11.1 Headaches (Migraine, Tension, Cluster) & Cranial Neuralgias

Headaches (Migraine, Tension, Cluster) & Cranial Neuralgias

Cephalalgia is among the top reasons for ambulatory primary care visits and emergency department consultations across the adult and geriatric lifespan. For the Adult-Gerontology Primary Care Nurse Practitioner (AGPCNP), clinical competency requires rapid, systematic differentiation between benign primary headache syndromes (such as migraine, tension-type, and cluster headaches) and life-threatening secondary headaches caused by intracranial hemorrhage, mass lesions, central nervous system infections, or systemic vasculitis.

Mastering headache evaluation demands an understanding of cranial nociceptive neuroanatomy, disciplined application of the SNOOP4 red-flag algorithm, fluency in evidence-based abortive and prophylactic pharmacology, and vigilance for catastrophic neuro-ophthalmologic emergencies such as Giant Cell Arteritis (GCA).

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1. Neuroanatomy & Pathophysiological Fundamentals

The brain parenchyma itself is entirely devoid of pain receptors (nociceptors). Cephalic pain arises exclusively from the activation of pain-sensitive intracranial and extracranial structures innervated by the trigeminal nerve (Cranial Nerve V), upper cervical nerves (C2 and C3), and the glossopharyngeal (CN IX) and vagus (CN X) nerves.

+-----------------------------------------------------------------------------+
|                   CRANIAL PAIN-SENSITIVE vs. INSENSATE STRUCTURES           |
|                                                                             |
|   PAIN-SENSITIVE STRUCTURES:                                                |
|   * Dura mater (especially base of skull and tentorium cerebelli)           |
|   * Dural venous sinuses and tributary cortical veins                       |
|   * Large intracranial arteries (Circle of Willis, proximal MCA/ACA/PCA)    |
|   * Meningeal arteries (Middle meningeal artery)                            |
|   * Cranial nerves with sensory afferents: CN V (Trigeminal), IX, X         |
|   * Cervical nerve roots: C2 (greater occipital nerve), C3                  |
|   * Extracranial structures: Scalp, pericranial muscles, temporal arteries, |
|     paranasal sinuses, teeth, temporomandibular joint (TMJ), eyes           |
|                                                                             |
|   INSENSATE STRUCTURES:                                                     |
|   * Brain parenchyma (cerebral cortex, basal ganglia, thalamus, cerebellum) |
|   * Ependymal lining of cerebral ventricles                                 |
|   * Choroid plexus                                                          |
|   * Most of the pia-arachnoid mater                                         |
+-----------------------------------------------------------------------------+

The Trigeminovascular System & Neurogenic Inflammation

The common final pathway for migraine and trigeminal autonomic cephalalgias is the Trigeminovascular System (TGVS). Unmyelinated C-fibers and thinly myelinated A-delta fibers from the ophthalmic division of the trigeminal nerve ($V_1$) innervate dural blood vessels. Activation of these fibers triggers antidromic release of vasoactive neuropeptides:

1. Calcitonin Gene-Related Peptide (CGRP): The principal mediator of neurogenic vasodilation, mast cell degranulation, and plasma protein extravasation.
2. Substance P & Neurokinin A: Induce localized sterile neurogenic inflammation, endothelial swelling, and edema.
3. Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP): Amplifies parasympathetic autonomic outflow and nociceptive sensitization.

+-----------------------------------------------------------------------------+
|                THE TRIGEMINOVASCULAR NOCICEPTIVE CASCADE                    |
|                                                                             |
|   Cortical Spreading Depression (CSD) / Hypothalamic Trigger                |
|                               |                                             |
|                               v                                             |
|   Trigeminal Ganglion Activation -> Release of CGRP, Substance P, PACAP     |
|                               |                                             |
|                               v                                             |
|   Meningeal Neurogenic Vasodilation, Mast Cell Degranulation & Inflammation |
|                               |                                             |
|                               v                                             |
|   Trigeminocervical Complex (TCC) -> Thalamus -> Somatosensory Cortex       |
|                               |                                             |
|                               v                                             |
|   Central Sensitization: Hyperalgesia, Cutaneous Allodynia & Photophobia    |
+-----------------------------------------------------------------------------+

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2. Red-Flag Screening: The SNOOP4 Decision Matrix

Before classifying a headache as a primary disorder, the AGPCNP must systematically evaluate for secondary etiologies using the validated SNOOP4 mnemonic. Any positive red flag mandates immediate neuroimaging and targeted diagnostic testing.

