PLANARY DISCUSSION

Physiotherapy in the Management of Migraine Headaches

CREATED BY:

5th TUTORIAL GROUP

PHARMACY DEPARTMENT

FACULTY OF MEDICAL AND HEALTH SCIENCE

MUHAMMADIYAH UNIVERSITY OF YOGYAKARTA

2018
Member’s Name:

20160350082 Facetha Intan Pramana

20160350100 Annisa Zulfarrahmah

20160350070 Rifka Syaida Fitria

20160350023 Dwi Asih Ramadhani

20160350067 Puji Septiana

20160350096 Suci Apriliyanti

20160350074 Firly Amila Nazar

20160350077 Isna Aura Dewayanti

20160350058 Hanan Nisa Prabaswari

20160350104 Avisena

20160350028 Linta Sabila Hanik

20160350050 Elma Safitri

 PREFACE

Praise and Gratitude we thank God Almighty, because it has been bestowed Thanks, Grace
and His gift so that we can arrange this paper properly and on time. In this paper we will discuss
about " Diarrhea Diseases And The Treatment".

This paper has been prepared by a variety of observations and some support from other
parties to help resolve the challenges and obstacles during work on this paper. Therefore, we would
like to thank the coach and also all those who have helped in the preparation of this paper.

We realize that there are still many fundamental flaws in this paper. Therefore, criticism
and suggestions from readers so we expect to enhance the next paper.

Final words I hope this paper can provide benefits for us all.

Yogyakarta, January 5th 2016

Writer
 CHAPTER I
INTRODUCTION

1.1 Purpose

1. Know deeply about primer headache,ecspectially about migraine type

2. Knowing how to manage the migraine with physiotherapy

1.2 Formulation of the problem

1. What is headache?
2. How is epidemiology, pathophysiology and etiology of headaches?
3. What are the types of headaches?
4. What are pharmacological and non-pharmacological therapies for migraine
headaches?

1.3 Background

Headache is pain or discomfort throughout the head area. Based on the cause is
classified by primary headache and secondary headache. Primary headache is no anatomy or
structural abnormality, namely migraine, tense lightheadedness, head of girl and other natural
heads. Secondary head pain is a clear function of anatomical or structural abnormalities and
progressive nature, including other non-vascular ones. Headache is a common problem that is
often encountered in everyday life. Headache appears as a result of stimulation of body parts in
the head and neck that are sensitive to pain. It is not only a physical problem as a cause, it is also
a dominant cause. For pain caused by physical factors that are easier to diagnose because the
patient will find other symptoms that accompany the headache, but not so possible with
problems caused by psychological factors. Headache that often arises in the community is the
head without salt, in other words is the strength of the head caused by psychological factors.

Headache is a symptom that can be caused by a variety of good or functional

abnormalities, and it is possible to determine the type of headache.
The prevalence of headaches for life is 96%, with female dominance. The global active
prevalence of tension headaches is around 40% and migraine is 10%. The majority of headaches
suffered are primary head fluids. Most often occur within 25 and 55 years and 3 times more
common in women.

Some headaches are very effective and very influential on a person's quality of life,
impose huge costs on health care and cannot be done directly. Only a small part of a special
headache disorder. For the large can be done by primary care doctors or general with a clinical
diagnosis that is really not special.

Cephalgia or headache are the most common symptoms in everyday life, about 90% of
every individual has ever experienced at least 1 time per year. Headache occupies the composition
of the number of patients most of those who came out went to the neurologist, the results of the
observations it was found that the incidence of diseases from clinical practice in the field in the
year 2003 found 10 major outpatient diseases, where cephalgia occupied rank first with a
percentage of 42% . Migraine itself is one type of primary headache classified by the International
Headache Society (IHS) and is a cause second primary headache after Tension Type Headache
(TTH). Migraine is marked with headaches that are generally unilateral with pulsating pain, and
location of pain is generally in the frontotemporal area.

One in 10 people have migraine. The patient’s history is the essential diagnostic tool.
Treatment options include acute rescue, lifestyle strategies, alternative remedies, and prophylactic
drugs. Most patients are managed in primary care; many never consult a doctor. The triptans have
improved acute treatment, and renewed scientific interest in migraine. Overuse of acute rescue
medication can lead to chronic daily headache.
 Chronic migraine is the term that the International Classification of Headache Disorders
(ICHD) uses to describe patients with frequent headaches, believed to be biologically migrainous
[Headache Classification Committee of the International Headache Society, 2013] The meaning
of the term ‘chronic migraine’ has evolved over the last two decades, as it has steadily replaced
earlier terminology such as ‘chronic daily headache’ and ‘transformed migraine’ [Olesen et
al. 2006; Zeeberg et al. 2009; Goadsby et al. 2010]. There is ongoing debate about whether a
further subdivision of the diagnosis should be created to specify patients who are refractory to
treatment [Martelletti et al. 2014]. The broader acceptance of the concept that migraine can be a
chronic condition has led to increasing interest in the pathophysiology, epidemiology, and
treatment of this condition [Diener et al. 2012].

