Headache
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Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief:Niloofarsadaat Eshaghhosseiny, MD[2] Cafer Zorkun, M.D., Ph.D. [3]
Synonyms and keywords: Cephalgia
Overview
Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
A headache is a condition of pain in the head; sometimes neck or upper back pain may also be interpreted as a headache. It ranks amongst the most common local pain complaints.
Historical Perspective
The first recorded classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories.
Pathophysiology
The brain in itself is not sensitive to pain, because it lacks pain-sensitive nerve fibers. Several areas of the head can hurt, including a network of nerves which extend over the scalp and certain nerves in the face, mouth, and throat. The meninges and the blood vessels do have pain perception. Headaches often result from traction to or irritation of the meninges and blood vessels. The muscles of the head may similarly be sensitive to pain.
Causes
The vast majority of headaches are benign and self-limiting. Common causes are tension, Neck pain, migraine, eye strain, dehydration, low blood sugar, and sinusitis. The vast majority of chronic headaches are multifactoral in nature. Much rarer are headaches due to life-threatening conditions such asmeningitis, encephalitis, cerebral aneurysms, extremely high blood pressure, and brain tumors. When the headache occurs in conjunction with a head injury the cause is usually quite evident. A large percentage of headaches among females are caused by ever-fluctuating estrogen during menstrual years. This can occur prior to, during or even midcycle menstruation.
Natural History, Complications and Prognosis
The prognosis of headache depends on the underlying cause.
Diagnosis
Laboratory Findings
Blood tests may help narrow down the differential diagnosis, but are rarely confirmatory of specific headache forms.
CT
Computed tomography (CT/CAT) scans of the brain or sinuses are commonly performed.
MRI
Magnetic resonance imaging (MRI) of the brain and sinuses are done in specific settings.
Treatment
Medical Therapy
Headaches may be successfully treated through medical therapies such as analgesisa and, in some cases, a tandem approach with implanted electrodes.
Primary Prevention
Some forms of headache, such as migraine, may be amenable to preventative treatment.
References
Historical Perspective
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Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
The first record of human headache has been known for 6000 years ago.In 17th Century migraine was recognized by Willis.The first recorded classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories.The idea of migraine may be a vascular disease revisited by Wolff and colleaguse in the 1940s.
Historical Perspective
Discovery
- The first record of human headache has been known for 6000 years ago.[1]
- The first recorded classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672.
- In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories.[2]
- In 17th Century migraine was recognized by Willis.
- The idea of migraine may be a vascular disease revisited by Wolff and colleagues in the 1940s.[3]
References
- ↑ Goadsby PJ, Holland PR, Martins-Oliveira M, Hoffmann J, Schankin C, Akerman S (2017). “Pathophysiology of Migraine: A Disorder of Sensory Processing”. Physiol Rev. 97 (2): 553–622. doi:10.1152/physrev.00034.2015. PMC 5539409. PMID 28179394.
- ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1212/01 Check
|pmid=value (help). - ↑ “Reorganized text”. JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
Pathophysiology
Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
The brain in itself is not sensitive to pain, because it lacks pain-sensitive nerve fibers. Several areas of the head can hurt, including a network of nerves which extend over the scalp and certain nerves in the face, mouth, and throat. The meninges and the blood vessels do have pain perception. Headaches often result from traction to or irritation of the meninges and blood vessels. The muscles of the head may similarly be sensitive to pain.
Pathophysiology
Physiology
- The normal pathophysiology of cluster can be understood as follows:
- vascular dilation,trigeminal nerve stimulation and histamine release.[1]
Pathogenesis
- The exact pathophysiology of cluster headache is not completely understood.
- It is understood that cluster headache is caused by either vascular dilation,trigeminal nerve stimulation and histamine release.[1]
- Previously thought cluster headache was a type of vascular headache, but current proof implies that pathophysiology of cluster headache includes the brain, trigeminovascular and cranial parasympathetic system.[2]
- One of the theories of migraine pain in patients without aura is extracranial arterial dilatation.[3]
Genetics
Genes involved in the pathogenesis of migraine include:
- MTDH
- LRP1
- TRPM8
The development of familial hemiplegic migraine is the result of multiple genetic mutations such as:
- CACNA1A
- ATP1A2
- SCN1A[4]
References
- ↑ 1.0 1.1 Weaver-Agostoni J (2013). “Cluster headache”. Am Fam Physician. 88 (2): 122–8. PMID 23939643.
