HEADACHE AND FACIAL PAIN

HEADACHE
Very common neurological symptom
Structures that are pain sensitive with in the skull are dura (sinuses and flax cerebri),
proximal parts of large pail blood vessels .These are innervated by trigeminal nerve
(Vth) and upper cervical nerves.
Brain parenchyma, ventricles and choriod plexus are pain insensitive
Common causes of headache and facial pain
Tension-type headache (persistent daily headache)
Migraine
Cluster headache
Raised intracranial pressure
Trigeminal neuralgia
Diagnostic approach for headache
1) Onset of headache
a) Acute
Causes if acute headache subachaniod haemorrhage and migraine, meningitis etc.
Sudden severe is a feature of serious neurological disease
Episodic headache is feature of migraine, cluster headache etc.
b) Chronic (more than few weeks)
Common causes for chronic headache are headache due to raised intra cranial
tension (ITC), tension headache, giant cell arteries etc.
2) location of headache
Unilateral classic migraine, cluster headache
Diffuse tension headache
Superficial pain - giant cell arteritis
Lesions of sinuses, teeth, eyes produce pain localized pain.
3) Associated symptoms and aggravating and reliving factors
Aura classical migraine
Fever- meningitis, encephalitis, tyhpoid
Nausea & vomiting migraine, raised ICT
Early morning hypertension, raised ICT
Increasing in bending forward frontal sinusitis

Features of increased ICT are

Worse in morning, improves through the day
Associated with morning vomiting
Worse bending forward
Worse with cough and straining
Relieved by analgesia

 Dull ache, often mild

Red flag signs of headache

Sudden onset of severe head ache.
Headache associated with neurological signs.
Onset of headache after 50 yrs.
Progressively worsening headache.
Headache not responding to treatment.

Migraine
Definition Migraine is recurrent headache associated with visual and gastrointestinal
disturbances.
Pathogenesis
Pathogenesis of migraine is largely unknown but various theories are
a) Genetic -There is definitive genetic predisposition in patients suffering with
migraine esp. in the familial types like familial hemiplegic migraine.
b) Vascular- Neurological symptoms like aura etc are caused by the intracranial
vasospasm and headache by extra cranial vasodilatation but vascular changes
alone may not alone explain all the symptoms of migraine.
c) Neural theory- Neuronal stimulation esp. of the upper brain stem can produce
migraine like headache and fortification spectrum. Pain of migraine may be due to
release of substance P in sensory ganglion.5HT plays important role in
pathogenesis of migraine. Final common pathway is trigeminal vascular system.
Clinical features
Classical triad of migraine is
a) Aura of focal neurological events
b) Paroxysmal headache
c) Nausea and vomiting
Patient with all the above 3 features are said to have classical migraine or
migraine with aura.
Patient without aura but with other 2 features are called migraine without aura or
common migraine (since it is more common than classical migraine)
Migraine starts at young age. 90% of the patient shave 1st attack before 40 yrs. It is
more common in females than males.
Most often episodes are paroxysmal ranging from 1-2 per year to 1-2 per day.
Phases of each episode
A) Aura
Aura is preceded by non-specific prodromes.
Typically takes a form of fortification spectrum(slinging zig zag
lines which march across visual fields)

 Sensory aura may be present.

B) Headache
May or may not be preceded by aura (depending the type)
Recurring, moderate to sever pulsating quality, either unilateral (esp.
in classical) or bilateral (esp. in common migraine) and associated
with nausea and vomiting.
Aggravating factors
Chocolate and Cheese & hunger.
Noise and flashes of lights
Premenstrual period and O.C pills
Relieving factors
Sleep
Analgesics
Pregnancy
During the episode patient may have scalp vessels tenderness.
Other types of migraine
a) Basilar migraine- headache associated with symptoms of brain stem dysfunction
like vertigo, dysarthria or diplopia
b) Hemiplegic migraine -migraine with hemiplegia (most often recovers fully) may
mimics stroke.
c) Opthalmoplegic migraine - Migraine with 3rd nerve palsy.
## If focal events occur without headache- Migraine equivalents
## If focal neurological events dont recover completely Complicated migraine
## A migraine attack lasting for more than 72 hrs is called status migrainosus.
Differential diagnosis
Subarachnoid haemorrhage-features are severe worst headache of life, loss of
conscious with out focal neurological deficits and associated with signs of
meningeal irritation.
Meningitis - fever , headache, and signs of meningeal irritation.
Investigations
Diagnosis of migraine is clinical
Imaging of brain is required only if atypical features are present like hemiplegia.
Treatment
Reassurance and avoidance of precipitating factors like OC pills etc are important
part of treatment.
Treatment of acute attack
a) NSAIDs
NSAIDs like paacetamol or aspirin with antiemetic like domperidone or
metacloprimide are very effective in reducing the headache.

