This document provides an overview of headaches, including their definition, epidemiology, classifications, causes, clinical features, management, and prognosis. It focuses specifically on tension headaches and migraines. Some key points: - Headaches are very common, with about 7 in 10 people experiencing at least one per year. Migraines affect 15-20% of women and 5-10% of men. - Headaches are classified as primary (not caused by an underlying condition) or secondary (caused by underlying issues). Migraines and tension headaches are examples of primary headaches. - Migraines involve severe throbbing pain that is often accompanied by nausea, sensitivity to light and sound. Tension

1. By Yahya Ibrahim
MBChB 3.
Dr. Bacwa.
HEADACHE

2. LEARNING OBJECTIVES
 Definition
 Epidemiology
 Classifications and pathophysiology
 Causes
 Clinical features
 Complications
 Managements
 Preventions
 Prognosis
 References

3. Definition
 A headache is a very common condition that
cause pain and discomfort in the head, scalp
or neck.
 Migraine headache is a complex, recurrent
headache disorder that is one of the most
common complaints in medicine.

4. EPIDEMIOLOGY
 It’s estimated that 7 in 10 people have at least
one headache each year.
 50% of the general population have
headaches during any given year and more
than 90% report a lifetime history of
headache.
 Approximately 70% of migraine patients have
first-degree relative with history of migraine.
 Primary headaches are a common problem in
the general population and one of the most
common complaints in neurology clinics.

5. CLASSIFICATIONS
 Primary headache are benign, recurrent
headaches not caused by underlying disease or
structural problems.
 Secondary headache are those caused by an
underlying disease. May be due to structural,
infective, inflammatory or vascular condition.

7. OTHER CAUSES
 External compression headache(a result of
pressure-causing headgear)
 Ice cream headache(commonly called brain
freeze)
 Rebound headaches(caused by overuse of pain
medication)
 Sinus headache(caused by inflammation
&congestion in sinus cavity)

9. History.
Ask about
 Headache location (e.g. hemicranial), severity and
 Character (e.g. throbbing vs non-throbbing)
 Associated symptoms, e.g. nausea, photophonia, phonophobia and
motion sensitivity
 Presence of autonomic symptoms, e.g. tearing or ptosis
 Relieving or exacerbating features, e.g. effect of posture
 Headache pattern. Is headache episodic and part of a pattern of
previous similar headaches?
 Age at onset and headache frequency
 Duration of headache episodes (helpful in distinguishing between
different primary headache types)
 Triggers
 Pattern of analgesic use
 Family history of headache
 Red flag’ symptoms – fever (meningitis, sinusitis).

10. Migraine headache
 A headache of very intensity, often accompany by
nausea and sensitivity to light and sound.
 (15–20% of women and 5–10% of men); in 90%,
onset is before 40 years of age.
 Migraine accounts for 10-20%of all headache in
adults
 1% chronic migraine (>15days/months)

11. Pathogenesis.
 Genetic factors play a part in causing the
neuronal hyper excitability.
 Migraine is polygenic but a rare form of familial
migraine is associated with mutations in the α-1
subunit of the P/Q-type voltage-gated calcium
channel or neuronal sodium channel (SCN1A),
and a dominant loss of function mutation in
potassium channel gene (TRESK) has recently
been identified in some patients with migraine
with aura.

12. Pathophysiology
Theories on the pathogenesis of migraine include:
 The vascular theory
 The neurovascular hypothesis
 The cortical spreading depression theory
 The serotogenic abnormalities hypothesis

13. Contn.
 Migraine is now thought to have a primarily
neurogenic rather than vascular basis.
 Spreading cortical depression-a wave of neuronal
depolarization followed by depressed activity
spreading slowly anteriorly across the cerebral
cortex from the occipital region-is thought to be
the basis of migraine with aura.
 Activation of trigerminal pain neurones is the
basis of headache.

