Headache/ Pain

Cluster Headache

Migraine

Trigeminal Neuralgia

Complex Regional Pain Syndrome-Reflex
Sympathetic Dystrophy

Low Back Pain

Tension-type Headache

Medication Overuse Headache

Menstrual Migraine
523
524
CLUSTER HEADACHE
Treatment
Drug Treatment
Attack treatment
Sumatriptan (Imigran)
 6 mg via subcutaneous injection
Ergotamine
 Sublingual tablets of ergotamine tartrate
 Oxygen inhalation,
 Repeated intravenous injections of dihydroergotamine;
Prophylactic treatment
Ergotamine (Cafergot, Migrainil)
 1 to 2 mg orally or rectally two times per day for no
more than a few weeks.
Verapamil (Isoptin)
 120 mg three times daily.
Lithium (Priadel, Prianil)
 Lithium carbonate, 900 mg/d.
Prednisone (Hostacortin)
 60 to 80 mg initially, tapered to zero in less than 4
weeks.
Methysergide (Deseril)
 1 to 3 mg/d for a period not longer than 4 to 5 months.
Drugs that are under investigation
 Valproate (Depakine) → pain relief in 60-73% of pts.
 Capsaicin, a constituent of hot peppers, depletes sensory
neurons of substance P and induces a painful burning
sensation when applied topically, twice daily for 7 days,
followed by improvement of headache.
525

Leuprolide is a gonadotropin-releasing hormone
analogue thought to enhance the pain-suppressing systems
of the hypothalamus.
 Transdermal clonidine (Catapres), administered for 1
week,
 Melatonin, 10 mg every evening for 14 days,
 Intranasal lidocaine (Lignocaine) 4% (in spray form)
 Tizanidine, (Sirdalud), a central muscle relaxant, was
given as adjunctive therapy along with conventional drugs
 Methylphenidate (Ritalin) is rapidly effective as an
attack-abolishing agent
Surgery
 Retrogasserian injections of glycerol
 Radiofrequency trigeminal rhizotomy
 Radiofrequency lesioning of the sphenopalatine ganglion
through an infrazygomatic approach
 Microvascular decompression of the trigeminal nerve
Other therapies
 Hyperbaric oxygen therapy
Oxygen inhalation
 100% oxygen, 7L/min, via facial mask for 15 minutes.
526
MIGRAINE
Diet and lifestyle
 Migraine attacks are triggered by cheese, chocolate,
citrus fruits, & red wine in 20% of cases. Such pts are
advised to avoid these foods & drinks.
Drug Treatment
Acute treatment
 Aspirin, paracetamol (acetaminophen), low-dose
codeine, ibuprofen (Brufen). naproxen (Naprosyn) or
diclofenac (Voltaren) may abort the attack
 Sumatriptan, (Imigran) zolmitriptan, (Zomig) rizatriptan,
(Maxalt) naratriptan (Naramig)
 Intramuscular and inhaled dihyroergotamine preparations
are popular
Prophylactic treatment
Simple analgesics
 Aspirin, 600 to 900 mg every 4 hours.
 Paracetamol (acetaminophen), 1 g every 4 hours.
 Two compound paracetamol/aspirin/codeine tablets
every 4 hours.
Antiemetics
 Phenothiazines (e.g., prochlorperazine) 5-mg tablets or
25-mg suppositories
 Gastrokinetic agents: metoclopramide (Primperan), 10mg tables; domperidone (Motilium), 10-mg tablets or 30mg suppositories.
 Antiemetics are also available as combination tablets
with aspirin or paracetamol (Panadol)
527
Nonsteroidal anti-inflammatory agents (NSAIDs)
 Ibuprofen (Brufen): 400 to 800 mg repeated after 4 hours
to a maximum of approximately 2 g/d.
 Naproxen (Naprosyn): 250 to 750 mg repeated every 4
hours to a maximum of 1250 mg daily.
 Diclofenac (Voltaren): 25 to 50 mg repeated to a
maximum of 150 mg/d.
Ergotamine and derivatives
 Ergotamine, sometimes combined with caffeine, is
available as 1-mg and 2-mg tablets and as 2-mg
suppositories (e.g., Cafergot).
 The ergotamine inhaler delivers 360 μg per metered
inhalation.
 The sublingual preparation is not recommended.
 Dihydroergotamine (Dihydergot) tablets are so poorly
absorbed that they are not recommended;
 DHE nasal preparation is now available (Migranal)
Triptans
 Sumatriptan (Imigran) 25-mg, 50-mg, or 100-mg tablets
taken orally; 20 mg by inhalation; or 6 mg by
subcutaneous autoinjecion.
 Zolmitriptan (Zomig): 2.5-mg tablets.
 Naratriptan: (Naramig) 2.5 mg tablets.
 Rizatriptan (Maxalt): 5-mg and 10-mg tablets and a melt
preparation.
Beta-blockers
 Propranolol (Inderal) 40 mg twice daily, increasing to
160 mg twice daily if necessary.
 Atenolol (Tenormin): 50 mg/d, increasing to 150 mg/d
 Metoprolol (Lopressor): 50 to 150 mg/d.
 Nadolol (Corgard): 40 to 160 mg/d.
528
Pizotifen and methysergide
 Pizotifen (Mosegor) 0.5 mg, increasing to 1.5 mg or
perhaps 3 mg at night.
 Methysergide (Deseril): 0.5 mg/d. increasing to a
maximum of 2 mg three times daily for no more than 6
consecutive months, and then a 1-month drug-free
interval.
Other prophylactic agents
 Valproate (Depakine): 200 mg twice daily, increasing to
approximately 1.6 g/d in divided doses.
 Amitriptyline (Tryptizol): 10 mg/d, increasing, if
necessary, to 100 mg/d.
 Flunarizine (Sibelium): 10 mg/d at night
529
TRIGEMINAL NEURALGIA
Treatment:
Drug Treatment
Drugs for trigeminal neuralgia
Drug
First report of use
Phenytoin (Epanutin)
1942
Antihistamines
1948
Carbamazepine (Tegretol)
1962
Clonazepam (Rivotril)
1975
Baclofen (Lioresal)
1980
Vlaproic acid (Depakine)
1980
L-Baclofen
1987
Oxcarbazepine (Trileptal)
1987
Proparacaine
1991
Lamotrigine (Lamictal)
1995
Gabapentin (Neurontin)
1997
Carbamazepine (Tegretol)
 Carbamazepine remains the drug of choice for the initial
drug treatment of trigeminal neuralgia.
 The initial dose is 200 to 300 mg/d in divided doses, or.
 Using slow-release preparations (Tegretol CR) in a
twice-daily regimen.
 Most patients respond to a dose within the range of 600
to 800 mg/d.
 Higher doses, up t o1600 mg/d, can be used
Phenytoin (Epanutin)
 300 mg/d. The drug can be given as a single dose before
bedtime.
Baclofen (Lioresal)
530

