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HEADACHE-A BASIC GUIDE
Kathleen
B. Digre, M.D.
Professor of Neurology, Ophthalmology
University of Utah
Objectives:
1.
Know the 4 histories to take on every patient with headache
2.
Differentiate between pain-sensitive and pain-insensitive structures
3.
Know the different types of primary headache.
4.
Know the difference between primary and secondary Headache
5.
Know the clinical features of headaches due to temporal arteritis,
brain tumors, and meningitis
6.
List factors that can transform a primary migraine disorder into a
chronic migraine
Headache is extremely common.
It is estimated that 70-80% of adults suffers from headache at
sometime in their lives. Even 38% of children have had headaches.
Headache can be a symptom of underlying structural pathology and
potentially dangerous. However, most headaches are benign, recurrent headaches.
They can cause difficulty with work and life; frequently, they are not
diagnosed correctly or treated appropriately.
Therefore, it is important to get a good history and do a complete
physical and neurological examination in all headache sufferers.
I. HISTORY
History
is the single most important clue to the
diagnosis of any headache condition since the examination is often normal.
There are five histories to take from patients who have headache.
A.
Family History: Determine if the patient is
genetically headache prone.
1.
Ask if the patient’s mother, father, sister
brother ever had a headache
2.
“Sinus headache” is usually recurrent
migraine
B.
The life history:
Determines what has happened with headaches over a person’s life
1.
Was there car sickness or night terrors as a
child (frequent associations to migraine)
2.
Was there episodic nausea or abdominal pain
as a child (another kind of migraine in children
3.
When did the migraines start (adolescence is
a frequent starting point)
4.
When in the life did they get worse:
patients with life-stressors (marriage, death of a relative, college,
new baby, moving) all can make underlying headaches worse
5.
Have the headaches changed over time?
C.
The attack history: Since many people have
more than one kind of headache it is important to ask query the events of
each headache type.
1.
Is this a new headache or an old headache
(new headaches need to be closely scrutinized for features which may signal a
secondary cause).
What kind of warning signals are there:
“Auras” are frequently neurologic symptoms occurring before an
attack (e.g. visual spots, lights, wavy vision, sparks, flashes, zigzag
lines, heat wave sensation. Numbness,
weakness, vertigo, fatigue, and yawning.)
2.
Where
is the headache? (unilateral,
bilateral, holocranial)
3.
How frequently does it occur? (every
day, 1 q month, rarely)
5. How long does it last? (Hours,
days, weeks)
6.
What type of pain is it? (Dull,
ache, throbbing, jabbing, burning, ice-pick)
7. When does it occur? (am,
pm, awaken from sleep)
8.
How does it come on? (sudden
onset, gradual build up)
9.
What are the associated symptoms? (nausea,
vomiting, photophobia,
phonophobia, lacrimation, red eye, stuffy nose, etc.)
10.
What factors bring it on? (diet, stress, menstruation)
11.
What factors relieve the headache?
(bed rest, dark room, medication, vomiting, pacing, ice packs, heat
packs)
12.
What are aggravating factors?
(movement, lack of sleep, sunlight, position changes, driving, stress)
13. How does it
leave? (suddenly, gradually)
D.
Medical history than affect, cause headaches:
1.
Medical
considerations: COPD, thyroid
disease - 40% have HA, hypertension, anemia
2.
Medications:
Prescriptions, Non-prescriptions;
especially over-the-counter caffeinated preparations combined with
aspirin or acetaminophen can cause rebound headache; Medications with
sympathomimetics may increase headache; Drug abuse (cocaine, amphetamine) all
can cause headache
3.
Psychiatric co-morbidities: abuse (sexual,
physical other); depression; anxiety all are associated with increased
headaches.
II.
PHYSICAL EXAMINATION AND NEUROLOGIC EXAMINATION:
A. General examination should include a thorough examination of the head and neck areas including the cervical spine,
tender temporal
arteries, bony swellings, TM Joint pain, local/focal tenderness.
B. Blood pressure
C. Ocular fundus - R/O
papilledema and look for spontaneous
venous pulsation
E.
Neurological examination should be completely
normal in primary headache disorders
III. Laboratory Investigation in headache:
A.
