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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. • rain parenchyma, ventricles and choriod plexus are pain insensitive Common causes of headache and facial pain • Tension!type headache (persistent daily headache) • "igraine • #luster headache • $aised intracranial pressure • Trigeminal neuralgia Diagnostic approach for headache %) Onset of headache a) Acute • #auses if acute headache subachaniod haemorrhage and migraine, meningitis etc. • Sudden severe is a feature of serious neurological disease • &pisodic headache is feature of migraine, cluster headache etc. b) Chronic (more than few weeks) • #ommon causes for chronic headache are headache due to raised intra cranial tension ('T#), tension headache, giant cell arteries etc. () location of headache • )nilateral * classic migraine, cluster headache • +iffuse * tension headache • Superficial pain ! giant cell arteritis • ,esions of sinuses, teeth, eyes produce pain locali-ed pain. .) Associated symptoms and aggravating and reliving factors • /ura *classical migraine • 0ever! meningitis, encephalitis, tyhpoid • 1ausea 2 vomiting * migraine, raised '#T • &arly morning *hypertension, raised '#T • 'ncreasing in bending forward * frontal sinusitis • • • • • Features of increased ICT are 3orse in morning, improves through the day /ssociated with morning vomiting 3orse bending forward 3orse with cough and straining $elieved by analgesia

!igraine Definition *"igraine is recurrent headache associated with visual and gastrointestinal disturbances. 8rogressively worsening headache.• +ull ache. features are said to have classical migraine or migraine (ith aura) • 8atient without aura but with other ( features are called migraine (ithout aura or common migraine (since it is more common than classical migraine) • "igraine starts at young age. 4eadache not responding to treatment. "athogenesis 8athogenesis of migraine is largely unknown but various theories are a) #enetic $There is definitive genetic predisposition in patients suffering with migraine esp. of the upper brain stem can produce migraine like headache and fortification spectrum. • 8hases of each episode /) Aura • /ura is preceded by non!specific prodromes. 0inal common pathway is trigeminal vascular system. 5nset of headache after 67 yrs. 8ain of migraine may be due to release of substance 8 in sensory ganglion. b) %ascular$ 1eurological 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. in the familial types like familial hemiplegic migraine.7 yrs. 4eadache associated with neurological signs. c) &eural theory$ 1euronal stimulation esp. often mild • • • • • ed flag signs of headache Sudden onset of severe head ache.'HT plays important role in pathogenesis of migraine. • Typically takes a form of fortification spectrum(slinging -ig -ag lines which march across visual fields) . 't is more common in females than males. • "ost often episodes are paroxysmal ranging from %!( per year to %!( per day. Clinical features #lassical triad of migraine is a) /ura of focal neurological events b) 8aroxysmal headache c) 1ausea and vomiting • 8atient with all the above . 97: of the patient shave %st attack before .

• Sensory aura may be present. headache. / migraine attack lasting for more than ?( hrs is called status migrainosus. 5ther types of migraine a) *asilar migraine! headache associated with symptoms of brain stem dysfunction like vertigo.rd nerve palsy.# pills • $elieving factors • Sleep • /nalgesics • 8regnancy • +uring the episode patient may have scalp vessels tenderness. . either unilateral (esp. Differential diagnosis • -ubarachnoid haemorrhage!features are severe worst headache of life. • !eningitis ! fever . c) Opthalmoplegic migraine ! "igraine with .  1oise and flashes of lights  8remenstrual period and 5. == 'f focal events occur without headache! !igraine e+uivalents == 'f focal neurological events don>t recover completely * Complicated migraine . Treatment of acute attac. Investigations • +iagnosis of migraine is clinical • 'maging of brain is re<uired only if atypical features are present like hemiplegia. • /ggravating factors  #hocolate and #heese 2 hunger. loss of conscious with out focal neurological deficits and associated with signs of meningeal irritation.. dysarthria or diplopia b) Hemiplegic migraine !migraine with hemiplegia (most often recovers fully) may mimics stroke. in classical) or bilateral (esp. moderate to sever pulsating <uality. ) Headache • "ay or may not be preceded by aura (depending the type) • $ecurring. in common migraine) and associated with nausea and vomiting. and signs of meningeal irritation. Treatment • $eassurance and avoidance of precipitating factors like 5# pills etc are important part of treatment. a) 1S/'+s • 1S/'+s like paacetamol or aspirin with antiemetic like domperidone or metacloprimide are very effective in reducing the headache.