An initial dosage is 15 mg/d in divided doses, increasing
to a maximum of 80 to 90 mg/d.
Clonazepam (Rivotril)
 Start at 0.5 mg/d, increasing, if possible, to a range of 4
to 8 mg/d. A therapeutic range for the drug of 0.04 to 0.23
μmol/L has been suggested.
Valproate sodium (Depakine)
 600 to 1200 mg/d.
Oxcarbazepine (Trileptal)
 600 to 3600 mg/d.
Interventional procedures
Glycerol rhizotomy
 Under local anesthesia, a standard 20-gauge spinal
needle is directed percutaneously through the foramen
ovale, using fluoroscopic control.
 Cerebrospinal fluid flow usually indicates that the needle
is in the trigeminal cistern.
 Using a nonionic iodine contrast medium, the cisternal
volume can be calculated, allowing the appropriate
volume of glycerol to be determined.
 The volume injected ranges from 0.2 to 0.5 ml
Radiofrequency thermal rhizotomy
 Radiofrequency lesions can selectively destroy
nociceptive fibers (unmyelinated C and poorly myelinated
A delta fibers) while preserving heavily myelinated fibers.
 A 20-gauge needle is inserted through the foramen ovale
under fluoroscopic control to reach the retrogasserian
portion of the nerve.
 Intravenous anesthesia is used.
 The electrode is guided through the needle, is final
position being determined by the patient’s response to
electrical stimulation.
531

Elicitation of paresthesia or pain a low current in the
distribution of the relevant division is sought.
 Preliminary lesion is produced at 60o to 70oC for 70
seconds.
 Additional lesions are induced with increasing
temperatures, the aim being to produce dense hypalgesia
in the relevant division.
Percutaneous balloon compression of the trigeminal nerve
 General anesthesia + atropine to block the bradycardia
that occurs in two thirds of subjects.
 Fluoroscopic control, a thin-walled, 14-gauge needle is
directed to the foramen ovale.
 Once the foramen is engaged, a fogarty catheter is
advanced to the entrance of Meckel’s cave.
 The balloon is inflated with Omnipaque (Nycomed)
producing a compression pressure of 650 to 950 mm Hg
for 1 to 1½ minutes.
 After deflation, the balloon & catheter are removed
together.
Surgery
Microvascular decompression
 Through a retromastoid craniectomy, the trigeminal
nerve is examined microsurgically for vascular
compression at or near is point of entry into the brain
stem.
 Intraoperative monitoring with brain stem auditory
evoked potentials (BAEPs) is recommended.
 The trigeminal nerve is visualized from the brain stem to
Meckel’s cave
 The nerve is decompressed of all vessels, both arterial
and venous.
532

