Migraine and other headaches Flashcards

1
Q

What is a migraine

A

Recurrent headache for 4-72hrs with visual and/or GI disturbance

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2
Q

Aetiology of migraine (as well as precipitants)

A

Genetic and environmental factors.

Precipitants: chocolate, cheese and too much/little sleep.

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3
Q

Pathophysiology of migraine

A

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

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4
Q

Types of migraines

A

Aura
Without aura
Variant

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5
Q

Clinical presentation of aura

A
Characteristically unilateral. 
Visual disturbance (zig zaggy lines). 
Photosensitivity. 
Nausea. 
Sometimes premonitory symptoms.
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6
Q

Clinical presentation of migraine without aura

A

Characteristically unilateral.
Photosensitivity.
Nausea.
Sometimes premonitory symptoms.

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7
Q

Clinical presentation of variant migraine

A

Unilateral motor or sensory symptoms resembling a stroke

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8
Q

What is aura

A

Cortical spreading depression

A self propogating wave of neuronal and glial depolarisation that spreads across the cortex

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9
Q

Epidemiology of migraine

A

More in women

Usually presents before 40

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10
Q

Diagnosis of migraine

A
Clinical
Exclude other causes:
Lab tests (CRP and ESR)
Lumbar puncture at times
Neuroimaging: Rule out mass lesions
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11
Q

Treatment of migraine

A

Passes in sleep
Painkillers: Paracetamol / NSAIDs
In severe: Triptans (serotonin agonsts)

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12
Q

Alternate definition of migraine

A

Recurrent throbbing headache often preceded by an aura and associated
with nausea, vomiting and visual changes

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13
Q

Special effects on body from a migraine aura

A

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

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14
Q

Aetiology of migraine

A

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

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15
Q

Risk factors of migraine

A

Strong genetic component thus family history
Female
Age - can occur at any age but majority have first migraine in adolescence

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16
Q

Pathophysiology of migraine

A
  • 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
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17
Q

Clinical presentation of migraine without aura

A

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)

18
Q

How long do migraines last

A

4-72 hours

19
Q

Clinical presentation of migraine with aura

A

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

20
Q

General migraine features

A
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
21
Q

what is aura

A

Cortical spreading depression is a self propogating wave of neuronal and glial depolarisation that spreads across the cortex

22
Q

Indications for neuro-imaging (CT/MRI)

A
  • Worst/severe headache - thunderclap headache - SAH
  • Change in pattern of migraine
  • Abnormal neurological exam
  • Onset >50yrs
  • Epilepsy
  • Posteriorly located headache
23
Q

Prevention of migraine

A

• 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

24
Q

What type of headache are the most chronic daily and recurrent

A

Tension headaches

25
Q

Epidemiology of Tension headaches

A

Commonest primary headache
Can be episodic or chronic
No organic cause

26
Q

What is meant by tension headaches being episodic or chronic

A
Episodic = <15 days/month
Chronic = >15 days/month for at least 3 months
27
Q

Aetiology/risk factors of tension headaches

A
Stress
Sleep deprivation
Bad posture
Hunger
Eyestrain
Anxiety
Noise
28
Q

Clinical presentation of tension headache

A
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)
29
Q

Differential diagnosis of tension headache

A

Migraine, cluster headache, giant cell arteritis, drug-induced headache

30
Q

Diagnosis of tension headache

A

Clinical from history

31
Q

Treatment of tension headache

A

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

32
Q

Describe medication overuse headaches

A
  • 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
33
Q

What headache is the most disabling of the primary headache disorders

A

Cluster headache

34
Q

Epidemiology of cluster headache

A
  • Distinct from migraine
  • Much rarer than migraine (1 per 1000)
  • MALES > females
  • Affects adults, typically between 20-40 yrs - Commoner in smokers
35
Q

Risk factors of cluster headache

A

Smoker
Male
Autosomal dominant gene has a role

36
Q

Diagnosis of cluster headache

A

Differential diagnosis = migraine
Diagnosis:
Clinical
At least 5 headache attacks fulfilling the above criteria

37
Q

Clinical presentation of cluster headache

A

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

38
Q

Ipsilateral cranial autonomic features of cluster headache

A

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

39
Q

Cluster headache - episodic vs chronic

A

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

40
Q

Treatment of acute attack of cluster headache

A

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)

41
Q

Prevention of cluster headache

A

**Calcium channel blocker e.g. VERAPAMIL is first line prophylaxis
Avoid alcohol during cluster period
Corticosteroids e.g. PREDNISOLONE may help during cluster