Clinical Approach to Headache
Comprehensive Practical Framework1. Symptom Overview
Understanding the clinical significance and classification of Headache
Headache is one of the most common symptoms encountered in clinical practice, affecting approximately 50% of the global adult population annually. It accounts for nearly 4% of all emergency department visits and is the fourth leading cause of disability worldwide according to the Global Burden of Disease study. In primary care settings, headache represents up to 5% of all consultations. While the vast majority of headaches are benign primary headache disorders, approximately 1-5% of patients presenting with headache have a serious underlying cause requiring urgent investigation and treatment.
Definition
Headache is defined as pain located anywhere in the region of the head or upper neck. It arises from activation of pain-sensitive structures including the meninges, blood vessels, muscles, periosteum, and cranial or cervical nerves. Notably, the brain parenchyma itself lacks pain receptors and cannot generate headache directly.
Primary Classification: Primary vs Secondary Headache
Primary Headaches (approximately 90%)
Headache disorders where the headache itself is the condition, without an underlying structural or systemic cause. These include migraine, tension-type headache, and trigeminal autonomic cephalalgias such as cluster headache.
Secondary Headaches (approximately 10%)
Headaches caused by an underlying condition such as infection, vascular abnormality, trauma, or mass lesion. Identifying secondary headaches is critical as they may represent life-threatening emergencies requiring immediate intervention.
Classification by Duration and Temporal Pattern
| Category | Duration | Common Causes | Clinical Significance |
|---|---|---|---|
| Acute Single Episode | Minutes to days (first occurrence) | Subarachnoid hemorrhage, meningitis, first migraine, thunderclap headache | Requires urgent evaluation to exclude life-threatening causes |
| Acute Recurrent | Episodic attacks with pain-free intervals | Migraine, cluster headache, tension-type headache | Pattern recognition aids diagnosis; prophylaxis may be indicated |
| Chronic Daily | 15 or more days per month for greater than 3 months | Chronic migraine, medication overuse headache, chronic tension-type | Evaluate for medication overuse; significant disability burden |
| Progressive | Gradually worsening over weeks to months | Intracranial mass, idiopathic intracranial hypertension, subdural hematoma | Red flag pattern requiring neuroimaging |
Classification by Character and Quality
| Character | Description | Typical Causes |
|---|---|---|
| Throbbing or Pulsatile | Rhythmic, beating quality often synchronized with heartbeat | Migraine, vascular headaches, fever-associated headache |
| Pressing or Tightening | Band-like pressure sensation, non-pulsatile | Tension-type headache, cervicogenic headache |
| Stabbing or Lancinating | Brief, sharp, electric shock-like pain | Trigeminal neuralgia, primary stabbing headache |
| Boring or Drilling | Deep, intense, penetrating quality | Cluster headache, other trigeminal autonomic cephalalgias |
| Explosive or Thunderclap | Maximum intensity reached within seconds to one minute | Subarachnoid hemorrhage, reversible cerebral vasoconstriction syndrome, pituitary apoplexy |
Classification by Location
Unilateral
Suggests: Migraine, cluster headache, trigeminal neuralgia, cervicogenic headache
Note: Strictly unilateral headache with autonomic features strongly suggests trigeminal autonomic cephalalgia
Bilateral
Suggests: Tension-type headache, medication overuse headache, systemic illness
Note: Bilateral pressing quality is characteristic of tension-type headache
Occipital or Posterior
Suggests: Cervicogenic headache, occipital neuralgia, posterior fossa lesion, Chiari malformation
Note: Associated neck stiffness requires meningitis evaluation
Classification by Associated Features
| Associated Feature | Clinical Significance | Consider |
|---|---|---|
| Nausea and vomiting | Common in migraine; also seen with raised intracranial pressure | Migraine; intracranial mass if progressive |
| Photophobia and phonophobia | Strongly associated with migraine | Migraine; meningitis if with fever and neck stiffness |
| Visual aura | Transient visual phenomena preceding headache | Migraine with aura |
| Autonomic features | Lacrimation, conjunctival injection, rhinorrhea, ptosis | Cluster headache and other trigeminal autonomic cephalalgias |
| Fever | Suggests infectious or inflammatory etiology | Meningitis, encephalitis, sinusitis, systemic infection |
| Focal neurological deficits | Red flag requiring urgent evaluation | Stroke, intracranial mass, complicated migraine |
Key Concept: The “Big Four” Primary Headache Disorders
- Tension-type headache — The most common primary headache, affecting up to 80% of the population at some point
- Migraine — Affects approximately 12% of the adult population; more common in women (3:1 ratio)
- Cluster headache — Rare but severe; affects approximately 0.1% of the population; more common in men
- Medication overuse headache — Affects 1-2% of the population; a critical diagnosis to identify as it prevents treatment success
Key Epidemiological Facts
- Migraine is the second leading cause of years lived with disability globally
- Tension-type headache has an estimated lifetime prevalence of 30-78%
- Peak age for migraine onset is between 25-55 years
- Approximately 3% of episodic migraine patients progress to chronic migraine annually
- Headache disorders cost the European economy approximately €27 billion annually in lost productivity
2. Pathophysiology and Mechanisms
Understanding the underlying mechanisms of Headache
Understanding headache pathophysiology is essential for rational diagnosis and treatment. The brain parenchyma itself is insensitive to pain; headache arises from activation of pain-sensitive structures including the meninges, blood vessels, periosteum, muscles, and cranial nerves. The trigeminovascular system plays a central role in most primary headache disorders, while secondary headaches result from direct stimulation or compression of pain-sensitive structures.
Pain-Sensitive Structures of the Head
| Structure | Innervation | Clinical Relevance |
|---|---|---|
| Dura mater and dural sinuses | Trigeminal nerve (V1 division), upper cervical nerves (C1-C3) | Inflammation or traction produces referred pain to forehead and vertex |
| Cerebral blood vessels | Trigeminal nerve and sympathetic fibers | Vasodilation and neurogenic inflammation in migraine |
| Extracranial arteries | Trigeminal and cervical nerves | Temporal artery tenderness in giant cell arteritis |
| Periosteum of skull | Trigeminal and cervical nerves | Pain from skull fractures, Paget disease, metastases |
| Muscles of scalp and neck | Cervical nerves, trigeminal nerve | Tension-type headache, cervicogenic headache |
| Paranasal sinuses | Trigeminal nerve (V1 and V2 divisions) | Sinusitis produces facial and frontal pain |
| Eyes and orbits | Trigeminal nerve (V1 division) | Acute glaucoma, orbital pathology |
The Trigeminovascular System
Central Pathway: The trigeminovascular system is the key anatomical substrate for headache, particularly migraine. Pain signals from intracranial structures travel via trigeminal afferents to the trigeminal nucleus caudalis in the brainstem, then ascend to the thalamus and cortex for conscious perception.
| Component | Structure | Function |
|---|---|---|
| Peripheral Receptors | Nociceptors on meningeal vessels and dura | Detect mechanical, thermal, and chemical stimuli |
| Primary Afferents | Trigeminal nerve (V1 ophthalmic division primarily) | Transmit pain signals to brainstem |
| First Synapse | Trigeminal nucleus caudalis (extends to C2 dorsal horn) | Initial processing; explains referred pain to occiput |
| Second Order Neurons | Trigeminothalamic tract | Ascend to thalamus |
| Thalamus | Ventral posteromedial nucleus | Relay to cortex; integration with other sensory input |
| Cortex | Somatosensory cortex, insula, cingulate cortex | Conscious perception of pain and emotional response |
Pathophysiology by Headache Type
Migraine
The Current Understanding of Migraine
Migraine is now understood as a neurovascular disorder involving dysfunction of brainstem and hypothalamic nuclei, cortical hyperexcitability, and activation of the trigeminovascular system. The aura is caused by cortical spreading depression, while the headache phase involves release of inflammatory neuropeptides including calcitonin gene-related peptide (CGRP).