Veins are generally coagulated, and arteries are separated
from the nerve with Teflon.
Partial sensory trigeminal rhizotomy
 Retromastoid craniectomy is used when:
1) There is no evidence of significant vascular contact with
the trigeminal nerve root or
2) Previous microvascular decompression has failed and
there is no significant vascular contact at the time of
reoperation.
 The procedure is done with concomitant measurement of
BAEPs.
 After the main sensory root has been identified, one third
to one half of the cross-sectional area of the sensory root
is cut about 2 to 5 mm from the pons.
Peripheral neurectomy
 Supraorbital neurectomy is performed through an
incision the eyebrow.
 All branches of the surpraobital and supratrochlear
nerves are divided and avulsed under magnification.
 Infraorbital neurectomy is performed via an intraoral
incision in the labiogingival sulcus.
 The infraorbital nerve is avulsed well into the
infraorbital foramen.
 Sectioning of the inferior alveolar nerve is
accomplished within the inferior alveolar canal.
Emerging therapies
Stereotactic radiosurgery
 Stereotactic MRI is performed to identify the
trigeminal nerve.
 The 4-mm radiosurgical isocenter is targeted at
the mid-portion of the trigeminal nerve about 2 to
533


4 mm anterior t o the junction of the nerve and
the brain stem.
The length of nerve irradiated at the 50% isodose
is 4 mm.
Approximately 70 Gy are delivered in 30
minutes.
534
COMPLEX REGIONAL PAIN SYNDROME
REFLEX SYMPATHETIC DYSTROPHY
Treatment
Diet and lifestyle
 Improve aerobic capacity
 Mobilize coping skills and psychological resources,
including mastery of relaxation, and stress management
techniques
 Attain and maintain ideal body weight.
Drug Treatment
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Standard dosage of non-steroidal anti-inflammatory drugs
(NSAIDs)
Agent
Dosage range, mg/d
Ibuprofen (Brufen)
1200-3200
Piroxicam (Feldene)
20
Naproxen (Naprosyn)
500-1000
Diclofenac (Voltaren)
100-225
Oxaprozin
1200-1800
Nabumetone (Nabugesic)
1000-2000
Etodolac (Napilac)
600-1200
t
Celecoxib * (Celebrex)
200-400
*Selective cyclooxygenase-2 inhibitor; it is claimed to have a
minimal effect on cyclooxygenase1 (platelet, gastrointestinal,
and renal function).
Opioids
 Tolerance and physical dependence occur, leading to the
need for dose escalation.
Antidepressants
 The standard dosage for antidepressants varies within
and between patients.
535
Anticonvulsants
 Gabapentin (Neurontin) 900 to 3600 mg/d in four
divided doses.
Alpha-adrenergic blockers
(e.g., prazosin and doxazosin)
 Doxazosin (Cardura) 1 mg at bedtime, increased as
tolerated by 1 mg/d until:
1) Postural hypotension or other adverse effects are
intolerable,
2) Symptoms reverse, or
3) A maximum dosage of 16 mg/d is reached.
 Prazosin (Minipress) 1 mg twice daily, increased as
tolerated by 1 mg/d until:
1) Postural hypotension or other adverse effects are
intolerable,
2) Symptoms reverse, or
3) A maximum dosage of 20 mg/d is reached.
Membrane stabilizers
 Anticonvulsants
 Mexiletine (Mexitil) and lidocaine (Xylocaine), by
infusion or topical application,
Corticosteroids
 Topical,
intravenous,
regional,
and
systemic
corticosteroids
Capsaicin
 Topical capsaicin in postherpetic neuralgia and diabetic
peripheral neuropathy, and in some cases of CRPS.
Interventional procedures
Regional anesthetic techniques
 Regional anesthetic techniques is based on two
argument:
536
1)
Provision of regional anesthesia facilitates more effective
passive physical therapy and
2) Temporary sympatholysis
 Intravenous regional sympatholysis (by guanethidine)
 Continuous conduction (epidural) blockade, combined
with aggressive physical therapy.
Neuromodulation
 The use of implanted spinal and peripheral nerve
stimulators in CRPS
 Psychological assessment is mandatory
Surgery
 Surgical sympathectomy is ineffective in CRPS
Physical/speech therapy and exercise
 The following techniques may be used: reactivation,
contrast baths, desensitization, flexibility, edema control,
peripheral electrical stimulation, isometric strengthening,
management of secondary myofascial pain, range of
motion (gentle), stress loading, isotonic strengthening,
general aerobic conditioning, postural normalization and
balanced use, ergonomics, movement therapies,
normalization of use, and vocational and functional
rehabilitation.
Other treatment
 As pain, impairment, disturbed sleep, and anxiety
progress, depression develops.
 Hostility, somatization, frustration, and abnormal illness
behavior may be seen.
 These changes should be treated with the somatic
components of the illness.
 Again, a comprehensive pain rehabilitation program may
be the best option.
537
LOW BACK PAIN



