Nyeri kepala

Yang dimaksudkan di sini adalah rasa sakit / nyeri pada satu area atau lebih
di kepala, muka, mulut, leher. Nyeri kepala bisa kronik, rekuren atau jarang.
Nyeri bisa ringan atau cukup berat yang mengganggu aktifitas sehari-hari.
Pada semua kasus, nyeri kepala menyangkut keterlibatan serabut saraf di
jaringan, otot, dan pembuluh darah yang terletak di kepala dan dasar
tengkorak.
Disini, nyeri kepala harus dibedakan dengan pusing (vertigo dan perasaan
melayang atau nggliyer (dizziness atau light headness. Dua hal terakhir tadi
sifat dan latar belakangnya memang berlainan.
Bangunan peka nyeri
!angunan peka nyeri di kepala apabila terstimulasi akan menimbulkan
perasaan nyeri. !angunan ini dapat dibedakan menjadi bangunan
intrakranial dan ekstrakranial. !angunan peka nyeri intrakranial meliputi
sirkulus "illisi dan lanjutannya ke proksimal, arteri meninges, #ena besar di
otak dan dura, bagian duramater dekat pembuluh darah, ner#i kraniales $,
$%%, %&,dan &, serta saraf spinal ser#ikal bagian atas ('(,). *ementara itu
jaringan otak bukan merupakan bangunan peka nyeri.
!angunan peka nyeri ekstrakranial meliputi +tot kepala dan leher, saraf
kutaneus dan kulit kepala, mukosa sinus paranasalis dan hidung, mata dan
orbita, telinga, gigi, saraf dan radiks serfikal, dan arteri karotis eksterna dan
cabangnya.
Lokasi nyeri
Nyeri yang berasal dari bangunan intrakranial tidak dirasakan di dalam
rongga tengkorak melainkan dirujuk ke bagian lainnya. *truktur
supratentorial dipersarafi oleh N.$, dan infratentorial oleh n.'(,) sehingga
lesi lobus oksipital direfer ke depan, Nyeri yang berasal dari duapertiga
bagian depan kranium, di fosa kranium tengah dan depan, serta di atas
tentorium serebeli dirasakan di daerah frontal, parietal dan temporal. dan
lesi serebellum direfer ke belakang. -agi pula bagian kaudal nukleus N $ dari
pertengahan pons sampai medulla spinalis segmen '), juga menerima
stimulus nyeri dari radiks serfikal atas selain dari N. .rigeminus. Nyeri ini
disalurkan melalui cabang pertama ner#us trigeminus.
Nyeri yang berasal dari bangunan di ba/ah tentorium serebeli di fosa
posterior (misalnya di serebelum biasanya diproyeksikan ke belakang
telinga, di atas persendian ser#iko-oksipital atau di bagian atas kuduk. Ner#i
kraniales %& dan & dan saraf spinal '(, dan ') berperan untuk perasaan di
bagian infratentorial. !angunan peka nyeri ini terlibat melalui berbagai cara
yaitu oleh peradangan, traksi, kontraksi otot dan dilatasi pembuluh darah.
Klasifikasi
Nyeri kepala primer mencakup 01 2 kasus nyeri kepala, di mana tidak
jelas kelainan sebagai penyebab yang mendasari.
Nyeri kepala sekunder didasari oleh suatu kelainan seperti penyakit
serebro#askuler, trauma kepala, infeksi, tumor, dan kelainan metabolik
(mis., diabetes, penyakit tiroid . Nyeri kepala juga bisa berasal dari sindrom
yang mengenai mata, telinga, leher, gigi, atau sinus. Pada kasus-kasus
seperti ini penyebabnya harus di cari dan diobati. !eberapa macam obat juga
dapat menimbulkan sakit kepala sebagai efek samping.
Neri kepala sekunder yang berat, mendadak, dan mengganggu yang timbul
setelah benturan di kepala, dan mengganggu aktifitas normal, atau disertai
kelainan lain (mis., kejang, disorientasi, gangguan keseimbangan, hilang
kesadaran, nyeri di mata atau telinga, demam harus die#aluasi sesegera
mungkin.
Nyeri kepala primer
1. Migren
3igren adalah nyeri kepala yang berdenyut yang sering unilateral dan
disertai mual, muntah, sensitif terhadap cahaya, suara, bau-bauan4 tidur
terganggu4 dan depresi. *erangan sering rekuren dan cenderung berkurang
beratnya dengan bertambahnya usia.
,., 3igren tanpa aura
,.( 3igren dengan aura
,.(.,. 3igren dengan aura tipik
,.(.(. Nyeri 5epala non migren dengan aura tipik
,.(.). 3igren dengan aura tipik tanpa sakit kepala
,.(.6. 3igren hemiplegi familial
,.(.7. 3igren hemiplegi sporadik
,.(.8. 3igren tipe !asiler
,.). *indrom periodik pada anak yang sering menjadi prekursor migren
,.).,. 3untah-muntah siklik
,.).(. 3igren abdominal
,.).). $ertigo paroksismal benigna pada anak
,.6. 3igren retina
,.7. 5omplikasi migren
,.7.,. 3igren kronik
,.7.(. *tatus migren
,.7.). 9ura persisten tanpa infark
,.7.6. 3igren infark
,.7.7. 3igren yang mencetuskan bangkitan
,.8. Probable migren
,.8.,. Probable migren tanpa aura
,.8.(. Probable migren dengan aura
,.8.). Probable migren kronik
2. Nyeri kepala tegang otot
Nyeri kepala tegang otot adalah bentuk yang paling sering dari nyeri
kepala primer. *erangan biasanya mulai pada umur pertengahan dan sering
disertai stres, kecemasan, dan depresi yang dapat timbul pada umur-umur
tersebut.
(.,. Nyeri kepala tegang otot episodik yang jarang
(.,.,. Nyeri kepala tegang otot episodik dengan nyeri tekan
perikranial
(.,.(. Nyeri kepala tegang otot episodik tanpa nyeri tekan perikranial
(.(. Nyeri kepala tegang otot episodik yang sering
(.(.,. Nyeri kepala tegang otot episodik dengan nyeri tekan
perikranial
(.(.(. Nyeri kepala tegang otot episodik tanpa nyeri tekan perikranial
(.). Nyeri kepala tegang otot kronik
(.).,. Nyeri kepala tegang otot kronik dengan nyeri tekan perikranial
(.).(. Nyeri kepala tegang otot kronik tanpa nyeri tekan perikranial
(.6. Probable tension type headache
(.6.,. Probable tension type headache episodik yang jarang
(.6.(. Probable tension type headache episodik yang sering
(.6.). Probable tension type headache kronik
2. Nyeri kepala kelompok dan nyeri kepala trigeminal-otonom
yang lain
Nyeri kepala kelompok berlangsung tiap hari selama masa berminggu-
minggu bahkan kadang-kadang bulan. *erangan bisa menghilang kemudian
muncul kembali pada musim yang sama pada tahun berikutnya.
).,. Nyeri kepala kelompok
).,.,. Nyeri kepala kelompok episodik
).,.(. Nyeri kepala kelompok kronik
).(. :emikrania paroksismal
).(.,. hemikrania paroksismal episodik
).(.(. hemikrania paroksismal kronik
).). Nyeri kepala neuralgi unilateral singkat dengan injeksi konjungtifa
dan lakrimasi
).6. Probable sefalgia trigeminal otonomik
).6.,. Probable nyeri kepala kelompok
).6.(. Probable hemikrania paroksismal
).6.). Probable *;N'.
4. Nyeri kepala Primer lainnya
6.,. Nyeri kepala menusuk primer
6.(. Nyeri kepala akibat batuk primer
6.). Nyeri kepala akibat olah raga primer
6.6. Nyeri kepala primer sehubungan aktifitas seksual
6.6.,. Nyeri kepala preorgasmik
6.).(. Nyeri kepala orgasmik
6.6. Nyeri kepala hypnic
6.7. Nyeri kepala thunderclap primer
6.8. :emikrania kontinua
6.<. Nyeri kepala harian persisten yang baru
Nyeri kepala sekunder
5. Nyeri kepala pada trauma
7.,. Nyeri kepala pasca trauma akut
7.,.,. Pada trauma kepala yang bermakna dan / atau gejala
konfirmasi
7.,.(. Pada trauma kepala ringan dan / atau tanpa gejala konfirmasi
7.(. Nyeri kepala pasca trauma kronik
7.(.,. Pada trauma kepala yang bermakna dan / atau gejala
konfirmasi
6. akit Kepala pada kelainan !askuler
8.,. Penyakit serebro#askuler iskemik akut
8.,.,. *erangan iskemik sepintas
8.,.(. *trok tromboemboli
8.(. Perdarahan intrakranial
8.(.,. Perdarahan intraserebral
8.(.(. Perdarahan subdural
8.(.). Perdarahan epidural
8.). Perdarahan subarahnoid
8.6. 3alformasi #askuler yang tidak ruptur
8.6.,. malformasi arteri#ena
8.6.(. aneurisma sakuler
8.7. 9rteritis
8.7.,. 9rteritis sel raksasa (arteritis temporalis
8.7.(. 9rteritis sistemik lain
8.7.). 9rteritis intrakranial primer
8.8. Nyeri arteri karotis atau #ertebralis
8.8.,. Diseksi arteri karotis atau #ertebralis
8.8.(. karotidinia (idopatik
8.8.). Nyeri kepala pascaendarterektomi
8.<. .rombosis #ena
8.=. :ipertensi arteri
8.=.,. >fek peninggian tekanan darah akut terhadap bahan luar
8.=.(. ?eokromasitoma
8.=.). :ipertensi maligna
8.=.6. Preeklamsi dan eklamsi
". Nyeri kepala pada kelainan intrakranial non!akuler
<.,. .ekanan intrakranial yang tinggi
<.,.,. Peninggian tekanan intrakranial benigna
<.,.(. hidrosefalus tekanan tinggi
<.(. .ekanan intrakranial yang rendah
<.(.,. Nyeri kepala setelah pungsi lumbal
<.(.(. Nyeri kepala pada fistula cairan serebrospinal
<.). %nfeksi intrakranial
<.6. *arkoidosis intrakranial dan penyakit inflamsi non-infeksi lainnya
<.7. Nyeri kepala sehubungan suntikan intratekal
<.7.,. >fek langsung
<.7.(. 5arena meningitis kimia
<.8. Neoplasma intrakranial
<.<. Nyeri kepala sehubungan kelainan intrakranial lain
#. akit kepala karena pemakaian $a%an atau peng%entiannya
=.,. Nyeri kepala karena penggunaan bahan akut
=.,.,. Nyeri kepala akibat nitrat/nitrit
=.,.(. Nyeri kepala akibat monosodium glutamat
=.,.). Nyeri kepala akibat '+
=.,.6. Nyeri kepala akibat alkohol
=.,.7. Nyeri kepala akibat bahan lain
=.(. Nyeri kepala akibat penggunaan bahan kronik
=.(.,. Nyeri kepala akibat >rgotamin
=.(.(. Nyeri kepala akibat analgetik
=.(.). !ahan lain
=.). Nyeri kepala akibat penghentian bahan (penggunaan akut
=.).,. Nyeri kepala akibat penghentian alkohol
=.).(. !ahan lain
=.6. Nyeri kepala akibat penghentian bahan (penggunaan kronik
=.6.,. *akit kepala penghentian ergotamin
=.6.(. *akit kepala penghentian kofein
=.6.). *akit kepala ketergantungan narkotik
=.6.6. !ahan lain
=.7. Nyeri kepala karena bahan tetapi tanpa mekanisme jelas
=.7.,. Pil antihamil atau estrogen
=.7.(. bahan lain
0. Nyeri kepala pada infeksi di luar kepala
0.,. %nfeksi #irus
0.,.,. %nfeksi fokal
0.,.(. %nfeksi sistemik
0.(. %nfeksi bakteri
0.(.,. %nfeksi fokal
0.(.(. %nfeksi sistemik
0.). *akit kepala pada infeksi lain
,1. Nyeri kepala pada kelainan metabolik
,1.,. :ipoksia
,1.,.,. Nyeri kepala pada ketinggian
,1.,.(. Nyeri kepala hipoksia
,1.,.). Nyeri kepala apnu tidur
,1.(. :iperkapnia
,1.). 'ampuran hipoksia dan hiperkapnia
,1.6. :ipoglikemi
,1.7. Dialisis
,1.8. Nyeri kepala pada kelainan metabolik lain
,,. Nyeri kepala atau /ajah pada kelainan kranium, leher, mata, telinga,
hidung, sinus, gigi, mulut, atau struktur /ajah dan kepala yang lain
,,.,. .ulang kranium
,,.(. -eher
,,.(.,. $ertebra serfikal
,,.(.(. .endonitis retrofaringeal
,,.). 3ata
,,.).,. @laukoma akut
,,.).(. gangguan refraksi
,,.).).:eteroforia atau heterotropia
,,.6. .elinga
,,.7.:idung dan sinus
,,.7.,. Nyeri kepala sinus akut
,,.7.(. Penyakit lain pada hidung dan sinus
,,.8. @igi, rahang, dan struktur yang berhubungan
,,.<. Penyakit pada sendi temporomandibular
,(. Neuralgia kranial, nyeri trunkus saraf dan nyeri deaferensasi
,(.,.
