causes, types, treatment of headache

1. HEADACHE
MODERATOR:-Dr.ARUN JOSHI MD [HOD]
GENERAL MEDICINE
PRESENTED BY:-Dr.SUBEG SINGH PGJR2

2. INTRODUCTION
• Headache is among the most common reasons patients
seek medical attention.
• Primary headaches
▫ Recurrent
▫ Benign
▫ No organic disease as their cause
• Secondary headaches
▫ Underlying organic disease

3. TYPES OF HEADACHE
• Primary headache disorders are
characterized by the lack of an identifiable and
treatable underlying cause.
• Migraine, tension-type, and cluster headaches
are examples
• Secondary headache disorders are those
associated with a variety of organic causes such
as trauma, cerebrovascular malformations, and
brain tumors.

4. International Headache
Society(IHS)
• Migraine
• Tension-Type
• Cluster
• Miscellaneous Headaches Unassociated with
Structural Lesion (e.g., cold stimulus headache,
benign exertional headache)
• Headache Associated with Head Trauma
• Headache Associated with Vascular Disorders
• Headache Associated with Nonvascular
Intracranial Disorder (e.g., high or low CSF
pressure, intracranial infection, or neoplasm)

5. • Headache Associated with Substances or their
Withdrawal (e.g., withdrawal from alcohol,
caffeine,ergotamine, narcotics)
• Headache Associated with Noncephalic Infection
(e.g., viral or bacterial infection)
• Headache Associated with Metabolic
Disorder(e.g., hypoxia, hypercapnia,
hypoglycemia, dialysis)
• Headache or Facial Pain Associated with
Disorder of Cranium, Neck, Eyes, Ears, Nose,
Sinuses, Teeth,Mouth, or Other Facial or Cranial
Structures
• Cranial Neuralgias, Nerve Trunk Pain and
Deafferentation Pain (e.g., compression,
demyelination, infarction, or inflammation.

6. Common Causes of Headache
• Primary Headache
• Type %
• Tension-type 69
• Migraine 16
• Idiopathic stabbing 2
• Exertional 1
• Cluster 0.1

7. Common Causes of Headache
• Secondary Headache
• Type %
• Systemic infection 63
• Head injury 4
• Vascular disorders 1
• Subarachnoid hemorrhage <1
• Brain tumor 0.1

8. Anatomy and Physiology of
Headache
• Relatively few cranial structures are pain-producing;
• the scalp,
• middle meningeal artery,
• dural sinuses,
• falx cerebri, and
• proximal segments of the large pial arteries.
• The ventricular ependyma, choroid plexus, pial veins,
and much of the brain parenchyma are not pain-
producing.

9. Pathophysiology Of Headache
* Two Suggested Theories For The
Pathophysiology Of Headaches / Migraines :
[1]Old : The Vascular Theory :
Intracranial vasoconstriction is responsible for
the aura of the migraine.
Headache is results from the subsequent rebound
dilatation which leads to the activation of the
perivascular nociceptive nerves.

10. Pathophysiology Of Headache
- [2]New : The Neurological Theory :
- Headaches/ Migraines are triggered by a
complex series of neural and vascular events ,
due to Neuronal hyper-excitability in
the cerebral cortex, especially in the occipital
cortex.

11. HISTORY IN HEADACHE
• Character & Pattern.
• Onset
• Duration & Frequency.
• Location & Radiation.
• Severity / Intensity / Impact.
• Relieving/ Aggravation Factors.
• Relation To Actions Or Events.
• Response To Treatment.
• Associated Symptoms.
• Previous Experience

12. PRIMARY HEADACHE SYNDROMES
• Tension type headache
• Migraine
• Trigeminal Neuralgia
• Atypical facial pain
• Cluster headache
• Benign paroxysmal
headaches

13. TENSION TYPE
• Most common-69%
• Episodic or chronic
• Gradual onset , radiate forward from occiput
• Bilateral, dull, tight, band like pain
• Less in morning, pain increase as day goes on
• No accompanying Nausea & Vomiting,
throbbing, sensitivity to light, sound or
movement

14. Pathophysiology
• Primary disorder of CNS pain modulation alone,
unlike migraine, which involves a more
generalized disturbance of sensory modulation.
.
• The name tension-type headache implies that
pain is a product of nervous tension, but there is
no clear evidence for tension as an etiology.
• Muscle contraction has been considered to be a
feature that distinguishes TTH from migraine,
but there appear to be no differences in
contraction between the two headache types.

