1. دکترمحمدرضانجفی استاد مغزواعصاب
Headaches
Dr. Mohammad Reza Najafi Professor of Neurology
دکترمحمدرضانجفی
استاد مغزواعصاب

2. Introduction Nearly everyone is subject to headache from time to time;
moreover, 40% of all people have severe headaches annually.
The brain mechanism that generates headaches is
activated by many factors.
Genetic factors probably augment
the system, so that some people are susceptible to
more frequent or more severe head pain.

3. Headache is usually a benign symptom and only occasionally
is a manifestation of a serious illness, such as
brain tumor, aneurysmal rupture or giant cell arteritis.
The first issue to resolve in the care of a patient with
headache is to differentiate benign and more ominous
causes.

4. Painful state characteristics
1- Quality
2- Severity
3- Location
4- Duration
5- Time course
6- Intensity
7- Mode of onset
8- Time - intensity curve
9- Conditions that produce , exacerebation, relieve
10- personality of patients

6. IHS Classification of Headache

7. Part I: The Primary Headaches
1. Migraine
2. Tension-type headache
3. Cluster headache and other trigeminal autonomic cephalalgias
4. Other primary headaches

8. Part II: The Secondary Headaches
5. Headache attributed to head and/or neck trauma
6. Headache attributed to cranial or cervical vascular disorder
7. Headache attributed to non-vascular intracranial disorder
8. Headache attributed to a substance or its withdrawal
9. Headache attributed to infection

9. 10. Headache attributed to disorder of homoeostasis
11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures
12. Headache attributed to psychiatric disorder

10. Part III: Cranial Neuralgias Central and Primary Facial Pain and Other Headaches
13. Cranial neuralgias and central causes of facial pain
14. Other headache, cranial neuralgia, central or primary facial pain

12. Tension-type headache (TTH)
Tension-type headache (TTH) represents one of the most costly diseases because of its very high prevalence.
TTH is the most common type of headache, and it is classified as episodic (ETTH) or chronic (CTTH).
It had various ill-defined names in the past including tension headache, stress headache, muscle contraction headache, psychomyogenic headache, ordinary headache, and psychogenic headache.

13. Episodic tension-type headache
At least 10 previous headaches fulfilling the following criteria; number of days with such headache fewer than 15 per month
Headaches lasting from 30 minutes to 7 days

14. Characteristics of tension type headache
At least 2 of the following pain characteristics: Pressing/tightening (nonpulsating) quality Mild or moderate intensity (may inhibit but does not prohibit activities) Bilateral location No aggravation from climbing stairs or similar routine physical activity Both of the following: No nausea or vomiting Photophobia and phonophobia absent or only one present Secondary headache types not suggested or confirmed

15. Chronic tension-type headache
Average headache frequency of more than 15 days per month for more than 6 months fulfilling the following criteria At least 2 of the following pain characteristics: Pressing/tightening (nonpulsating) quality Mild or moderate intensity (may inhibit but does not prohibit activities) Bilateral location No aggravation from climbing stairs or similar routine physical activity Both of the following: No vomiting No more than one of the following: nausea, photophobia, or phonophobia Secondary headache types not suggested or confirmed

16. Pathophysiology of TTH
Pathogenesis of TTH is complex and multifactorial, with contributions from both central and peripheral factors.
In the past, various mechanisms including vascular, muscular (ie, constant overcontraction of scalp muscles), and psychogenic factors were suggested.
The more likely cause of these headaches is believed now to be abnormal neuronal sensitivity and pain facilitation, not abnormal muscle contraction.

18. Various evidence suggests that, like migraine, TTH is associated with exteroceptive suppression (ES2), abnormal platelet serotonin, and decreased cerebrospinal fluid beta-endorphin.

19. Epidemiology Frequency
Rasmussen et al reported a lifetime prevalence of TTH of 69% in men and 88% in women in the Danish population.[2] The patient may experience more than one primary headache syndrome.

20. Tension headache

21. Sex Women are slightly more likely to be affected than men
Sex Women are slightly more likely to be affected than men. The female-to-male ratio for TTH is approximately 1.4:1. In CTTH, female preponderance is 1.9:1. Age TTH can occur at any age, but onset during adolescence or young adulthood is common. It can begin in childhood.

22. History
Tension-type headaches (TTHs) are characterized by pain that is usually mild or moderate in severity and bilateral in distribution. Unilateral pain may be experienced by 10-20% of patients. Headache is a constant, tight, pressing, or bandlike sensation in the frontal, temporal, occipital, or parietal area (with frontal and temporal regions most common).

24. Physical
Patients with TTH have normal findings on general and neurologic examinations. Some patients may have tender spots or taut bands in the pericranial or cervical muscles (trigger points).

