MyEClinic
MyEClinic
Health Dictionary Find a Doctor

Tension headache

For patient information, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Muscle contraction headache; headache – benign; headache – tension; chronic headaches – tension; rebound headaches – tension; stress headache

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

A common primary headache disorder, characterized by a dull, non-pulsatile, diffuse, band-like (or vice-like) pain of mild to moderate intensity in the head, scalp or neck. The subtypes are classified by frequency and severity of symptoms. There is no clear cause even though it has been associated with muscle contraction and stress. Tension headaches, which were renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches. The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive pathways, environmental and genetic factors. It includes hypersensitivity of central and peripheral nociceptive pathways: lack of habituation, Nitric oxide and combination of genetic and envirommental factors. The exact cause of tension-type headaches is still unknown. Multiple pathophysiologic mechanisms explain the possible etiologies or causative factors. Differential diagnosis if tension type headache includes; Migraine, Cluster headache, Secondary headaches such as Medication overuse, Sinus headache and Cervicogenic headache. Tension headache is one of the most common type of headaches. Tension-type headache (TTH) is the most prevalent headache in the general population. Tension-type headache (TTH) is the second-most prevalent disorder in the world. A Danish Registry showed 1 year prevalances of infrequent episodic, frequent episodic and and chronic TTH were 63.5, 21.6 and 0.9% respectively. Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor; stress, sleep deprivation, irregular meal time (hunger), eyestrain. Diagnostic criteria for tension-type headache is specified by the International Classification of Headache Disorders, 3rd edition (ICHD-3). Tension-type headache pain is often described as a constant pressure, as if the head were being squeezed in a vise. The pain is frequently bilateral which means it is present on both sides of the head at once. Tension-type headache pain is typically mild to moderate, but may be severe. In contrast to migraine, the pain does not increase during exercise. Tension type headache may have following examination findings: Increased pericranial muscle (head, neck or shoulders) and myofascial tissue tenderness on manual palpation. Increased number of myofacial trigger points: frontal, temporal, masseter, ptrygoid, sternocleidomastoid, splenius, and trapezius mucles. Neuro-imaging is generally not indicated for patients with TTH. Usually indicated if abnormal neurologic examination findings or atypical presentation or presentation not fulfilling the ICHD-3 criteria. Neuro-imaging with an magnetic resonance imaging (MRI) scan with and without contrast is preferred to non-contrast computed tomography (CT) scan. MRI is usually indicated to rule out underlying structural brain lesion or to evaluate brain and pituitary gland in patient presenting with typical features or highly suspicious of TTH. Episodic tension-type headaches generally respond well to over-the-counter analgesics, such as paracetamol, ibuprofen or aspirin. Simple analgesic monotherapy such as NSAIDS or aspirin are recommended (Grade 1A) for episodic TTH treatment requiring patients. Simple analgesic monotherapy is used in combination with caffeine for TTH patients who are unresponsive or have a poor response to analgesic monotherapy (Grdae 2A). Combination therapies including opioids or butalbital are not recommended as first line agents for TTH Rx (Grade 1C). Inpatient treatment for severe TTH can be treated in addition to the above mentioned treatment with chlorpromazine, metoclopramide, combination of metoclopramide and diphenhydramine and intramuscular ketorolac. TTH prevention and prophylactic treatment is generally indicated for chronic TTH and frequent episodic TTH. Data regarding pharmacologic prevention and prophylactic treatment is limited and not well established. Drugs that can be used are; TCA (amitriptyline), SSRI (mirtazapine, venlafaxine), and anticonvulsants (gabapentin, topiramate). Behavioral treatments include; relaxation, biofeedback, and CBT. For patients with frequent episodic or chronic TTH, combined Rx with TCA plus stress management therapy is recommended rather than alone therapy with TCA or behavioral therapy alone. (Grade 2B). For patients with frequent episodic or chronic TTH, having preference for pharmacologic therapy rather than behavioral therapy, TCA with amitriptyline is recommended. (Grade 2B). For patients with frequent episodic or chronic TTH, not needing pharmacologic therapy, electromyography biofeedback combined with relaxation therapy is recommended. (Grade 2B). For patients with frequent episodic or chronic TTH, who cannot tolerate or require more effective treatments such as amitriptyline and biofeedback, accupuncture (Grade 2B) or physical therapy (Grade 2C) is recommended.