When to suspect secondary disorders that
require further laboratory investigations:
1.
Unexplainable and abnormal worsening of
previously existing migraines.
2.
Dramatic or unusual change in character of
the prodrome or the headache previously present.
3.
Headaches awakening the patient in the middle
of the night (provided it is not a cluster headache).
4.
Headaches much worse when recumbent or with
coughing, sneezing, Valsalva.
5.
Unusually severe headache of sudden onset
("worst headache of my life").
6. Focal
deficits that do not disappear after the headache is over.
7. Any
abnormal neurologic finding.
8. Beginning of headaches at an older age
without neither a previous history nor a positive family history.
B.
What tests to consider
1.
CBC with ESR
2. Chemistries Na, K,
Ca++, glucose, BUN/Cr
3. Urine analysis
4.
VDRL/FTA
5.
Imaging
a. CT Sinus if sinus disease expected.
b. Cervical Spine Film:
For occipital headache
c. Brain CT Scan: If any part of the history is worrisome for a bleed, or if any part of the neurological examination is abnormal. CT is especially good if you suspect intra-cranial hemorrhage.
d. MR Scan--Most Headaches: More sensitive- Look at brain, and soft tissue
e. CSF examination if SAH, infection, or increased intracranial pressure is suspected
IV. WHAT CAUSES HEAD PAIN?
A. Pain Sensitive Structures
1.
Intracranial
a. Pain Sensitive
Cranial sinuses and afferent veins
Arteries/Veins of the dura mater
Arteries of the base of the brain and their major branches
Parts of the dura mater (in the vicinity of large vessels)
b. Insensitive to Pain
Parenchyma of the brain
Ependyma, choroid plexus
Pia mater, arachnoid membrane, parts of the dura mater
2. Extracranial
a. Pain Sensitive
Skin, scalp, fascia, muscles
Mucosa
Arteries (veins: less sensitive)
b. Insensitive to Pain
Skull (periosteum slightly sensitive)
4. Nerves: Trigeminal, facial, vagal, glossopharyngeal 2nd and 3rd cervical nerves
B. Mechanism of Head pain
1.
Vessels: distension,
traction, dilation of intra-cranial and extracranial arteries and veins.
2.
Nerves: compression,
traction, spasm, interstitial inflammation, trauma of cranial cervical
nerves.
3. Muscle: voluntary, involuntary spasm, inflammation of cranial/cervical muscles
C. Pain Pathways
1.
Structures above the tentorium cerebelli result in pain in front of a
line drawn from the ears across the top of the head.
This area is generally subserved by the V cranial nerve.
The pain is referred to the head and the face.
2. Structures below the tentorium cerebelli are served by the Cranial nerves 1X, X, C2, C3. The pain is referred to the posterior 1/3 of the head, the upper neck, ear and throat.
3.
The major nucleus of headache pain is the
spinal nucleus of V. All
portions of V synapse with in the nucleus, cross, and are carried within
spinothalamic pathways to ventral posterior medial nucleus of the thalamus.
4.
CN IX and X are important for headache pain;
they are related to the spinal nucleus of V and spinothalamic pathways with
termination in the thalamus.
V. CLASSIFICATION OF HEADACHE DISORDER
Classification of headache disorder revolves on the general concept of understanding that headaches can be primary or secondary. Primary Headache disorders are due to a primary genetic predisposition and start in response to trigger factors or just occur spontaneously. Whereas Secondary Headache is due to some definable condition such as brain tumor, increased or decreased intracranial pressure, inflammation of blood vessels and so forth. The International Headache Society (HIS) has classified all primary and secondary headaches with definitions that are used in research and also to communicate a specific headache diagnosis.
A. PRIMARY HEADACHE DISORDERS
1. Migraine
a.
WHAT IS MIGRAINE: Migraine is a Primary Headache disorder
1)
Attacks lasting 4-72 hours, average 12 to 48
hours
2)
At least 2 of the following:
a)
Unilateral head pain
b) Throbbing or pulsating
quality
c) Moderate to
severe pain affecting ability to function
d) Worsening of
pain with routine activity
3) At least one of the following:
Nausea and/or vomiting; Sensitivity to light and sound
4)
It is not the amount of pain that makes it a
migraine, but what
comes with it
5)
Five previous attacks fulfilling the above
criteria should have occurred prior to diagnosis of migraine.