Patients with chronic headaches have in the past experienced the adverse effects of lack of
education about headaches, and therapeutic nihilism. There is now no excuse for either of these
factors to impact upon the management of these patients. As this article will show, it is almost
always possible to make a specific diagnosis in patients with chronic migraine, and by making this
diagnosis one opens up a substantial number of treatment options.
 CHAPTER II
LITERATURE REVIEW

2.1 EPIDEMIOLOGY

Migraines occur in almost 30 million people in the United States and 75 % of them are
women. Migraines can occur at any age but usually appears at the age of 10-40 years and the
incidence rate decreases after age 50 years. Migraines without aura are more common than
migraines which is accompanied by aura with a percentage of 9: 1.3 The prevalence of
headaches in the USA shows 1 in 6 people (16.54%) or 45 million people suffer from chronic
headaches and 20 million from 45 million it is a woman. 75% of the amount above is tension
type headache which results in a decrease in the concentration of learning and work 62.7%.
Onset of migraine occurs under 30 years of age in 80% of cases and decreases with age. The risk
of developing migraine is increasing large in people who have a family history of migraine
sufferers. About 75% to 80% of migraine sufferers have family members close to having
headaches.

2.2 Definition and classification of headache

Definition

Headache is pain or discomfort on the whole area of the head with the lower boundary
from chin to the back area of head (occipital area and some part of the neck) (Sjahrir, 2008).
Headache is generally classified as primary headache and pain secondary head, then divided into
certain types of headaches. Primary headache disorders are "idiopathic" headaches, pain head that
is not related to pathological conditions or other causes underlying. Based on neurological
examinations and imaging tests usually normal, no matter how severe the symptoms are. More
primary headache events often occurs compared to secondary headaches. Secondary headache is
headache associated with underlying pathological conditions, such as presence of brain tumors,
aneurysms, inflammatory diseases. With inspection neurological and imaging tests have been
shown to help in pain diagnostics secondary head.

Classification

1. Primary Headaches
Primary headaches is a non-associated headache with pathology or other abnormalities
that cause it. This headache is still divided based on the symptoms profile to:

A. Migraine
Migraine has two major subtypes. Migraine without aura and migraines with aura.
Migraine with aura is mainly characterized by neurological symptoms usually
precedes or sometimes accompanies headaches. Some the patient also experiences
the premonitory phase (sign phase), occurs several hours or days before headaches,
and the phase of resolution. That gives a sign and symptoms resolutions such as
repeated yawning, fatigue and stiff and / or sore neck.
a. Migraine without Aura
Recurrent headache with manifestations of attack for 4-72 hours.
Characteristics are unilateral, throbbing, moderate or heavy, getting heavy with
routine physical activity and followed with nausea and or photophobia and
phonophobia.
b. Migraine with Aura
Repeated attacks, survive in minutes, are completely unilateral reversible be it
visual, sensory or other symptoms of the central nervous system which usually
develops gradually and is followed by headache and related migraine
symptoms.

B. Tension Type Headache

Tension type headache is very common, with a prevalence of age living in the
general population ranged between 30% and 78% in the study different, and has a
very high socio-economic impact.
a. Rare Episode Tension Type Headache
 Episodes of headache that are rare, bilateral, pressing or binding and mild to
moderate intensity, lasting minutes to days. The pain does not worsen with
routine and unrelated physical activity with nausea, but photophobia or
phonophobia may be present.
b. Frequent Episode Tension Type Headache
Episodes of headache that are rare, bilateral, pressing or binding and mild to
moderate intensity, lasting minutes to days. The pain does not worsen with
routine and unrelated physical activity with nausea, but photophobia or
phonophobia may be present.
c. Chronic Tension-type Headache
A disorder develops from tense episodes of headache often, with episodes of
headaches daily or very often, bilaterally, pressing or binding quality and mild
to moderate intensity, lasts hours to days, or does not stop. The pain doesn’t get
worse with routine physical activity, but may be related to nausea mild,
photophobia or phonophobia.

C. Trigeminal Autonomic Cephalalgias (TACs)

a. Cluster Type Headache
Severe, tight and unilateral pain in the orbital, supraorbital, temporal or in
combination, lasts 15 - 180 minutes and occurs from once every day to eight
times a day. Pain associated with ipsilateral conjunctival injection, lacrimation,
nose clogged, rhinorrhoea, forehead and sweaty face, miosis, ptosis and/or
eyelid edema, and/or with anxiety.
b. Paroxysmal Hemicrania
Severe, tight and unilateral pain in the orbital, supraorbital, temporal or in
combination, lasting 2 - 30 minutes and happens several times every day.
Attacks related to injection conjunctiva, lacrimation, nasal congestion,
rhinorrhoea, forehead and sweaty face, miosis, ptosis and / or ipsilateral eyelid
edema. There is a definite response to indomethacin.