14.  Prodromal symptoms last 15mins-1hr or more.
 There is decrease in cerebral blood flow due to
vasocntriction at the onset of an attach resulting
in focal disturbances of cortical
function,particulary in the occipital and parietal
lobes.
 Causing visual disturbances, nausea, tingling of
limbs ,transient aphasia and vague weakness of
one side

15. Migraine triggers.
 Stress
 Emotion
 Sex
 Glare-flickering light/light glare
 Hypoglycaemia
 Altered sleep pattern
 Menses
 Physical exertion
 Alcohol
 Smoking
 Excess caffein/withdrawal
 Odors( perfume, exhaust fumes, paint solvents)
 Food containig tyramine, nitrates, phenyl ethylamine, aspartame,
chocolate.
 Drugs
 Estrogen
 Nitroglyceride
 cocaine, theophylline

16. Clinical features of Migraine
 Malaise
 Irritability or behavioral change for some hours or
days
 Phonophobia
 Vomiting lasting from 4 to 72hrs
 Photophobia

17. Migraine without aura
Previously used terms:
 Common migraine; hemicrania simplex
Description:
 Recurrent headache disorder manifesting in
attacks lasting 4-72 hours
 Typical characteristics of headache are unilateral
location, pulsating quality, moderate or severe
intensity, aggravation by routine physical activity
and association with nausea and/or photophobia
and phonophobia

18. Diagnostic criteria.

19. Migraine with aura
Previously used terms:
 Classic, or classical migraine; complicated
migraine
Description:
 Recurrent attacks, lasting minutes, of unilateral
fully reversible visual, sensory or other CNS
symptoms that usually develop gradual and usually
followed by headache and associated with
migraine symptoms.

20.  Aura is a complex neurological symptoms that
occurs usually before the headache of but it may
begin after the pain phase has commenced or
continue to headache phase
 Visual aura is the most common occuring in over
90% of patients
 Is risk factors for ischemic stroke
 4 phase: prodrome, aura, headache and resolution
or postdrome

21. Management
 Pharmacological agents can be classified as
acute or prophylactic.
 Acute aims to reverse or at least stop progression
of a headache.
 It is most effective when given with in 15 min of
pain onset and when pain is mild.

22. Contn.
Treatment of acute episode:-
First lline include NSAIDS and paracetamol.
• Paracetamol 1 g every 6 hours
• Or Ibuprofen 400 mg every 6-8 hours
• Or Acetylsalicilic acid 300-900 mg every 4-6
hours (max 4 gr daily)

23. If not improving,
Selective serotonin receptor (5-HT1)agonists
 Naratriptan 2.5-mg tablet at onset; may repeat once after 4 h
 Rizatriptan 5–10-mg tablet at onset; may repeat after2h(max 30
mg/d)
 Sumatriptan 50–100-mg tablet at onset; may repeat after 2 h
(max 200 mg/d)
 Frovatriptan 2.5-mg tablet at onset, may repeat after 2 h (max
5 mg/d)
 Almotriptan 12.5-mg tablet at onset, may repeat after 2 h (max
25 mg/d)
 Eletriptan 40 or 80 mg
 Zolmitriptan 2.5-mg tablet at onset; may repeat after 2 h (max
10 mg/d)

24. Ergot alkaloids
 Ergotamine 1 mg, One or two tablets at onset,
then one tablet q½h (max 6 per day, 10 per week)
 Dihydroergotamine (Migrainal Nasal Spray);
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
 Caffeine. Concurrent adminstrationof caffeine
improves both the rate and extent of absorption
of ergotamine.

25. Parenteral
 Dihydroergotamine (DHE-45 ) 1 mg IV, IM, or
SC at onset and q1h (max 3 mg/d, 6 mg per
week)
 Sumatriptan 6 mg SC at onset (may repeat once
after 1 h for max of 2 doses in 24 h)

26. Cont.
Dopamine Receptor Antagonists
1.Oral
 Metoclopramide 5–10 mg/d
 Prochlorperazine 1–25 mg/d
2.Parenteral
 Chlorpromazine 0.1 mg/kg IV at 2 mg/min; max
35 mg/d
 Metoclopramide 10 mg IV
 Prochlorperazine 10 mg IV

27. Prophylactic medications.
Indications.
1. Frequency of migraine attacks is greater than 2
per month
2. Overused or failed abortive treatment
3. Duration of attacks longer than 24 hrs
4. Headaches cause major disruption of patients
lifestly, with significant disability that lasts 3 or
more days
5. Use of abortive medication more than 2 weeks
6. Risk of permanent neurological injury

28. Contn.
Medications.
1. Antiepileptic drugs
2. Beta blockers
3. Tricyclic antidepressant
4. Calcium channel blockers
5. NSAIDS
6. Botulinum toxin

29. Tension headache
 Tension-type headache(TTH) is the most common
type of headache and is experienced to some degree
by the majority of the population.
 TTH is chronic head-pain syndrome characterized by
bilateral tight, bandlike discomfort.
 Pain typically builds slowly, fluctuates in severity, and
may persist more or less continuously for many days.
 Headache may be episodic or chronic.
 Headaches are without accompanying features such
as nausea, vomiting, photophobia, osmophobia,
throbbing, and aggravation by movement.