6) Migraine
Headaches are often familial.
6)
It is
important to differentiate migraine with/without aura.
7)
Can be seen in the EPISODIC or CHRONIC form:
a)
EPISODIC migraine is <15 days/month
b)
CHRONIC migraine is >15 days/month
b.
MIGRAINE
WITHOUT AURA: (Common
Migraine): Patients may have
non-specific prodromes and severe headaches; they can be unilateral; they,
too, are often accompanied by nausea, vomiting, photo-phono-phobias.
1) IHS CRITERIA FOR
MIGRAINE WITHOUT AURA:
a)
At least five attacks fulfilling B-D.
b) Attacks lasting about 2 hours (untreated, unsuccessfully treated).
c) At least two of the following characteristics:
1)
Unilateral location
2)
Pulsating quality
3)
Moderate or severe intensity (inhibits or
prohibits daily activities)
4)
Aggravation by walking stairs or similar
routine activity.
d)
At least one of the following:
1)
Nausea and/or vomiting
2)
Photophobia and phonophobia
e)
At least one of the following:
1) History, physical, and neurological examinations don’t suggest other disorders.
2) History and/or physical and/or neurological examination does suggest such disorder, but it is ruled out by appropriate investigations.
3) Such disorder is present, but attacks do not occur for the first time in close temporal relation to the disorder.
2)
Subtypes of Migraine without Aura (Common Migraine)
a)
Menstrual Migraine: Headaches occurring only during the week before,
or the week of menstruation.
b)
Weekend Migraine: This type usually occurs after a strenuous,
stressful work-week; the onset of the headache ensues when the subject
relaxes.
c)
Abdominal Migraine: This type is usually seen in children.
d)
Exertional Migraine; Orgasmic Migraine; Weight Lifters
Migraine. These often occur during strenuous exercise or Valsalva
maneuvers. Occasionally the
differential diagnosis may include aneurysm rupture.
c. MIGRAINE WITH AURA: (Classic
Migraine): Refers to a vascular
headache with a well-defined aura or prodrome.
Frequently prodromes have a duration of minutes to 1 hour; they
usually terminate before the onset of the headache. Frequently a severe
headache follows; it is often unilateral and contralateral to the side of the
symptoms.
1) IHS
CRITERIA FOR MIGRAINE WITH AURA:
a)
At least two attacks fulfilling B.
b) At least three of the
following characteristics:
1)
One or more fully reversible aura symptom
indicating focal cerebral cortical and/or brain stem dysfunction.
2)
At least one aura symptom develops gradually
over more than four mintues or two or more symptoms occur in succession.
3)
No aura symptom lasts more than 60 minutes.
If more than one aura symptom is present, accepted duration is
proportionally increased
4)
Attack follows aura with a free interval of
less than 60 minutes (may also begin before or simultaneously with the aura).
c) At least one of the
following:
1)
History, physical, and neurological
examination do not suggest other disorders.
2)
History and/or physical and/or neurological
examinations do suggest such disorder, but it is ruled out by appropriate
investigations.
3)
Such
disorder is present, but attacks do not occur for the first time in close
temporal relation to the disorder
2) Common prodromes:
a) Visual disturbances:
-scotomas in visual field
quadrants
-bright flashes of light
-wavy vision
-fortification spectra
b)
Aphasia
c)
Vertigo
d)
Numbness around mouth and hand (cheiro-oral)
3)
Subtypes of Classic Migraine or Migraine with Aura
a)
Ophthalmoplegic migraine: A type of classic migraine; which consists
of attacks of weakness of the extra-ocular muscles served by the third nerve
and usually follows the headache. It
is frequently found in the young. Occasionally,
the deficit will persist. The
pupil may or may not be involved.
b)
Hemiplegic Migraine: A rare condition characterized by migrainous
episodes associated with hemiplegia which can outlast the headaches; these
can be familial; often seen in young women.
