oral presentation about Pharmacological And Non-Pharmacological Treatment Of Primary Headaches

1. By
Wael Ezzat
Assistant Lecturer of Neurology
Cairo University
2015

2. ©International Headache
Society 2003/5
1. Migraine
2. Tension-type headache
3. Cluster headache
and other trigeminal autonomic cephalalgias
4. Other primary headaches

4. Goals Of Acute Treatment:
 Treat attacks rapidly and consistently without
recurrence.
 Restore the patient’s ability to function.
 Minimize the use of back-up and rescue
medications.

5.  Optimize self-care and reduce subsequent use
of resources.
 Be cost effective for overall management.
 Have minimal or no adverse events.

6.  Lipton and colleagues (2000b), after surveying
various approaches to acute migraine
treatment, described three strategies for
treating diagnosed acute migraine, which they
called :
1. step care across attacks
2. step care within attacks (also called staged
care)
3. stratified care.

7. Step Care Across Attacks:
 In this approach, the least expensive non-
specific medication is selected by the physician
for the patient to use first
 ‘‘step up’’ to the next drug, until finally
reaching a specific, more effective medication
IF
Failed

8. Step Care Within Attacks:
 This approach involves starting with a non-
specific, less expensive medication first
 the patient take the specific medication at that
point.
 The specific drug would be used during an
attack only if the lower-level medicine had
failed
IF
Failed

9.  nonsteroidal anti-inflammatory drugs
(NSAIDs)
 over-the-counter medication
 prescribed nonspecific medication
 step up to the triptan during the attack
IF
Failed

10. Stratified Care:
Two types of stratified care have been described
first would be to evaluate the characteristics of the
attack itself:
 The severity of the peak intensity of the attack

11.  The time to peak intensity, ie, How much time
is available to achieve adequate treatment
before the patient is disabled?
 Presence of associated symptoms, eg, nausea,
vomiting, phonophobia, and photophobia
 Time to associated symptoms

12. The second type of stratified care is that which is
based on disability or impact of the migraine on
the patient over time
 In this form of stratified care, a disability or
impact assessment tool is used:
 Migraine Disability Assessment Scale (MIDAS)
 Headache Impact Test (HIT)-6

14. 1) NSAIDS
2) ASA
3) Acetaminophen (APAP);
4) Combinations Of ASA, APAP, And
Aspirin/Amphetamine/Caffeine(AAC);
5) Neuroleptics
6) Antiepilepsy Drugs (AEDS);
7) Aminobutyric (GABA) Agonists, Such As Baclofen
8) Antihistamines
9) Mild Vasoconstrictor/ Sedative/APAP Mixtures
(Isometheptene/ Dichloralphenazone/APAP)
10) Barbiturate Mixtures (Butalbital/Caffeine With Either
ASA Or APAP)

15. 11) Opioids:
 Oral opioid combinations may be considered
when sedation will not put the patient at risk
and/or the risk for abuse has been addressed.
 Parenteral opioids may be considered a choice
only in a supervised setting and again when
sedation will not put the patient at risk and/or
the risk for abuse has been addressed.

16. 1- TRIPTANS:
Oral triptans can be divided into two clinical
groups:
Group I: Triptans with fast onset, relatively high
headache response, and pain-free rates at 2 hours.

17.  Group II: Triptans have slower onset and lower
efficacy rates

19. 2- ERGOTS:
 The ergot alkaloids were the first specific anti-
migraine therapy available.
 The two used for acute treatment of migraine,
dihydroergotamine (DHE) and ergotamine
(ET)

20.  vasoconstriction by stimulating alpha-
adrenergic and 5-HT receptors, although ET is
a more potent vasoconstrictor.
 Both can inhibit the actions of norepinephrine
(NE) and are venoconstrictors.
 Clinically, ergots are difficult to use. The oral
bioavailability of ET is less than 1%. Because
most of the drug is metabolized during the first
pass through the liver.

21.  Oral ET is appropriate for patients with slowly
evolving migraine without early-onset nausea.
 The patient should take one 1-mg tablet at the start
of an attack, with a maximum total dose of 6 mg
per attack.
 Even this 1-mg dose, is often nauseating. Nausea
may indicate that the dose is too high.
 Even more important than limiting total dosage is
restricting ET use to no more than 2 days per week
with an interval of at least 4 days in between usage
days to prevent drug-induced headache

22.  the use of narcotics as rescue treatment for
status migrainosus should be avoided.
 a variety of IM or IV treatments can be used
together or separately
 The only contraindication that of mixing
triptans and ergots in the same day, and that of
avoiding triptans and ergots in patients with
vascular disease.