| Phase | Mechanism | Clinical Manifestation |
|---|---|---|
| Prodrome | Hypothalamic activation | Fatigue, food cravings, mood changes, yawning |
| Aura | Cortical spreading depression — wave of neuronal depolarization followed by suppression | Visual scintillations, sensory symptoms, speech disturbance |
| Headache | Trigeminovascular activation; CGRP release; neurogenic inflammation; peripheral and central sensitization | Throbbing unilateral pain, photophobia, phonophobia, nausea |
| Postdrome | Recovery phase with persistent neuronal dysfunction | Fatigue, cognitive impairment, residual sensitivity |
Tension-Type Headache
Peripheral Mechanism
- Increased pericranial muscle tenderness
- Myofascial trigger points
- Peripheral sensitization of muscle nociceptors
Central Mechanism
- Central sensitization at trigeminal nucleus
- Impaired descending pain modulation
- Reduced pain thresholds
Cluster Headache
| Feature | Mechanism | Clinical Correlation |
|---|---|---|
| Circadian pattern | Hypothalamic pacemaker dysfunction (suprachiasmatic nucleus) | Attacks occur at same time daily; seasonal clustering |
| Severe unilateral pain | Intense trigeminovascular activation | Orbital, supraorbital, or temporal pain |
| Autonomic features | Trigeminal-autonomic reflex activation via superior salivatory nucleus | Lacrimation, conjunctival injection, rhinorrhea, ptosis, miosis |
Mechanisms of Secondary Headaches
| Condition | Mechanism of Pain | Treatment Implication |
|---|---|---|
| Subarachnoid hemorrhage | Meningeal irritation by blood; acute rise in intracranial pressure; arterial spasm | Neurosurgical emergency; prevent vasospasm |
| Meningitis | Inflammation of meninges; raised intracranial pressure | Antimicrobial therapy; reduce inflammation |
| Intracranial mass lesion | Traction on pain-sensitive structures; raised intracranial pressure; hydrocephalus | Address underlying lesion; manage intracranial pressure |
| Idiopathic intracranial hypertension | Elevated cerebrospinal fluid pressure; papilledema | Weight loss; acetazolamide; cerebrospinal fluid diversion if severe |
| Giant cell arteritis | Granulomatous vasculitis of medium and large arteries; ischemia | Urgent high-dose corticosteroids to prevent blindness |
| Cervicogenic headache | Referred pain from C1-C3 via trigeminocervical nucleus convergence | Address cervical pathology; physical therapy |
| Medication overuse headache | Central sensitization; downregulation of serotonin receptors; altered pain modulation | Withdrawal of offending medication; prevention is key |
Key Neurotransmitters and Therapeutic Targets
Calcitonin Gene-Related Peptide (CGRP)
Role: Potent vasodilator; key mediator of neurogenic inflammation in migraine
Clinical relevance: CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab) are effective migraine prophylaxis
Serotonin (5-HT)
Role: 5-HT1B/1D receptors on trigeminal neurons inhibit CGRP release and cause vasoconstriction
Clinical relevance: Triptans are 5-HT1B/1D agonists used for acute migraine treatment
Dopamine
Role: Involved in prodromal symptoms including nausea and yawning
Clinical relevance: Dopamine antagonists (metoclopramide, prochlorperazine) effective for migraine-associated nausea
Often Overlooked Mechanism: Cervicogenic Contribution
The trigeminocervical complex explains why neck pathology can cause headache and why headache can cause neck pain. Afferents from C1-C3 converge with trigeminal afferents in the trigeminal nucleus caudalis. This convergence means that cervical spine pathology (such as osteoarthritis, disc disease, or whiplash) can produce referred pain to the head, and primary headache disorders frequently present with neck pain and tenderness. Always examine the cervical spine in headache patients.
Central Sensitization: Why Headaches Become Chronic
Central sensitization is a state of heightened excitability in central pain pathways that develops with repeated headache attacks. It explains:
- Why pain thresholds decrease over time (allodynia during attacks)
- Why episodic headache transforms to chronic headache
- Why early treatment of attacks is more effective than delayed treatment
- Why medication overuse perpetuates chronic headache
3. History Taking
A comprehensive approach to eliciting the Headache history
Red Flags — Require Urgent Evaluation
- Thunderclap onset — Maximum intensity within seconds suggests subarachnoid hemorrhage
- New headache after age 50 — Consider giant cell arteritis, mass lesion, or subdural hematoma
- Progressive worsening pattern — Suggests space-occupying lesion or chronic subdural
- Fever with neck stiffness — Meningitis until proven otherwise
- Papilledema — Raised intracranial pressure requiring urgent imaging
- Focal neurological deficits — Stroke, mass lesion, or complicated migraine
- Altered consciousness or confusion — Encephalitis, intracranial hemorrhage, or mass effect
- Headache triggered by Valsalva — Chiari malformation or posterior fossa lesion
- History of malignancy — Brain metastases or leptomeningeal disease
- Immunocompromised state — Opportunistic infections, atypical presentations
- Postural component — Worse when lying suggests raised pressure; worse when upright suggests low pressure
Red Flag Mnemonic: “SNOOP4”
Use the mnemonic “SNOOP4” to screen for secondary headache causes:
- S — Systemic symptoms (fever, weight loss) or Systemic illness (malignancy, HIV, pregnancy)
- N — Neurological symptoms or signs (focal deficits, altered consciousness, seizures)
- O — Onset sudden (thunderclap headache reaching maximum in less than 1 minute)
- O — Older age of onset (new headache after age 50 years)
- P — Pattern change (first or worst headache, progressive headache, change from prior pattern)
- P — Positional (worse lying down or worse upright)
- P — Precipitated by Valsalva (cough, strain, exertion)
- P — Papilledema
Systematic History: The “HEADACHE” Approach
Use the mnemonic “HEADACHE” to ensure comprehensive history taking:
- H — How did it start? (Sudden versus gradual onset; first episode or recurrent)
- E — Evolution and duration (How long does each episode last? Is it getting worse over time?)
- A — Associated symptoms (Nausea, vomiting, photophobia, phonophobia, aura, autonomic features, fever)
- D — Description of pain (Character: throbbing, pressing, stabbing; Severity: 0-10 scale)
- A — Area and radiation (Location: unilateral versus bilateral; frontal, temporal, occipital; radiation to neck)
- C — Circumstances and triggers (Stress, sleep, foods, menses, exertion, posture, time of day)
- H — History of headache and treatments (Prior diagnosis, medications tried, response to treatment, frequency of analgesic use)
- E — Effect on life and Examination findings (Disability, work impact, warning symptoms, prior investigations)
Targeted Questions by Suspected Cause
| Suspected Cause | Key Features | Ask This Question |
|---|---|---|
| Migraine | Unilateral, throbbing, moderate-severe, with nausea and photophobia | “Does light or noise bother you during the headache? Do you feel nauseated or need to lie down in a dark room?” |
| Tension-type headache | Bilateral, pressing, mild-moderate, no significant nausea | “Does it feel like a tight band or pressure around your head? Can you continue your normal activities during the headache?” |
| Cluster headache | Strictly unilateral, severe, orbital pain with autonomic features | “Does your eye water or become red on the same side? Do you feel restless and need to pace during attacks?” |
| Medication overuse headache | Daily or near-daily headache, regular analgesic use | “How many days per month do you take painkillers or migraine medications? Do you take them preventively?” |
| Subarachnoid hemorrhage | Thunderclap onset, worst headache of life | “Did the headache reach its worst intensity within seconds? Is this the worst headache you have ever experienced?” |
| Meningitis | Fever, neck stiffness, photophobia, altered mental status | “Do you have a fever? Does bending your neck forward cause pain? Have you been more confused than usual?” |
| Giant cell arteritis | Age over 50, scalp tenderness, jaw claudication, visual symptoms | “Does your scalp hurt when you brush your hair? Do you get pain in your jaw when chewing? Have you had any changes in vision?” |
| Idiopathic intracranial hypertension | Young obese female, daily headache, transient visual obscurations, pulsatile tinnitus | “Do you get brief episodes where your vision goes dark or grey? Do you hear a whooshing sound in your ears in time with your heartbeat?” |
| Intracranial mass lesion | Progressive headache, morning predominance, worse with Valsalva | “Is the headache worst when you wake up in the morning? Does it get worse when you cough, strain, or bend forward?” |
| Cervicogenic headache | Unilateral, starts in neck, triggered by neck movement or posture | “Does the headache start in your neck and spread to your head? Does turning or tilting your head trigger the pain?” |
| Trigeminal neuralgia | Brief lancinating pain in trigeminal distribution, triggered by touch | “Is the pain like an electric shock? Does touching your face, eating, or talking trigger the pain?” |
Understanding the Temporal Pattern
| Pattern | Typical Duration | Suggests | Key Question |
|---|---|---|---|
| Seconds to minutes | 1 second to 2 minutes | Trigeminal neuralgia, primary stabbing headache, SUNCT/SUNA | “Does each episode of pain last only seconds?” |
| 15 minutes to 3 hours | 15-180 minutes | Cluster headache, paroxysmal hemicrania | “Do attacks last between 15 minutes and 3 hours?” |
| 4 to 72 hours | 4-72 hours untreated | Migraine | “If untreated, how long does the headache typically last?” |
| Hours to days | 30 minutes to 7 days | Tension-type headache | “Can the headache last all day or even several days?” |
| Continuous daily | Present most of the day, most days | Chronic migraine, medication overuse headache, new daily persistent headache | “Is the headache present more days than not? When was your last completely headache-free day?” |
Medication and Treatment History
Medications That Can Cause or Worsen Headache
- Vasodilators — Nitrates, calcium channel blockers, phosphodiesterase inhibitors (sildenafil)
- Hormones — Combined oral contraceptives, hormone replacement therapy
- Analgesic overuse — Simple analgesics used greater than 15 days per month; triptans, opioids, or combination analgesics used greater than 10 days per month
- Proton pump inhibitors — Particularly with long-term use
- Nonsteroidal anti-inflammatory drugs — Paradoxically can cause medication overuse headache
- Dipyridamole — Potent vasodilator
- Caffeine withdrawal — Headache within 24 hours of cessation
Critical Questions About Medication Use
- Frequency: “How many days per month do you take any painkiller for headache?”