An abnormality in the calcium channel on
chromosome19 has been associated with hemiplegic migraine.
c) Basilar Migraine: Is characterized by total loss of vision, tinnitus, diplopia, vertigo, gait
ataxia, dysarthria, paresis, variable sensory symptoms in the limbs. These symptoms
precede
the headache phase; it is often seen in young girls
d)
Retinal Migraine: Is still another type of migrainous event in which
focal deficits are related to dysfunction of the retina.
In this form of migraine, temporary monocular photopsia, scotomata, or
visual loss occur. These
symptoms can occur during the headache phase and occasionally, may not be
associated with a subsequent headache. If
there is no headache, the episodes are designated migraine equivalents
e)
Migraine Aura without Headache (Migraine Equivalents).
As people get older, frequently the aura is present without headache.
Here typical auras are present as mentioned above, but no headache
ensues.
2.
CLUSTER HEADACHE: It is an important variant of migraine since it
requires special treatment.
a.
IHS
CRITERIA FOR CLUSTER HEADACHE
1)
At least five attacks fulfilling below.
a)
Severe unilateral orbital, supraorbital
and/or temporal pain lasting 15 to 180 minutes untreated.
b)
Attack is associated with at least
one of the following signs on the side of pain:
(1)
Conjunctival injection
(2)
Lacrimation
(3)
Nasal Congestion
(4)
Rhinorrhea
(5)
Forehead and facial sweating
(6)
Miosis
(7)
Ptosis
(8)
Eyelid edema
b.
These are unilateral
headaches almost always occurring on the same side associated with flushing,
sweating, rhinorrhea, lacrimation, ptosis, and occasionally, Horner's
syndrome.
c.
It occurs most frequently in men (5-7:1).
d.
It is brief -- usually 10 minutes to 1 hour.
e.
The name "cluster" is used because the pain tends to cycle
or cluster around a season or time. Patients
have several headaches each week with periods of time (months, years) in
between of being headache free.
f.
EPISOIDC CLUSTER is a cluster period with
remissions in between attack periods.
CHRONIC
CLUSTER is a cluster period without remission for more than 12 months.
g.
The pathophysiology is unclear, however, the “generator” for
cluster appears to be in the hypothalamus.
Parasympathetic stimulation (rhinitis, tearing) and sympathetic
depression (Horner’s syndrome)
h. Headache types often confused for cluster include: Migraine (common); Benign Paroxysmal Hemicrania;
Raeder's
Trigeminal Syndrome, Sluder's Neuralgia (sphenopalatine ganglion neuralgia)
3. TENSION HEADACHE is on of the most common headache forms.
Almost one-half of patients with headache suffer from this type.
It is a primary headache type that many people may experience.
a.
Definition: An ache or
tightness around the head (band-like sensation) or occipital headache.
It is not usually associated with visual or gastrointestinal symptoms.
b.
Clinical History:
onset mid-like afternoon
band-like sensation
tender scalp
pressure
usually does not remit
worse as the day goes on
c.
Signs: tender
scalp and neck muscles
d.
There is much confusion and little data about
the way stress in peoples' lives contribute to this form.
e.
Types:
CHRONIC TENSION HEADACHE >15 days/month
EPISODIC TENSION HEADACHE
<15 days/month
f. IHS
CRITERIA FOR EPISODIC TENSION-TYPE HEADACHE:
1)
Average frequency of attacks, 15 days/month for 6 months fulfilling critera 2-4
below.
2)
At least two of the following pain characteristics:
a)
Pressing/tightening quality
b)
Mild or moderate severity (may inhibit, but does not
prohibit activities)
c)
Bilateral location
d)
No aggravation by walking stairs or similar routine physical activity
3)
Both of the following:
a)
No vomiting
b)
No more than one of the following: nausea, photophobia, or phonophobia
4)
At least one of the following:
a)
History, physical, and neurological
examinations do not suggest the
disorders.
b) History and/or physical, and/or neurological do suggest other disorders, but it is ruled
out by appropriate investigations
4.
PATHOPHYSIOLOGY OF MIGRAINE HEADACHE
a. Vascular
Theory:
This theory was introduced by Wolff in the early 1940's. It is
believed that migraines are caused by very active vasculature.
The aura is believed to be associated with vasoconstriction; the
headache phase is thought to be associated with vasodilatation.
