Migraine and other headaches Flashcards
What is a migraine
Recurrent headache for 4-72hrs with visual and/or GI disturbance
Aetiology of migraine (as well as precipitants)
Genetic and environmental factors.
Precipitants: chocolate, cheese and too much/little sleep.
Pathophysiology of migraine
Changes in brainstem blood flow
-> unstable trigeminal nerve nucleus and nuclei in the basal thalamus
-> release of vasoactive neuropeptides (CGRP and substance P)
-> neurogenic inflammation; vasodilatation and plasma protein extravasation.
Aura: Cortical spreading depression is a self propogating wave of neuronal and glial depolarisation that spreads across the cortex
Types of migraines
Aura
Without aura
Variant
Clinical presentation of aura
Characteristically unilateral. Visual disturbance (zig zaggy lines). Photosensitivity. Nausea. Sometimes premonitory symptoms.
Clinical presentation of migraine without aura
Characteristically unilateral.
Photosensitivity.
Nausea.
Sometimes premonitory symptoms.
Clinical presentation of variant migraine
Unilateral motor or sensory symptoms resembling a stroke
What is aura
Cortical spreading depression
A self propogating wave of neuronal and glial depolarisation that spreads across the cortex
Epidemiology of migraine
More in women
Usually presents before 40
Diagnosis of migraine
Clinical Exclude other causes: Lab tests (CRP and ESR) Lumbar puncture at times Neuroimaging: Rule out mass lesions
Treatment of migraine
Passes in sleep
Painkillers: Paracetamol / NSAIDs
In severe: Triptans (serotonin agonsts)
Alternate definition of migraine
Recurrent throbbing headache often preceded by an aura and associated
with nausea, vomiting and visual changes
Special effects on body from a migraine aura
A migraine aura may affect the patients eyesight with visual phenomena such as fortification spectra (zig-zag lines), shimmering or scotomas (black holes in visual field), but may also result in pins and needles (tingling), dysphasia and rarely weakness of limbs and motor function
Aetiology of migraine
CHOCOLATE
- Chocolate
- Hangovers
- Orgasms
- Cheese
- Oral contraceptives
- Lie-ins
- Alcohol
- Tumult - loud noise
- Exercise
Also chemical imbalance may be present or changes in the brainstem and its interactions with the trigeminal nerve
Risk factors of migraine
Strong genetic component thus family history
Female
Age - can occur at any age but majority have first migraine in adolescence
Pathophysiology of migraine
- Changes in brainstem blood flow lead to an unstable trigeminal nerve nucleus and nuclei in the basal thalamus
- Cortical spreading depression - self-propagating wave of neuronal and glial depolarisation that spreads across the cerebral cortex is thought to cause the aura of migraine and leads to the release of inflammatory mediators which impact on the trigeminal nerve nucleus
- This results in release of vasoactive neuropeptides including calcitonin-gene- related peptide (CGRP) and substance P; this then results in the process of neurogenic inflammation - vasodilation and plasma protein extravasation - leading to pain that propagates all over the cerebral cortex
Clinical presentation of migraine without aura
2 of following:
Unilateral; Pulsing; Moderate/severe pain in head; Aggravated by routine physical activity
During headache at least 1 of:
Nausea and/or vomiting
Photophobia or sound sensitive
(not attributable to another disorder)
How long do migraines last
4-72 hours
Clinical presentation of migraine with aura
At least 2 attacks
Unliateral, pulsatile headache
Aura precedes the attack by minutes and may persist during it:
Visual - chaotic cascading, jumbling, distorting lines, dots or zigzags; Scotoma (black hole in visual field); Hemianopia
Somatosensory - Paraesthesiae (pins and needles) spreading from fingers to face
General migraine features
At least 2 of: - Unilateral pain - Throbbing-type pain - Moderate to severe intensity - Motion sensitivity (headache made worse with head movement of physical activity • At least 1 of: - Nausea/vomiting - Photophobia/phonophobia - Normal examination with no other attributable cause