+-----------------------------------------------------------------------------+
|                     THE SNOOP4 RED-FLAG DECISION MATRIX                     |
|                                                                             |
|   S - SYSTEMIC SYMPTOMS / SIGNS                                             |
|       - Fever, night sweats, unexplained weight loss, chills                |
|       - Underlying systemic disease: HIV/AIDS, active malignancy, immunosuppression|
|       - Differential: Bacterial/fungal meningitis, encephalitis, brain      |
|         abscess, metastatic intracranial neoplasm.                          |
|                                                                             |
|   N - NEUROLOGIC SYMPTOMS / SIGNS                                           |
|       - Focal deficits (hemiparesis, visual field cuts, aphasia, ataxia)    |
|       - Altered mental status, confusion, personality change, seizures      |
|       - Differential: Ischemic stroke, intracranial hemorrhage, neoplasm,   |
|         dural arteriovenous fistula, cavernous sinus thrombosis.            |
|                                                                             |
|   O - ONSET: SUDDEN / "THUNDERCLAP"                                         |
|       - Reaches maximal peak intensity within seconds to <1 minute          |
|       - "Worst headache of my life"                                        |
|       - Differential: Subarachnoid Hemorrhage (SAH), Reversible Cerebral    |
|         Vasoconstriction Syndrome (RCVS), cervical artery dissection,       |
|         pituitary apoplexy.                                                 |
|                                                                             |
|   O - OLDER AGE OF ONSET (AGE >= 50 YEARS)                                  |
|       - New-onset headache or progressive change in headache phenotype      |
|       - Differential: Giant Cell Arteritis (GCA), primary brain neoplasm,   |
|         chronic subdural hematoma, normotensive hydrocephalus.              |
|                                                                             |
|   P1 - PATTERN CHANGE OR PROGRESSIVE HEADACHE                               |
|       - Progressive worsening in frequency, severity, or character         |
|       - Failure to respond to standard guideline-directed therapies         |
|       - Differential: Space-occupying lesion, chronic meningitis, subdural. |
|                                                                             |
|   P2 - PAPILLEDEMA                                                          |
|       - Bilateral optic disc swelling on fundoscopic examination            |
|       - Differential: Idiopathic Intracranial Hypertension (IIH), mass      |
|         lesion, cerebral venous sinus thrombosis (CVST), malignant HTN.     |
|                                                                             |
|   P3 - PRECIPITATED BY VALSALVA, COUGH, EXERTION, OR SEXUAL ACTIVITY       |
|       - Sudden headache triggered by coughing, sneezing, bending over       |
|       - Differential: Chiari I malformation, posterior fossa mass, aneurysm.|
|                                                                             |
|   P4 - POSITIONAL VARIATION                                                 |
|       - Worsens dramatically when upright / standing -> Low CSF pressure /  |
|         spontaneous intracranial hypotension (SIH / CSF leak).              |
|       - Worsens dramatically when recumbent / awakens patient from sleep -> |
|         Elevated Intracranial Pressure (ICP / mass lesion / hydrocephalus). |
+-----------------------------------------------------------------------------+

Diagnostic Neuroimaging Algorithms

• Emergent Non-Contrast Head CT: The initial test of choice for suspected acute Subarachnoid Hemorrhage (SAH) or acute intracranial bleeding. Sensitivity is $>98%$ within the first 6 hours of headache onset, declining to $\sim 85%$ at 24 hours.
• Lumbar Puncture (LP): Mandatory if thunderclap headache is present and non-contrast CT is negative or equivocal. Evaluate for elevated opening pressure, persistent red blood cells in tubes 1 through 4, and xanthochromia (yellow CSF discoloration via spectrophotometry resulting from hemoglobin degradation, appearing 6–12 hours post-bleed).
• Brain MRI with and without IV Gadolinium Contrast: The superior modality for evaluating structural lesions, posterior fossa pathology, cerebellopontine angle tumors, pituitary apoplexy, pachymeningeal enhancement (CSF leaks), leptomeningeal carcinomatosis, and cerebral venous sinus thrombosis (MRV).

