This document provides information on Dr. Ganta Rajasekhar's academic qualifications and areas of interest in neurology. It then discusses approaches to evaluating headache, classifications of primary and secondary headache disorders, migraine pathogenesis and management, tension-type headache, and trigeminal autonomic cephalalgias. Evaluation and treatment strategies for acute migraine, preventive migraine therapy, medication overuse headache, and special headache conditions are covered. Common questions in headache management are also addressed.

1. Dr GANTA. RAJASEKHAR
MD(GEN MED),Dch,DM(NEUROLOGY)
NIMS,HYDERABAD
Asst Professor
Department Of Neurology ,SVMC,Tirupathi.
• Academics.
• Presented platform paper on Role of thymectomy in Myasthenic Gravis.
• Presented platform paper on NBIA spectrum disorders
• Research paper on Ftd and Overlap dementia syndromes.
• Areas of interest
• Stroke,Epilepsy,paediatric neurology.
• .

2. HEADACHE
Dr Ganta.Raja Sekhar
DM(Neurology)
NIMS,HYDERABAD
Asst Professor
Dept Of Neurology
SV Medical College
TIRUPATI

3. HEADACHE
APPROACH TO THE PATIENT

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

5. PRIMRY
HEADACHE
90-95%
SECONDARY
HEADACHES
3-5%
PAINFUL
CRANIAL
NEUROPATHIES
1-2%

6. Common Causes of Headache
Primary Headache Secondary Headache
Type % Type %
63
Tension-type 69
Migraine 16
Systemic
infection
Head injury 4
2 1
Idiopathic
stabbing
Exertional 1
Cluster 0.1
Vascular
disorders
Subarachnoid <1
hemorrhage
Brain tumor 0.1

7. Primary Headache Disorders
 More common
 Migraine, with or without aura
 Tension type Headache(TTH)
 Cluster Headache
 Less common
 Paroxysmal hemicrania.
 SUNCT (short-lasting unilateral
neuralgiform headache attacks
with conjunctival injection and
tearing).
 Primary Stabbing Headache.
 Primary Cough Headache.
 Cold-stimulus.
 Benign cough.
 Benign exertional.

8. Secondary Headache Disorders
• Associated with non-vascular intracranial
disorder
• Benign intracranial
hypertension
• Intracranial infection
• Low CSF pressure
• Associated with noncepalic infection
• Viral infection
• Bacterial infection
• Associated with vascular disorders
• Subarachnoid hemorrhage
• Acute ischemic cerebrovascular disorder
• Unruptured vascular
malformation
• Arteritis
• Carotid or vertebral artery pain
• Venous thrombosis
• Arterial hypertension

9. Secondary Headache Disorders
• Associated with head
trauma
Acute post-traumatic
headache
• Associated with substance
use or withdrawal
Acute use or exposure
Chronic use or exposure
• Associated with
metabolic disorders
• Hypoxia
• Hypercapnia
• Mixed
hypoxia &
hypercapnia
• Dialysis

10. 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.

11. Common Theories of Migraine Pathogenesis
 Theories on the pathogenesis of migraine include
 The vascular theory
 The cortical spreading depression theory(CSD)
 The neurovascular hypothesis
 The serotonergic abnormalities hypothesis
 The integrated hypothesis.

13. Clinical Evaluation of Acute, New-Onset Headache
• In new-onset and severe headache, the probability of finding a potentially
serious cause is considerably greater than in recurrent headache.
• Patients with recent onset of pain require prompt evaluation and
appropriate treatment.
• In most cases,CT or MRI study.
• In some circumstances, Lumbar puncture (LP),
Eyes by fundoscopy,
Intraocular pressure measurement, and refraction,
Cranial arteries by palpation is required.

