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170 Chi Tim HUNG, Steven H.S. WONG
seizure, mania or anxiety. Monitoring of serum
level would be advisable at intervals to keep within
the antiepileptic dose range, although some authors
found this not useful [15]. All these preparations
are contraindicated in pregnant women or those
contemplating pregnancy, unless contraceptives are
taken concurrently, because of possible neural tube
defects. Rarely, liver dysfunction may occur and
regular monitoring of liver function is necessary.
Other adverse effects include nausea, alopecia,
tremor and weight gain.
Besides valproate, newer anticonvulsants found
to be effective for migraine prophylaxis include
gabapentin and topiramate. Gabapentin (1800–
2400 mg daily) was found to be superior to placebo
in a double-blind study [62]. Topiramate (100–200
mg daily) was proven to be effective in migraine
prophylaxis in two large placebo-controlled, dose-
ranging trials [95, 11].
Antidepressants
Amitriptyline is useful in migraine prophylaxis,
especially when associated with tension-type
headache. e mechanism is probably through
modulation of neurotransmitter release. e use of a
sub-depressant dosage is good enough. Drowsiness
is a major drawback and affects drug compliance.
e drug can be started in a small dose such as 10
to 12.5 mg at night followed by a gradual increase
over the next few weeks. Tolerance to drowsiness
usually occurs after a week. e selective serotonin
reuptake inhibitors like fluoxetine have also been
found to be useful for prophylaxis.
Nortriptyline and dothepin can be tried if patients
cannot tolerate amitriptyline. e use of tricyclics
in elderly patients should be made with caution
because of the anticholinergic side effects.
Methysergide
Methysergide is the most effective prophylactic
agent for migraine because of the 5HT
2
receptor
antagonist effect. In view of the well-known
complication of retroperitoneal fibrosis, it is
reserved for prophylaxis of severe recurrent
migraine when all other medications and therapies
have failed. It is contraindicated in hypertension,
cardiopulmonary disease, liver disease, and kidney
and collagen diseases. It should not be used for
more than 6 months without a break in treatment
of 1 to 2 months to prevent retroperitoneal fibrosis
[76]. For those who have received treatment for
6 months or longer, periodic auscultation of the
heart, chest X-ray, CT or MRI of the abdomen
and urinalysis should be performed. e other
serotonin antagonist, cyproheptadine, is also useful
as prophylaxis. It is commonly used in children and
causes weight gain. Side effects are less serious than
with methysergide.
Non-steroidal anti-inammatory drugs
Apart from being useful for aborting migraine,
NSAIDs are useful as prophylactic agents. Naproxen
has been found to be very useful especially for
preventing premenstrual attacks. Indomethacin
has been found to be very effective for some daily
headache syndromes. e NSAIDs can cause
gastrointestinal and renal side effects. Gastric
protection should be considered when prescribing
these agents as a prophylaxis. e prostaglandin
analogue misoprostol is useful for protection.
Because of the potential to induce abortion,
misoprostol has to be used with caution in any
woman who has the potential to become pregnant.
Miscellaneous medications
Some of the monoamine oxidase inhibitors like
phenelzine or pizotyline have also been found to be
effective. ey are reserved until other treatments
fail. Botulinium toxin type A (Botox) has been tried
for migraine treatment. An open-label study found
it to be an effective, well-tolerated treatment for
migraine [7]. In a double-blind vehicle-controlled
study, pericranial injection of botulinium toxin type
A was shown to reduce the frequency and severity
of migraine attacks [93]. Further large-scale studies
are needed to define the role of botulinium toxin in
migraine treatment.
Role of regional blocks in
migraine
e role of regional blocks for migraine is limited. e
procedure can be tried when all methods have failed.
is is also a good time to review the diagnosis of
migraine. Trigger point injections and various nerve
blocks have been tried. Trigger point inactivation
by dry needling of the neck region was shown in
a randomised placebo-controlled trial involving
85 patients to be of similar efficacy to metoprolol
in the prophylactic treatment of migraine [41]. In
another uncontrolled series, therapeutic blockade
of the greater occipital or supraorbital nerves using
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Headache 171
0.5 to 1 ml of 0.5% bupivacaine repeatedly on
alternate days was shown to improve the pain in
85% of patients. ese patients had failed multiple
drug combinations before the injections [17].