- Type: “What medications do you use — over-the-counter or prescription?”
- Escalation: “Are you needing to take more medication than you used to?”
- Preventive use: “Do you ever take painkillers to prevent a headache from starting?”
- Prior preventives: “Have you tried any daily medications to prevent headaches? What happened?”
- Response: “Do your current medications actually stop the headache, or just take the edge off?”
Medication Overuse Headache Thresholds
- Simple analgesics (paracetamol, NSAIDs): Risk increases with use on 15 or more days per month
- Triptans, opioids, ergotamines, or combination analgesics: Risk increases with use on 10 or more days per month
- Medication overuse headache should be suspected in any patient with chronic daily headache and frequent analgesic use
Social, Occupational, and Family History
Lifestyle and Social Factors
- Sleep: Sleep deprivation and oversleeping are both migraine triggers; sleep apnea causes morning headache
- Caffeine: Both excess consumption and withdrawal can cause headache
- Alcohol: Red wine commonly triggers migraine; alcohol triggers cluster headache during cluster periods
- Stress: Major trigger for tension-type headache and migraine
- Diet: Missed meals, dehydration, and specific foods (aged cheese, processed meats, MSG) may trigger migraine
- Exercise: Both lack of exercise and exertional headache are relevant
Occupational and Other Factors
- Screen time: Prolonged computer use associated with tension-type headache
- Posture: Poor ergonomics contribute to cervicogenic headache
- Carbon monoxide exposure: Occupational or faulty heating — causes bilateral throbbing headache
- Shift work: Circadian disruption may trigger cluster headache
- Recent trauma: Post-traumatic headache after head injury
- Family history: Migraine has strong genetic component (70% concordance in monozygotic twins); family history of aneurysm relevant
Assessing Headache Impact and Disability
Key Questions for Impact Assessment
- “How many days in the past month have you missed work or school because of headache?”
- “How many days was your productivity reduced by half or more?”
- “How many family or social activities have you missed?”
- “On a scale of 0-10, how much does headache affect your quality of life?”
- “Do you feel anxious about when the next headache will come?”
Consider using validated tools such as the Migraine Disability Assessment (MIDAS) or the Headache Impact Test (HIT-6) for formal assessment.
4. Physical Examination
A systematic head-to-toe approach for Headache
Systematic Framework: Use the “General to Specific” approach for complete examination of patients presenting with headache. Begin with vital signs and general inspection, proceed to focused neurological examination, and complete with specific targeted examinations based on clinical suspicion.
General Inspection
- Appearance: Does the patient appear unwell, toxic, or in distress? Photophobia (wearing sunglasses, avoiding light)?
- Level of consciousness: Alert and oriented? Any confusion, drowsiness, or agitation?
- Posture and behavior: Lying still (migraine) versus pacing and restless (cluster headache)?
- Skin: Rash (meningococcal disease), pallor, or diaphoresis?
- Obvious abnormalities: Facial asymmetry, ptosis, proptosis, or visible scalp lesions?
Vital Signs
| Vital Sign | What to Look For | Clinical Significance |
|---|---|---|
| Temperature | Fever (greater than 38°C) | Meningitis, encephalitis, brain abscess, sinusitis, systemic infection |
| Blood Pressure | Severe hypertension (greater than 180/120 mmHg) | Hypertensive emergency can cause headache; also Cushing reflex in raised intracranial pressure |
| Heart Rate | Bradycardia with hypertension | Cushing reflex suggesting raised intracranial pressure |
| Respiratory Rate | Abnormal pattern | Irregular breathing may indicate brainstem involvement |
| Oxygen Saturation | Hypoxia | May indicate carbon monoxide poisoning (normal SpO2 with CO poisoning); respiratory compromise |
Head and Face Examination
Scalp and Skull
- Palpate temporal arteries: Tenderness, nodularity, reduced pulsation (giant cell arteritis)
- Scalp tenderness: Localized (temporal arteritis) versus diffuse (scalp allodynia in migraine)
- Pericranial muscle tenderness: Temporalis, frontalis, occipitalis, sternocleidomastoid, trapezius (tension-type headache)
- Trigger points: Greater occipital nerve at nuchal line; supraorbital notch
- Signs of trauma: Bruising, lacerations, Battle sign, raccoon eyes
Face and Sinuses
- Sinus tenderness: Palpate and percuss over frontal and maxillary sinuses
- Facial sensation: Test all three trigeminal divisions
- Jaw claudication: Ask patient to open and close mouth repeatedly
- Temporomandibular joint: Tenderness, clicking, reduced opening
- Facial symmetry: Assess at rest and with movement (facial nerve function)
Eye Examination
| Component | What to Assess | Clinical Significance |
|---|---|---|
| Visual acuity | Test each eye separately | Reduced acuity may indicate giant cell arteritis, optic neuritis, or papilledema |
| Visual fields | Confrontation testing | Homonymous defects suggest posterior circulation pathology; enlarged blind spot with papilledema |
| Pupillary responses | Direct, consensual, and swinging light test | Anisocoria with ptosis suggests Horner syndrome (cluster headache, carotid dissection) or third nerve palsy (posterior communicating artery aneurysm) |
| Eye movements | Test in all directions; assess for diplopia | Sixth nerve palsy may be false localizing sign of raised intracranial pressure; third nerve palsy with “down and out” eye |
| Fundoscopy | Optic disc margins, venous pulsations, hemorrhages | Papilledema indicates raised intracranial pressure; spontaneous venous pulsations when present suggest normal pressure |
| Conjunctiva and eyelid | Injection, lacrimation, ptosis, lid edema | Ipsilateral autonomic features in cluster headache and other trigeminal autonomic cephalalgias |
Fundoscopy is Essential
Fundoscopy should be performed in all patients presenting with new headache, headache with red flags, or headache with any neurological symptoms. Papilledema is the most important finding to exclude, as it indicates raised intracranial pressure and warrants urgent neuroimaging. The absence of papilledema does not exclude raised pressure, particularly if acute.
Neck Examination
Meningeal Signs
- Neck stiffness: Resistance to passive neck flexion with chin to chest
- Kernig sign: With hip flexed to 90°, pain or resistance on knee extension
- Brudzinski sign: Spontaneous hip and knee flexion when neck is passively flexed
- Jolt accentuation: Worsening headache with horizontal rotation of head 2-3 times per second
Cervical Spine
- Range of motion: Assess flexion, extension, rotation, and lateral flexion
- Tenderness: Palpate spinous processes and paraspinal muscles
- Trigger points: Upper trapezius, levator scapulae, suboccipital muscles
- Reproduction of headache: Does neck movement or sustained posture trigger the headache?