Low back problems are extremely common.
LBP is a symptom & not a specific disease.
Although 90% of pts with LBP have self-limited disease,
recurrent attacks of pain are common & 10% of pts develop
chronic LBP.
 In general, LBP is over-evaluated & over-treated.
 The physician's job, when evaluating a pt with acute LBP, is
to look for “red flag”- symptoms & signs that should prompt
additional evaluation & treatment.
 Without “red flag” conditions, LBP should be treated with
“comfort control” measures only e.g., activity modification
& analgesics.
 Surgery should be reserved for pts with progressive
compressive radiculopathy.
 Neurologists should be involved in the evaluation &
treatment of pts with LBP.
Major Sources of Low Back & Referred LL Pain
Spondylogenic:
 Bones
 Muscles
 Ligaments & tendons
 Joints
 Discs
Neurogenic:
 CNS
 Nerve roots
 Lumbar or Sacral plexus
 Peripheral nerves
 Meninges
538
Viscerogenic:
 Pancreas
 Bowel
 Kidneys
 Ureter
 Bladder
 Uterus
 Ovaries
 Prostate
Vascular:
 Abdominal aortic aneurysm
 Atherosclerotic peripheral vascular disease
Psychogenic:
 With or rarely without an additional source of pain
Treatment:
Diet & lifestyle:
 Abstinence from tobacco may help to prevent LBP.
 Occupational LBP occurs in settings of heavy work, lifting,
prolonged sitting or standing, bending & twisting, vibration,
monotonous work, job dissatisfaction, & poor relationships
with co-workers.
 Bed rest.
Drug Treatment:
 NSAIDs.
 Acetaminophen.
 Muscle relaxants are useful in acute LBP.
 Tramadol is useful in chronic LBP.
 Opioid analgesics are reserved for acute severe LBP.
 Nortriptyline (Aventyl) is useful in chronic LBP.
 Oral corticosteroids are not recommended for LBP.
539
Interventional Procedures:
 Comfort control measures include injection of
corticosteroids, local anesthetics, & other substances
including opioid analgesics.
 Epidural injections of a corticosteroid, a local anesthetic, or
both has no role in acute LBP without radiculopathy,
however they are useful for short-term relief of radicular
pain.
 Epidural steroid injections may be of short-term benefit for
chronic LBP, but epidural steroids are not more effective
than injections of a local anaethetic or a muscle relaxant.
 There are facet joint injections, epidural injections, and local
injections.
Surgery:
 Fracture with instability, infection, tumor, and cauda equina
syndrome require urgent or emergent surgical consultation
for possible stabilization, culture, biopsy or removal, and
decompression respectively.
 For patients without any of these conditions, there are two
categories of surgery to consider; surgery directed at a
herniated lumbar disk to relieve nerve root compression and
various attempts at fusion to improve stability of the
lumbosacral spine and help relieve pain.
 Operations directed at a herniated disk are considered in
patients with lingering acute, subacute, or acute
superimposed on chronic LBP with sciatica.
 Operations to fuse the spine are performed in patients with
chronic LBP with or without radicular pain.
540

Chymopapain injection into the nucleus pulposus is
considered a surgical procedure and is compared with
surgical intervention.
Surgery for herniated disc:
 Surgery for acute LBP with sciatica should not be
considered for the first 1 month after onset of symptoms.
 Lumbar disk surgery should only be considered if:
1) The patient has sciatica in addition to LBP, and the
sciatica is both severe and disabling;
2) The pain or associated neurologic deficits persist without
improvement for greater than 4 weeks or progress; and
3) There is strong physiologic evidence of dysfunction of a
specific nerve root with confirmation of disk herniation
at the appropriate level on an imaging study.
 Surgical discectomy provides effective short-term and
intermediate relief of symptoms for carefully selected
patients with sciatica who fail to improve with conservative
therapy and may improve the patient's chances of regaining
lost neurologic function; it is not clear that such surgery has
a beneficial effect on long-term outcomes.
 Standard discectomy and microdiscectomy are similarly
efficacious.
 Automated percutaneous discectomy and laser discectomy
are not recommended.
 Chemonucleolysis (dissolving the nucleus pulposus by
enzyme injection) using chymopapain is an acceptable
treatment, but is less efficacious than standard or
microdiscectomy.
 Chymopapain injection is less invasive than discectomy, but
the results are poorer and lead to significantly greater need
for a second intervention.
Lumbar fusion for the treatment of chronic LBP:
541