2. Secondary Headaches
 Secondary headaches is headache due to other diseases so there is an increase in
intracranial pressure or headache clearly there are anatomical and structural
abnormalities.
A. Headache due to trauma in the head and/or neck
B. Headache due to cranial or cervical vascular disorders
C. Headache due to intracranial non-vascular disorders
D. Headache due to substance or withdrawal
E. Headache due to infection
F. Headache due to homeostasis disorders
G. Headache or facial pain due to cranial, neck, eyes, ears, nose, sinus cavity, teeth,
mouth disorders, or other facial or cranial structures
H. Headache due to psychiatric disorders

2.3 ETIOLOGY

The cause of migraine is still unknown, but there are several factors or triggers that can
cause it to occur migraine. Migraine trigger factors :

Triggers from food:

1) alcohol
2) Caffeine / withdrawal caffeine
3) Chocolate
4) Fermentation food
5) Monosodium glutamate
6) Saccharin
7) Food that contain nitrate or tyramine

Triggers from environment :

1) dazzling light that quite bright
2) Highness
3) noisy
4) sharp smell
5) cigarette smoke
6) weather changes

Triggres from physiologist factor :

1) sleep excess or insomnia
2) fatigue
3) menstruation or menopause
4) hungry
5) excess activity
6) stress or pasca stress

2.4 Pathophysiology of Headache

1. Pathophysiology of Tension-type headache

 Regarding the pathophysiology of migraine,3) traditionally the vascular theory, according
to which vasoconstriction occurs during an aura whereafter dilatation leads to headache, has been
widely believed. However, recently, two theories for the pathophysiology of migraine are
suggested and have become the focus of attention. One is the neuronal theory,4) according to
which the excessive excitement of nerve cells in the cerebral cortex is the origin of migraine. The
other is the trigeminovascular theory that focuses on the relationship between the trigeminal
nerves and intracranial vessels (Moskowitz5) underscored the relationship between the trigeminal
nerves and intracranial vessels, especially dural vessels, and indicated that unmyelinated C-
fibers, which originate from the trigeminal ganglion, are distributed among the dural vessels.
Furthermore, they revealed that neurogenic inflammation occurs in the dural vessels if the
trigeminal nerves are electronically or chemically stimulated. Therefore they thought that
neurogenic inflammation, which originates in the trigeminovascular system, could serve as a
migraine model. Consequently the trigeminovascular theory was suggested. A summary of this
theory is shown in Fig. 1. In other words, some kind of stimulation acts on the axons in the
trigeminal nerves, which are found around the dural vessels, and vasoactive neuropeptides
(substance P (SP), neurokinin A (NKA), calcitonin gene-related peptide (CGRP), etc.) are
released. These in turn cause neurogenic inflammation (vasodilatation, leakage of plasma
protein, and mast cell degranulation). This causes both anterograde and retrograde conduction in
the trigeminal nerves. According to this theory, anterograde conduction reaches the trigeminal
nuclei, and is then transmitted to the thalamus and cerebral cortex. This message is felt as pain.
Retrograde conduction, on the other hand, further activates a release of vasoactive neuropeptides
on the periphery of the trigeminal nerves. In addition, it is demonstrated that sumatriptan acts on
5-HT1B receptors in the intracranial vascular smooth muscle to constrict the vessels, and it also
inhibits the release of neuropeptides by binding to 5-HT1D receptors which are found in the
trigeminal nerves around the blood vessels. Furthermore, Moskowitz presented an article in
which this unknown stimulation is considered as the cortical spreading depression found during
an aura. This theory seems to be an organic combination of the traditional vascular and neuronal
theories.

2. Pathophysiology of Tension-type headache

 Tension-type headache (TTH) is the most common form of headache, and chronic tension-
type headache (CTTH) is one of the most neglected and difficult types of headache to treat. The
pathogenesis of multifactorial and varies between forms and individuals. Peripheral mechanisms
(myofascial nociception) and central mechanisms (sensation and inadequate endogenous pain
control) are intermingled: the former predominate in infrequent and frequent TTH, whereas the
latter predominate in CTTH. Acute therapy is effective for episodes of TTH, whereas preventive
treatment - which is indicated for frequent and chronic TTH - is, on average, not effective. For
most patients with CTTH, the combination of drug therapies and non-drug therapies (such as
relaxation and stress management techniques or physical therapies) is recommended. There is
clearly an urgent need to improve management of patients who are disabled by headache. This
review summarizes the present knowledge on TTH and discusses some of its more problematic
features.

3. Pathophysiology of Cluster Headache

The pathophysiology of cluster headache is not fully understood. Current theories implicate
mechanisms such as vascular dilation, trigeminal nerve stimulation, and circadian effects.
Histamine release, an increase in mast cells, genetic factors, and autonomic nervous system
activation may also contribute. Acute cluster headache has been shown to involve activation of
the posterior hypothalamic gray matter, and is inherited as an autosomal dominant condition in
about 5% of patients.2 Having a first-degree relative with cluster headache increases the risk 14-
to 39-fold.
 One study showed an association between cluster headache and the HCRTR2 gene.
Disturbed circadian rhythms have been suggested as a possible contributor because headaches
often begin during sleep.

2.5 CLINICAL MANIFESTATIONS

Overall clinical manifestations of migraine sufferers vary each individual. There are 4
common phases that occur in migraine sufferers. But not everything must be experienced by
each individual.

1. productive phase.
This phase is experienced by around 40-60% of migraine sufferers. Symptoms in the form of
mood changes, irritable, depression or euphoria, feelings of weakness, excessive sleep and want
certain types of food. This symptom appears a few hours or days before headache.

2. Aura phase

Aura is a complex focal neurological symptom that precedes or accompany a migraine

attack. This phase appears gradually for 5-20 minutes. Auras can be motoric, sensory, visual or
combined sensations among them. Visual aura 64% appears in patients and is a symptom most
common neurological. Aura in migraine is usually lost a few minutes and then headaches appear.