Neurological Examination
Mental Status
- Level of consciousness: Glasgow Coma Scale if impaired
- Orientation: To person, place, time, and situation
- Attention and concentration: Serial 7s, spell “WORLD” backwards
- Speech: Dysarthria or dysphasia
Cranial Nerves
| Cranial Nerve | Key Tests | Relevance to Headache |
|---|---|---|
| II (Optic) | Acuity, fields, fundoscopy, RAPD | Papilledema; optic neuritis; giant cell arteritis |
| III, IV, VI (Oculomotor, Trochlear, Abducens) | Eye movements, pupil size and reactivity | Third nerve palsy in aneurysm; sixth nerve palsy in raised intracranial pressure |
| V (Trigeminal) | Facial sensation in V1, V2, V3; corneal reflex; muscles of mastication | Trigeminal neuralgia; cavernous sinus pathology |
| VII (Facial) | Facial symmetry at rest and movement | Lower motor neuron pattern in Bell palsy; upper motor neuron pattern in stroke |
| VIII (Vestibulocochlear) | Hearing, nystagmus | Acoustic neuroma; vestibular migraine |
| IX, X (Glossopharyngeal, Vagus) | Palate movement, gag reflex, voice | Brainstem lesions |
| XI (Accessory) | Shoulder shrug, head turn against resistance | Trapezius involvement in tension-type headache |
| XII (Hypoglossal) | Tongue protrusion, look for deviation or fasciculations | Brainstem or base of skull pathology |
Motor, Sensory, and Coordination
Motor
- Pronator drift
- Power in upper and lower limbs
- Tone
- Deep tendon reflexes
- Plantar responses
Sensory
- Light touch
- Pin prick
- Proprioception
- Vibration sense
- Dermatomal pattern if abnormal
Coordination
- Finger-to-nose test
- Heel-to-shin test
- Rapid alternating movements
- Gait assessment
- Romberg test
Expected Findings by Etiology
| Condition | General/Vital Signs | Head and Neck | Neurological |
|---|---|---|---|
| Migraine | Often normal; may appear uncomfortable | Scalp allodynia during attack; pericranial tenderness | Usually normal; rarely transient focal signs with aura |
| Tension-type headache | Normal | Pericranial muscle tenderness; trigger points | Normal |
| Cluster headache | Restless, pacing; may appear agitated | Ipsilateral ptosis, miosis, conjunctival injection, lacrimation, rhinorrhea | Normal between attacks; partial Horner during attack |
| Meningitis | Fever, tachycardia, may be hypotensive | Neck stiffness; positive Kernig and Brudzinski; photophobia | Altered consciousness; may have focal signs |
| Subarachnoid hemorrhage | May have hypertension; may be drowsy or comatose | Neck stiffness (develops over hours); photophobia | May have focal signs; third nerve palsy suggests posterior communicating artery aneurysm |
| Giant cell arteritis | May have low-grade fever | Tender, thickened, non-pulsatile temporal arteries; scalp tenderness; jaw claudication | May have visual loss (AION); rarely stroke |
| Idiopathic intracranial hypertension | Often obese young female | May have pulsatile tinnitus | Papilledema; sixth nerve palsy; enlarged blind spots |
| Intracranial mass | Variable; may have signs of malignancy | Usually normal | Papilledema; focal signs depending on location |
| Cervicogenic headache | Normal | Reduced cervical range of motion; tenderness; headache reproduced by neck movement | Normal |
Important Teaching Point
Normal examination is extremely common in headache patients! The majority of patients presenting with headache, including those with migraine, tension-type headache, and medication overuse headache, will have completely normal physical examination findings between attacks. A normal examination does not exclude serious pathology — the history and pattern of headache remain the most important diagnostic tools. Conversely, any abnormal findings should prompt further investigation.
Special Maneuvers and Tests
| Test | How to Perform | Positive Finding Suggests |
|---|---|---|
| Valsalva maneuver | Ask patient to bear down or cough | Worsening headache suggests raised intracranial pressure, Chiari malformation, or posterior fossa lesion |
| Positional testing | Compare headache severity lying versus standing | Worse lying down: raised intracranial pressure; Worse standing: intracranial hypotension (post-lumbar puncture, CSF leak) |
| Temporal artery palpation | Palpate along course of superficial temporal arteries bilaterally | Tenderness, nodularity, or absent pulse suggests giant cell arteritis |
| Cervical flexion-rotation test | Flex neck fully then rotate; compare range bilaterally | Asymmetric restriction suggests C1-C2 dysfunction (cervicogenic headache) |
| Trigger point examination | Apply pressure to occipital, temporal, and cervical muscles | Reproduction of typical headache suggests myofascial contribution |
5. Differential Diagnosis
Systematic approach organized by probability and clinical features
The differential diagnosis of headache is vast, but a systematic approach based on temporal pattern, associated features, and red flags allows efficient narrowing of possibilities. The first priority is always to identify or exclude secondary causes that require urgent intervention.
Step-by-Step Diagnostic Approach:
- Step 1: Screen for red flags using SNOOP4 — if present, investigate for secondary causes urgently
- Step 2: Classify by temporal pattern — acute single episode, acute recurrent, or chronic daily
- Step 3: Consider the most common causes first — migraine, tension-type headache, medication overuse headache
- Step 4: Match clinical features to specific diagnoses using ICHD-3 criteria
Acute New-Onset Headache (First or Worst Headache)
Critical Point
A first severe headache or “worst headache of life” must be evaluated urgently. Subarachnoid hemorrhage must be excluded in any thunderclap headache, even if examination is normal.
| Probability | Condition | Key Features | Red Flags |
|---|---|---|---|
| MUST EXCLUDE FIRST | Subarachnoid hemorrhage | Thunderclap onset; worst headache ever; may have neck stiffness, vomiting, altered consciousness | Sudden onset to maximum intensity; loss of consciousness; meningism |
| MUST EXCLUDE | Meningitis or encephalitis | Fever; neck stiffness; photophobia; altered mental status; rash in meningococcal disease | Fever; altered consciousness; seizures; petechial rash |
| MUST EXCLUDE | Cervical artery dissection | Unilateral head or neck pain; may follow minor trauma; Horner syndrome; focal neurological signs | Neck pain; Horner syndrome; stroke symptoms in young patient |
| LESS COMMON | Reversible cerebral vasoconstriction syndrome | Recurrent thunderclap headaches over days to weeks; triggered by exertion, Valsalva, or drugs | Recurrent thunderclap; triggered by vasoactive substances |
| LESS COMMON | Cerebral venous sinus thrombosis | Progressive headache; may have seizures; focal signs; risk factors include pregnancy, OCP use, thrombophilia | Progressive course; seizures; papilledema; hypercoagulable state |
| LESS COMMON | Pituitary apoplexy | Sudden severe headache; visual field defects; ophthalmoplegia; may have hypopituitarism | Known pituitary adenoma; visual loss; altered consciousness |
| COMMON (once serious causes excluded) | First migraine attack | Unilateral; throbbing; moderate-severe; nausea; photophobia; lasts 4-72 hours | None if typical features; diagnose only after excluding secondary causes |
| COMMON | Primary thunderclap headache | Sudden severe headache with negative investigations; diagnosis of exclusion | Must exclude all secondary causes first |
Acute Recurrent Headache (Episodic Pattern)
| Probability | Condition | Approximate Frequency | Key Distinguishing Features |
|---|---|---|---|
| VERY COMMON | Episodic tension-type headache | Up to 80% lifetime prevalence | Bilateral; pressing or tightening; mild-moderate; no nausea; no significant photophobia; can continue activities |
| COMMON | Migraine without aura | 12% of adults; 18% of women | Unilateral (can be bilateral); pulsating; moderate-severe; nausea and/or vomiting; photophobia and phonophobia; worse with activity; 4-72 hours |
| COMMON | Migraine with aura | 5-6% of adults | Visual aura (most common): scintillating scotoma, zigzag lines; sensory aura; speech disturbance; aura develops over 5-60 minutes; headache follows within 60 minutes |
| LESS COMMON | Cluster headache | 0.1% of population; male predominance 3:1 | Strictly unilateral orbital/supraorbital pain; severe or very severe; 15-180 minutes; restlessness; ipsilateral autonomic features (lacrimation, conjunctival injection, rhinorrhea, ptosis, miosis); occurs in clusters |