30. Pathophysiology.
 Tension-type headache is incompletely understood,
and some consider that it is simply a milder version
of migraine; certainly, the original notion that it is
due primarily to muscle tension (hence the
unsatisfactory name) has long since been
dismissed.
 In contrast to migraine, pain is usually mild to
moderate severity, bilateral and relatively
featureless, with tight band sensations, pressure
behind the eyes.
 TTH is often attributed to cervical spondylosis,
refractive errors or high blood pressure evidence for
such associations is poor.
 Depression is also a frequent co-morbid feature.

31. Clinical features.
 Headache characterised as ‘dull’, ‘tight’ or like a
‘pressure’, and there may be a sensation of a
band round the head or pressure at the vertex.
 Headache is of constant character and
generalised, but often radiates forwards from the
occipital region.
 May be episodic or persistent.
 There is no associated vomiting or photophobia.
 Tenderness may be present over the skull
vault or in the occiput.

32. Classification
ICHD CLASSIFICATION
1. Infrequent episodic tension-type headache
2. Frequent episodic tension-type headache
3. Chronic tension-type headache

33. Infrequent episodic TTH
 Infrequent episodes of headache, typically
bilateral, pressing or tightening in quality and of
mild to moderate intensity, lasting minutes to days
 Infrequent episodic type tension-type headache:
one or fewer episodes per month.

34. Diagnostic criteria.
a) At least 10 episodes of headache occurring on<1
day per month on average (<12 days per year) &
fulfilling criteria b-d.
b) Lasting from 30 minutes to 7 day.
c) At least two of the following
• Bilateral location
• Pressing or tightening quality
• Mild or moderate intensity
• Not aggravated by physical activity
d) Both of the following:
No nausea or vomiting
No more than one of photophobia or phonophobia
episode.

35. Frequent episodic TTH.
 Frequent episodic type tension-type headache:
more than one, but fewer than 15 episodes per
month for three or more months.

36. Diagnostic criteria.
a) At least 10 episodes of headache occurring on 1-
14 days per month on average of >3 months.
b) Lasting from30 min to 7 days.At
c)At least two of the following;
• Bilateral location
• Pressing tightness quality
• Mild or moderate intensity
d) Both of the following
• No N/V
• No more than one photophobia or phonophobia

37. Chronic tension-type headache.
 Chronic tension-type headache: more than 15
episodes per month for three or more months.

38. Management
Acute treatment.
 Simple analgesics such as acetaminophen, aspirin or
NSAIDS
 Behavioral approaches including relaxation can also be
effective
 Limit acute treatment to 2-3 days perweek.
Preventative.
Non pharmacological:
 Proper sleep
 Stress management
 Acupuncture
 Physical therapy
Pharmacological:
 TCAs

39. Trigeminal autonomic
cephalalgias
 TACs are characterized by relatively short lasting
attacks of head pain associated with cranial
autonomic symptoms, such as lacrimation,
conjunctival injection or nasal congestion
 Includes
1. Cluster headache
2. Paroxysmal hemicrania
3. SUNCT-Short-lasting, Unilateral, Neuralgiform
headache attacks with Conjunctival injection
and Tearing

40. CLUSTER HEADACHES
 So called because these headaches occurs
during a short time span.
 The cluster then occurs periodically.
 Atypical cluster of headaches may last 4-8
weeks with 1-2 headaches/day during the
cluster.
 They may be distinctly seasonal.
 Young adult men are more affected then women.
 Although uncommon, it is the most common of
the trigeminal autonomic cephalalgia syndromes.

41. Cause and mechanism of cluster
headache
 Cause not clear
 Probably due to paroxysmal parasympathetic
discharge mediated through the greater
superficial pertrosal nerve and sphenopalatine
ganglion.
 Functional imaging stuies have suggeste
abnormal hypothalamic activity.