14. Headache Symptoms thatSuggest a SeriousUnderlying
Disorder
 "Worst" headache ever"
First severe headache.
 Subacute worsening over days or weeks .
Abnormal neurologic examination.
Fever or unexplained systemic signs.
 Vomiting that precedes headache.
 Pain induced by bending, lifting, cough.
 Pain that disturbs sleep or presents immediately upon awakening.
 Onset after age 55
 Pain associated with local tenderness, e.g., region of temporal artery

15. Migraine
• Migraine is a neurovascular disease caused by neurogenic inflammation and characterized by
severe, recurring headaches.
• It usually characterized by the severe pain on one side of the head as compare to the pain in rest of
the head.
• second most common cause of headache,
Women > men.
• It is usually an episodic headache associated with certain features such as sensitivity to light,
sound, or movement; nausea and vomiting often accompany the headache.

16. Migraine contd…
 Glare, bright lights, sounds, or other afferent stimulation,
 Hunger, excess stress, physical exertion, stormy weather,
 Barometric pressure changes,
 Hormonal fluctuations during menses.
 Lack of or excess sleep,
 Alcohol or other chemical stimulation
• Headache can be initiated or amplified by various Triggers

17. Classification of Migraine headache
1)Migraine without Aura or common migraine
Does not give any warning signs before the onset of headache.
It occurs in about 70 to 80% of migraine patients
2)Migraine with Aura
Give some warning signs “ called aura” before the actual headache begins.
20 to 30% migraine sufferers experience aura.
The most common aura is visual and may include both
positive and negative (visual field defects) features.
.

18. Positive Scotoma. Additional structures One side loss of perception.
Zigzag structure
Negative
scotoma. Loss
of local
awareness of
local structure

19. Classification of Migraine headache contd.
3)Retinal migraine- It involves attacks of monocular scotoma or even blindness of one eye
for less than an hour and associated with headache.
4)Childhood periodic syndromes that involve cyclical vomiting (occasional intense periods
of vomiting), abdominal migraine (abdominal pain, usually accompanied by nausea), and
benign paroxysmal vertigo of childhood (occasional attacks of vertigo). They may be
precursors or associated with migraine.
5)Complications of migraine describe migraine headaches and/or auras that are unusually
long or unusually frequent, or associated with a seizure or brain lesion
6)Migraine with Brainstem Aura(Basilar Migraine)
Females>Males(Dysarthia,Vertigo,Tinnitus,Diploplia,Ataxia,Hypacusis)

20. Symptoms Accompanying
Severe Migraine
Symptom PatientsAffected, %
Nausea 87
Photophobia 82
Lightheadedness 72
Scalp tenderness 65
Vomiting 56
Visual disturbances 36
Paresthesias 33
Vertigo 33
Photopsia 26
Alteration of consciousness 18
Diarrhea 16
Fortification spectra 10
Syncope 10
Seizure 4
Confusional state 4

21. CHRONIC MIGRAINE
Headache occurring on 15 or more days/ month for more than
three months, which, on at least eight days/month, has the features
of migraine headache.

23. TENSION-TYPE HEADACHE (TTH)
• Tension-type headache is very common, with a lifetime prevalence in
the general population ranging in different studies between 30% and
78%. It has a high socio-economic impact.
2.1 Infrequent episodic tension-type headache
2.2 Frequent episodic tension-type headache
2.3 Chronic tension-type headache

24. TRIGEMINAL AUTONOMIC CEPHALALGIAS (TACs)
3.1 Cluster headache.
3.2 Paroxysmal hemicrania.
3.3 Short-lasting unilateral neuralgiform headache attacks(SUNCT).
3.4 Hemicrania continua.

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

30. MODE OF ACTION
 ERGOTAMINE
• Structurally similar to amines serotonin dopamine
• Causes constriction of blood vessels
• Wide range of effect
 TRIPTANS
• Serotonin is involved in migraine attack
• Triptans mimic the action of serotonin
• Triptans act on receptors at smooth muscle cells of brain vessels1B/1D/1F
Receptors.
• They are an advance over ergots