15. • Primary disorder of CNS pain modulation
• 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

16. 2 Theories
Muscle tension around head and neck
Malfunctioning pain filter located in brain stem,
brain misinterprets information and interprets
this signal as pain. One of the main
neurotransmitters which is probably involved is
serotonin

17. Management
• Paracetamol,Aspirin,NSAIDs
• Behavioral approach-relaxation
• Amitriptyline

18. Treatment: Tension-Type Headache
• The pain of TTH can generally be managed with
simple analgesics such as acetaminophen,
aspirin, or NSAIDs.
• Behavioral approaches including relaxation can
also be effective.
• TRIPTANS in pure TTH are NOT HELPFUL,
although triptans are effective in TTH when the
patient also has migraine.

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

20. ©International Headache Society 2003/4ICHD-II. Cephalalgia 2004; 24 (Suppl 1)
1. Migraine
1.1 Migraine without aura
1.2 Migraine with aura
1.3 Childhood periodic syndromes that are
commonly precursors of migraine
1.4 Retinal migraine
1.5 Complications of migraine
1.6 Probable migraine
ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1. Migraine
1.1 Migraine without aura
1.2 Migraine with aura
1.3 Childhood periodic syndromes that are
commonly precursors of migraine
1.4 Retinal migraine
1.5 Complications of migraine
1.6 Probable migraine

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

22. 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

23. Rare aura:
• Vertigo
• Aphasia
• Hemiparesis
• Delirium
Migraine with limb weakness-Hemiplegic
migraine
Symptoms of aura do not resolve leaving
permanent neurological damage-Complicated
migraine

24. Common Migraine or Migraine
without AURA
• Paroxysmal headache
• Vomiting +/-
• NO AURA

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

26. Clinical phases of a migraine
attack
Vulnerability
Prodrome
Aura
Pain
Postdrome
Attack Initiation

27. Triggers
• Flashing lights
• Loud sounds
• Strong odors
• Stress
• Hunger
• Fatigue
• Alcohol
• Smoking
• Menstruation
• Pregnancy
• Menopause
• Oral Contraceptives
• Sleep changes
• Caffeine
• Chocolate
• Tyramine
• MSG

28. Pathophysiology of Migraine
• Cortical spreading
depression
• Vascular
• Low Serotonin
• Melanopsin receptor

29. Cortical spreading depression
• Dysfunction of ion channels-Quick
depolarization(activation) followed by long-
lasting depression over an area of cortex
• Release of inflammatory mediators
• Irritation of cranial nerve roots-trigeminal

30. Vascular
Vasoconstriction of blood vessels in brain-Aura
(begins in occipital lobe)
Vasodilatation of scalp blood vessels
Inflammation
Pain

31. Migraine Pain-Trigeminovascular
• Key pathway for pain is trigeminovascular input
from meningeal vessels
• Modulation of trigeminovascular input comes
from dorsal raphe nucleus, locus coeruleus and
nucleus raphe magnus

32. Presymptomatic hyperexcitabilty increases brain stem response to triggers
Release of Neurotransmitters
(5-HT, NE, DA, GABA, Glutamate, NO, CGRP, Substance P, Estrogen)
Neurotransmitters activate the Trigeminal Nucleus
Dilation of
Meningeal
blood vessels
(Throbbing)
Activation of
Area Postrema
NAUSEA &
VOMITING
Activation of
Cortex and
Thalamus
(Head pain)
Activation of
Hypothalamus
(Hypersensitivity)
Activation of
cervical
trigeminal
system (Muscle
spasm)

35. TREATMENT GOALS FOR
MIGRANE

36. Management
• Acute attack-
aspirin/paracetamol+metoclopromide/
domperidone
• Severe attack-Sumatriptan
• Frequent attacks-
Propranolol,Amitriptyline,Sodium valproate or
Topiramate

37. MIGRAINE MANAGMENT
Non pharmacological treatment
• Identification of triggers
• Meditation
• Relax techniques
• Psychotherapy
Pharmacological treatment
• Abortive treatment
• Preventive treatment

38. INDICATION OF PROPHYLAXIS
• Patients who have very frequent headaches
(more than 2-3/week)
• Attack duration> 48hrs
• Headache severity is extreme
• Migraine attacks are accompanied by severe
aura
• Contraindication to acute treatment
• Unacceptable adverse effects occur with acute
migraine treatment
• Patients preference

40. CLUSTER HEADACHES
• Cluster headaches derive their name from a
characteristic pattern of recurrent headaches
that are separated by periods of remission that
last from months to even years.
• During those periods when clusters of headaches
are experienced, the headaches usually occur at
least once daily.
• The headache generally is unilateral, occurs
behind the eye, reaches maximal intensity over
several minutes, and lasts for <3 hours.