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3. Primary Headache Syndromes: Comparative Taxonomy

+---------------------------------------------------------------------------------------------------------+
|                              PRIMARY HEADACHE COMPARATIVE MATRIX                                        |
|                                                                                                         |
|   FEATURE              MIGRAINE                    TENSION-TYPE (TTH)          CLUSTER HEADACHE         |
|   ---------------------------------------------------------------------------------------------------   |
|   Gender Ratio (F:M)   3 : 1                       1.2 : 1                     1 : 3 to 1 : 4 (Male!)   |
|   Onset Age            15 - 35 years               20 - 40 years               20 - 50 years            |
|   Pain Location        Unilateral (60-70%)         Bilateral (diffuse, band)   Strictly Unilateral      |
|                        Fronto-temporal / ocular    Occipital, frontal, neck    Periorbital, retro-orbital|
|   Pain Quality         Throbbing, pulsating        Pressing, tightening, dull  Excruciating, piercing,  |
|                                                    "vice-like" headband        "hot poker in eye"       |
|   Pain Severity        Moderate to severe          Mild to moderate            Extremely Severe (10/10) |
|   Duration             4 to 72 hours               30 minutes to 7 days        15 to 180 minutes        |
|   Attack Frequency     1-4 per month (episodic)    Variable (episodic/chronic) 1-8 per day during cluster|
|   Aggravation by       YES (prefers quiet, dark    NO (routine activity does   NO (patient is AGITATED, |
|   Routine Activity     room; stays immobile)       not worsen pain)            paces floor, rocks body) |
|   Associated GI        Nausea, vomiting,           ABSENT (no true nausea;     Absent or mild           |
|   Symptoms             anorexia                    anorexia may occur)                                  |
|   Associated Sensory   Photophobia AND             Photophobia OR              Photophobia/phonophobia  |
|   Sensitivities        Phonophobia (both classic)  phonophobia (not both)      ipsilateral to pain only |
|   Autonomic Signs      Infrequent / mild           ABSENT                      PROMINENT & IPSILATERAL: |
|                                                                                Lacrimation, rhinorrhea, |
|                                                                                ptosis, miosis, sweating |
|   Preceding Aura       Present in 25-30%           ABSENT                      ABSENT                   |
|                        (visual scintillations)                                                          |
+---------------------------------------------------------------------------------------------------------+

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4. Migraine: Pathophysiology, Diagnosis & Management

Diagnostic Criteria (ICHD-3)

Migraine without Aura requires at least 5 attacks fulfilling the following:

1. Attack duration lasting 4 to 72 hours (untreated or unsuccessfully treated).
2. Headache has at least two of the following four characteristics:
   • Unilateral location
   • Pulsating (throbbing) quality
   • Moderate or severe pain intensity
   • Aggravation by or causing avoidance of routine physical activity (e.g., walking, climbing stairs)
3. During headache, at least one of the following is present:
   • Nausea and/or vomiting
   • Photophobia AND phonophobia
4. Not better accounted for by another ICHD-3 diagnosis.

Migraine with Aura occurs in $\sim 25%$ of patients. The aura represents a wave of neuronal and glial depolarization followed by sustained inhibition known as Cortical Spreading Depression (CSD). Aura features:

• Visual disturbances (scintillating scotomas, fortification spectra, photopsias, homonymous visual cuts) are most common ($>90%$).
• Sensory symptoms (unilateral paresthesias, numbness spreading across hand and face).
• Speech/language disturbances (dysphasia).
• Characteristics: Spreads gradually over $\ge 5$ minutes, each individual symptom lasts 5–60 minutes, and the headache typically follows within 60 minutes.