26. Causes
Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor.
Stress - Usually occurs in the afternoon after long stressful work hours
Sleep deprivation
Uncomfortable stressful position and/or bad posture
Irregular meal time (hunger)
Eyestrain

27. Differential Diagnoses
Aseptic Meningitis Lyme Disease Migraine Headache Migraine Variants Pseudotumor Cerebri

28. Laboratory Studies
The diagnosis of tension-type headache (TTH) is clinical. As with the other primary headaches, no specific diagnostic test is available for TTH. Occasionally, studies may be required to exclude secondary headache disorders.

29. Imaging Studies
Neuroimaging studies are important to rule out secondary causes of headache, including neoplasms and cerebral hemorrhage. MRI imaging shows the greatest detail of cerebral structures and is especially useful in evaluating the posterior fossa. CT scan with contrast is a viable alternative but is inferior to MRI for viewing structures in the posterior fossa. Neuroimaging is indicated if the headaches are atypical in any way or if they are associated with abnormalities in the neurologic examination.

30. Migraine Headache Practice Essentials
Migraine is a complex disorder characterized by recurrent episodes of headache, most often unilateral and in some cases associated with visual or sensory symptoms—collectively known as an aura—that arise most often before the head pain but that may occur during or afterward.
Migraine is most common in women and has a strong genetic component.

31. Signs and symptoms Typical symptoms of migraine include the following:
Throbbing or pulsatile headache, with moderate to severe pain that intensifies with movement or physical activity
Unilateral and localized pain in the frontotemporal and ocular area, but the pain may be felt anywhere around the head or neck
Pain builds up over a period of 1-2 hours, progressing posteriorly and becoming diffuse
Headache lasts 4-72 hours
Nausea (80%) and vomiting (50%), including anorexia and food intolerance, and light-headedness
Sensitivity to light and sound

32. Features of migraine aura are as follows:
May precede or accompany the headache phase or may occur in isolation Usually develops over 5-20 minutes and lasts less than 60 minutes Most commonly visual but can be sensory, motor, or any combination of these Visual symptoms may be positive or negative The most common positive visual phenomenon is the scintillating scotoma, an arc or band of absent vision with a shimmering or glittering zigzag border

33. Physical findings during a migraine headache may include the following:
Cranial/cervical muscle tenderness Horner syndrome (ie, relative miosis with 1-2 mm of ptosis on the same side as the headache) Conjunctival injection Tachycardia or bradycardia Hypertension or hypotension Hemisensory or hemiparetic neurologic deficits (ie, complicated migraine) Adie-type pupil (ie, poor light reactivity, with near dissociation from light)

34. Diagnosis The diagnosis of migraine is based on patient history.
IHS diagnostic criteria are that patients must have had at least 5 headache attacks that lasted 4-72 hours (untreated or unsuccessfully treated) and that the headache must have had at least 2 of the following characteristics :
Unilateral location
Pulsating quality
Moderate or severe pain intensity
Aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)

35. In addition, during the headache the patient must have had at least 1 of the following:
Nausea and/or vomiting
Photophobia and phonophobia
Finally, these features must not have been attributable to another disorder.

36. Classification of migraine
Migraine without aura (formerly, common migraine)
Probable migraine without aura
Migraine with aura (formerly, classic migraine)
Probable migraine with aura
Chronic migraine
Chronic migraine associated with analgesic overuse
Childhood periodic syndromes that may not be precursors to or associated with migraine
Complications of migraine
Migrainous disorder not fulfilling above criteria

37. Migraine variants include the following:
Childhood periodic syndromes Late-life migrainous accompaniments Basilar-type migraine Hemiplegic migraine Status migrainosus Ophthalmoplegic migraine Retinal migraine

38. migraine variant
A migraine variant may be suggested by focal neurologic findings, such as the following, that occur with the headache and persist temporarily after the pain resolves: Unilateral paralysis or weakness - Hemiplegic migraine Aphasia, syncope, and balance problems - Basilar-type migraine Third nerve palsy with ocular muscle paralysis and ptosis, including or sparing the pupillary response - Ophthalmoplegic migraine

39. Testing and imaging studies
Selection of laboratory and/or imaging studies to rule out conditions other than migraine headache is determined by the individual presentation (eg, erythrocyte sedimentation rate and C-reactive protein levels may be appropriate to exclude temporal/giant cell arteritis).
Neuroimaging is not necessary in patients with a history of recurrent migraine headaches and a normal neurologic examination.

45. What is a Migraine Aura?

50. Migraine Triggers Food Disturbed sleep pattern Hormonal changes Drugs
Physical exertion
Visual stimuli
Auditory stimuli
Olfactory stimuli
Weather changes
Hunger
Psychological factors

51. Triggers: Changes in Daily Cycles

52. Triggers: Environment or Diet

53. Triggers: Mental

54. Migraine Major Forms: Migraine without aura (common) 70%
Migraine with aura (classical) 25%
Migraine variants and complicated migraine 5%

55. Phases of Acute Migraine
Prodrome
Aura
Headache
Postdrome

56. The Stages of a Migraine Attack
Migraine is more than just head pain. Migraine is a process that can start long before head pain begins.
The process of headache is generally believed to come in phases: preheadache (prodrome and aura), headache, and postheadache.
The migraine process can begin at any phase, and not all phases present themselves (either in every migraine or at all).
The process of migraine can also stop at any phase: in some cases sufferers have an aura; however, the headache never develops.
The variability inherent in the migraine process and symptoms makes multiple migraine treatment options extremely important.
Reference: Cady RK. Early intervention in the treatment of migraine. Headache Q. 2001;12(suppl 1):3-8.