Cerebral blood flow studies have found distinctly decreased blood flow
during the aura phase. Recently,
this theory has been revived tying in sympathetic/parasympathetic and
trigeminal nerve effects on vasculature.
b. Biochemical
Theories (primary or secondary)
Serotonin is a major candidate for a vasoactive mediator in migraine.
Some propose migraine to be a low plasma serotonin syndrome.
It is found in platelets and can be altered in migraine.
5-HIAA, a major metabolite, is increased in migraine.
Most new migraine drugs affect serotonin in some way.
c. Unified
Hypothesis:
We inherit ability to get migraine.
There is a neural generator in the trigeminal systems which can be
triggered by various environmental factors (stress, light, noise, sleep (too
much or lack of) food). A
neurological signal triggers a vascular response by various neurotransmitters
medications including serotonin. A
local inflammation in the vessel occurs and pain is experienced.
The “generator” has been shown to set up electrical “spreading
depression” first hypothesized by Leao.
d. Other
biochemical theories:
1)
Epinephrine, norepinephrine have been found
in some subjects to decrease just prior to early stages of migraine.
This theory is often used to explain weekend migraine.
2)
Bradykinin has been isolated from
perivascular, extracellular fluid during migraine attacks.
3)
Histamine is reported to have increased
levels during cluster attacks. Many
studies conducted, but not much evidence.
4)
Prostaglandins are a primary focus in
headache research. They have a relationship to platelets and vasoactivity.
Prostaglandin inhibitors are part of the anti-migrainous regimen.
5)
Substance P - A pain transmitter at distal
site
B.
SECONDARY HEADACHE DISORDERS
1. Temporal arteritis:
is an inflammatory condition of the cranial arteries. The headache is usually bitemporal with severe temporal
artery and scalp tenderness. It
is a disease of older people usually greater than 60 years of age. The erythrocyte sedimentation rate is usually (if not always)
elevated. An elevated C-reactive
protein may also be helpful..
Other associated symptoms and signs may include polyarthralgia
rheumatica, jaw claudication, weight loss and anemia.
The importance of this headache is that it can lead to blindness due
to arteritic involvement of the cilioretinal arteries, central retinal
artery, or ophthalmic artery. Examination
reveals tender temporal arteries. Diagnosis
is made by temporal artery biopsy and treatment is with immediate steroid
therapy.
2. Brain Tumor
Headache Or Headaches Associated With Intracranial Hypertension:
Many people with tumors of the brain have headaches. Although
there is no particularly typical headache type, these patients may be
awakened at night by headache (without cluster symptoms), or may experience
projectile vomiting. The
headache often is on the side of the tumor.
Change of the headache to bioccipital signifies increased intracranial
pressure.
Similarly,
patients with intracranial hypertension without headache, may have frequent
if not chronic headaches. Papilledema
may be present. A complete
workout for increased intracranial pressure should be done including MR and
MRI. Idiopathic intracranial
hypertension affects obese women of childbearing age.
A spinal tap is crucial to measure the opening pressure and be sure of
normal CSF.
3.
Low-pressure headaches are worse when the patient is upright
and better when the patient lies down. Diagnosis
can be made clinically. MR may
show meningeal enhancement and low lying cerebellar tonsils.
CSF pressure may not be detected on lumbar puncture
4.
Headache of Meningeal Irritation (Meningitis, subarachnoid hemorrhage)
Headache accompanying subarachnoid hemorrhage
are usually sudden at onset and severe -
"The sudden onset of the worst
headache of my life". The
headache may be associated with neck stiffness or muscle rigidity.
Kernig’s and Brudzinski's sign may be elicited.
Kernig's sign: with
patient supine, flex hip to 90 degrees with the knees flexed.
When knee is extended, pain will be produced in the back of the neck.
(Can also see in herniated disk and back syndromes.)
Brudzinski’s sign: Passive
flexion of the neck induced involuntary hip flexion.
5. Sinus Headache -Pain
is frequently localized over the sinuses and associated with nasal or
pharyngeal drainage. Often
present in the morning, it disappears with an upright posture and may
increase in stooping over. Often
inhalant sympathomimetic drugs (e.g., Neosynephrine) will alleviate pain.
Many complain they have "sinus headache" when they actually
have migraine.
