Migraine Headache: Difference between revisions

No edit summary
No edit summary
Line 148: Line 148:
== Causes  ==
== Causes  ==


add text here <br>  
Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brain stem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater.&nbsp;<ref name="Merck Manual" />
 
 
 
Common causes include:&nbsp;<br>
 
*Vasodilators (eg, Nitroglycerin)<ref name="Neurology" />
*Skipping meals<ref name="Merck Manual" />
*Weather changes<ref name="Merck Manual" />
*Sleep deprivation<ref name="Merck Manual" />
*Stress<ref name="Merck Manual" /><ref name="Neurology" /><br>
*Head trauma, neck pain, or temporomandibular joint dysfunction can trigger or exacerbate a migraine<ref name="Merck Manual" />
*Hormonal factors: fluctuating estrogen levels are a potent migraine trigger. Many women have onset of migraine at menarche, severe attacks during menstruation (menstrual migraine: appear to be more frequently in migraine with aura<ref name="Pathology" />) and worsening migraine during menopause.<ref name="Merck Manual" /> Oral contraceptives and other hormone therapy occasionally trigger or worsen migraine and have been associated with stroke in women who have migraine with aura.<ref name="Merck Manual" />&nbsp;Pregnancy can either exacerbate or relieve migraine attacks.
*Certain foods can precipitate a migraine attack (including, but not limited to):<br>
**tyramine-containing chesses<ref name="Neurology" />
**meat, such as hot dogs or bacon, with nitrate preservatives<ref name="Neurology" />
**chocolate containing phenylethylamine but not chocolate alone<ref name="Neurology" />
**food additives such as monosodium glutamate, a commonly used flavor enhancer<ref name="Neurology" />
**Coffee and alcohol (especially red wine)<ref name="Pathology" /><ref name="Merck Manual" />
**Sugar (in vulnerable individuals)<ref name="Pathology" />
*Genetics: There is a positive family history of migraine in about 60% of cases, which suggests a hereditary factor.<ref name="Pathology" />&nbsp;All twin studies done so far (comparison of concordance rates between monozygotic and dizygotic twins) show that migraine has a genetic component in addition to environmental factors.<ref name="Genetics of Migraine">Ducros A, Tournier-Lasserve E, Bousser MG. The Genetics of Migraine. Lancet Neurology 2002; 1: 285-293.</ref>&nbsp;Familial hemiplegic migraine (FHM), a rare type of migraine with aura, is the only form in which a monogenic mendelian ode of inheritance has been clearly established.<ref name="The Genetics of Migraine" />


== Systemic Involvement  ==
== Systemic Involvement  ==

Revision as of 05:44, 7 March 2010

Welcome to PT 635 Pathophysiology of Complex Patient Problems This is a wiki created by and for the students in the School of Physical Therapy at Bellarmine University in Louisville KY. Please do not edit unless you are involved in this project, but please come back in the near future to check out new information!!

Original Editors - Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Lead Editors - Your name will be added here if you are a lead editor on this page.  Read more.

Definition/Description[edit | edit source]

Migraine is a chronic, episodic primary headache.  Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brainstem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).[1]

Symptoms typically last 4 to 72 hours and may be severe. Pain is often but not always unilateral, throbbing, worse with exertion, and accompanied by autonomic symptoms (eg, nausea; sensitivity to light, sound, or odors).  Fortification spectra and other transient focal neurologic deficits occur in a few patients, usually just before the headache, also known as aura.[1] Diagnosis of migraine can usually be made by history alone.  Treatment includes lifestyle changes (diet, exercise, sleeping habits), medications including NSAIDs, analgesics, serotonin receptor agonists, beta blockers, calcium channel blockers, and antiemetics.[1][2]

Prevalence[edit | edit source]

Migraine headaches are the second most common type of primary headache. An estimated 28 million people in the United States (about 12% of the population) will experience migraine headaches at some point.[2] Lifetime prevalence is 18% for women and 6% for men in the US.  It most commonly begins during puberty or young adulthood, waxing and waning in frequency and severity over the ensuing years and usually diminishing after age 50.[1] In 90% of migraineurs, the first attack generally develops before the age of 40 years.  In women the frequency of headaches is highest during their reproductive years, when estrogen levels are higher, and decreases to some extent after menopause. About 45% of cases of migraine emerge during childhood or adolescence. Migraine with aura is more likely to develop at an earlier age than migraine without aura.[2]

