Headache

Question 1

Why do headaches occur?

Answer 1

in response to activation of pain receptors located around Extracranial and
Intracranial vessels, Meninges; Can also occur due to pain receptors on Scalp, Neck and Facial
Muscles, Paranasal Sinuses, Eyes and Teeth

Question 2

Causes of secondary headaches

Answer 2

Raised ICP
Infections
GCA
Intracranial haemorrhages 
Low CSF volume 
Post traumatic headache
Acute glaucoma

Question 3

Concerning presentations of headache

Answer 3

New onset severe headache without previous history especially in 50_+
Need to exclude secondary headache

Question 4

What should be included in a headache history

Answer 4

SOCRATES, Autonomic symptoms, Headache pattern and frequency, Duration, Pattern of Analgesia use, Family History

Question 5

Red flag symptoms

Answer 5

Fever, Sudden onset <1 minute, Features of raised ICP, Jaw Claudication

Question 6

What examinations should be done in headaches?

Answer 6

Fundoscopy for Papilloedema; Temporal Arteries palpated for Pulselessness and Tenderness;
Examination usually normal in Primary disorders

Question 7

When should neuroimaging be used in headache investigation?

Answer 7

Neuroimaging only if indication of underlying secondary cause; Older patients with red flag
symptoms require CT Head; ESR for Giant Cell Arteritis

Question 8

Migraine: What is it

Answer 8

Commonest cause of Episodic headache (Females 2×); Most diagnosed before middle age
• Associated with sensory sensitivity e.g. Light, Sound, Movement; May be associated with
Nausea and Vomiting; Spectrum of severity;
• Usually greatly affects the individual; May transform into a chronic daily headache

Question 9

Aetiology behind migraines: Genetic factors

Answer 9

Genetic factors leading to neuronal hypersensitivity;
Sodium and Potassium channels have been implicated;
thought to be a neurogenic rather than vascular basis

Question 10

Aetiology of Aura

Answer 10

Aura thought to be due to spreading of Cortical
depression – Wave of depolarisation followed by
depressed activity spreading from Occipital to Frontal

Question 11

Aetiology behind migraines: Trigeminovascular system

Answer 11

Innervation of large
intracranial vessels and dura by Ophthalmic branch of
Trigeminal; Activation of Trigeminal pain neurones resulting in pain
o Release of Vasoactive peptides including Calcitonin Gene-Related Peptide (CGRP) and
Serotonin (5-HT) by activated; Meningeal inflammation and Vasodilation as a result
o Peripheral and Central Sensitisation occurs – Innocuous stimuli becomes perceived out of proportion

Question 12

Presentation of Migraines

Answer 12

Starts around puberty; Increasing prevalence into adulthood; Scalp might be tender to touch
during episodes (Allodynia); Preference for dark and quiet environment

Question 13

Migraine Triggers

Answer 13

Triggers can include Sleep, Stress, Hormonal Factors (e.g. Menstrual Migraine, COCP, Menopause), Eating (Skipping meals and alcohol), Sensory stimuli (Loud sounds, Physical exertion, Minor head injuries

Question 14

Aura

Answer 14

Approximately 25% suffer focal neurological symptoms before headache phase (Aura);
Evolves over 5-20 minutes, rarely lasts longer than 60 minutes, followed immediately with
headache; Visual Aura is the commonest type
o Shimmering, Teichopsia (Fortification Spectra), Fragmentation of the image, Patches of loss of vision (Scotomas),Hemianopia/Tunnel vision
o Positive sensory symptoms (Tingling, Dysphasia, Loss of motor function) may occur

Question 15

Diagnostic Pitfalls

Answer 15

Sometimes males 50+ present with Acephalgic Migraines Aura, might be
confused with Transient Ischaemic Attack
o TIA is typically more acute, and presents more with negative symptoms
o Might have history of typical Migraine Aura in early adulthood

Question 16

Vertigo

Answer 16

Overlap with Basilar Migraine; Associated with brainstem aura symptoms including
Perioral Paraesthesia, Diplopia, Unsteadiness and rarely reduced LOC

