Nervous system


Episodic throbbing disabling headache usually associated with nausea and of > 6 months duration with normal neurological examination. 


International Headache Society (IHS) classification of primary headaches:

  • Migraine
  • Tension headache
  • Trigeminal autonomic cephalalgias (of which cluster headache is the most prominent variety)
  • Group 4 “other primary headache disorders”: Consists of 10 rare headache syndromes with well-established primary nature
    • Benign exertional headaches
    • Primary stabbing headaches (“jabs and jolts syndrome”)
Primary headache disorders. | Lee, V., Ang, L. L., Soon, D., Ong, J., & Loh, V. (2018). The adult patient with headache. Singapore medical journal, 59(8), 399–406. doi:10.11622/smedj.2018094


Episodic throbbing disabling headache usually associated with nausea and of > 6 months duration with normal neurological examination. 
  • Episodic migraine (EM): Distinguished by recurrent, slowly developing attacks with lateralized and reversible visual, sensory, speech/language, motor, brainstem, or retinal symptoms; attacks are accompanied or followed by headache and migraine symptoms
    • Migraine without aura (common migraine) (M/C, 80%)
    • Migraine with aura (classical migraine)
  • Chronic migraine (CM): Migraines experienced ≥ 15 days/month
Distinguishing features of episodic migraine (EM) and chronic migraine (CM) | Moriarty, M., & Mallick-Searle, T. (2016). Diagnosis and treatment for chronic migraine. The Nurse practitioner, 41(6), 18–32. doi:10.1097/01.NPR.0000483078.55590.b3

Rare variants:

  • Ophthalmoplegic migraine: Transient unilateral CN III palsy (reversible) → ptosis
  • Basilar type migraine: Transient posterior cerebellar symptoms (reversible
    • Ataxia, tinnitus, diplopia, vertigo
  • Hemiplegic migraine: Transient hemiplegia (reversible)
  • Familial hemiplegic migraine (seen in children)
  • Retinal migraine: Transient monocular visual loss


Trigeminovascular complex (centre for pain in migraine):

Pathophysiology of migraine: The trigeminovascular input from the meningeal vessels passes through the trigeminal ganglion and synapses in the trigeminocervical complex. The peripheral release of molecules results in vasodilation, plasma leakage and mast cell degranulation within the dura mater, while central release can cause activation of second-order neurons leading to the pain of migraine attacks. Trigeminal activation can mediate parasympathetic responses via the pterygopalatine ganglion. | Goadsby PJ, Lipton RB, Ferrari MD. Migraine—current understanding and treatment. N Engl J Med. 2002; 346:257–70. [PubMed: 11807151]

Pathogenic hypothesis:

  • Vascular theory:
    • Intracerebral blood vessel vasoconstriction
    • Intracranial/extracranial blood vessel vasodilation
  • Serotonin theory:
    • ↓ Serotonin

Aura phenomenon:

The Calgary Guide |
  • Cortical spreading depression: Propagating wave of depolarization followed by neural suppression
Animation of the cortical spreading depression | By User:S. JähnichenBrain_bulbar_region.svg: Image:Brain human sagittal section.svg by Patrick J. Lynch; Image:Brain bulbar region.PNG by DO11.10; present image by Fvasconcellos. – Brain_bulbar_region.svg, CC BY 2.5,


Prodrome (60% cases):

  • Onset: 2 hours-2 days before aura or pain
  • Symptoms:
    • Altered mood, irritability, depression/euphoria
    • Fatigue
    • Craving for certain foods
    • Stiff muscles (especially neck)
    • Constipation/diarrhoea
    • Sensitivity to smells/noise

Aura: Only in classical migraine

Transient focal neurological phenomenon that occurs before or during the headache.
  • Visual aura (M/C) > Auditory > Sensory
    • Visual aura: Zigzag lines (fortification spectra), scintillating scotomas
  • Onset≤ 60 minutes before headache


  • Increase in frequency & severity over time
  • Localization:
    • Unilateral → holocranial
    • Frontotemporal > orbital
  • Throbbing/pounding quality
  • Duration: 4-72 hr
  • Associated conditions:
    • Nausea, vomiting
    • Photophobia/phonophobia/osmophobia (patient prefers dark, quiet room)


Stepped care across migraine attacks
Stepped care across migraine attacks: Preventive therapy, in addition, may be indicated at any stage. In general, initiation of preventive therapy is indicated in patients who are adversely affected on ≥2 days per month despite acute treatment optimized according to the stepped care approach. | NSAID, non-steroidal anti-inflammatory drug. | Eigenbrodt, A.K., Ashina, H., Khan, S. et al. Diagnosis and management of migraine in ten steps. Nat Rev Neurol 17, 501–514 (2021).

Acute migraine:

  • Analgesics or NSAIDs (mild attacks)
  • Triptans (5HT 1B/1D agnoists) (moderate-to-severe attacks)
    • Constrict blood vessels and block pain pathways in the brain
    • M/effective: Rizatriptan, Eletriptan
    • Others: Sumatriptan, Zolmitriptan
  • Ergot alkaloids (if triptans ineffective)
    • Dihydroergotamine
  • Opiates (severe cases)

Preventive medications:

  • 1st line: Propranolol. tricyclic antidepressants (TCA), topiramate
  • 2nd line: Telmisartan, venlafaxine, valproate
  • 3rd line: Pizotifen (5-HT 2C agonist), flunarizine (CCB), clonidine

Novel treatments:

  • Monoclonal antibody: Erenumab (CGRP antagonist)
  • Greater occipital nerve block
  • Onabotulinum toxin A
  • Supraorbital transcutaneous stimulation
Ten-step approach to the diagnosis and management of migraine.
Ten-step approach to the diagnosis and management of migraine | CGRP, calcitonin gene-related peptide; MOH, medication overuse headache; NSAID, non-steroidal anti-inflammatory drug. aSodium valproate is absolutely contraindicated in women of childbearing potential. bCGRP monoclonal antibodies target CGRP or its receptor. | Eigenbrodt, A.K., Ashina, H., Khan, S. et al. Diagnosis and management of migraine in ten steps. Nat Rev Neurol 17, 501–514 (2021).

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