Historical Perspective

Tension headaches, which were renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches. In the earlier days, it was known as stress or tension headache, muscle-contraction headache, psychomyogenic headache, and psychogenic headache.

Classification

Tension-type headaches can be episodic or chronic. Episodic tension-type headaches are defined as tension-type headaches occurring less than 15 days a month, whereas chronic tension headaches occur 15 days or more a month for at least 6 months. Tension-type headaches can last from minutes to days or even months, though a typical tension headache lasts 4-6 hours.

Pathophysiology

The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive pathways, environmental and genetic factors. It includes hypersensitivity of central and peripheral nociceptive pathways: lack of habituation, Nitric oxide and combination of genetic and envirommental factors.

Causes

The exact cause of tension-type headaches is still unknown. Multiple pathophysiologic mechanisms explain the possible etiologies or causative factors.

Differential Diagnosis

Differential diagnosis if tension type headache includes; Migraine, Cluster headache, Secondary headaches such as Medication overuse, Sinus headache and Cervicogenic headache.

Epidemiology and Demographics

Tension headache is one of the most common type of headaches. Tension-type headache (TTH) is the most prevalent headache in the general population. Tension-type headache (TTH) is the second-most prevalent disorder in the world. A Danish Registry showed 1 year prevalances of infrequent episodic, frequent episodic and and chronic TTH were 63.5, 21.6 and 0.9% respectively. A United States study showed that the 1 year prevalences of episodic and chronic TTH were 38.3 and 2.2%. Females have a higher prevalence compared to males. Limited data suggests TTH to be more prevalent in whites compared to black in the US, irrespective of sex. A recent study showed that TTH prevalence peaking in the 4th decade. A Danish study showed decreasing prevalence of TTH with increasing age.

Risk Factors

Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor; stress, sleep deprivation, irregular meal time (hunger), eyestrain. Other triggers of tension headaches include: alcohol , caffeine, colds, the flu, or a sinus infection, dental problems such as jaw clenching or teeth grinding, excessive smoking and fatigue or overexertion.

Natural History, Complications and Prognosis

Tension headache is considered to have a high socioeconomic impact, being the most common type of headache. It is a life long condition and usually results in reduced quality of life and marked functional disability. Tension type headache if left untreated or undiagnosed, is found to be associated with increased risk of depression and suicide, due to its huge socioeconomic impact. Tension headaches that occur as a symptom of another condition are usually relieved when the underlying condition is treated. Frequent use of pain medications in patients with tension-type headache may lead to the development of medication overuse headache.

Diagnosis

Diagnostic criteria

Diagnostic criteria for tension-type headache is specified by the International Classification of Headache Disorders, 3rd edition (ICHD-3).

History and Symptoms

Tension-type headache pain is often described as a constant pressure, as if the head were being squeezed in a vise. The pain is frequently bilateral which means it is present on both sides of the head at once. Tension-type headache pain is typically mild to moderate, but may be severe. In contrast to migraine, the pain does not increase during exercise.

Physical Examination

Tension type headache may have following examination findings: Increased pericranial muscle (head, neck or shoulders) and myofascial tissue tenderness on manual palpation. Increased number of myofacial trigger points: frontal, temporal, masseter, ptrygoid, sternocleidomastoid, splenius, and trapezius mucles.

Laboratory Findings

Laboratory investigations, such as electrophysiologic testing (eg, evoked potential, electroencephalography) and examination of the cerebrospinal fluid, are not found to be helpful and needs more studies for further evaluation.