| LESS COMMON | Paroxysmal hemicrania | Rare; female predominance | Similar to cluster but shorter attacks (2-30 minutes); more frequent (greater than 5 per day); absolute response to indomethacin |
| LESS COMMON | Hemicrania continua | Rare | Continuous strictly unilateral headache with autonomic features and migrainous features; absolute response to indomethacin |
| LESS COMMON | Primary stabbing headache | 2% of population | Brief stabs lasting seconds; single or series; often in migraine patients; no autonomic features |
| LESS COMMON | Primary exertional headache | 1% of population | Brought on by physical exertion; pulsating; lasts minutes to 48 hours; must exclude subarachnoid hemorrhage and arterial dissection on first presentation |
| LESS COMMON | Primary headache associated with sexual activity | 1% of population; male predominance | Occurs during sexual activity; may be thunderclap at orgasm; must exclude subarachnoid hemorrhage initially |
Chronic Daily Headache (15 or more days per month for greater than 3 months)
| Probability | Condition | Approximate Frequency | Key Distinguishing Features |
|---|---|---|---|
| VERY COMMON | Medication overuse headache | 1-2% of population; up to 50% of chronic daily headache | Daily or near-daily headache; regular use of acute medications (simple analgesics ≥15 days/month; triptans/opioids/combination ≥10 days/month); headache worsens despite treatment |
| COMMON | Chronic migraine | 2% of population | Headache on ≥15 days/month; at least 8 days with migraine features; evolved from episodic migraine; often coexists with medication overuse |
| COMMON | Chronic tension-type headache | 2-3% of population | Headache on ≥15 days/month; bilateral pressing quality; mild-moderate; minimal nausea; pericranial tenderness often present |
| LESS COMMON | New daily persistent headache | Rare | Daily headache from onset; patient can pinpoint exact date it started; may follow viral illness; featureless or migraine-like; often refractory to treatment |
| LESS COMMON | Hemicrania continua | Rare | Continuous strictly unilateral headache; autonomic features; migrainous exacerbations; responds completely to indomethacin |
Secondary Headaches: Causes to Consider
Vascular
Subarachnoid hemorrhage
Intracerebral hemorrhage
Ischemic stroke
Cerebral venous sinus thrombosis
Arterial dissection (carotid, vertebral)
Giant cell arteritis
Reversible cerebral vasoconstriction syndrome
Hypertensive emergency
Infectious and Inflammatory
Bacterial meningitis
Viral meningitis
Encephalitis
Brain abscess
Sinusitis
Systemic infection with fever
HIV-related headache
Post-infectious headache
Structural and Pressure-Related
Brain tumor (primary or metastatic)
Idiopathic intracranial hypertension
Intracranial hypotension (CSF leak)
Subdural hematoma
Hydrocephalus
Chiari malformation
Post-traumatic headache
Colloid cyst of third ventricle
Other Secondary Causes
Medication overuse headache
Cervicogenic headache
Acute glaucoma
Temporomandibular disorder
Trigeminal neuralgia
Carbon monoxide poisoning
Altitude headache
Obstructive sleep apnea
Drug-Induced Headache
| Drug or Drug Class | Mechanism | Characteristics | Time to Resolution After Stopping |
|---|---|---|---|
| Simple analgesics (paracetamol, NSAIDs) | Central sensitization; altered pain modulation with chronic use | Daily dull headache; improves briefly after dose then recurs | 2-4 weeks; may worsen initially during withdrawal |
| Triptans | Serotonin receptor changes; rebound effect | Migraine-like features; increasing frequency of use | 1-2 weeks; withdrawal may trigger migraine attacks |
| Opioids | Opioid-induced hyperalgesia; dependence | Daily headache; requires increasing doses; associated with other opioid side effects | 2-4 weeks; significant withdrawal symptoms |
| Combination analgesics (with caffeine or codeine) | Combined mechanisms; caffeine withdrawal adds component | Most likely to cause medication overuse headache | 2-4 weeks; caffeine withdrawal headache in first days |
| Nitrates (GTN, isosorbide) | Vasodilation; nitric oxide-mediated | Immediate headache after dose; throbbing; dose-related | Resolves within hours of dose; tolerance may develop |
| Phosphodiesterase inhibitors (sildenafil, tadalafil) | Vasodilation via nitric oxide pathway | Throbbing headache; facial flushing; dose-related | Resolves within hours as drug effect wears off |
| Calcium channel blockers | Vasodilation | Throbbing headache; may occur at initiation or dose increase | Days to weeks; may resolve with continued use |
| Dipyridamole | Vasodilation; adenosine potentiation | Throbbing headache; common at initiation | Often improves over days; may need dose reduction |
| Hormone therapy (estrogen, oral contraceptives) | Fluctuations in estrogen levels | May trigger or worsen migraine; occurs with pill-free interval | Variable; consider continuous regimen or alternative |
| Proton pump inhibitors | Unknown; possibly related to magnesium depletion | Chronic headache with long-term use | Weeks after discontinuation |
| Caffeine withdrawal | Adenosine receptor upregulation; rebound vasodilation | Bilateral throbbing headache; fatigue; begins 12-24 hours after last caffeine | Peaks at 1-2 days; resolves within 1 week |
Headache in Special Populations
Headache in Patients Over 50
- Giant cell arteritis: Temporal headache; jaw claudication; scalp tenderness; visual symptoms; elevated ESR and CRP
- Subdural hematoma: May follow minor trauma; progressive; fluctuating consciousness
- Brain metastases: History of malignancy; progressive; focal signs
- Trigeminal neuralgia: Peak incidence 50-70 years
- Medication-related: Polypharmacy increases risk
Headache in Pregnancy
- Pre-eclampsia/eclampsia: After 20 weeks; hypertension; proteinuria; visual disturbance; hyperreflexia
- Cerebral venous thrombosis: Increased risk peripartum
- Pituitary apoplexy: Pituitary enlarges in pregnancy
- Posterior reversible encephalopathy syndrome: Associated with pre-eclampsia
- Migraine: Often improves in pregnancy; may worsen postpartum
Quick Reference: “If You See This, Think This”
| Clinical Clue | Think This First | Next Step |
|---|---|---|
| Thunderclap onset (maximum in seconds) | Subarachnoid hemorrhage until proven otherwise | CT head immediately; if negative, lumbar puncture at 12 hours |
| Fever + neck stiffness + headache | Meningitis | Blood cultures; lumbar puncture (if no contraindication); empiric antibiotics immediately |
| New headache age greater than 50 + scalp tenderness | Giant cell arteritis | Urgent ESR and CRP; start prednisolone before biopsy |
| Unilateral headache + ipsilateral red eye + lacrimation | Cluster headache (or other trigeminal autonomic cephalalgia) | High-flow oxygen; subcutaneous sumatriptan; refer neurology |
| Daily headache + taking painkillers most days | Medication overuse headache | Identify offending medication; plan supervised withdrawal |
| Headache worse lying down + papilledema | Raised intracranial pressure (mass, idiopathic intracranial hypertension) | Urgent CT/MRI; if normal and idiopathic intracranial hypertension suspected, lumbar puncture with opening pressure |
| Headache worse when upright + recent lumbar puncture | Post-dural puncture headache (intracranial hypotension) | Conservative management; epidural blood patch if severe or persistent |
| Unilateral headache + Horner syndrome | Carotid or vertebral artery dissection | Urgent CT or MR angiography of head and neck |
| Morning headache in obese patient with snoring | Obstructive sleep apnea | Sleep study; assess for other causes of raised intracranial pressure |
| Headache + jaw claudication + visual symptoms in elderly | Giant cell arteritis with threatened vision | Emergency high-dose corticosteroids; same-day ophthalmology review |
| Brief electric shock pains triggered by touch | Trigeminal neuralgia | MRI brain with trigeminal protocol; carbamazepine |
| Bilateral headache with household contacts affected | Carbon monoxide poisoning | Remove from environment; measure carboxyhemoglobin; high-flow oxygen |
6. Diagnostic Investigations
A stepwise, cost-effective approach guided by clinical suspicion
The majority of primary headache disorders are diagnosed clinically based on history and a normal examination. Investigations are indicated when red flags are present, when secondary headache is suspected, or when the diagnosis is uncertain. The key principle is targeted investigation based on clinical suspicion rather than routine screening.