what is aura
Cortical spreading depression is a self propogating wave of neuronal and glial depolarisation that spreads across the cortex
Indications for neuro-imaging (CT/MRI)
- Worst/severe headache - thunderclap headache - SAH
- Change in pattern of migraine
- Abnormal neurological exam
- Onset >50yrs
- Epilepsy
- Posteriorly located headache
Prevention of migraine
• If more than 2 attacks a month, or acute treatment required more than
2x a week
• Beta blocker e.g. PROPRANOLOL (not for asthmatics)
• Tricyclic anti-depressant e.g. AMITRIPTYLINE , S/E; drowsiness, dry mouth and reduced vision
• Anti-convulsant e.g. TOPIRAMATE, S/E; reduced memory
What type of headache are the most chronic daily and recurrent
Tension headaches
Epidemiology of Tension headaches
Commonest primary headache
Can be episodic or chronic
No organic cause
What is meant by tension headaches being episodic or chronic
Episodic = <15 days/month Chronic = >15 days/month for at least 3 months
Aetiology/risk factors of tension headaches
Stress Sleep deprivation Bad posture Hunger Eyestrain Anxiety Noise
Clinical presentation of tension headache
Usually has one of the following: • Bilateral • Pressing/tight non-pulsatile • Mild/moderate intensity • +/- scalp muscle tenderness Without vomiting or sensitivity to head movement, no aura Not aggravated by physical activity Tight band-like sensation Pressure behind eyes, mild-moderate pain Headaches can last from 30 mins to 7 days (Not attributed to other disorder)
Differential diagnosis of tension headache
Migraine, cluster headache, giant cell arteritis, drug-induced headache
Diagnosis of tension headache
Clinical from history
Treatment of tension headache
Reassurance and lifestyle advice e.g. regular exercise, avoidance of triggers
Stress relief e.g massage or acupuncture
Symptomatic treatment for episodes occurring >2 days a week:
• ASPIRIN
• PARCETAMOL
• NSAIDs e.g. IBUPROFEN
*NO OPIOIDS
Describe medication overuse headaches
- Worsens whilst on regular analgesia especially on OPIOIDS
- Other causes are mixed analgesics e.g. paracetamol + codeine/opiates,
ergotamine and triptans - Common reason for episodic headache becoming chronic daily headache
What headache is the most disabling of the primary headache disorders
Cluster headache
Epidemiology of cluster headache
- Distinct from migraine
- Much rarer than migraine (1 per 1000)
- MALES > females
- Affects adults, typically between 20-40 yrs - Commoner in smokers
Risk factors of cluster headache
Smoker
Male
Autosomal dominant gene has a role
Diagnosis of cluster headache
Differential diagnosis = migraine
Diagnosis:
Clinical
At least 5 headache attacks fulfilling the above criteria
Clinical presentation of cluster headache
Rapid onset of EXCRUCIATING pain AROUND ONE EYE, TEMPLE or FOREHAND
Pain is unilateral
Rises to crescendo over minutes and lasts 15-60 mins (1 or 2 a day usually at the same time)
Often nocturnal/early morning (wakes people)
Sometime vomiting
Episodic or chronic
Ipsilateral cranial autonomic features of cluster headache
Eye may become watery and bloodshot with lid swelling, lacrimation,
Facial flushing
Rhinorrhea (blocked nose)
Miosis (excessive pupil constriction) +/- ptosis (drooping or falling of upper eyelid) - seen in 20% of attacks
Cluster headache - episodic vs chronic
Episodic - clusters last 4-12 weeks and are followed by pain-free periods of months or even 1-2 yrs before the next cluster
Chronic - attacks for >1 year without remission
Treatment of acute attack of cluster headache
No analgesics
100% 15L O2 for 15mins via non-rebreathable mask (not if COPD)
Triptan (selective serotonin (5HT) agonist) e.g. SC SUMATRIPTAN:
(Triptans are serotonin receptor agonists - this reduces vascular inflammation)
Prevention of cluster headache
**Calcium channel blocker e.g. VERAPAMIL is first line prophylaxis
Avoid alcohol during cluster period
Corticosteroids e.g. PREDNISOLONE may help during cluster