33. PREVENTIVE THERAPY
• Beta blockers – e.g.. Propanolol
• Calcium channel blocker – eg.verapamil,Flunarazine
• TCA – amitriptylene
• SSRI’s –fluoxetine,Venlaflaxine
• Anticonvulsant- - sodium valproate,Topiramite
• Anti histaminic – cyproheptadine.
NEED FOR PROPHYLACTIC TREATMENT
• Abortive drugs should not be used for more than 2-3 times a week

34. MIGRAIN PREVENTION

35. Drugs approved
• Antiepileptic drugs
• Level A- divalproex sodium/ sodium
valproate
• Level A- Topiramate
• Level C- carbamazepine
• Level U- Gabapentin
• Antidepressants
• Level B – Amitryptiline
• Level B – Venlafaxine
• Level U – Fluoxetine
• Level U – Fluvoxamine
• Level U -- Protryptiline

36. • B-Blockers
• Level A- Propranolol
• Level A- Metoprolol
• Level A- Timolol
• Calcium-channel blockers
• Verapamil- level U
• Nimodipine- Level U
• Diltiazem- Level U
• Level B- Atenolol
• Level C- Nebivolol
• Level U-
Bisoprolol
Drugs approved

37. First line drugs
• Propranolol,
• Timolol,
• Amitriptyline,
• Divalproex,
• sodium valproate,
• Topiramate
Second line drugs
• Gabapentin,
• Dihydroergotamine,
• Candesartan,
• Lisinopril,
• Atenolol, nadolol,
Metoprolol,
• Fluoxetine,
• Verapamil, Flunarizine
• Magnesium,
• Riboflavin, coenzyme Q10,
• Botulinum toxin type A,

38. Severity of attacks
 Mild -can continue his or her usual activities with only minimal disruption.
 Moderate -activities are significantly impaired.
 Severe -unable to continue his or her normal activities and can function only with
severe discomfort and impaired efficiency.

39. Question 1-Acute/Abortive
• First-line
• Mild to moderate NSAIDs
• Moderate to severe Triptans
• Ergotamine- lower relapse rates, very poor bioavailability,side
effects
• C/I - opioids

40. Question 2-When to start treatment?
1. Recurring migraines, significantly interfere with ADL, despite acute treatment
(e.g., two or more attacks a month or infrequent but produce profound
disability)
2. Frequent headaches (more than 2 a week) or a pattern of increasing
attacks over time.
3. Contraindication or failure or Adverse events oroveruse of acute therapies.
4. Patient preference.
5. Presence of uncommon migraine conditions, including hemiplegic
migraine, basilar migraine, migraine with prolonged aura, or migrainous
infarctions

42. Question 3-What treatment to start?
 Initiate therapy with medications that have the highest level of evidence-
based efficacy with the lowest effective dose.
 Increase it slowly and give each drug an adequate trial of 2 to 3 months to
achieve clinical benefit.

43. Question 4-Treatment of relapse
 Treatment of relapse within the same attack after initial efficacy-
• repeat same drug-if still- naproxen 500mg or tolfenamic acid 200mg.
 Patients who consistently experience relapse-
• Use drugs with less relapse rate –
• Naratriptan, eletriptan, frovatriptan , Ergotamine, Naproxen, tolfenamic acid

44. Question 5 - Nonresponders
• Drug should be
tried in three attacks
Given for 6-8 weeks without side-effects
dose titrated before it is rejected for lack of efficacy
• Step one: simple oral analgesic ± anti-emetic
• Step two: rectal analgesic ± anti-emetic
• Step three: specific anti-migraine drugs
• Step four: combinations- 1 + 3 f/b 2 + 3

45. Other drugs used in prophylaxis
• limited or uncertain efficacy
• OnabotulinumtoxinA - licensed for prophylaxis of
patients with more than 15 headache days per
month, of which at least eight days are with migraine.
• Clonidine
• Verapamil MR 120-240mg bd
• Fluoxetine 20 - 40mg od
• co-enzyme Q10
• Transcranial magnetic stimulation

46. Question 6 - When to stop treatment?
 If after 3 to 6 months headaches are well controlled, consider tapering or
discontinuing treatment.
 Withdrawal is best achieved by tapering the dose over 2-3weeks.