CT

Neuro-imaging is generally not indicated for patients with TTH. Usually indicated if abnormal neurologic examination findings or atypical presentation or presentation not fulfilling the ICHD-3 criteria. Neuro-imaging with a non-contrast computed tomography (CT) scan is usually indicated to rule out underlying structural brain lesion or to evaluate brain and pituitary gland in patient presenting with typical features or highly suspicious of tension-type headache.

MRI

Neuro-imaging is generally not indicated for patients with TTH. Usually indicated when abnormal neurologic examination findings or atypical presentation or presentation not fulfilling the ICHD-3 criteria. Neuro-imaging with an magnetic resonance imaging (MRI) scan with and without contrast is preferred to non-contrast computed tomography (CT) scan. MRI is usually indicated to rule out underlying structural brain lesion or to evaluate brain and pituitary gland in patient presenting with typical features or highly suspicious of TTH.

Treatment

Medical Therapy

Episodic tension-type headaches generally respond well to over-the-counter analgesics, such as paracetamol, ibuprofen or aspirin. Simple analgesic monotherapy such as NSAIDS or aspirin are recommended (Grade 1A) for episodic TTH treatment requiring patients. Simple analgesic monotherapy is used in combination with caffeine for TTH patients who are unresponsive or have a poor response to analgesic monotherapy (Grdae 2A). Combination therapies including opioids or butalbital are not recommended as first line agents for TTH Rx (Grade 1C). Inpatient treatment for severe TTH can be treated in addition to the above mentioned treatment with chlorpromazine, metoclopramide, combination of metoclopramide and diphenhydramine and intramuscular ketorolac.

Prevention

TTH prevention and prophylactic treatment is generally indicated for chronic TTH and frequent episodic TTH. Data regarding pharmacologic prevention and prophylactic treatment is limited and not well established. Drugs that can be used are; TCA (amitriptyline), SSRI (mirtazapine, venlafaxine), and anticonvulsants (gabapentin, topiramate). Behavioral treatments include; relaxation, biofeedback, and CBT. For patients with frequent episodic or chronic TTH, combined Rx with TCA plus stress management therapy is recommended rather than alone therapy with TCA or behavioral therapy alone. (Grade 2B). For patients with frequent episodic or chronic TTH, having preference for pharmacologic therapy rather than behavioral therapy, TCA with amitriptyline is recommended. (Grade 2B). For patients with frequent episodic or chronic TTH, not needing pharmacologic therapy, electromyography biofeedback combined with relaxation therapy is recommended. (Grade 2B). For patients with frequent episodic or chronic TTH, who cannot tolerate or require more effective treatments such as amitriptyline and biofeedback, accupuncture (Grade 2B) or physical therapy (Grade 2C) is recommended.

References


Template:WikiDoc Sources

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

Tension headaches, which were renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches. In the earlier days, it was known as stress or tension headache, muscle-contraction headache, psychomyogenic headache, and psychogenic headache.

Historical Perspective

  • Tension headaches, which were renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches.
  • In the earlier days, it was known as stress or tension headache, muscle-contraction headache, psychomyogenic headache, and psychogenic headache.[1][2][3]


References

  1. ↑ Jensen RH (February 2018). “Tension-Type Headache – The Normal and Most Prevalent Headache”. Headache. 58 (2): 339–345. doi:10.1111/head.13067. PMID 28295304.
  2. ↑ Martelletti P, Birbeck GL, Katsarava Z, Jensen RH, Stovner LJ, Steiner TJ (February 2013). “The Global Burden of Disease survey 2010, Lifting The Burden and thinking outside-the-box on headache disorders”. J Headache Pain. 14: 13. doi:10.1186/1129-2377-14-13. PMC 3620501. PMID 23565711.
  3. ↑ “Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition”. Cephalalgia. 38 (1): 1–211. January 2018. doi:10.1177/0333102417738202. PMID 29368949.