Characteristics/Clinical Presentation[edit | edit source]

add text here

Associated Co-morbidities[edit | edit source]

add text here

Medications[edit | edit source]

According to Clinical Neurology (6th ed)[3], the following medications are generally used:

1. Acute Treatment:

Simple Analgesics

  • Aspirin
  • Naproxen Sodium
  • Ibuprofen
  • Acetominophen

Comments: May cause gastric pain or bleeding and rebound headache if used frequently.

Ergot Preparations

  • Ergotamine/caffeine (Cafergot)

Comments: May cause nausea and vomiting (N/V); contraindicated by pregnancy or coronary or peripheral vascular disease (PVD)

  • Dihydroergotamine

Comments: Use with metoclopramide (antiemetic)

Narcotic analgesics

  • Codeine/aspirin
  • Codeine/aspirin/acetominophen
  • Meperidine
  • Butorphanol

5-HT agonists (Serotonin Receptor Agonists)

  • Sumariptan (Imitrex)
  • Rizatriptan (Maxalt)
  • Zolmitriptan (Zomig)
  • Naratriptan (Amerge)
  • Almotriptan (Axert)
  • Frovatriptan (Frova)
  • Eletriptan (Relpax)

Comments:10% incidence N/V; contraindicated by pregnancy or coronary or PVD, and with monoamine oxidase inhibitors (MAOI)

Other Agents

    • Caffeine/butalbital/aspirin (Fiorinal)
  • Prochlorperazine

Comments: Can cause hypotension and drug-induced dystonia

2. Prophylactic Treatment

Antiinflammatory agents: 

  • Aspirin
  • Naproxen Sodium

Comments: May cause gastric pain or bleeding

Tricyclic Antidepressants

  • Amitriptylline
  • Nortriptyline
  • Protriptyline
  • Doxepin

Comments: May cause dry mouth, urinary retention, and sedation; contraindicated in glaucoma or prostatism

Beta Blockers

    • Nadolol
  • Atenolol
  • Timolol
  • Metoprolol

Comments: Listed in descending order of efficacy; symptomatic bradycardia may occur at high doses; contraindicated in asthma and congestive heart failure; not to be used with calcium blockers

Ergot Alkaloids

  • Methergine

Comments: Occurrence of retroperitoneal fibrosis with urethral obstruction and mediastinal fibrosis, although uncommon, should be monitored withe creatinine, ultrasonography, or intravenous urograms, and chest x-rays every 6 months; a drug holiday every 6 months is prudent

Cyproheptadine Comments: Drowsiness common early in treatment

Anticonvulsants

  • Phenytoin
  • Valproic acid
  • Topiramate
  • Gabapentin

Calcium Channel Antagonists

  • Verapamil
  • Nicardipine
  • Flunarizine

Comments: Contraindicated by severe left ventricular dysfunction, hypotension, sick sinus syndrome without artificial pacemaker, or second- or third-degree AV nodal block; constipation is most common side effect; not for use with beta blockers

3. Other Agents

  • Prochlorperazine
  • Hydroxyzine
  • Metoclopramide

Comments: Adjunct to treatment; improves enteric drug absorption and reduces nausea; dystonia and akathisia may occur and respond to IV benedryl

Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]

Diagnosis is based on characteristic symptoms and a normal physical (including neurologic) examination. Typical cases without worrisome findings do not require CNS imaging. Patients requiring very urgent CT or MRI to look for hemorrhage, increased intracranial pressure, and other structural causes of headache include those with:

  • Sudden-onset thunderclap headache*
  • Altered mental status, including seizure
  • Focal neurologic deficits
  • Papilledema**
  • Severe hypertension


  • Thunderclap headache: is an abrupt severe headache that may be a sign of bleeding in the brain and requires immediate medical attention.
  • Papilledema: an optic disc swelling that is secondary to elevated intracranial pressure.[4]

