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

 +ull ache, often mild

ed flag signs of headache Sudden onset of severe head ache. 4eadache associated with neurological signs. 5nset of headache after 67 yrs. 8rogressively worsening headache. 4eadache not responding to treatment.

!igraine
Definition *"igraine is recurrent headache associated with visual and gastrointestinal disturbances. "athogenesis 8athogenesis of migraine is largely unknown but various theories are a) #enetic $There is definitive genetic predisposition in patients suffering with migraine esp. in the familial types like familial hemiplegic migraine. b) %ascular$ 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. c) &eural theory$ 1euronal stimulation esp. of the upper brain stem can produce migraine like headache and fortification spectrum. 8ain of migraine may be due to release of substance 8 in sensory ganglion.'HT plays important role in pathogenesis of migraine. 0inal common pathway is trigeminal vascular system. 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 . 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. 97: of the patient shave %st attack before ;7 yrs. 't is more common in females than males. "ost often episodes are paroxysmal ranging from %!( per year to %!( per day. 8hases of each episode /) Aura /ura is preceded by non!specific prodromes. Typically takes a form of fortification spectrum(slinging -ig -ag lines which march across visual fields)

 Sensory aura may be present. ) Headache "ay or may not be preceded by aura (depending the type) $ecurring, moderate to sever pulsating <uality, either unilateral (esp. in classical) or bilateral (esp. in common migraine) and associated with nausea and vomiting. /ggravating factors #hocolate and #heese 2 hunger. 1oise and flashes of lights 8remenstrual period and 5.# pills $elieving factors Sleep /nalgesics 8regnancy +uring the episode patient may have scalp vessels tenderness. 5ther types of migraine a) *asilar 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 ! "igraine with .rd nerve palsy. == 'f focal events occur without headache! !igraine e+uivalents == 'f focal neurological events don>t recover completely * Complicated migraine ,, / migraine attack lasting for more than ?( hrs is called status migrainosus. Differential diagnosis -ubarachnoid haemorrhage!features are severe worst headache of life, loss of conscious with out focal neurological deficits and associated with signs of meningeal irritation. !eningitis ! fever , headache, and signs of meningeal irritation. Investigations +iagnosis of migraine is clinical 'maging of brain is re<uired only if atypical features are present like hemiplegia. Treatment $eassurance and avoidance of precipitating factors like 5# pills etc are important part of treatment. Treatment of acute attac. a) 1S/'+s 1S/'+s 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) 6!4T agonists %) Triptans &.g. Sumatriptan, ri-atriptan These drugs 6!4T receptor agonists These are potent vasoconstrictors of extra cranial arteries $oute of admistration can be oral, sublingual, subcutaneous, nasal spray or parental ('" or 'V). "ost rapid response is seen with parental route +ose *oral Sumatriptan !67!%77mg () &rgotime &rgotime preparations should be avoided as they increase the incidence of dependence. "rophyla/is Indication *more than . attacks per week +rugs commonly used in prophylaxis a) 8ropranolol sustain release!@7!%A7 mg Bday b) /mitriptyline !%7!67mg Bday c) 5ther drugs that can be used are valproate, SS$'s and verapamil. C01-TE HEADACHE 2!I# AI&O1- &E1 A0#IA) There is a 6C% predominance of males and onset is usually in the third decade. #haracteristic syndrome comprises periodic, severe, unilateral periorbital pain accompanied by unilateral lacrimation, nasal congestion and conDunctival inDection, very severe pain, is characteristically brief (.7!97 minutes). Typically, the patient develops these symptoms at a particular time of day. 5ccur repeatedly for a number of weeks, followed by a respite for a number of months before another cluster occurs again. 8athogenesis remains unknown. /cute attacks are usually halted by subcutaneous inDections of Sumatriptan or by inhalation of %77: oxygen. Standard migraine therapies are ineffective. "rophyla/is $ Verapamil (@7!%(7 mg @!hourly) is the drug of choice. 5ther drugs * lithium, methysergide or short courses of corticosteroids. TE&-IO&$T3"E HEADACHE or "E -I-TE&T DAI03 HEADACHE "ost common type of headache. The pain is usually constant and generali-ed, dull, tight or like a EpressureE, and there may be a sensation of a band round the head. 8ain may continue for weeks or months without interruption ( unlike migraine) and is not associated vomiting or photophobia. 8oorly responsive to ordinary analgesia. 8athogenesis &motional strain or anxiety is a common precipitant.

!anagement $eassurance. &xcessive use of analgesics, particularly of codeine, may actually worsen the headache (analgesic headache). 8hysiotherapy (with muscle relaxation and stress management) is usually beneficial. /mitriptyline (%7 mg increased gradually to .7!67 mg) may be necessary. 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.

Definition! Trigeminal neuralgia is a condition characteri-ed by excruciating paroxysms of pain in distribution of the fifth nerve. "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. superior crebellar is cause for idiopathic trigeminal neuralgia. 5ther causes for compression can pla<ue of multiple sclerosis, aneurysms, and neurofibroma. Clinical features The disorder occurs almost exclusively in middle!aged and elderly women. "ost often pain involves manidibular and maxillary division and very rare in ophthalmic division of trigeminal nerve.

 8ain often is experienced as single Dabs 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) /nother characteristic feature is the initiation of pain by stimuli applied to certain areas on the face, lips, or tongue (Ftrigger -onesF) or by movement of these parts. 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. Differential diagnosis Temporal arteritis ! elderly women with superficial not shock like with high &S$. 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.common side effects are di--iness, sedation and agranucytosis 8henytion can also be used. b) Surgical treatment Surgical therapy should be offered only if drug treatment fails. 3idely applied procedure is heat ablation of the trigeminal (gasserian) ganglion, a method termed radiofre+uency thermal rhi5otomy) 'nDection of glycerol in "eckelEs 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 "icrovascular decompression can also be done with very good results but is a maDor surgical procedure.