Tension Headache

• Peripheral mechanism—muscular tension: Sustained contraction of cervical, temporal, and occipital muscles (trapezius, sternocleidomastoid, masseter) creates mechanical nociceptive input through sustained tension and reduced blood flow. Electromyographic studies demonstrate elevated baseline muscle tension in chronic TTH sufferers. This mechanism explains the pressing/tightening quality and bilateral distribution but does not fully account for central pain modulation abnormalities.

• Central sensitization and pain processing dysfunction: Functional neuroimaging and neurochemical studies reveal impaired pain inhibition through the descending noradrenergic and serotonergic pathways originating in the brainstem (locus coeruleus and dorsal raphe nucleus). Cerebrospinal fluid analysis demonstrates reduced levels of serotonin (5-HT) metabolites and abnormal substance P concentrations. Reduced activity in the anterior insula and dorsolateral prefrontal cortex indicates impaired pain modulation. The periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) show altered responsiveness to nociceptive input, resulting in a lowered pain threshold (allodynia).

• Neuromodulator deficiency and stress physiology: Chronic TTH involves dysregulation of multiple neurotransmitter systems including serotonin (5-HT), norepinephrine (NE), dopamine, and γ-aminobutyric acid (GABA). Elevated substance P and reduced endogenous opioid activity contribute to pain amplification. Psychophysiological stress activates the hypothalamic-pituitary-adrenal (HPA) axis chronically, increasing cortisol exposure and perpetuating muscle tension through brainstem and spinal cord facilitation of nociception. Metabolic dysfunction in mitochondrial energy production and accumulation of lactate in muscular tissue may contribute to fatigue-related pain exacerbation.

• Stress and psychological factors: Acute and chronic psychosocial stressors (work pressure, relationship conflict, major life changes), anxiety, depression, and personality traits (perfectionism, trait anxiety) represent the strongest modifiable risk factors. The temporal relationship between stressor intensity and headache frequency is often reported by patients.

• Muscular factors: Poor ergonomics (prolonged computer use, inadequate desk setup), cervical muscle tension disorders, forward head posture, and myofascial trigger points in occipital and cervical muscles. Bruxism and temporomandibular joint dysfunction may exacerbate symptoms.

• Sleep disturbance: Insomnia, sleep apnea, and non-restorative sleep patterns impair pain modulation and predispose to chronic TTH through reduced descending inhibition.

• Comorbid psychiatric conditions: Major depressive disorder, generalized anxiety disorder, and somatic symptom disorder co-occur in 40-80% of chronic TTH cases, representing both etiologic and perpetuating factors.

• Genetic predisposition: Family history of headache increases risk; twin studies suggest 40% heritability, implicating genetic variation in pain modulation pathways.

• Medication overuse: Analgesic use ≥10-15 days/month paradoxically perpetuates chronic TTH through central sensitization and rebound phenomena.

• Female sex and age: Women have 1.5-2.5 times higher prevalence; peak incidence occurs in 30-50-year-old age groups.

• Social and environmental factors: Lower socioeconomic status, occupational stress, poor social support, and trauma history increase TTH burden.

Cardinal Symptoms

• Bilateral pain distribution: Characteristically affects frontal, temporal, or occipital regions symmetrically; described as diffuse, non-throbbing, and spreading across the head like a "band" or "vice."

• Pain quality: Pressing, tightening, squeezing, or compressive sensation (never described as throbbing or pulsatile, which suggests migraine). Pain is typically steady without fluctuation.

• Intensity and duration: Mild to moderate severity (allowing continued function, unlike migraine), ranging 30 minutes to 7 days. Episodic TTH averages 30 minutes; chronic daily tension headaches may persist continuously.

• Absence of prominent nausea/vomiting: Gastrointestinal symptoms are minimal or absent, distinguishing TTH from migraine. Mild photophobia or phonophobia may occur but not both prominently.

• Associated features: Anhedonia, anxiety, irritability, difficulty concentrating, sleep disturbance, and fatigue commonly accompany chronic TTH.

Physical Examination Findings

• Palpable neck/scalp muscle tension: Increased muscle tone in trapezius, sternocleidomastoid, and cervical paraspinal muscles; tenderness to palpation in myofascial trigger points.