Question 17

Hemiplegic Migraine

Answer 17

Rare, Autosomal Disorder which causes Hemiparesis/Coma and

Headache with recovery within 24hrs; Might have permanent Cerebellar signs

Question 18

Migraine Management: Lifestyle

Answer 18

Avoidance of Trigger Factors, Lifestyle Modification

Question 19

Migraine Management: Analgesia

Answer 19

High-dose dispersible Aspirin or Naproxen is often effective with Antiemetic
treatment e.g. Metoclopramide if necessary; Repeated use might lead to further headaches
• Triptans (5-HT1B/D Agonists) e.g. Sumatriptan are specific for Migraine; Useful if vomiting
prevents oral medication, or if medical therapy fails
o Avoided in Vascular disease and should not be overused
• CGRP Antagonists e.g. Telcagepant are possible treatments

Question 20

Migraine Prophylaxis

Answer 20

If >1-2 attacks/month and debilitating
o 3-6 months of treatment sufficient to reduce frequency and severity by 50%; Not effective if there is ongoing Analgesic overuse
o Anticonvulsants – Valproate, Topiramate
o Beta-Blockers – Slow release Propranolol
o Tricyclic Antidepressants – E.g. Amitriptyline
o Botulinum toxin – 31 injections over Scalp/Neck repeated every 3 months

Question 21

Tension Type Headache

Answer 21

• Overlap with Migraine Headache; No diagnostic tests, unknown if biological distinct
• Pain is usually mild/moderate severity, Bilateral and relatively featureless
• Tight band sensations, pressure behind eyes and burning sensation; Depression is common
comorbid feature;

Question 22

Tension Type Headache Management

Answer 22

Simple analgesia (Paracetamol, NSAIDs) often effective; Avoid overuse
o Physiotherapy – Massage, Ice packs, Relaxation
o Frequent or Chronic Tension Type Headache might respond to Migraine Suppression; Tricyclic Antidepressants being used first-line

Question 23

Cluster Headache

Answer 23

• Distinct and rarer than Migraines (1 in 1000); Affects adults, mostly males between 20-40;
Recurrent bouts (Clusters) of Unilateral, Retro-orbital Pain; Parasympathetic activation of
same eye leading to Redness/Tearing, Nasal Congestion and even Transient Horner’s
• Patients prefer to move about/rock back and forth (C/f Migraine Headache)
• Attacks usually shorter than Migraines; May occur several times a day especially during sleep;
Hypothalamic function implicated during attacks

Question 24

Cluster Headache: Treatment

Answer 24

Analgesia are unhelpful; Subcutaneous Sumatriptan for Acute headache; High flow O2;
Verapamil, Lithium, Steroids might help terminate Clusters

Question 25

Chronic Daily Headache: Criteria

Answer 25

• >15 days per month for at least 3 months; Affects 4% of population
• May possible causes (including Secondary Headache); Migraine is probably responsible for
majority of cases (Chronic Migraine)

Question 26

Medication Overuse Headaches

Answer 26

Overuse of Analgesia, Triptans; Especially in Migraine, associated with use of >10 doses a month might lead to development of Chronic headache
o Period of Transient worsening of Headache after drug withdrawal; Might be helped with introduction of Migraine Suppression medications
o Inpatient analgesic withdrawal with IV/IM Dihydroergotamine

Question 27

Trigeminal Autonomic Cephalgia

Answer 27

Primary Headache disorder characterised by Unilateral

Trigeminal distribution pain and prominent ipsilateral autonomic features

Question 28

Paroxysmal Hemicrania

Answer 28

Rare condition like Cluster Headache; Briefer attacks and more frequent, does not occur in clusters; Rapid and complete response to Indomethacin

Question 29

Short-lasting Unilateral Neuralgiform Headache with Conjunctival Injection and Tearing
(SUNCT)

Answer 29

Short attacks, frequently occurs in bouts; Presents like Trigeminal Neuralgia
Treat with Lamotrigine

Question 30

Primary Stabbing Headache

Answer 30

Momentary Jabs/Stabs of Localised pain; Symptoms
wax and wane, more common in patients with other Primary Headache Disorders; Responds
well to Indomethacin

Question 31

Primary Cough Headache

Answer 31

Sudden Sharp Head pain on coughing; No underlying cause,
Intracranial pathology must be excluded; Responds well to Indomethacin; LP to removal CSF
can help relieve