57. PRODROME
Vague premonitory symptoms that begin from 12 to 36 hours before the aura and headache
Symptoms include
Yawning
Excitation
Depression
Lethargy
Craving or distaste for various foods
Duration – 15 to 20 min

58. AURA Aura is a warning or signal before onset of headache Symptoms
Flashing of lights
Zig-zag lines
Difficulty in focussing
Duration : min

59. HEADACHE
Headache is generally unilateral and is associated with symptoms like:
Anorexia
Nausea
Vomiting
Photophobia
Phonophobia
Tinnitus
Duration is 4-72 hrs

60. POSTDROME (RESOLUTION PHASE)
Following headache, patient complains of
Fatigue
Depression
Severe exhaustion
Some patients feel unusually fresh
Duration: Few hours or up to 2 days

61. MIGRAINE: CLINICAL FEATURES
Migraine Without Aura
Migraine With Aura
No aura or Prodrome
Aura or prodrome is present
Unilateral throbbing headache may be accompanied by nausea and vomiting
Unilateral throbbing headache and later becomes generalised
During headache, patient complains of phonophobia and photophobia
Patient complains of visual disturbances and may have mood variations

62. MIGRAINE - PATHOPHYSIOLOGY
VASCULAR THEORY
Intracerebral blood vessel vasoconstriction – aura
Intracranial/Extracranial blood vessel vasodilation – headache
SEROTONIN THEORY
Decreased serotonin levels linked to migraine
Specific serotonin receptors found in blood vessels of brain
PRESENT UNDERSTANDING
Neurovascular process, in which neural events result in activation of blood vessels, which in turn results in pain and further nerve activation

63. NEUROVASCULAR PROCESS

64. Arterial Activation
Release of Neurotransmitter
Worsening of Pain

66. Cascade of events underlying migraine
Pain / headache
Triggers
Brain excitability
Trigeminovascular
activation
CASCADE OF EVENTS
A whole series of events occur during a migraine attack before involvement of the TRIGEMINAL NERVE and its peripheral blood supply.
Cascade of neurochemical events
Afferent firing via
trigeminal nerve
Lumen NO
glutamate
5-HT
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67. How Migraine Works 3
Changes in nerve cell activity and blood flow
may result in visual disturbance, numbness or tingling, and dizziness. 4
Chemicals in the brain cause blood vessel dilation and inflammation of the surrounding tissue 5
The inflammation irritates the trigeminal nerve, resulting in severe or throbbing pain 2
Electrical impulses spread to other regions of the brain. 1
Migraine originates deep within the brain

68. Prognosis
Migraine is a chronic condition, but prolonged remissions are common. One study showed that among persons who had migraine during childhood, 62% were migraine free for more than 2 years during puberty and as young adults but that only 40% were still migraine free at age 30 years.

69. The severity and frequency of migraine attacks tend to diminish with increasing age. After 15 years of suffering migraines, approximately 30% of men and 40% of women no longer have migraine attacks.

70. Cluster Headache 
Cluster headache (CH), also known as histamine headache, is a primary neurovascular primary headache disorder, the pathophysiology and etiology of which are not well understood.[1]
As the name suggests, CH involves a grouping of headaches, usually over a period of several weeks.
According to the diagnostic criteria developed by the International Headache Society (IHS), CH has the following characteristics

71. The patient experiences attacks of severe or very severe, strictly unilateral pain (orbital, supraorbital, or temporal pain) that last minutes and occur from once every other day to 8 times a day

72. The attacks are associated with 1 or more of the following (all ipsilateral):
conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis, or eyelid edema

73. Cluster Headache Classification
CH may be usefully classified into 2 main forms as follows: Episodic CH, in which at least 2 cluster phases lasting 7 days to 1 year are separated by a cluster-free interval of 1 month or longer Chronic CH, in which the clusters occur more than once a year without remission or the cluster-free interval is shorter than 1 month

78. Medication overuse headaches
Affects 1 in 50 adults
Females:males 5:1
First noted with phenacetin/ergotamine
More common with aspirin/ NSAIDs/paracetamol/codeine/DF118
Can take several weeks to resolve after medication withdrawl
Key feature-pre-emptive use of analgesia

79. Medication overuse headaches-cont.
Low doses daily carry larger risk than higher doses weekly
Esp common if using simple analgesia more days than not per month
Using triptans, codeine >10days per month
Worse on awakening in the morning
Worse after physical exertion