Approach to Headache Flashcards

1
Q

How common is migraine?

A

20% of women

5-10% of men

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2
Q

What is migraine?

A

Idiopathic headache syndrome (genetic)

May be preceded by aura but over 2/3 are not

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3
Q

What is the typical presentation of migraine?

A

Recurrent, episodic headache

Really bad pain (moderate to severe, building over minutes)

Unilateral

Pulsating

Aggravated by exercise

+ one or both of N+V, and photo- or phono-phobia

Sometimes accompanied by vertigo

Patient just “doesn’t feel right” (distracted, confused, irritable)

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4
Q

What changes of brain activity occur during migraine aura?

A

Slowly spreading wave of reduced activity (cortical spreading depression of Leao; measured in cm/min)

Probably glial rather than neuronal

Often with occipital onset

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5
Q

What visual disturbances are often reported with migraine aura?

A

Scintillating scotoma

Monochromatic patterns (e.g. wavy lines, fortification spectra, water effects)

Creeping hemi or quandrantanopia

Monocular changes rare (but retinal migraine does exist)

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6
Q

What kinds of phenomena can be seen with a migraine aura?

A

Visual

Sensory (e.g. parasthesia)

Motor (e.g. weakness)

Speech centre (e.g. dysphasia)

Brainstem (e.g. in basilar migraine)

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7
Q

What causes headache in migraine?

A

Much less clear

Trigeminal pain (meningeal and facial innervation, serotonin receptors involved)

Almost certainly a brainstem event, but there are secondary meningeal vessel changes, and pain amplification occurs in scalp and head (allodynia; this feedback loop can be broken by botullinum toxin)

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8
Q

Describe the typical presentation of tension-type headache

A

Mild to moderate

Band-like: bilateral, pressing

Not associated with exercise induction, N+V, photo- or phono-phobia

I.e. a “normal headache”

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9
Q

What is chronic daily headache? What are the different types?

A

Headache on most days, most of the day

Chronic migraine (evolves from migraine without aura) or chronic tension-type (individually mild headaches but persistence distressing)

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10
Q

What can make a headache chronic?

A

Bad luck: severe migraine, chronic daily headache as a primary headache

Bad treatment: medication overuse headache

Bad neck: cervicogenic

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11
Q

What medications can cause chronic headache?

A

Opiates

Triptans

Ergots

Possibly paracetamol but probably not NSAIDs

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12
Q

Describe the typical pattern of medication overuse headache

A

More than 10 days a month (twice a week)

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13
Q

What is the mechanism of medication overuse headache?

A

Chronic changes rather than just tolerance; upregulation of pain receptors

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14
Q

Mx of medication overuse headache

A

Medication withdrawal (but have withdrawal headaches for weeks; however patients are often surprisingly compliant with stopping medication)

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15
Q

What clinical feature may accompany a cervicogenic headache?

A

Muscular neck pain (nearly ubiquitous)

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16
Q

What features may accompany the thunderclap headache characteristic of SAH?

A

May have neurological Sx/signs, e.g. weakness/sensory loss, impairment of consciousness (common; depth of coma marks prognosis)

Photo- or phono-phobia

N+V

Can be unilateral headache (headache is meningeal)

17
Q
A
18
Q

How can SAH be distinguished from migraine?

A

Onset is extremely abrupt in SAH

19
Q

DDx for primary thunderclap headache

A

SAH

Sexual and exertional headaches

Vasospastic headache

Primary thunderclap headache (although not well-described entity)

20
Q

Dx of SAH

A

Plain CT

Lumbar puncture if CT normal but there is a good story (will be more accurate once xanthochromia develops)

21
Q

Signs/Sx of raised ICP

A

Diffuse headache, variable in severity but often progressive

Prominent nausea

Papilloedema (peripheral visual loss or transient blindness)

Diplopia (CNVI palsy)

Worsening of Sx with increases in ICP (e.g. valsalva - cough or straining, morning headache) and better with reduced ICP (e.g. when standing)

May also have Sx of underlying lesion

22
Q

26 year old woman with transient, objective L sided weakness and sensory disturbance makes acute presentation to ED, but her sensory and motor Sx then fully resolved

DDx?

A

Migraine aura (high prior probability)

TIA

Focal seizure

Hypoglycaemia

Vasospastic headache

Functional eurological disorder

Others: non-seizure tumour Sx, periodic paralysis, paroxysmal dyskinesia, mitochondrial disorder, etc

23
Q

Does EEG diagnose seizure?

A

No, just predicts recurrence (sometimes)

24
Q

Distinguish between migraine, TIA and focal seizure in terms of the typical pattern of involvement

A

Migraine: cortical, brainstem

TIA: cortical, brainstem

Focal seizure: cortical, mesial temporal (invokes memory phenomena)

25
Q

Distinguish between migraine, TIA and focal seizure in terms of the typical onset

A

Migraine: acute with sensorimotor march over minutes

TIA: acute, immediate

Focal seizure: acute with sensorimotor march over seconds

26
Q

Distinguish between migraine, TIA and focal seizure in terms of the typical offset

A

Migraine: gradual, often stepwise, intermixed with new Sx

TIA: gradual

Focal seizure: distinct (Todd’s paresis)

27
Q

Todd’s paresis

A

Focal weakness in a part of the body after a seizure

28
Q

Distinguish between migraine, TIA and focal seizure in terms of the typical Sx character

A

Migraine: often active parasthesia, weakness usually varies

TIA: usually negative Sx (e.g. weakness, numbness)

Focal seizure: often active parasthesia, clonus or dystonia prior to weakness

29
Q

Outline some distinguishing clinical features of migraine, TIA and focal seizure

A

Migraine: N+V, headache (may be mild with fronto-parietal aura), photo- or phono-phobia, more likely in young

TIA: CV Hx (CV RFs, PHx of MI/stroke/PVD), very common in those >65

Focal seizure: dyscognitive phase, previous stereotyped events