Comparisons of instrumented (placement of metallic
hardware) and non-instrumented fusions indicate that
instrumented fusion has a higher fusion rate, does not
improve clinical outcomes, and is probably associated with
higher complication rates.
 Most patients who have acute or chronic idiopathic or
discogenic LBP should be managed non-operatively.
 Operative treatment results in some improvement in about
75% of patients, but significant pain relief and recovery of
function are seen in 50% or less.
Assistive devices:
 Shoe insoles (inserts into both shoes) to help reduce LBP
may be helpful for patients with acute low back problems
who stand for long periods of time.
 Shoe lifts, in which the heel or sole (or both) of one shoe is
built up might be helpful in treating or preventing LBP for
patients with leg length discrepancies of more than 2 cm.
 Lumbar corsets and support belts have not been proven
helpful for treating patients with acute low back problems.
Physical therapy and exercise:
 Patients may be taught self-application of heat or cold to the
back at home.
 Low stress aerobic exercise can help to prevent inactivityinduced debilitation and is recommended for patients with
acute LBP.
 Exercise therapy is not more effective than other
conservative treatments including no intervention for acute
LBP.
 Exercise therapy (such as specific back, abdominal, flexion,
extension, static, dynamic, strengthening, stretching, or
542
general aerobic exercises) is effective for treatment of
chronic LBP;
 Exercise therapy is probably no more effective than passive
physical therapy for chronic LBP.
Other therapies:
 Acupuncture is not more effective than placebo or sham
needling for the treatment of chronic LBP.
 Acupuncture is not recommended for acute LBP.
 Behavior therapy.
 Spinal manipulation can be helpful for patients with acute
low back problems without radiculopathy within the first
month after onset of symptoms. It is not recommended for
patients with radiculopathy, or for those with chronic LBP
 Patient education can include spoken, printed, and
audiovisual materials and educational programs.
 Back schools (a structured program of education about LBP,
usually in a group setting) may be effective for patients with
recurrent and chronic LBP in occupational settings.
 Spinal traction is not recommended in the treatment of
patients with acute LBP or chronic LBP.
 Transcutaneous electrical nerve stimulation (TENS) is not
recommended for the treatment of acute LBP.
 Percutaneous electrical nerve stimulation is more effective
than TENS or exercise therapy in providing short-term pain
relief and improved physical function in patients with
chronic LBP.
Emerging therapies:
 Vertebroplasty is a promising new therapy for patients with
compression fractures of the spine who do not improve with
conservative management.
543

Intradiscal electrothermal anuloplasty may prove helpful for
chronic LBP due to disk degeneration without nerve
impingement.
Pediatric considerations:
 LBP is much less common in children than in adults.
 Degenerative conditions basically do not occur in children.
 Mechanical, developmental, inflammatory, infectious, and
neoplastic etiologies should be considered in children with
LBP.
TENSION-TYPE HEADACHE

Primary headaches represent some of the most costly
diseases in modern society,
544

Tension-type headache and migraine represent two different
diseases, although coexisting in many patients.
 Simple analgesics and non steroidal anti-inflammatory drugs
(NSAIDs) for the treatment of acute headache and low dose
tricyclic antidepressants are still the mainstays of
treatment, although new promising therapies are emerging.
Diagnostic criteria for episodic tension-type headache
A. At least 10 previous headache episodes fulfilling criteria B
through D listed below.
B. Number of days with such a headache is less than 180 days
per year (or less than 15 per month).
C. At least two of the following pain characteristics:
1. Pressing or tightening (non-pulsating quality).
2. Mild or moderate severity.
3. Bilateral location.
4. No aggravation by walking stairs or similar routine
physical activity.
D. Both of the following:
1. No nausea or vomiting.
2. Photophobia and phonophobia are absent; one but not the
other is present.
E. At least one of the following:
1. History, physical, and neurologic examinations do not
suggest one of the disorders listed in group 5 through 11
(symptomatic disorders).
2. History, physical, and neurologic examinations suggest
such a disorder, but it is ruled out by appropriate
investigations.
3. Such a disorder is present, but tension-type does not occur
for the first time in close temporal relation to the
disorder.
Diagnostic criteria for chronic tension-type headache
545
A. Average headache frequency more than 15 days per month or
more (more than 180 days per year) for 6 months or more,
fulfilling criteria B through D listed below.
B. At least two of the following pain characteristics:
1. Pressing or tightening (non-pulsating quality).
2. Mild or moderate severity.
3. Bilateral location.
4. No aggravation by walking stairs or similar routine
physical activity.
C. Both of the following:
1. No vomiting.
2. No more than one of the following:
Nausea, photophobia, or phonophobia.
D. At least one of the following:
1. History, physical, and neurologic examinations do not
suggest one of the disorders listed in group 5 through 11
(symptomatic disorders).
2. History, physical, and neurologic examinations suggest
such a disorder, but it is ruled out by appropriate
investigations.
3. Such a disorder is present, but tension-type does not occur
for the first time in close temporal relation to the
disorder.
Treatment:
Diet and lifestyle:
546

