm. Headache 1991; 31:210.
  54. Hindfelt B, Olivecrona H. Cerebral arteriovenous malformation and cluster-like headache. Headache 1991; 31:514.
  55. Gawel MJ, Willinsky RA, Krajewski A. Reversal of cluster headache side following treatment of arteriovenous malformation. Headache 1989; 29:453.
  56. Chang YH, Luo CB, Wang SJ, Chen SP. Cluster headache and middle meningeal artery dural arteriovenous fistulas: A case report. Cephalalgia 2018; 38:1792.
  57. Bellamio M, Anglani M, Mainardi F, et al. Cluster headache: When to worry? Two case reports. Cephalalgia 2017; 37:491.
  58. Park KI, Chu K, Park JM, Kim M. Cluster-like Headache Secondary to Cerebral Venous Thrombosis. J Clin Neurol 2006; 2:70.
  59. Wang SJ, Hung CW, Fuh JL, et al. Cranial autonomic symptoms in patients with pituitary adenoma presenting with headaches. Acta Neurol Taiwan 2009; 18:104.
  60. Kou L, Huang J, Xu Y, et al. Cluster-Like Headache Secondary to Anamnesis of Sphenoid Ridge Meningioma: A Case Report and Literature Review. Front Neurol 2019; 10:23.
  61. Taub E, Argoff CE, Winterkorn JM, Milhorat TH. Resolution of chronic cluster headache after resection of a tentorial meningioma: case report. Neurosurgery 1995; 37:319.
  62. Massie R, Sirhan D, Andermann F. Chronic cluster-like headache secondary to an epidermoid clival lesion. Can J Neurol Sci 2006; 33:421.
  63. Malissart P, Ducros A, Labauge P, et al. Carotid paraganglioma mimicking a cluster headache. Cephalalgia 2014; 34:1111.
  64. Appelbaum J, Noronha A. Pericarotid cluster headache. J Neurol 1989; 236:430.
  65. Jiménez-Jiménez FJ, García-Albea E, Zurdo M, et al. Giant cell arteritis presenting as cluster headache. Neurology 1998; 51:1767.
  66. Edvardsson B. Cluster headache associated with acute maxillary sinusitis. Springerplus 2013; 2:509.
  67. Gross SG. Dental presentations of cluster headaches. Curr Pain Headache Rep 2006; 10:126.
  68. Douglas VP, Douglas KAA, Rizzo JF 3rd, Chwalisz BK. Case report: Orbital myositis triggering oxygen-responsive cluster headache. Cephalalgia 2020; 40:313.
  69. Tomsak RL. Ophthalmologic aspects of headache. Med Clin North Am 1991; 75:693.
  70. Scorticati MC, Raina G, Federico M. Cluster-like headache associated to a foreign body in the maxillary sinus. Neurology 2002; 59:643.
Topic 3326 Version 24.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