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Complex neurological disorder that affects multiple cortical, subcortical and brainstem areas that regulate autonomic, affective, cognitive and sensory functions

Primary Headache- the disorder is the headache itself ( as in migraine , tension type headache and cluster headache ) Secondary Headache -headache is a symptom of a secondary abnormality such as dental pain , SAH or brain tumour

How common-Migraine has a prevalence of about 12 % globally and contributes to around 40-50 % of the overall headache burden Chronic migraine affects 1-2 % of global population Most common severe primary headache disorder Second most disabling disease worldwide Frequently starts in childhood , particularly around puberty and affects women ↑ than men ( 3 : 1 female to male ratio ) Migraine is the most prevalent neurological disorder in men Affects people during the formative and most productive periods of their lives – between age 15-49 with a peak prevalence between ages 35-39 yrs Tends to run in families and as such is considered a genetic disorder- some estimates quote heritability to be as high as 50 % and with a likely polygenic multifactorial inheritance The more disabling the migraine ↑ likely there is to be familial connection

It is no more considered to be a disorder of blood vessels new evidence indicates that migraine represents a highly choreographed interaction between major inputs from both the peripheral and CNS with the trigeminovascular system and the cerebral cortex among the main players
 An attack of migraine can last from hours to days with 4 distinct phases
 24-48 hrs before the headache onset. These may include changes in mood and activity , irritability , fatigue , food cravings, repetitive yawning, stiff neck and phonophobia
 seen in about one third of patients with migraine. Aura can be positive ( added symptoms ) or negative ( loss of function ) and can manifest as visual , sensory or motor symptoms. These are fully reversible headache can be uni or bilateral and often described as throbbing or pulsatile accompanied by nausea , photophobia and phonophobia or both This phase has not been defined by ICHD-3 but studies indicate that its characteristic symptoms reflect those observed during premonitory phase

Disease burden -Second highest cause of years lost due to disability , interfering significantly with occupational , educational , household , family and social responsibilities Second highest contributor to neurological disease burden after stroke Unlike progressive neurological disorders like Parkinson’s disease and multiple sclerosis migraine does not lead to a permanent physical disability or sequelae It is believed that the burden of migraine is generally underestimated Economic cost $ 19.6 billion annually for US and 27 billion euros in EU and about £ 6 billion in UK alone Hence migraine is a public health problem of great impact on both the individual and society

Diagnosis -migraine without aura Headache has at least two of the following characteristics unilateral location pulsating quality ( ie varying with heartbeat ) moderate or severe pain intensity aggravation by or causing avoidance of routine physical activity
( eg walking or climbing stairs ) During headache at least one of the following
 nausea and / or vomiting photophobia and or phonophobia Not attributed to another disorder 
( history and examination do not suggest a secondary headache disorder or , if they do , it is ruled out by appropriate investigations or headache attacks do not occur for the 1st time in close temporal relation to the other disorder ) Migraine without aura is the commonest subtype of migraine

Assess severity and nature of attacks 
( consider using scale as MIDAS- available via
uploads/2015/01/MIDAS.pdf?7a7d37 )

○ Quality of attacks- intensity and site of pain , spread , associated symptoms
○ Timing and frequency
○ Possible causes- triggers , predisposing factors
○ Family history
○ Relieving factors
○ Ask about general health between attacks
○ If more than one type of headache is present
 Headache diary- for a minimum of 8 weeks
 Not always possible to identify- may be multiple
 Internal triggers include
○ menstrual cycle 
○ altered sleep patterns
○ stress
○ relaxation after stress ( weekend migraine )
 External triggers
○ specific food ( if happens within 6 hrs of intake and effect is easily reproducible )
○ strong smells
○ bright light
○ dehydration and missed meals or excessive heat
○ jet lag
○ strenuous exercise ( if not used to )
○ trauma ( particularly in children

Migraine without aura – Most common subtype – about 70-90 % people experience this type

Seen in about 25 % of people with migraine – aura can be positive or negative ( absence loss of function )

Migraine can be termed chronic if there are atleast 15 headaches days monthly including 8 migraine days per month for atleast 3 months. Chronic migraine is more debilitating and associated with increased headache related burden and greater psychiatric and medical comorbidities

A migraine with predominantly brainstem aura , initially thought to be due to spasm of basilar artery. Unknown aetiology. Aura symptoms can inlcude vertigo , dysarthria , diplopia , tinnitus , impaired hearing , lack of co-ordination , confusion and sometimes LOC

Rare subtype in which aura manifests as motor weakness ( unilateral weakness ) and may also include other forms of aura impairment in vision speech or sensation