Question 32

Primary Sex Headache

Answer 32

Explosive Headache at/before Orgasm; Might resolve spontaneously
after severe attacks; Intracranial bleeding (SAH) must be excluded

Question 33

Raised Intracranial Pressure

Answer 33

Worst on waking, Coughing, Straining, Sneezing; Often presents
with Vomiting; Momentary Bilateral Visual Loss with Bending/Coughing (Associated with
Papilloedema, may not be present if acute ICP); Neuroimaging is mandatory; If Papilloedema exists without lesions seen on neuroimaging (e.g. Mass lesions, Venous Sinus Thrombosis,
Hydrocephalus), Idiopathic Intracranial Hypertension might be the cause; LP to confirm ICP

Question 34

Idiopathic Intracranial Hypertension: Signs

Answer 34

Results from reduced CSF resorption (Occurs at
Superior Sagittal Sinus through Arachnoid Villi); More common in Younger Overweight Female
patients, associated with Polycystic Ovaries; Presents with Headache, Transient Obscuration due to Papilloedema; Lateral Rectus Palsy (False Localising Sign); Increased ICP

Question 35

Idiopathic Intracranial Hypertension: Investigations

Answer 35

Neuroimaging is normal but ventricles might appear smaller and “slit-like”

Question 36

Idiopathic Intracranial Hypertension: Causes

Answer 36

o Sagittal Sinus Thrombosis can cause similar picture – TRO by MR Venography
o ? Drug causes – Tetracycline, Vitamin A supplements
o Usually self-limiting; Optic nerve damage can result
from longstanding Severe Papilloedema,progressive loss of Peripheral Visual Fields

Question 37

Idiopathic Intracranial Hypertension: Treatment

Answer 37

Acetazolamide and Thiazide Diuretics reduce CSF
production; LP to relieve pressure; VP Shunt might
be necessary, or Optic Nerve Sheath Fenestration to
protect vision

Question 38

Low Pressure Headache

Answer 38

Low CSF Volume (Low Pressure) Headache – Seen most often after LP; CSF leaks might also occur spontaneously, leading to postural headache (Worse on standing, Better when lying flat)
o History of vigorous Valsalva manoeuvres before
onset (Straining, Coughing)

Question 39

Low Pressure Headache: Management

Answer 39

o Leptomeningeal enhancement might be seen on MRI (Not always present)
o Site of leak might be within the spine; Treatment by injection of autologous blood
into Spinal Epidural space (Blood patch) or Surgical repair of dural tear
o IV Caffeine, Bed rest sometimes effective

Question 40

Trigeminal Neuralgia

Answer 40

• More common onset 60-70yrs; Hypertension is the main risk factor; Compression of Trigeminal nerve by enlarged vascular loop near Pons; May be seen on MRI
o Younger patients more likely to have Multiple Sclerosis or CPA tumours e.g. Acoustic Schwannomas, Meningiomas rather than Trigeminal Neuralgia

Question 41

Trigeminal Neuralgia: Presentation

Answer 41

Presents as knife/electric like pain lasting seconds along Trigeminal distributions; Pain most commonly commences in Mandibular division
Bilateral pain is rare; Usually due to brainstem lesion e.g. Demyelination in MS
Episodes might occur many times a day with refractory period between
Trigged by stimulation of specific areas on face
Might be in remission for months/years before invariably recurring

Question 42

Trigeminal Neuralgia: Management

Answer 42

Carbamazepine reduces severity; Oxcarbazepine, Lamotrigine (VgNa Blockade) and Gabapentin (Increases GABA biosynthesis) might be useful
Percutaneous Selective Ablation of Trigeminal Ganglion (Recurrence might occur),
Microvascular Decompression of Nerve in Posterior Fossa (High long-term success)

Question 43

Atypical Facial Pain

Answer 43

Not along distribution of Trigeminal, no trigger points; Multiple aetiology, might be somatic manifestation of depression; TCAs and Neuropathic pain
medication might help

Question 44

Other causes of facial pain

Answer 44

Trigeminal Autonomic Cephalgias, Migraine,

Carotid Dissection and Giant Cell Arteritis