Template:WikiDoc Sources

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

Tension-type headaches can be episodic or chronic. Episodic tension-type headaches are defined as tension-type headaches occurring less than 15 days a month, whereas chronic tension headaches occur 15 days or more a month for at least 6 months. Tension-type headaches can last from minutes to days or even months, though a typical tension headache lasts 4-6 hours.

Classification

Tension headache may be classified into 3 subtypes depending upon the frequency and duration of episodes:[1] This classification is based upon underlying pathophysiology, impact on quality of life, and the treatment approach. Each of the 3 subtype is futher classified as with or without pericranial muscle tenderness.

  • Infrequent episodic
    • Headache episodes < 1 day a month
  • Frequent episodic
    • Headache episodes 1 to 14 days a month
  • Chronic
    • Headaches 15 or more days a month



References

  1. ↑ “Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition”. Cephalalgia. 38 (1): 1–211. January 2018. doi:10.1177/0333102417738202. PMID 29368949.


Template:WikiDoc Sources

Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive pathways, environmental and genetic factors. It includes hypersensitivity of central and peripheral nociceptive pathways: lack of habituation, Nitric oxide and combination of genetic and envirommental factors.

Pathophysiology

The pathophysiology for tension type headache is multifactorial and generally includes increased sensitivity of central and peripheral nociceptive pathways, environmental and genetic factors.[1][2][3][4][5]

Hypersensitivity of central and peripheral nociceptive pathways:

  • Increased sensitivity of central and peripheral nociceptive pathways has a central role in the pathogenesis of tension type headache.[2]
  • Hypersensitivity of central nociceptive pathways and central nervous system is more commonly involved with chronic type tension headache.[6]
  • Hypersensitivity of peripheral nociceptive pathways and peripheral nervous system is more commonly involved with episodic type tension headache.[7] [8]
    • Peripheral factors:[9][10]
      • Active and latent trigger points (Increased muscle tenderness)[11]
      • Forward head posture[12]
      • Decreased neck mobility[13][14]
      • Increased levels of interleukin-1 beta (inflammatory mediator)

Lack of Habituation:

  • Lack of habituation is also observed to be an important pathogenetic factor in a subset population of tension type headache
  • Low pain, electrical and thermal thresholds in patients with chronic tension type headache may suggest abnormal limbic-controlled descending pain pathways secondary to underlying deficient descending inhibition.[15]

Nitric oxide:

  • NO is one of the most importanr chemical mediator involved in the pathogenesis of tension type headache[16]
  • Nitric oxide synthase inhibitors have a potent antinociceotive effect[17]

Genetic factors:

  • Genetic factors have a strong association in the pathogenesis of chronic tension headaches compared to episodic.[3]
  • First degree relatives of chronic TTH have 3 times higher risk of developing chronic TTH compared to the general population[4]
  • Chronic TTH has a complex multifactorial inheritance[5]

Environmental factors:

  • Several studies have shown that episodic TTH may be caused by a variety of genes in combination with environmental factors.