+-----------------------------------------------------------------------------+
|                        PHASES OF A MIGRAINE ATTACK                          |
|                                                                             |
|   1. PRODROME (Premonitory: 24-48 hours before pain)                        |
|      - Yawning, food cravings (carbohydrates), neck stiffness, mood swings, |
|        fluid retention, polyuria (hypothalamic activation).                 |
|                               |                                             |
|                               v                                             |
|   2. AURA (5-60 minutes; present in ~25-30%)                                |
|      - Visual fortification spectra, scintillations, sensory paresthesias.  |
|                               |                                             |
|                               v                                             |
|   3. HEADACHE (4-72 hours)                                                  |
|      - Unilateral throbbing pain, photophobia, phonophobia, nausea,         |
|        cutaneous allodynia (pain triggered by brushing hair/light touch).   |
|                               |                                             |
|                               v                                             |
|   4. POSTDROME ("Migraine Hangover": 24-48 hours post-resolution)          |
|      - Cognitive slowing ("brain fog"), exhaustion, dizziness, euphoria.   |
+-----------------------------------------------------------------------------+

Acute (Abortive) Pharmacotherapy

Treatment must be initiated at the earliest onset of pain (during the mild phase or early headache phase) to prevent central sensitization.

+-----------------------------------------------------------------------------+
|                   STRATIFIED ACUTE MIGRAINE ABORTIVE LADDER                 |
|                                                                             |
|   [MILD TO MODERATE ATTACKS]                                                |
|   - Simple NSAIDs: Naproxen sodium (500-550 mg), Ibuprofen (400-800 mg)     |
|   - Combination Analgesics: Acetaminophen + Aspirin + Caffeine (Excedrin)   |
|   - Adjunctive Antiemetics: Metoclopramide (10 mg) or Prochlorperazine      |
|     (10 mg) PO/IV (promotes gastric motility, enhances NSAID absorption)    |
|                                     |                                       |
|                                     v                                       |
|   [MODERATE TO SEVERE ATTACKS / NSAID-REFRACTORY]                           |
|   1. TRIPTANS (5-HT1B/1D Receptor Agonists)                                 |
|      - Sumatriptan: 50-100 mg PO (repeat in 2h, max 200 mg/24h),           |
|        6 mg SC (onset 10-15 min; max 12 mg/24h), 20 mg nasal spray.         |
|      - Zolmitriptan: 2.5-5 mg PO/ODT/nasal spray.                           |
|      - Rizatriptan: 5-10 mg PO/ODT (reduce to 5 mg if taking Propranolol!). |
|      - Eletriptan: 20-40 mg PO (high potency, lipophilic).                  |
|      - Naratriptan / Frovatriptan: Slower onset, longer half-life (26h);     |
|        ideal for menstrually related migraine and prevention of recurrence. |
|                                                                             |
|   2. DITANS (5-HT1F Receptor Agonist)                                       |
|      - Lasmiditan: 50-100-200 mg PO. Lacks vasoconstrictive activity!       |
|      - SAFE in CAD, stroke, PVD, uncontrolled HTN.                          |
|      - Warning: CNS sedation (patient CANNOT drive for >= 8 hours!).        |
|                                                                             |
|   3. GEPANTS (Small-Molecule Oral CGRP Antagonists)                         |
|      - Ubrogepant: 50-100 mg PO.                                            |
|      - Rimegepant: 75 mg PO/ODT (dual-acting: acute abortive & every-other- |
|        day preventive!).                                                    |
|      - Zavegepant: 10 mg nasal spray (rapid non-oral option).               |
|      - No vasoconstriction! Safe in cardiovascular disease. No MOH risk!   |
+-----------------------------------------------------------------------------+

Absolute Contraindications to Triptans and Ergot Derivatives:

• Ischemic coronary artery disease (angina, history of myocardial infarction, coronary vasospasm / Prinzmetal angina).
• History of ischemic stroke or Transient Ischemic Attack (TIA).
• Peripheral vascular disease (claudication, ischemic bowel disease).
• Uncontrolled or severe hypertension ($\text{BP} \ge 160/100\text{ mmHg}$).
• Hemiplegic migraine or migraine with brainstem aura (basilar migraine).
• Concurrent use of Monoamine Oxidase Inhibitors (MAOIs) or within 24 hours of another triptan or ergotamine derivative.

