Headache Headache is a pain in the head. It results from disorders that affect pain-sensitive...

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Headache Headache is a pain in the head. It results from disorders that affect pain-sensitive structures of the head and neck .

description

Pain-Sensitive Structures: - the venous sinuses (eg, sagittal sinus); a) Within the Cranial Vault - the venous sinuses (eg, sagittal sinus); - the anterior and middle meningeal arteries; - the dura at the base of the skull; - the trigeminal (V), glossopharyngeal (IX), and vagus (X) nerves; - the proximal portions of the internal carotid artery and its branches near the circle of Willis; - the brainstem periaqueductal gray matter; - the sensory nuclei of the thalamus.

Transcript of Headache Headache is a pain in the head. It results from disorders that affect pain-sensitive...

Page 1: Headache Headache is a pain in the head. It results from disorders that affect pain-sensitive structures of the head and neck.

Headache

Headache is a pain in the head. It results from disorders that affect pain-sensitive structures of the head and neck.

Page 2: Headache Headache is a pain in the head. It results from disorders that affect pain-sensitive structures of the head and neck.

Pain-Sensitive Structures:a) Within the Cranial Vault - the venous sinuses (eg, sagittal sinus); - the anterior and middle meningeal arteries; - the dura at the base of the skull; - the trigeminal (V), glossopharyngeal (IX), and

vagus (X) nerves; - the proximal portions of the internal carotid

artery and its branches near the circle of Willis; - the brainstem periaqueductal gray matter; - the sensory nuclei of the thalamus.

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b) Extracranial Pain-Sensitive Structures - the periosteum of the skull; - the skin; the subcutaneous tissues of skull; - muscles, and arteries of skull; - the neck muscles; - the second and third cervical nerves; - the eyes, ears, teeth, paranasal sinuses, - oropharynx; and the mucous membranes of the

nasal cavity.

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Causes of Headache and Facial Pain according to the mode of onset:

Acute onset (over minutes, hours, days):   Common: Subarachnoid hemorrhage, Other cerebrovascular

diseases, Meningitis or encephalitis, Ocular disorders (glaucoma, acute iritis)  

Less common: Seizures, Lumbar puncture, Hypertensive encephalopathy, Coitus 

 Subacute onset (over weeks, months): Giant cell (temporal)

arteritis, Intracranial mass (tumor, subdural hematoma, abscess), Pseudotumor cerebri (benign intracranial hypertension), Trigeminal neuralgia, Glossopharyngeal neuralgia, Posttherpetic neuralgia, Hypertension (including pheochromocytoma and the use of monoamine oxidase inhibitors plus tyramine), Atypical facial pain

  Chronic (over years): Migraine, Cluster headache, Tension

headache, Cervical spine disease, Sinusitis, Dental disease

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Tension Headache

It is chronic headache of unapparent cause that lack enough features characteristic of migraine or cluster headache.

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The underlying pathophysiologic mechanism is unknown, and tension is unlikely to be primarily responsible. Contraction of neck and scalp muscles, which has also been proposed as the cause, is probably a secondary phenomenon.

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It is either episodic or chronic (i.e: present > 15 days per month). The chronic disorder begins after age 20. It is characterized by frequent (often daily) attacks of nonthrobbing, bilateral occipital head pain that is not associated with nausea, vomiting, or prodromal visual disturbance. The pain is sometimes likened to a tight band around the head or pressure over the vertex. Women are more commonly affected than men. It is more at evening than morning. Relieved by preoccupation & exaggerated by isolation & stress. It does not interfere with daily living activities or awake patient from sleep.

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Although tension headache and migraine have been traditionally considered two distinct disorders, many patients have headaches that exhibit features of both. Thus, some patients who are classified as having tension headaches experience throbbing headaches, unilateral head pain, or vomiting with attacks. In consequence, it may be more accurate to view tension headache and migraine as representing 2 opposite poles of a single clinical spectrum.