24. Non-pharmacological Treatment:

25.  Behavioural lifestyle changes & Behavioural
Therapy.
 Anxiety management, psychotherapy and
physiotherapy.
 Biofeedback.

26. Why And When To Use Migraine preventive
Medications?
 United States Evidenced-based Guidelines for
Migraine—Preventive Treatment:
1. Recurring migraine that significantly interferes
with the patient’s daily routine despite acute
treatment (eg, two or more attacks a month that
produce disability that lasts 3 or more days, or
headache attacks that are infrequent but produce
profound disability).

27. 2. Failure of, contraindication to, or troublesome side
effects from acute medications.
3. Overuse of acute medications.
4. Special circumstances, such as hemiplegic migraine or
attacks with a risk of permanent neurological injury.
5. Very frequent headaches (more than two a week), or a
pattern of increasing attacks over time, with the risk of
developing medication overuse headache.
6. Patient preference, that is, the desire to have as few
acute attacks as possible

28.  Serotonin antagonists were developed based
on the concept that migraine is due to excess 5-
hydroxytryptamine (5-HT).
 Antidepressants down-regulate 5-HT2 and -
adrenergic receptors.
 Anticonvulsant medications decrease
glutamate and enhance –aminobutyric acid
(GABA)A, and block sodium or calcium
channels.

29. The major medication groups for preventive migraine
treatment include:
1) Anticonvulsants: Valproate, gabapentin,
topiramate
2) Antidepressants: TCA, SSRI, MAO-I
3) Beta-adrenergic blockers: Propranolol,
metoprolol, atenolol
4) Calcium Channel Antagonists: Verapamil,
flunarizine
5) Serotonin Antagonists: Methysergide
6) Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
7) Neurotoxins
8) Others (including riboflavin, minerals, and herbs).

30. Principles Of Preventive Therapy:
 Start the chosen drug at a low dose and increase it
slowly until therapeutic effects develop, the max.
dose for the chosen drug is reached, or side effects
become intolerable.
 Give each treatment an adequate trial. A full
therapeutic trial may take 2 to 6 months.
 Avoid interfering, overused, and contraindicated
drugs. To obtain maximal benefit from preventive
medication, the patient should not overuse
analgesics, opioids, triptans, or ergot derivatives.

31.  Re-evaluate therapy. Migraine headaches may improve
independent of treatment. Many patients experience
continued relief with a lower dose of the medication,
and others may not require it at all.
 Be sure that a woman of childbearing potential is
aware of any potential risks, and pick the medication
that will have the least adverse effect on a fetus.
 To maximize compliance, involve patients in their
care.
 Consider comorbidity.

32. ß-Adrenergic Blockers:
 The most widely used class of drugs in
prophylactic migraine treatment, are
approximately 50% effective in producing a
greater than 50% reduction in attack frequency.
 Evidence consistently showed propranolol to
be effective for migraine prevention in a daily
dose of 120 mg to 240 mg.

33.  All beta-blockers can produce behavioral
adverse events, such as drowsiness, fatigue,
lethargy, sleep disorders, nightmares,
depression, memory disturbance and
hallucinations, indicating that they all affect the
central nervous system (CNS).

34. Antidepressants:
 Only tricyclic antidepressants (TCAs) have proven efficacy
in migraine.
 Adverse events are common with TCA use:
Antimuscarinic adverse include dry mouth, a metallic taste,
epigastric distress, constipation, dizziness, mental confusion,
tachycardia, palpitations, blurred vision, and urinary retention.
Antihistaminic activity may be responsible for carbohydrate
cravings, which contribute to weight gain.
Adrenergic activity is responsible for the orthostatic
hypotension, reflex tachycardia, and palpitations.

35. Principles of antidepressant use:
 With the exception of protriptyline, TCAs are
sedating. Start with a low dose of the chosen
TCA at bedtime.
 If the TCA is too sedating, switch from a
tertiary TCA (amitriptyline, doxepin) to a
secondary TCA (nortriptyline, protriptyline).
 Bipolar patients can become manic on
antidepressants.