Although the trigeminovascular system is involved
in the pathogenesis of migraine, the place of
various nerve blocks including trigeminal ganglion
blocks in true migraine is undetermined. Further
randomised trials are needed.
Cluster Headache
Clinical features
Cluster headache is not as frequently encountered
as migraine, but it is often confused with migraine.
In contrast to migraine (Table 10.03), cluster
headache affects males more than females with
onset in the late 20s [60]. It can, however, affect
any age group. e diagnosis of cluster headache
is exclusively clinical. Explicit diagnostic criteria
have been laid down in the revised version of the
International Classification of Headache Disorders
(Table 10.08) [65, 16].
e typical feature is the clustering. Cluster refers
to the periodicity of the attacks, which may occur
every day or a few times a day. ere should be
long stretches of time in a year when the patient
is completely pain free. e regularity of headache
may be very pronounced in some individuals,
recurring at the same time each day and commonly
occurring at night. For nocturnal cluster headache,
the pain usually comes 90 minutes after the onset of
sleep, coinciding with the first rapid eye movement
(REM) phase. It can occur in the non-REM phase.
Oxygen desaturation associated with partial airway
obstruction at sleep can precede the headache,
leading to the hypothesis of hypoxaemia as a factor
in pathogenesis. e attacks occur about one to
three times each day. e headache is unilateral;
bilateral pain is uncommon, occurring in 6% of
cases [60]. e pain is intense; it peaks in about
10 to 15 minutes and lasts 15 minutes to 3 hours.
A prolonged headache is not common. e pain
is described as non-throbbing, excruciating and
penetrating. It is commonly felt in the region of the
trigeminal innervation and hence can be confused
with other facial pains such as trigeminal neuralgia.
Sometimes the pain may be confined to the
maxillary region and is called lower-half headache.
Pain may also be felt in the extratrigeminal area
(18%). In the majority (78%) of patients, the site
and side of the pain remains unchanged. During
an attack, the carotid artery, but not the temporal
artery, may be tender to palpation.
Another characteristic, not shared by other types
of headache, is the presence of autonomic features
during an attack. ese are thought to be due to
sympathetic paresis or parasympathetic overactivity
and consist of ipsilateral lacrimation, conjunctival
injection, nasal stuffiness and rhinorrhoea. Ptosis
and miosis can occur and should be looked for.
Ptosis may become permanent after repeated attacks
(6%) [60]. e scalp and face may also become
tender. Nausea or vomiting does not occur.
e facial features of patients suffering from
cluster headache are characteristic and have been
described as giving a “lionine facial appearance”
[34]. ese patients typically have a ruddy
complexion with deep furrows on the face, vertical
headache creases, asymmetric facial crease, orange
peel facial skin, nasal telangiectasia, and a broad
chin and skull. ey are generally tall and rugged
looking. ese patients tend to continue work
despite the frequent headache and may be heavy
smokers and drinkers.
Table 10.08 IHS diagnostic criteria for cluster
headache [38]
Diagnostic criteria
A At least five attacks fulfilling criteria B–D
B Severe or very severe unilateral orbital,
supraorbital, and/or temporal pain that lasts
15–180 min if untreated
C Headache is accompanied by at least one of
the following:
1. Ipsilateral conjunctival injection and/or
lacrimation
2. Ipsilateral nasal congestion and/or
rhinorrhoea
3. Ipsilateral eyelid oedema
4. Ipsilateral forehead and facial sweating
5. Ipsilateral miosis and/or ptosis
6. A sense of restlessness or agitation
D Attacks have a frequency from one every other
day to eight per day
E Not attributed to any other disorder
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172 Chi Tim HUNG, Steven H.S. WONG
e preceding description refers to the episodic
cluster headache. ere is a variant where the
clustering is less obvious and headache occurs
every day at roughly the same time. is is
chronic cluster headache. Other variants include
the chronic paroxysmal hemicrania (CPH) and
similar disorders like cluster-tic syndrome, cluster-
vertigo and cluster-migraine. In contrast to cluster
headache, CPH is seen mostly in women. e
distinguishing feature lies in the short duration
of each attack, lasting 5 to 10 minutes, but the
attacks occur five to 20 times per day. e response
to indomethacin is dramatic. Indomethacin may
act via inhibition of the neurogenic inflammation.