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Treatment of Tension Headache:

a) Acute phase therapy (during the attack) : aspirin, other non-steroidal anti-inflammatory drugs,

acetaminophen (2 tab x 3 per day, tab 325 mg), ergotamine, or dihydroergotamine.

b) prophylactic treatment – only in chronic form – (after end of acute

attack – to prevent new attacks) Amitriptyline (Tryptizol)® a tricyclic antidepressant (10-175 mg

at bed time, tab 10, 25, 50, 75, 100, 150) or imipramine (Tofranil)® are often effective, and propranolol is useful in some cases. Although many patients respond to benzodiazepines such as diazepam, 5–30 mg/d orally, or chlordiazepoxide (Librium)®, 10–75 mg/d orally, these drugs should be used sparingly because of their addictive potential.

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Migraine

Migraine, the most common cause of headache, afflicts approximately 15% of women and 6% of men. A useful definition of migraine is a benign and recurring syndrome of headache, nausea, vomiting, and/or other symptoms of neurologic dysfunction in varying admixtures.

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Triggering factors:• red wine• menses (so ask about the effect of

menstrual cycle on headache)• hunger (so avoid fasting)• lack of sleep• glare• estrogen• worry• perfumes

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Relieving factors:

• sleep (the patient have a desire to sleep when attack come)

• pregnancy• exhilaration• triptans

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Pathogenesis: It is multifactoriala) Genetic factors: It is of polygenic + strong environmental factors. The aggregation of migraine within families has long been recognized (+ve

family history). Consistent mendelian patterns of inheritance have not been found Concordance rates in monozygotic twins of only 28–52% A rare subtype of migraine with aura, familial hemiplegic migraine, has a

straightforward autosomal dominant mode of inheritance. b) Vascular theory: Intracranial vasoconstriction and extracranial vasodilatation have long

been held to be the respective causes of the aura and headache phases of migraine. This theory applied only for classic migraine & even here it is weak theory.

c) Neuronal theory: Increase in activation of dorsal raphe (serotonergic cells) & locus cereulus

(adrenergic cells) lead to 2 results: a. increase in blood flow in mid-brain & pons causing headache, b. activation in lateral geniculate body, visual cortex, superior colliculus, retina causing aura.

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Clinical Features: MIGRAINE WITHOUT AURA (COMMON MIGRAINE) In this syndrome no focal neurologic disturbance

precedes the recurrent headaches. Migraine without aura is by far the more frequent

type of vascular headache. The International Headache Society criteria for

migraine include moderate to severe head pain, pulsating quality, unilateral location, aggravation by walking stairs or similar routine activity,

attendant nausea and/or vomiting, photophobia and phonophobia, and multiple attacks, each lasting ˃ 2 hr, up to 72 h, (10 hr as average)

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Migraine with Aura (Classic Migraine) In classic migraine headache is preceded by transient neurological

symptoms—the aura. The most common auras are scintillation scotomas (fortification spectra) that occurs in 10 % of patients start as small paracentral scotomas then slowly enlarge and spread peripherally into C-shape with illuminating zigzag borders lasting 20-25 minutes. A throbbing unilateral headache ensues with or following these prodromal features. The frequency of headache varies, but ˃ 50% of patients experience no more than one attack per week. The duration of episodes is ˃ 2 hours and less than 1 day in most patients. Remissions are common during the second and third trimesters of pregnancy and after menopause. Between 40-70 years especially in the elderly, prodromal symptoms may occur without headache (migraine equivalents). Although hemicranial pain is a hallmark of classic migraine, headaches can also be bilateral. Bilateral headache, therefore, does not exclude the diagnosis of migraine, nor does an occipital location—a characteristic commonly attributed to tension headaches. During the headache, prominent associated symptoms include nausea, vomiting, photophobia, phonophobia, irritability, and lassitude. Uncommonly, migraines are associated with frank neurologic deficits that accompany, or persist beyond resolution of the pain phase. These may include hemiparesis, hemisensory loss, speech dysfunction, or visual disturbance.