Causes[edit | edit source]

Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brain stem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater. [1]


Common causes include: 

  • Vasodilators (eg, Nitroglycerin)[5]
  • Skipping meals[1]
  • Weather changes[1]
  • Sleep deprivation[1]
  • Stress[1][5]
  • Head trauma, neck pain, or temporomandibular joint dysfunction can trigger or exacerbate a migraine[1]
  • Hormonal factors: fluctuating estrogen levels are a potent migraine trigger. Many women have onset of migraine at menarche, severe attacks during menstruation (menstrual migraine: appear to be more frequently in migraine with aura[2]) and worsening migraine during menopause.[1] Oral contraceptives and other hormone therapy occasionally trigger or worsen migraine and have been associated with stroke in women who have migraine with aura.[1] Pregnancy can either exacerbate or relieve migraine attacks.
  • Certain foods can precipitate a migraine attack (including, but not limited to):
    • tyramine-containing chesses[5]
    • meat, such as hot dogs or bacon, with nitrate preservatives[5]
    • chocolate containing phenylethylamine but not chocolate alone[5]
    • food additives such as monosodium glutamate, a commonly used flavor enhancer[5]
    • Coffee and alcohol (especially red wine)[2][1]
    • Sugar (in vulnerable individuals)[2]
  • Genetics: There is a positive family history of migraine in about 60% of cases, which suggests a hereditary factor.[2] All twin studies done so far (comparison of concordance rates between monozygotic and dizygotic twins) show that migraine has a genetic component in addition to environmental factors.[6] Familial hemiplegic migraine (FHM), a rare type of migraine with aura, is the only form in which a monogenic mendelian ode of inheritance has been clearly established.[7]

Systemic Involvement[edit | edit source]

add text here

Medical Management (current best evidence)[edit | edit source]

add text here

Physical Therapy Management (current best evidence)[edit | edit source]

add text here

Alternative/Holistic Management (current best evidence)[edit | edit source]

add text here

Differential Diagnosis[edit | edit source]

Due to the complexity of the pathophysiology and signs and symptoms attributed to migraine headaches, differential diagnosis is crucial for determining whether the headache is a medical emergency or a non-life threatening headache from other causes.  The following is a criteria developed by the International Headache Society classifying each type of headache into either primary, secondary, or other causes of headache with subclasses for each category for specific diagnosis. 

IHS Classification of Headaches[8]

This classification is hierarchical and you must decide how detailed you want to make your diagnosis. This can range from the first-digit level to the fourth. First one gets a rough idea about which group the patient belongs to. Then one obtains information allowing a more detailed diagnosis. The desired detail depends on the purpose. In general practice only the first- or second-digit diagnoses are usually applied whilst in specialist practice and headache centres a diagnosis at the third- or fourth-digit levels is appropriate.

Part I: The Primary Headaches[8]

1. Migraine

   1.1. Migraine without aura

   1.2. Migraine with aura

          In younger patients, several unusual disorders can mimic migraine with aura:[1]

  • Dissection of the carotid or vertebral artery
  • Antiphospholipid antibody syndrome
  • Cerebral vasculitis
  • Moyamoya disease
  • CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
  • MELAS (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes) syndrome

         In older patients, migraine with aura can be mistaken for a transient ischemic attack, especially when the aura occurs            without headache. [1]

   1.3. Childhood periodic syndromes that are commonly precursors of migraine

   1.4. Retinal migraine

   1.5. Complications of migraine

   1.6. Probable migraine

2. Tension-Type Headache (TTH)

   2.1. Infrequent episodic tension-type headache

   2.2. Frequent episodic tension-type headache

   2.3. Chronic tension-type headache

   2.4. Probable tension-type headache

3. Cluster Headache and Other Trigeminal Autonomic Cephalgias

   3.1. Cluster headache

   3.2. Paroxysmal hemicrania

   3.3. Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

   3.4. Probable trigeminal autonomic cephalgia

4. Other Primary Headaches

Part II: The Secondary Headaches:[8]