- ↑ May A, Schwedt TJ, Magis D, Pozo-Rosich P, Evers S, Wang SJ (2018). “Cluster headache”. Nat Rev Dis Primers. 4: 18006. doi:10.1038/nrdp.2018.6. PMID 29493566.
- ↑ Amin FM, Asghar MS, Hougaard A, Hansen AE, Larsen VA, de Koning PJ; et al. (2013). “Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study”. Lancet Neurol. 12 (5): 454–61. doi:10.1016/S1474-4422(13)70067-X. PMID 23578775.
- ↑ Andreou AP, Edvinsson L (2019). “Mechanisms of migraine as a chronic evolutive condition”. J Headache Pain. 20 (1): 117. doi:10.1186/s10194-019-1066-0. PMC 6929435 Check
|pmc=value (help). PMID 31870279.
Causes
Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
The vast majority of headaches are benign and self-limiting. Common causes are tension,Neck pain, migraine, eye strain, dehydration, low blood sugar, and sinusitis. Much rarer are headaches due to life-threatening conditions such as meningitis, encephalitis, cerebral aneurysms, extremely high blood pressure, and brain tumors. When the headache occurs in conjunction with a head injury the cause is usually quite evident. A large percentage of headaches among females are caused by ever-fluctuating estrogen during menstrual years. This can occur prior to, during or even midcycle menstruation.
Causes
Common Causes
- Tension headache
- Neck pain
- Migraine
- Eye strain
- Dehydration
- Low blood sugar
- Sinusitis.
Causes by alphabetical order
- Amoxicillin
- Aprepitant
- Busulfan
- Carmustine
- Ceftibuten
- Cimetidine
- Cycloserine
- Desmopressin
- Didanosine
- Doripenem
- Eculizumab
- Efavirenz
- Eribulin
- Etonogestrel
- Exemestane
- Flunisolide
- Flurbiprofen
- Pegylated interferon alfa-2a
- Histrelin
- Hydroxyzine
- Hydroxocobalamin
- Interferon gamma
- Ivacaftor
- Levonorgestrel
- Lomefloxacin hydrochloride
- Loratadine
- Mebendazole
- Micafungin sodium
- Mifepristone
- Milnacipran hydrochloride
- Multiple endocrine neoplasia type 1
- Natalizumab
- Oprelvekin
- Oritavancin
- Papaverine
- Pirfenidone
- Plerixafor
- Pyrantel pamoate
- Ribavirin
- Siltuximab
- Sipuleucel-T
- Stavudine
- Sunitinib
- Temozolomide
- Teniposide
- Tigecycline
- triptorelin pamoate
- Trovafloxacin mesylate
- Von Willebrand factor
- Voriconazole
References
Differentiating Headache from other Diseases

For the WikiDoc page for this topic, click here Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]
Differential diagnosis of headache includes: Migraine, tension-type headache, cluster headache, seizure, meningitis, encephalitis, neurosyphilis, SAH, subdural hematoma, brain tumor, hypertensive encephalopathy, brain abscess, multiple sclerosis, hemorrhagic stroke, Wernickes encephalopathy, and drug toxicity etc.[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]
| Disease | History and Physical Examination | PMHx | Diagnostic approach | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Bilateral | Throbbing character | Autonomic symptoms | Fever | Photophobia | Aphasia | LOC | Aura | Nause/
Vomiting |
Rash | Neck stiffness | Vision changes | Neurologic deficits | Labs and CSF findings | CT/MRI | Gold standard test | ||
| Migraine | – | + | – | – | + | – | – | + | + | – | – | + | – | Trigger factors, family hx | – | – | Clinical assesment |
| Tension-type headache (TTH) | + | – | – | – | – | – | – | – | – | – | – | – | – | stress, genetics | – | – | Clinical assesment |
| Cluster headache | – | – | + | – | – | – | – | – | – | – | – | + | – | episodic history | – | – | Clinical assesment |
| Seizure | + | – | – | – | – | +/- | + | +/- | – | – | – | – | +/- | Hx of seizures | prolactin level | +/- mass lesion | EEG [20] |
| Meningitis | + | – | – | + | +/- | +/- | – | – | +/- | +/- | + | – | + | Hx of fever, malaise | <math>\uparrow</math>WBC