It may also reduce cerebral blood flow through
vasoconstriction.
Apart from CPH, migraine, cervicogenic headache,
temporal arteritis, trigeminal neuralgia and
postherpetic neuralgia, brain tumours must be
distinguished from cluster headache [73]. Applying
pressure at the trigger areas in the suboccipital
region can reproduce cervicogenic headache. Such
features are lacking in cluster headache, unless
they occur together. Temporal arteritis usually
occurs in older patients with malaise, myalgia, an
inflamed temporal artery and a high erythrocyte
sedimentation rate. e eye signs of cluster
headache are unique and if present would make
diagnosis much easier.
Pathogenesis
As with migraine, cluster headache has a neurogenic
element. e trigeminal nerve and the trigeminal
vascular system are involved. e site of pain
correlates with the ophthalmic and maxillary
divisions of the trigeminal nerve. Unlike migraine,
surgical treatment of the trigeminal nerve by
radiofrequency thermocoagulation may bring about
pain relief. is demonstrates the involvement of
the trigeminal nerve. A more complicated neural
network involving the Vth, VIIth, IXth and Xth
cranial nerves is likely. e multiple sources of
sensory input mean that reduction of input from
any of these sources may bring about temporary
relief of pain. Procedures such as sphenopalatine
ganglion injection, occipital nerve injection or
intervention on the trigeminal nerve have been
found to be useful.
e cluster pattern may imply a dysfunction of
the clock mechanism in the hypothalamus where
activation of both the anterior and posterior
hypothalamus is necessary to explain the symptoms.
Hypoxaemia seems to be another important factor
in the genesis of pain. It is hypothesised that the
chemoreceptors of the carotid bodies may be
dysfunctional in cluster headache patients during
cluster periods [45].
Management
In contrast to migraine, the acute attacks of cluster
headache are fairly short lived and frequent. e
headache may have subsided before drugs can take
effect. Also large doses of drugs may be needed in
order to abort every attack. Prophylactic treatment
therefore is more important than abortive
treatment.
Abortive treatment is, however, useful for attacks
that are of longer duration. Oxygen inhalation
6–7 litres/minute for 15 minutes at the onset of
headache will abort the attack in 75% of patients
[103] and if pain recurs repeated inhalation will be
useful. Otherwise the 5HT
1
agonists ergotamine
[103], dihydroergtamine and sumatriptan [75]
can be used. For sumatriptan, the subcutaneous
route in a dose of 6 mg is preferred for its fast
onset. Dexamethasone in a dose of 8 mg can also
relieve the pain. Local anaesthetic blocks using 4%
lignocaine intranasally have been reported to be
useful 44, 80]. Strong opioid is not advised because
attacks are short lived and frequent.
Prophylactic treatment should be instituted
whenever the patient is within the cluster period.
Drugs have to be continued until the headaches
are completely absent for at least 2 weeks and then
tapered [60]. When the patient goes into the next
cluster period, medication has to be restarted again.
Due consideration should be given when choosing
the particular drug.
Calcium channel blockers have been advocated to
be the first-line prophylactic treatment. ey act
via inhibiting calcium dependent smooth muscle
contraction and the neuronal release of serotonin.
Verapamil is commonly employed in a dose of 360–
480 mg daily (120 mg 3 to 4 times daily). Adverse
effects include constipation and water retention.
Lithium in a dose of 600–900 mg daily is effective.
e effectiveness will be known within a week.
Blood levels have to be monitored closely to
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Headache 173
avoid toxicity (normal range 0.6–1.2 mmol/L).
Patients must maintain a normal salt diet because
hyponatraemia can increase lithium toxicity. e
effectiveness may decrease with prolonged use and
sometimes transforms chronic cluster headache into
episodic cluster headache. Concurrent ergotamine
or verapamil may be needed to maintain a pain free
state. is double or triple therapy will be useful
for difficult headaches. A combination of lithium
with verapamil is the most effective treatment for
chronic cluster headache. Adverse effects include
tremor, which responds to propanolol, and thyroid
dysfunction. Neurotoxicity is a sign of frank toxicity
and presents with confusion, ataxia and cerebellar
signs.
e role of methysergide is more established for
young episodic cluster headache sufferers. It is
probably less effective for the chronic form. e
safety rule for use of methysergide deliberated
previously still applies. e drug should never be
given in doses of more than 6 mg.