*elanjutnya yang akan dibicarakan adalah nyeri kepala tegang otot, nyeri
kepala kelompok, dan migren.
Nyeri kepala tegang otot dan kelompok
&nsidens and Pre!alensi
Di 9merika *erikat, lebih dari 67 juta orang Atermasuk lebih dari )) juta
penderita asma, diabetes, dan sakit jantung Amengalami nyeri kepala
kronik, rekuren. (= juta dari padanya menderita migren setiap tahun.
!erkisar <72 to 012 dari semua orang yang mengeluh nyeri kepala kronik,
atau sering, menderita nyeri kepala tegang otot. Nyeri kepala tegang otot
lebih banyak pada /anita dari pria. Nyeri kepala kelompok utamanya pada
pria berumur antara (1 dan 61 tahun.
Penye$a$
Nyeri kepala tegang otot disebabkan oleh stres, ketegangan otot, dilatasi
pembuluh darah, perubahan posisi, batuk atau bersin yang berlebihan, dan
demam. 5ondisi fisik dan mental yang dapat mengakibatkan ketegangan otot
kronik dan sakit kepala B
kecemasan
9rtritis pada leher atau #ertebra
Penyakit degenerasi pada tulang atau diskus #ertebra
Depresi
@angguan sendi temporomandibular
9da beberapa faktor pemicu yang diketahui menyertai nyeri kepala
kelompok, termasuk obat-obatan yang menyebabkan dilatasi atau
konstriksi pembuluh darah dan alkohol. %ni menimbulkan dugaan bah/a
perubahan dalam dinding pembuluh darah di kepala mempunyai peranan
sebagian.
!eberapa peneliti percaya bah/a kadar rendah endorphins dapat
menyebabkan nyeri kepala yang sering, berat, atau kronik. >ndorphins
adalah bahan penghilang nyeri yang ditemukan di otak.
ymptoms
Nyeri kepala tegang otot
Nyeri kepala tegang otot biasanya menimbulkan nyeri yang tumpul, menetap
pada kedua sisi kepala. Nyeri biasanya meningkat dalam beberapa jam.
!eberapa penderita nyeri kepala tegang otot mengatakan bah/a bila
memburuk, nyeri berkembang dengan munculnya nyeri yang berdenyut.
Nyeri kepala tegang otot pernah diuraikan sebagai tekanan atau ikatan di
sekeliling kepala, sepertinya tali yang ditarik kencang mengelilingi kepala
atau kepala merasa dijepit.
Nyeri tekan pada otot didaerah leher, dasar tengkorak, kulit kepala, dahi,
/ajah, rahang, bahu, atau lengan atas bisa ditemukan pada penderita nyeri
kepala tegang otot. 5ulit kepala dan dahi mungkin terasa nyeri pada
sentuhan. !eberapa orang nampak giginya terkatup.
Nyeri kepala kelompok
+rang yang mengalami nyeri kepala kelompok bisa merasakan sampai = kali
serangan sehari, setiap kali berlangsung ,7- sampai 67 menit atau lebih
lama. *erangan nyeri sering datang saat pagi-pagi buta dan membangunkan
pasien dari tidur.
Nyeri pada nyeri kepala kelompok biasanya unilateralB terletak di sekitar
satu mata dan hampir selalu pada satu sisi kepala. !isa disertai hidung
mampet dan mata berair.
Nyeri bisa terasa sangat hebat pada kebanyakan penderita, sering diuraikan
seperti pisau atau paku ditusukkan ke dalam kepala. !erbaring bisa
membuat nyeri kepala betambah parah. !eberapa orang mondar-mandir dan
bergerak terus, tetapi tanpa perbaikan.
'iagnosis
Diagnosis nyeri kepala tegang otot dan kelompok didasarkan pada keluhan
dan pemeriksaan medis yang menyeluruh pada pasien, seperti berikutB
Pemeriksaan mata
'iri-ciri nyeri kepala
5ebiasaan tidur
Ci/ayat keluarga
Ci/ayat medis
+bat-obat yang diminum
Pemeriksaan darah
Pemeriksaan neurologis
Pemeriksaan fungsi tiroid, hati , dan ginjal
Pemeriksaan Imaging otak mungkin dibutuhkan untuk menyingkirkan
berbagai masalah medis serius yang mendasari, seperti tumor otak, strok,
infeksi, and malformasi #askuler (e.g., aneurisma.
Pemeriksaan imaging yang mungkin dilakukan B
>>@ (electroencephalogram untuk menilai aktifitas otak
'9. (computer aDial tomography or 3C% (magnetic resonance
imaging scan untuk melihat jaringan dan struktur sekitar, pada , dan
di dalam otak
?oto kepala, atau 3C9 (magnetic resonance angiography untuk
menilai pembuluh darah otak
Pemeriksaan laboratorium dan imaging dapat membantu menyingkirkan
penyebab sekunder nyeri kepala, seperti berikutB
.umor otak
9neurisma otak
hipertensi
infeksi (mis., meningitis, sinusitis, infeksi telinga
arteritis temporalis
neuralgia trigeminus
Pengo$atan
Nyeri kepala tegang otot
Nyeri kepala tegang otot biasanya dapat diobati dengan baik dengan
mengatur pola hidup dan penggunaan analgesik (mis., aspirin, ibuprofen,
acetaminophen. !ila nyeri kepala berat atau sering, harus hati dengan
penggunaan analgetik yang berlebihan, yang bisa menimbulkan nyeri kepala
rebound.
Pada nyeri kepala rebound, kadar yang tinggi dari obat di dalam badan
sebenarnya menyebabkan nyeri kepala. Pada kebanyakan kasus , nyeri
kepala rebound membaik bila obat-obat di hentikan.
Nyeri kepala tegang otot yang tidak mempan obat penghilang nyeri dapat
diberikan antidepresan atau obat mengurangi kecemasan, seperti
amitriptylin, nortriptylin or desipramin.
!eberapa pasien nyeri kepala tegang otot merasakan membaik dengan
pengobatan sekunder dengan mengurangi efek dari stres dan tegangan di
badan, menggunakan pijat, meditasi dan biofeedback. !ila cocok,
psikoterapi dapat menolong beberapa pasien untuk belajar mengatasi lebih
baik keadaan stres yang dapat menimbulkan sakit kepala.
Nyeri kepala kelompok
3engobati nyeri kepala kelompok terdiri atas mengurangi nyeri yang tak
tertahankan, dan memutus atau memperpendek episode nyeri. +bat-obat
untuk keadaan akut sama yang digunakan untuk migrenB
sumatriptan (%imitreDEAsuntikan atau sprai nasal. .riptan lain
peroral juga bisa efektif.
D:> (3igranalEAsuntikan atau sprai nasal. Fuga digunakan pada
migren. >fek samping berupa mual dan diGGiness.
,112 oDygenAdihirup dari oksigen tangki. Diberikan bila obat-obat
tidak memberikan perbaikan. Dapat digunakan di rumah.
Narkotik (e.g., codeine Aperoral. .idak bekerja cukup cepat,
mempersingkat nyeri kepala.
Prednison adalah kortikosteroid, merupakan bahan kimia yang poten yang
dibentuk alamiah dalam badan. Diberikan dosis tinggi pada a/alnya dan
kemudian di tapering selama beberapa hari atau minggu, tergantung
respons. +bat ini paling baik bila diberikan jangka pendek. Penggunaan
jangka panjang dapat menimbulkan banyak efek samping serius sebab
mempunyai banyak fungsi dalam badan. >fek samping potensial seperti
peninggian tekanan intraokuler, osteoporosis, perubahan tingkah laku, ulkus,
dan diabetes.
Lithium karbonat -ithium dapat meningkatkan kadar dopamin dan
norepinefrin di otak. Diberikan peroral, biasanya ( kali sehari, untuk
memutus nyeri kepala kelompok. 5onsentrasi lithium darah harus dimonitor
ketat dengan pemeriksaan darah berulang. Efek samping seperti tremor,
cepat haus, mual, dan sering kencing. -ithium karbonat khususnya
digunakan untuk mengobati episode manik dari pasien manik depresi.
Verapamil melebarkan pembuluh darah. !isa diminum ( kali sehari. Efek
samping berupa mual, diGGiness, dan konstipasi. $erapamil khususnya
untuk mengobati angina, hipertensi dan aritmia.

M&()*N
3igren adalah nyeri kepala yang berdenyut yang sering unilateral dan
disertai mual, muntah, sensitif terhadap cahaya, suara, bau-bauan4 tidur
terganggu4 dan depresi. *erangan sering rekuren dan cenderung berkurang
beratnya dengan bertambahnya usia.
+ipe
5lasifikasi migren didasarkan pada keluhan yang timbul. *udah diuraikan di
atas.
Dua bentuk yang laGim adalah migren dengan aura dan migren tanpa aura
yang akan diuraikan berikut.
!entuk yang lebih jarangB
3igren basiler
karotidinia
migren tanpa sakit kepala
migren oftalmoplegi
status migren
&n,idens and Pre!alensi
3igren mengenai sekitar (6 juta orang di 9*. !isa pada setiap umur, tetapi
biasanya mulai antara umur ,1 dan 61 tahun dan berkurang setelah 71
tahun. !eberapa orang mengalamai beberapa kali serangan se bulan,
sementara yang lainnya hanya mengalami beberapa kali seumur hidupnya.
!erkisar <72 penderita migren adalah /anita.
Penye$a$
Penyebab migren tidak diketahui. 5ondisi ini bisa akibat dari satu rentetan
reaksi dari **P yang disebabkan oleh perubahan pada badan atau
lingkungan. *ering ada ri/ayat keluarga menderita sakit tersebut, sehingga
diduga penderita migren menerima /arisan kepekaan terhadap pemicu yang
menghasilkan inflamasi pada pembuluh darah dan saraf sekitar otak,
menyebabkan nyeri.
Pemi,u
Pemicu adalah setiap stimulus yang memulai proses atau reaksi. Pemicu
migren yang laGim dikenal B
9lkohol (mis., anggur merah
?aktor lingkungan (mis., cuaca, ketinggian, perubahan daerah /aktu
3akanan yang mengandung kafein (mis., kopi, coklat, monosodium
glutamate (3*@4 pada makanan 'ina, dan nitrat (mis., makanan
yang diproses, hot dogs
'ahaya yang menyilaukan
Perubahan hormon pada /anita
-apar
5urang tidur
+bat-obatan (beli sendiri dan diresepkan
Parfum
*tres
(e-ala dan Kelu%an
Nyeri migren sering diuraikan sebagai nyeri berdenyut yang bertambah
dengan aktifitas rutin, batuk, mengedan, atau merendahkan kepala. Nyeri
kepala sering begitu berat sehingga mengganggu aktifitas harian dan dapat
membangunkan orang tersebut. *erangan nyeri membuat tidak berdaya, dan
sering merasa lelah dan lemah terus begitu sakit kepala hilang.
3igren khasnya dimulai di satu area pada satu sisi kepala, kemudian meluas
dan meningkat intensitasnya di atas , sampai ( jam dan perlahan-lahan
mereda. !isa berakhir dalam (6 jam, dan pada beberapa kasus , beberapa
hari.
9da keluhan penyerta seperti mual, muntah, peka terhadap cahaya
(fotofobia, atau peka terhadap suara (fonofobia. .angan dan kaki dapat
merasa dingin dan berkeringat dan bau yang tidak enak dapat tidak diterima.
Migren dengan aura ditandai oleh fenomena neurologis (aura yang
dirasakan ,1 H )1 menit sebelum sakit kepala. 5ebanyakan aura adalah
#isual dikatakan sebagai terang menyilaukan sekeliling benda atau pada
bagian tepi lapangan pandang (disebut scintillating scotomas atau garis-
garis GigGag , bayangan berombak, atau halusinasi. Yang lain merasakan
hilang penglihatan sementara.
9ura non#isual seperti kelemahan motorik, kelainan bicara atau bahasa,
diGGiness, #ertigo, and kesemutan atau baal (parestesia /ajah, lidah, or
ekstremitas.
Migren tanpa aura adalah tipe yang paling sering dan bisa mengenai satu
sisi kepala atau keduanya (bilateral. 5elelahan atau perubahan mood dapat
dialami pada hari sebelum sakit kepala. 3ual, muntah, peka cahaya
(fotofobia sering ada pada migren tanpa aura.
Migren arteri basiler menyebabkan gangguan pada arteri basiler di batang
otak. 5eluhan berupa nyeri kepala hebat, #ertigo, penglihatan doubel, bicara
pelo dan koordinasi otot yang terganggu. !entuk ini terutama pada orang
muda.