<math>\uparrow</math>Protein <math>\downarrow</math>glucose |
+/- | CSF analysis[21] |
| Encephalitis | + | +/- | – | + | +/- | +/- | – | – | – | +/- | + | – | + | Hx of fever, malaise | elevated WBC, low glucose | + | CSF PCR |
| Brain tumor[22] | + | – | – | – | – | +/- | – | – | +/- | – | – | +/- | +/- | weight loss, fatigue | neuromarkers,
Cancer cells[23] |
+/- mass | MRI |
| Subdural hemorrhage | -/+ | +/- | – | – | – | +/- | – | – | – | – | – | +/- | +/- | Trauma, fall | Xanthochromia | + | CT w/o contrast |
| Subarachnoid hemorrhage | -/+ | +/- | – | – | +/- | +/- | – | – | – | – | +/- | +/- | +/- | thunderclap headache | <math>\uparrow</math>opening pressure, xanthochromia | + | CT w/o contrast |
| Hypertensive encephalopathy | + | +/- | – | – | +/- | – | – | – | – | – | – | +/- | – | Hypertension | UA +/- | +/- | clinical assessment |
| CNS abscess | -/+ | – | – | + | – | +/- | – | – | +/- | +/- | +/- | +/- | +/- | History of drug abuse, endocarditis, immunosupression | ↑ leukocytes, ↓ glucose and ↑ protien | + | MRI |
| Conversion disorder | -/+ | – | – | – | – | +/- | – | – | – | – | +/- | +/- | +/- | History of emotional stress | – | – | Diagnosis of exclusion |
| Multiple sclerosis | -/+ | – | – | – | – | – | – | – | – | – | – | + | +/- | History of relapses and remissions | ↑ CSF IgG levels
(monoclonal bands) |
+ | MRI |
| Hemorrhagic stroke | -/+ | +/- | – | – | – | +/- | – | – | – | – | – | +/- | +/- | HTN | – | + | CT scan without contrast[24][25] |
| Neurosyphilis[26][27] | -/+ | – | – | – | – | – | +/- | – | – | +/- | – | +/- | +/- | STIs | ↑ Leukocytes and protein | + | CSF VDRL-specifc
CSF FTA-Ab -sensitive[28] |
| Wernicke’s encephalopathy | -/+ | – | – | – | – | +/- | – | – | – | – | – | +/- | +/- | History of alcohal abuse | blood ethanol levels | +/- | Clinical assesment and lab findings |
| Drug toxicity | -/+ | – | – | +/- | – | – | +/- | – | +/- | – | +/- | +/- | +/- | Medication hx | Drug levels | – | Drug screen test |
| Metabolic disturbances | -/+ | – | – | – | – | – | – | – | +/- | – | – | +/- | +/- | Underlying CKD, CLD | Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia | – | Cause dependent |
| Sinusitis | -/+ | – | – | +/- | – | – | – | – | – | – | – | – | – | allergies, seasonal | leukocytosis | + | CT |
Diagnsotic Labs For Meningitis
Diagnosis of meningitis, is based on clinical presentation in combination with CSF analysis. CSF analysis has major role for diagnosis and rule out other possibilities. The following table summarizes the CSF findings in different types of meningitis.[2][3][4][5][6]
| Cerebrospinal fluid level | Normal level | Bacterial meningitis[5] | Viral meningitis[5] | Fungal meningitis | Tuberculous meningitis[29] | Neoplastic meningitis[2] |
|---|---|---|---|---|---|---|
| Cells/ul | < 5 | >300 | 10-1000 | 10-500 | 50-500 | >4 |
| Cells | Lymphocyte | Leukocyte > Lymphocyte | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte | Lymphocyte > Leukocyte |
| Total protein (mg/dl) | 45-60 | Typically 100-500 | Normal or slightly high | High | Typically 100-200 | >50 |
| Glucose ratio (CSF/plasma)[3] | > 0.5 | < 0.3 | > 0.6 | <0.3 | < 0.5 | <0.5 |
| Lactate (mmols/l)[4] | < 2.1 | > 2.1 | < 2.1 | >3.2 | > 2.1 | >2.1 |
| Others | Intra-cranial pressure (ICP) = 6-12 (cm H2O) | CSF gram stain, CSF culture, CSF bacterial antigen | PCR of HSV-DNA, VZV | CSF gram stain, CSF india ink | PCR of TB-DNA | CSF tumour markers such as alpha fetoprotein, CEA |
References
- ↑ “National guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage”. Ann. Clin. Biochem. 40 (Pt 5): 481–8. September 2003. doi:10.1258/000456303322326399. PMID 14503985.
