2 Migraine
2 Migraine
2 Migraine
Clinical Picture
What Symptoms Occur During a Migraine Attack?
Migraineurs have recurrent, severe, and disabling attacks of headache, often unilateral and pulsating, along with
symptoms of sensory disturbance, such as light, sound, and odor sensitivity. Nausea and neck stiffness are other
common symptoms, and symptoms can be aggravated by movement.
Some patients experience dizziness during attacks.
About 2030% of patients experience aura and neurological symptoms (e.g., visual disturbances), which usually
precede the headache phase of an attack.
Premonitory symptoms such as yawning, irritability, tiredness, cravings, and difficulty concentrating sometimes
precede headache onset.
Epidemiology
How Many People Are Affected by Migraine?
Women: about 1318% of the population
Men: about 510% of the population
Numbers may be lower in Asian populations
Chronic Migraine
About 4% of the adult population experiences chronic headache, i.e., headache on 15 or more days a month. About half
of this group has chronic migraine, and the other half has chronic tension-type headache [7].
Pathophysiology
Migraine Pathophysiology
Migraine was considered to be vascular in origin for much of the 20th century [6], but today it is considered to be a
disorder of the brain, with abnormalities in the vasculature occurring secondary to the primary neuronal events. Migraine
has a strong inherited component, and a large genetic study suggests the involvement of glutamate pathways in migraine
pathogenesis [1]. Genetic variations on chromosome 19 have been reported for rare forms of familial hemiplegic migraine
(FHM1 and 2).
Definition/Diagnosis/Differential Diagnosis
The International Classification of Headache Disorders
Distinguishes primary headache syndromes from secondary, symptomatic headache diseases. Migraine and tension-
type headache are the most common types of primary headache. The classification of primary headache disorders is
based on a phenomenological (operational) categorization. In contrast, secondary headaches, which have to be ruled
out, are classified according to their etiology (e.g., headache attributed to a tumor or a vascular abnormality). Some
types of migraine can be classified based on genetic markers (familial hemiplegic migraine).
Defines episodic migraine as migraine attacks occurring on fewer than 15 days a month and chronic migraine as
attacks occurring on 15 or more days a month.
Other potential causes of headache such as intracranial/spinal pathology, musculoskeletal pathology,
inflammatory/autoimmune diseases, systemic illnesses, or drug-related headaches have to be ruled out by clinical
history, neurological examination, and additional diagnostic tests, when appropriate, in order to diagnose migraine.
Therapy
How Can Migraine Attacks Be Treated?
Simple analgesics (e.g., aspirin, acetaminophen/paracetamol)
NSAIDs (e.g., naproxen, ibuprofen, diclofenac)
Triptans (e.g., sumatriptan)
Second choice treatment: ergot derivatives (e.g., dihydroergotamine)
In the future, CGRP-receptor antagonists such as telcagepant may be a new option for the treatment of acute attacks
[3].
Compound analgesics, such as those containing aspirin, acetaminophen/paracetamol, and caffeine have been shown
to be more effective than single analgesics. However, they are thought to increase the risk of medication overuse
headache (see below).
Medication Overuse
Is defined as consumption of triptans, ergotamine, opioids, or combination analgesics on 10 days or more per month,
or simple analgesics on 15 days or more a month.
Is an important issue in migraine therapy and needs to be identified and managed.
Can produce rebound headache.
Can reduce the efficacy of preventive therapy.
Can mask the headache phenotype.
Neuromodulation Approaches
The efficacy of migraine therapy using electrostimulation of peripheral nerves is currently being investigated in studies
(see the fact sheet on Neuromodulation in Primary Headaches). Results are pending.
References
[1] Anttila V, Stefansson H, Kallela M, et al. Genome-wide association study of migraine implicates a common susceptibility variant on
8q22.1. Nat Genet 2010;42:86973.
[2] Dalkara T, Nozari A, Moskowitz MA. Migraine aura pathophysiology: the role of blood vessels and microembolisation. Lancet
Neurol 2010;9:30917.
[3] Goadsby PJ, Sprenger T. Current practice and future directions in the prevention and acute management of migraine. Lancet
Neurol 2010;9:28598.
[4] Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache
Disorders, 2nd edition. Cephalalgia 2004;24(Suppl 1):9160.
[5] Lashley K. Patterns of cerebral integration indicated by the scotomas of migraine. Arch Neurol Psychiatry 1941;46:3319.
[6] Moskowitz MA, Buzzi MG, Sakas DE, Linnik MD. Pain mechanisms underlying vascular headaches: progress report 1989. Rev
Neurol (Paris) 1989;145:18193.
[7] Scher AI, Stewart WF, Lipton RB. Epidemiology of chronic daily headache. In: Goadsby PJ, Silbersten SD, Dodick DW, editors.
Chronic daily headache for clinicians. Ontario: BC Decker; 2005. p. 311.