36. Clinical use:
 Patients with coexistent depression are more
tolerant and require higher doses of
amitriptyline. Start at a dose of 10 mg to 25 mg
at bedtime. The dose ranges from 10 mg/d to
400 mg/d.
 Doxepin is a sedating tertiary amine TCA. Start
at a dose of 10 mg at bedtime. The dose ranges
from 10 mg/ d to 300 mg/d.

37. Selective Serotonin Reuptake Inhibitors:
 Evidence for the effectiveness of SSRIs in
headache management is disappointing.
 They are helpful for patients with comorbid
depression because their tolerability profile is
superior to tricyclics.

38. Calcium Channel Antagonists:
 Two types of calcium channels exist: calcium
entry channels, which allow extracellular
calcium to enter the cell, and calcium release
channels, which allow intracellular calcium to
enter the cytoplasm.

39. Mechanism of action in migraine:
 The mechanism of action of the calcium
channel antagonists in migraine prevention is
uncertain.
 prevent hypoxia of cerebral neurons,
contraction of vascular smooth muscle, and
inhibition of the Ca2+-dependent enzymes
involved in prostaglandin formation.

40. Adverse events:
 Patients often report an initial increase in
headache. Headache improvement often
requires weeks of treatment.
 Adverse events with nifedipine were frequent
(54%) and included dizziness, edema, flushing,
headache, and mental symptoms.

41. Clinical use:
 Verapamil is available as a 40-mg, 80-mg, or
120-mg tablet or as a 120-mg, 180-mg, or 240-
mg sustained release preparation. Start at a
dose of 80 mg 2 to 3 times a day, with a
maximum of 640 mg a day in divided doses.
 Flunarizine dose is 5 mg/d to 10 mg/d.

42. Anticonvulsants:
 Anticonvulsant medication is increasingly
recommended for migraine prevention because
of placebo-controlled, double-blind trials that
prove it to be effective.

44. Nonsteroidal anti-inflammatory drugs:
 Aspirin (650 mg/d) decreased headache
frequency.
 Other NSAIDs that may be effective in migraine
prophylaxis include sodium naproxen, fenoprofen,
ketoprofen, and tolfenamic acid
 Although NSAIDs are effective, they must be used
with caution because of their gastrointestinal and
renal function adverse events.

45. Angiotensin-converting enzyme inhibitors and
angiotensin II receptor antagonists:
 Schrader and colleagues (2001) conducted a
double-blind, placebo controlled, crossover
study of lisinopril, an angiotensin-converting
enzyme inhibitor, in migraine prophylaxis.
Days with migraine were reduced by at least
50%.

46. Botulinum toxin:
 Silberstein and colleagues (2000) evaluated the
safety and efficacy of pericranial botulinum
toxin type A injections as prophylactic
treatment of chronic moderate to severe
episodic migraine.
 The 25-U but not the 75-U botulinum toxin
type A treatment group fared significantly
better than the placebo group.

47. Medicinal Herbs, Vitamins, and Minerals:

48.  Feverfew (Tanacetumparthenium).
 Petasites hybridus root (butterbur).
 Riboflavin: with placebo in migraineurs in a
randomized trial of 3 months’ duration.
Riboflavin was significantly superior to
placebo in reducing attack frequency, headache
days, and migraine index.

49.  Coenzyme Q10: 150 mg/d was effective for
prevention of migraine headaches in an open-
label trial.
 Magnesium supplementation.

50.  Pascual and colleagues (2003) found that
combining a beta-blocker and sodium
valproate could lead to an increased benefit for
patients whose migraine was resistant to either
alone.
 Further Controlled trials are needed to
determine the true advantage of this
combination treatment in episodic and chronic
migraine.

51.  Patients suffering from long-duration chronic
daily headache often present not only with
acute medication overuse, but also with
psychiatric and somatic comorbidity, low
frustration tolerance, and both physical and
emotional dependence.

52. The essential features of an effective treatment
regimen include a combination of the following
steps:
1. Educating the patient, establishing
expectations and a follow-up plan.
2. Identifying, addressing, and treating
psychiatric and somatic comorbidities.

53. 3. Using non-pharmacological therapies when
appropriate:
 Biofeedback and relaxation therapy.
 Cognitive behavioral therapy.
 Individual/family counseling as necessary.
 Dietary instructions, chronobiological therapy, and
sleep hygiene.
 Daily exercise program.