- ↑ 2.0 2.1 2.2 Le Rhun E, Taillibert S, Chamberlain MC (2013). “Carcinomatous meningitis: Leptomeningeal metastases in solid tumors”. Surg Neurol Int. 4 (Suppl 4): S265–88. doi:10.4103/2152-7806.111304. PMC 3656567. PMID 23717798.
- ↑ 3.0 3.1 3.2 Chow E, Troy SB (2014). “The differential diagnosis of hypoglycorrhachia in adult patients”. Am J Med Sci. 348 (3): 186–90. doi:10.1097/MAJ.0000000000000217. PMC 4065645. PMID 24326618.
- ↑ 4.0 4.1 4.2 Leen WG, Willemsen MA, Wevers RA, Verbeek MM (2012). “Cerebrospinal fluid glucose and lactate: age-specific reference values and implications for clinical practice”. PLoS One. 7 (8): e42745. doi:10.1371/journal.pone.0042745. PMC 3412827. PMID 22880096.
- ↑ 5.0 5.1 5.2 5.3 Negrini B, Kelleher KJ, Wald ER (2000). “Cerebrospinal fluid findings in aseptic versus bacterial meningitis”. Pediatrics. 105 (2): 316–9. PMID 10654948.
- ↑ 6.0 6.1 Brouwer MC, Tunkel AR, van de Beek D (2010). “Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis”. Clin Microbiol Rev. 23 (3): 467–92. doi:10.1128/CMR.00070-09. PMC 2901656. PMID 20610819.
- ↑ Vermeulen M, Hasan D, Blijenberg BG, Hijdra A, van Gijn J (July 1989). “Xanthochromia after subarachnoid haemorrhage needs no revisitation”. J. Neurol. Neurosurg. Psychiatry. 52 (7): 826–8. doi:10.1136/jnnp.52.7.826. PMC 1031927. PMID 2769274.
- ↑ Wasay M, Mekan SF, Khelaeni B, Saeed Z, Hassan A, Cheema Z, Bakshi R (June 2005). “Extra temporal involvement in herpes simplex encephalitis”. Eur. J. Neurol. 12 (6): 475–9. doi:10.1111/j.1468-1331.2005.00999.x. PMID 15885053.
- ↑ Glaser CA, Honarmand S, Anderson LJ, Schnurr DP, Forghani B, Cossen CK, Schuster FL, Christie LJ, Tureen JH (December 2006). “Beyond viruses: clinical profiles and etiologies associated with encephalitis”. Clin. Infect. Dis. 43 (12): 1565–77. doi:10.1086/509330. PMID 17109290.
- ↑ Meltzer EO, Hamilos DL (May 2011). “Rhinosinusitis diagnosis and management for the clinician: a synopsis of recent consensus guidelines”. Mayo Clin. Proc. 86 (5): 427–43. doi:10.4065/mcp.2010.0392. PMC 3084646. PMID 21490181.
- ↑ Rasmussen BK, Jensen R, Schroll M, Olesen J (1991). “Epidemiology of headache in a general population–a prevalence study”. J Clin Epidemiol. 44 (11): 1147–57. doi:10.1016/0895-4356(91)90147-2. PMID 1941010.
- ↑ Kelman L (October 2004). “The premonitory symptoms (prodrome): a tertiary care study of 893 migraineurs”. Headache. 44 (9): 865–72. doi:10.1111/j.1526-4610.2004.04168.x. PMID 15447695.
- ↑ Laurell K, Artto V, Bendtsen L, Hagen K, Häggström J, Linde M, Söderström L, Tronvik E, Wessman M, Zwart JA, Kallela M (September 2016). “Premonitory symptoms in migraine: A cross-sectional study in 2714 persons”. Cephalalgia. 36 (10): 951–9. doi:10.1177/0333102415620251. PMID 26643378.
- ↑ Charlotte E. Grayson and The Cleveland Clinic Neuroscience Center (October 2004). “Cluster Headaches”. WebMD. Retrieved 2006-09-22.
- ↑ Drummond PD (October 1994). “Sweating and vascular responses in the face: normal regulation and dysfunction in migraine, cluster headache and harlequin syndrome”. Clin. Auton. Res. 4 (5): 273–85. doi:10.1007/BF01827433. PMID 7888747.
- ↑ Drummond PD (June 2006). “Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache”. Cephalalgia. 26 (6): 633–41. doi:10.1111/j.1468-2982.2006.01106.x. PMID 16686902.
