HEADACHE

PRIMARY HEADACHE SYNDROMES

• Tension type headache

• Migraine• Trigeminal Neuralgia• Atypical facial pain• Cluster headache• Benign paroxysmal

headaches

TENSION TYPE

•Most common-69%•Episodic or chronic•Gradual onset , radiate forward from

occiput•Bilateral, dull, tight, band like pain•Less in morning, pain increase as day

goes on •No accompanying N,V, throbbing,

sensitivity to light, sound or movement

Pathophysiology

• Primary disorder of CNS pain modulation• Precipitating factorsStress: usually occurs in the afternoon after long

stressful work hours or after an exam Sleep deprivation Uncomfortable stressful position and/or bad

posture Irregular meal time (hunger) Eyestrain Caffeine withdrawal Dehydration

2 Theories

Muscle tension around head and neckMalfunctioning pain filter located in brain

stem, brain misinterprets information and interprets this signal as pain. One of the main neurotransmitters which is probably involved is serotonin

Management

•Paracetamol,Aspirin,NSAIDs•Behavioral approach-relaxation•Chronic-amitriptyline

MIGRAINE

•2nd most common-16%•15% women and 6% men•Severe, episodic, unilateral,throbbing

pain• Nausea,Vomiting• Sensitivity to light ,sound, movement• Genetic predisposition

Classical Migraine or Migraine with AURA

Symptom TriadParoxysmal headachenausea &/or vomitingaura of focal neurological events(visual) 20-25%

AURA

• flashing lights, silvery zigzag lines moving across visual field over a period of 20 minutes sometimes leaving a trail of temporary visual field loss• Sometimes-Auditory ,Olfactory, gustatory

hallucinations• Sensory aura-spreading front of tingling

and numbness, from one body part to another

Rare aura:• Vertigo• Aphasia• Hemiparesis• DeliriumMigraine with limb weakness-

Hemiplegic migraineSymptoms of aura do not resolve leaving

permanent neurological damage-Complicated migraine

Common Migraine or Migraine without AURA

•Paroxysmal headache•Vomiting +/-•NO AURA

Simplified Diagnostic Criteria for MIGRAINE

At least 2 of the following:

+ At least 1 of the following:

• Unilateral pain• Throbbing pain• Aggravation by

movement• Moderate or severe

intensity

• Nausea/vomitting• Photophobia and

phonophobia

Clinical phases of a migraine attack

Vulnerability

Prodrome

Aura

Pain

Postdrome

Attack Initiation

Triggers

• Flashing lights• Loud sounds• Strong odors• Stress• Hunger• Fatigue• Alcohol• Smoking

• Menstruation• Pregnancy• Menopause• Oral Contraceptives• Sleep changes• Caffeine• Chocolate• Tyramine• MSG

Pathophysiology of Migraine

•Cortical spreading depression

•Vascular• Low Serotonin • Melanopsin receptor

Cortical spreading depression of LEAO•Dysfunction of ion channels-Quick

depolarization(activation) followed by long-lasting depression over an area of cortex

•Release of inflammatory mediators

•Irritation of cranial nerve roots-trigeminal

Vascular

Vasoconstriction of blood vessels in brain-Aura

(begins in occipital lobe)

Vasodilatation of scalp blood vessels

Inflammation

Pain

Migraine Pain-Trigeminovascular•Key pathway for pain is trigeminovascular

input from meningeal vessels

•Modulation of trigeminovascular input comes from dorsal raphe nucleus, locus coeruleus and nucleus raphe magnus

Management

•Acute attack-aspirin/paracetamol+metoclopromide/ domperidone

•Severe attack-Sumatriptan•Frequent attacks-

Propranolol,Amitriptyline,Sodium valproate or Topiramate

Trigeminal Neuralgia

• Lancinating pain in 2nd and 3rd divisions of trigeminal nerve

• >50yrs• Severe,

brief ,repetitive pain causing patient to flinch

• Precipitated by touching trigger zones—washing, shaving, eating, cold wind

Pathophysiology

•Compression of trigeminal N by aberrant loop of cerebellar arteries as nerve enters brainstem

•Other benign compressive lesions

•Multiple sclerosis- TN occurs due to plaque of demyelination in trigeminal root entry zone

Management

•Carbamazepine-DOC•Intolerant-Gabapentin/Pregabalin•Injection of alcohol into peripheral branch

of nerve•Posterior craniotomy to relieve vascular

compression of trigeminal nerve

Atypical facial pain

•Persistent idiopathic facial pain•Continuous,

burning/crushing,unremittent, centred over maxilla usually left side

•Middle aged women•Early form of trigeminal neuralgia•Rx-Amitriptyline, Gabapentin

Other causes of facial pain

Sinusitis • Frontal-pain more in morning, decreases

as day progresses, stooping and blowing nose increase pain• Ethmoid and Sphenoid-pain over vertex,

less in morning and increase gradually

Post herpetic neuralgia-continuous, burning pain sensitive to light touch, shingles

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