No specific relation between diet and tension-type headache,
although alcohol and chocolate may precipitate headache in
some individuals.
 A balanced diet with regular meals and avoiding alcohol
consumption can be recommended.
Drug Treatment:
The acute episode:
Acetylsalicylic acid (ASA) (Aspirin)
 Start with 500 mg once per day early in the acute episode.
 May be increased to 1000 mg, and repeated, maximally 4 g
per day.
Acetaminophen:
 Starting with 500 mg once per day early in the acute
episode.
 May be increased to 1000 mg and repeated, maximally to 4
g per day.
NSAIDs:
 Ibuprofen (Brufen) starting with 200 mg once per day in the
acute episode, eventually increasing to 400 mg. Dosage can
be repeated, up to 1800 mg per day.
 Ketoprofen-starting with 25 mg in the acute episode,
eventually increasing to 50 mg. Dosage can be repeated up
to 200 mg per day.
Muscle relaxants:
 Tizanidine (Sirdalud) was reported to be effective in the
reduction of pain intensity.
547
Pharmacologic treatment paradigm for the acute episode of
tension-type headache. Physicians should start the patient on the
lowest dosage of simple analgesics and increase gradually in the
following headache episodes.
Triptans:
 The effect of migraine-specific drugs in tension-type
headache is controversial.
 Subcutaneous injections of 6 mg of sumatriptan (Imigran)
had some effect in patients with chronic tension-type
headache.
 In episodic tension-type headache, there was a pronounced
effect of 6 mg sumatriptan subcutaneously in patients with
coexisting migraine.
 The use of triptans should be restricted to migraine.
Prophylactic treatment:
Tricyclic antidepressants (TCAs):
 Starting with 10 mg once per day before bedtime, increase
with 10 mg weekly to effect or side effects.
548
Treatment paradigm of the chronic tension-type headache.
Physicians should start therapy with diary recordings, be aware
of any mental and muscular stress, recommend a daily exercise
program, and suggest, eventually, a low dose of amitriptyline in
slowly increasing dosages of 10 mg weekly until effect or side
effects.
Other antidepressants:
 As imipramine (Tofranil) and buspirone (Buspar), a 5 HT1A
agonist, have a prophylactic effect in chronic tension-type
headache.
Selective seritonin reuptake inhibitors (SSRIs):
 The effect of SSRIs in those patients with coexisting
depression and headache appear to be favorable.
Other prophylactics:
 Sodium valproate (Depakine) plays no role in the treatment
of pure tension-type headache.
 NSAIDs are also reported to have a prophylactic effect.
Botulinum toxin:
 Injections of botulinum toxin type A (Botox A) in pericranial
muscles have a prophylactic effect.
549
Nonpharmacologic treatment:
Cervical manipulation:
 Amitriptyline (Tryptizol) had a better prophylactic effect
during active treatment periods whereas the long-term effect
was in favor of cervical manipulation.
Relaxation and biofeedback:
 Various forms of muscle relaxation with or without EMG
biofeedback reduce pain intensity and frequency by 40% to
60% of their pretreatment values.
 EMG biofeedback is better than simple muscle relaxation
alone, whereas the combination of muscle relaxation and
EMG biofeedback is favorable.
Acupuncture:
 Acupuncture is frequently applied to headache patients,
(chronic tension headache) → a significant pain reduction of
31%.
Psychologic treatment:
 Tension-type headache frequently is precipitated by stress.
 Relaxation therapy and stress management may be helpful.
 If depression or anxiety is a significant finding, a specific
treatment strategy for these disorders should be initiated.
Electrical stimulation:
 Percutaneous electrical nerve stimulation in chronic
tension-type headache noted a significant reduction in
frequency and intensity during active treatment.
Physical therapy and exercise:
Physical therapy:
 Various treatment modalities such as hot and cold packs,
ultrasound, and electrical stimulation, improvement of
posture, relaxation, and exercise programs are applied.
Usually biweekly for 6 to 8 weeks.
550
Spinal manipulation:
 Widely used although substantial evidence for the effect is
relatively scarce.
Emerging therapies:
 Easy soluble NSAIDs, eventually the selective COX2inhibitors with fewer gastrointestinal side effects, are
promising for treating the acute episode.
 Nitric oxide is of interest in chronic pain. Infusions of
glyceryl trinitrate produce headache in most subjects. The
nitric oxide synthase inhibitors may thus relieve the
headache,
 Botulinum toxin injected into the pericranial muscles is a
promising new strategy for chronic tension-type headache.
 Other (nontricyclic) antidepressants should be investigated,
e.g. paroxetine, fluvoxamine and mianserin.
551
MEDICATION OVERUSE HEADACHE