3. Headache Phase

Migraine headaches are usually throbbing, unilateral and usually starting in the
frontotemporal and ocular regions. Then after 1-2 hours diffusely spread posteriorly. The attack
lasted for 4-72 hours in adults and in children usually 1-48 hours. Intensity moderate to severe
pain and interfere with daily activities.

4. Postdormal or Recovery Phase

The patient feels tired, irritable, concentration decreases and occurs mood changes. Patients
can fall asleep for a long time.

2.6 Symptoms Of Headache :

Symptoms Of Migraine Headache :

a) Prodromal : Symptoms before migraine occurs, include changes in mood, changes in

feelings, fatigue and muscle tension.

b) Aura : Visual disturbances before migraine.

c) Headache : Migraine is characterized by pain such as throbbing, unilateral or bilateral,

accompanied by nausea and vomiting, sensitive to light and sound.

d) Headaches will stop even if they are not treated, usually the pain will come down

during sleep.

e) Postdromal : Other signs such as not being able to eat, fatigue, not concentrating.

Symptoms Of Tension Type Headache :

a) Characterized by mild or moderate pain that can occur bilaterally and in the frontal,

temporar and occipital pariental regions.

b) Will experience photophobia and phonophobia.

c) Pericranial muscles or neck muscles will experience lumps and pain if pressed, this

can occur in some patients.

d) Can be caused by anxiety, stress and depression.

Symptoms Of Cluster Headache :

a) Pain is periodic and unilateral and in one peroide usually occurs for 15 minutes to 3

hours.

b) Caused by abnormal blood vessel activity that causes dilation.

c) Symptoms will occur unilaterally redness of the face

d) There are no symptoms of nausea and sensitivity to light and sound

 CHAPTER III
DISCUSSION
Pharmacological treatment for primary headache

Non- Pharmacological treatment for primary headache

For migraine:

Prevention management should begin by identifying and avoiding factors that can trigger the
headaches. Behavioral changes (relaxation therapy, biofeedback, cognitive therapy) are
preventive measures that can be carried out by patients who tend to be well tolerated by patients.

For tension headache:

Non-pharmacological therapies for tension headaches include convincing counseling and effort
as well as stress management, relaxation training, or various physical therapies (eg hot or cold
compresses, ultrasound, nerve stimulation with electricity, massage, acupuncture, blocking the
occipital nerves)

For the cluster headache:

for non-pharmacological therapy and preventing attacks, patients must avoid possible trigger
factors, including the following:
- daytime sleep or other important changes in their sleep habits.
alcohol, especially during the cluster period
- Prolonged exposure to chemicals such as cleaning fluids or oil paints.
- extreme anger or emotion.
- prolonged physical activity.
- extreme change in altitude.

Pharmacological treatment for primary headache:

For migraine:

Triptans

Despite twenty years of clinical experience with the serotonin 1B/1D receptor agonists, this class
of medication still has not enjoyed widespread use in the ED setting. One explanation for this is
the lack of parenteral options—to this day, sumatriptan remains the only injectable triptan
available in the US. Another likely cause of its infrequent use is the perception of cardiovascular
risk. Though cardiac events have been infrequent, the difficulty of risk stratifying migraine
patients in acute pain may cause practitioners to choose alternates. Side effects, which are often
short-lived, occurred in 50% of patients receiving subcutaneous sumatriptan in the ED setting.
This rate is twice that of placebo treated patients. Cheaper alternatives are available, as
sumatriptan will soon be available as a generic medication. Nevertheless, when it is effective,
subcutaneous sumatriptan can rapidly and completely relieve migraine headache, allowing
patients to return promptly to their usual daily activities.

Data from a meta-analysis demonstrate that subcutaneous sumatriptan was almost three times as
likely to relieve headache as placebo. By two hours, 60% of sumatriptan subjects were pain free,
versus 12% of placebo subjects. Sustained headache response (attaining headache relief and
maintaining it for 24 hours) was achieved in 49% of sumatriptan subjects, almost three times as
many as placebo. In the ED setting, the median time to headache relief with subcutaneous
sumatriptan was 34 minutes. However, a large proportion of those who respond to sumatriptan
will suffer a headache recurrence within 24 hours of ED discharge.
When choosing a suitable population for subcutaneous sumatriptan, the most reasonable
candidates include those who report previous response to sumatriptan. Recent literature describes
a phenomenon referred to as cutaneous allodynia which may be associated with migraine
headaches. Cutaneous allodynia is defined as the sensation of pain in response to normally non-
noxious touch stimuli, such as brushing one’s hair, taking a hot shower, or putting one’s hair
back in a ponytail. This phenomenon, hypothetically, is a manifestation of involvement of
ascending pain pathways within the central nervous system. The presence of cutaneous allodynia
has been associated with decreased responsiveness to subcutaneous sumatriptan. This
phenomenon has not been well studied outside of headache sub-specialty populations and may
be confounded by chronicity of the underlying headache disorder. Inadvertent administration of
sumatriptan during pregnancy has not resulted in a marked increase in birth defects, though
safety cannot yet be assured. Therefore, in pregnant patients, alternate therapies should be used.
Triptan nasal sprays are available but do not yet have a well-defined role in the ED.

In summary, subcutaneous sumatriptan may be considered for the treatment of acute migraine,
dosed as a one-time 6mg dose. Additional doses are unlikely to be more effective. For patients
with a history of good response to triptans, subcutaneous sumatriptan should be considered a
first-line therapy. For patients who are triptan naïve, the ED setting may not be the most
appropriate location for a first dose.