 These drugs should be taken at the onset of headache

b) 5-HT agonists
1) Triptans E.g. Sumatriptan, rizatriptan
These drugs 5-HT receptor agonists
These are potent vasoconstrictors of extra cranial arteries
Route of admistration can be oral, sublingual, subcutaneous, nasal spray or
parental (IM or IV). Most rapid response is seen with parental route
Dose oral Sumatriptan -50-100mg
2) Ergotime
Ergotime preparations should be avoided as they increase the incidence of
dependence.
Prophylaxis
Indication more than 3 attacks per week
Drugs commonly used in prophylaxis
a) Propranolol sustain release-80-160 mg /day
b) Amitriptyline -10-50mg /day
c) Other drugs that can be used are valproate, SSRIs and verapamil.
CLUSTER HEADACHE (MIGRAINOUS NEURALGIA)
There is a 5:1 predominance of males and onset is usually in the third decade.
Characteristic syndrome comprises periodic, severe, unilateral periorbital pain
accompanied by unilateral lacrimation, nasal congestion and conjunctival injection,
very severe pain, is characteristically brief (30-90 minutes).
Typically, the patient develops these symptoms at a particular time of day.
Occur repeatedly for a number of weeks, followed by a respite for a number of
months before another cluster occurs again.
Pathogenesis remains unknown.
Acute attacks are usually halted by subcutaneous injections of Sumatriptan or by
inhalation of 100% oxygen.
Standard migraine therapies are ineffective.
Prophylaxis Verapamil (80-120 mg 8-hourly) is the drug of choice.
Other drugs lithium, methysergide or short courses of corticosteroids.
TENSION-TYPE HEADACHE or PERSISTENT DAILY HEADACHE
Most common type of headache.
The pain is usually constant and generalized, dull, tight or like a 'pressure', and
there may be a sensation of a band round the head.
Pain may continue for weeks or months without interruption ( unlike migraine) and
is not associated vomiting or photophobia.
Poorly responsive to ordinary analgesia.
Pathogenesis Emotional strain or anxiety is a common precipitant.

Management
Reassurance.
Excessive use of analgesics, particularly of codeine, may actually worsen the
headache (analgesic headache).
Physiotherapy (with muscle relaxation and stress management) is usually
beneficial.
Amitriptyline (10 mg increased gradually to 30-50 mg) may be necessary.
TRIGEMINAL NEURALGIA (TIC DOULOUREUX)
The trigeminal (fifth cranial) nerve supplies sensation to the skin of the face and
anterior half of the head.

Definition- Trigeminal neuralgia is a condition characterized by excruciating paroxysms

of pain in distribution of the fifth nerve.
Pathogenesis
Symptoms result from compression resulting in ectopic generation of action
potentials from afferent fibers of fifth nerve root before it enters the pons.
Etiology
Most often this compression is due to artery esp. superior crebellar is cause for
idiopathic trigeminal neuralgia.
Other causes for compression can plaque of multiple sclerosis, aneurysms, and
neurofibroma.
Clinical features
The disorder occurs almost exclusively in middle-aged and elderly women.
Most often pain involves manidibular and maxillary division and very rare in
ophthalmic division of trigeminal nerve.

 Pain often is experienced as single jabs or clusters, and lasts more than a few
seconds or a minute or two but may be so intense that the patient winces, hence the
term tic.
Another characteristic feature is the initiation of pain by stimuli applied to certain
areas on the face, lips, or tongue ("trigger zones") or by movement of these parts.
Objective signs of sensory loss cannot be demonstrated on examination.
Investigations
Trigeminal neuralgia is purely clinical and neuroimaging studies are not necessary
Only in young patients or bilateral symptoms or objective sensory loss should be
investigated.
Differential diagnosis
Temporal arteritis - elderly women with superficial not shock like with high ESR.
Cluster headache
Pain arising from sinuses and teeth
Treatment
a) Pharmacological treatment
Drug therapy with oral carbamazepine is the initial treatment of choice
Usual dose of carbamazepine is 100 to 200mg/day.common side effects are
dizziness, sedation and agranucytosis
Phenytion can also be used.
b) Surgical treatment
Surgical therapy should be offered only if drug treatment fails.
Widely applied procedure is heat ablation of the trigeminal (gasserian)
ganglion, a method termed radiofrequency thermal rhizotomy.
Injection of glycerol in Meckel's cave.
Success of both the procedure is only short term and most patients have
recurrence
These procedures result in partial numbness of the face and carry a risk of
corneal denervation with secondary keratitis
Microvascular decompression can also be done with very good results but is
a major surgical procedure.