References

  1. ↑ “Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition”. Cephalalgia. 38 (1): 1–211. January 2018. doi:10.1177/0333102417738202. PMID 29368949.
  2. ↑ 2.0 2.1 Jensen R (2003). “Peripheral and central mechanisms in tension-type headache: an update”. Cephalalgia. 23 Suppl 1: 49–52. doi:10.1046/j.1468-2982.2003.00574.x. PMID 12699459.
  3. ↑ 3.0 3.1 Ulrich V, Gervil M, Olesen J (June 2004). “The relative influence of environment and genes in episodic tension-type headache”. Neurology. 62 (11): 2065–9. doi:10.1212/01.wnl.0000129498.50793.8a. PMID 15184615.
  4. ↑ 4.0 4.1 Russell MB, Ostergaard S, Bendtsen L, Olesen J (May 1999). “Familial occurrence of chronic tension-type headache”. Cephalalgia. 19 (4): 207–10. doi:10.1046/j.1468-2982.1999.019004207.x. PMID 10376164.
  5. ↑ 5.0 5.1 Russell MB, Iselius L, Ostergaard S, Olesen J (February 1998). “Inheritance of chronic tension-type headache investigated by complex segregation analysis”. Hum. Genet. 102 (2): 138–40. doi:10.1007/s004390050666. PMID 9521579.
  6. ↑ Bezov D, Ashina S, Jensen R, Bendtsen L (February 2011). “Pain perception studies in tension-type headache”. Headache. 51 (2): 262–71. doi:10.1111/j.1526-4610.2010.01768.x. PMID 21029081.
  7. ↑ Bendtsen L, Fumal A, Schoenen J (2010). “Tension-type headache: mechanisms”. Handb Clin Neurol. 97: 359–66. doi:10.1016/S0072-9752(10)97029-2. PMID 20816435.
  8. ↑ Schmidt-Wilcke T, Leinisch E, Straube A, Kämpfe N, Draganski B, Diener HC, Bogdahn U, May A (November 2005). “Gray matter decrease in patients with chronic tension type headache”. Neurology. 65 (9): 1483–6. doi:10.1212/01.wnl.0000183067.94400.80. PMID 16275843.
  9. ↑ Bendtsen L (June 2000). “Central sensitization in tension-type headache–possible pathophysiological mechanisms”. Cephalalgia. 20 (5): 486–508. doi:10.1046/j.1468-2982.2000.00070.x. PMID 11037746.
  10. ↑ Ashina S, Bendtsen L, Ashina M (December 2005). “Pathophysiology of tension-type headache”. Curr Pain Headache Rep. 9 (6): 415–22. doi:10.1007/s11916-005-0021-8. PMID 16282042.
  11. ↑ Bendtsen L, Fernández-de-la-Peñas C (December 2011). “The role of muscles in tension-type headache”. Curr Pain Headache Rep. 15 (6): 451–8. doi:10.1007/s11916-011-0216-0. PMID 21735049.
  12. ↑ Fernández-de-Las-Peñas C, Cuadrado ML, Pareja JA (May 2007). “Myofascial trigger points, neck mobility, and forward head posture in episodic tension-type headache”. Headache. 47 (5): 662–72. doi:10.1111/j.1526-4610.2006.00632.x. PMID 17501847.
  13. ↑ Fernández-de-Las-Peñas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA (September 2006). “Myofascial trigger points and their relationship to headache clinical parameters in chronic tension-type headache”. Headache. 46 (8): 1264–72. doi:10.1111/j.1526-4610.2006.00440.x. PMID 16942471.
  14. ↑ Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, Gerwin RD, Pareja JA (March 2006). “Trigger points in the suboccipital muscles and forward head posture in tension-type headache”. Headache. 46 (3): 454–60. doi:10.1111/j.1526-4610.2006.00288.x. PMID 16618263.
  15. ↑ Bendtsen L (December 2003). “Central and peripheral sensitization in tension-type headache”. Curr Pain Headache Rep. 7 (6): 460–5. doi:10.1007/s11916-003-0062-9. PMID 14604505.
  16. ↑ de Tommaso M, Ceci E, Pica C, Trojano M, Delussi M, Franco G, Livrea P, Ruggieri M (July 2012). “Serum levels of N-acetyl-aspartate in migraine and tension-type headache”. J Headache Pain. 13 (5): 389–94. doi:10.1007/s10194-012-0448-3. PMC 3381063. PMID 22527035.
  17. ↑ Fischer M, Wille G, Klien S, Shanib H, Holle D, Gaul C, Broessner G (August 2012). “Brain-derived neurotrophic factor in primary headaches”. J Headache Pain. 13 (6): 469–75. doi:10.1007/s10194-012-0454-5. PMC 3464472. PMID 22584531.


Template:WikiDoc Sources

Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

The exact cause of tension-type headaches is still unknown. Multiple pathophysiologic mechanisms explain the possible etiologies or causative factors.