Dihydroergotamine

Ergotamine has been used for the treatment of migraine for more than 100 years. Its
hydrogenated derivative, dihydroerogtamine has been available for over 50 years as a parenteral
option and is better tolerated than its precursor. Though largely replaced by the triptans because
of the latter’s greater selectivity for serotonin receptors, dihdryoergotamine may still play a
useful second-line role for some ED patients. When compared head-to-head, sumatriptan has
greater initial efficacy, though dihydroergotamine is less likely to allow recurrence of headache,
and so it may be useful in patients with a history of recurrence after treatment.
Dihydroergotamine is often administered with an anti-emetic, because it commonly induces
nausea. When choosing an anti-emetic, one of the anti-migraine anti-emetics, discussed below,
would be preferred.
Dihydroergotamine, when administered as monotherapy, is less likely than sumatriptan to relieve
the pain or the functional disability associated with an acute migraine attack. Both medications
are associated with an assortment of adverse events, including chest pain (more common with
sumatriptan), nausea (more common with dihydroergotamine), drowsiness, flushing, neck
stiffness, vertigo, weakness, and injection site reactions. When compared to chlorpromazine,
dihydroergotamine alone was more likely to result in use of rescue medication.

Dihydroergotamine can be administered in doses of 0.5 to 1mg, infused as a slow intravenous

drip. It is commonly co-administered with intravenous metoclopramide 10mg. It should be
avoided in patients with uncontrolled hypertension, risk of atherosclerotic vascular disease, and
pregnancy.

The anti-emetic dopamine-antagonists

An increasing evidence base demonstrates that this diverse class of medications is the most
appropriate first-line treatment of acute migraine in the ED setting, though mechanistic data for
this class’s efficacy is still lacking. Anti-migraine action is probably mediated through
dopamine-receptor blockade, albeit this has not yet been demonstrated.

Anti-migraine efficacy has been well-demonstrated in multiple high quality clinical trials for
chlorpromazine, Metoclopramide, prochlorperazine, and droperidol In general, these medications
are inexpensive, well-tolerated and at least as efficacious, if not more so, than any agent to which
they have been compared. Therefore, these medications should be considered first-line therapy
for acute migraine in the ED setting.

Of the four agents mentioned above, chlorpromazine has fallen out of favor because of profound
orthostasis that may accompany administration of this medication. Of the remaining three agents,
droperidol is probably the most effective, with two hour headache relief rates approaching 100%.
The ideal dose, as determined by a high quality dose finding study is 2.5mg. This medication is
commonly used and exceedingly safe, but a recent FDA warning about QT prolongation has
caused some clinicians to perform an EKG prior to medication administration.
Prochlorperazine administered in doses of 10mg is also highly effective, though not quite as
effective as droperidol . Metoclopramide is typically administered as a 10mg intravenous dose
but has been well-tolerated and efficacious when administered as repeated successive doses of
20mg.

Metoclopramide, prochlorperazine, and droperidol can all be accompanied by extra-pyramidal

symptoms, particularly akathisia, which often goes unrecognized. Prophylactic administration of
diphenhydramine is a reasonable course of action, as is slower intravenous drip rates .

The anti-emetic trimethobenzamide and the anti-psychotic haloperidol have also demonstrated
efficacy and tolerability for acute migraine attacks, though as of this writing, fewer data are
available to determine the relative efficacy of these two agents.

Metoclopramide has a favorable pregnancy rating and a long history of use for treatment of
hyperemesis gravidarum. It is the most appropriate parenteral agent for treatment of acute
migraine in pregnancy.

Non-steroidal anti inflammatory drugs

Non-steroidal anti-inflammatory drugs are a main-stay of outpatient migraine therapy,

particularly for less severe migraine attacks. The parenteral non-steroidal ketorolac has
demonstrated efficacy for the acute treatment of migraine. Its overall efficacy is comparable to
meperidine , though less than the anti-emetics. In patients without contra-indications to non-
steroidals, such as peptic ulcer disease or chronic kidney disease, this medication dosed at 30mg
IV or 60mg IM is a reasonable treatment option, either as primary treatment or as adjuvant
therapy for acute migraine.

Opioids

Opioids, particularly meperidine, are still the most widely used medications for the treatment of
acute migraine in North American EDs . Standard critiques of opioid use for migraine include
the following: decreased efficacy, high rate of adverse effects, increased rate of recurrence of
migraine within the short term, increased rate of ED recidivism, and association with chronic
migraine, though specific data for all of these is underwhelming. A recent meta-analysis
demonstrated that meperidine is less efficacious for the treatment of acute migraine and
burdened by more side effects than regimens containing DHE . Additionally, meperidine is
probably less efficacious than the anti-emetics while allowing a higher rate of return visits to the
ED, though a lower rate of extra-pyramidal side effects. Finally meperidine is no better than
ketorolac, with a similar side effect profile. Some data suggest that meperidine is associated with
an increased rate of return visit to the ED and may be associated with decreased responsiveness
to triptans . In short, there are ample reasons to recommend avoidance of meperidine as a first-
line treatment of migraine. In patients with infrequent episodic migraine and a history of
excellent response to this medication, it still may be a reasonable option.

