Erfan Bashar
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Headache Secondary Causes

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.

A secondary headache is headache caused by another disorder. This is the safety side of headache medicine: the headache is not the final diagnosis but the alarm bell.

Subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space, usually around the brain where cerebrospinal fluid (CSF) circulates. It classically presents with sudden severe headache, often described as the worst headache of life, with possible nausea, vomiting, neck stiffness, loss of consciousness, meningeal signs, pupil abnormalities, focal signs, hyperreflexia, or extensor plantar responses. The mechanism is direct: blood in the subarachnoid space irritates the meninges and raises intracranial pressure. Meningeal irritation explains neck stiffness and light discomfort, while raised pressure and vascular injury explain vomiting, altered consciousness, and focal signs. Suspected SAH needs urgent evaluation, usually starting with noncontrast CT when presentation is acute.

Post-dural puncture headache

Post-dural puncture headache (PDPH) follows puncture of the dura, classically after lumbar puncture or neuraxial anesthesia, when CSF leaks out and lowers CSF pressure. The clinical clue is posture: the headache is usually worse upright and better lying down. That makes mechanical sense, because low CSF pressure allows traction on pain-sensitive intracranial structures when the patient stands. Conservative measures may help, but persistent or severe cases can require an epidural blood patch, which works by sealing the leak rather than masking the pain.

Tumor or raised intracranial pressure

Tumor-related headache is secondary because a mass or raised intracranial pressure drives the pain. The danger clues are progression, new neurological deficits, seizures, papilledema, morning worsening, vomiting, or headache triggered by cough or Valsalva maneuvers. Raised pressure hurts not because brain tissue feels pain but because pressure stretches pain-sensitive meninges, vessels, and cranial structures.

Giant cell arteritis

Suspect giant cell arteritis in any patient over 50 with a new or altered headache plus jaw claudication, fever or constitutional symptoms, visual disturbance, or vascular abnormality. New headache affects about two-thirds of patients. Jaw claudication affects about half: pain on chewing that eases with rest. Visual symptoms affect 20–30%, with permanent vision loss in roughly 8%, usually from anterior ischaemic optic neuropathy.

The action rule is absolute: start high-dose glucocorticoids immediately on suspicion and never wait for biopsy. Complete temporal artery biopsy within 2 weeks of starting steroids. Without visual loss, prednisone 40–60 mg daily continues until symptoms and inflammatory markers resolve, then tapers over 12–18 months. Threatened or established visual loss calls for intravenous methylprednisolone 500–1000 mg daily for 3 days, then high-dose oral steroids.

Medication-overuse headache

Medication-overuse headache is secondary because repeated exposure to acute headache medication maintains the pattern. A patient may start with migraine, treat attacks more and more frequently, and end with the rescue medication sustaining a chronic headache loop. This is why the medication history belongs in every headache assessment: ask not only what the patient takes but on how many days per month they take it. Breaking the loop is covered in /notes/neurology/headache-treatment/.

Trigeminal neuralgia

Brief shock-like facial pain that is triggerable by touch or chewing belongs to trigeminal neuralgia rather than headache proper. It has its own drug and procedure ladder, covered in /notes/neurology/headache-trigeminal-neuralgia/.

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