Medication overuse headache is common.
Simple analgesics, caffeine-containing analgesics, butalbitalcontaining analgesics, opioids, ergotamine, and triptans may
cause medication overuse headache.
Proposed 1994 criteria for medication overuse
At least one of the following for at least 1 month:
1. Simple analgesic use (more than 1000 mg of acetylsalicyclic
acid or acetaminophen) more than 5 days per week.
2. Combination analgesics (caffeine, barbiturate-containing
medication--more than three tablets per day) more than 3
days per week.
3. Opioids (more than one tablet per day) more than 2 days per
week.
4. Ergotamine use (1 mg orally or 0.5 mg rectally) more than 2
days per week.
Treatment:
 Patients suffering from drug-induced headache can be
difficult to treat, often exhibiting depression, low frustration
tolerance, and physical and emotional dependency.
 Detoxification may require hospitalization.
Diet and lifestyle:
 Chronobiologic interventions, such as maintaining regular
meal and sleep times and limiting stress.
 Biofeedback, stress management, and cognitive behavior
therapy are effective in migraine and daily headache.
552
Drug Treatment:
Outpatient strategies:
 Two outpatient strategies are advocated to taper the
overused medication;
1) gradually substituting a long-acting NSAID
2) abruptly discontinue the overused drug and either
substitute
an
NSAID
or
use
intramuscular
dihydroergotamine (DHE) or corticosteroids.
 Two recent strategies; 6-day course of prednisone, and low
dosage tizanidine (Sirdalud) in combination with long acting
NSAIDs.
 If high doses of a butalbital-containing analgesic are
abruptly discontinued, low dosage phenobarbital, tapering
from 60 to 15 mg at night for 1 week, should be given.
 Naproxen sodium (Naprosyn), 550 mg orally twice per day
for 1 week and 1 extra tablet daily, may be given as needed;
after 1 week, its use should be decreased by 1 day per week
until the patient is using the drug only 3 days per week.
 Supplemented naproxen with low dosage tizanidine (average
dosage 3.6 mg for every hour of sleep) reported a 68%
response rate.
 Alternatively, prednisone (60 mg per day for 2 days, 40 mg
orally for 2 days, then 20 mg orally for 2 days) is given at
the time of abrupt detoxification.
Rescue medications:
 Opioids may be appropriate rescue medications for patients
with episodic migraine; however, they are contraindicated
when detoxifying a patient who is overusing medication.
 Neuroleptics and antinauseants are frequently used.
553
Outpatient transitional medicine strategies:
Naproxen, prednisone, and tizanidine:
 Naproxen (Naprosyn) 500 mg by mouth twice per day or
naproxen sodium 550 mg twice per day for 7 days then as
required, or prednisone (Hostacortin) 60 mg per day for 2
days, 40 mg orally for 2 days, then 20 mg orally for 2 days.
 Naproxen sodium may be supplemented by tizanidine
(Siradalud) 2 to 6 mg by mouth for every hour of sleep.
Inpatient strategies:
Repetitive intravenous steroids:
 Solu-Medrol 100 to 200 mg intravenously every 12 hours for
3 days.
Repetitive neuroleptics:
 Prochlorperazine (Compazine) at 25 mg administered
rectally every 6 hours as required; 5 to 10 mg
intramuscularly or intravenously every 8 hours;
chlorpromazine (Neurazine) 25 mg orally every hour as
required, maximum of 5 dosages per day. 12.5 to 25 mg
intravenously after 250 cc saline bolus, and droperidol 1.25
to 2.5 mg intravenously every 6 hours or 1.25 to 2.5 mg
intravenously every hour with a maximum of 10 mg per 24
hours.
Dihydroergotamine:
 Following 10 mg of intravenous metoclopramide
(Primperan), DHE at 0.5 mg is administered intravenously.
Subsequent dosages are adjusted based on pain relief and
side effects. Most patients eventually take DHE 1.0 mg
intravenously every 8 hours.
554
Repetitive intravenous valproate:
 Intravenous valproate (Depakine) 500 mg every 8 hours was
as effective as DHE and metoclopramide (in this case 0.5 mg
of DHE with 5 mg metoclopramide (Primperan) every 6
hours) with few side effects.
Infusion center treatment:
 Many treatments that used to be given only in an inpatient
setting are now being administered in outpatient infusion
centers, after which patients are sent home.
Emerging therapies:
Intravenous propofol:
 Propofol (Diprivan) 20 to 30 mg intravenous push, repeat
every 5 minutes based on patient alertness, blood pressure,
and respiration.
 The average dosage in a published outpatient study was 110
mg.
Physical therapy and exercise:
 Exercise is effective as a migraine preventive, although it
has little role in the acute treatment of analgesic overuse
headache.
 Physical therapy may be useful in patients with muscular
neck pain or jaw pain.
Pediatric considerations:
 Children and adolescents may develop drug overuse
headache.
 Children are given low dosages of intravenous DHE (0.1 to
0.5 mg intravenously every 8 hours).
555
MENESTRUAL MIGRAINE