Medication Overuse Headache (MOH / "Rebound Headache")

• Definition (ICHD-3): Headache occurring on $\ge 15\text{ days/month}$ in a patient with a pre-existing headache disorder, resulting from regular overuse of acute headache medications for $>3\text{ months}$:
  • $\ge 10\text{ days/month}$ of triptans, ergots, opioids, or combination analgesics (e.g., acetaminophen/aspirin/caffeine or butalbital combinations).
  • $\ge 15\text{ days/month}$ of simple analgesics (acetaminophen, NSAIDs).
• Clinical Picture: Dull, daily or near-daily, diffuse morning headache that briefly improves after taking the offending medication but recurs predictably as the drug wears off.
• Management: Complete withdrawal/weaning of the overused acute medication, patient education, initiation of non-overused prophylactic bridge therapy (e.g., topiramate, CGRP monoclonal antibodies, or a 10-day prednisone taper).

Preventive (Prophylactic) Migraine Pharmacotherapy

Indications for Preventive Therapy:

• $\ge 4$ headache days per month or $\ge 8$ migraine days per month.
• Attacks causing significant disability or interference with daily activities despite acute therapy.
• Contraindication to, intolerance of, or failure of acute abortive medications.
• Patient preference or presence of rare migraine variants (hemiplegic migraine, brainstem aura).
• Risk of medication overuse headache.

+---------------------------------------------------------------------------------------------------------+
|                         EVIDENCE-BASED PREVENTIVE PHARMACOTHERAPY MATRIX                                |
|                                                                                                         |
|   DRUG CLASS           AGENT & DOSING              CLINICAL PEARLS & COMORBIDITY MATCHING CONTRAINDICATIONS|
|   ---------------------------------------------------------------------------------------------------   |
|   Beta-Blockers        Propranolol (40-160 mg/d)   First-line for young, non-smokers;     Asthma, severe COPD,   |
|                        Metoprolol (50-200 mg/d)    ideal for concurrent HTN, angina,      bradycardia, 2nd/3rd  |
|                        Timolol (20-30 mg/d)        or essential tremor.                   degree AV block.      |
|                                                                                                         |
|   Anticonvulsants      Topiramate (50-100 mg/d)    Promotes WEIGHT LOSS; ideal for obese  History of nephrolith-|
|                                                    patients or idiopathic intracranial    iasis (kidney stones),|
|                                                    HTN. Side effects: paresthesias,       glaucoma, pregnancy   |
|                                                    cognitive slowing ("Dopamax").        (teratogenic: clefts).|
|                                                                                                         |
|                        Divalproex Sodium           High efficacy; beneficial in bipolar   PREGNANCY (neural tube|
|                        / Valproate (500-1500 mg/d) disorder or epilepsy. Side effects:    defects!), hepatic    |
|                                                    weight gain, alopecia, tremor, PCOS.   disease, pancreatitis.|
|                                                                                                         |
|   Tricyclic            Amitriptyline (10-75 mg QHS) First-line for concurrent INSOMNIA,  Cardiac conduction    |
|   Antidepressants      Nortriptyline (10-75 mg QHS) chronic tension headache, depression, abnormalities, QTc    |
|   (TCAs)                                           or fibromyalgia. Promotes sedation.    prolongation, glaucoma|
|                                                    Anticholinergic (dry mouth, constip).  urinary retention/BPH.|
|                                                                                                         |
|   SNRIs                Venlafaxine (75-150 mg/d)   Excellent for comorbid GAD, panic,     Uncontrolled hyper-   |
|                        Duloxetine (60 mg/d)        or chronic musculoskeletal/neuropathic tension (monitor BP). |
|                                                                                                         |
|   CGRP Monoclonal      Erenumab (Aimovog 70/140mg) Subcutaneous monthly injections.       Severe constipation,  |
|   Antibodies           Fremanezumab (Ajovy)        Targets CGRP Receptor (Erenumab) or    uncontrolled hyper-   |
|   (Anti-CGRP mAbs)     Galcanezumab (Emgality)     CGRP Ligand (others). High efficacy,   tension (Erenumab),   |
|                        Eptinezumab (Vyepti IV Q3M) excellent tolerability, no organ tox.  pregnancy.            |
|                                                                                                         |
|   OnabotulinumtoxinA   Botox (155 units across     Indicated EXCLUSIVELY for CHRONIC      Eaton-Lambert, ALS,   |
|                        31 injection sites Q12W)    MIGRAINE (>= 15 headache days/month    myasthenia gravis.    |
|                                                    with >= 8 migraine days for >3 months).                      |
+---------------------------------------------------------------------------------------------------------+

