Section 5 Headaches and Facial Pain
Chapter
Patients with tension headaches
43 Natacha Telusca, Chrystina Jeter, and Kingsuk Ganguly
Case study
A 35-year-old female with past medical history signifi-
cant for anxiety and depression presents with complaints
of headaches that have been worsening for over 3 years.
She reports that the pain starts in the back of her neck
and moves to the forehead. The pain is described as a
tightening band around her forehead. The characteristic
of the pain has been the same over the years, but the
frequency has increased. She does not have any associ-
ated symptoms such as nausea, vomiting, blurry vision,
photophobia, or photophonia. She is single and works as
an attorney at a prestigious law firm. She uses aspirin
and Tylenol, which provide some relief.
1. What is the differential diagnosis?
 Tension-type headache
Occipital neuralgia

 Headache, migraine
 Headache, cluster
 Sinusitis
 Meningitis
 Trigeminal neuralgia
2. What is the epidemiology of these
headaches?
Headache is a major public health problem affecting a
large segment of the world population. The patient in
the above case study is likely suffering from a tension-
type headache (TTH), which is the most prevalent type
of headache.[1] A Danish population-based study
reported that the overall prevalence of TTH
is 79–87%, and 2–5% for chronic TTH (CTTH).[2]
TTH is slightly less common in men then women with
a male to female ratio of 4:5.[3] Some of the reported
Case Studies in Pain Management, ed. Alan David Kaye and Rinoo V. Shah. Published by Cambridge University Press.
© Cambridge University Press 2015.
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risk factors for developing TTH include poor self-rated
health, inability to relax after work, and poor sleeping
patterns.[3,4] The reported average age of onset of
TTH is 25–30.[3] The global societal burden of TTH
is substantial and greater than that of migraine.[1]
Despite the high socioeconomic burden, TTH is the
least studied of the primary headaches.[5]
The second edition of the International Classifica-
tion of Headache Disorders (ICHD) classified TTH into
three main subtypes: infrequent episodic TTH, frequent
episodic TTH, and chronic episodic TTH.[5] The cri-
teria for infrequent TTH headache are episodes less
than 1 day a month. Frequent episodic TTH is defined
as at least 10 episodes occurring on 1 to 14 days per
month. Chronic episodic TTH is described as having
more headaches occurring on more than 15 days per
month. Frequent TTH does not have significant impact
on the individual, and chronic TTH has major impact
on quality of life.[5]
3. Describe the clinical presentation
In comparison to all of the primary headaches, TTH
has the least features, which makes the diagnosis one
of exclusion.[3] Patients with TTH typically present
with bilateral, pressing, or tightening pain.[6] The
pain is usually mild to moderate in intensity and is
not aggravated by routine physical activity; patients
usually do not have nausea, severe photophobia, or
phonophobia.[6] A detailed history, general physical,
and neurologic exam are important to make the cor-
rect diagnosis. In addition to the general history and
physical exam, a 4- to 6-week headache diary is a very
useful tool that can help the clinician to ensure the
correct diagnosis of TTH.[7] The diary can also help
differentiate between mild migraines and TTH.[8]
Furthermore, the diary helps to identify triggers and
 Chapter 43: Patients with tension headaches