54. 4. Discontinuing all potentially offending
medications and caffeine by outpatient or
inpatient detoxification procedures.
5. Instituting a program of acute care and
preventive pharmacological therapy.

55. Addressing Risk Factors for
Chronic/Transformed Migraine:
 risk factors for developing chronic migraine
have been identified. Some of them are not
modifiable (gender, age, etc), but others
(obesity, depression, caffeine and medication
overuse, snoring) should be addressed.
 even though it is not yet known whether this
will translate into better outcomes once chronic
migraine is already established

57.  Most of the commonly used preventive agents for
primary chronic daily headache have not been
evaluated in well designed, double-blind studies.
They are usually the same medications that are
tried for migraine prevention.
Alpha2-agonists:
 Clonidine 0.05 mg/d to 0.3 mg/d
 Guanfacine 1 mg

58. Anticonvulsants:
 Divalproex sodium 500 mg/d to 1500 mg/d
 Gabapentin 300 mg to 3000 mg
 Levetiracetam 1500 mg to 4500 mg
 Topiramate 50 mg to 200 mg
 Zonisamide 100 mg to 400 mg

59. Beta-blockers:
 Atenolol 25 mg to 100 mg
 Metoprolol 50 mg to 200 mg
 Nadolol 20 mg to 240 mg
 Propranolol 60 mg to 240 mg
 Timolol 10 mg to 30 mg

60. Calcium channel antagonists:
 Verapamil 240 mg to 960 mg
 Nimodipine 40 mg 3 times a day
 Diltiazem 30 mg to 60 mg 3 times a day
 Amlodipine 2.5 mg to 10 mg every day

61. Serotonergic agents:
 Methylsergide 2 mg to 12 mg
 Cyproheptadine 2 mg to 16 mg
 Pizotifen 1.5 mg to 3 mg

62. Antidepressants:
 Monoamine oxidase inhibitors: Phenelzine 30
mg/d to 90 mg/d
 Tricyclic antidepressants: Amitriptyline 20 mg
to 150 mg, Nortriptyline 20 mg to 100 mg
 Selective serotonin reuptake inhibitors:
Fluoxetine 10 mg to 40 mg, Sertraline 50 mg to
100 mg, Paroxetine 10 mg to 30 mg,
Venlafaxine 37.5 mg to 225.0 mg, Mirtazapine
15 mg to 45 mg

63.  Miscellaneous:
 Montelukast sodium 10 mg to 20 mg
 Lisinopril 10 mg to 40 mg
 Botulinum toxin A injection 25 units to 150 units
(intramuscular)
 Chelated magnesium glycinate 400 mg/d to 600
mg/d
 Riboflavin 100 mg/d

64.  A combination of pharmacological, non-
pharmacological, behavioral, and sometimes
physical interventions is usually necessary for a
favorable outcome in medication overuse
headache.
 Most studies suggest the benefit and necessity of
detoxifying the patient from the overused
medication (when present), followed by an
intensive, long term treatment plan. If patients
discontinue their overused medications, they
frequently improve considerably, and, if they do
not, they are usually difficult to treat effectively

65. Outpatient Setting:
Patients who can usually be successfully treated
as outpatients include those who:
 Understand the concept of medication overuse
headache and its consequences in terms of
prognosis.
 Are motivated to participate and follow the
regimens prescribed.

66.  Are willing to take an active role in their
treatment, including keeping headache
calendars.
 Understand that they will initially worsen
before they improve.
 Have no psychiatric comorbidity that will
prevent outpatient participation.
 Have support of family or friends and their
workplace.

67. Basically, three non–mutually exclusive
outpatient approaches to ‘‘bridge’’ from frequent
daily use to intermittent use are used:
 First approach involves tapering the overused
medication gradually while an effective
preventive therapy is established.
 Second approach is to abruptly discontinue the
overused drug, institute a transitional
medication or medication bridge to break the
cycle of headache, and subsequently taper the
transitional

68.  Third approach is to combine the two strategies by
eliminating the rebound medication rapidly,
adding a preventive medication rapidly, and also
supplying a temporary bridge to give the patient
the maximum chance to improve without
drastically worsening first.
 Generally, ergots, non-opioids, and triptans can be
abruptly discontinued in some people. On the
other hand, opioids, barbiturates, and
benzodiazepines are usually withdrawn slowly,
perhaps over 2 weeks or more, depending on
duration of use.