- ↑ Ekbom K (August 1990). “Evaluation of clinical criteria for cluster headache with special reference to the classification of the International Headache Society”. Cephalalgia. 10 (4): 195–7. doi:10.1046/j.1468-2982.1990.1004195.x. PMID 2245469.
- ↑ Sandrini G, Antonaci F, Pucci E, Bono G, Nappi G (December 1994). “Comparative study with EMG, pressure algometry and manual palpation in tension-type headache and migraine”. Cephalalgia. 14 (6): 451–7, discussion 394–5. doi:10.1046/j.1468-2982.1994.1406451.x. PMID 7697707.
- ↑ Jensen R, Fuglsang-Frederiksen A (June 1994). “Quantitative surface EMG of pericranial muscles. Relation to age and sex in a general population”. Electroencephalogr Clin Neurophysiol. 93 (3): 175–83. doi:10.1016/0168-5597(94)90038-8. PMID 7515793.
- ↑ Manford M (2001). “Assessment and investigation of possible epileptic seizures”. J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557. PMID 11385043.
- ↑ Carbonnelle E (2009). “[Laboratory diagnosis of bacterial meningitis: usefulness of various tests for the determination of the etiological agent]”. Med Mal Infect. 39 (7–8): 581–605. doi:10.1016/j.medmal.2009.02.017. PMID 19398286.
- ↑ Morgenstern LB, Frankowski RF (1999). “Brain tumor masquerading as stroke”. J Neurooncol. 44 (1): 47–52. PMID 10582668.
- ↑ Weston CL, Glantz MJ, Connor JR (2011). “Detection of cancer cells in the cerebrospinal fluid: current methods and future directions”. Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
- ↑ Birenbaum D, Bancroft LW, Felsberg GJ (2011). “Imaging in acute stroke”. West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
- ↑ DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). “ACR Appropriateness Criteria® on cerebrovascular disease”. J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
- ↑ Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
- ↑ Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
- ↑ Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
- ↑ Caudie C, Tholance Y, Quadrio I, Peysson S (2010). “[Contribution of CSF analysis to diagnosis and follow-up of tuberculous meningitis]”. Ann Biol Clin (Paris). 68 (1): 107–11. doi:10.1684/abc.2010.0407. PMID 20146981.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
The prevalence of cluster headache is approximately 3 to 150 per 100,000 individuals worldwide.*Worldwide Prevalence of patient with secondary headache is approximately 18%. The prevalence of Migraine headache is estimated to be 12 to 15 percent of general population.The prevalence of frequent episodic tension type headache is 21.6 percent.Patients of all age groups may develop headache.Cluster headache commonly affects individuals between 20 to 40years of age.Cluster headache usually affects women of the Aferican -American and Caucasians.women are more commonly affected by migraine than men. Men are more commonly affected by cluster than women. The male to female ratio is approximately 2.5 to 1.
Epidemiology and Demographics
Prevalence
- The prevalence of cluster headache is approximately 3 to 150 per 100,000 individuals worldwide.[1]
- Worldwide Prevalence of patient with secondary headache is approximately 18%.[2]
- The prevalence of Migraine headache is estimated to be 12 to 15 percent of general population.[3]
- The prevalence of frequent episodic tension type headache is 21.6 percent.[4]
Age
- Patients of all age groups may develop headache.
- Cluster commonly affects individuals between 20 to 40years of age. [5]
- The incidence of tension type headache peaked in the fourth decade.[4]
Race
- Cluster headache usually affects women of the Aferican -American and Caucasians.[6]
Gender
- women are more commonly affected by migraine than men.
- Men are more commonly affected by cluster than women. The male to female ratio is approximately 2.5 to 1.[1]
References
- ↑ 1.0 1.1 Wei DY, Yuan Ong JJ, Goadsby PJ (2018). “Cluster Headache: Epidemiology, Pathophysiology, Clinical Features, and Diagnosis”. Ann Indian Acad Neurol. 21 (Suppl 1): S3–S8. doi:10.4103/aian.AIAN_349_17. PMC 5909131. PMID 29720812.
- ↑ Do TP, Remmers A, Schytz HW, Schankin C, Nelson SE, Obermann M; et al. (2019). “Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list”. Neurology. 92 (3): 134–144. doi:10.1212/WNL.0000000000006697. PMC 6340385. PMID 30587518.