When choosing among opioids, scant data are available to help guide a clinician. Parenteral
morphine and hydromorphone have not been subjected to comparative clinical trials.
Intramuscular butorphanol is more efficacious than meperidine and is as efficacious and well-
tolerated as DHE + metoclopramide. Opioids should not be withheld on principle--in general,
this class of medication is highly effective, safe, and well-tolerated for the management of acute
pain. However, for this one ailment, better agents are available.

Valproic acid

A more recent addition to the anti-migraine armamentarium, this anti-epileptic medication has
seemed beneficial in open-label studies, though it has performed less well in randomized trials. It
is not an unreasonable choice as a final treatment prior to admission, and should not be
considered a first line medication. Valproic acid is often administered in doses between 500mg
and 1gm as a slow intravenous drip over thirty minutes.

Recurrence of migraine after ED discharge

No matter the treatment used, migraines frequently recur after ED discharge. Two-thirds of
patients report headache within 24 hours of ED discharge; half of these are moderate or severe in
intensity. Fifty percent of patients report functional disability within 24 hours of ED discharge. It
is difficult to predict who will suffer headache after discharge. Risk factors include a history of
headache recurrence, longer duration of headache, more severe pain at baseline or persistent pain
at discharge. It is a reasonable to educate all patients as to the likelihood of recurrence.

A recent meta-analysis demonstrated that one dose of parenteral dexamethasone administered in

the ED can decrease the rate of recurrence of headache after ED discharge, with a number
needed to treat of nine. Dexamethasone may begin to be effective within several hours.

Doses of dexamethasone demonstrating efficacy have ranged from 10mg to 24mg, without a
clear dose-response curve. In general, one dose of dexamethasone was very well-tolerated, and
may now be considered first-line therapy to decrease the recurrence of headache after ED
discharge.

It is less clear what additional medications should be offered to treat the recurrence of headache
after ED discharge. Non-steroidals, such as naproxen, or triptans, such as sumatriptan, are
reasonable options, though data are not available.

A substantial proportion of migraine patients who use the ED continue to suffer from their
underlying headache disorder over the months after ED discharge. It is reasonable practice to
start patients who suffer from episodic migraines on an oral medication for use during their next
migraine attack, particularly if neurology or headache specialty appointments will be difficult to
obtain. If non-steroidals, acetaminophen, or aspirin have not proved sufficient for the patient
previously, consider starting the patient on a triptan medication, assuming low cardiovascular
risk, or a combination of metoclopramide taken with a non-steroidal drug or salicylate. An
evidence-based approach to outpatient care stratifies patients based on headache-related
disability at baseline. Thus patients with substantial headache-related functional disability at
baseline (i.e., frequently miss work or social activities) benefit from a triptan and patients
without as much functional disability can be started on cheaper alternatives such as a prescription
non-steroidal with or without metoclopramide. Though baseline headache-related functional
disability scores are less useful in the ED setting, this model is a useful framework to approach
migraine care at the time of discharge.

Frequent ED migraine visitors

Although they represent fewer than 10% of all ED headache patients, frequent ED users account
for 50% of visits in some institutions. The reasons why patients frequent the ED are not well
understood. Although it could represent “drug-seeking” behavior, it may also be a marker for
poorly treated migraine. Headache patients who frequent the ED tend to know their disease well
and request specific medications, often opioids. Although effective ED-based approaches to the
frequent visitor have not been reported in the headache literature, individual EDs should develop
a uniform departmental approach to the chronic pain patient, so that the pain and social needs of
the patient can be addressed appropriately. Physician to physician variability in management
leads to unpleasant confrontations for the physician and uncomfortable situations for the patients,
who at times are forced to beg for analgesia within the throes of an acute migraine.

Some data demonstrate a decrease in the frequency of ED visits for chronic headache patients
who participated in a comprehensive headache management program, which offered headache
education and multidisciplinary care. These programs were effective at decreasing the burden of
illness and healthcare costs in patients with chronic headaches, though only select patients were
able to benefit from these programs.

We could not find any evidence-based ED-appropriate strategies for addressing a patient’s opioid
for migraine requirements from the perspective of the individual clinician. This is a difficult
problem for an emergency clinician in the middle of a busy shift. Potential strategies include
offering a non-opioid therapy in conjunction with a lower opioid dose, referring to an appropriate
outpatient clinician, and initiating a preventative therapy at the time of discharge. It is not clear
how best to handle infrequent ED users who report complete and persistent relief after one dose
of opioid. On the one hand, one should not deny effective analgesics to patients who respond
well to a particular therapy. On the other hand, there is an association between this particular
class of therapy, chronic migraine, and ED recidivism.

Special concerns for a pediatric population

Migraine incidence begins to peak in early adolescence and may be a concern for children as
young as five or six years. In general, the presentation of pediatric migraine is more atypical, as
children may present with bilateral headache of shorter duration and without the combination of
photo- and phonophobia. There is a smaller evidence base for the treatment of pediatric
migraine, partly because of a very high placebo-response rate in this population. Management of
pediatric migraine often consists of simple analgesics, such as ibuprofen or acetaminophen,
which seem to be as efficacious in this population as oral triptans. The anti-emetic dopamine
antagonists are commonly used , though efficacy data is inferential and to date, limited to
prochlorperazine. The pediatric population also suffers several variants of cyclical pediatric pain
and vomiting syndromes linked to migraine. These are particularly difficult to diagnose because
they lack associated headache. Cyclical vomiting, benign paroxysmal vertigo of childhood, and
abdominal migraine are associated with development of migraine in adulthood.

