definition - types of headaches symptoms & signs Pathophysiology -diagnosis and treatment of primary headache syndromes

1. HEADACHE
Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine

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CONTENTS
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4
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Diagnosis
PREVENTION
&TREATMENT
INTRODUCTION
TYPES
PRIMARY
HEADACHE
SYNDROMES

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1 INTRODUCTION

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Introduction
 Definition : A headache is a pain or discomfort in the
head , scalp , or neck
 One of the most common of all human physical
complaints.
 Headache is actually a symptom rather than a disease
a stress response, vasodilation (migraine),skeletal
muscle tension (tension headache), or a combination
of factors.

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Worldwide problem
 Up to 25% of adults have a severe
headache each year
 Up to 4% have daily or near-daily
headache
 Lifetime prevalence: 90% or more
 Significant suffering and economic loss

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2 TYPES

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Classification
I. PRIMARY HEADCHE
 A headache that is not caused by another
underlying disease, trauma or medical condition.
 Accounts for about ninety percent of all headaches.

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 Intrinsic dysfunction of the nervous system
 Most patients presenting with headache have primary
headache syndromes
 Episodic headache: more common
 Chronic headache: attacks occurring more frequently
than 15 days/month for more than 6 months
Cont.

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 <2% of headaches in primary care offices
 Caused by exogenous disorders:
o Head trauma
o Vascular disease
o Neoplasms
o Substance abuse or withdrawal
o Infection/Inflammation
o Metabolic disorders
o others
II. SECONDARY HEADCHE

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3 PRIMARY HEADACHE SYNDROMES

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 PRIMARY HEADACHE SYNDROMES
 Tension type headache
 Migraine
 Trigeminal Neuralgia
 Cluster headache
 Others

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I- TENSION TYPE
 Most common-69%
 Episodic or chronic
 Primary disorder of CNS pain
modulation
 seen equally in both sexes

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 Precipitating factors
 Stress: usually occurs in the afternoon after long stressful work
hours or after an exam
 Sleep deprivation
 Uncomfortable stressful position and/or bad posture
 Irregular meal time (hunger)
 Eyestrain
 Caffeine withdrawal
 Dehydration

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Symptoms & Signs
 Gradual onset , radiate forward from occiput
 Bilateral, dull, tight, band like pain
 Less in morning, pain increase as day goes on
 No accompanying N,V, throbbing, sensitivity to
light, sound or movement

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 Management
 Paracetamol,Aspirin,NSAIDs
 Behavioral approach-relaxation
 Chronic-amitriptyline

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II- MIGRAINE
 2nd most common-16%
 15% women and 6% men
 Severe, episodic, unilateral,throbbing pain
 Nausea,Vomiting
 Sensitivity to light ,sound, movement
 Genetic predisposition

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Pathophysiology
 Different theories suggest different causes
I. Vascular theory :
 vasoconstriction followed by vasodilation with resulting in
changes in blood flow causes the throbbing pain .
II. Second theory :
 pain results from muscular tension
III. Biochemical changes:
 changes in serotonin level

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Triggers
 Flashing lights , Loud sounds , Strong odors
 Stress
 Hunger
 Fatigue
 Smoking
 Menstruation , Pregnancy , Menopause , Oral Contraceptives
 Sleep changes
 Caffeine ,Chocolate ,Tyramine

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Classical Migraine or
Migraine with AURA
 Symptom Triad
 Paroxysmal headache
 nausea &/or vomiting
 aura of focal neurological events(visual) 20-25%

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 AURA:
 Flashing lights, silvery zigzag lines moving across visual
field over a period of 20 minutes
 Sometimes leaving a trail of temporary visual field loss
 Sometimes-Auditory ,Olfactory, gustatory hallucinations
 Sensory aura-spreading front of tingling and numbness,
from one body part to another

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Common Migraine or
Migraine without AURA
 Paroxysmal headache
 Vomiting +/-
 NO AURA