Karotidinia, juga disebut nyeri kepala separuh ba/ah atau migren /ajah,
menimbulkan nyeri dalam, tumpul, dan kadang-kadang nyeri menusuk di
rahang atau leher. !iasanya ada nyeri tekan dan pembengkakan pada arteri
karotis di leher. >pisod bisa timbul beberapa kali seminggu dan berakhir
beberap menit sampai beberapa jam. .ipe ini lebih laGim pada orang tua.
Migren tanpa nyeri kepala ditandai oleh adanya aura tanpa sakit kepala.
%ni terjadi pada pasien dengan ri/ayat migren dengan aura.
Migren oftalmoplegia mulai dengan nyeri kepala di mata dan disertai
muntah. !egitu nyeri kepala berjalan, kelopak mata jatuh (ptosis dan saraf
yang menggerakkan bola mata mengalami paralisis. Ptosis bisa menetap
selama beberapa hari atau minggu.
Status migren adalah bentuk yang jarang dengan nyeri yang hebat yang
biasanya berlangsung lebih dari <( jam. Pasien mungkin membutuhkan
pera/atan.
'iagnosis
Diagnosis migren didasarkan ri/ayat keluhan, pemeriksaan fisik, dan
pemeriksaan neurologis. Pemeriksaan dilakukan untuk menyingkirkan
kelainan neurologis lain dan serebro#askuler, seperti berikutB
9neurisma serebri (pelebaran pembuluh darah di otak
%nfark serebri (strok di otak
.rombosis sinus #ena di otak (gumpalan darah dalam selaput yang
menutupi otak
hidrosefalus (kelebihan cairan otak
perdarahan intraserebral (perdarahan dalam tengkorak
cairan otak yang sedikit ('*?
3eningitis (peradagan selaput otak dan med.spinalis
blok sinus nasalis
nyeri kepala pasca iktus (terjadi setelah strok atau bangkitan
.umor
Pemeriksaan
Computed axial tomography ('. scan dilakukan untuk menyingkirkan
kelainan otak yang mendasari bila migren masih baru atau bila ada
perubahan ciri atau kekerapan. '. scan juga mencakup menyuntikkan
kontras kemudian mengambil rentetan D-rays.
Eletroenephalography (>>@ merekam signal listrik dalam otak
menggunakan elektrode yang ditempatkan pada permukaan kulit kepala.
Pemeriksaan ini untuk menemukan malfungsi aktifitas otak (mis.,
bangkitan.
Spinal tap (lumbar puncture is dilakukan untuk menemukan infeksi dan
menetapkan kadar sel darah putih, glukosa, dan protein dalam cairan otak.
Pemeriksaan ini mencakup mengambil sejumlah kecil cairan dan memeriksa
diba/ah mikroskop.
Magneti resonane imaging (3C% scan and magneti resonane
angiography (3C9 dapat dilakukan untuk e#aluasi lebih lengkap. 3C%
menghasilkan bayangan otak yang jelas yang memanfaatkan energi
elektromagnetik. 3C9 menghasilkan bayangan pembuluh darah otak dan
digunakan untuk menemukan aneurisma dan kelainan #askuler lain.
Pengo$atan
Perlu analisa ri/ayat migren pasien untuk memutuskan program pengobatan
yang sesuai. .ujuan pengobatan adalah untuk mencegah atau mengurangi
jumlah serangan migren (disebut pengobatan profilaksi dan untuk
meredakan keluhan dan memperpendek lama migren (disebut pengobatan
abortif.
Pengobatan profilaksi
+bat-obat profilaksi (pencegahan dapat diresepkan pada pasien dengan
nyeri kepala yang sering () atau lebih sebulan yang tidak mempan
pengobatan abortif. Pertama dicoba satu obat (monoterapi, tetapi kombinasi
obat-obat mungkin diperlukan. !anyak dari obat-obat ini mempunyai efek
samping yang tidak diinginkan. !ila migren terkontrol, dosis obat dapat
diturunkan atau dihentikan.
!eta blokers (e.g., propranolol I%nderalEJ, atenolol I.enorminEJ adalah
obat yang lebih disukai. +bat-obat ini mempengaruhi laju denyut jantung.
.idak boleh pada pasien asma dan harus digunakan dengan hati-hati pada
pasien diabetes.
Efek samping terdiri atas gangguan gastrointestinal, insomnia, tekanan
darah rendah (hipotensi, denyut jantung melambat (bradikardi, dan
disfungsi seksual. !eberapa betablocker masuk ke dalam susu ibu dan dapat
menyebabkan masalah pada bayi yang disusui.
"bat#obat antibangkitan seperti asam #alproat (DepakoteE, topiramat
(.opomaDE, and gabapentin (NeurontinE mungkin efektif dalam
pengobatan migren.
Efek samping meliputi mual, rasa tidak enak gastrointestinal, sedasi,
kerusakan hati, dan tremor.
Calium hannel blokers (e.g., #erapamil, amlodipine INor#ascEJ
menghambat dilatasi arteri dan meblok pelepasan serotonin. .idak boleh
diminum oleh pasien payah jantung atau blok jantung.
Efek samping mencakup konstipasi, muka merah (flushing, tekanan darah
rendah, rash, dan mual.
$riyli antidepressants (.'9s4 e.g., amitryptaline I>la#ilEJ,
nortryptaline IPamelorEJ, desipramine INorpraminEJ memblok reabsorbsi
serotonin dan butuh minggu untuk efektif.
Efek samping meliputiB
konstipasi
mulut kering
hipotensi
takhikardi
retensi urine
disfungsi seksual
berat badan bertambah
Dosis tinggi .'9 dapat menimbulkan bangkitan, strok, dan serangan
jantung. Penghentian mendadak obat-obat ini dapat menyebabkan sakit
kepala, mual, malaise,dan dapat memperberat efek samping.
Seleti%e serotonin reuptake inhibitors (**C%s4 e.g., paroDetine
IPaDilEJ, fluoDetine IProGacEJ, sertraline IKoloftEJ biasanya lebih baik
ditoleransi dari .'9, tetapi tidak seefektif .'9.
Efek samping mencakup mual, insomnia, disfungsi seksual,dan hilangnya
nafsu makan.
Methysergide maleate (e.g., DeserilE, *ansertE dapat diberikan pada
pasien dengan migren yang sering, berat.
Efek samping terdiri atas insomnia, ngantuk, kepala ringan, dan rambut
rontok. +bat tersebut tidak boleh pada pasien penyakit arteri koroner dan
harus dihentikan selama )-6 minggu setelah )-6 bulan penggunaan sebab
dapat menyebabkan fibrosis retroperitoneal, 5eadaan di mana pembuluh
darah di abdomen menebal, yang mengurangi aliran darah ke organ.
Pengo$atan .$ortif
3igren yang ringan dan jarang bisa membaik dengan obat-obat beli sendiri.
Nyeri kepala berat disertai keluhan penyerta perlu diresepkan obat-obatan.
*elama migren, orang sering lebih suka beristitahat, atau tidur sendiri di
ruang gelap& ukup tenang. 3enempelkan bungkusan es di kepala atau
menekan arteri yang menonjol di depan telinga pada sisi yang sakit dapat
mengurangi sementara rasa sakit.
'nalgesik (mis., aspirin, ibuprofen, acetaminofen meredakan nyeri kepala
sementara dan harus diminum saat gejala pertama migren. +bat-obat ini
sangat efektif untuk migren yang jarang (kurang dari ) perbulan dan nyeri
kepala yang tetap timbul dengan obat-obat profilaksi (breakthrough
headaches.
*ering menggunakan analgesik (mis., lebih dari 6 kali seminggu dapat
menyebabkan nyeri kepala LreboundM dan dapat mengganggu pengobatan
profilaski. 9cetaminofen kadang dikombinasi dengan obat-obat lain untuk
membuat bahan analgesik (mis., 3idrinE.
Efek samping yang disebabkan oleh aspirin dan ibuprofen (mis., 9d#ilE,
3otrinE adalah gangguan pencernaan dan perdarahan. +bat-obat ini harus
diminum saat makan dan digunakan hati-hati. %buprofen tersedia dalam
bentuk suppositoria, yang bisa berguna bila migren disertai mual dan muntah
yang hebat.
(eseptor serotonin (mis, %mitreDE, 9mergeE, 9DertNO,<6 adalah obat
yang bekerja cepat, biasanya ditoleransi dengan baik, laGim digunakan untuk
mengobati migren. .ersedia dalam bentuk oral, suntikan dan, dan bentuk
semprotan hidung dan dapat digunakan setiap saat sakit kepala.
Efek samping adalah muka merah, perasaan tidak enak, kesemutan, dan
mual.
Ergots (e.g., 'afergotE, 3ioranalE dapat digunakan oral atau suppositoria
dan sering digunakan bersama obat anti mual, seperti prochlorperaGine
('ompaGineE. +bat ini harus diminum saat gejala pertama migren muncul
dan tidak efektif bila sakit kepala sudah berdenyut.
Efek samping adalah rasa tidak enak pencernaan, diGGiness, strok, dan
hipertensi. >rgots jangan diminum oleh pasien sakit jantung, #askuler, hati,
dan ginjal.
Pen,ega%an
3encegah pemicu, menangani stres, dan minum obat profilaksi dapat
mencegah migren. Dengan membuat catatan migren, dapat membantu
mengetahui pemicu dan menilai efektifitas penanganan pre#entif. Pasien
harus mencatat hal-hal berikutB
9ktifitas
?aktor emosi (mis. *ituasi stres
?aktor lingkungan (mis., cuaca, perubahan ketinggian
3akanan dan minuman
+bat-obat (yang dibeli bebas dan diresepkan
'iri-ciri migren (mis., beratnya, lamanya
?aktor fisik (mis., penyakit, kelelahan
Pola tidur
$ehnik penanganan stres (mis., biofeedback, hipnosis dan aktifitas yang
mengurangi stres (mis., meditasi, yoga, latihan dapat membantu mencegah
migren.
Tension-type headache
How to recognize this common condition
Loretta Mueller, DO
VOL 111 / NO 4 / APRIL 2002 / POSTGRADUATE MEDICINE
CME learning objectives
To review accurate diagnosis of tension-type headache
To better understand the pathophysiology, precipitating factors, and societal
impact of tension-type headache
Preve!:
Tension-type headache is the most prevalent headache type, affecting most women and
men at some time in their lives, and can impair job productivity and interfere with family
and social time. However, despite its impact, tension-type headache is also the most
misunderstood headache type. Because of these misperceptions, many affected people are
reluctant to see medical treatment. !n this article, "r #ueller discusses possible triggers
of tension-type headache, appropriate evaluation, and management with pharmacologic,
nonpharmacologic, and alternative therapies.
Mueller L. Tension-type, the forgotten headache: how to recognize this common but
undertreated condition. Postgrad Med 22!"""#$%:2&-&
Up to $$% of women and &'% of men e(perience tension-type headache during their
lifetime )*+. The word ,tension, implies that this type of headache can be attributed
entirely to tension or stress, which may mae people with this type of headache reluctant
to consult a physician. -hysician misperceptions that tension-type headaches are mild,
benign, self-treatable conditions due solely to stress may further trivialize the problem.
,Tension-type, is a headache classification developed in *'$$ by the !nternational
Headache .ociety )!H.+ )table *+. !t refers to a condition characterized by bilateral mild
to moderate pain and pressure that often is described as similar to that of having ,a vise
around the head., .ome patients with tension-type headache may e(perience severe pain
and mared disability.
Ta"le 1# I$ter$ato$al %ea&a'(e So'et) &a*$o+t' 'rtera ,or te$+o$-t).e
(ea&a'(e
Pr/ar) &a*$o++
1# Headache has at least two of the following characteristics:
Bilateral pain
-ressure
#ild to moderate pain
/o increased pain with physical e(ertion
2# 'nd no more than one of the following:
.ensitivity to light
.ensitivity to sound
0# 'nd neither of the following0:
/ausea
1omiting
4# 'nd duration of 23 minutes to 4 days
Su"&v+o$ &a*$o++
1# 5pisodic )6*7 days8mo+ or chronic )9*7 days8mo for 9& mo+
2# :ssociated with or not associated with coe(isting pericranial muscle tenderness00
0;hronic tension-type headache may include one of these symptoms.
00"iagnosed by manual palpation or electromyographic studies.
'dapted from (eadache )lassification )ommittee of the *nternational (eadache +ociety
#2%.
Tension-type headache usually is not associated with migrainelie symptoms, such as
nausea, vomiting, increased pain with physical e(ertion, photophobia, and phonophobia.
.tress may be one of many precipitating factors, but the underlying cause is unnown.
<esearch advances into this nonvascular headache have not ept pace with e(citing new
migraine discoveries.
: central mechanism that is not unlie the mechanism of the serotonin abnormalities of
migraine is one liely cause of tension-type headache, with muscular tenderness being
either a contributing factor or an epiphenomenon. -hysician and patient education
directed at addressing the reduced =uality of life and wor productivity due to tension-
type headache may stimulate further research and increase healthcare use by the $7% of
people with tension-type headache who do not see treatment )2+.