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Treatment:a) During the acute attack: 1st start with simple analgesia + anti-emetic Simple analgesia like: Aspirin 650-1300 mg/d or Paracetamol (Emidol)® 650-1300mg/d Diclofenac potassium (Voltfast)® powder Anti-emetic like: Metoclopramide (Plasil)® ampoule 10 mg I.V or

S.C injection or Prochlorperazine (Stemetil)® 2.5-10 mg I.M or I.VIf no response so ADD to the above one of the following:1. Ergot preparations: they act by causing vasospasm & are of 2 types:a. non-selective 5 HT agonists like:Dihydroergotamine ampoule (1 mg/cc) 1-2 mg I.M or S.C or 0.75-1.25 mg I.V injction. Nasal spray (4 mg/cc) (2 mg/spray=0.5cc) 1 spray to each nostril

repeated in 15 minutes Ergotamine/caffeine (Migrail)® or (Cafergot) ® tab or suppositories

(1/100 mg), (2/100 mg) 2-6 tab / w max. 10 tab / w or ¼ -2 supp. / w max. 5 supp. / w

Side effect: nausea, vomitingContraindicated in pregnancy, coronary or peripheral vascular

diseases & HT

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b.Triptan (selective 5 HT agonist) like:Sumatriptan tab (25,50,100 mg/tab) 200 mg/d orally nasal spray (5,20 mg/spray) 40 mg/d ampoule (6 mg/ampoule) 12 mg/d S.C Side effect & contraindications are the same for previous

group. In addition they must never use in combination with them.

2. Narcotics like:Mepredine (50,100 mg tab or ampoule) 50-200 mg orally or

I.M injection.Paracetamol/Codeine (Cetapar)® : 30-120 mg Codeine /

day

For mild attack use oral preparations, while nasal spray for moderate one & injectable forms in sever cases.

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These drugs to be of maximum effect they

should be used as early as possible before the onset of headache phase in classic migraine & as early as possible when the symptom start in common migraine.

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b) Prophylactic treatment (to prevent new attacks): It is indicated if the patient have 3 or more attacks per months or if there is C.I to acute phase therapy.

We use one of the following agents:a.Anticonvulsants like Na valiprait (Depakine)® tab 250-1000 mg bid or

Topiramate (Topamax)® 50-100 mg/d÷2 or Gabapentin (Neurontin)® tab 900-2400 mg/d÷3

b.B blockers like Propranolol tab 20-160 mg bid SRP 60-320 mg qd or bid we use them preferably for patients with prominent visual aura. Side effects: symptomatic bradycardia, bronchospasm, hypotension, exercise

intolerance, impotence, sedation, depression.c.Tricyclic antidepressants like Amitriptyline (Tryptizol)® (10,25,50,75,100,150

mg/tab) 10-175 mg at bed time. Side effects: dry mouth, urinary retention, dilated pupils ; so they are

contraindicated in B.P.H & glaucoma. we use them preferably for patients with anxiety, insomnia or depression.d.Calcium channel blockers Verapamil (Isoptine)® (40, 80, 120 mg/tab)

80 mg tid 240 mg qd or bid SRP. They are not for use with B blockers. They cause constipation & not used in

hypotension, L.V heart failure, S.S.S, 2nd or 3rd degree heart block.e.Cyproheptadine (a serotonine antagonist & antihistamine) (4-8 mg tid orally).

Commonly it cause drowsiness in the early stage of treatment.

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Meperidine, Paracetamol & (Paracetamol + Codeine) Cetapar® are the only drugs to be used for treatment of migraine during pregnancy.

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Avoid the triggering factors.

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There is a slight increase in the risk of thromboembolic stroke in patients who suffer from migraine, particularly migraine with aura. This risk is considerably elevated by concomitant use of oestrogen-based contraception.

FOR THAT WE SHOULD INSTRACT FOR THAT WE SHOULD INSTRACT THE FEMALE PATIENT WITH MIGRAIN THE FEMALE PATIENT WITH MIGRAIN TO USE ALTERNATIVE TO USE ALTERNATIVE CONTRACEPTION METHOD.CONTRACEPTION METHOD.