6. Post-Traumatic
Headache Frequently
headaches or migraines will occur variably after head injury.
In people predisposed to migraine, trauma may set these headaches off.
Often headaches do not resolve until litigation surrounding the injury
resolves.
7.
Trigeminal Neuralgia Characterized
by lancinating pains in the distribution of the trigeminal
nerve lasting seconds. Paroxysms
of pain are triggered by brushing teeth or light touch.
In younger individuals trigeminal neuralgia is caused demyelination,
and in older individuals it is caused by a vascular loop on the nerve root
entry zone.
8. Other
Headaches Related to Medical Disorders
Fever
Carbon Monoxide Exposure
COPD with high PCO2
Hypothyroidism
Cushing's Disease
Hypertension
Renal Dialysis
Carcinoid Tumor
Cervical spine Disease - Arthritis
Sleep Apnea
D. CHRONIC DAILY HEADACHE is frustrating to both patients and doctors.
1.
Primary
Chronic Daily Headache is the most common
a.
Chronic
Migraine
b.
Chronic
Tension-type headache
c.
Chronic
Cluster Headache
2.
Chronic
migraine is usually due to some transformational factor
a. Analgesic overuse can transform episodic migraine to chronic migraine
1) Characteristics
a)
chronic headaches associated with relief by analgesics requiring
frequent administration
b)
may have superimposed migraine
c)
sleep disturbance is common
2) Especially prominent
with caffeine and narcotics
3)
If you can stop the analgesic alone, chronic headache improves in
50%. If you restore sleep, 75% improve.
b. Depression
1)
Frequent familial predisposition
2)
May also have migraines
3)
Must treat depression
c. Hormonally
induced headache
d.
Chronic headache
associated with sexual abuse or internal
psychiatric conflict; multiple personality and dissociation
1)
Usually chronic migraine
2)
Daily headache unresponsive to almost all medications
3)
Sleep disorder
4)
Need to work on the conflict to resolve the headache
e. Internal
psychiatric conflict
f. Cervical
(neck) pathology
g Post-traumatic
headache
3.
Secondary Headache disorders also cause
chronic daily headache. The most
common causes of chronic daily headache due to secondary headache include:
a.
Increased intracranial pressure (pseudotumor
cerebri, or real tumor, venous thrombosis)
b.
Decreased intracranial pressure
c.
Arnold Chiari Malformation
d.
Chronic meningitis (e.g. Epstein Barr Virus;
virus)
e.
Metabolic disorders:
Sleep apnea, hypothyroidism, high altitude headache
f.
Post-traumatic disorders
g.
Inflammatory conditions: arthritis, systemic lupus
TREATMENT OF MIGRAINE HEADACHES
A.
Identify and treat known
exacerbating conditions:
1.
stress reduction
2.
medication over use (analgesic)
3.
lack of sleep or too much sleep
4.
diet
5.
hormone irregularities; medication
6.
light, sound,
smell
B.
Symptomatic Treatment of Migraine
1. The basic treatment is to alleviate the nausea, relieve the pain, and in some cases, sedate the patient. The
choice
of medication depends on the patient's needs.
a. ANTI-EMETICS to relieve the GI symptoms.Metaclopramide (Reglan), prochlorperazine (compazine),
hydroxyzine
(vistaril), promethazine (phenergan) suppositories are useful in a severely
nauseated person.
b. PAIN
RELIEF
1.
Aspirin
2.
Isometheptene (Midrin)
3.
Ergotamine:
(Cafergot, Dihydroergotamine)
4.
Triptans are “designer drugs” for
headache; all have some affect
on serotonin. Very effective. Cannot
be used in patients with underlying heart disease
a.
Sumatriptan (Imitrex)
b.
Zolmitriptan (Zomig)
c.
Naratriptan (Amerge)
d.
Rizatriptan (Maxalt)
e.
Almotriptan (Axert)
5.
EMERGENCY ROOM/OFFICE VISIT -
non-narcotic treatment for an acute headache
a.
IV Prochlorperazine (Compazine) (1 mg/min) -
10 mg IV
b.
Sumatriptan (Imitrex) 6 mg SQ
c.
IV DHE--pre treat nausea (Reglan or phenergan)
d.
