Tension-type Headache

01Pathophysiology

Tension-type headache is the most common primary headache disorder worldwide, yet its pathophysiology remains less studied compared to migraine. The current understanding divides the mechanism into peripheral and central components, and recognizing this distinction is important because it explains why episodic and chronic forms behave differently.

In episodic TTH, the dominant mechanism is peripheral myofascial nociception. Increased muscle tone and tenderness in the pericranial muscles (temporalis, frontalis, masseter, sternocleidomastoid, and trapezius) generate nociceptive input through stimulation of peripheral pain receptors. This is triggered or worsened by physical and emotional stress, sustained poor posture, and jaw clenching. The pain is transmitted via the trigeminal nerve (V1) and upper cervical nerve roots (C2-C3) to the trigeminocervical complex in the brainstem. Because the nociceptive drive is peripheral and intermittent, the headache is self-limited and mild.

As episodic TTH becomes more frequent, repeated nociceptive bombardment leads to central sensitization. This is the hallmark of the transition to chronic TTH. In this state, second-order neurons in the trigeminal nucleus caudalis become hyperexcitable, meaning that even normal, non-painful stimuli can be interpreted as painful (allodynia). Additionally, there is impaired descending inhibitory pain modulation from supraspinal structures, including the periaqueductal gray (PAG) and the rostral ventromedial medulla. In essence, the brain loses its ability to "turn down" the pain signal. This is why chronic TTH patients have persistent daily headaches even in the absence of ongoing peripheral muscle tension.

An important concept to internalize is that the pericranial tenderness seen on exam directly correlates with headache frequency and intensity. This means the physical exam finding of tender pericranial muscles is not incidental but reflects the underlying pathophysiological driver.

Serotonin and nitric oxide have been implicated in chronic TTH. Reduced platelet serotonin levels and increased nitric oxide contribute to central sensitization and lowered pain thresholds. This explains the rationale for using tricyclic antidepressants (amitriptyline), which modulate serotonergic pathways, as first-line prophylaxis in chronic TTH.

02Classification and Clinical Manifestation

The International Classification of Headache Disorders, 3rd edition (ICHD-3) classifies TTH based on frequency of headache days. Each subtype can occur with or without pericranial tenderness.

by Frequency

Core Diagnostic Features

A crucial exam point: the moment you see pulsating quality, unilateral location, worsened by physical activity, nausea/vomiting, and BOTH photophobia and phonophobia, you are looking at migraine, not TTH.

03Diagnostic Workup

TTH is a clinical diagnosis. There is no laboratory test or imaging study that confirms it. The diagnosis is made by applying the ICHD-3 criteria to the patient's history and ensuring the neurological examination is completely normal.

The best initial test is a thorough history focused on headache character, location, intensity, duration, frequency, aggravating/alleviating factors, and associated symptoms. Physical examination should include palpation of the pericranial muscles bilaterally. Tenderness on palpation is the single most reproducible objective finding in TTH.

Neuroimaging (CT or MRI) is NOT indicated for patients who meet the criteria for TTH and have a normal neurological exam. Ordering imaging in this scenario is a common exam distractor. Neuroimaging is reserved only for the presence of red flags (mnemonic: SNOOP):

If a vignette presents a typical TTH with no red flags and asks for the "next best step," the answer is reassurance and treatment, not imaging. This is a commonly tested principle.

04Management and Treatment

Acute Management

For infrequent and frequent episodic TTH, simple analgesics are the mainstay. NSAIDs (ibuprofen, naproxen, aspirin) are preferred over acetaminophen due to superior evidence. Acetaminophen is an alternative when NSAIDs are contraindicated (peptic ulcer disease, renal insufficiency, aspirin-exacerbated respiratory disease).

A critical exam principle: triptans are NOT indicated for TTH. Triptans are serotonin 5-HT1B/1D receptor agonists that target the trigeminovascular mechanism of migraine. Since TTH does not involve trigeminovascular activation or meningeal vasodilation, triptans have no role. If a vignette describes a classic TTH and offers triptans as an answer choice, it is a distractor.

Opioids and barbiturate-containing combination analgesics (butalbital) should be avoided. They carry high risk of dependence and are the leading causes of medication overuse headache (MOH).

Medication Overuse Headache Prevention

This is one of the most tested concepts surrounding TTH management. Analgesic use must be limited to:

• Simple analgesics (NSAIDs, acetaminophen): no more than 15 days per month

• Combination analgesics, triptans, opioids: no more than 10 days per month

If a patient with episodic TTH develops a pattern of daily or near-daily headache with escalating analgesic use, medication overuse headache must be suspected and the offending agent must be withdrawn.

Prophylactic Management

Prophylaxis is indicated when headache frequency reaches the chronic threshold ($\ge \backslash geq$ 15 days/month) or when episodic TTH is frequent enough to cause significant disability or risk of medication overuse.

Amitriptyline is the first-line prophylactic agent. It works by inhibiting serotonin and norepinephrine reuptake, thereby enhancing descending inhibitory pain modulation. The starting dose is 10 to 25 mg at bedtime, titrated upward every 1 to 2 weeks as tolerated. The therapeutic dose is typically 25 to 75 mg/day. A minimum trial of 4 to 6 weeks at therapeutic dose is required before judging efficacy. Common side effects include sedation, dry mouth, constipation, and weight gain. It is contraindicated in patients with cardiac conduction abnormalities (obtain a baseline ECG in older adults).

If amitriptyline is not tolerated, nortriptyline (less sedating, less anticholinergic) or mirtazapine are alternatives. Venlafaxine (an SNRI) is another second-line option, particularly useful when comorbid depression is present.

Non-Pharmacologic Therapy

Non-pharmacologic approaches are first-line for infrequent episodic TTH and adjunctive for all other subtypes. EMG biofeedback has the strongest evidence and works by training patients to reduce pericranial muscle tension. Cognitive behavioral therapy (CBT) targets the stress and maladaptive pain behaviors that perpetuate the headache cycle. Physical therapy with focus on posture correction and cervical/shoulder stretching is also beneficial.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common trap in TTH questions is confusing it with migraine. Test writers deliberately craft vignettes where the headache is bilateral and the patient does not appear severely ill, tempting students to choose "migraine" based on superficial pattern recognition. The discriminating features to look for are: TTH is non-pulsating, not worsened by activity, and lacks nausea/vomiting. If the vignette includes any combination of pulsating quality, unilateral location, nausea, or activity-worsening, you are being directed toward migraine.

A second common trap is the next-best-step question for a typical TTH without red flags. Students frequently choose "order MRI brain" because the question stem describes a headache, and headache triggers an instinct to image. The correct answer is to treat with an NSAID and reassure. Imaging is only warranted when red flags are present, and the absence of red flags is the entire point of the question.

The third trap involves chronic TTH and medication overuse. A vignette will describe a patient whose episodic headaches have become daily, and who is now taking ibuprofen every day. Students may choose "start amitriptyline" or "switch to a stronger analgesic." The correct answer is to identify and withdraw the overused medication first, because prophylaxis will fail if MOH is not addressed.

Finally, remember that triptans are never correct for TTH. If a classic TTH vignette offers sumatriptan as an option, it is always a distractor. Triptans target the trigeminovascular mechanism of migraine and have no efficacy in TTH.

The core competency being tested in TTH questions is the ability to distinguish primary headache disorders from each other and from secondary causes based on pattern recognition of headache quality, associated features, and physical exam findings, and then to match the correct treatment to the correct diagnosis without reflexively ordering unnecessary workup.