Epidemiologic factors
/early $3% of the population will e(perience a tension-type headache at some time. :n
estimated *-year prevalence of $&% in women and &2% in men means that it is more
probable to have e(perienced a tension-type headache than not )*+. Headache is one of
the *3 chief complaints of patients seen in primary care practices, and >4% of headaches
are tension-type )2+. "uring childhood there is no male or female predominance for
tension-type headache, but during adulthood it is more commonly e(perienced by women
)female-male ratio, 7:>+ )>+. ?irst onset of tension-type headache is before age @3 in >3%
of affected persons, between ages @3 and >3 in >3%, and between ages >3 and 73 in *$%
)2+. Three percent of the general population )7% of women and @% of men+ e(perience
chronic tension-type headache, defined as more than *$3 headache days per year )*+.
-revalence of chronic tension-type headache increases with ageA the inverse is true for
episodic tension-type headache.
Societal impact
Because of its high prevalence and wide spectrum of disability, tension-type headache
has greater socioeconomic impact than any other headache type. :bout $@3 annual
wordays for every *,333 persons are lost on account of tension-type headache )versus
@43 days on account of migraine+ )7+. The reduced productivity of those who remain at
wor despite headache has an even greater impact. Bverall, tension-type headaches have
a negative effect on the emotional life of affected persons, resulting in mared reductions
in =uality of life and fre=uency of social and family activities. "espite this, less than *7%
of people with tension-type headache see medical attention )2+. -roposed reasons for
this disparity are lac of respect, empathy, and understanding by physiciansA fear of not
being taen seriouslyA trivialization of the disorder by media advertising and joesA and
the widespread misperception that the headaches have a purely psychological basis.
Diagnosis
There are no objective diagnostic marers for tension-type headache. :n accurate
diagnosis relies on comprehensive history taing, which is helpful in eliminating
secondary, potentially life-threatening diagnoses )table @+. The principal feature of
tension-type headache is mild to moderate pressure-type pain, usually on both sides of the
head, often described as occurring in the frontal or occipital areas or as a band around the
head. :ssociated symptoms may include fatigue, irritability, and difficulty concentrating,
but migrainelie symptoms usually are absent. Tension-type headaches typically last 23
minutes to * wee, but some people e(perience them daily.
Ta"le 2# D,,ere$tal &a*$o+t' 'o$+&erato$+ $ te$+o$-t).e (ea&a'(e
Pr/ar) &a*$o++
/onvascular: Tension-type
1ascular: #igraine or cluster
Se'o$&ar) 1or*a$'2 &a*$o++
1ascular disorders
.ubarachnoid hemorrhage
.ubdural hematoma
Cnruptured arteriovenous malformation or aneurysm
!schemic cerebrovascular disease
Temporal arteritis
:rterial hypertension
;erebral venous thrombosis
/onvascular intracranial disorders
Benign intracranial hypertension
!ntracranial hypotension after lumbar puncture
!ntracranial neoplasm
!ntracranial infection or meningitis
.ubstances that act as triggers
#edications )eg, nitrates, over-the-counter drugs+
?oods )eg, monosodium glutamate, alcohol+
5(posures )eg, carbon mono(ide+
<ebound )eg, caffeine, analgesic, ergot+
#etabolic disorders
Hypo(ia )eg, chronic obstructive pulmonary disease, sleep apnea+
Hypercapnia
Hypoglycemia
:bnormalities of e(tracranial structures
5yes )eg, glaucoma, refractive errors+
5ars and sinuses )eg, infectious sinusitis, barosinusitis+
Teeth and jaws )eg, temporomandibular joint disorder+
.ull )eg, -agetDs disease, multiple myeloma+
/ec )eg, spondylosis, cervical dis disease+
The !H. criteria further classify tension-type headaches into an episodic form )occurring
on fewer than *7 days a month+ and a chronic form )occurring on *7 or more days a
month for more than & months+ based on headache fre=uency and the presence or absence
of a coe(isting disorder of pericranial muscles )identified as tenderness to manual
palpation or increased surface amplitude tracings on electromyography+. -ericranial
muscle abnormalities are not associated with any distinguishing clinical characteristics or
specific treatments.
-hysical e(amination is rarely helpful in diagnosis but should focus on detailed
funduscopic and neurologic evaluations. "iagnostic studies are not re=uired unless the
history or physical e(amination reveals features that suggest an organic cause: atypical
headache features not meeting !H. criteria, sudden onset of or change in headache, late
first onset of headache )after age 73+, or abnormal physical e(amination findings.
Eenerally, a severe headache of sudden onset is best evaluated by computed tomography
of the head without contrast and, possibly, lumbar puncture to rule out subarachnoid
hemorrhage. #agnetic resonance imaging )#<!+ of the brain is preferred for evaluating
chronic progressive headaches because it has higher sensitivity for tumors, aneurysms,
and posterior fossa lesions. !nterestingly, nonspecific white matter abnormalities are an
incidental finding on #<! scans in many patients with tension-type headache as well as
in patients with migraine )2@% and 2>%, respectively, versus 4.>% in controls+ )&+.
Faboratory studies may be indicated to identify suspected secondary causes of headache
)eg, temporal arteritis, anemia, thyroid or metabolic abnormalities, Fyme disease+ or to
monitor for to(ic effects from headache medication. 5lectrocardiography may be
performed before prescribing of drugs that potentially alter conduction times )ie, tricyclic
antidepressants+ or cause vasoconstriction. .tandardized psychometric testing may
identify comorbid psychiatric disorders, but these abnormalities may be the result of
chronic headache pain.
Precipitating factors
Tension-type headache triggers are not always identifiable or consistent, and multiple
triggers may have the additive effect of lowering the threshold of headache activation. !n
the past, studies have demonstrated few tension-type headache triggers other than
emotional stressA more recent studies have found similar headache precipitants for both
tension-type headache and migraine )table 2+.
Ta"le 0# Pote$tal tr**er+ o, te$+o$-t).e (ea&a'(e
.tress )eg, everyday hassles, family crises, heavy worloads, unpleasant wor or social
situations+
;hange in sleep regimen )eg, shift wor, oversleeping+
.ipping meals
;ertain foods )eg, caffeine, alcohol, cheese, chocolate+
-hysical e(ertion
5nvironmental factors )eg, sun glare, odors, smoe, ambient noise, fluorescent lighting,
sustained postures at video terminals or while driving+
?emale hormonal changes )eg, menses, menopause, pregnancy, e(ogenous hormone use+
#edications used for concomitant medical conditions )eg, nitrates, selective serotonin
reuptae inhibitors, antihypertensives+
Bveruse of headache medication )eg, analgesic and caffeine combinations, butalbital
compounds, opiates, ergot+
*nformation from ,asmussen #-%.
1arious medical conditions may e(acerbate tension-type headache but rarely are an
underlying cause. Tension-type headaches may be aggravated by barosinusitis from
allergic or structural turbinate congestion or by functional disturbances of the masticatory
muscles around the temporomandibular joint from clenching, bru(ism, or malocclusion.
Head trauma--even a mild whiplash injury not associated with a blow to the head or loss
of consciousness--may initiate or e(acerbate tension-type headache, possibly on a chronic
basis. That patients with first onset of tension-type headache after trauma have a genetic
predisposition for the disorder is suspected but unproven )$+.
.tress is undoubtedly the most common precipitant, triggering up to $3% of tension-type
headaches. 5motions have biochemical effects in the body, and mental stress alone can
elicit muscle contraction through the limbic system. .tudies have demonstrated that,
compared with control groups, patients with tension-type headache have similar major
stressful life events but perceive more events as ,hassles, and have less effective coping
strategies )eg, avoidance, self-criticism, lac of use of social supports+ )'+. The increased
prevalence of comorbid an(iety, depression, and somatoform disorders among people
with tension-type headache is still debated. !t is uncertain whether these disorders can
initiate, contribute to, or maintain tension-type headachesA whether they are the result of a
chronic pain conditionA or whether they are due to a genetic susceptibility and serotonin
abnormalities.
Pathophysiologic mechanisms
The cause of tension-type headache is unnown, but most research has focused on a
peripheral mechanism pertaining to pericranial muscle tenderness, thus e(plaining the
previous term ,muscle contraction headache., <esearchers who have attempted to find
correlations between subjective complaints of pericranial muscle tension and
electromyographic changes during a headache have had conflicting results. !n fact,
electromyographic readings indicating tenderness are usually greater in patients with
migraine than in patients with tension-type headache during a headache )*3+. .ustained
muscle contraction from physical or emotional causes may compress intramuscular
arterioles, causing ischemia, accumulation of no(ious metabolites, or both, which results
in localized tenderness )'+.
:nother hypothesis, favored by physicians who believe migraine and tension-type
headache are part of a continuum of the same underlying disorder, is that tension-type
headache has a purely central mechanism and that muscle tension is an epiphenomenon
)**+. .tudies that suggest a shared disorder with migraine have found reductions in
platelet or serum serotonin, epinephrine, norepinephrine, and dopamine levelsA these
findings appear to support the idea that an alteration in serotoninergic and
monoaminergic central systems results in depressed pain suppression and activated pain
pathways in tension-type headache )*@+. ;hronic tension-type headache also may be
associated with central opioid hypofunction with decreased cerebrospinal fluid beta-
endorphin levels.
The cause of tension-type headache is most liely multifactorial and best described by
BlesenDs vascular-myogenic-supraspinal model )*2+. !t is the convergence of multiple
pain pathways--vascular, myogenic, supraspinal, or all of these--that enter the caudate
nucleus of the trigeminovascular system and, in combination with other precipitating
factors in a predisposed person, determine whether the headache activation threshold is
met )*3+. : genetic predisposition has been suggested by studies that found a threefold
increased incidence of chronic tension-type headache in families )*>+.
Treatment
?ew people with tension-type headache consult a physician for treatmentA a recent study
)*7+ found that &3% of those reporting severe headaches used only over-the-counter
medications. #any get ade=uate relief with over-the-counter abortive medications, but
others e(perience a mared reduction in function and =uality of life. "aily or nearly daily
use of over-the-counter analgesics at recommended or higher-than-recommended dosages
can lead to gastrointestinal to(icity, renal to(icity, and hepatoto(icityA analgesic
nephropathy is the leading cause of drug-induced renal failure. !nappropriately fre=uent
use )9@ days a wee+ of over-the-counter or prescription abortive medications--especially
simple analgesics containing caffeine, caffeinated beverages, butalbital combination
products, narcotics, or ergotamines--may cause or maintain a chronic daily headache
pattern called analgesic rebound )*&+. !n analgesic rebound, headache fre=uency and
severity typically increase, and patients re=uire regular dosing of the offending
medication to avoid becoming incapacitated by headache.
: comprehensive therapeutic approach, incorporating both nonpharmacologic and
pharmacologic means, is successful for over '3% of patients with tension-type headache.
/onpharmacologic approaches include regulation of sleep and meal schedules, avoidance
of headache precipitants, and training in rela(ation techni=ues )table >+. #any patients
see alternative therapiesA however, vitamins )eg, riboflavin+, minerals )eg, magnesium,
calcium+, and herbal therapies )eg, feverfew+, which have been found to benefit people
with migraine, have not been ade=uately studied in patients with tension-type headache.
#ost headache therapies have a >3% placebo response, which usually is dependent on the
patientDs faith in both the treatment and the physician prescribing it.
Ta"le 4# No$.(ar/a'olo*' a..roa'(e+ to treat/e$t o, te$+o$-t).e (ea&a'(e
Re*ulato$ o, l,e+t)le
#aintain regular sleep schedule
5at regular meals
:void nown dietary triggers
Eet regular aerobic e(ercise
M$/3ato$ o, e/oto$al +tre++or+
-lan ahead and avoid stressful situations
Fearn biofeedbac
#editate
!ncrease undemanding leisure activities, hobbies, social events
Fearn other rela(ation techni=ues )eg, progressive muscle rela(ation, visualization+
;onsider individual or family psychotherapy
Avo&a$'e o, e$vro$/e$tal .re'.ta$t+
Gear sunglasses
:void smoe, strong odors, and noisy areas
#aintain proper postureA limit sustained positions
P()+'al t(era.) te'($4ue+
Heat, ice, ultrasound, transcutaneous electrical nerve stimulation
#assage or cervical traction
.tretching and strengthening e(ercises for cervical musculature
Trigger point stretching, compression, injection )any or all+
O+teo.at(' or '(ro.ra't' /a$.ulato$
Alter$atve t(era.e+
:cupuncture
:cupressure
Therapeutic touch
:romatherapy )eg, peppermint, green apple+
Topical salves )eg, salicylic acid, piro(icam H?eldeneI, etoprofen HBrudis, BruvailI+
E&u'ato$ a$& (ea&a'(e +u..ort *rou.+
/ational Headache ?oundation )$$$-&>2-777@, www.headaches.org+
:merican ;ouncil for Headache 5ducation )$33-@77-:;H5, www.achenet.org+
-sychological stressors or comorbidities should be addressed for the best possible
therapeutic outcome. : physician cannot change a patientDs life circumstance but may be
able to alter a patientDs perspective about life events and the amount of stress they cause.