- ↑ Lipton RB, Stewart WF, Diamond S, Diamond ML, Reed M (2001). “Prevalence and burden of migraine in the United States: data from the American Migraine Study II”. Headache. 41 (7): 646–57. doi:10.1046/j.1526-4610.2001.041007646.x. PMID 11554952.
- ↑ 4.0 4.1 Russell MB, Levi N, Saltyte-Benth J, Fenger K (2006). “Tension-type headache in adolescents and adults: a population based study of 33,764 twins”. Eur J Epidemiol. 21 (2): 153–60. doi:10.1007/s10654-005-6031-3. PMID 16518684.
- ↑ Weaver-Agostoni J (2013). “Cluster headache”. Am Fam Physician. 88 (2): 122–8. PMID 23939643.
- ↑ Reed C, Gordon S (1966). “Anaemia and polycythaemia in haemorrhagic telangiectasia”. Med J Aust. 1 (11): 449–51. doi:10.5694/j.1326-5377.1966.tb72472.x. PMID 5909131.
Risk Factors
Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Common risk factors in the development of headache may be occupational, environmental, and genetic.Common risk factors in the development of migraine divided in three categories: non-modifiable, modifiable, and putative. Non-modifiable risk factors include female gender, age, white race, low educational level, socioeconomic status, and genetic factors.Modifiable risk factors include,obesity, medication overuse,stressful life events, caffeine overuse, other pain syndromes.
Risk Factors
The most risk factors in the development of headache are: [1][2]
- Brain tumors
- Brain infection
- Intracranial hypertension
- Anxiety
- Arthritis in neck or spine
- Degenerative bone or disk disease in the neck or spine
- Depression
- Temporomandibular joint disorders
- Drugs, such as nitrates
- Alcohol
- Environmental changes, such as changes in barometric pressure and altitude, inclement weather, or high winds.
Common Risk Factors
- Common risk factors in the development of headache may be occupational, environmental, and genetic.
- Common risk factors in the development of migraine include:
- age
- female gender
- white race
- genetic factors
- Obesity
- Medication overuse
- Stressful life events
Less Common Risk Factors
- Less common risk factors in the development of migraine include:
- Caffeine overuse
- Snoring
- Other pain syndromes[1]
References
- ↑ 1.0 1.1 Bigal M (2009). “Migraine chronification–concept and risk factors”. Discov Med. 8 (42): 145–50. PMID 19833063.
- ↑ Bentley RE (1971). “The on-line applications of a small digital computer to a gamma scintillation camera”. Br J Radiol. 44 (517): 77. PMID 5539409.
Natural History, Complications and Prognosis
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Editor-In-Chief: Robert G. Schwartz, M.D. [1], Piedmont Physical Medicine and Rehabilitation, P.A.; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
The symptoms of cluster headache usually decreased with age.13% of patients with initial episodic cluster headache may progress to develop chronic cluster headache.33% of patients with initial episodic cluster headache may progress to episodic pattern.
Natural History, Complications, and Prognosis
Natural History
- The symptoms of cluster headache usually decreased with age.
- 13% of patients with initial episodic cluster headache may progress to develop chronic cluster headache.
- 33% of patients with initial episodic cluster headache may progress to episodic pattern.[1]
Complications
- Status migrainosus: The migraine episode lasts more than 72 hours.
- Persistent aura without infarction: The symptoms of aura last for more than a week in the absence of any neuroimaging findings suggestive of infarction.
- Migrainous infarction: The symptoms of aura last for more than a week in the context of any neuroimaging findings suggestive of infarction in the corresponding brain territory.
- Seizure triggered by a migrainous aura[2]
Prognosis
- 13% of patients with initial episodic cluster headache may progress to develop chronic cluster headache.
- 33% of patients with initial episodic cluster headache may progress to episodic pattern.[1]
References
- ↑ 1.0 1.1 Wei DY, Yuan Ong JJ, Goadsby PJ (2018). “Cluster Headache: Epidemiology, Pathophysiology, Clinical Features, and Diagnosis”. Ann Indian Acad Neurol. 21 (Suppl 1): S3–S8. doi:10.4103/aian.AIAN_349_17. PMC 5909131. PMID 29720812.
- ↑ Headache Classification Committee of the International Headache Society (IHS) (2013). “The International Classification of Headache Disorders, 3rd edition (beta version)”. Cephalalgia. 33 (9): 629–808. doi:10.1177/0333102413485658. PMID 23771276.
References
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Case Studies
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