and there may be a sensation of a band round the head. severe. followed by a respite for a number of months before another cluster occurs again. ri-atriptan • These drugs 6!4T receptor agonists • These are potent vasoconstrictors of extra cranial arteries • $oute of admistration can be oral. is characteristically brief (. • Typically. Sumatriptan. unilateral periorbital pain accompanied by unilateral lacrimation. • Standard migraine therapies are ineffective. . • 5ther drugs * lithium. nasal spray or parental ('" or 'V). • /cute attacks are usually halted by subcutaneous inDections of Sumatriptan or by inhalation of %77: oxygen. subcutaneous. the patient develops these symptoms at a particular time of day. nasal congestion and conDunctival inDection. • The pain is usually constant and generali-ed. TE&-IO&$T3"E HEADACHE or "E -I-TE&T DAI03 HEADACHE • "ost common type of headache. dull. • 8oorly responsive to ordinary analgesia. • #haracteristic syndrome comprises periodic. • 5ccur repeatedly for a number of weeks. very severe pain. "rophyla/is $ • Verapamil (@7!%(7 mg @!hourly) is the drug of choice. sublingual. SS$'s and verapamil.• These drugs should be taken at the onset of headache b) 6!4T agonists %) Triptans &. C01-TE HEADACHE 2!I# AI&O1. tight or like a EpressureE. "ost rapid response is seen with parental route • +ose *oral Sumatriptan !67!%77mg () &rgotime • &rgotime preparations should be avoided as they increase the incidence of dependence. • 8ain may continue for weeks or months without interruption ( unlike migraine) and is not associated vomiting or photophobia.7!97 minutes).g. methysergide or short courses of corticosteroids. • 8athogenesis &motional strain or anxiety is a common precipitant. • 8athogenesis remains unknown. "rophyla/is • Indication *more than .&E1 A0#IA) • There is a 6C% predominance of males and onset is usually in the third decade. attacks per week • +rugs commonly used in prophylaxis a) 8ropranolol sustain release!@7!%A7 mg Bday b) /mitriptyline !%7!67mg Bday c) 5ther drugs that can be used are valproate.

superior crebellar is cause for idiopathic trigeminal neuralgia. . Definition! Trigeminal neuralgia is a condition characteri-ed by excruciating paroxysms of pain in distribution of the fifth nerve. particularly of codeine. • /mitriptyline (%7 mg increased gradually to . aneurysms. T I#E!I&A0 &E1 A0#IA 2TIC DO10O1 E14) • The trigeminal (fifth cranial) nerve supplies sensation to the skin of the face and anterior half of the head. "athogenesis • Symptoms result from compression resulting in ectopic generation of action potentials from afferent fibers of fifth nerve root before it enters the pons. Etiology • "ost often this compression is due to artery esp. • 5ther causes for compression can pla<ue of multiple sclerosis. • "ost often pain involves manidibular and maxillary division and very rare in ophthalmic division of trigeminal nerve. • &xcessive use of analgesics.!anagement • $eassurance. Clinical features • The disorder occurs almost exclusively in middle!aged and elderly women. • 8hysiotherapy (with muscle relaxation and stress management) is usually beneficial. may actually worsen the headache (analgesic headache).7!67 mg) may be necessary. and neurofibroma.

• 3idely applied procedure is heat ablation of the trigeminal (gasserian) ganglion. • Cluster headache • 8ain arising from sinuses and teeth Treatment a) 8harmacological treatment • +rug therapy with oral carbama-epine is the initial treatment of choice • )sual dose of carbama-epine is %77 to (77mgBday. hence the term tic) • /nother characteristic feature is the initiation of pain by stimuli applied to certain areas on the face. lips. • Objective signs of sensory loss cannot be demonstrated on e/amination) Investigations • Trigeminal neuralgia is purely clinical and neuroimaging studies are not necessary • 5nly in young patients or bilateral symptoms or obDective sensory loss should be investigated. sedation and agranucytosis • 8henytion can also be used. .• 8ain often is experienced as single Dabs or clusters. b) Surgical treatment • Surgical therapy should be offered only if drug treatment fails. • 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 • "icrovascular decompression can also be done with very good results but is a maDor surgical procedure. or tongue (Ftrigger -onesF) or by movement of these parts. and lasts more than a few seconds or a minute or two but may be so intense that the patient winces.common side effects are di--iness. Differential diagnosis • Temporal arteritis ! elderly women with superficial not shock like with high &S$. a method termed radiofre+uency thermal rhi5otomy) • 'nDection of glycerol in "eckelEs cave.