Half of women with migraine report that menstruation is an
important trigger of headache episodes.
 Abnormal CNS response to normal fluctuations in hormones
is the likely underlying cause of menstrual migraine.
 Abortive therapy works well for menstrual-related migraine
attacks.
 For women with refractory menstrual migraine, hormonal
therapy can be tried.
Diagnostic criteria for migraine headache without aura
A. At least five attacks fulfilling criteria B through D.
B. Headache lasts 4 to 72 hours (untreated or unsuccessfully
treated).
C. Headache has 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 physical
activity.
D. During headache, at least one of the following occurs:
1. Nausea or vomiting.
2. Photophobia and phonophobia.
E. At least one of the following is present:
1. History or physical or neurologic examinations do no
suggest an organic disorder
2. History or physical or neurologic examinations do suggest
an organic disorder, but it is ruled out by appropriate
investigations.
3. Such a disorder is present, but migraine attacks do not
occur for the first time in close temporal relation to it.
556
Diagnostic criteria for migraine headache with aura
A. At least two attacks fulfilling criterion B.
B. At least three of the following characteristics are present:
1. One or more fully reversible aura symptoms occur,
indication brain dysfunction.
2. At least one aura symptom develops gradually over more
than 4 minutes; two or more symptoms occur in
succession.
3. No single aura symptom lasts more than 60 minutes.
4. Headache follows aura with a free interval of less than 60
minutes (may also begin before or simultaneously with
the aura).
C. History, physical examination, and, where appropriate,
diagnostic tests exclude a secondary cause.
Treatment:
Diet and lifestyle:
 Dietary and lifestyle factors are frequently mentioned as
possible triggers for migraine headaches.
 Regular and adequate amounts of sleep, avoidance of
excessive stress or tension, and regular meals are all
beneficial in generic migraine.
 Biofeedback-assisted relaxation training has been shown to
be helpful in migraine and is useful both in modifying acute
attacks and in preventing future attacks.
Drug Treatment:
Abortive therapy:
 The majority of patients with menstrual associated migraine
will do well with abortive therapy only.
 The triptans are highly preferred for first-line therapy.
 Nonspecific therapies, especially those containing
barbiturates or caffeine, are a frequent cause of rebound
(analgesic-induced) headaches.
557

Because they cause constriction of coronary arteries, triptans
and ergotamine compounds are recommended for use only
in those patients who do not have evidence of or risk factors
for coronary artery disease.
Nonspecific over-the-counter (OTC) medications:
Aspirin,
ibuprofen,
naproxen
sodium,
and
aspirin/acetaminophen/caffeine:
 Aspirin at 500 to 650 mg every 4 to 6 hours. Ibuprofen
(Brufen) at 400 mg every 4 to 6 hours. Naproxen sodium at
500 mg every 4 to 6 hours. Aspirin/acetaminophen/ caffeine
(AAC) at 2 tablets every 6 hours.
Butalbitoal-containing products:
 Two tablets every 4 to 6 hours.
Triptan:
 Sumatriptan (Imigran) autoinjector at 6 mg administered via
subcutaneous injection every 2 hours--maximum of two
injections per day.
 Sumatriptan (Imigran) nasal spray at 20 mg sprayed in one
nostril, and may be repeated after 2 hours--maximum of two
sprays per day.
 Sumatriptan (Imigran) tablet at 50 mg starting dose every 2
hours--maximum of 200 mg per day (some patients will
prefer a 100 mg dose).
 Zolmitriptan (Zomig) tablets at 2.5 mg every 2 hours-maximum of 10 mg per day.
 Rizatriptan (Maxalt) tablet at 10 mg every 2 hours-maximum of 30 mg per day. Reduce dosage to 5 mg
(maximum of 15 mg per day) for patients on propranolol
(Inderal).
 Naratriptan (Naramig) tablet at 2.5 mg every 2 hours-maximum of 5 mg per day.
558
Short-term scheduled prophylaxis of anticipated attacks (miniprophylaxis):
Perimenstrual use of NSAIDs: naproxen sodium and fluriprofen:
 For naproxen sodium (Naprosyn), a dosage of 550 mg orally
twice per day appears to be optimal. Flurbiprofen 100 mg
orally three times per day is also often employed.
Danazol:
 This drug suppresses the pituitary-ovarian axis; 200 to 600
mg per day as studied in late luteal phase dysphoric disorder
(LLPDD).
Tamoxifen (Tamofen)
 5 to 15 mg per day for the last 7 days of the luteal phase.
Bromocriptine (Parlodel)
 2.5 mg three times per day continuously as studied in an
open-label trial.
Continuous oral contraceptive regimens:
 One tablet per day—skipping the pill-free week.
Mini-prophylaxis with triptans:
 Sumatriptan (Imigran) at 25 mg three times per day.
 Naratriptan (Naramig) at 1 mg orally twice per day for 5
days perimenstrually.
Short-term estrogen supplementation:
 Estrogen patch at 100 g
Ergot and derivatives:
 Ergotamine tartrate at 1 mg at the hour of sleep or three
times daily for 5 days perimenstrually.
 Dihydroergotamine, for prevention of menstrual migraine.
Magnesium and vitamin therapy:
 360 mg of magnesium prolidone carboxylic acid.
559
Interventional procedures:
 Treatment with oophorectomy causing abrupt surgical
menopause may worsen migraine.
 The use of continuous estrogen replacement postoperatively
may alone account for many reported responses to
oophorectomy.
 Trials of medical oophorectomy using gonadotropin
releasing hormone analogues are underway.
560