?amily or individual psychotherapy, or both, may help patients to modify perfectionistic
standards, environmental demands, and maladaptive coping mechanismsA e(press their
anger and emotions effectivelyA and develop a less critical self-perception. !n some cases,
family members should be involved in treatment to identify and address family behaviors
that may unconsciously reinforce secondary gains and enabling behaviors in the patient.
Eenerally, families should deemphasize concerns regarding headaches and encourage the
patient to maintain as normal a lifestyle as possible.
!f pharmacologic agents are indicated, abortive medications to relieve headaches may be
used alone for infre=uent headaches )occurring on * or @ days a wee+ or in addition to a
daily prophylactic medication for more fre=uent or severe headaches. -rophyla(is should
be considered if significant disability occurs with attacs, if abortive medication cannot
be used because of comorbid conditions or a history of substance abuse, or if preventive
medication enhances the abortive medication effect. The mainstays of abortive therapy
are analgesics and muscle rela(ants )table 7+. .imple over-the-counter analgesics and
non-steroidal antiinflammatory drugs )/.:!"s+ have been found to be effective in
clinical trials. Fittle scientific evidence is available to support the effectiveness of muscle
rela(ants. Butalbital analgesic combinations with or without codeine have been found to
provide effective pain relief for tension-type headache )*4+A the barbiturate compound
helps relieve the an(iety component of pain. ;affeine, used as an analgesic adjuvant in
over-the-counter and prescription barbiturate combinations, increases the absorption,
pea concentration, and analgesic potency of medication as much as >3%. The mild
central nervous system stimulant effect of caffeine counteracts the sedative effects of
barbiturates or opioids. : combination of isometheptene, dichloralphenazone, and
acetaminophen also is indicated for tension-type headache. !nterestingly, sumatriptan
succinate )!mitre(+, which typically is used for migraine, has been found to be effective
in subgroups of patients with tension-type headache who e(perience fre=uent vascular
headache =ualities )ie, throbbing, increased pain with e(ertion, photophobia, and
phonophobia+ )*$+. .umatriptan has not been found to be effective in patients with
tension-type headache who do not report these vascular =ualities.
Ta"le 5# P(ar/a'olo*' treat/e$t o, te$+o$-t).e (ea&a'(e
A"ortve t(era.)
.imple analgesics without caffeine
.imple analgesic combinations with caffeine
/onsteroidal anti-inflammatory drugs
#uscle rela(ants with or without an analgesic combination
!sometheptene, dichloralphenazone, and acetaminophen compounds
Barbiturate or analgesic compounds
/arcotic analgesics
Pro.()la't' t(era.)
/onsteroidal anti-inflammatory drugs
Tricyclic antidepressants
.edating )eg, amitriptyline H;l H5lavilI, do(epin H;l H.ine=uanI, trimipramine
maleate H.urmontilI+
!ntermediate sedation )eg, nortriptyline H;l H:ventyl H;l -ulvules, -amelorI,
imipramine H;l HTofranilI+
/onsedating )eg, protriptyline H;l H1ivactilI, desipramine H/orpraminI+
.elective serotonin reuptae inhibitors
)eg, fluo(etine H;l H-rozacI, sertraline H;l HJoloftI,
paro(etine H;l H-a(ilI, citalopram hydrobromide H;ele(aI+
Bther antidepressants )eg, trazodone H;l
H"esyrelI, bupropion H;l HGellbutrinI,
venlafa(ine H5ffe(orI, nefazodone H;l H.erzoneI+
#onoamine o(idase inhibitors )eg, phenelzine
sulfate H/ardilI, isocarbo(azid H#arplanI+
:bortive migraine therapy has advanced from a stepped-care to a stratified-care
approach, but no such schema has been proposed for tension-type headache. Table &
illustrates a proposed stratified-care approach that emphasizes choosing medications on
the basis of headache fre=uency and disabilityA the stepped-care approach involves
beginning treatment of all patients with the weaest medications and slowly advancing to
stronger medications on the basis of response. !n a stratified-care model, more effective
medications, such as barbiturate or opioid combination analgesics, or both, may be
considered first-line therapy for patients e(periencing more disabling headachesA this is
true as long as the headaches are not fre=uent )6@ days a wee+ and the patient is at low
ris for habituation and has no history of substance abuse.
Ta"le 6# Strat,e&-'are a..roa'( to te$+o$-t).e (ea&a'(e /a$a*e/e$t "a+e& o$
,re4ue$') a$& &e*ree o, &+a"lt)7
I$,re4ue$t
Fow disability
/onpharmacologic approaches only
Bver-the-counter simple analgesics with or without caffeine )eg, 5(cedrin, Tylenol+
/onsteroidal anti-inflammatory drugs )eg, :napro(, #otrin+
/o prophyla(is
High disability
/arcotic analgesics )eg, ?ioricet Gith ;odeine ;apsules, 1icodan+
/onsteroidal anti-inflammatory drugs with or without analgesic adjuvant ):napro(,
#otrin+
#uscle rela(ants
Barbiturate and analgesic compounds
!sometheptene compound
:n(iolytics
;onsider prophyla(is
8re4ue$t
Fow disability
/onpharmacologic approaches only
Bver-the-counter simple analgesics without caffeine
/onsteroidal anti-inflammatory drugs
;onsider prophyla(is
High disability00
#uscle rela(ants
/onsteroidal anti-inflammatory drugs
!sometheptene compounds
-rophyla(is indicated
0Headache fre=uency: infre=uent, 6@ days per weeA fre=uent, 9@ days per wee. Fow
disability means no to moderate impairment in function. High disability means moderate
to severe impairment.
00High potential for analgesic overuseA avoid caffeine products, barbiturate compounds,
an(iolytics, and narcotic analgesics.
Tricyclic antidepressants are the mainstay of prophylactic therapy for tension-type head-
ache )*'+. .election of a tricyclic antidepressant is usually based on the presence of sleep
disturbances, with poor sleepers receiving the more sedating drugs. The average
maintenance dose of most tricyclic antidepressants is 73 to 47 mg daily )e(cept
protriptyline hydrochloride H1ivactilI, which is dosed differently+. 5ffective dosage
varies among patients and is unrelated to serum drug levels or antidepressant properties.
"espite their improved side effect profile, selective serotonin reuptae inhibitor
antidepressants are less reliable for headache prophyla(is. :typical antidepressant classes
have potential but unproven benefits. ;yclobenzaprine hydrochloride )?le(eril+, a muscle
rela(ant, has a chemical structure similar to that of the tricyclic antidepressants and has
been found to be an effective prophylactic agent for tension-type headache but is not
approved for long-term use )@3+. /.:!"s also may be used prophylactically.
.ome physicians who feel strongly that migraine and tension-type headache are common
entities propose that all migraine prophylactics are also effective for tension-type
headacheA however, few controlled studies of beta blocers, calcium channel blocers, or
anticonvulsants used for tension-type headache are available. Botulinum to(in type :
)Boto(+ has been studied as a potential headache treatment when injected into the
frontalis muscle, but further studies are needed to identify the group of patients who are
best suited for this treatment )@*+.
5fforts to foster a collaborative relationship with patients, maing them active
participants in their care, are liely to achieve higher treatment success rates. -atients
should be educated about realistic treatment e(pectations. The physician should e(plain
that a >- to $-wee drug trial at full therapeutic doses may be re=uired because of delayed
effectiveness, that combinations of medications may be re=uired, and that overuse of
caffeine or analgesics negates treatment effect.
-reventive medications are not a cureA successful therapy is considered to be a 73%
reduction in headache fre=uency, a reduction in headache intensity or duration, an
enhancement of abortive medication effect, or all of these. Gor around patient biases
against certain drug classes or their potential for side effects )eg, weight gain, fatigue+
while maintaining safety and efficacy.
Treatment is a balance between medication efficacy and adverse effects. Headache is a
dynamic condition, and routine follow-up is re=uired to reassess the need for medication
adjustments and to reinforce nonpharmacologic regimens. Ghen patients are doing well,
reduction of dosages of preventive medications should be attempted. 5(acerbation of
headache occurs at times regardless of potential triggers or medical regimens. The art of
headache treatment is nowing when to maintain therapy and reassure patients, when to
mae minor adjustments in medications, and when to change the entire treatment
regimen.
Conclusion
<ecent advances in the treatment and understanding of migraine have overshadowed
concerns about tension-type headache, the most prevalent headache disorder. Because of
its high prevalence and wide spectrum of disability, tension-type headache is the most
important headache type in regard to reduction in wor productivity, =uality of life, and
socioeconomic impact.
?uture research endeavors will address the pathophysiology of tension-type headache,
whether peripheral, central, psychological, or multifactorial. Gell-controlled clinical
trials are needed to clarify the best treatment approaches and determine whether standard
migraine medications may be used for tension-type headache. -atient education and more
aggressive treatment regimens would liely increase use of the healthcare system and
decrease the large indirect economic cost attributable to this often inade=uately treated
disorder.
References
*. Ra+/u++e$ 9:, ;e$+e$ R, S'(roll M, et al# 5pidemiology of headache in a
general population: a prevalence study. K ;lin 5pidemiol *''*A>>)**+:**>4-74
@. %ea&a'(e Cla++,'ato$ Co//ttee o, t(e I$ter$ato$al %ea&a'(e So'et)#
;lassification and diagnostic criteria for headache disorders, cranial neuralgias
and facial pain. ;ephalalgia *'$$A$).uppl 4+:@'-2>
2. : study of headache in /orth :merican primary care: report from the :mbulatory
.entinel -ractice /etwor. K < ;oll Een -ract *'$4A24)23@+:>33-2
>. 8re&/a$ AP, &e Sola Pool N, vo$ Stor'( T;# Tension headache. K:#:
*'72A*7*:*4>-4
7. Ra+/u++e$ 9:, ;e$+e$ R, Ole+e$ ;# !mpact of headache on sicness absence
and utilisation of medical services: a "anish population study. K 5pidemiol
;ommunity Health *''@A>&)>+:>>2-&
&. De 9e$e&tt+ G, Lore$3ett A, S$a C, et al# #agnetic resonance imaging in
migraine and tension-type headache. Headache *''7A27)7+:@&>-$
4. Ra+/u++e$ 9:# #igraine and tension-type headache in a general population:
precipitating factors, female hormones, sleep pattern and relation to lifestyle. -ain
*''2A72)*+:&7-4@
$. <a/a*u'( M# !ncidence of headache and severity of head injury. Headache
*''@A2@)'+:>@4-2*
'. Gla++ DE# Tension headache and some psychiatric aspects of headache. Headache
L *''@A2)2+:@&@-'
*3. ;e$+e$ R# -athophysiological mechanisms of tension-type headache. ;ephalalgia
*'''A*')&+:&3@-@*
**. Ole+e$ ;, ;e$+e$ R# Eetting away from simple muscle contraction as a
mechanism of tension-type headache. )5ditorial+ -ain *''*A>&)@+:*@2->
*@. Ca+tllo ;, Mart$e3 8, Lera R, et al# -lasma monoamines in tension-type
headache. Headache *''>A2>)'+:72*-7
*2. Ole+e$ ;# ;linical and pathophysiological observations in migraine and tension-
type headache e(plained by integration of vascular, supraspinal and myofascial
inputs. -ain *''*A>&)@+:*@7-2@
*>. Ru++ell M9, I+elu+ L, O+ter*aar& S, et al# !nheritance of chronic tension-type
headache investigated by comple( segregation analyses. Hum Eenet
*''$A*3@)@+:*2$->3
*7. L.to$ R9, Da/o$& S, Ree& M, et al# #igraine diagnosis and treatment: results
from the :merican #igraine .tudy !!. Headache @33*A>*)4+:&2$->7
*&. De$er %C, D'(*a$+ ;, S'(ol3 E, et al# :nalgesic-induced chronic daily
headache: long-term results of withdrawal therapy. K /eurol *'$'A@2&)*+:'-*>
*4. 8re&/a$ AP, DSero 8;# .ymptomatic treatment of chronically recurring
tension headache. ;lin Ther *'$4A*3)*+:&'-$*
*$. Ca&) R:, Gutter/a$ D, Saer+ ;A, et al# <esponsiveness of non-!H. migraine
and tension-type headache to sumatriptan. ;ephalalgia *''4A*4)7+:7$$-'3
*'. Da/o$& ML, Solo/o$ GD# Tension-type headache. !n: "iamond #F, .olomon
E", eds. "iamond and "alessioDs the practicing physicianDs approach to headache.
