Migraine Flashcards
what is the definition of migrane?
Episodic migraine with or without aura or chronic migraine, featureful headaches, moderate to severe pain, >4 hours without treatment
Migraine without aura:
A. 5 attacks fulfilling B-D
B. Attacks last 4-72 hours
C. Two of the following, Unilateral, Pulsing, Moderate/severe, Aggravation by routine physical activity
D. During headache at least one of, Nausea and /or vomiting, Photophobia and phonophobia
E. Not attributed to another disorder
Aura:
Visual- Fortification Spectra, usually followed by a headache
what is the epidemiology of migraine?
Early to mid life presentation
Very common
what is the aetiology of migrane?
Genetic component
Exacerbating factors
what are the risk factors for migraine?
Family history Female Obese Stress Medication overuse Sleep disorders
what is the pathophysiology of migraine?
The headache of migraine results from neurogenic inflammation of first-division trigeminal sensory neurons that innervate the large vessels and meninges of the brain. This causes a change in the way that pain is processed by the brain. Increased neuronal activity can be demonstrated in areas of the brainstem during migraine, and this persists even when the headache is relieved by triptans. It is not known whether this brainstem activation reflects the cause of migraine (the so-called brainstem generator) or signifies activation of endogenous pain-control systems.
When activated, the trigeminal neurons release substances that cause dilation of meningeal blood vessels, leakage of plasma proteins into surrounding tissue, and platelet activation. Peptides including calcitonin gene-related peptide, substance P, and bradykinin are released, resulting in sensitisation of peripheral nociceptors. This peripheral sensitisation results in increased nociceptive inputs into the trigeminal sensory nucleus, and ultimately in central sensitisation, so that non-painful stimuli (for example, light touch) are interpreted as pain.
Aura:
Aura is caused by neuronal dysfunction. A wave of neuronal excitation spreads anteriorly in the cortex, at a rate of 3-5 mm/minute (which correlates temporally with the reported rate of change in visual symptoms). This is followed by a prolonged period of decreased neuronal activity, and finally neuronal recovery. Cortical depression causes release of excitatory amino acids and other mediators of excitation, resulting in activation of nociceptors in adjacent dura and blood vessels, leading in turn to activation of the trigeminal sensory nucleus. How these neurons are triggered in migraine without aura is unknown, but one hypothesis is that cortical spreading depression in migraine without aura occurs in ‘silent’ areas of the brain that do not produce recognisable symptoms of aura.
what are the key features of migraine?
Risk factors Prolonged headaches Nausea Decreased ability to function Headache worse with activity Sensitivity to light Noise sensitivity, aura
what are the signs of migraine?
risk factors
what are the symptoms of migraine?
Prolonged headaches Nausea Decreased ability to function Headache worse with activity Sensitivity to light Noise sensitivity, aura
how is migraine diagnosed?
clinically
what are the differential diagnoses for migraine?
Tension
Cluster
Medication overdose
how are migraines managed?
Offer combination therapy for acute treatment of migraine with:
– an oral triptan and an NSAID, or
– an oral triptan and paracetamol
• For people who prefer only one drug, consider monotherapy with oral triptan, NSAID, aspirin (900 mg) or paracetamol for the acute treatment of migraine
• Consider an anti-emetic in addition to other acute treatment for migraine even in the absence of nausea and vomiting
• Do not offer ergots or opioids for acute treatment of migraine.
Preventative:
• Offer topiramate or propranolol
• If both Topiramate and propranolol are unsuitable or ineffective, consider:
– a course of up to 10 sessions of acupuncture over 5–8 weeks or
– gabapentin (up to 1200 mg per day) > now Amitriptyline instead
• For people who are already having treatment with preventive such as amitriptyline, and whose migraine is well controlled, continue the current treatment as required
• Advise people with migraine riboflavin (400mg once a day) may be effective
• Botulinum toxin type A is recommended for the prophylaxis of chronic migraine:
– if not responded to at least three prior pharmacological prophylaxis therapies and
– whose condition is appropriately managed for medication overuse
how is migraine monitored?
Patients with migraine should be monitored regularly to assess disability and treatment needs, which may vary over time. It is helpful to ask patients to keep a headache diary or calendar to assess triggers, headache frequency and characteristics, other symptoms, and medication use (including effectiveness)
what are the complications of migraine?
Pregnancy complications
Status migrainosus
Migrainous infarction
what is the prognosis for migraine?
Most patients with episodic migraine do well with treatment. In population-based surveys the frequency of migraine headaches decreases with age.