69. Tapering Strategies:
 The general idea is to move from the patient’s
pattern of medicating continuously on a pain-
contingent basis to a scheduled taper.
 One must avoid medicating at mild to
moderate intensities during this phase and use
migraine-specific medications (triptans,
dihydroergotamine, ergotamine tartrate) only
for severe headache and limited to 2 or fewer
times a week.

70. Tapering over-the-counter medication:
 Most over-the-counter medications can be
stopped abruptly unless they contain caffeine,
in which case they may be tapered slowly over
a few weeks.
 If someone is overusing an acetaminophen
compound, he or she can be switched to an
NSAID, which should be gradually tapered

71. Tapering caffeine:
 Caffeine often relieves headaches when used
acutely in patients who are not overusing it
chronically.
 when it is overused on a daily basis, caffeine
withdrawal can be associated with increased
headache.
 It is important to taper caffeine slowly, over the
course of several weeks.

72. Tapering opiates:
 Taper the opiate 10% to 15% every day over 7 to 10
days.
 Adding clonidine 0.05 mg or 0.1 mg bid or tid
during withdrawal of an opiate tends to reduce
withdrawal symptoms.
 Various sleep-promoting medications e.g, tricyclic
antidepressants, atypical antipsychotics may help
patients with opiate dependency issues
complaining lack of ability to fall asleep.

73. Tapering ergotamine:
 Tapering ergotamine tartrate is to switch the
patient to intravenous dihydroergotamine and
taper it slowly over a few days.
 Dihydroergotamine itself is a useful bridge
therapy for most overuse headache syndromes.

74. Tapering triptans:
 If a patient is having increased headaches and
taking triptans 3 or more days per week on an
ongoing basis, taper to one tablet per day, and
a short course of a steroid or an NSAID can be
used concomitantly to attempt to decrease any
withdrawal symptoms.

75. Transitional therapy:
 No matter what medication is being tapered, a
very useful technique is to use a 3- to 7-day taper
of oral steroids, either prednisone starting at 60
mg/d or dexamethasone starting at 4 mg/d to 12
mg/d.
 The mechanism of action is unknown but is
presumed to be related to decreasing neurogenic
inflammation in the meninges.
 A second adjunctive therapy is to use a short
course of daily triptan in patients who are not
overusing them.

76. Ambulatory infusion treatment:
 Patients who do not need hospital-level care
but cannot be safely or adequately treated as
outpatients can be considered for ambulatory
infusion treatment.
 patient will receive intravenous medications,
sometimes 2 or 3 times per day for several
days, until withdrawal is complete.

77. Inpatient Strategy:
 If outpatient treatment fails.
 If outpatient treatment is unsafe or unlikely to
be effective.
 if significant somatic and/or psychiatric
comorbidity is present.

78.  The use of repetitive intravenous
dihydroergotamine preceded by an antiemetic.
 A test dose of 0.25 mg of dihydroergotamine,
followed by 0.5 mg of dihydroergotamine tid, with
each dose preceded by an antiemetic medication.
 Metoclopramide and ondansetron work well and
are often tried orally but are even more effective
intravenously.
 The repetitive intravenous administration of
dihydroergotamine is a safe and effective means of
rapidly controlling intractable headache.

79.  Dihydroergotamine is usually well tolerated
except for following side effects:
1. Nausea
2. Diarrhea
3. Transient Increase In Headache
 contraindicated in:
1. Uncontrolled Hypertension,
2. Coronary, Cerebral And Peripheral Vascular
Disease.

80.  For those who are unable to tolerate
dihydroergotamine or when it is contraindicated,
A 2.5-mg to 12.5-mg dose of intravenous
chlorpromazine diluted in saline and preceded by
hydration, given every 6 hours for 2 days, is
effective in some patients.
 Other medications that have been used
intravenously are magnesium sulfate, propofol,
diphenhydramine, ketorolac, and divalproex
sodium.

81. Daily use of opioids:
 The role of opioids in the management of chronic
benign pain remains controversial.
 The available evidence suggests that opioids are a
risk factor for medication overuse headache, and
patients who overuse opioids have elevated
headache relapse rates after withdrawal treatment.
 For patients with frequent and disabling
headaches that remain intractable after usual
treatment approaches, daily opioids will help a
small percentage, but this has to be weighed
against the potential for harm.

