Tension Headache

Populations and Risk Factors

• Most common primary headache — affects approximately 40–80% of the population at some point; prevalence peaks between ages 30 and 39; slightly more common in women (~3:2)
• Occupational risk: Prolonged static postures (computer operators, desk workers, drivers, students) producing sustained contraction of cervical and cranial muscles; forward head posture is the most common biomechanical contributor
• Psychological stress: Anxiety, depression, and emotional tension are strongly associated; stress increases muscle tension through sympathetic activation and reduces pain threshold through central mechanisms
• Oromandibular dysfunction (TMD): Jaw clenching, bruxism, and temporomandibular joint dysfunction are significant contributing factors through shared myofascial connections between masticatory and cervical muscles
• Medication overuse: Chronic use of analgesics (>15 days/month for simple analgesics, >10 days/month for triptans/opioids/combinations) can produce medication-overuse headache (MOH/rebound headache) that perpetuates the cycle
• Sleep disturbance: Both insufficient sleep and oversleeping can trigger episodes
• Caffeine: Both excessive intake and withdrawal are triggers
• Cervical spine dysfunction: C1–C2 restriction, facet joint dysfunction, and reduced cervical ROM are commonly associated

Causes and Pathophysiology

Peripheral Mechanism (Episodic TTH)

• Myofascial trigger points (TrPs) in the pericranial and cervical muscles are the primary pain generators in episodic tension headache. TrPs in the upper trapezius, SCM, suboccipitals, temporalis, frontalis, and masseter refer pain to the head in patterns that replicate the headache distribution.
• Upper trapezius TrP referral: Pain refers unilaterally along the posterolateral neck to the temporal region and behind the eye — one of the most common headache referral patterns
• SCM TrP referral: Sternal division refers to the ipsilateral forehead, periorbital region, and vertex; clavicular division refers to the ipsilateral forehead, ear, and mastoid area — SCM referral patterns can mimic migraine or cluster headache distribution
• Suboccipital TrP referral: Deep aching pain wrapping from the occiput forward over the skull toward the ipsilateral eye — the suboccipitals are the most consistently involved muscles in chronic TTH
• Temporalis TrP referral: Temporal and retro-orbital pain; frequently associated with TMD and bruxism
• Sustained muscle contraction reduces local blood flow, produces ischemia, and sensitizes peripheral nociceptors in the muscle and fascia, generating ongoing pain signals. This peripheral sensitization maintains the headache as long as the muscle tension persists.

Central Sensitization (Chronic TTH)

• In chronic tension headache (>15 days/month for >3 months), the pathophysiology shifts from primarily peripheral (muscle-driven) to primarily central. Prolonged nociceptive input from pericranial muscles sensitizes second-order neurons in the trigeminal nucleus caudalis and the cervical dorsal horn (C1–C3).
• Central sensitization lowers the pain threshold and amplifies normal sensory input — pressure that would be non-painful in a healthy individual becomes painful (allodynia). Pericranial tenderness becomes generalized rather than localized to specific TrPs.
• Impaired descending inhibition: Chronic pain reduces the effectiveness of descending pain-modulating pathways from the periaqueductal gray and rostral ventromedial medulla, further amplifying pain perception.
• The clinical implication is that chronic TTH may persist even after the peripheral muscle trigger is addressed — central sensitization requires additional strategies (regular treatment, stress management, sleep hygiene, possibly medication) beyond acute TrP deactivation.

Trigeminocervical Nucleus and Cervicogenic Overlap

• The trigeminocervical nucleus (TCN) is the convergence zone where afferent input from the trigeminal nerve (V1, V2, V3 — innervating the head and face) and the upper cervical nerves (C1–C3 — innervating the suboccipital muscles, upper cervical joints, and posterior scalp) converge on shared second-order neurons.
• This convergence explains why cervical dysfunction (C1–C2 restriction, suboccipital hypertonia) produces headache: nociceptive input from the cervical spine is processed through the same neurons as trigeminal headache signals, and the brain cannot distinguish the source — cervical pain is perceived as headache.
• This mechanism also creates the clinical overlap between tension headache and cervicogenic headache — both share suboccipital muscle involvement and C1–C2 dysfunction as contributors, and both respond to cervical manual therapy. The key differentiator is that cervicogenic headache is consistently associated with cervical movement restriction and cervical provocation testing, while TTH may occur without identifiable cervical signs.

Signs and Symptoms

Episodic Tension Headache (<15 days/month)

• Bilateral, non-pulsating pressure or tightness — described as a "band," "vice," or "cap" around the head
• Mild to moderate intensity — does not prevent activities (distinguishes from migraine)
• No nausea or vomiting (mild anorexia possible but not the prominent nausea/vomiting of migraine)
• No aura (visual, sensory, or speech disturbance)
• No significant photophobia or phonophobia (mild sensitivity possible but not both, and not prominent)
• Duration: 30 minutes to 7 days per episode
• Pericranial muscle tenderness on palpation — the most consistent physical finding

Chronic Tension Headache (>15 days/month for >3 months)

