Session 9: Headaches Flashcards by Don J

Types of headache.

Primary

Secondary

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How do primary and secondary headaches usually differ?

Primary are usually more gradual and also chronic

Secondary tend to have an acute onset and also life/sight-threatening

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Give examples of primary headache disorders.

Tension headache

Migraine

Cluster headache

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Give life-threatening secondary headaches.

SAH

Subdural haemorrhage

Extradural haemorrhage

Venous sinus thrombosis

Meningitis, encephalitis, abscess

Space occupying lesion such as a tumour

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Give sight-threatening secondary headaches

Closed angle glaucoma

Temporal / Giant cell arteritis

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Give other causes of secondary headaches

Drug side effects such as from coffee, analgesics, vasodilators.

Hypertension

Pre-eclampsia

Phaeochromocytoma

Medication over-use

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How will clinical examination differ between primary and secondary headaches.

Primary will usually have normal clinical examination

Secondary usually not

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Explain the process of history taking of headaches.

SQITARS

PMH with previous headaches, or conditions that can cause secondary headaches.

Drug history of analgesics or other medicaiton that can cause headache.

FH of migraines

Social history with difficulty sleeping? alcohol/caffeine? diet? triggers? Dehydration?

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Give a common drug that can cause headaches.

CCBs

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Red flags of headaches.

SNOOP

Systemic signs and disorders such as meningitis, HIV, pregnancy

Neurologic smpyomts due to SOL, intracranial haemorrhage or glaucoma

Onset new or changed and patient is over 50 - malignancy or giant cell arteritis

Onset in thunderclap presentation (SAH)

Papilloedema etc… - raised ICP

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Clinical examination of headaches.

Temperature

Neurological examination

CVS if needed

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Why is blood pressure and pulse rate measured in headaches?

Raised ICP can cause bradycardia and hypotension

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Rank primary headache disorders from most common to least.

Tension-type headaches

Migraines

Cluster headaches

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Pathophysiology of tension-type headache.

Thought to be due to tension in muscles of head and neck.

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Epidemiology of tension-type headaches.

F>M

Young onset (20-39 y/o)

First onset after >50 y/o is uncommon

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Explain the pain of TTH

Generalised usually in frontal and occipital region

Tight/band like radiating to neck

Mild-moderate intensity where patient can carry out tasks that they are doing

Worse at the ned of the day (may be cortisol related)

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Aggravating and relieving factors of TTH.

Stress, poor posture and lack of sleep

Often responds to simple analgesics.

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Associated symptoms and clinical examination findings.

Can be slightly nauseous

Should not find anything on clinical examination

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Epidemiology of migraines.

F>M

Common

Presents early-mid life

Most have first attack by 30

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Pathophysiology of migraines.

Vasodilation of meningeal blood vessels is a possible theory.

Explain the pain of migraines.

Unilateral, usually temporal or frontal.

Throbbing and pulsating

Moderate-severe and often disabling

Prolonged headaches (4-72 hours)

Triggers and relieving factors of migraines.

Certain food (cheese and chocolate)

Menstrual cycle

Stress

Lack of sleep

Usually simple analgesics is enough. May need triptans.

Can usually go lie in a dark room.

Associated symptoms and clinical examination findings.

Nausea

Vomiting

Aura

Photophobia

Phonophobia

Usually clinical exam is normal.

What is aura?

The signs/feeling before the onset of a migraine

What is medication over-use headache?

More common in women than men. A headache that present on at least **15 days/month** It occurs in patients with **pre-existing headache disorders** where they have been using regular analgesics at least **10 days/month** to try to relieve it. However the headache is not responding to medication anymore and has even gotten worse.

Common co-morbidities of medication over-use headaches.

Depression Sleep disturbances

Treatment of medication over-use headaches.

Discontinue medication. This will cause the headache to worsen before it gets better. Can take up to 2 months to resolve. This makes doctors struggle with adherence of patients.

Pathophysiology of medication over-use headaches.

Upregulation of pain receptors in meninges.

Epidemiology of cluster headaches.

M \> F 1/1000 Usually begins at 30-40 years of age.

Explain the pain of cluster headaches.

**Unilateral** and around or behind one eye. It is a **sharp, stabbing and penetrating pain** It goes on for 15 min to 3 hours and occur in **clusters** with periods of remission (3m-3y)

Triggers and relieving factors of cluster headaches.

Alcohol Cigarettes Volatile smells Warm temp Lack of sleep Usually simple analgesics is ineffective so can give **high flow oxygen** and **triptans**.

Associated symptoms and clinical examination findings.

Can give **ipsilateral** autonomic (decreased symp) symptoms such as ptosis, red and watery eyes, blocked runny nose. Clinical examination will show autonomic features.

Explain the pain of space-occupying lesion.

**Gradual and progressive** (gets worse) Usually described as **dull** Mild in severity and worse in the mornings. Usually worse early mornings and on waking.

Why is SOL headaches worse in the morning?

Due to higher ICP in the morning.

Aggravating and relieving factors of SOL headaches.

Worsened with posture (**leaning forwards**) Cough Valsalva manoeuvre (**essentially anything raising ICP**) Simple analgesics can help early on.

Associated symptoms of SOL headaches.

Nausea Vomiting Focal neurological or visual symptoms Can also have behavioural and personality changes.

Clinical examination findings of SOL headaches.

Focal unilateral neurological signs Papilloedema

Epidemiology of trigeminal neuralgia.

F\>M 25/100000 50-60 years of age

Pathophysiology of trigeminal neuralgia

Compression of CN V due to loop of a blood vessel. 5% is due to a tumour or skull base abnormalities or AV malformations.

Explain the pain of TN.

**Unilateral** Pain felt in 1 or more division of CN V. Sharp, stabbing and often described as an electric shock. Lasts few seconds to a few minutes but **severe** **Sudden onset**

Triggers and relieving factors.

Light touch to face/scalp, eating, cold wind, combing hair SImple analgesics are not effective so can be hard to treat.

Associated symptoms and clinical examination findings.

Preceding symptoms such as tingling, numbness and pain that can radiate to areas within CN V distribution. Clinical examination is normal

What is temporal/giant cell arteritis?

Vasculitis involving small and medium sized arteries of head.

Epidemiology of temporal arteritis.

F\>M \> 50 years and even most common in \>75 years **Consider this a diagnosis in any \>50 y/o with abrupt onset of headache + visual disturbance or jaw claudication.**

Which artery is commonly involved in temporal arteritis (most often seen)?

Superficial temporal artery

Risks of temporal arteritis.

Risk of irreversible loss of vision due to ischaemia of CN II (opthalmic artery involved)

Symptoms of giant cell arteritis.

Headache Jaw claudication Scalp tenderness Loss of vision Claducation of extremities Fever, night sweats and weight loss Myalgia

Investigations of headaches.

Investigate accordingly if suspect haemorrhage Headache diary for chronic headaches Imaging