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5. Trigeminal Autonomic Cephalalgias: Cluster Headache

Cluster headache is the most prevalent of the Trigeminal Autonomic Cephalalgias (TACs). It is characterized by severe, unremitting, strictly unilateral lancinating pain centered in the orbital, supraorbital, or temporal region, associated with prominent cranial parasympathetic autonomic symptoms.

Epidemiology & Clinical Presentation

• Male-to-Female Predominance: Historically 4:1 to 3:1 (most common in young to middle-aged adult males, age 20–50).
• Strong Association: Heavy cigarette smoking ($>85%$) and alcohol consumption (alcohol predictably triggers attacks during active cluster periods).
• Periodicity / Circadian Clock: Attacks occur with striking circadian regularity (often awakening the patient precisely 1–2 hours after falling asleep, coinciding with REM sleep, earning the moniker "alarm clock headache"). Cluster periods typically last 6 to 12 weeks, followed by remissions lasting months to years.
• Behavioral Hallmark: Unlike migraineurs who retreat to a quiet, dark room and lie completely motionless, cluster headache patients exhibit profound psychomotor agitation and restlessness (pacing the floor, rocking, holding or hitting their head).

+-----------------------------------------------------------------------------+
|                        CLUSTER HEADACHE CLINICAL PROFILE                    |
|                                                                             |
|   EXCRUCIATING UNILATERAL PERIORBITAL PAIN (15 - 180 MINUTES)               |
|                                  +                                          |
|   AT LEAST ONE IPSILATERAL CRANIAL AUTONOMIC SIGN:                          |
|   * Conjunctival injection (red eye) and/or Lacrimation (tearing)           |
|   * Nasal congestion and/or Rhinorrhea (runny nostril)                      |
|   * Eyelid edema (puffy lid)                                                |
|   * Forehead and facial sweating / flushing                                 |
|   * Miosis (constricted pupil) and/or Ptosis (drooping lid) -> Partial      |
|     Horner's Syndrome caused by third-order sympathetic fiber compression   |
|     within the carotid canal edema.                                         |
|   * Sensation of fullness in the ear                                        |
|                                  +                                          |
|   RESTLESSNESS / AGITATION (Pacing, unable to lie recumbent)                |
+-----------------------------------------------------------------------------+

Stepwise Management of Cluster Headache

1. Acute Abortive Therapy:

   • 100% High-Flow Oxygen: The definitive, non-pharmacologic first-line abortive treatment. Administer 12 to 15 L/min via a non-rebreather mask for 15 to 20 minutes with the patient sitting upright. Provides relief in $>75%$ of patients within 10–15 minutes without rebound or medication overuse toxicity.
   • Subcutaneous Sumatriptan: 6 mg SC (onset within 5–10 minutes). Highly effective. (Oral triptans are ineffective due to slow gastrointestinal absorption relative to the rapid 15-to-180-minute attack duration).
   • Intranasal Zolmitriptan: 5–10 mg nasal spray administered into the nostril contralateral to the pain (if ipsilateral nostril is congested).

2. Transitional (Bridge) Prophylaxis:

   • Oral Corticosteroid Burst: Prednisone 60–80 mg daily tapered over 10–14 days, or greater occipital nerve (GON) block with bupivacaine/triamcinolone. Rapidly halts attacks while waiting for maintenance prophylactic drugs to reach steady-state therapeutic levels.

3. Maintenance Prophylaxis (Initiated on Day 1 of Cluster Period):

   • Verapamil: The gold-standard, first-line prophylactic agent. Starting dose 240 mg daily, titrated upward every 2 weeks (up to 480–960 mg/day under specialist care). Mandatory baseline and titration ECG monitoring to detect PR interval prolongation, AV nodal block, and bradycardia.
   • Galcanezumab (Emgality): 300 mg SC at the onset of the cluster period and then monthly until the end of the cluster period (specifically FDA-approved for episodic cluster headache).
   • Lithium Carbonate: Second-line agent (target serum level 0.6–1.0 mEq/L; monitor renal function and TSH).