47. Question 7 - If complications occur?
 Patients with nausea and vomiting -sumatriptan subcutaneously or as a nasal
spray.
(1/2 cc = 6 mg)

48. Question 7 - Dosages
• Sumatriptan - 25 mg orally, increase the dose in increments of
50 mg to a maximum of 300 mg per day.
• NSAIDs - Aspirin 600-900mg,
• Ibuprofen 400-600mg,
• Naproxen 750-825mg,
• Diclofenac-potassium 50-100mg

49. Dosages
• Drugs
• Amitryptyline
• Divalproex
/Valproate
• Propranolol
• Topiramate
Dose in adults
(mg/d)
10-50
500-1000
80-240
50-100

50. Question 8 - medication-induced (rebound) headache
 Use of triptans on 10 or more days a month or analgesics on 15 or more days a
month is inappropriate for migraine and is associated with a clear risk.
 Taper the drug over weeks and use alternative

51. Question 9 - Status migranosus
• Fluids
• NSAIDs - Acetaminophen 1 gm IV, Naproxen , diclofenac 50
im,
ketorolac 30mgiv,
• Triptans- sumatriptan 6mg sc-best studied
• DHE - 1mg iv/im
• Antidopaminergic Agents- iv metoclopramide,
Prochlorperazine
and chlorpromazine (Level B)
• Corticosteroids-dexamethasone- should be offered to these
patients to prevent recurrence of headache (Should offer—
Level B)
• Opioids- only to pregnant patients who are refractory to all
• Magnesium, propofol – unknown
• Lignocaine, opioid, octreotide - avoid

52. Question 10 - Contraindications
• Triptans - During the aura phase, within 24 hours of the administration of DHE,
cardiac risk factors, cardiac disease or uncontrolled hypertension, pregnant
• Beta-blockers - asthma, chronic obstructive pulmonary disease, insulin-dependent
diabetes mellitus, heart block or failure, or peripheral vascular disease.
• Calcium-channel -pregnant patients, hypotension, congestive heart failure or
arrhythmia
• Amitryptiline -severe cardiac, glaucoma, hypotension, seizure disorder and use of a
monoamine oxidase inhibitor.

53. Question 11 - Special situations
Co-morbidity Drug
• Hypertensio
n
• Angina
• Depression
• Insomnia
• Under
weight
• Epilepsy
• Mania
β blockers
Calcium channel
blockers Tricyclic
antidepressants
Tricyclic
antidepressants
Tricyclic
antidepressants
Sodium valproate
Sodium valproate

54. Question 12 - Special situations
• Co-
morbidity
• Epilepsy
• Depression
• Obesity
Drugs to be
avoided
Tricyclic
antidepressant
s β blockers
Tricyclic
antidepressants
, valproate

55. Question 13 - Menstrual migraine
• Acute - Same as for nonmenstrual attacks
• There is no concern regarding medication overuse unless used > 15days/ month
• Prophylaxis - Tried for a minimum of three cycles at maximum dose before it is
deemed ineffective.
 Mefenamic acid 500mg tds - from the onset of menstruation until the last day
of bleeding.
 Frovatriptan for 6 days (5mg bd on day 1; 2.5mg bd on days 2-6)
 Patients who do not respond to standard preventive measures may benefit from
hormonal therapy. Perimenstrual Estrogen supplementation with estradiol (0.5
mg orally twice a day, or Transdermal estrogen 7-day patch 50μg ) may be
beneficial.