high intake of analgesics.[8] The general and neuro- 5. Treatment

logic physical exam is typically normal. Brain imaging
The management of TTH involves non-
is required if the clinical picture is unclear and sec-
pharmacological treatments, pharmacologic treat-
ondary causes are suspected.[3]
ments, and invasive procedures. Patients with chronic
TTH often have associated psychosocial factors such
4. What is the pathophysiology of as stress, anxiety, and depression that can aggravate
tension-type headache? their pain,[9] therefore it is vital to identify and
treat significant comorbidities concurrently.[8] Non-
TTH has a very complex mechanism, which is not
pharmacologic managements are commonly used and
fully understood. Many factors may contribute to the
encouraged as part of the treatment for TTH; however
development of TTH including genetic predisposition,
the evidence for the efficacy of many of the treatments
environmental, psychological, peripheral, and central
is lacking.[8] Some of the common modalities include
factors.[9] There is a clear relationship between TTH
electromyography (EMG) biofeedback, CBT, relax-
and psychologic distress and poor coping skills.[10]
ation training, and acupuncture. A recent review by
Patients with frequent TTH tend to have higher rates
Sun-Edelstein and Mauskop concluded that EMG
of anxiety and depression.[10] A study by Janke et al
biofeedback (BFB) is effective in the treatment of
showed that depression increases susceptibility to
TTH, and CBT and relaxation training may have
TTH following laboratory stress, and was correlated
some benefits.[18] Stress management therapy,
with increased paracranial muscle tenderness.[11] In
including relaxation and cognitive coping skills, is a
patients with frequent headaches, depression could
modestly effective treatment for TTH.[19]
exacerbate central sensitization increasing vulnerability
Acupuncture is used in the prophylactic treatment
to TTH.[11]
for TTH; however there is lack of evidence for its
Peripheral factors have been studied and shown to
efficacy. A Cochrane review by Linde et al including
have an association with TTH. Patients with TTH
11 trials with 2317 participants concluded that there is
tend to have increased pericranial muscle tenderness
insufficient evidence to support the use of acupunc-
and myofascial trigger points,[12] and there is a posi-
ture in the treatment of TTH.[20]
tive correlation with the increased tenderness and the
Interventional treatments that are used in the treat-
intensity and frequency of TTH.[13] Fernández-de-
ment of TTH include cervical epidural steroid injec-
las-Peñas et al reported that patients with chronic
tion, occipital nerve blocks, and upper cervical facet
TTH have increased pericranial muscle tenderness
injections. There are limited studies to support the
and decreased pressure pain thresholds in compari-
effectiveness of these procedures. However, these pro-
son to healthy controls.[14]
cedures are relatively safe and provide an integral part
Though the exact mechanism of increased tender-
of multimodal care by attempting to target the pain
ness is not fully understood, there are several proposed
generator. Occipital and supraorbital nerve stimulation
mechanisms including sensitization of peripheral myo-
play a role in occipital neuralgia and migraines.
fascial nociceptors, sensitization of second-order neuron
Similarly, these neuromodulatory procedures may be
at the level of the spinal dorsal horn/trigeminal nucleus,
beneficial in chronic TTH that is refractory to more
sensitization of supraspinal neurons, and decreased anti-
conservative treatments. A study by Leinisch-Dahlke
nociceptive activity from supraspinal structures.[15]
found that occipital nerve blockage is not an effective
Central sensitization due to recurrent stimuli from
treatment for TTH.[21]
pericranial muscle tissues may play a role in the conver-
The two most common analgesics used in the acute
sion of episodic to chronic TTH.[12] Buchgreitz et al
treatment of TTH are acetaminophen and aspirin.[22]
showed that there is a close relation between altered pain
Randomized controlled studies have shown that
perception and chronification of headache.[13]
500 and 1000 mg aspirin,[22] 1000 mg of acetamino-
Patients with chronic TTH have an increased
phen,[22,23] and 375 mg of Naproxen[23] are effective
number of active trigger points in the suboccipital
treatments for acute TTH. Preventive treatment should
muscles, and in the upper trapezius, sternocleidomas-
be considered in patients with CTTH. Tricyclic
toid and temporalis muscles,[16] higher headache
antidepressants have been shown to be an effective
intensity, and longer headache duration than those
prophylactic treatment. Amitriptyline has been shown
with latent trigger points.[17]

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 Chapter 43: Patients with tension headaches

Table 43.1 Acute therapy of tension-type headache; Bendtsen et al recommended the following drugs for acute therapy of tension-type
headache[3]

Treatment Dose Remark

Ibuprofen 200–800 mg Gastrointestinal side effects, risk of bleeding
Ketoprofen 25 mg Same side effects as for ibuprofen
Aspirin 500–1000 mg Same side effects as for ibuprofen
Naproxen 375–550 mg Same side effects as for ibuprofen
Diclofenac 12.5–100 mg Same side effects as for ibuprofen, only doses 12.5–25 mg tested in TTH
Paracetamol 1000 mg (oral) Less risk of gastrointestinal side effects as compared with NSAIDs
Caffeine comb. 65–200 mg See below*
* “Combination with caffeine 65–200 mg increases the efficacy of ibuprofen and paracetamol but possibly also increases the risk for
developing medication overuse headaches.”[3]

to decrease the frequency and duration of headache,

Table 43.2 Drugs for prophylactic therapy of tension-type
headache; Bendtsen et al. recommended the following drugs
and intake of analgesics.[24] A randomized placebo-
for prophylactic therapy of tension-type headache[3] controlled trial by Holroyd et al comparing amitriptyl-
ine and nortriptyline showed that combined therapy of
Treatment Daily dose antidepressant medication and stress management
Drug of first choice provide good outcome relative to single therapy.[19]
Amitriptyline 30–75 mg
Drugs of second choice
Mirtazapine 30 mg
6. Conclusion
Venlafaxine 150 mg
TTH is a common problem affecting a large segment
of the population. The pathophysiology is not fully
Drugs of third choice understood. A detailed history, general physical and
Clomipramine 75–150 mg neurologic exam, and headache diary are essential to
Maprotiline 75 mg
ensure the correct diagnosis. Tables 43.1 and 43.2 can
Mianserin 30–60 mg
be used to guide treatment.

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