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6. Tension-Type Headache (TTH)

Tension-Type Headache is the most prevalent primary headache disorder worldwide, affecting up to 70–80% of the adult population.

Clinical Presentation & Diagnostic Criteria

• Quality: Dull, steady, non-throbbing, pressing or tightening sensation, classically described as a tight "band around the head," "vice," or "cap."
• Location: Bilateral, fronto-occipital, or generalized across the vertex and neck muscles.
• Severity: Mild to moderate intensity (does not prohibit activities of daily living).
• Distinguishing Pertinent Negatives:
  • NO aggravation by routine physical activity (walking, bending).
  • NO severe nausea or vomiting (anorexia may occur).
  • May have photophobia OR phonophobia, but NEVER both.
• Physical Exam Findings: Tenderness upon manual palpation of pericranial muscles (frontalis, temporalis, masseter, trapezius, and sternocleidomastoid).

Evidence-Based Management

• Acute Therapy: First-line simple analgesics—Acetaminophen (650–1000 mg), Ibuprofen (400 mg), Naproxen sodium (500 mg), or Aspirin (650–1000 mg). Avoid opioid- or butalbital-containing combinations due to high dependency and rebound risk.
• Chronic TTH Prophylaxis ($\ge 15\text{ days/month}$ for $>3\text{ months}$):
  • Amitriptyline: 10–25 mg QHS titrated up to 50–75 mg QHS (first-line drug of choice; modulates central pain processing).
  • Non-pharmacologic: Cognitive behavioral therapy (CBT), biofeedback, physical therapy, trigger point relaxation, and sleep hygiene.

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7. Cranial Neuralgias & Critical Secondary Headaches

+---------------------------------------------------------------------------------------------------------+
|                            CRANIAL NEURALGIAS & URGENT SECONDARY HEADACHES                              |
|                                                                                                         |
|   DISORDER             CLINICAL PRESENTATION       DIAGNOSTIC WORKUP       FIRST-LINE CLINICAL MANAGEMENT|
|   ---------------------------------------------------------------------------------------------------   |
|   Trigeminal           Unilateral, paroxysmal,     Clinical diagnosis.     1. CARBAMAZEPINE (100-200 mg  |
|   Neuralgia            electric-shock, stabbing    MRI Brain with thin     BID, titrate to 400-1200mg/d).|
|   (Tic Douloureux)     pain in CN V2/V3 divisions. cuts of posterior fossa 2. Monitor: CBC (aplastic     |
|                        Lasts seconds to <2 min.    to rule out vascular    anemia/agranulocytosis), LFTs,|
|                        Triggered by: light touch,  compression (SCA) or    electrolytes (hyponatremia). |
|                        shaving, brushing teeth,    Multiple Sclerosis      3. Screen HLA-B*1502 in Asian |
|                        eating, wind on face.       (demyelinating plaques). ancestry (Stevens-Johnson!). |
|                                                                            4. Alt: Oxcarbazepine, Baclofen|
|                                                                                                         |
|   Giant Cell           Age >= 50. New temporal     1. ESR (>50 mm/h, often 1. IMMEDIATE HIGH-DOSE        |
|   Arteritis (GCA /     headache, scalp tenderness  >100) and CRP.          SYSTEMIC CORTICOSTEROIDS:    |
|   Temporal Arteritis)  (pain brushing hair),       2. Definitive: TEMPORAL Prednisone 40-60 mg PO daily |
|                        JAW CLAUDICATION (pain      ARTERY BIOPSY (>= 2 cm  (or IV Methylprednisolone    |
|                        chewing; high specificity), segment). Biopsy shows  1 g/d for visual loss).      |
|                        Amaurosis fugax, fever,     granulomatous pan-      2. DO NOT DELAY STEROIDS for |
|                        association with PMR        arteritis with giant    biopsy! Prevents PERMANENT   |
|                        (polymyalgia rheumatica).   cells.                  BLINDNESS (AION).            |
|                                                                                                         |
|   Idiopathic           Young, obese female (90%).  1. Fundoscopy: Bilateral 1. Aggressive WEIGHT LOSS.   |
|   Intracranial         Diffuse headache worse      PAPILLEDEMA.            2. ACETAZOLAMIDE (500-2000    |
|   Hypertension (IIH /  recumbent, transient visual 2. Brain MRI/MRV:       mg/day; carbonic anhydrase   |
|   Pseudotumor          obscurations (graying out), Empty sella, flattened  inhibitor to reduce CSF).    |
|   Cerebri)             PULSATILE TINNITUS ("whoosh sclera, transverse      3. Topiramate (aids weight   |
|                        in ears"), CN VI palsy      sinus stenosis; NO mass.loss and reduces ICP).       |
|                        (horizontal diplopia).      3. LP: OPENING PRESSURE 4. Surgical shunt / optic    |
|                                                    > 250 mm H2O; normal CSF nerve sheath fenestration   |
|                                                    cytology/chemistry.     if progressive vision loss.  |
+---------------------------------------------------------------------------------------------------------+