In contrast to migraine treatment, the long term use
of ergotamine in prophylaxis of cluster headache
is well justified and will not lead to rebound
headaches. Bedtime use of ergotamine (1 mg) is
useful for nocturnal cluster headache and one to
two doses can be administered daily. Ergotamine
can be combined with verapamil and works best
for episodic cluster headache.
In refractory cluster headaches, prednisone 40 mg
daily in divided doses can be tried. It is important
to keep the duration of steroid treatment as short
as possible, preferably not longer than 3 to 4 weeks.
Headache may recur when the steroid dose is
reduced or terminated.
Among the newer approaches and similar to
migraine prophylaxis, valproate has been tried,
with inconsistent results [39, 26]. Similarly,
several open-label studies have yielded conflicting
results with topiramate [109, 52]. Other drugs
that have been investigated include capsaicin [58],
melatonin [49], methylphenidate [66], baclofen
[40], clonidine [50], eletriptan [112], gabapentin
[48] and botulinum toxin A [27].
Sphenopalatine ganglion blocks using local
anaesthetics like cocaine or lignocaine have been
reported to bring about pain relief in cluster
headache. Occipital nerve injections with lignocaine
and methylpredniosolone can also bring about
remissions for weeks [74].
Neuroablative and intracranial surgical interventions
have also been reported. Neuroablation carries
with it some morbidity and mortality. It should be
considered only when the pain is uncontrollable by
drugs, and when the affected site is strictly unilateral.
A psychological assessment should establish that
the patient is stable without susceptibility to
addiction. Neuroablation of the trigeminal nerve
using radiofrequency or glycerol is the commonest
procedure. Both procedures are safe. To achieve best
results, both the ophthalmic and maxillary branches
have to be lesioned. e cornea may be insensitive
after the procedure and protection of the cornea
must be taken to avoid corneal ulcers. Excellent
results have been obtained in 76% of patients. e
procedure can be repeated for pain recurrence. e
use of radiosurgery using a gamma knife has just
been reported on a few patients [28]; it is too early
to draw conclusions about its role. Intracranial
surgery with resection of the greater petrosal nerve
and nervus intermedius has been reported but
the results are not encouraging. Morbidity and
mortality with craniotomies are great.
Tension-Type Headache
Clinical features
Tension-type headache is highly prevalent and it is
the most common headache type. Again it is divided
into the episodic type and the chronic tension
headache (Table 10.09). In a Danish population-
based study, the lifetime prevalence of tension-type
headache was found to be as high as 69% in men
and 88% in women [78]. In a survey in Baltimore
County [85], the prevalence for episodic tension
headache was 38.3%, with women more commonly
affected than men (1:1.16) in all age groups, race or
education levels. Prevalence peaks in the 30- to 39-
year age group and increases with education levels
in both sexes. About half of those who have received
graduate school education have been afflicted with
the disorder. In contrast, the chronic tension type
headache is much less prevalent (2.2%). Although
females are more affected, prevalence decreases
with increasing education. e chronic type has
a greater societal and individual impact than the
episodic type. ese patients tend to report more
lost working days.
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174 Chi Tim HUNG, Steven H.S. WONG
Table 10.09 IHS diagnostic criteria for tension-
type headache [38]
Diagnostic criteria
TTH
(2.X)
A At least 10 episodes fulfilling criteria
B–E. Number of days/month with such
headache: <1 (episodic infrequent), 1–
14 (episodic frequent), or >15 (chronic)
B Headache lasting from 30 min to 7 days
C At least two of the following pain
characteristics present:
1. Pressing/tightening (nonpulsating)
quality
2. Mild or moderate intensity (may
inhibit, but does not prohibit
activities)
3. Bilateral location
4. No aggravation by walking, stairs or
similar routine physical activity
D Both of the following:
1. No nausea or vomiting (anorexia
may occur)
2. Photophobia and phonophobia are
absent, or one but not both may be
present
E Not attributed to another disorder
TTH
(2.X.1)
Associated with pericranial tenderness
A Fulfils criteria for 2.X
B Increased tenderness on pericranial
manual palpation
TTH
(2.X.2)
Not associated with pericranial
tenderness
A Fulfils criteria for 2.X. Not associated
with increased pericranial tenderness
TTH = tension-type headache; X = the correspondent digit for
infrequent episodic (1), frequent episodic (2), or chronic (3).