83. Abortive Therapy:
 The goal of abortive therapy for cluster headache is
fast, effective, and consistent relief.
 Abortives need to show effect usually within 20
minutes as the attacks are short in duration.
 There is no role in cluster headache for over-the-
counter agents and little if any need for opiates.

84. Sumatriptan:
 Subcutaneous sumatriptan is the most effective
medication for the symptomatic relief of cluster
headache.
 Injection or nasal spray are both efficacious, but
injection is more effective.
 Sumatriptan is contraindicated in:
1. Uncontrolled hypertension
2. History of myocardial infraction or stroke.

85. Oxygen:
 Oxygen inhalation is an excellent abortive therapy
for cluster headache.
 Typical dosing is 100% oxygen given via a face
mask at 7 L/min to 10 L/min for 20 minutes.
 oxygen is completely effective at aborting an attack
if taken when the pain is at maximal intensity,
while in others, the attack is only delayed for
minutes to hours rather than completely alleviated.

86.  Oxygen is a very attractive therapy as it is
completely safe and can be used multiple times
during the day.

87. Other:
 Other effective abortives include ergotamine
suppositories and dihydroergotamine (DHE)
nasal spray or intramuscular injection.

88. Transitional Therapy:
 Short-term preventive treatment that bridges the time
between cluster diagnosis and when the true
traditional maintenance preventive agent becomes
efficacious.
 Transitional preventive agents are started at the same
time the maintenance preventive medication is begun.
 The transitional preventive agent should provide the
patient with almost immediate pain relief and allow
the patient to be headache free or nearly headache free
while the maintenance preventive medication dose is
being raised to an effective level

90. Occipital nerve blockade:
 Occipital nerve blockade using a combination
of an anesthetic (eg, lidocaine) and steroid (eg,
triamcinolone) will not only break an ongoing
single attack of cluster, but when used inter-
ictally can prevent cluster attacks from coming
on for at least 1 to 2 days and sometimes for up
to 6 weeks.

91. Preventive Therapy:
 Preventive agents are absolutely necessary in patients
with cluster headache unless the cluster periods last for
less than 2 weeks.
 Preventive medications are used only while the patient
is in cycle and are tapered off once a cluster period has
ended.
 Continuing a preventive agent even after the patient
has gone out of cycle does not appear to prevent a
subsequent cluster period from starting.
 Polypharmacy is not discouraged in cluster headache
prevention.

92. Verapamil:
 First-line preventive therapy for both episodic and
chronic cluster headache.
 It can be used safely in conjunction with sumatriptan,
ergotamine, corticosteroids, as well as other preventive
agents.
 The initial starting daily dosage of verapamil is 80 mg
tid. dosages are typically increased by 80 mg every 3 to
7 days.
 Constipation is the most common side effect, but
dizziness, edema, nausea, fatigue, hypotension, and
bradycardia may also occur.

93. Valproic acid:
 Divalproex sodium ER (500 mg): dose range 500
mg to 3000 mg.
Lithium carbonate:
 considered a mainstay of cluster prevention, but its
narrow therapeutic window and high side effect
profile make it less desirable than other newer
preventive agents.
 Dose range 300 mg to 900 mg

94. Topiramate:
 Dose range 50 mg to 400 mg (typical dose 75
mg or less).
Melatonin:
 Serum melatonin levels are reduced in patients
with cluster headache, particularly during a
cluster period.
 Dose 9 mg at bedtime.

95. Surgical Treatment:
Surgical treatment of cluster headache should
only be considered:
 After a patient has exhausted all medical
options.
 When a patient’s medical history precludes the
use of typical cluster abortive and preventive
medications.

96. Surgical Techniques:
 Surgery on the cranial parasympathetic system:
The parasympathetic autonomic pathway can
be interrupted by sectioning the greater
superficial petrosal nerve or the sphenopalatine
ganglion.
 Surgery on the sensory trigeminal nerve:
alcohol injection into supraorbital and
infraorbital nerves, alcohol injection into the
trigeminal ganglion.

97.  Radiofrequency thermocoagulation: is the most
commonly used surgical technique for cluster
headache, and it provides one of the best options for
pain relief.
 Hypothalamic stimulation (New strategy):
There has always been a suggestion that a hypothalamic
influence over cluster headache is based on the circadian
rhythmicity of the syndrome and the neuro-hormonal
changes identified in cluster headache patients.
with electrode implantation into the posterior inferior
hypothalamus. Almost every patient has had a
tremendous reduction in cluster frequency, and some
have become pain free.