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Diagnosis
 Simplified Diagnostic Criteria for MIGRAINE
At least 2 of the following + At least 1 of the following:
o Unilateral pain
o Throbbing pain
o Aggravation by
movement
o Moderate or severe
intensity
o Nausea/vomitting
o Photophobia and phonophobia

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Management
 Non drug treatmenr
 Preventive therapy
 Abortive therapy

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Management
 Non drug treatment
 Avoid headache triggers: foods, drugs, activities
 Avoid frequent abortive treatment
 Stop smoking
 Normalize sleeping and eating
 Exercise
 Relaxation and biofeedback
 Psychotherapy

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Management
 Preventive Treatment
 Tricyclic antidepressants (first-line)
o Amitriptyline
 Beta-blockers (first-line)
o Atenolol, nadolol
 Ca++ channel blockers – less effective
o Verapamil most commonly used

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Management
 Preventive Treatment
 Anticonvulsants (second-line; valuable)
 Valproate and topiramate are quite effective
 Gabapentin
 Lamotrigine, levetiracetam
 Pregabalin

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Management
 Preventive Treatment
 Ergots: Rarely used for prevention
o Side effects may be problematic
o Methysergide: fibrosis (use 6 months max)
 MAOIs: Can be very effective
o Tyramine-free diet a must
o Numerous drug interactions

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Management
 Abortive Treatment
 Simple and combined analgesics e.g NSAIDs.
 Mixed analgesics (barbiturate plus simple analgesics)
 Ergot derivatives
 Triptans
 Opioids

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Management
 Triptans:
 Serotonin 5-HT1 agonists
 Reduce neurogenic inflammation
 Most effective if used at onset of headache or aura, though may
be helpful at other phases
 Used specifically for migraine
 For nonresponders, try ergots (also act on NE, DA, other
receptors)

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Management
 Other Agents
 Antiemetics/Neuroleptics:
o often combined with abortive agents
o Prochlorperazine, hydroxyzine, promethazine, metoclopramide

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 Drugs To Avoid
 Butorphanol nasal spray
 Meperidine
 Overuse of any short-acting analgesic (opioids,
triptans)

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III- Trigeminal Neuralgia
 Lancinating pain in 2nd and 3rd divisions of
trigeminal nerve
 >50yrs
 Severe, brief ,repetitive pain causing patient
to flinch
 Precipitated by touching trigger zones:
washing, shaving, eating, cold wind

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Pathophysiology
 Compression of trigeminal N by aberrant loop of
cerebellar arteries as nerve enters brainstem
 Other benign compressive lesions
 Multiple sclerosis: occurs due to plaque of
demyelination in trigeminal root entry zone

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Management
 Carbamazepine
 Intolerant-Gabapentin/Pregabalin
 Injection of alcohol into peripheral branch of nerve
 Posterior craniotomy to relieve vascular compression of
trigeminal nerve

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IV- CLUSTER HEADACHE
 Headaches occur during a short time span.
 The cluster then recurs periodically.
 A typical cluster of headaches may last 4-
8weeks with 1-2 headaches/day during the
cluster.
 Patient may be free 6months to 1year before
another cluster of headache occurs.
 Male to Female ratio 5:1

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Symptoms & Signs
 Abrupt onset of headache originating in the eye and spreading
over the temporal area.
 Pain extremely severe and last 20-60minutes
 The headache associated with
 Nasal stuffiness
 Rhinorrhoea
 Redness of the Eye
 Flush and edema of the cheek

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Management
 Acute:
 Oxygen inhalation 100%
 Triptans/ergots
 Indomethacin

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Management
 Chronic/Preventive:
 Verapamil, lithium
 Valproate, topiramate
 Prednisone burst
 Melatonin
 Ergots

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Medication Overuse Headache
 Persistent, recurring headache in the setting of regular
analgesic use
 Continues until medication is stopped
 Often responsible for “transformation” of episodic into
chronic headache

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46. Thanks
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