• Reduced cervical range of motion: Limitations in neck flexion/extension and rotation, often with pain on passive stretch.

• Normal neurologic exam: Crucially, the neurologic examination is completely normal—no focal neurologic deficits, no papilledema, normal mental status, and normal reflexes/sensation. Any abnormal neurologic finding should prompt investigation for secondary pathology.

• No signs of meningismus or increased intracranial pressure: Absence of neck stiffness (Kernig/Brudzinski signs negative), normal pupillary responses, and normal extraocular movements.

• Vital signs normal: No hypertension, fever, or tachycardia.

Clinical Diagnostic Approach

ICHD-3 Diagnostic Criteria for Episodic Tension-Type Headache

1. 1.At least 10 headaches fulfilling criteria B-D occurring on 1-14 days/month for ≥3 months (frequency threshold)
2. 2.Lasting 30 minutes to 7 days
3. 3.At least two of the following pain characteristics:

• Bilateral location
• Pressing or tightening quality (not pulsating)
• Mild or moderate intensity (does not prohibit activity)
• Not aggravated by routine physical activity

1. 1.Both of the following:

• No nausea or vomiting (anorexia may occur)
• Photophobia OR phonophobia may be present, but not both

1. 1.Not attributed to another ICHD-3 diagnosis

History and Red Flag Assessment

• Headache characterization: Use structured questioning addressing onset (acute vs. gradual), frequency, duration, location, radiation, quality, severity, and temporal pattern. Ask about triggers (stress, poor posture, weather changes, caffeine), relieving factors (rest, massage, analgesics), and associated symptoms.

• Red flags requiring imaging/investigation:
• Sudden-onset "thunderclap" headache (subarachnoid hemorrhage)
• Headache with fever, neck stiffness, altered consciousness (meningitis/encephalitis)
• Progressive headache with focal neurologic deficits, papilledema, or consciousness changes (mass lesion, hydrocephalus)
• Headache following head trauma
• Headache in elderly or immunocompromised patient with new onset
• Headache with systemic symptoms (weight loss, malaise, night sweats suggesting malignancy or infection)
• Headache with visual loss, scalp tenderness, or jaw claudication in patients >50 years (temporal arteritis)
• Headache with focal neurologic signs (stroke, arterial dissection)

Physical Examination

• Mental status and orientation (rule out encephalitis/toxic-metabolic states)
• Fundoscopic exam (papilledema, retinal hemorrhages)
• Cranial nerves II-XII (focal CNS pathology)
• Motor/sensory/cerebellar function (myelopathy, mass effect)
• Meningeal signs (Kernig sign, Brudzinski sign)
• Neck and shoulder muscle examination (palpation for trigger points, range of motion)
• Blood pressure (hypertension as secondary cause)

Laboratory Testing

• Complete blood count, comprehensive metabolic panel, thyroid-stimulating hormone: Only if systemic illness suspected (anemia, metabolic disease, hypothyroidism)
• Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP): If temporal arteritis suspected in patients >50 years with new-onset headache
• Lumbar puncture: Only if meningitis/encephalitis clinically suspected (fever, neck stiffness, altered mental status); contraindicated if papilledema present

Imaging

• Red flag symptoms or signs present
• Atypical headache features (focal onset, progressive severity, change in headache pattern)
• Abnormal neurologic examination
• Suspicion of secondary pathology (mass, vascular lesion, inflammation)
• First severe headache or significant change from baseline

• MRI brain (preferred modality): Provides superior soft tissue contrast for detection of structural lesions, tumors, demyelinating disease, and arterial/venous abnormalities. T1, T2, FLAIR, and gradient echo sequences assess for pathology. No contrast needed for routine TTH workup.

• CT head (non-contrast or with contrast): More rapid, sensitive for acute hemorrhage and bone lesions; preferred if acute stroke or SAH suspected. Lower soft tissue contrast than MRI.