5. Headache attributed to head and/or neck trauma

   5.1. Acute post-traumatic headache

   5.2. Chronic post-traumatic headache

   5.3. Acute headache attributed to whiplash injury (S13.4)

   5.4. Chronic headache attributed to whiplash injury (S13.4)

   5.5. Headache attributed to traumatic intracranial haematoma

   5.6. Headache attributed to other head and/or neck trauma (S06)

   5.7. Post-craniotomy headache

6. Headache attributed to Cranial or Cervical Vascular Disorder

   6.1. Headache attributed to ischemic stroke or transient ischemic attack

   6.2. Headache attributed to non-traumatic intracranial hemorrhage (I62)

   6.3. Headache attributed to unruptured vascular malformation (Q28)

   6.4. Headache attributed to arteritis (M31)

   6.5. Carotid or vertebral artery pain (I63.0, I63.2, I65.0, I65.2 or I67.0)

   6.6. Headache attributed to cerebral venous thrombosis (CVT) (I63.6)

   6.7. Headache attributed to other intracranial vascular disorder

7. Headache attributed to non-vascular intracranial disorder

8. Headache attributed to a substance or its withdrawal

9. Headache attributed to infection

10. Headache attributed disorder of homeostasis

11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures

12. Headache attributed to psychiatric disorder

Part III: Cranial Neuralgias, Central and Primary Facial Pain and Other Headaches[8]

13. Cranial Neuralgias and Central Causes of Facial Pain

14. Other Headache, Cranial Neuralgia, Central or Primary Facial Pain


Pathologic Conditions Causing Headache[2]:

  • Subdural Hematoma: Mild to severe, intermittent headache; neurologic symptoms include fluctuating consciousness
  • Subarachnoid Hemorrhage: Sudden onset, severe and constant headache; elevated BP; can cause change in consciousness
  • Increased Intracranial Pressure (ICP): Mild to severe headache; neurologic symptoms include hemiparesis, visual changes, and brainstem symptoms, such as vomiting, altered consciousness
  • Meningitis, viral and bacterial: Severe headache with radiation down neck; acute illness and fever; positive Kernig's sign
  • Brain abscess: Mild to severe headache; local or distant infection; fever may not be present; neurologic signs consistent with local site of infection
  • Central nervous system: Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
  • Central nervous system neoplasm: Localized headache and focal neurologic symptoms; cranial nerve symptoms often seen
  • Toxicity: Generalized headache, pulsating; other signs of toxicity may be present
  • Sinusitis: Frontal or dull headache, usually worse in the morning; increased pain in cold damp air; nasal discharge
  • Otitis media, mastoiditis: Feeling of fullness in ear, stabbing pains in head, vertigo, and tinnitus

Case Reports[edit | edit source]

add links to case studies here (case studies should be added on new pages using the case study template)

Resources
[edit | edit source]

add appropriate resources here

Recent Related Research (from Pubmed)[edit | edit source]

see tutorial on Adding PubMed Feed

Extension:RSS -- Error: Not a valid URL: Feed goes here!!|charset=UTF-8|short|max=10

References[edit | edit source]

see adding references tutorial.

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M. The Merck Manual of Diagnosis and Therapy 18th ed. Whitehouse Station:Merck Research Laboratories; 2006: 1847-1849
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist 3rd ed. St. Louis: Saunders Elsevier; 2009: 1551-1559.
  3. Aminoff MJ, Greenberg DA, Simon RP. Clinical Neurology 6th ed. New York: Lange Medical Books/McGraw-Hill; 2005: 85-90.
  4. Gossman MV, Giovannini J. Papilledema. 2009. Available at: http://emedicine.medscape.com/article/1217204-overview. Accessed on March 6, 2010.
  5. 5.0 5.1 5.2 5.3 5.4 5.5 Cite error: Invalid <ref> tag; no text was provided for refs named Neurology
  6. Ducros A, Tournier-Lasserve E, Bousser MG. The Genetics of Migraine. Lancet Neurology 2002; 1: 285-293.
  7. Cite error: Invalid <ref> tag; no text was provided for refs named The Genetics of Migraine
  8. 8.0 8.1 8.2 8.3 IHS Classification of Headaches. Available at: http://ihs-classification.org/en/02_klassifikation/. Accessed March 5, 2010.