For Tension:

Acetaminophen, aspirin, ibuprofen, naproxen, ketoprofen, indomethacin, and ketorolac are quite
effective. High-dose NSAIDs and a combination of aspirin or acetaminophen with butalbital or
codeine (rarely combined) are effective choices. The use of a combination of butalbital with
codeine should be avoided if it possible. Acute treatment for episodic headaches should not
exceed 2 days / week to prevent chronic disease. Preventive medication should be considered if
an increase in the frequency of headaches (more than 2 times a week), the duration (more than 3-
4 hours), or the severity will lead to excessive drug use or a substantial activity disorder. TCA
groups are more often used for the prevention of these tension headaches. Tetracyclic
antidepressants, especially amitriptyline, 25-150 mg per day, are recommended for patients with
chronic headaches.

For cluster:

ACUTE THERAPY
The main options for acute therapy are shown in the Table. The 5HT 1b/1d agonists, in particular
the triptans, are the most effective acute medications for cluster headache. Because a rapid onset
of action is essential, only injectable and intranasal formulations should be considered for most
patients.

Subcutaneous Sumatriptan
Subcutaneous (SC) sumatriptan 6 mg is the acute treatment of choice for most patients with
cluster headache. It has been shown to be effective in well-done clinical trials,11 with 36% of
patients pain-free within 10 minutes and 46% within 15 minutes. It is a short-acting drug and is
only approved for up to 2 doses per day. Patients with a high frequency of cluster headache
attacks (more than 2 per day) may tend to exceed this amount. It is important therefore to start a
transitional therapy quickly in such patients.

Intranasal Zolmitriptan
Intranasal zolmitriptan 5 mg is a good alternative12,13 for patients who cannot tolerate self-
injection or if the cost of SC sumatriptan is an issue. It often provides good relief, although it is
slower than SC sumatriptan. The proportion of patients with a pain-free response was superior to
placebo at 15 minutes after dosing, and pain-free rates at 30 minutes were found to be 38.5%
with the 5 mg dose.12 The 10 mg nasal spray dose in more effective but not generally available.
.
Dihydroergotamine
Dihydroergotamine (DHE) is another injectable alternative for the acute treatment of cluster
headache, but one for which there is little formal evidence for efficacy. In a retrospective study,
intravenous DHE was found to render most patients headachefree within 2 days, and 16%
became headache-free after the first dose.15 DHE can be self-administered subcutaneously or
intramuscularly at home and as an injectable medication has the potential for a rapid onset of
action. As a result of its long half-life, it may protect patients with frequent attacks from further
attacks for as long as 12 hours, for example overnight. For routine use for individual attacks, SC
sumatriptan is a more evidence-based and faster agent.

Others
Among other options, intranasal sumatriptan has the most evidence for efficacy. Intranasal
zolmitriptan has stronger evidence for efficacy, however, and also stronger evidence for
substantial direct absorption through the nasal mucosa16 that would be expected to allow for a
faster onset of action. There is also some evidence for efficacy of oral zolmitriptan in acute
cluster headache treatment, and some patients, particularly those with longer attacks, find oral
triptans helpful. They can be expected to be slower than intranasal zolmitriptan, and their
evidence for efficacy is less strong. They are therefore not recommended for routine use. There
is little evidence for efficacy of DHE nasal spray in cluster headache, and in clinical use, the
intranasal triptans are generally superior.
Non-steroidal anti-inflammatory drugs are not usually helpful for cluster attacks, and the
usefulness of opiate analgesics is very limited. Neither is recommended for routine use.

Self medication for migraine

Self-medication is defined as the use of drugs to treat self-diagnosed disorders or symptoms, or

the intermittent or continued use of a prescribed drug for chronic or recurrent disease or
symptoms. Medicines are usually selected by consumers for symptoms that they regard as
troublesome to require drug therapy but not to justify the consultation of a prescriber. It is also
defined as the acquisition of medicines and self-administering them (or administering them to the
children) with the aim of treating perceived illness

Over the counter (OTC) medication are those medications which can be dispensed by the
pharmacist without referring back to a written prescription. The National Medicines and Poisons
Board (NMPB) have developed a list that contains all medication that can be dispensed without a
prescription. To promote rational use of medicines the pharmacists when dispensing any
medication should provide ap-propriate counseling to the patients. Counseling should be done
with special care when dispensing OTC medicines

OTC : Over the counter

 Can be found in supermarket, drugstore. Without prescribe. Example :

Paracetamol

 Can be found in drugstore without prescribe. Example: CTM, antimo, Bufect

For headache we can use paracetamol or bufect (ibuprofen)

Prophylactic therapy

A prophylactic therapy is a medication or a treatment designed and used to prevent a disease

from occurring.

Patients for whom prophylactic therapy is indicated have the following migraine features:

 More than 2 headaches per month, but fewer than 8 (>8 attacks per month usually
indicate overuse of abortive therapy)
 Headaches less frequent but more prolonged (>2 days' duration) or severe attacks leading
to substantial disability
 Migraines are refractory to abortive treatment measures
 Therapies for acute attacks are intolerable, contraindicated, or overused (>2 per week)
 Migraines are predictable in occurrence
 The patient has other migraine conditions such as migraine with prolonged aura or
hemiplegic migraine

Pharmacologic options for migraine prophylaxis include calcium channel blockers, beta -
blockers, antidepressants, ergot-alkaloid, and anticonvulsants. These medications, however, may
have limited efficacy, and can be poorly tolerated.