&th ed. -hiladelphia: GB .aunders, *''':*@7-2&
@3. La$'e ;=, A$t(o$) M# ;yclobenzaprine in the treatment of chronic tension
headache. #ed K :ust *'4@A@:*>3'-**
@*. =(eeler A%# Botulism To(in :, adjunctive therapy for refractory headaches
associated with pericranial muscle tension. Headache *''$A2$)&+:>&$-4*
A fresh look at migraine therapy
New treatments promise improed management
Se)/our Da/o$&, MD
VOL 10> / NO 1 / ;ANUAR< 2001 / POSTGRADUATE MEDICINE
CME learning objectives
To become familiar with the pathophysiology and clinical features of migraine
To learn the common signs of various types of migraine
To understand the various options available for acute and prophylactic therapy of
migraine
.r .iamond discloses financial interests in or connection with the following pharmaceutical companies:
/la0o 1ellcome, 1yeth-'yerst, 2ayer, Merc3, 'stra4eneca, )arnric3, 2ristol-Myers +5uibb, and 'bbott.
This is the second of four articles on headache
This page is best viewed with a browser that supports tables.
Preve!: :bout @& million :mericans, nearly 43% of them women, are challenged by
persistent, sometimes incapacitating migraine headaches. :lthough treatment has
improved dramatically during the last decade, migraine headaches continue to raise
diagnostic dilemmas and management =uestions among primary care physicians. !n this
article, "r "iamond discusses diagnosis, current management, and prophylactic measures
that can offer hope to many patients.
.iamond +. ' fresh loo3 at migraine therapy: new treatments promise impro6ed
management. Postgrad Med 2"!"7#"%:$7-8
The malady nown as migraine was identified thousands of years ago and is nown
throughout all civilizations on earth. The earliest recorded description of headache dates
to #esopotamia in >333 B;. :retaeus of ;appadocia )*23 to @33 :"+ devised the first
true description of migraine as a distinct entity because of its unilateral occurrence,
association with nausea, regular recurrence, and paro(ysms of pain separated by pain-free
intervals. Because the pain was unilateral, :retaeus called this type of headache
,heterocrania., Ge now use the word ,hemicrania,, which literally means ,half a head.,
:retaeus also recognized the differences between acute headache attacs that lasted for
days )cephalalgia+ and chronic headaches )cephalea+.
Classification of headache
#any elaborate classifications of headache have been formulated, including the *'&@
recommendations of the :d Hoc ;ommittee on ;lassification of Headache of the
/ational !nstitutes of Health )*+. The most recent effort was published in *'$$ by the
!nternational Headache .ociety )@+. These classifications are comple( and lengthy and
are used primarily for research purposes. Therefore, they are difficult to translate into
clinical practice.
#y colleague "onald K. "alessio, #", and ! devised a practical classification of
headache for clinical use )2+. Ge classified headaches into three primary categories )table
*+: vascular )migraine, cluster+ headache, tension-type )muscle contraction+ headache,
and organic )traction, inflammatory+ headache. Ge also subdivided migraine into three
types: migraine with aura )classic+, migraine without aura )common+, and complicated
migraine )hemiplegic, ophthalmoplegic, and basilar artery migraine+.
Ta"le 1# Cla++,'ato$ o, (ea&a'(e
Va+'ular
#igraine
Gith aura
Githout aura
;omplicated
MHemiplegic
MBphthalmoplegic
MBasilar artery ;luster )histamine+
To(ic vascular
Hypertensive
Te$+o$-t).e 1/u+'le 'o$tra'to$2
"epressive e=uivalents and conversion reactions
;hronic an(iety states
;ervical osteoarthritis
;hronic myositis
Or*a$'
#ass lesions )tumors, edema, hematomas, cerebral hemorrhage+
"iseases of eye, ear, nose, throat, and teeth
:rteritis, phlebitis
Bcclusive vascular disease
:typical facial pain
Temporomandibular joint dysfunction
;ranial neuralgias )facial, glossopharyngeal+
: large number of patients have coe(isting migraine and tension-type headache, which
we consider an overlapping category. This combination headache is sometimes called
mi(ed headache syndrome, transformed migraine, or chronic daily headache. -atients
who have these headaches usually can differentiate the severe headache that has migraine
characteristics and occurs two to five times a month from the chronic daily headache that
is less severe )>+.
Pathophysiology
:lthough the pathophysiology of migraine has not been firmly established, we owe a
great deal of our nowledge about migraine pathophysiology to Harold E. Golff, #".
"uring the *'23s, "r Golff did e(tensive research on migraine, including performing a
craniotomy on a patient who was having an acute migraine attac. He observed initial
cerebral vasoconstriction, followed by e(tracranial and intracranial vasodilation )7+. He
also noted that sterile inflammation surrounded the affected vessel and secondary muscle
contraction was present.
Bn the basis of this information, "r Golff formulated the vascular theory of migraine. He
also noted that certain vasoactive substances found in the inflamed tissue around the
blood vessels contained catecholamines, histamine, serotonin, peptides, prostaglandins,
and the slow-reacting substance of anaphyla(is, which is an acidic lipid. "r Golff
speculated that prolonged migraine attacs )lasting @> to >$ hours+ seemed to be related
to sterile inflammation. :s a result of "r GolffDs findings, corticosteroids were used for
treating prolonged migraine headaches.
The wor of .icuteri and associates )&+ and ;urran and colleagues )4+ confirmed the role
of serotonin and its metabolites during all phases of a migraine attac. These
investigations demonstrated that serotonin-releasing agents can induce migrainelie
attacs. The fact that many of the newer drugs used for management of acute migraine
are serotonin receptor agonists further implicates serotonin as a ey player in migraine
pathogenesis.
/eurologic theories of migraine have also been proposed. .tudies by Blesen and
associates )$+ suggested that migraine results from an abnormal firing of a brain neuron.
.preading depression, a part of the neurologic theory, could e(plain the prodrome or aura
of migraine. #osowitz )'+ identified the trigeminal ganglion as a factor in inducing
neurogenic dural inflammation and the subse=uent vascular pattern of the migraine
attac. Bther, more recent investigations suggested that substance - )*3+, calcitonin )**+,
and nitric o(ide )*@+ are all active in the dural inflammatory cascade that occurs with or
causes the vascular changes.
Definition of migraine
:lthough several definitions of migraine have been formulated, we rely on the definition
developed by the Gorld ?ederation of /eurology )*2+. !t defines migraine as ,a familial
disorder characterized by recurrent attacs of headache widely variable in intensity,
fre=uency, and duration. :ttacs are commonly unilateral and are usually associated with
anore(ia, nausea, and vomiting. !n some cases, they are preceded by, or associated with,
neurological and mood disturbances.,
The definitive characteristic of migraine with aura is the occurrence of a neurologic
symptom comple( 7 to 23 minutes before the onset of an acute migraine attac.
;omplicated migraine is described as a migraine attac associated with focal neurologic
symptoms that may persist after the headache disappears. Bphthalmoplegic, hemiplegic,
and basilar artery migraine are considered forms of complicated migraine.
:mong adults who have migraine, about 43% are women and, of those, about 43% report
a relationship between acute migraine attacs and menstruation. #enstrual migraine
attacs can occur immediately before, during, or after menses. However, some women
may also have attacs at other times of the month. #any women report a decrease in or
complete remission of migraine attacs after the first trimester of pregnancy.
Clinical features
#igraine is not a daily headache. ?re=uency varies from a few headaches each wee to
one or two episodes each year. #ost often, attacs occur two to eight times a month.
:verage duration is > to @> hours, although some patients complain of headache lasting
several days )status migrainosus+. The degree of severity varies from moderate to
incapacitating.
-atients who have migraine headaches often describe them as throbbing or pulsating.
:lthough migraine pain is usually unilateral, it can occur on both sides of the head. -ain
often affects the frontal and temporal regions but may be localized behind the eye. :lso,
pain can radiate across the head and to other regions of the face and nec.
Because of its association with nausea, vomiting, photophobia, phonophobia, dizziness,
tinnitus, and blurred vision, migraine is often depicted as a ,sic, headache. .ymptoms
can influence the selection of abortive and pain-relieving medication, as well as the route
of administration. #igraine headaches are often e(acerbated by physical activity.
:lthough migraine can first occur in childhood or as late as age 73, it usually starts
during adolescence or young adulthood. !n childhood migraine, boys and girls are
affected e=ually until puberty, when the predominance shifts to girls )&3% to 43%+. Cp to
43% of migraineurs report a family history of similar headaches.
T(e !ar$$* .(a+e
:s stated earlier, the two major types of migraine are differentiated by the presence of an
aura )prodromata+. The aura consists of focal neurologic symptoms localized to the
cerebral corte( or brainstem that may initiate or accompany the headache phase.
.ymptoms develop gradually over 7 to @3 minutes and are attributed to initial
vasoconstriction. The aura typically lasts less than an hour.
The symptoms of the aura usually include such visual phenomena as flashing lights,
zigzag or jagged lines, blind spots, difficulty in focusing, and distorted perception.
.ometimes visual images are out of focus or appear to be unusually large or small.
:nother occasional warning symptom is difficulty in speech, such as inability to find the
right word or use of wrong words. : complete inability to spea occurs on rare
occasions. .ome patients are not able to understand what has been said. :lso, headache
may be preceded by motor aphasia.
.ome patients who have migraine attacs, with or without aura, also have vague
premonitory symptoms that start from *@ to 2& hours before the actual headache occurs.
The symptoms usually begin imperceptibly and develop slowly. -remonitory symptoms
vary and may range from one e(treme to the other )eg, from euphoria to withdrawal,
hyperactivity to sluggishness, e(treme hunger to anore(ia, diarrhea to constipation,
fre=uent urination to fluid retention+.
Bther premonitory symptoms include yawning and fatigue, difficulty focusing, changes
in personality, slurred speech, impaired concentration, irritability, agitation, sensitivity to
light or sound, stiff nec, general muscle weaness, sensitive sin, and thirst. .ome
people have a feeling of well-being, become unusually talative, and notice a surge of
energy. The personDs face may be pale, and the eyes may appear dar, heavy, or sunen.
:lthough the migraine victim is not aware of these warning signs, friends or relatives
may notice them.
1ariations in hormone levels trigger headaches in many women, and fatigue,
oversleeping, or sipping a meal can bring on migraine in some people. #edications have
also been implicated in migraine attacs, including such agents as nitroglycerin,
reserpine, indomethacin )!ndocin+, oral contraceptives, and cyclic estrogen replacement
drugs. -sychological factors, such as an(iety, depression, repressed hostility, anger, and
fear, can play a role as well.
Treatment
#igraine treatment can be divided into four types: general measures, abortive therapy,
pain relief measures, and prophylactic therapy. .tatus migrainosus may re=uire that
additional strategies be tried.
Ge$eral /ea+ure+
:n important step in migraine management is identifying and avoiding headache triggers.
Because migraine patients are particularly sensitive to changes in routine, regular sleep
and meal schedules should be maintained. :lthough stress cannot be avoided, training in
coping strategies or stress management may be beneficial. .imilarly, a significant number
of migraine sufferers appear to be obsessive, compulsive, and rigid, although this
hypothesis has been debated. They may create environments that present enormous
challenges. ?or e(ample, a woring mother returns to school and also participates in a
number of volunteer activities. !n many cases, a migraine sufferer endures a stressful
period but then has a severe headache once the stress is alleviated.
;ertain activities often trigger acute migraine attacs, such as looing at bright lights or
the sun or watching a flicering or out-of-focus television program or film. ! recommend
use of tinted glasses during times of e(posure to bright light for my migraine patients. !n
addition, flying or being at high altitudes, where the o(ygen tension and concentration are
usually lower than normal, can precipitate migraine attacs. :cetazolamide )"azamide,
"iamo(+, a diuretic and carbonic anhydrase inhibitor, taen the day before and the day of
flying, may help patients who have migraine related to altitude changes. ;hanges in
barometric pressure have also been identified as a migraine trigger, and migraine patients
may be especially sensitive to weather conditions.
A"ortve t(era.)
Cntil the early *''3s, only a few drugs were available for the acute treatment of
migraine. #any physicians started with over-the-counter analgesics or prescription
nonnarcotic nonsteroidal anti-inflammatory drugs )/.:!"s+, progressed through the
ergotamine drugs, and used narcotics as a last resort in patients who had acute migraine
attacs. #any times, management involved a litany of trial and error before a suitable
drug was found. Gith the introduction of the triptans, early intervention with these
migraine-specific drugs may act to reverse the migraine cascade.
.ince then, advances have been made in pharmacologic therapy for migraine.
/evertheless, management of the migraine patient still re=uires fre=uent office visits,
open communication between physician and patient, and an understanding by both
physician and patient of the intricacies of drug treatment and interactions. ?or e(ample,
the route of administration is important in obtaining relief because it impacts the speed of
action. :lthough oral administration is the simplest, it may not be appropriate for many
of the 43% of migraineurs who have associated nausea and vomiting. -arenteral
administration offers the =uicest action, but self-injection may not be the optimal choice
for many patients. : trip to the physicianDs office or emergency department delays the
relief so badly needed.