41. • Unilateral lacrimation, rhinorrhea, and facial
flushing may accompany the cluster headache.
• by alcohol, naps, and vasodilating drugs.
• common in males than females.

43. Pathophysiology
• Not commonly undestood.
• The cyclic nature of attack implicates a
pathogenesis of hypothalamic dysfunction with
resulting alterations in circadian rhythms.
• During a cluster headache, thermography shows
increased peri-orbital heat emission ipsilateral
to the head pain.
• Also, patients commonly report flushing in the
same area, and these observations suggest that
extracranial vasodilation occurs.
• Abnormal plasma levels of melatonin, growth
hormone,testosterone, and prolactin have been
reported

44. • occur commonly at night
• Attacks occur suddenly, with pain peaking
quickly after onset and generally lasting 15 to
180 minutes.
• Auras are not present with cluster headaches.
• The pain is excruciating, penetrating,and of a
boring intensity in orbital, supraorbital, and
temporal unilateral locations.
• The headache can be accompanied by
conjunctival injection, lacrimation, nasal
stuffiness, rhinorrhea, eyelid edema, facial
sweating, miosis/ptosis, and restlessness or
agitation.
• During the cluster period, attacks occur from
once every other day to eight times per day

45. TREATMENT
• 1. abortive
• 2.prophylactic
• [1]ABORTIVE
• Oxygen
The standard acute treatment of cluster headache
is inhalation of 100% oxygen by at a rate of 7 to 10
L/min for 15 to 25 minutes

46. • Ergotamine Derivatives
• All forms of ergotamine have been used
• Intravenous dihydroergotamine results in the
quickest response and repeated administration
for 3 to 7 days can break the cycle of frequent
cluster headache attacks.
• Ergotamine tartrate also has provided effective
relief sublingually or rectally

47. • TRIPTANS
• The quick onset of subcutaneous and intranasal
triptans make them safe and effective abortive
agents for cluster headaches.
• Subcutaneous sumatriptan (6 mg) is the most
effective agent.
• oral zolmitriptan(10 mg) also used

48. PROPHYLACTIC
• Verapamil, the preferred calcium channel
blocker for the preventionof cluster headaches,
is effective in approximately 70% of patients.
• The beneficial effects of verapamil often appear
after 1week of therapy

49. • LITHIUM
• Lithium carbonate is effective for episodic and
chronic cluster headache attacks and can be
used in combination with verapamil.
• The usual dose is 600mg to 1.2g/day,
• starting dose of 300 mg twice daily.
• Initial side effects are mild and include tremor,
lethargy, nausea,diarrhea, and abdominal
discomfort

50. • ERGOTAMINE
• an efficacious agent for prophylactic as well as
abortive therapy of cluster headaches.
• A 2mg bedtime dose is beneficial for the
prevention of nocturnal headache attacks.
• Daily use of 1 to 2 mg ergotamine alone or in
combination with verapamil or lithium can
provide effective prophylaxis in patients
refractory to other agents

51. • MRTHYSERGIDE
In patients unresponsive to other therapies,
methysergide 4 to 8 mg/day in divided doses is
usually effective in shortening the course of
cluster headache.
• CORTICOSTEROIDS
• Corticosteroids are useful for inducing
remission.
• Therapy is initiated with 40 to 60 mg/day
prednisone and tapered over approximately 3
weeks.
• Relief appears within 1 to 2 days of initiating
therapy ster headaches

52. 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

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

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

55. Atypical facial pain
• Persistent idiopathic facial pain
• Continuous, burning/crushing,unremittent,
centred over maxilla usually left side
• Middle aged women
• Early form of trigeminal neuralgia
• Rx-Amitriptyline, Gabapentin

56. Other causes of facial pain
Sinusitis
• Frontal-pain more in morning, decreases as day
progresses, stooping and blowing nose increase
pain
• Ethmoid and Sphenoid-pain over vertex, less in
morning and increase gradually

58. Post herpetic
neuralgia-continuous,
burning pain
sensitive to light
touch, shingles

59. REREFERENCES
ERENCES
• ADAMS & VICTOR’S Principles of Neurology 9th edition
chapter 10 headache page no 162.
• DAVIDSON’S Principles & Practice of Medicine 22nd edition
chapter 26 page no 1156.
• HARRISON’S Principles of Internal Medicine 19th edition
chapter 21 page no 107 volume 1.
• API TEXT BOOK OF MEDICINE 10th edition part 2 volume
1 page no 25.

60. THANK YOU