e headache is symmetrical and of non-disabling
severity. Vascular features like throbbing, nausea
and photophobia are absent. If laterality of
pain is prominent (10–20%), the diagnosis
of tension headache should be reviewed. In
these circumstances, the headache is probably
accompanied by various vascular phenomena and
the term tension vascular headache should be
applied. Tension-type headache is not associated
with any prodrome or aura. Intensity of pain ranges
from mild to moderate. e character of the pain is
dull and non-throbbing (pulsating in 10%). People
describe the pain as a feeling of tightness, pressure
and constriction (hat-band like). e intensity of
the headache is fairly constant over time and in
some patients, the headache can persist for a long
time. e distribution of the headache is commonly
bifrontal and bioccipital. Sometimes occipital or
suboccipital localisation may occur. During the
attack, the site of pain can change in half of the
subjects. Involvement of the neck is common in
the trapezius and interscapular regions. Tender
spots or sharply localised nodules can be found
in the pericranial muscles and cervical muscles.
ese spots are found significantly more than in
controls even in headache free periods. ere may
be accentuation of pain as the day progresses. e
frequency may be high at times, becoming daily
and continuous.
Tension-type headache and migraine are now
considered as two ends of the benign recurrent
headache spectrum [88, 102]. ey frequently
coexist together. Migraine may start off as a tension-
type headache that gains features of migraine
when it increases in severity. Differentiation may
be difficult when the two exist together. Routine
physical activity aggravates migraine and has no
effect on tension-type headache. In chronic tension-
type headache, the diagnostic criteria are the same
as the episodic type, except nausea is allowed.
Depression may be a prominent feature in chronic
tension headache, which may be the result of the
pain instead of the cause for the headache.
Pathogenesis
Tension-type headache was originally thought to be
due to stress or tension causing sustained contraction
of head muscles leading to tissue ischaemia and
pain. Hence in the past it has been called muscle
contraction headache. Recent studies have cast
doubt on this simple theory. ere is no difference
in the incidence of sustained muscle contraction
in migraine and tension headache sufferers. ere
is also no correlation between muscle contraction,
muscle tenderness and headache [2]. ere is now
evidence that migraine and tension-type headache
share the same pathogenesis because both are
associated with:
• Muscle tenderness
• Abnormal electromyogram
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Headache 175
• Abnormally low platelet serotonin
• Abnormally decreased cerebrospinal fluid
beta-endorphin level.
Tension-type headache is now hypothesised to
be another clinical manifestation of abnormal
neuronal sensitivity that facilitates pain
transmission. It is likely that the cause of tension-
type headache is multifactorial. e peripheral
mechanism is most likely in the episodic tension-
type headache. is involves the sustained muscle
contraction and tissue ischaemia. It can occur in
otherwise normal individuals triggered by physical
stress, such as abnormal posture, or psychological
stress. Central neuronal sensitivity is important
for those with chronic tension-type headache [43].
e nucleus caudalis of the trigeminal complex is
the major relay nucleus for head and neck pain. It
receives nociceptive input from the blood vessels
and pericranial muscles and synapses with various
supraspinal nuclei. A certain group of neurons in
the ventromedulla nucleus is postulated to facilitate
pain transmission. is sensitises the nucleus
caudalis and renders the myofascial nociceptor
hypersensitive. Emotional stress may also reduce
endogenous antinociception mechanisms. e
central sensitisation of nociception and the
decreased activity in antinociceptive systems
result in chronic tension headache. Sensitisation
of the nucleus caudalis hence can result in normal
non-painful stimuli being perceived as painful
producing trigger spots and overlapping symptoms
with migraine.
Management
e peripheral and central mechanisms must be
considered in the treatment. Similarly the treatment
can be divided into psychological, physical and
pharmacological.