Tr.ta$+? "iscovery of the 7-hydro(ytryptamine* )7-HT*+ receptor agonists ),triptans,+
has brought about remarable advances in the treatment of migraine )*>+. These drugs
have demonstrated efficacy in aborting migraine attacs and have variable affinity for the
7-HT*:, 7-HT*B, 7-HT*", and 7-HT*? receptors. Their antimigraine effect is e(erted by way
of a receptor-mediated neural pathway in both the central nervous system and the
trigeminal nerve, at which point neurogenic inflammation is bloced.
.umatriptan succinate )!mitre(+, the first triptan to be approved for migraine abortive
therapy in the early *''3s, originally was available only for subcutaneous injections.
/ow sumatriptan can be given by oral or intranasal routes, as well as by injection. !t is
usually well tolerated and causes only minor side effects )eg, flushing, tingling, nec or
chest tightness or pain, nausea, throat discomfort+. !f the first dose of sumatriptan offers
at least partial headache relief, a second dose can be given an hour later or anytime within
the ne(t @> hours if the headache recurs. However, a 7-day hiatus should be maintained
between days of use. .umatriptan should not be used in patients with basilar or
hemiplegic migraine, ischemic heart disease, or -rinzmetalDs angina and cannot be used
concomitantly with ergotamine preparations or monoamine o(idase inhibitors )#:B!s+.
.everal oral second-generation 7-HT*B8*" agonists have been developed in the past few
years. !n *''$, the C. ?ood and "rug :dministration )?":+ approved naratriptan
):merge+, rizatriptan benzoate )#a(alt, #a(alt-#FT+, and zolmitriptan )Jomig+ for
migraine therapy. !t should be noted that none of the triptans can be used concomitantly
with ergotamine derivatives nor should they be used in patients with basilar or
hemiplegic migraine, ischemic heart disease, or -rinzmetalDs angina.
/aratriptan has a longer half-life than the other triptans and remains active in the blood
vessels for up to & hours. !t has a low incidence of side effects, the most common of
which are nausea and vomiting. /aratriptan holds promise for management of menstrual
migraine because it has a long half-life. !n addition, it can be used with #:B!s.
<izatriptan is absorbed rapidly, and its effects can be noted within 23 minutes of
ingestion. !t is well tolerated but can cause a few mild side effects )eg, bitter taste,
dizziness, fatigue, sleepiness, nausea+. <izatriptan is the only triptan currently available
in an orally disintegrating tablet, which offers patients a convenient alternative if they
prefer not to tae water with their migraine medication. The formulation =uicly
dissolves on the tongue and is absorbed through the gastrointestinal tract. !t does not
e(acerbate the nausea often associated with an acute migraine attac.
Jolmitriptan is also absorbed =uicly and alleviates migraine attacs faster than some of
the other triptans. !t appears to be effective in alleviating associated symptoms, including
nausea and sensitivity to light and sound. !ts side effects are similar to those with
sumatriptan and include nausea, dizziness, pricling or tingling of the sin, drowsiness,
warm or cold sensations, jaw pain, and tightness of the nec or throat.
Three new triptans )eletriptan H<elpa(I, almotriptan, frovatriptan+ may be available in the
near future.
Er*ota/$e &ervatve+? 5rgotamine tartrate preparations are vasoconstrictors that have
been used in migraine abortive therapy for more than 73 years. These agents are available
for oral administration in combination with caffeine. 5rgotamine is also available for
sublingual administration, but in the Cnited .tates, it is no longer available in the
parenteral form. :n ade=uate dose should be taen as early as possible in a migraine
attac to achieve a ma(imum response.
To prevent ergotamine rebound headaches or ergotism, care should be taen to remain
within the limits of the recommended dosage. 5rgotamine derivatives should not be used
in patients with cerebrovascular, cardiovascular, peripheral vascular, ischemic heart,
renal, or hepatic diseasesA sepsisA or severe hypertension. !n addition, ergotamine
preparations should be used cautiously in patients with peptic ulcer and recent infection
and should not be used in pregnancy.
"ihydroergotamine mesylate )".H.5. >7, #igranal+ has also been used safely and
effectively in the abortive therapy of migraine, and it has recently been ,rediscovered,
because of its action as a 7-HT*" receptor agonist. !t also has a potent effect at a number
of other biogenic amine receptor sites. Cnlie ergotamine tartrate, dihydroergotamine is
associated with a lower incidence of nausea and is more of a venoconstrictor than an
arterial vasoconstrictor. !t can also be used to help patients who are ergotamine-
dependent withdraw from ergotamine use.
"ihydroergotamine is available for intramuscular, subcutaneous, and intravenous
injection and as a nasal spray. !t also has been successfully used in repeated intravenous
doses in patients with intractable migraineA a dose of 3.7 mg given as an intravenous push
over @ to 2 minutes, in combination with *3 mg of the antiemetic8antivertigo drug
metoclopramide, may be repeated every $ hours for 2 days in these cases.
Because of its vasoconstrictive properties, dihydroergotamine is contraindicated in
patients who have peripheral vascular disease, ischemic heart disease, -rinzmetalDs
angina, uncontrolled hypertension, hemiplegic or basilar migraine, impaired hepatic or
renal function, or sepsis, as well as in pregnant women. !t should not be used
concomitantly with other 7-HT* agonists or ergotamine preparations. :lso,
dihydroergotamine should not be given to patients who have ris factors for coronary
heart disease );:"+ unless a cardiovascular evaluation provides satisfactory clinical
evidence that a patient is reasonably free of ;:", ischemic myocardial disease, and other
significant cardiovascular disorders.
?or patients with ris factors predictive of ;:" who have a satisfactory cardiovascular
evaluation, the first dose of dihydroergotamine should be given in a physicianDs office.
Because cardiac ischemia can occur in the absence of clinical symptoms, consideration
should be given to obtaining an electrocardiogram after the first dose is given to a patient
with nown ris for ;:".
I+o/et(e.te$e /u'ate? !n patients who cannot tolerate ergotamine or in whom
ergotamine derivatives are contraindicated, isometheptene may be an effective
alternative. Fie ergotamine, isometheptene has cerebral vasoconstrictive actions. !t is
available in a preparation that also contains acetaminophen and dichloralphenazone, a
mild sedative.
A+.r$ a$& NSAID+? :spirin and other of the /.:!"s )eg, ibuprofen, napro(en
sodium+ have been used successfully in migraine abortive therapy. /.:!"s stabilize
proteins and inhibit formation of active prostaglandins. They also inhibit inflammation
through their effects on chemota(is, phagocytosis, lysosomal enzyme release, and inin
generation.
P(e$ot(a3$e+? The phenothiazines chlorpromazine hydrochloride )Thorazine+ and
prochlorperazine );ompazine+ have been used effectively in the emergency department
setting for the abortive treatment of acute migraine. 5fficacy of these drugs is attributed
to their antinauseant and sedative effects. !n addition, their dopaminergic and adrenergic
actions may trigger specific mechanisms involved in aborting migraine.
L&o'a$e? : recent report )*7+ has suggested that use of intranasal lidocaine is helpful
for abortive treatment of acute migraine. : 73% reduction in headache was noted by 77%
of patients who used lidocaine. However, relapse was common and occurred early after
treatment. !n selected patients, this treatment has demonstrated significant benefit.
Pa$ rele, /ea+ure+
:bortive therapy may not completely resolve a migraine attac, and analgesics may be
needed to alleviate pain. Bver-the-counter analgesics )eg, aspirin, acetaminophen,
ibuprofen, napro(en sodium, etoprofen+ may be effective. However, overconsumption
of these analgesics, particularly those containing caffeine, can produce serious side
effects. Githdrawal from caffeine-containing drugs may trigger caffeine withdrawal
headache. Therefore, these drugs should be avoided in patients who have fre=uent
migraine attacs.
The first over-the-counter agent approved by the ?": for relief of migraine pain was the
combination of aspirin, acetaminophen, and caffeine )5(cedrin #igraine+. This
combination agent is suggested for the acute treatment of mild to moderate headache
without associated vomiting and disability. <ecently, two other nonprescription
preparations of ibuprofen ):dvil #igraine, #otrin #igraine+ have also received approval
for the relief of migraine pain. !n addition, a parenteral /.:!", etorolac tromethamine
)Toradol+, offers analgesia that is nonnarcotic and nonhabituating, and it has a low side-
effect profile. The drug is given intramuscularly in a &3-mg dose.
:mong the other options for pain relief are use of narcotic analgesics, antiemetics,
phenothiazines, and cold pacs. /arcotic analgesics )eg, codeine, meperidine
hydrochloride H"emerol H;lI, methadone hydrochloride H"olophine H;l, #ethadoseI+,
preferably administered parenterally, are effective for pain relief but are potentially
habituating. :s with other pain syndromes, these drugs should not be used in patients
with fre=uent migraine attacs and should never be used for daily headaches.
:ntiemetics and phenothiazines, given parenterally or rectally, may be indicated in some
migraine patients. The phenothiazines )including promethazine hydrochloride H:nergan,
-henerganI, chlorpromazine, and prochlorperazine+ are also useful because of their
sedative and antinauseant action. .ome antiemetics, such as trimethobenzamide
hydrochloride and metoclopramide, have little sedative effect. However, metoclopramide,
a 7-HT2 receptor agonist, enhances absorption of oral medications and has been used
effectively in combination with intravenous dihydroergotamine. This use of
metoclopramide occasionally causes nervousness and tremor.
Transnasal butorphanol tartrate ).tadol /.+ is a totally synthetic mi(ed agonist-
antagonist opioid analgesic that originally was available for parenteral administration. !ts
=uic absorption through the nose is enhanced by its lipophilic nature. The highly
vascular character of the nasal mucosa speeds uptae and absorption. ;aution must be
e(ercised because of the possibility of habituation to butorphanol, and it should not be
prescribed for patients who have daily headaches.
;old pacs have been used by migraine patients for many years. :pplication of ice bags
or commercially manufactured ice pacs to the site of the pain, along with gentle
pressure, may reduce the pulsating pain associated with acute migraine attacs.
Pro.()la't' t(era.)
-rophylactic drug therapy should be considered in patients who have more than two acute
migraine attacs per month. !t may also be considered in patients who have attacs that
seriously compromise daily activities or that last several days.
9eta "lo'@er+? ?or the past two decades, the beta blocers have been recognized for their
efficacy in migraine prevention. <esearchers have suggested that beta blocers without
intrinsic sympathomimetic activity are more beneficial than those possessing such
activity. -ropranolol hydrochloride )Betachron 5-<, !nderal+, timolol maleate
)Blocadren+, and nadolol );orgard+, all of which lac intrinsic sympathomimetic activity,
are recognized as effective migraine prophylactic agents. 5ach of these drugs is
considered nonselective and should not be used in patients with pulmonary disorders.
?or patients with asthma and other respiratory disorders, treatment with a cardioselective
beta blocer, such as metoprolol )Fopressor, Toprol NF+, is indicated. Beta blocers are
also contraindicated in patients with congestive heart failure and atrioventricular
conduction disturbances. !n addition, beta blocers should be used cautiously in patients
who use insulin, oral hypoglycemics, or #:B!s.
A$t'o$vul+a$t &ru*+? "ivalproe( sodium )"epaote+ has shown efficacy in migraine
prophyla(is. !t may be of particular use in migraineurs with concomitant convulsive
disorders, because it has the potential for preventing seizures. "ivalproe( should be
avoided in patients who have a history of hepatitis or abnormal liver function. <ecently,
an e(tended-release formulation that can be used once a day received ?": approval.
NSAID+? The use of /.:!"s has become increasingly common for prophylactic
management of migraine. :cceptance of /.:!" therapy was accelerated by the results
of a randomized study of more than @@,333 male physicians who used low-dose aspirin or
placebo every other day )*&+. :bout &% of those on active medication had migraine
attacs, compared with 4.>% of the placebo group. :lthough this decrease in headache
fre=uency )@3%+ was modest, the results suggest that /.:!" therapy may be effective in
migraine prevention. .everal /.:!"s have demonstrated prophylactic efficacy in
decreasing the fre=uency and severity of migraine.
Cal'u/ '(a$$el "lo'@er+? ;alcium channel blocers may be considered in migraine
prophyla(is, particularly in patients refractory to beta blocer therapy. The rationale for
using these agents stems from their effect on intracranial vasoconstriction. /imodipine
)/imotop+ appears to have mared selectivity for the cerebral vasculature, and verapamil
hydrochloride );alan, !soptin, 1erelan+ has also demonstrated antiplatelet effects.
Al.(a-a&re$er*' "lo'@er+? ?or patients who e(perience food-related migraine,
clonidine hydrochloride );atapres+ has demonstrated efficacy. ;lonidine, an alpha
agonist, has also been observed as beneficial for patients undergoing opiate withdrawal.
A$t&e.re++a$t+? :ntidepressants have shown continued efficacy in migraine
prophyla(is for several decades. The tricyclic drugs, particularly amitriptyline
hydrochloride )5lavil+, are believed effective in headache prevention because of
analgesic actions independent of their antidepressant effects. Cse of antidepressants is
preferred for the treatment of coe(isting migraine and tension-type headaches.