42. Clinical features.
 Abrupt onset of headache originating in the eye and
spreading over the temporal area.
 Pain extremely severe and last 15-180 min
 Unilateral lacrimation
 Nasal congestion
 Conjunctival injection
 Eyelid oedma
 Forehead and facial sweating
 Sensation of fullness in ears
 Miosis and/or ptosis
 Pts. Are often highly agitated during the headache
phase

43. Management.
 Tryptan – sumatriptan 6 mg SC is rapid in onset
and usually shorten attacks to 10-15 min
 Sumatriptan (20mg) and zolmitrptan (5mg) nasal
sprays are both effective in acute cluster
headache
 DHE.

44. THUNDERCLAP HEADACHE
 Thunderclap also referred to as a lone acute
severe headache. It is sudden onset that takes
seconds to minutes to reach maximum intensity
 Clinical features are;
- Vomiting and nausea
- Fainting
- Pain felt anywhere in your neck

45. CAUSES OF THUNDERCLAP
HEADACHE
 Subarachnoid hemorrhage(10-25% of all causes)
 Cerebral venous sinus thrombosis
 Cervical artery dissection
 Hypertensive emergency
 Spontaneous intracranial
hypotension(unexplained low csf pressure)
 Stroke

46. COMPLICATIONS
1.Permanent brain damage
2.Migraine-triggered stroke or seizure
3.Migraine rises risk of heart attack and early death
4.Loss of motivation to go do work
5.Isolation from social activities

47. Management
a. Non pharmacological.
• Drink water,inadequte hydration may lead you to
develop a headache
• Limit alcohol
• Get adequate sleep
• Avoid foods high in histamine
• Perfect your posture. Good posture can help your
muscle tensing

48. Contn.
b. Pharmacological
• Treatment of acute attack consists of simple
analgesia with aspirin,paracetamol,or NSAID
• Anti emesis eg metoclopramide
• In severe attacks use triptans e.g. sumatriptan
• Inhalation of 100% oxygen

49. Medication overuse headache.
 With increasing availability of over-the-counter medication,
 headache syndromes perpetuated by analgesia intake are
 becoming much more common.
 Medication overuse headache (MOH) can complicate any headache
syndrome but is especially common with migraine and chronic
tension-type headache.
 The most frequent culprits are compound analgesics (particularly
 codeine and other opiate-containing preparations) and triptans and
MOH is usually associated with use on more than 10–15 days per
month.
 Management is by withdrawal of the responsible analgesics.
 Patients should be warned that the initial effect will be to exacerbate
the headache, and migraine prophylactics may be helpful in
reducing the rebound headaches.
 Relapse rates are high, and patients often need help and support in
withdrawing from analgesia; a careful explanation of this
paradoxical concept is vital.

50. Trigeminal neuralgia.
 This is characterised by unilateral lancinating facial
pain, most commonly involving the second and/or
third divisions of the trigeminal nerve territory,
usually in patients over the age of 50 years.
Pathophysiology.
 Mostly idiopathic but there is a suggestion that it
may be due to an irritative lesion involving the
trigeminal root zone, in some cases an aberrant
loop of artery.
 Other compressive lesions, usually benign, are
occasionally found.
 Trigeminal neuralgia associated with multiple
sclerosis may result from a plaque of demyelination
 in the brainstem.

51. Clinical features.
 The pain is repetitive, severe and very brief
(seconds or less).
 It may be triggered by touch, a cold wind or
eating.
 Physical signs are usually absent, although the
spasms may make the patient wince and sit
silently (tic douloureux).
 There is a tendency for the condition to remit and
relapse over many years.
 Rarely, theremay be combined features of
trigeminal neuralgia and cluster headache
(‘cluster–tic’).

52. Management
 A low dose carbamezapine and increase
gradually, according to effect.
 In patients who cannot tolerate carbamazepine
oxcarbazepine, gabapentin, pregabalin,
amitriptyline or glucocorticoids may be effective
alternatives, but if medication is ineffective or
poorly tolerated, surgical treatment should be
considered.
 Decompression of the vascular loop encroaching
on the trigeminal root is said to have a 90%
success rate.
 Otherwise, localised injection of alcohol or phenol
into a peripheral branch of the nerve may be

53. Prevention
A practicing these easy steps will help you avoid
many common headache triggers
1. Maintain good posture, and move around during
the day
2. Get the right pillows
3. Stay consistent
4. Get an appropriate amount of sleep
5. Stick to a healthy diet and exercise regimen
6. Drink water
7. Manage stress

54. References
 Davidson’s principles and practice of medicine
23rd edition.
 Kumar and clark clinical medicine 8th Edition.