NUR AINA BINTI AB KADIR

GENERAL PRINCIPLES

• Associated features are the disorders itself

PRIMARY

• Exogenous disordersSECONDARY

COMMON CAUSES OF HEADACHE

ANATOMY&PHYSIOLOGY

• Peripheral nociceptors are stimulated tissue

injury,visceral distension

• Pain producing pathways of the peripheral/ CNS are

damaged/activated inappropiately

• Cranial structures(pain producing): scalp, middle

meningeal artery, dural sinuses, falx cerebri, proximal

segments of the large pial arteries

CLINICAL EVALUATION OF ACUTE, NEW ONSET HEADACHE

• New& severe VS recurrent over many years• Probability of finding a potentially serious cause & need

prompt evaluation, proper treatment• 1st step: complete neurologic examination• Abnormal examination/history of recent-onset headache

CT/MRI study• General evaluation of acute headache might include the

investigation of CVS & renal status by BP monitoring & urine examination

Cont..

• Psychological state : relationship exist between head pain and depression

• Underlying recurrent headache disorders may be activated by pain follows otologic/ endodontic surgical procedures.

HEADACHE SYMPTOMS THAT SUGGEST A SERIOUS UNDERLYING DISORDER

• “WORST” headache ever• 1st severe headache• Subacute worsenig over days/weeks• Abnormal neurologic examination• Fever/unexplained systemic signs• Vomiting that precedes headache• Pain induced by bending,lifting,cough• Pains that disturbs sleep/presents immediately upon awakening

• Known systemic illness• Onset after age 55• Pain associated with local tenderness eg.: region of temporal artery

MIGRAINE• Second most common cause of headache

• Episodic headache with certain features such as sensitivity to light, sound, and movement

• Headache often accompanied by nausea and vomiting

• A benign and recurring syndrome of headache associated with other symptoms of neurologic dysfunction in varying admixtures.

• Sensitive to environmental and sensory stimuli

PATHOPHYSIOLOGY1) Vascular theory

2) Cortical spreading depression

• Activation of cells in the trigeminal vasoactive neuropeptides,

calcitonin gene–related peptide (CGRP), at vascular terminations of the

trigeminal nerve and within the trigeminal nucleus.

• Centrally, the second-order trigeminal neurons cross the midline and

project to ventrobasal and posterior nuclei of the thalamus for further

processing.

• Other brainstem region : nucleus locus coeruleus in the pons and the

rostroventromedial medulla.

PATHOPHYSIOLOGY

3) Involvement of neurotransmitter 5-hydroxytryptamine- methysergide : first drug capable of preventing migraine attacks- triptans : potent agonists of 5-HT1B, 5-HT1D, 5-HT1F

PATHOPHYSIOLOGY

4) Role of dopamine- migraine symptoms can be induced by dopaminergic stimulation- dopamine receptor antagonists are effective especially when given parenterally or concurrently with other antimigraine agents

PATHOPHYSIOLOGY

• Migraine has a strong genetic component5) Familial hemiplegic disorders

- rare type of migraine with aura

FHM MUTATIONS

FHM1 CAY2.1 (P/Q)-type voltage-gated calcium channel CACNA1A gene

FHM2 Na+-K+ATPase ATP1A2 gene

FHM3 Neuronal voltage gated sodium channel SCN1A

• Hormonal influences – usually occur during menstruation

• Contraceptive pill - exacerbate migraine in many patients

• Dietary precipitants - cheese, chocolate, red wine

• Psychological stress - pt tend to have attacks at

weekends/beginning of a holiday (may be associated with

vasodilatation of extracranial vessels, but may be due to

disturbed neuronal activity in the hypothalamus

DIAGNOSIS & CLINICAL FEATURESRepeated attacks of headache lasting 4-72 hours in patients with a normal physical examination, no other reasonable cause for the headache and:At least 2 of the following features