:ntidepressant therapy also may prove helpful in patients refractory to other standard
forms of treatment. !n these patients, a trial of the #:B!s should be considered.
A$t(+ta/$e a$& +eroto$$ "lo'@er+? ;yproheptadine hydrochloride )-eriactin+ is the
agent of choice in childhood migraine because it blocs both histamine and serotonin
receptors. .ide effects include drowsiness and weight gain. 5fficacy in adults is minimal.
Met()+er*&e? : lysergic acid derivative, methysergide maleate ).ansert+ is closely
lined to ergotamine. !n addition to its vasoconstrictor actions, methysergide also appears
to bloc the inflammatory mechanisms of serotonin. :lthough it has shown efficacy in
migraine prevention, it is not widely used because of its serious side effects with
prolonged therapy. Ghen it is used, patients should be evaluated at monthly intervals to
rule out pulmonary, coronary, or retroperitoneal fibrosis, as well as peripheral vascular
disease. !f a patient has been maintained on methysergide for & consecutive months, a >-
to &-wee drug hiatus must be ordered and an intravenous urographic study should be
performed to rule out retroperitoneal fibrosis.
Statu+ /*ra$o+u+
!n patients who have this disorder, migraine attacs are unrelenting and refractory to
conventional therapy. ?or some migraine attacs that persist for more than @> hours, the
treatment of choice is adrenocorticosteroid therapy, such as de(amethasone or
methylprednisolone in dose pacs. .terile inflammation is considered the cause of these
prolonged migraine attacs.
Ghen migraine persists, the associated symptoms )eg, nausea, vomiting+ may pose a
threat to the patientDs well-being. "ehydration can become a problem, and hospitalization
may be needed for intravenous fluid replacement and to monitor serum electrolytes.
!ntravenous dihydroergotamine )3.7 mg+ given with metoclopramide )*3 mg+ every $
hours for @ days has demonstrated efficacy in treating status migrainosus. This therapy
avoids use of habituating narcotic analgesics.
Summary
.uccessful management of migraine headaches involves identifying and avoiding
headache triggers and using appropriate abortive therapy once a headache is recognized.
-ain relief measures include over-the-counter analgesics, parenteral /.:!" therapy
when needed, and use of antiemetics and cold pacs. /arcotic analgesics are best used
only as a ,last resort, measure.
-rophylactic therapy should be considered for patients who have more than two acute
migraine attacs each month or whose daily activities are seriously compromised by
headaches. ?or the patient in whom status migrainosus threatens well-being,
hospitalization and more intensive therapy may be needed.
References
*. ;lassification of headache. :d Hoc ;ommittee on ;lassification of Headache.
K:#: *'&@A*4')&+:4*4-$
@. ;lassification and diagnostic criteria for headache disorders, cranial neuralgias
and facial pain. Headache ;lassification ;ommittee of the !nternational Headache
.ociety. ;ephalalgia *'$$A$).uppl 4+:*-'&
2. Da/o$& S, Dale++o D;# The practicing physicianDs approach to headache. /ew
Oor: #edcom, *'42:@
>. Da/o$& S# #igraine headache. !n: "iamond #F, .olomon E", eds. "iamond
and "alessioDs the practicing physicianDs approach to headache. &th ed.
-hiladelphia: GB .aunders, *''':>&-43
7. =ol,, %G# Headache and other head pain. @d ed. /ew Oor: B(ford Cniversity
-ress, *'&2
&. S'uter 8, Te+t A, A$+el/ 9# Biochemical investigations in headache: increase
in hydro(yindoleacetic acid e(cretion during migraine attacs. !nt :rch :llergy
*'&*A*':77-$
4. Curra$ DA, %$ter"er*er %, La$'e ;=# Total plasma serotonin, 7-
hydro(yindoleacetic acid and p-hydro(y-m-metho(ymandelic acid e(cretion in
normal and migrainous subjects. Brain *'&7A$$)7+:''4-*3*3
$. Ole+e$ ;, Lar+e$ 9, Laurt3e$ M# ?ocal hyperemia followed by spreading
oligemia and impaired activation of r;B? in classic migraine. :nn /eurol
*'$*A')>+:2>>-7@
'. Mo+@o!t3 MA# The neurobiology of vascular head pain. :nn /eurol
*'$>A*&)@+:*74-&$
*3. Goa&+") P;, E&v$++o$ L, E@/a$ R# <elease of vasoactive peptides in the
e(tracerebral circulation of humans and the cat during activation of the
trigeminovascular system. :nn /eurol *'$$A@2)@+:*'2-&
**. Goa&+") P;, E&v$++o$ L, E@/a$ R# 1asoactive peptide release in the
e(tracerebral circulation of humans during migraine headache. :nn /eurol
*''3A@$)@+:*$2-4
*@. 9u33 MG, Mo+@o!t3 MA# The antimigraine drug, sumatriptan )E<>2*47+,
selectively blocs neurogenic plasma e(travasation from blood vessels in dura
mater. Br K -harmacol *''3A'')*+:@3@-&
*2. Crt'(le) M# "efinition of migraine. !n: ;ochrane :, ed. Bacground to
migraine: third migraine symposium. /ew Oor: .pringer 1erlag, *'43:*$*-@
*>. Perout@a S;# "evelopments in 7-hydro(ytryptamine receptor pharmacology in
migraine. /eurol ;lin *''3A$)>+:$@'-2'
*7. Ma3el+ M, S'ott 9, Co(e$ =, et al# !ntranasal lidocaine for treatment of
migraine: a randomized, double-blind, controlled trial. K:#: *''&A@4&)>+:2*'-
@*
*&. 9ur$* ;E, Peto R, %a$$e@e$+ C%# Fow-dose aspirin for migraine prophyla(is.
K:#: *''3A@&>)*2+:*4**-2
Cluster headaches
Three enigmas surround cluster headaches:
Ghy do they beginP
Ghy do they stopP
Ghy do they start againP
/o one has been able to e(plain the peculiar periodicity of cluster headaches, even
though, as with all headache types, theories abound.
Eoadsby )*+ suggests that cluster headache should be termed neurovascular headache. He
used a nitroglycerin spray to initiate typical cluster attacs in nine patients with chronic
cluster headaches. The patientsD brains were then studied by using positron emission
tomography. He found that the cluster headaches affected three areas of the brain, two of
which are associated with any painful stimulus. The area most activated by cluster
headache was the ipsilateral hypothalamic gray matter. Because the hypothalamus can be
associated with periodic illness of any sort, it could be postulated that an e(planation for
the intermittent nature of cluster headache is at hand.
Eoadsby also noted that the vasodilation associated with cluster headache is a ,secondary
phenomenon,, a result of activation of the trigeminal vascular system. !t remains to be
resolved whether this is correct or whether the vasodilation is primary and the other
changes are secondary.
Cl$'al ,$&$*+
;luster headaches are characterized by e(cruciating, sharp, penetrating pain that typically
lasts 23 to >7 minutes )range, *3 minutes to > hours+. They usually occur once or twice a
day )but may occur up to *3 times per day+ for * to > months. #ost patients then
e(perience a remission of months or years.
;luster headaches and migraine have many similarities but also many differences. !n
contrast to migraine, cluster headaches are more prevalent in men, are not preceded by an
aura, always occur unilaterally with pain recurring on the same side in subse=uent
headaches, and usually are not associated with a positive family history of cluster
headache.
The headache often occurs during sleep )usually within * hour after falling asleep+ and is
severe enough to wae the patient. The mean age at onset is @4 to 23 years.
;haracteristically, cluster headache is associated with ipsilateral lacrimation, rhinorrhea,
nasal congestion, and conjunctival injection. The pain is distributed unilaterally over the
oculotemporal, oculofrontal, or temporal facial region. : partial HornerDs syndrome with
miosis and ptosis may occur on the ipsilateral side.
S(ort-ter/ treat/e$t
B(ygen inhalation is effective and relatively safe for the symptomatic treatment of cluster
headache )@+. ! generally prescribe it as first-line treatment. The mechanism of action is
unnown but probably involves a mared reduction in cerebral blood flow that results in
concomitant pain reduction. -atients should be told to begin therapy at the onset of an
attac by administering *33% o(ygen through a face mas at a rate of 4 to $ F8min for *3
to *7 minutes. : nasal cannula should not be used because nasal congestion may impede
inhalation. -atients should assume a sitting position, either upright or leaning forward,
and should avoid hyperventilation, which may limit o(ygen saturation.
5rgotamine preparations are more convenient than o(ygen treatment, but the relatively
slow onset of action of the oral products often limits their usefulness in cluster headache
treatment )2+. .ublingual ergotamine has a more rapid onset of action, which may render
it useful for cluster headache treatment. : single dihydroergotamine meslyate )".H.5.
>7+ injection may be useful in an emergency department or office setting.
No$+tero&al a$t-$,la//ator) &ru*+? Theoretically, many drugs used in the abortive
or symptomatic treatment of migraine also should be effective in cluster headaches.
However, because of the e(tremely brief nature of cluster headaches, most oral
preparations do not provide relief. The nonsteroidal anti-inflammatory drug )/.:!"+
napro(en sodium given in a 773-mg dose at the onset of an attac may be of some use in
these situations because of its relatively fast absorption. This drugDs usefulness is limited,
however, to those patients whose headaches last longer than >7 minutes. Because of
/.:!"sD potential to cause serious gastrointestinal bleeding and ulcers, patients
e(periencing several attacs a day must carefully adhere to the manufacturerDs
recommendations for total daily dose.
L&o'a$e $o+e &ro.+? .ome patients may feel relief with the local anesthetic lidocaine
hydrochloride in the form of nose drops. Fidocaine >% topical solution )Nylocaine+ is
available by prescription and may be dispensed in a dropper bottle )>+. Gith the head
tilted bacward and turned toward the ipsilateral side, patients should instill *7 drops in
the nostril on the affected side at the onset of headache. The dose may be repeated after
*7 minutes, if needed.
Fidocaine may be used two times per headache, up to four times per day. To facilitate the
administration of lidocaine, phenylephrine hydrochloride 3.7% nasal drops may be used
to clear congested nasal passages. .ide effects of lidocaine nasal drops may include
nervousness and dizziness. .ome patients allergic to lidocaine may show signs of
hypersensitivity.
Tr.ta$+? The triptans, particularly sumatriptan succinate )!mitre(+, are effective for
short-term treatment of cluster headache )7+. Eenerally, sumatriptan is used in patients
who e(perience one or two cluster headaches each day.
Pro.()la't' treat/e$t
Because of both the limited usefulness of drugs for cluster headache pain and the intense
nature of the pain, prophylactic treatment is essential. ;luster headaches that occur only
during sleep may be treated with nightly administration of ergotamine. However, attacs
that occur at various times of day or night may be prevented by routine use of
methysergide maleate ).ansert+, verapamil hydrochloride );alan, !soptin, 1erelan+,
lithium, or prednisone, either alone or in combination )&-$+. ?or e(ample, ! may prescribe
a combination of prednisone )&3 to $3 mg8day+ and verapamil )@>3 mg8day+ first )figure
*: not shown+. ! am careful to limit prednisone use to 4 to *> days. !t may be necessary to
increase the verapamil dose or to continue the therapy through the cluster headache
period.
!f this combination fails, ! usually try methysergide )@ mg three times daily+, but again, !
limit treatment to * to @ months. #ethysergide should not be given with other drugs
e(cept pain relievers such as hydrocodone bitartrate )1icodin+. !f methysergide is
ineffective, lithium or valproic acid )"epaene, "epaote+, or both, can be used, often
with verapamil. Treatment must be individualized if multiple drug failures occur.
;hronic cluster headache can be treated prophylactically with verapamil or lithium, or
both. 1alproic acid used alone or with verapamil often is effective. Bccasionally, a
patient responds to intranasal application of capsaicin five or si( times per day. Bccipital
nerve blocs may relieve cluster attacs briefly, but ! have found that subse=uent
injections become less effective. -atients with chronic cluster headache may become
resistant to a previously successful prophylactic medication. These patients may re=uire
polypharmacy or, eventually, inpatient treatment.
?or hospitalized patients with the rare intractable cluster headache, ! use
dihydroergotamine given intravenously every $ hours. .ome patients become headache-
free during treatment, and remission is often sustained after discharge from the hospital.
!f hospitalization and all prophylactic efforts fail, neuroablative procedures may be
considered. :t this point, ! sometimes refer patients to the "iamond Headache ;linic for
histamine desensitization )'+, a benign procedure that can produce striing results.
.urgical procedures include sphenopalatine ganglionectomy, radiofre=uency
thermocoagulation of the trigeminal ganglion, and section of the trigeminal nerve )*3-
*@+. However, the corneal anesthesia that results from these procedures puts the
ipsilateral eye at ris. Cse of glycerol injection into the trigeminal cistern to treat
intractable cluster headache has resulted in significant pain relief and poses no ris to the
cornea )*3+.