Chlorpromazine (Thorazine) (watch BP)
e.
Ketorolac (Toradol) (30-60 mg IM)
f.
Hydroxyzine (Vistaril)/Promethazine (Phenergan)
c. SEDATION
1.
Hydroxyzine 75 (Vistaril) and Promethazine 75
(Phenergan)
2.
Chloral hydrate (up to 2 grams)
3.
Narcotic medication should be avoided in
migraine treatment, since these headaches are often life-long and the
patients are young, the potential for addiction is high. LIMIT 20/MONTH.
C.
Prevention of Migraine - (if the
symptoms are too frequent; if the symptoms are too severe).
C. Prevention of Migraine - (if the symptoms are too frequent; if the symptoms are too severe)
1.
First Line Treatment of Migraine
a.
Propranolol, Nadolol and Timolol.
b.
Naproxen sodium (Anaprox)
c.
Amitriptyline: (Nortriptyline Imipramine, Desipramine, Doxepin)
d.
Calcium Channel Blockers: Verapamil, Nifedipine
e.
Anticonvulsants: Valproic
Acid (Depakoate) approved for use in migraine; others used:
Gabapentin (Neurontin); Topiramate (Topomax); Lamotrigine (Lamictal)
f.
Antidepressants may be helpful with co-morbid
depression - Fluoxetine (Prozac), Sertraline (Zoloft), Venlafaxine (Effexor),
Paroxetine (Paxil), Nefazodone (Serazone), and Mirtazipine (Remeron) if
depression is present.
2. Second Line of
Treatment
a.
Other anti-platelet medications.
(Omega 3 Fish Oil tid)
b.
Riboflavin- 400 mg
c.
Cyproheptadine - can be
used in children; effective with allergic individuals.
d.
Methysergide - is effective but because of its potentially serious
side effects, probably should not be used unless all other medications have
failed. (Retroperitoneal and
valvular fibrosis).
e.
MAO inhibitors
f.
Phenytoin
g.
Prednisone – only short courses to break a cluster cycle or
intractable migraine
D.
ACUTE TREATMENT OF CLUSTER HEADACHE
1.
Oxygen 10 liters/FM 15 minutes
(each attack)
2.
Lidocaine 2% nose drops:
3.
Sumatriptan: SQ or Nasal Spray
4.
Ergotamine: sub-lingual, Nasal Spray
5.
Ergotamine: intramuscular or sub Q
E.
PREVENTION OF CLUSTER HEADACHES
1.
Lithium
2.
Indomethacin (also good for paroxysmal hemicrania)
3.
Methysergide 2MG QID
6 months at a time with 1 month holiday
4.
Prednisone (burst and taper only)
5.
Cafergot: BID
6.
Calcium Channel Blocker - Verapamil
7.
Depakote
8.
Neurontin
F.
PATIENT EDUCATION
1.
Recognition of chronic analgesic overuse headaches.
2.
Know headache type and management for each
3.
Self management techniques
4.
Reading materials:
“Headache Relief” by Rapaport & Sheftell
“Hope for your Headache Problem” by Diamond & Vye
“Taking Control of Your Headaches” by Duckro, Richardson and Marshall
“Migraine: The Complete Guide” written by ACHE
1994
5.
American Association for Study of Headache
875 Kings Highway Suite
200
Woodbury NJ
08096
Telephone (609) 845-0322
FAX (609) 384-5811
6.
National Headache Foundation
428 W. St. James Place
2nd Floor
Chicago, IL 60614-2750
Toll Free (800) 843-2256
http://www.headache.org
BIBLIOGRAPHY
1.
Dalessio DJ (ed): Wolff's
Headache and Other Head Pain. Oxford University Press, 2001.
2.
Neurology Clinics Headache Volume 1:2, May 1983, WB Saunders.
3.
Raskin NH, Headache, NY: Churchill
Livingston, 1988.
4.
Blau JN, ed. Migraine, Baltimore:
The Johns Hopkins University Press, 1987.
5.
Silberstein SD, Lipton RB, Goadsby PJ, Headache in Clinical
Practice, Oxford: 1515 Medical Media, 1998
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Last updated: 10/05/2002 © 2000-2002 John Rose, MD University of Utah School of Medicine