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Summary Table

Domain	Detail
Risk Factors	Female sex, psychological stress, anxiety/depression, poor posture, sleep deprivation, excessive screen time, jaw clenching
Etiology	Peripheral myofascial nociception (episodic form) progressing to central sensitization (chronic form); no single structural lesion
Patient Presentation	Bilateral, band-like or pressure-type headache of mild-to-moderate intensity; patient can usually continue daily activities; no nausea or vomiting
Classic Physical Exam	Pericranial muscle tenderness on palpation (temporalis, masseter, sternocleidomastoid, trapezius); normal neurological exam; no papilledema
Key Diagnostic Results	Entirely clinical diagnosis using ICHD-3 criteria; no labs or imaging needed in the absence of red flags; neuroimaging is normal when obtained
Management	Acute: NSAIDs or acetaminophen. Prophylactic (chronic form): amitriptyline. Non-pharmacologic: stress management, physical therapy, biofeedback
Keywords	"Band-like," "pressing/tightening quality," "bilateral," "non-pulsating," "not worsened by physical activity," "no nausea or vomiting"

1. Pathophysiology

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.

2. Classification 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

Subtype	Frequency Criteria	Clinical Features
Infrequent Episodic TTH	< 1 day/month (< 12 days/year)	Mild bilateral pressing headache, short duration (30 min to 7 days), no nausea, no vomiting; photophobia OR phonophobia may be present (but not both); rarely requires medical attention
Frequent Episodic TTH	1 to 14 days/month for > 3 months (12 to 180 days/year)	Same quality as above but more frequent; begins to cause disability; may require abortive therapy; risk of progression to chronic form with analgesic overuse
Chronic TTH	$\geq$ 15 days/month for > 3 months ($\geq$ 180 days/year)	Headache may be daily and unremitting; mild nausea is permitted (but NOT moderate/severe nausea or vomiting); photophobia OR phonophobia allowed (not both); pericranial tenderness is commonly present; central sensitization is the dominant mechanism

Core Diagnostic Features

Feature	Requirement
Location	Bilateral
Quality	Pressing or tightening (non-pulsating)
Intensity	Mild to moderate
Effect of physical activity	Not aggravated by routine physical activity (walking, climbing stairs)
Nausea/Vomiting	Absent in episodic forms; mild nausea allowed in chronic form; vomiting always absent
Photophobia/Phonophobia	One or the other may be present, but NOT both simultaneously
Duration per episode	30 minutes to 7 days

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.

3. Diagnostic Workup

Test	Role	Expected Finding
Clinical history and physical exam	Best initial and confirmatory test	Bilateral, pressing, non-pulsating headache with pericranial tenderness; normal neurological exam
Headache diary	Adjunct for classification	Documents frequency to distinguish episodic vs. chronic
CT/MRI Brain	Only if red flags present	Normal (used to exclude secondary causes)
ESR / CRP	If age > 50 with new headache	Normal (rules out giant cell arteritis)
Lumbar puncture	If papilledema or thunderclap headache	Normal opening pressure and CSF (rules out idiopathic intracranial hypertension or subarachnoid hemorrhage)

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):

Red Flag	Concern
Systemic symptoms (fever, weight loss) or secondary risk factors (HIV, cancer)	Infection, metastasis
Neurological deficits or abnormal exam	Intracranial mass, stroke
Onset sudden (thunderclap)	Subarachnoid hemorrhage
Onset after age 50	Giant cell arteritis, mass
Pattern change (progressive worsening, change in character)	Secondary headache

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.

4. Management and Treatment

Setting	Treatment	Details
Acute (episodic)	Ibuprofen	400 mg PO, may repeat every 6-8 hours; max 1200 mg/day
Acute (episodic)	Naproxen sodium	220 to 550 mg PO once, may repeat in 12 hours
Acute (episodic)	Acetaminophen	1000 mg PO, may repeat every 6 hours; max 3000 mg/day (2000 mg/day in liver disease)
Acute (episodic)	Aspirin	500 to 1000 mg PO once
Prophylaxis (chronic)	Amitriptyline	10 to 25 mg PO at bedtime, titrate up to 75 mg; minimum trial of 4 to 6 weeks
Prophylaxis (chronic)	Nortriptyline	Alternative to amitriptyline if sedation is intolerable; 10 to 25 mg at bedtime, titrate up
Prophylaxis (chronic)	Mirtazapine	15 to 30 mg at bedtime; second-line
Prophylaxis (chronic)	Venlafaxine	150 mg/day; second-line
Non-pharmacologic	Physical therapy, biofeedback, cognitive behavioral therapy, stress management	Adjunct to all pharmacologic therapy; first-line for infrequent episodic TTH

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 ($\geq$ 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.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Migraine without aura	Can also be bilateral in up to 40% of cases; moderate intensity overlaps	Migraine is pulsating, worsened by physical activity, and associated with nausea/vomiting and BOTH photophobia and phonophobia; TTH has none of these
Chronic migraine	Headache $\geq$ 15 days/month, overlaps with chronic TTH frequency	Chronic migraine requires $\geq$ 8 days/month meeting migraine criteria (pulsating, unilateral, nausea, or triptan-responsive); chronic TTH does not meet migraine criteria on any day
Medication overuse headache	Daily headache in a patient with a history of TTH	Ask about analgesic frequency: if simple analgesics > 15 days/month or combination analgesics > 10 days/month, MOH is the primary diagnosis; headache improves after drug withdrawal
Cervicogenic headache	Can be bilateral and pressing; pericranial/cervical tenderness	Cervicogenic headache is triggered by neck movement or sustained posture and associated with reduced cervical range of motion; pain originates from the occipital region and radiates forward
Idiopathic intracranial hypertension (IIH)	Bilateral, daily headache in a young woman	IIH causes papilledema, pulsatile tinnitus, transient visual obscurations, and elevated opening pressure on LP (> 25 cmH2O); TTH has a completely normal exam
Giant cell arteritis (GCA)	New daily headache, bilateral, pressing quality	GCA occurs in patients > 50 years old with jaw claudication, scalp tenderness, elevated ESR (often > 50 mm/hr), and visual symptoms; temporal artery biopsy is confirmatory
TMJ disorder	Bilateral facial/head pain; tender muscles on palpation	Pain is localized to the preauricular area and worsened by chewing; clicking or crepitus of the temporomandibular joint on exam

6. Traps 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.

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