Headache Flashcards
Why do headaches occur?
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
Causes of secondary headaches
Raised ICP Infections GCA Intracranial haemorrhages Low CSF volume Post traumatic headache Acute glaucoma
Concerning presentations of headache
New onset severe headache without previous history especially in 50_+
Need to exclude secondary headache
What should be included in a headache history
SOCRATES, Autonomic symptoms, Headache pattern and frequency, Duration, Pattern of Analgesia use, Family History
Red flag symptoms
Fever, Sudden onset <1 minute, Features of raised ICP, Jaw Claudication
What examinations should be done in headaches?
Fundoscopy for Papilloedema; Temporal Arteries palpated for Pulselessness and Tenderness;
Examination usually normal in Primary disorders
When should neuroimaging be used in headache investigation?
Neuroimaging only if indication of underlying secondary cause; Older patients with red flag
symptoms require CT Head; ESR for Giant Cell Arteritis
Migraine: What is it
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
Aetiology behind migraines: Genetic factors
Genetic factors leading to neuronal hypersensitivity;
Sodium and Potassium channels have been implicated;
thought to be a neurogenic rather than vascular basis
Aetiology of Aura
Aura thought to be due to spreading of Cortical
depression – Wave of depolarisation followed by
depressed activity spreading from Occipital to Frontal
Aetiology behind migraines: Trigeminovascular system
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
Presentation of Migraines
Starts around puberty; Increasing prevalence into adulthood; Scalp might be tender to touch during episodes (Allodynia); Preference for dark and quiet environment
Migraine Triggers
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
Aura
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
Diagnostic Pitfalls
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
Vertigo
Overlap with Basilar Migraine; Associated with brainstem aura symptoms including
Perioral Paraesthesia, Diplopia, Unsteadiness and rarely reduced LOC
Hemiplegic Migraine
Rare, Autosomal Disorder which causes Hemiparesis/Coma and
Headache with recovery within 24hrs; Might have permanent Cerebellar signs
Migraine Management: Lifestyle
Avoidance of Trigger Factors, Lifestyle Modification
Migraine Management: Analgesia
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
Migraine Prophylaxis
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
Tension Type Headache
• 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;
Tension Type Headache Management
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
Cluster Headache
• 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
Cluster Headache: Treatment
Analgesia are unhelpful; Subcutaneous Sumatriptan for Acute headache; High flow O2;
Verapamil, Lithium, Steroids might help terminate Clusters
Chronic Daily Headache: Criteria
• >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)
Medication Overuse Headaches
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
Trigeminal Autonomic Cephalgia
Primary Headache disorder characterised by Unilateral
Trigeminal distribution pain and prominent ipsilateral autonomic features
Paroxysmal Hemicrania
Rare condition like Cluster Headache; Briefer attacks and more frequent, does not occur in clusters; Rapid and complete response to Indomethacin
Short-lasting Unilateral Neuralgiform Headache with Conjunctival Injection and Tearing
(SUNCT)
Short attacks, frequently occurs in bouts; Presents like Trigeminal Neuralgia
Treat with Lamotrigine
Primary Stabbing Headache
Momentary Jabs/Stabs of Localised pain; Symptoms
wax and wane, more common in patients with other Primary Headache Disorders; Responds
well to Indomethacin
Primary Cough Headache
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
Primary Sex Headache
Explosive Headache at/before Orgasm; Might resolve spontaneously
after severe attacks; Intracranial bleeding (SAH) must be excluded
Raised Intracranial Pressure
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
Idiopathic Intracranial Hypertension: Signs
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
Idiopathic Intracranial Hypertension: Investigations
Neuroimaging is normal but ventricles might appear smaller and “slit-like”
Idiopathic Intracranial Hypertension: Causes
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
Idiopathic Intracranial Hypertension: Treatment
Acetazolamide and Thiazide Diuretics reduce CSF
production; LP to relieve pressure; VP Shunt might
be necessary, or Optic Nerve Sheath Fenestration to
protect vision
Low Pressure Headache
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)
Low Pressure Headache: Management
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
Trigeminal Neuralgia
• 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
Trigeminal Neuralgia: Presentation
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
Trigeminal Neuralgia: Management
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)
Atypical Facial Pain
Not along distribution of Trigeminal, no trigger points; Multiple aetiology, might be somatic manifestation of depression; TCAs and Neuropathic pain
medication might help
Other causes of facial pain
Trigeminal Autonomic Cephalgias, Migraine,
Carotid Dissection and Giant Cell Arteritis