Diagnostic Criteria Summary - Mnemonic "TT HEAD"

• Two or more characteristics (bilateral, pressing, mild-moderate, not worsened by activity)
• Ten or more headaches per month (episodic)
• Head pressing/tightening quality
• Exclusion of nausea/vomiting (only anorexia allowed)
• Absence of prominent autonomic features
• Duration 30 minutes to 7 days

Acute/Abortive Therapy (for individual headache episodes)

• First-line: Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Ibuprofen 400-600 mg orally or naproxen sodium 550 mg orally are effective and well-tolerated
• Mechanism: Inhibition of cyclooxygenase (COX-1 and COX-2), reducing prostaglandin synthesis and peripheral nociception
• Efficacy achieved within 60-90 minutes; use at headache onset for optimal benefit
• Contraindications: Severe gastroesophageal reflux disease, peptic ulcer disease, severe renal impairment, cardiovascular disease

• Alternative first-line: Acetaminophen 500-1000 mg
• Mechanism: Central analgesic action through monoamine system modulation and cannabinoid receptor interaction
• Safer in patients with NSAID contraindications; lower efficacy than NSAIDs
• Maximum 3-4 grams daily to avoid hepatotoxicity

• Second-line: Combination analgesics
• Acetaminophen + aspirin + caffeine (Excedrin): Caffeine (65-100 mg) enhances analgesic efficacy through adenosine antagonism and vasoconstriction
• Effective for episodic TTH but risk of medication overuse if used >10-15 days/month

• Avoid opioids: Not recommended due to poor efficacy in TTH, high dependence risk, and paradoxical medication overuse headache development with chronic use

• Muscle relaxants: Limited evidence; tizanidine or cyclobenzaprine may have modest benefit if significant muscle tension present, but sedation limits use

Preventive/Prophylactic Therapy (for frequent/chronic TTH)

• First-line: Tricyclic antidepressants (TCAs)
• Amitriptyline 10-100 mg daily (usual effective range 25-75 mg at bedtime) is most extensively evidence-supported
• Mechanism: Blocks reuptake of serotonin and norepinephrine, enhancing descending pain inhibition from brainstem; anticholinergic and antihistamine properties promote sleep
• Efficacy: 40-60% headache reduction in 60-70% of patients; therapeutic effect develops over 4-8 weeks, requiring gradual titration
• Advantages: Low cost, once-daily dosing, concurrent management of comorbid depression/anxiety/insomnia
• Adverse effects: Sedation (often beneficial for sleep), anticholinergic effects (dry mouth, constipation, urinary retention), weight gain, orthostatic hypotension. Slower titration reduces side effects.
• Contraindications: Recent myocardial infarction, uncontrolled arrhythmias, narrow-angle glaucoma, urinary retention

• Second-line: Selective serotonin reuptake inhibitors (SSRIs)
• Sertraline 50-200 mg daily or paroxetine 20-40 mg daily are alternatives, particularly when depression/anxiety prominent
• Mechanism: Selective inhibition of serotonin reuptake, increasing synaptic 5-HT availability and enhancing descending pain inhibition
• Efficacy: 30-50% less effective than amitriptyline for TTH specifically; 4-6 weeks to therapeutic effect
• Advantages: Better tolerability than TCAs; useful when concurrent depression/anxiety exists
• Adverse effects: Sexual dysfunction, initial anxiety exacerbation, SIADH (hyponatremia), activation/agitation in some patients

• Third-line: Other agents with supportive evidence
• Venlafaxine (SNRI) 75-225 mg daily: Dual 5-HT and NE reuptake inhibition; moderate evidence (fewer studies than amitriptyline)
• Mirtazapine 15-30 mg daily: Tetracyclic antidepressant; beneficial when insomnia prominent; weight gain common
• Topiramate 25-100 mg daily: Anticonvulsant with proposed GABA-enhancement

Disease-related complications

• Chronification (episodic → chronic TTH): Repeated nociceptive input sustains central sensitization in the trigeminocervical complex and degrades descending inhibition, so headache days accumulate. Signaled by a patient reporting ≥15 headache days/month for ≥3 months (ICHD-3 threshold) and escalating analgesic use.
• Medication overuse headache (MOH): Per ICHD-3, regular intake of simple analgesics on ≥15 days/month, or combination analgesics, triptans, ergots, or opioids on ≥10 days/month for >3 months, converts an episodic pattern into a daily, refractory, early-morning headache. The signal is a headache that worsens as the analgesic wears off and improves only after withdrawal. The American Headache Society's Choosing Wisely list explicitly warns against prolonged or frequent over-the-counter analgesic use for headache.
• Psychiatric and functional morbidity: Depression, anxiety, insomnia, and work absenteeism cluster with chronic TTH bidirectionally through shared monoaminergic dysfunction.