A full explanation to the patient allays the anxiety
about the presence of occult disease like brain
tumour. Patients should be made aware of the
importance of the peripheral mechanism of the
headache such as muscle contraction, and that
muscle contraction may be related to posture
or a stress reaction of the patient. Relaxation
techniques can be taught. ese sometimes bring
about good results. Patient compliance to the
relaxation technique is important, emphasising
the importance of adequate explanation and
reassurance. Biofeedback may be useful [71].
e use of drugs depends on the severity and
character of symptoms. If features of vascular
headache predominate, an antimigraine regimen
should be tried. Otherwise simple analgesics such
as aspirin, paracetamol and NSAIDs and muscle
relaxants such as diazepam can be used to abort the
attack. Prophylactic drug treatment in the form of
tricyclic antidepressants such as amitriptyline can
be useful to reduce the number and severity of
attacks.
Physical treatments like TENS, topical heat/cold
therapy or acupuncture have been reported. Trigger
point injections using local anaesthetics or dry
needling can be tried. Because of the varied nature
of the disease, the results are not uniformly in favour
and the attending risks cannot be ignored [9].
Cervicogenic Headache
Abnormalities of the cervical spine have been
reported to produce anterior or posterior headache
[25, 104]. Sjaastad described this as cervicogenic
headache in 1983 [97] and proposed a set of
diagnostic criteria in 1990 [98]. ere is some
dispute as to whether cervicogenic headache is a
real entity, even after the publication of diagnostic
criteria proposed by Sjaastad and by the IASP in
1998 [99] and IHS in 2004 (Table 10.10) [38]. Part
of this controversy is related to the different criteria
employed by different authors. More importantly,
it is sometimes difficult to differentiate it from
other primary headaches. Sometimes tension-
type headache or migraine is incorrectly described
as cervicogenic headache simply because of the
occipital location of the pain.
e syndrome described by Sjaastad [98] includes
unilateral headache without side-shift triggered by
head and neck movements. In contrast to migraine,
the pain starts in the neck and radiates to the head.
ere is significant neck involvement with reduction
in the range of movement of the neck. Pain may be
precipitated by mechanical stimulation and may
radiate diffusely to the ipsilateral arm or shoulder.
ese features are typical in cervicogenic headache
but absent in migraine. ere is no clear-cut criterion
in the literature to differentiate cervicogenic
headache trigger points from myofascial trigger
points. Although the IASP criteria use the positive
response to diagnostic greater occipital nerve
block to differentiate it from primary headache
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176 Chi Tim HUNG, Steven H.S. WONG
Table 10.11 Presentations of aura in migraine
Visual symptoms (most common)
• Negative disorders:
Hemianopsia
Quadrantopsia
Scintillating scotoma
• Positive disorders:
Teichopsia (fortification spectrum)
Photopsia (flickering of light)
Macro/microsomatognosia
Other visual hallucinations
Sensory symptoms
• Numbness starting from hand (unilateral) and
spreading to face and tongue
• Perioral tingling
• Paraesthesia
Auditory symptoms
• Vertigo/tinnitus
• Auditory hallucinations
Olfactory symptoms
• Olfactory hallucinations
Motor symptoms
• Hemiparesis
• Dysarthria
• Dysphasia
Table 10.10 IHS diagnostic criteria for cervicogenic
headache [38]
Diagnostic criteria
A Pain, referred from a source in the neck and
perceived in one or more regions of the head
and/or face, fulfilling criteria C and D
B Clinical, laboratory, and/or imaging evidence
of a disorder or lesion within the cervical
spine or soft tissues of the neck known to
be or generally accepted as a valid cause of
headache
C Evidence that the pain can be attributed to the
neck disorder or lesion based on at least one
of the following conditions:
1. Demonstration of clinical signs that
implicate a source of pain in the neck
2. Abolition of headache after diagnostic
block of a cervical structure or its nerve
supply by use of a placebo or other
adequate control
D Pain resolves within 2 months after successful
treatment of the causative disorder or lesion
disorders, this test is not specific [51]. Radiological
abnormalities of the cervical spine are common in
the elderly and the positive predictive value of such
abnormalities is low. Neck structures definitely
play a role in the pathophysiology of some of these
headaches. However, the clinical patterns indicating
a neck-headache relationship still have not been
adequately defined.
Treatment for headache related to the cervical spine
is symptomatic and geared towards the cervical spine
pathology [8]. Physiotherapy, simple analgesics and
trigger point injections will be of help [9].
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