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8. Geriatric & Lifespan Considerations in Cephalalgia

• New-Onset Headache in the Older Adult: Any new-onset headache in an adult aged $\ge 50$ years is considered a secondary headache until proven otherwise. The differential diagnosis must prioritize Giant Cell Arteritis, intracranial neoplasm (primary or metastatic), chronic subdural hematoma (following trivial or unrecognized falls), and ischemic/hemorrhagic stroke.
• Vascular Comorbidities & Pharmacotherapy: Due to high rates of occult coronary artery disease, peripheral arterial disease, and cerebrovascular atherosclerosis in older adults, triptans and ergotamines must be avoided unless cardiovascular safety is objectively confirmed. Gepants (ubrogepant, rimegepant) and ditans (lasmiditan, with sedation counseling) represent safer alternatives.
• Beers Criteria Cautions:
  • Avoid tricyclic antidepressants (amitriptyline) for migraine prophylaxis in frail older adults due to potent anticholinergic toxicity (urinary retention, severe dry mouth, constipation, blurred vision, acute delirium, and elevated fall risk).
  • Avoid long-term simple NSAID use due to high risks of peptic ulcer disease, acute kidney injury, fluid retention, and worsening of baseline hypertension.

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9. Board-Yield Summary & Clinical Pearls

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|                       ANCC AGPCNP CLINICAL EXAM PEARLS                      |
|                                                                             |
|   * Migraine + Uncontrolled HTN / CAD / Prior Stroke -> STRICTLY AVOID      |
|     TRIPTANS AND ERGOTS! Prescribe Gepants (Rimegepant/Ubrogepant) or Ditans|
|     (Lasmiditan) instead.                                                   |
|                                                                             |
|   * Suspected Giant Cell Arteritis (GCA) -> START ORAL PREDNISONE (60 MG)   |
|     IMMEDIATELY before obtaining the temporal artery biopsy! Waiting for a  |
|     biopsy risks irreversible Anterior Ischemic Optic Neuropathy (AION) and |
|     permanent bilateral blindness.                                          |
|                                                                             |
|   * Cluster Headache Acute Attack -> First-line is 100% HIGH-FLOW OXYGEN    |
|     (12-15 L/min via non-rebreather mask) + Subcutaneous Sumatriptan 6 mg.  |
|     Oral medications are too slow!                                          |
|                                                                             |
|   * Medication Overuse Headache (MOH) -> Occurs when abortive agents are    |
|     used >= 10 days/month (triptans/combination analgesics) or >= 15 days/   |
|     month (NSAIDs/acetaminophen) for >3 months. Must taper/wean offending   |
|     drug and initiate prophylactic bridge therapy.                          |
|                                                                             |
|   * Trigeminal Neuralgia -> First-line medication is CARBAMAZEPINE. Check   |
|     baseline CBC (agranulocytosis risk), LFTs, and test for HLA-B*1502 in   |
|     patients of Asian descent to prevent fatal Stevens-Johnson syndrome.    |
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