98. Indomethacin:
 CPH is one of the rare headache disorders that
by definition is totally responsive to
indomethacin.
 The normal starting dosage of indomethacin is
one 25-mg tablet tid for 3 days; this dose can be
increased to two tablets (50 mg) tid.

99.  Most individuals will respond with a dosage of
150 mg/d, and the response can be dramatic
with quick dissipation of headache symptoms.
 Side effects of indomethacin therapy are
mainly gastrointestinal disturbances with
either dyspepsia or ulcer development and
serious renal implications with long-term
indomethacin usage.

100. Other agents:
 Cyclooxygenase (COX)-2 inhibitors have given relief of
CPH in some patients, but the dose required may be
higher than that normally prescribed for arthritis.
 verapamil in a dose of 240 mg/d to 320 mg/d.
 Acetylsalicylic acid, naproxen, and a piroxicam
derivative have demonstrated some effect in a small
number of cases.
 Prednisone is effective in high doses for controlling
CPH but is not considered an adequate chronic therapy
regimen because of its side effect profile.
 Acetazolamide was effective in a single case report.

101. Indomethacin:
 HC is defined by its responsiveness to
indomethacin. The response to indomethacin is
one of the most dramatic treatment responses in
headache. Patients can literally become pain free
after their first dose of indomethacin regardless of
duration of their headaches.
 Some authors have suggested an indomethacin-
resistant form of HC, although this is controversial.

102. Other agents:
 ibuprofen, piroxicam-beta and naproxen.
 Recently several authors have documented that
the COX-2 inhibitors rofecoxib and celecoxib
have shown effect in HC.

103. Medical TTT:
 Preventive agents that have previously been
tried include aspirin, paracetamol,
indomethacin, naproxen, ergotamine, DHE,
sumatriptan, prednisone, methysergide,
verapamil, valproate, lithium, propranolol,
amitriptyline, and carbamazepine

104.  Carbamazepine has shown partial effect in
some patients. Combining carbamazepine and
a short course of corticosteroids at the onset
may be more efficacious than starting with
carbamazepine alone.
 Azathioprine was shown to be somewhat
effective in one patient.

105. Surgical Treatment:
 Gamma Knife.
 Microvascular decompression of the trigeminal
nerve.
 Balloon compression of retro-ganglionic fibers.
 Hypothalamic stimulation was recently shown
to be efficacious in a single case of refractory
SUNCT.

107.  Behavioral medicine maintains an important
place in the management of chronic headache
disorders, alongside the use of appropriate
medication, physical therapies, and
anesthesiological procedures when
appropriate.
 Behavioral treatment can increase the
effectiveness of pharmacotherapy.

108. Behavioral Tools for Assessment and Management
of Stress-Related Risk Factors:
 Ask direct questions.
 Use headache diaries.
 Apply behavioral analysis.
 Employ and refer for stress management therapies.
 Modify headache-related and health behavior.

109. Psychiatric Comorbidity— Clinical Syndromes:
 American Psychiatric Association (DSM-IV) classifies
psychiatric disorders in two general categories:
 Clinical Syndromes (Axis I)
 Personality Disorders (Axis II)
 presence of comorbid psychiatric clinical syndromes
can contribute to the intractability of migraine.
 Migraine increases the risk for comorbid psychiatric
disorders, such as anxiety and depression, and the
presence of comorbid disorders contributes to a poorer
prognosis for headache treatment.

110.  Biofeedback is a mind-body technique that
helps teach patients how to influence their
autonomic nervous systems.
 This is done by attaching an electronic "cue"
(usually a "beep," tone or visual image on a
screen) to a measurable physiologic process.

111.  The three most common types of biofeedback
therapy are:
 Thermal biofeedback - which measures skin
temperature.
 Electromyography - measures muscle tension.
 Neurofeedback - measures brain wave activity.

112. Clinical biofeedback techniques are now widely used
to treat list of conditions. These include:
 Migraine headaches, tension headaches, and many
other types of pain.
 Disorders of the digestive system.
 High blood pressure and its opposite, low blood
pressure.
 Cardiac arrhythmias.
 Paralysis and other movement disorders.

113. Thank you