Treatment-related complications

• NSAIDs: COX-1 inhibition removes gastroprotective prostaglandins and afferent arteriolar vasodilation → dyspepsia, GI bleeding (melena, drop in hemoglobin), AKI, hypertension, and fluid retention. Overt GI hemorrhage is an emergency.
• Acetaminophen: NAPQI accumulation with glutathione depletion causes centrilobular hepatic necrosis; transaminases in the thousands with rising INR signal fulminant failure — an emergency requiring N-acetylcysteine.
• Tricyclic antidepressants (amitriptyline): Anticholinergic burden produces dry mouth, constipation, urinary retention, confusion in the elderly, and can precipitate acute angle-closure glaucoma (painful red eye, mid-dilated fixed pupil, halos) — an ophthalmologic emergency. Sodium-channel blockade in overdose causes QRS widening and ventricular arrhythmia, treated with IV sodium bicarbonate — an emergency.
• SSRIs/SNRIs: Hyponatremia from SIADH, and serotonin syndrome (clonus, hyperthermia, agitation) when combined with TCAs, triptans, or tramadol — an emergency. All antidepressants carry an FDA boxed warning for suicidality in patients under 25.
• Topiramate: Carbonic anhydrase inhibition → non-anion-gap metabolic acidosis, kidney stones, paresthesias, and angle-closure glaucoma; teratogenic (oral clefts).
• Missed secondary headache: Anchoring on "tension headache" delays diagnosis of giant cell arteritis (permanent vision loss — start high-dose glucocorticoids before biopsy per the ACR/Vasculitis Foundation guideline), subarachnoid hemorrhage, or cerebral venous thrombosis.

• The buzzword triad: bilateral, pressing/tightening (non-pulsatile), band-like or vice-like, mild-to-moderate, not worsened by routine activity, with a completely normal neurologic exam. If the stem says throbbing, unilateral, worse with stairs, or vomiting, the answer is migraine, not TTH.
• The single best next step in a classic stem: no neuroimaging. A stable headache meeting ICHD-3 criteria with a normal neurologic examination requires reassurance, trigger/lifestyle counseling, and a simple analgesic — the American Headache Society Choosing Wisely list specifically advises against CT or MRI for stable headaches with a normal exam, and ACR Appropriateness Criteria reserve imaging for red flags.
• The association examiners test: analgesic frequency. Always ask "how many days per month do you take something?" A daily headache in someone using OTC analgesics most days is medication overuse headache, and the management is withdrawal of the offending drug plus initiation of prophylaxis — not a stronger analgesic.
• Prophylaxis answer: amitriptyline (TCA) is the best-supported preventive for frequent or chronic TTH; it works by enhancing serotonergic/noradrenergic descending inhibition, takes 4–8 weeks, and is dosed at bedtime. Nonpharmacologic options with real evidence — cognitive behavioral therapy, biofeedback, relaxation training, and exercise — are frequently the correct "add-on."
• Common distractor — triptans: sumatriptan and other 5-HT1B/1D agonists are ineffective in pure TTH; a "response to a triptan" points toward migraine. Likewise, opioids and butalbital-containing combinations are wrong answers in every TTH vignette given dependence and MOH risk.
• Autonomic features change the diagnosis: strictly unilateral orbital pain with lacrimation, ptosis, rhinorrhea, and agitation is cluster headache (high-flow oxygen plus subcutaneous sumatriptan), not TTH.
• Age >50 with new headache plus scalp tenderness, jaw claudication, or vision change → check ESR/CRP and start glucocorticoids immediately for giant cell arteritis; biopsy follows, it does not precede treatment.
• TTH is a clinical diagnosis by exclusion of red flags — labs and LP have no routine role.