56. Question 14 - Migraine and hormones
• Combined hormonal contraceptives- contraindication
• Progestogen-only contraception is acceptable- no thrombotic risk
• HRT in menopause not contraindicated- no evidence that risk of
stroke is elevated or reduced by the use of HRT

57. Question 15 - Pregnancy
• Avoid ergot, valproate, lisinopril and candesartan
• Beta blockers, propranolol, topiramate, amitriptyline and gabapentin (relative)
• Triptans- limited knowledge, so better to avoid

58. Question 16-MIGRAINE IN CHILDREN
Acute treatment
First choice: ibuprofen 10 mg/kg
Second choice: paracetamol 15 mg/kg
Third choice: sumatriptan/Almotriptan nasal spray 10-20 mg
Prophylaxis
Flunarizine (calcium channel blocker) 5-10 mg
Propranolol 40-80 mg.
• Non-drug therapy very effective
• Trigger avoidance and simple analgesics

59. 17. HEADACHE ATTRIBUTED TO ARTERIAL HYPERTENSION
• Headache, often bilateral and pulsating, caused by arterial hypertension, usually
during an acute rise in systolic (to 180 mmHg) and/or diastolic (to 120 mmHg)
blood pressure.
• It remits after normalization of blood pressure.

60. DIAGNOSTIC CRITERIA
A. Any headache fulfilling criterion C
B. Hypertension, with systolic pressure 180 mmHg and/or diastolic pressure 120
mmHg, has been demonstrated
C. Evidence of causation demonstrated by either or both of the following:
1. Headache has developed in temporal relation to the onset of hypertension
2. Either or both of the following:
a) Headache has significantly worsened in parallel with worsening hypertension
b) Headache has significantly improved in parallel with improvement in
hypertension

61. 10.3 HEADACHE ATTRIBUTED TO ARTERIAL HYPERTENSION
Comments: Mild (140–159/90–99 mmHg) or moderate (160–179/100–109
mmHg) chronic arterial hypertension do not appear to cause headache.
Whether moderate hypertension predisposes to headache remains controversial,
but there is some evidence that it does.

62. Question 18 - Non-pharmacologic therapy
• May be combined with preventive therapy
• Behavioral treatments –
– relaxation training,
– cognitive-behavioral training (stress-management training).
• Physical treatment –
– acupuncture,
– cervical manipulation,
– mobilization therapy

63. RECENT
DRUGS

64. GEPTANS AND DITAN
Rimegepant, a CGRP receptor antagonist in orally disintegrating tablet form approved in
2020, has shown efficacy in the acute treatment of migraine in adults in a pair of phase 3
studies.
Ubrogepant is an orally administered CGRP receptor antagonist approved in December 2019
for the acute treatment of migraine with and without aura in adults.
Lasmiditan is a selective serotonin (5-HT1F) receptor agonist (ditan) that was approved in
2019 by the FDA for the acute treatment of migraine with and without aura in adults. The
vasoconstrictive effects of triptans have been attributed to their 5-HT1B agonist activity.

65. Thank you

67. Clinical feature Migraine Cluster headache Tension headache
Family history Yes No Yes
Sex More females More males More females
Onset Variable During sleep Under stress
Location Usually unilateral
in adults
Behind/around
one eye
Bilateral in band
around head
Character/severity Pulsatile
Throbbing
Excruciating/
sharp
Steady
Dull Persistent
Tightening/pressing
30 min to 7 days
Frequency/
duration
2–72 h/attack
1 attack/year to
>8 per month
15–90 min/attack
1–8 attacks/day
for 3–16 weeks
1–2 bouts/year
3–4 attacks/week
to 1–2 attacks/year
Mild photophobia
Associated
symptoms
Visual aura
Phonophobia
Photophobia
Pallor
Nausea/vomiting
Sweating
Facial flushing
Nasal congestion
Ptosis
Lacrimation
Conjunctival injection
Pupillary changes
Mild phonophobia
Anorexia

68. • Currently, the major prophylactic medications for migraine work via one of the
following mechanisms:
• 5-HT2 antagonism - Methysergide
• Regulation of voltage-gated ion channels - Calcium channel blockers
• Modulation of central neurotransmitters - Beta blockers, tricyclic antidepressants
• Enhancing gamma-aminobutyric acid-ergic (GABAergic) inhibition - Valproic acid,
gabapentin
• Prevention of acetylcholine from presynaptic membrane – Botulinum toxin
• Calcitonin gene-related peptide (CGRP) inhibitors – Erenumab, fremanezumab,
galcanezumab, eptinezumab