Causes

The exact cause of tension-type headaches is still unknown. In the past, persistent or sustained pericranial muscle contracture and tenderness was thought to be the main etiology of tension type headache. Excessive stress leading to muscle contraction was also considered a suspected cause of tension type headache.

References

  1. ↑ Ulrich V, Gervil M, Olesen J (June 2004). “The relative influence of environment and genes in episodic tension-type headache”. Neurology. 62 (11): 2065–9. doi:10.1212/01.wnl.0000129498.50793.8a. PMID 15184615.
  2. ↑ Russell MB, Ostergaard S, Bendtsen L, Olesen J (May 1999). “Familial occurrence of chronic tension-type headache”. Cephalalgia. 19 (4): 207–10. doi:10.1046/j.1468-2982.1999.019004207.x. PMID 10376164.
  3. ↑ Russell MB, Iselius L, Ostergaard S, Olesen J (February 1998). “Inheritance of chronic tension-type headache investigated by complex segregation analysis”. Hum. Genet. 102 (2): 138–40. doi:10.1007/s004390050666. PMID 9521579.
  4. ↑ de Tommaso M, Ceci E, Pica C, Trojano M, Delussi M, Franco G, Livrea P, Ruggieri M (July 2012). “Serum levels of N-acetyl-aspartate in migraine and tension-type headache”. J Headache Pain. 13 (5): 389–94. doi:10.1007/s10194-012-0448-3. PMC 3381063. PMID 22527035.
  5. ↑ Fischer M, Wille G, Klien S, Shanib H, Holle D, Gaul C, Broessner G (August 2012). “Brain-derived neurotrophic factor in primary headaches”. J Headache Pain. 13 (6): 469–75. doi:10.1007/s10194-012-0454-5. PMC 3464472. PMID 22584531.


Template:WikiDoc Sources

Differentiating Tension Headache from other Diseases

Differentiating Tension Headache from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

Differential diagnosis of tension-type headache includes; Migraine, Cluster headache, Secondary headaches such as Medication overuse, Sinus headache and Cervicogenic headache.

Differential diagnosis

Differential diagnosis of tension-type headache includes[1][2][3][4]

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.[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]


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 [24]
Meningitis + – – + +/- +/- – – +/- +/- + – + Hx of fever, malaise <math>\uparrow</math>WBC

<math>\uparrow</math>Protein

<math>\downarrow</math>glucose

+/- CSF analysis[25]
Encephalitis + +/- – + +/- +/- – – – +/- + – + Hx of fever, malaise elevated WBC, low glucose + CSF PCR
Brain tumor[26] + – – – – +/- – – +/- – – +/- +/- weight loss, fatigue neuromarkers,

Cancer cells[27]

+/- 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[28][29]
Neurosyphilis[30][31] -/+ – – – – – +/- – – +/- – +/- +/- STIs ↑ Leukocytes and protein + CSF VDRL-specifc

CSF FTA-Ab -sensitive[32]

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.[6][7][8][9][10]

Cerebrospinal fluid level Normal level Bacterial meningitis[9] Viral meningitis[9] Fungal meningitis Tuberculous meningitis[33] Neoplastic meningitis[6]
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)[7] > 0.5 < 0.3 > 0.6 <0.3 < 0.5 <0.5
Lactate (mmols/l)[8] < 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