Indications for Investigation:
- Any red flag present (SNOOP4 criteria)
- First or worst headache
- Change in established headache pattern
- Abnormal neurological examination
- Headache not responding to appropriate treatment
- Atypical features that do not fit a primary headache diagnosis
- Patient over 50 with new headache (to exclude giant cell arteritis and secondary causes)
Baseline Investigations When Secondary Cause Suspected
| Investigation | Purpose | What to Look For | Practical Points |
|---|---|---|---|
| Full blood count | Screen for infection, anemia, malignancy | Leukocytosis (infection); anemia; thrombocytosis | Non-specific but useful baseline |
| Erythrocyte sedimentation rate (ESR) | Screen for giant cell arteritis and inflammatory conditions | ESR greater than 50 mm/hr concerning for giant cell arteritis; use age-adjusted normal (age/2 for men; (age+10)/2 for women) | Essential in all patients over 50 with new headache |
| C-reactive protein (CRP) | Inflammatory marker; complements ESR | Elevated in giant cell arteritis, infection, inflammatory conditions | More sensitive than ESR for acute inflammation; use both for giant cell arteritis |
| Urea and electrolytes | Assess for metabolic causes; baseline before contrast imaging | Hyponatremia can cause headache; renal function for contrast safety | Routine baseline investigation |
| Glucose | Hypoglycemia and hyperglycemia can cause headache | Low glucose; diabetic ketoacidosis | Check in acute presentations |
| Thyroid function tests | Thyroid disease associated with headache | Hypothyroidism or hyperthyroidism | Consider in chronic headache workup |
Neuroimaging: CT versus MRI
| Modality | Best For | Limitations | When to Choose |
|---|---|---|---|
| CT head (non-contrast) | Acute hemorrhage; large masses; hydrocephalus; skull fractures | Poor sensitivity for posterior fossa; misses small lesions; radiation exposure | First-line for emergency presentations; suspected subarachnoid hemorrhage; trauma |
| CT head with contrast | Suspected mass lesion; infection; inflammatory conditions | Contrast reactions; requires adequate renal function | When mass or infection suspected and MRI not immediately available |
| CT angiography (CTA) | Aneurysms; arterial dissection; cerebral venous thrombosis | Radiation; contrast required; may miss small aneurysms | Suspected subarachnoid hemorrhage with negative CT; suspected dissection |
| CT venography (CTV) | Cerebral venous sinus thrombosis | Contrast required; radiation | When cerebral venous thrombosis suspected |
| MRI brain | Posterior fossa; white matter lesions; pituitary; subtle pathology; venous thrombosis | Time; availability; contraindications (pacemakers, some implants); claustrophobia | Preferred for non-emergency workup; posterior fossa symptoms; pituitary pathology |
| MR angiography (MRA) | Aneurysms; dissection; vasculitis; reversible cerebral vasoconstriction syndrome | May miss small aneurysms; flow artifacts | Follow-up of known aneurysm; suspected vasculitis; recurrent thunderclap |
| MR venography (MRV) | Cerebral venous sinus thrombosis | May have flow-related artifacts | Suspected cerebral venous thrombosis; young patient with papilledema |
Key Points on Neuroimaging
- CT is the first-line emergency investigation — fast, widely available, excellent for acute hemorrhage
- MRI is superior for most non-emergency indications — better soft tissue resolution, no radiation, better for posterior fossa
- CT for subarachnoid hemorrhage has 98% sensitivity within 6 hours — sensitivity drops to 93% at 24 hours and continues to fall thereafter
- Negative CT does not exclude subarachnoid hemorrhage — lumbar puncture required if clinical suspicion remains
Lumbar Puncture
Indications
- Suspected meningitis or encephalitis
- Suspected subarachnoid hemorrhage with negative CT
- Suspected idiopathic intracranial hypertension (measure opening pressure)
- Suspected intracranial hypotension (measure opening pressure)
- Suspected carcinomatous meningitis
- Suspected central nervous system infection in immunocompromised patients
Key Findings
- Opening pressure: Normal 10-20 cm H2O; greater than 25 cm H2O suggests raised pressure
- Xanthochromia: Yellow discoloration from bilirubin; positive from 12 hours to 2 weeks after subarachnoid hemorrhage
- Cell count: Pleocytosis in infection; predominantly neutrophils in bacterial meningitis; lymphocytes in viral/TB
- Protein: Elevated in infection, inflammation, malignancy
- Glucose: Low CSF:serum ratio (less than 0.4) in bacterial meningitis
Contraindications to Lumbar Puncture
- Signs of raised intracranial pressure with risk of herniation — perform CT first
- Focal neurological signs — image first to exclude mass lesion
- Coagulopathy or anticoagulation (may need reversal or alternative approach)
- Local infection at puncture site
- Unstable patient — stabilize first; do not delay antibiotics for suspected meningitis
Targeted Investigations by Suspected Etiology
If Suspecting Subarachnoid Hemorrhage
First-Line Tests
- CT head (non-contrast): Sensitivity 98% within 6 hours; look for blood in basal cisterns, sylvian fissure, interhemispheric fissure
- Lumbar puncture (if CT negative): Perform at least 12 hours after headache onset; look for xanthochromia (spectrophotometry) and raised red blood cell count that does not clear
Second-Line Tests
- CT angiography: To identify source of hemorrhage (aneurysm, AVM)
- MRI/MRA: If CT and lumbar puncture equivocal; more sensitive for subacute blood
- Digital subtraction angiography: Gold standard for aneurysm detection; may be needed if CTA negative but high suspicion
If Suspecting Giant Cell Arteritis
First-Line Tests
- ESR: Typically greater than 50 mm/hr; may be greater than 100 mm/hr; normal ESR does not exclude giant cell arteritis (10-20% have normal ESR)
- CRP: Usually elevated; more sensitive than ESR
- Platelet count: Reactive thrombocytosis common
Definitive Tests
- Temporal artery biopsy: Should be performed within 2 weeks of starting steroids; skip lesions mean negative biopsy does not exclude diagnosis
- Temporal artery ultrasound: “Halo sign” of arterial wall edema; operator-dependent; increasingly used as first-line
- PET-CT or MRA: For large vessel vasculitis assessment
If Suspecting Idiopathic Intracranial Hypertension
First-Line Tests
- MRI brain with MRV: Exclude mass lesion and venous thrombosis; look for empty sella, flattened posterior globe, tortuous optic nerves
- Fundoscopy: Papilledema; may be asymmetric
- Visual field testing: Enlarged blind spot; peripheral constriction
Confirmatory Tests
- Lumbar puncture: Opening pressure greater than 25 cm H2O (measured in lateral decubitus position); normal CSF composition
- OCT (optical coherence tomography): Quantify optic nerve head swelling; monitor response to treatment
If Suspecting Meningitis
First-Line Tests
- Blood cultures: Obtain before antibiotics if possible; positive in 50% of bacterial meningitis
- Lumbar puncture: Cell count, protein, glucose, Gram stain, culture, PCR for viruses
- CT head before lumbar puncture if: Immunocompromised, history of CNS disease, new seizure, papilledema, altered consciousness, focal neurological deficit
Additional Tests
- Meningococcal and pneumococcal PCR: Especially if antibiotics given before lumbar puncture
- CSF viral PCR panel: HSV, VZV, enterovirus
- Cryptococcal antigen: In immunocompromised patients
- TB PCR and culture: If subacute presentation or risk factors
Empiric Treatment Trials as Diagnostic Tools
Therapeutic Trial Approach
For certain headache disorders, response to specific treatment can confirm the diagnosis. This approach is particularly useful when investigations are normal and a primary headache disorder is suspected.
| Suspected Condition | Treatment Trial | Expected Response | Interpretation |
|---|---|---|---|
| Paroxysmal hemicrania | Indomethacin 25mg three times daily, increasing to 75mg three times daily | Complete resolution within 1-2 days | Absolute response to indomethacin is diagnostic criterion; no response excludes diagnosis |
| Hemicrania continua | Indomethacin 25mg three times daily, increasing to 75mg three times daily | Complete resolution within 1-2 days | Absolute response required for diagnosis; partial response suggests other diagnosis |
| Cluster headache | High-flow oxygen (12-15 L/min via non-rebreather) or subcutaneous sumatriptan 6mg | Significant improvement within 15-20 minutes | Good response supports diagnosis; helps confirm in unclear cases |
| Medication overuse headache | Withdrawal of overused medication | Improvement within 2-4 weeks (often worsening in first 1-2 weeks) | Resolution or significant improvement confirms diagnosis |
| Cervicogenic headache | Greater occipital nerve block with local anesthetic | Temporary relief of headache | Response supports cervicogenic contribution; helps guide further treatment |
| Trigeminal neuralgia | Carbamazepine 100mg twice daily, titrating up | Significant reduction in attack frequency and severity | Good response supports diagnosis; continue if effective |
Quick Reference: Which Investigation When?
| Clinical Scenario | First Investigation | Additional Investigations |
|---|---|---|
| Thunderclap headache | CT head (non-contrast) immediately | Lumbar puncture at 12 hours if CT negative; CTA if subarachnoid hemorrhage confirmed |
| Fever + headache + neck stiffness | Blood cultures, then lumbar puncture (CT first if contraindications) | Do not delay antibiotics for investigations |
| New headache age greater than 50 | ESR and CRP (same day) | MRI brain; temporal artery biopsy or ultrasound if giant cell arteritis suspected |
| Headache with papilledema | MRI brain with MRV | Lumbar puncture with opening pressure (after imaging excludes mass) |
| Progressive headache over weeks | MRI brain with contrast | Guided by findings; consider lumbar puncture if imaging normal |
| Headache with focal neurological signs | CT head (emergency) or MRI brain (urgent) | MRA/CTA if vascular cause suspected |
| Typical migraine pattern, normal examination | No investigation required | Clinical diagnosis; investigate only if atypical features or treatment failure |
| Chronic daily headache with analgesic overuse | Usually no investigation required | Consider MRI if first presentation or atypical features |
7. Pattern Recognition and Clinical Decision-Making
Practical algorithms and decision pathways
Step 1: Is This Urgent?