Plus at least 1 of the following features

Unilateral pain Nausea/vomiting

Throbbing pain Photophobia and phonophobia

Aggravation by movement

Moderate or severe intensity

TREATMENT

• NON PHARMACOLOGIC MANAGEMENT– Identify and avoid of specific headache triggers– Change of lifestyles– Reduce stress

TREATMENT

• ACUTE ATTACK THERAPIES FOR MIGRAINE– Mild migraine : oral agents– Severe attacks : parenteral therapy – Drugs : • 5-HT1B/1D receptor agonists• Ergot alkaloids• NSAIDs• Dopamine receptor antagonists

•Simple Analgesics•Acetaminophen, aspirin, caffeine : Two tablets or caplets q6h (max 8 per day)

•NSAIDs•Naproxen :220–550 mg PO bid

•5-HT1 Agonists•Oral•Ergotamine One 2 mg sublingual tablet at onset

•Nasal•Dihydroergotamine •Prior to nasal spray, the pump must be primed 4 times; 1 spray (0.5 mg) is administered, followed in 15 min by a second spray

Cont..

• Parenteral• Dihydroergotamine : 1 mg IV, IM, or SC at onset and q1h • Sumatriptan:6 mg SC at onset • Dopamine Antagonists• Oral• Metoclopramide :5–10 mg/d• Parenteral• Chlorpromazine 0.1 mg/kg IV at 2 mg/min; max 35

mg/d

OTHER• Other• Oral• Acetaminophen, 325 mg, plus dichloralphenazone, 100 mg,

plus isometheptene, 65 mg• Two capsules at onset followed by 1 capsule q1h (max 5

capsules)• Nasal• Butorphanol 1 mg (1 spray in 1 nostril), may repeat if

necessary in 1–2 h• Parenteral• Narcotics

TREATMENT

• PREVENTIVE TREATMENT

– Frequency of attacks is >2 per month

– Duration of attacks is >24 hours

– Disturb patient's lifestyle, with significant disability

that lasts 3 or more days

– Acute attack therapies fails or is overused

DRUGS DOSES

Antiepileptic drugs : valproate

400-600 mg bid

Beta blockers : propranolol 40-120mg bid

Tricyclic antidepressants :amitriptyline

10-75 mg at night

Serotonergic drugs:methysergide

1-4 mg qd

Pizotifen 0.5-2 mg qid

SECONDARY HEADACHE

MENINGITIS

INTRACRANIALHEMORRHAGE

BRAIN TUMOR

TEMPORALARTERITIS

GLAUCOMA

• MENINGITIS• Acute,severe headache

with neck stiff, fever• Lumbar puncture is

mandatory• Striking accentuation of

pain with eye movement

• INTRACRANIAL HEMORRHAGE

• Acute,severe headache with stiff neck,no fever suggest subarachnoid hemorrhage

• BRAIN TUMOR• Chief complaints of headache-

30%• Pain: intermittent deep, dull

aching of moderate intensity• Disturb sleep:10%• Vomitingheadcahe by weeks:

posterior fossa brain tumors• h/o amenorrhea& galactorrhea

prolactin-secreting pituitary adenoma/PCOS

• Head pain appear abruptly after bending, lifting,coughing posterior fossa mass, a Chiari malformation, low CSF volume

• GLAUCOMA• Prostrating headache with

nausea& vomiting• Starts with severe eye pain• On P/E: eye is often red with a

fixed,moderately dilated pupil

TEMPORAL ARTERITIS

• Inflammatory disorder of arteries(extracranial carotid circulation)• Common disorder of elderly• Half of the patient with untreated TA blindness • Symptoms: headache, polymyalgia rheumatica, jaw claudication,

fever and weight loss • Pain usually appears gradually over a few hours before peak

intensity is reached; occasionally, it is explosive in onset. • The quality of pain:throbbing; it is almost invariably described as

dull and boring, with superimposed episodic stabbing pains

REFERENCE

• Harrison’s Principle of Internal Medicine, 18th Edition, Volume 1

• Davidson’s Principles and Practice of Medicine, 22nd Edition

• http://emedicine.medscape.com/article/1142556