• Same quality as episodic but more persistent and disabling
• May develop mild migrainous features (slight photophobia OR phonophobia, not both) — blurring the distinction from chronic migraine
• Generalized pericranial tenderness (not just specific TrPs) — indicates central sensitization
• Medication overuse often co-exists — rebound headache from analgesic overuse perpetuates chronicity
• Significant impact on quality of life, work productivity, and psychological well-being
• Associated with depression, anxiety, and sleep disturbance in a bidirectional relationship

Headache Comparison Table

Assessment Profile

Subjective Presentation

• Chief complaint: "It feels like a tight band around my head"; "There's pressure on both sides of my head"; "My neck and shoulders are so tight and it gives me a headache"; "I get headaches almost every day, especially after work"
• Pain quality: Dull, pressing, tightening — non-pulsating; bilateral or diffuse; described as "band," "vice," "helmet," or "weight on my head"; not aggravated by routine physical activity (walking, climbing stairs)
• Onset: Gradual onset over hours; often begins in the afternoon after sustained posture or stress; episodic form has clear triggers; chronic form may be constant with fluctuating intensity
• Aggravating factors: Sustained postures (computer work, driving, reading), emotional stress, jaw clenching, poor sleep, eye strain, caffeine withdrawal, end of day/afternoon; does NOT worsen with routine physical activity (walking, bending) — unlike migraine
• Easing factors: Rest, relaxation, massage, over-the-counter analgesics (episodic form); chronic form may not respond to simple analgesics; stretching, heat to neck and shoulders; stress reduction
• Red flags: "Worst headache of my life" or sudden severe onset (thunderclap headache) → emergency referral; rule out subarachnoid hemorrhage. Headache with fever, neck stiffness, and altered consciousness → meningitis; emergency referral. New headache in patient over 50 → temporal arteritis screen (ESR). Progressive headache with focal neurological signs → space-occupying lesion; urgent referral. Headache after head trauma → post-concussion evaluation.

Observation

• Local inspection: No visible abnormality specific to TTH; jaw clenching or tooth grinding wear patterns may be visible; temporalis muscle may appear prominent if chronic clenching is present
• Posture: Forward head posture (FHP) — the most consistent postural finding; rounded shoulders; increased cervical lordosis with suboccipital extension ("poking chin"); elevated and protracted shoulders; upper-crossed syndrome pattern (tight upper trapezius/levator scapulae/pectorals with weak deep cervical flexors/lower trapezius)
• Gait: Normal — gait abnormalities are not a feature of TTH; if present, investigate other causes

Palpation

• Tone: Hypertonicity in pericranial and cervical muscles — upper trapezius (most commonly bilateral), SCM, suboccipitals, temporalis, frontalis, masseter, cervical paraspinals, levator scapulae; bilateral involvement is characteristic; hypertonia is the sustained contraction type (protective/postural guarding), not spastic (velocity-dependent UMN)
• Tenderness: Pericranial muscle tenderness is the defining palpation finding. Specific tender points and trigger points in: (1) upper trapezius — refers to temporal region and behind eye; (2) SCM — sternal division refers to forehead and periorbital area, clavicular division to forehead and ear; (3) suboccipitals — refers from occiput forward over skull toward ipsilateral eye; (4) temporalis — temporal and retro-orbital pain; (5) masseter — jaw and temporal area. In chronic TTH, tenderness becomes generalized rather than localized (central sensitization). Referred path tenderness: TrP referral patterns from upper trapezius, SCM, and suboccipitals reproduce the headache distribution — confirming myofascial contribution; active TrPs that reproduce the patient's headache on palpation are the primary treatment targets.
• Temperature: Normal; no thermal changes specific to TTH; warmth over hypertonic muscles may be mildly increased from sustained contraction (metabolic activity) but not clinically significant
• Tissue quality: Taut bands and palpable nodules (trigger points) in affected muscles; ropy, fibrotic texture in chronically hypertonic upper trapezius and suboccipitals; reduced fascial mobility in the cervicothoracic junction; suboccipital muscles may feel dense and shortened from chronic forward head posture

Motion Assessment

• AROM: Cervical ROM may be limited in rotation and lateral flexion (most commonly bilateral, unlike cervicogenic headache which is typically unilateral); upper cervical extension often restricted (suboccipital shortening); shoulder elevation ROM typically full but may provoke neck tension and headache; the restriction pattern is non-capsular (muscle guarding, not joint capsule)
• PROM / end-feel: Muscular/spasm end-feel at the limits of cervical rotation and lateral flexion — yielding but guarded; not the firm/bony end-feel of cervical spondylosis; slow sustained overpressure may improve range as muscles relax (warm-up effect); end-feel improves after treatment (unlike structural restriction)
• Resisted testing: Typically normal strength — TTH does not produce weakness; pain may be provoked with sustained isometric contraction of involved muscles (cervical extension, jaw clenching, sustained shoulder elevation) that reproduces the headache; this confirms the myofascial mechanism

Special Test Cluster

Headache red flag screening: Before treating any headache patient, rule out secondary headache causes. Ask: Is this a new or changed headache pattern? Was the onset sudden? Is there fever, neck stiffness, weight loss, visual changes, or focal neurological symptoms? Is the patient over 50 with new headache? Any "yes" answer requires medical evaluation before MT treatment.

Differential Assessment