  1. ↑ Berk T, Ashina S, Martin V, Newman L, Vij B (December 2018). “Diagnosis and Treatment of Primary Headache Disorders in Older Adults”. J Am Geriatr Soc. 66 (12): 2408–2416. doi:10.1111/jgs.15586. PMID 30251385.
  2. ↑ Lipton RB, Cady RK, Stewart WF, Wilks K, Hall C (May 2002). “Diagnostic lessons from the spectrum study”. Neurology. 58 (9 Suppl 6): S27–31. doi:10.1212/wnl.58.9_suppl_6.s27. PMID 12011271.
  3. ↑ Lipton RB, Stewart WF, Cady R, Hall C, O’Quinn S, Kuhn T, Gutterman D (2000). “2000 Wolfe Award. Sumatriptan for the range of headaches in migraine sufferers: results of the Spectrum Study”. Headache. 40 (10): 783–91. doi:10.1046/j.1526-4610.2000.00143.x. PMID 11135021.
  4. ↑ Rasmussen BK (February 1995). “Epidemiology of headache”. Cephalalgia. 15 (1): 45–68. doi:10.1046/j.1468-2982.1995.1501045.x. PMID 7758098.
  5. ↑ “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.
  6. ↑ 6.0 6.1 6.2 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.
  7. ↑ 7.0 7.1 7.2 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.
  8. ↑ 8.0 8.1 8.2 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.
  9. ↑ 9.0 9.1 9.2 9.3 Negrini B, Kelleher KJ, Wald ER (2000). “Cerebrospinal fluid findings in aseptic versus bacterial meningitis”. Pediatrics. 105 (2): 316–9. PMID 10654948.
  10. ↑ 10.0 10.1 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ Charlotte E. Grayson and The Cleveland Clinic Neuroscience Center (October 2004). “Cluster Headaches”. WebMD. Retrieved 2006-09-22.
  19. ↑ 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.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ Manford M (2001). “Assessment and investigation of possible epileptic seizures”. J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557. PMID 11385043.
  25. ↑ 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.
  26. ↑ Morgenstern LB, Frankowski RF (1999). “Brain tumor masquerading as stroke”. J Neurooncol. 44 (1): 47–52. PMID 10582668.
  27. ↑ 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.
  28. ↑ Birenbaum D, Bancroft LW, Felsberg GJ (2011). “Imaging in acute stroke”. West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
  29. ↑ 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.
  30. ↑ 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.
  31. ↑ Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  32. ↑ 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.
  33. ↑ 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.

Template:WikiDoc Sources

Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

Tension headache is one of the most common type of headaches. Tension-type headache (TTH) is the most prevalent headache in the general population. Tension-type headache (TTH) is the second-most prevalent disorder in the world. A Danish Registry showed 1 year prevalances of infrequent episodic, frequent episodic and and chronic TTH were 63.5, 21.6 and 0.9% respectively. A United States study showed that the 1 year prevalences of episodic and chronic TTH were 38.3 and 2.2%. Females have a higher prevalence compared to males. Limited data suggests TTH to be more prevalent in whites compared to black in the US, irrespective of sex. A recent study showed that TTH prevalence peaking in the 4th decade. A Danish study showed decreasing prevalence of TTH with increasing age.

Epidemiology and Demographics

Tension headache is one of the most common type of headaches.[1][2]

  • Tension-type headache (TTH) is the most prevalent headache in the general population
  • Tension-type headache (TTH) is the second-most prevalent disorder in the world[3]
  • A Danish Registry showed 1 year prevalances of infrequent episodic, frequent episodic and and chronic TTH were 63.5, 21.6 and 0.9% respectively.
  • A United States study showed that the 1 year prevalences of episodic and chronic TTH were 38.3 and 2.2%
  • Females have a higher prevalence compared to males.[4]
  • Limited data suggests TTH to be more prevalent in whites compared to black in the US, irrespective of sex.[5]
  • A recent study showed that TTH prevalence peaking in the 4th decade
  • A Danish study showed decreasing prevalence of TTH with increasing age.[6]