| Clinical Scenario | Urgency Level | Immediate Action |
|---|---|---|
| Thunderclap headache (maximum intensity within seconds) | EMERGENT | Immediate CT head; if negative, lumbar puncture at 12 hours; do not discharge without excluding subarachnoid hemorrhage |
| Headache with fever, neck stiffness, altered consciousness | EMERGENT | Blood cultures; empiric antibiotics immediately; lumbar puncture (CT first if focal signs or reduced consciousness) |
| Headache with new focal neurological deficit | EMERGENT | Urgent CT head; consider stroke pathway if appropriate; neurology review |
| Headache with papilledema | EMERGENT | Urgent MRI brain with venography; do not perform lumbar puncture until imaging excludes mass |
| New headache age greater than 50 with scalp tenderness or visual symptoms | URGENT (same day) | ESR and CRP immediately; start prednisolone 60mg if giant cell arteritis suspected; do not wait for biopsy |
| Severe cluster headache attack | URGENT | High-flow oxygen 12-15 L/min; subcutaneous sumatriptan 6mg; arrange neurology follow-up |
| Progressive headache worsening over days to weeks | URGENT (within days) | MRI brain with contrast; baseline bloods including ESR and CRP; neurology referral |
| Typical migraine in patient with established diagnosis | ROUTINE | Acute treatment; assess for medication overuse; consider prophylaxis if frequent |
| Chronic daily headache, stable pattern, normal examination | ROUTINE | Assess for medication overuse; review diagnosis; optimize management; routine neurology referral if refractory |
Step 2: Classify by Temporal Pattern
Acute Single Episode
First or worst headache
Proceed to Algorithm A — exclude secondary causes
Acute Recurrent
Episodic with pain-free intervals
Proceed to Algorithm B — classify primary headache type
Chronic Daily
15 or more days per month
Proceed to Algorithm C — assess for medication overuse and transformation
Step 3: Follow the Appropriate Algorithm
Algorithm A: Acute New-Onset Headache
| Clinical Scenario | Most Likely Diagnosis | Action |
|---|---|---|
| Thunderclap onset + worst headache ever | Subarachnoid hemorrhage until excluded | CT head immediately; lumbar puncture if CT negative (at 12 hours); CTA if blood found |
| Fever + neck stiffness + photophobia | Meningitis | Blood cultures; empiric antibiotics; lumbar puncture (CT first if indicated) |
| Unilateral headache + Horner syndrome + neck pain | Carotid or vertebral dissection | Urgent CTA or MRA head and neck; anticoagulation if confirmed |
| Age greater than 50 + new headache + jaw claudication + visual symptoms | Giant cell arteritis | ESR and CRP; start prednisolone 60mg immediately; arrange temporal artery biopsy within 2 weeks |
| Recurrent thunderclap headaches + recent vasoactive drug use | Reversible cerebral vasoconstriction syndrome | MRA; stop offending agents; supportive care; monitor for complications |
| Progressive headache + risk factors for thrombosis + papilledema | Cerebral venous sinus thrombosis | MRV or CTV; anticoagulation if confirmed |
| No red flags + typical migraine features + first attack | First migraine (diagnosis of exclusion in acute setting) | Treat acutely; arrange follow-up; advise to return if different or worsening |
Algorithm B: Acute Recurrent Headache
| Clinical Features | Likely Diagnosis | Action |
|---|---|---|
| Unilateral, pulsating, moderate-severe, nausea, photophobia, phonophobia, 4-72 hours, worse with activity | Migraine without aura | Acute treatment (NSAID, triptan); lifestyle modification; consider prophylaxis if ≥4 attacks/month or significant disability |
| As above with preceding visual or sensory aura lasting 5-60 minutes | Migraine with aura | As for migraine; avoid combined oral contraceptives; consider aspirin for vascular risk |
| Bilateral, pressing, mild-moderate, no nausea, no photophobia, 30 minutes to 7 days | Episodic tension-type headache | Simple analgesia PRN; stress management; limit analgesic use to prevent medication overuse |
| Strictly unilateral orbital pain, severe, 15-180 minutes, ipsilateral autonomic features, restlessness, occurs in clusters | Cluster headache | Acute: oxygen 12-15 L/min or sumatriptan SC; Transitional: prednisolone or greater occipital nerve block; Preventive: verapamil; refer neurology |
| Strictly unilateral, frequent attacks (greater than 5/day), 2-30 minutes, autonomic features | Paroxysmal hemicrania | Indomethacin trial (must have complete response); MRI brain to exclude structural cause |
| Brief stabbing pains lasting seconds, variable location, no autonomic features | Primary stabbing headache | Reassurance; indomethacin if frequent; often associated with migraine |
| Lancinating pain in trigeminal distribution, triggered by touch, eating, or talking | Trigeminal neuralgia | MRI brain with trigeminal protocol; carbamazepine; refer neurology or neurosurgery |
Algorithm C: Chronic Daily Headache
Key Question: Is the patient using acute medications on 10 or more days per month?
| Clinical Features | Likely Diagnosis | Action |
|---|---|---|
| Daily headache + analgesics ≥15 days/month OR triptans/opioids/combination ≥10 days/month | Medication overuse headache (likely with underlying chronic migraine or chronic tension-type) | Educate patient; plan medication withdrawal (abrupt or tapered); bridging therapy; start preventive; expect 2-4 weeks worsening before improvement |
| Headache ≥15 days/month + ≥8 days with migraine features + evolved from episodic migraine | Chronic migraine | Address medication overuse if present; preventive therapy (topiramate, amitriptyline, propranolol, CGRP antibody); lifestyle modification |
| Headache ≥15 days/month + bilateral pressing + mild-moderate + minimal nausea | Chronic tension-type headache | Amitriptyline first-line preventive; address stress, sleep, posture; limit analgesics; consider physiotherapy |
| Daily headache from onset + patient recalls exact start date + no prior headache history | New daily persistent headache | MRI brain to exclude secondary cause; try preventives as for chronic migraine; often refractory |
| Continuous strictly unilateral + autonomic features + complete response to indomethacin | Hemicrania continua | Indomethacin (diagnostic and therapeutic); gastric protection; MRI if not done |
“What Do I Do If…” Decision Reference
| Clinical Situation | Immediate Action | Next Step |
|---|---|---|
| CT negative but still suspect subarachnoid hemorrhage | Do not discharge; arrange lumbar puncture at 12 hours from headache onset | If xanthochromia positive or RBC elevated and not clearing, proceed to CTA; neurosurgery referral |
| Patient with headache refuses lumbar puncture | Document detailed discussion of risks; explain possibility of missed subarachnoid hemorrhage | Consider CTA as alternative (lower sensitivity for small bleeds); safety-net advice; arrange follow-up |
| Suspected giant cell arteritis but normal ESR | Do not exclude giant cell arteritis on ESR alone (10-20% have normal ESR); check CRP | If clinical suspicion high, start prednisolone and arrange temporal artery biopsy or ultrasound |
| Migraine not responding to triptans | Ensure correct timing (early in attack); adequate dose; try different triptan | Consider adding NSAID; assess for medication overuse; review diagnosis; consider preventive |
| Patient taking painkillers daily but resistant to stopping | Educate about medication overuse headache cycle; explain it prevents other treatments working | Offer supported withdrawal plan; consider bridging therapy; start preventive; arrange follow-up |
| Headache in pregnancy | Assess for pre-eclampsia (blood pressure, proteinuria, symptoms); check for red flags | MRI (no gadolinium) if imaging needed; paracetamol for acute treatment; avoid triptans in first trimester and NSAIDs in third |
| Cluster headache attack in emergency department | High-flow oxygen 12-15 L/min via non-rebreather mask OR subcutaneous sumatriptan 6mg | Arrange urgent neurology follow-up; consider starting verapamil or prednisolone bridge; provide home oxygen prescription |
| Post-lumbar puncture headache | Confirm orthostatic nature (worse upright, better lying flat); analgesia; fluids; caffeine | If severe or persistent beyond 48-72 hours, consider epidural blood patch |
| Headache with aura lasting longer than 60 minutes | Consider stroke or TIA if symptoms atypical; assess for migraine with prolonged aura | MRI brain; if acute stroke suspected, follow stroke pathway; neurology review |
| Patient requests opioids for migraine | Explain opioids are not first-line for migraine and increase risk of medication overuse headache | Offer appropriate alternatives (NSAIDs, triptans, antiemetics); address pain and disability concerns; investigate underlying issues |
Troubleshooting Refractory Headache
Ask These Questions When Headache Does Not Respond to Treatment
- Is the diagnosis correct? — Reconsider differential; look for red flags missed; consider secondary causes
- Is there medication overuse? — Most common reason for treatment failure in chronic headache
- Was the treatment adequate? — Correct drug? Adequate dose? Sufficient duration (preventives need 2-3 months)?