β-Blockers in migraine prophylaxis

 Daily dose range (the most effective dose or dose range is shown in parentheses)
β-Blockers in migraine prophylaxis

 Propranolol hydrochloride (should be specifically considered as first-line

agent)*: 40 to 320 mg (80-240 mg)
 Timolol maleate (should be specifically considered as first-line agent)*: 20 to 30
mg
 Nadolol: 40 to 240 mg
 Metoprolol tartrate: 50 to 300 mg (200 mg)
 Atenolol: 50 to 200 mg (100 mg)
 Side effects
 Fatigue
 Bradycardia
 Dizziness
 Depression
 Impotence
 Bronchospasm
 Nausea (adverse effects are less frequent than with the other first-line agents)

Tricyclic antidepressants in migraine prophylaxis

 Daily dose range (the most effective dose range is shown in parentheses)
 Amitriptyline hydrochloride (should be specifically considered as first-line
agent): 10 to 300 mg (30-150 mg)
 Doxepin hydrochloride: 10 to 200 mg (50-150 mg)
 Imipramine hydrochloride: 10 to 200 mg (50-150 mg)
 Nortriptyline hydrochloride: 10 to 150 mg (50-150 mg)
 Protriptyline hydrochloride: 15 to 40 mg
 Side effects
Tricyclic antidepressants in migraine prophylaxis

 Anticholinergic effects (dry mouth, constipation, blurred vision)

 Sedation
 Postural hypotension
 Agitation
 Tremor
 Seizures

Anticonvulsant: Divalproex sodium and valproic acid in migraine prophylaxis

 Side effects
 Nausea
 Vomiting
 Tremor
 Weight gain
 Hair loss
 Drowsiness
 Ataxia
 Hepatotoxicity

Calcium channel blockers in migraine prophylaxis

 Daily dose range (most effective dose shown in parentheses)

 Verapamil hydrochloride: 120 to 480 mg (240 mg)
 Nifedipine: 30 to 90 mg
 Diltiazem: 120 to 360 mg
 Nimodipine: 60 to 120 mg
 Side effects
 Constipation (especially verapamil)
 Dizziness
Tricyclic antidepressants in migraine prophylaxis

 Hypotension
 Peripheral edema
 Weight gain

Ergot-Alkaloid

 Methysergide

CHAPTER IV
CONCLUSION

1. the type of headache that is suffered by Mr. Am is migraine

2. Swamedikasi done by Mr. Am is appropriate because paracetamol is one of the free drug
classes
3. Pharmacological therapy was changed from monotherapy to polytherapy, namely a
combination of aspirin + pct + caffeine
4. Migraine prophylaxis therapy can be done if the frequency of migraine attacks is more
than 2 days / week
5. Non-pharmacological therapy for migraines is to avoid the trigger factors
 Bibliography
 Anurogo, Dito. Penatalaksanaan Migren. RS PKU Muhammadiyah Palangkaraya,
Kalimantan Tengah. 2012.
 Ikawati, Zullies.2014.Farmakologi Penyakit Sistem Syaraf Pusat.yogyakarta: Bursa Ilm
 Hartono. LA. (2007). Stres & stroke. Yogyakarta : Kanisus
http://medicalexpress.com/news/2014-03- migraine-stress-let-down.html diakses pada 2
oktober 2018 via internet

 Headache Classification Subcommitee of the International Headache Society. The

International Headache Classification Disorder: 2nd Edition. Cephalgia 2004; 24 Suppl
1:1-160
 Sjahrir, H. 2004. Nyeri Kepala 1,2 &3. Kelompok Studi Nyeri Kepala. Perhimpunan
Dokter Spesialis Saraf Indonesia
 SS Jatmiputri, M Belladonna, FEP Mundhofir. 2017. PENGARUH STRES KERJA
TERHADAP KEJADIAN NYERI KEPALA PADA PEKERJA GROUND HANDLING
(Studi Kasus di Bandara Ahmad Yani Semarang). Diponegoro University: Semarang.

.
Contents
PLANARY DISCUSSION ............................................................................................................. 1

Physiotherapy in the Management of migraine Headaches ............................................................ 1

CHAPTER I .................................................................................................................................... 4

INTRODUCTION .......................................................................................................................... 4

1.1 Purpose .................................................................................................................................. 4

1.2 Formulation of the problem................................................................................................... 4

1.3 Background ........................................................................................................................... 4

CHAPTER II................................................................................................................................... 7

LITERATURE REVIEW .............................................................................................................. 7

2.1 EPIDEMIOLOGY ................................................................................................................ 7

2.2 Definition and classification of headache ............................................................................. 7

2.3 ETIOLOGY ......................................................................................................................... 10

2.4 Pathophysiology of Headache ............................................................................................. 11

2.5 CLINICAL MANIFESTATIONS....................................................................................... 14

CHAPTER III ............................................................................................................................... 17

DISCUSSION ............................................................................................................................... 17

Pharmacological treatment for primary headache ..................................................................... 17

Self medication for migraine ..................................................................................................... 27

Prophylactic therapy.................................................................................................................. 28