Extremely rare subtype with repeated attacks of monocular visual disturbance , including scintillations , scotoma or blindness , associated with migraine headache

recurrent gastrointestinal disturbance 
○ cyclical vomiting syndrome
○ abdominal migraine benign paroxysmal vertigo benign paroxysmal torticollis


Follows trauma to head – look for symptoms suggestive of epidural or subdural haematoma Sudden with a rapid time to peak headache intensity
○ from a few seconds to 5 mins
○ suspect subarachnoid haemorrhage → arrange immediate admission Develops simultaneously with a sudden onset neurological impairment of
○ speech , sensation power or consciousness
○ impairment lasts > 1 hr → suspect TIA or CVA Associated 
○ fever
○ impaired consciousness
○ neck stiffness
○ photophobia Tenderness over temporal artery and 
person > 50 yrs age → Temporal arteritis Associated with features indicating
 ↑ risk of a space occupying lesion or idiopathic 
intracranial hypertension Severe unilateral eye pain
○ red eye
○ fixed and dilated pupils
○ hazy cornea
○ diminished vision Suspected Carbon Monoxide 
poisoning- exposure +
○ impaired consciousness
○ chest pain
○ wide range of neurological deficits


New headache with features of ↑ ICP as
○ papilledema ○ vomiting
○ posture related headache
○ headache waking them from sleep- think of
 ♦ SOL ♦ idiopathic intracranial hypertension New headache with focal neurological symptoms or
Non focal neurological symptoms as
○ blackout ○ change in personality
○ memory Unexplained headache that become progressively worse 
previous h/o cancer , HIV New onset of epileptic seizures


Status migrainosus- a debilitating migraine attack lasting more than 72 hours Persistent aura without infarction – aura symptoms persisting for 1 week without evidence of infarction on neuroimaging Migrainous infarction – one or more aura symptoms occurring in association with an ischaemic brain lesion in the appropriate territory demonstrated by neuroimaging , with onset during the course of a typical migraine with aura attack Migraine aura-triggered seizure – a seizure triggered by an attack of migraine with aura


  1. GBD 2016: still no improvement in the burden of migraine UweReuter The Lancet Neurology Volume 17, Issue 11, November 2018, Pages 929-930

  2. Monteith T.S. (2019) Chronic Migraine: Epidemiology, Mechanisms, and Treatment. In: Green M., Cowan R., Freitag F. (eds) Chronic Headache. Springer, Cham ( Abstract )
  3. Manack AN, Buse DC, Lipton RB. Chronic migraine: epidemiology and disease burden. Curr Pain Headache Rep. 2011;15(1):70-78. doi:10.1007/s11916-010-0157-z ( Abstract )
  4. Burch RC, Buse DC, Lipton RB. Migraine: Epidemiology, Burden, and Comorbidity. Neurol Clin. 2019;37(4):631-649. doi:10.1016/j.ncl.2019.06.001 ( Abstract )
  5. Bigal ME, Lipton RB. The epidemiology, burden, and comorbidities of migraine. Neurol Clin. 2009;27(2):321-334. doi:10.1016/j.ncl.2008.11.011 ( Abstract )
  6. Kadian R, Shankar Kikkeri N, Kumar A. Basilar Migraine. [Updated 2020 Apr 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  7. Kumar A, Samanta D, Emmady PD, et al. Hemiplegic Migraine. [Updated 2020 Apr 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  8. IHS Classification
  9. Peter J. GoadsbyPhilip R. HollandMargarida Martins-OliveiraJan HoffmannChristoph Schankin, and Simon Akerman Physiological Reviews 2017 97:2553-622
  10. Dodick, D.W. (2018), A Phase‐by‐Phase Review of Migraine Pathophysiology. Headache: The Journal of Head and Face Pain, 58: 4-16. doi:10.1111/head.13300
  11. Guidelines for All Healthcare Professionals in the Diagnosis and Management of Migraine , Tension Type Headache , Cluster Headache , Medication overuse Headache ; British Association for the Study of Headache 3rd Edition ( 1st revision ) 2010
  12. EFNS guideline on the drug treatment of migraine – revised report of an EFNS task force S Evers et al European Journal of Neurology 2009 , 16: 968-981
  13. IHS Classification ICHD – II accessed via
  14. Migraine : Multiple Processes , Complex Pathophysiology Rami Burstein , Rodrigo Noseda and David Borsook The Journal of Neuroscience 29 April 2015 , 35 (17 ) : 6619-6629 ; doi : 10 .1523/JNEUROSCI.0373-15.2015
  15. Shankar Kikkeri N, Nagalli S. Migraine with Aura. [Updated 2020 Jan 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  16. Pietrobon D, Moskowitz MA. Pathophysiology of migraine. Annu Rev Physiol. 2013;75:365-391. doi:10.1146/annurev-physiol-030212-183717


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