- Was adherence good? — Check patient actually taking medication as prescribed
- Are there multiple headache types? — Patient may have migraine AND tension-type AND medication overuse
- Are there comorbidities? — Depression, anxiety, sleep disorders, and chronic pain conditions affect headache outcomes
- Are there perpetuating factors? — Ongoing stress, poor sleep, caffeine excess, hormonal factors
- Does the patient need specialist referral? — Neurology or headache specialist for complex or refractory cases
When to Refer to Neurology or Headache Specialist
Urgent Referral
- Suspected secondary headache requiring specialist investigation
- Cluster headache (for initiation of oxygen and verapamil)
- New neurological deficit with headache
- Trigeminal neuralgia (for diagnosis confirmation and treatment)
- Idiopathic intracranial hypertension with visual compromise
Routine Referral
- Diagnostic uncertainty despite appropriate workup
- Chronic migraine not responding to first-line preventives
- Medication overuse headache with failed withdrawal attempts
- Consideration for CGRP monoclonal antibodies or botulinum toxin
- Significant disability despite appropriate management
- Patient request for specialist opinion
8. Clinical Pearls and Pitfalls
Practical wisdom — learn from successes and avoid common mistakes
Must-Know Clinical Pearls
The history is everything: In headache diagnosis, approximately 90% of the diagnosis comes from a careful history. Examination and investigations serve mainly to confirm or exclude suspected diagnoses.
Thunderclap headache demands action: Any headache reaching maximum intensity within seconds to one minute must be investigated for subarachnoid hemorrhage, regardless of other features. A negative CT does not exclude subarachnoid hemorrhage — lumbar puncture is required.
Giant cell arteritis is a medical emergency: In any patient over 50 with new headache, always consider giant cell arteritis. Start steroids immediately if suspected — do not wait for biopsy. Vision loss is preventable but irreversible once established.
Medication overuse is the most common cause of treatment failure: Always ask about analgesic use in chronic headache. Patients taking acute medications on more than 10-15 days per month cannot improve until this is addressed.
Normal examination does not mean benign: Many serious conditions (subarachnoid hemorrhage, early meningitis, giant cell arteritis) can present with normal neurological examination. The pattern and tempo of headache are more important than examination findings.
Cluster headache is often misdiagnosed: Average delay to diagnosis is 5-7 years. Look for the triad: strictly unilateral severe pain, short duration (15-180 minutes), and ipsilateral autonomic features. Restlessness during attacks distinguishes it from migraine.
Indomethacin-responsive headaches: Paroxysmal hemicrania and hemicrania continua have an absolute response to indomethacin — this is both diagnostic and therapeutic. Always trial indomethacin in appropriate clinical scenarios.
Preventive medications need time: Most headache preventives take 6-8 weeks to show effect at adequate doses. Do not abandon a preventive trial too early — patients often stop medications prematurely.
Critical Pitfalls to Avoid
Discharging thunderclap headache with negative CT: CT sensitivity for subarachnoid hemorrhage decreases significantly after 6 hours and continues to fall. Lumbar puncture is mandatory if subarachnoid hemorrhage is suspected and CT is negative or delayed.
Excluding giant cell arteritis based on normal ESR: Up to 20% of patients with biopsy-proven giant cell arteritis have normal ESR. Always check CRP as well, and treat empirically if clinical suspicion is high.
Attributing all headaches to “migraine” without systematic assessment: Migraine is common but secondary causes can coexist. Always screen for red flags and consider whether the presentation is truly typical for migraine.
Prescribing opioids for recurrent primary headache: Opioids are associated with worse outcomes in headache, increase risk of medication overuse headache, and should almost never be used for migraine or tension-type headache.
Failing to ask about medication use: Patients often do not volunteer information about over-the-counter analgesic use. Specifically ask “How many days per month do you take ANY painkiller?”
Ordering MRI for every headache: Neuroimaging is not indicated for typical primary headache with normal examination. Inappropriate imaging increases costs, delays diagnosis, and may find incidental abnormalities causing unnecessary anxiety.
Delaying antibiotics in suspected meningitis: If bacterial meningitis is suspected, give empiric antibiotics immediately. Do not wait for CT or lumbar puncture results. Every hour of delay increases mortality.
Ignoring the cervical spine: Cervicogenic headache is underdiagnosed. The trigeminocervical complex means neck pathology commonly causes headache. Always examine the cervical spine in headache patients.
Key Takeaways
- Primary headaches (migraine, tension-type, cluster) account for approximately 90% of headaches, but secondary causes must always be considered and excluded when red flags are present.
- Use the SNOOP4 mnemonic to screen for red flags: Systemic symptoms, Neurological signs, Onset sudden, Older age, Pattern change, Positional, Precipitated by Valsalva, Papilledema.
- Thunderclap headache requires immediate investigation — CT within 6 hours has 98% sensitivity for subarachnoid hemorrhage, but lumbar puncture is needed if CT is negative.
- Giant cell arteritis should be considered in every patient over 50 with new headache. ESR and CRP should be checked, and steroids started immediately if suspected.
- Medication overuse headache affects 1-2% of the population and is the most common cause of chronic daily headache that fails to respond to treatment.
- The diagnosis of primary headache is clinical — neuroimaging is indicated only when red flags are present, the pattern changes, or there is diagnostic uncertainty.
- Cluster headache is frequently misdiagnosed. Look for strictly unilateral severe attacks with autonomic features and restlessness. Treat acutely with high-flow oxygen or subcutaneous sumatriptan.
- Paroxysmal hemicrania and hemicrania continua have an absolute response to indomethacin — this response is diagnostic.
- A normal neurological examination does not exclude serious pathology. The tempo and pattern of headache are the most important diagnostic features.
- Prevention is better than cure — patients with frequent migraines benefit from preventive therapy, but this requires adequate dosing and duration (at least 8 weeks).
Quick Reference Algorithm
Systematic Approach to Headache:
- Screen for red flags (SNOOP4) — if present, investigate urgently for secondary causes
- Classify by temporal pattern — acute single, acute recurrent, or chronic daily
- Take a detailed history using HEADACHE mnemonic — onset, evolution, associated features, description, area, circumstances, prior history, effect on life
- Perform focused examination — vital signs, fundoscopy, neurological examination, cervical spine, temporal arteries if age over 50
- Make a working diagnosis — match clinical features to ICHD-3 criteria for primary headaches; investigate if secondary cause suspected
- Assess for medication overuse — in any patient with frequent headache, specifically ask about analgesic use
- Initiate appropriate treatment — acute treatment, lifestyle modification, and preventive therapy when indicated
- Arrange follow-up — reassess response, monitor for medication overuse, adjust treatment as needed
- Refer to specialist if — diagnostic uncertainty, treatment failure, or complex presentations
Common Presentations: Pattern Recognition
| Pattern | Think | Key Action |
|---|---|---|
| Unilateral + throbbing + nausea + photophobia + 4-72 hours | Migraine | NSAID or triptan acutely; preventive if ≥4/month |
| Bilateral + pressing + mild-moderate + can continue activities | Tension-type headache | Simple analgesia; limit use to prevent medication overuse |
| Unilateral orbital + severe + 15-180 min + eye waters + restless | Cluster headache | Oxygen or sumatriptan SC; start verapamil |
| Daily headache + painkillers most days + not improving | Medication overuse headache | Withdraw offending medication; start preventive |
| Age >50 + new headache + scalp tender + jaw pain + vision changes | Giant cell arteritis | Steroids immediately; temporal artery biopsy |
| Thunderclap + worst headache ever + neck stiffness | Subarachnoid hemorrhage | CT head; lumbar puncture if CT negative |
| Fever + neck stiffness + photophobia + confusion | Meningitis | Antibiotics immediately; blood cultures; lumbar puncture |
| Worse lying down + papilledema + obese young woman | Idiopathic intracranial hypertension | MRI with MRV; lumbar puncture with opening pressure |