References

  1. ↑ Jensen RH (February 2018). “Tension-Type Headache – The Normal and Most Prevalent Headache”. Headache. 58 (2): 339–345. doi:10.1111/head.13067. PMID 28295304.
  2. ↑ Martelletti P, Birbeck GL, Katsarava Z, Jensen RH, Stovner LJ, Steiner TJ (February 2013). “The Global Burden of Disease survey 2010, Lifting The Burden and thinking outside-the-box on headache disorders”. J Headache Pain. 14: 13. doi:10.1186/1129-2377-14-13. PMC 3620501. PMID 23565711.
  3. ↑ “Global, regional, and national burden of migraine and tension-type headache, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016”. Lancet Neurol. 17 (11): 954–976. November 2018. doi:10.1016/S1474-4422(18)30322-3. PMC 6191530. PMID 30353868.
  4. ↑ Couch JR (December 2005). “The long-term prognosis of tension-type headache”. Curr Pain Headache Rep. 9 (6): 436–41. doi:10.1007/s11916-005-0024-5. PMID 16282045.
  5. ↑ Wang SJ, Liu HC, Fuh JL, Liu CY, Lin KP, Chen HM, Lin CH, Wang PN, Hsu LC, Wang HC, Lin KN (July 1997). “Prevalence of headaches in a Chinese elderly population in Kinmen: age and gender effect and cross-cultural comparisons”. Neurology. 49 (1): 195–200. doi:10.1212/wnl.49.1.195. PMID 9222190.
  6. ↑ Schwartz BS, Stewart WF, Simon D, Lipton RB (February 1998). “Epidemiology of tension-type headache”. JAMA. 279 (5): 381–3. doi:10.1001/jama.279.5.381. PMID 9459472.


Template:WikiDoc Sources

Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor; stress, sleep deprivation, irregular meal time (hunger), eyestrain. Other triggers of tension headaches include: alcohol , caffeine, colds, the flu, or a sinus infection, dental problems such as jaw clenching or teeth grinding, excessive smoking and fatigue or overexertion.

Risk Factors

Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor;

  • Stress – Usually occurs in the afternoon after long stressful work hours
  • Sleep deprivation
  • Uncomfortable stressful position and/or bad posture
  • Irregular meal time (hunger)
  • Eyestrain

Other triggers of tension headaches include:


References

Template:WikiDoc Sources

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Overview

Tension headache is considered to have a high socioeconomic impact, being the most common type of headache. It is a life long condition and usually results in reduced quality of life and marked functional disability. Tension type headache if left untreated or undiagnosed, is found to be associated with increased risk of depression and suicide, due to its huge socioeconomic impact.

Natural history, Complications and Prognosis

  • Tension headache is considered to have a high socioeconomic impact, being the most common type of headache.[1]
  • It is a life long condition and usually results in reduced quality of life and marked functional disability.[2]
  • Tension headaches that occur as a symptom of another condition are usually relieved when the underlying condition is treated.[3]
  • Frequent use of pain medications in patients with tension-type headache may lead to the development of medication overuse headache.
  • Tension type headache if left untreated or undiagnosed, is found to be associated with increased risk of depression and suicide, due to its huge socioeconomic impact.[4]

References

  1. ↑ “Global, regional, and national burden of migraine and tension-type headache, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016”. Lancet Neurol. 17 (11): 954–976. November 2018. doi:10.1016/S1474-4422(18)30322-3. PMC 6191530. PMID 30353868.
  2. ↑ Couch JR (December 2005). “The long-term prognosis of tension-type headache”. Curr Pain Headache Rep. 9 (6): 436–41. doi:10.1007/s11916-005-0024-5. PMID 16282045.
  3. ↑ Wang SJ, Liu HC, Fuh JL, Liu CY, Lin KP, Chen HM, Lin CH, Wang PN, Hsu LC, Wang HC, Lin KN (July 1997). “Prevalence of headaches in a Chinese elderly population in Kinmen: age and gender effect and cross-cultural comparisons”. Neurology. 49 (1): 195–200. doi:10.1212/wnl.49.1.195. PMID 9222190.
  4. ↑ Schwartz BS, Stewart WF, Simon D, Lipton RB (February 1998). “Epidemiology of tension-type headache”. JAMA. 279 (5): 381–3. doi:10.1001/jama.279.5.381. PMID 9459472.


Template:WikiDoc Sources

Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters
External Links

Template:Diseases of the nervous system


Template:WikiDoc Sources

Looking for the patient version?

Back to the patient-friendly article

Imprint

Privacy Policy

Terms and Conditions

© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH