Neurosurgery notes/Functional/Craniofacial pain/Trigeminal autonomic cephalalgias (TACs)/Cluster headache

Cluster headache

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Trigeminal autonomic cephalalgias (TACs)

General

  • AKA histaminic migraine.

Numbers

  • Male : female ratio is ≈ 5:1.
  • 25% of patients have a personal or family history of migraine.

IHS Criteria

  1. At least 5 attacks fulfilling B-D
  1. Severe unilateral orbital, supra-orbital and/or temporal pain lasting 15-180 minutes untreated
  1. Headache associated with at least one of the following signs: Conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis, eyelid oedema
  1. Frequency once every other day to 8 per day

Mechanism

  • Actually a neurovascular event, distinct from true migraine.
  • Multiple theorise
    • Circadian periodicity
      • Abnormalities of the hypothalamus,
    • Involvement of the trigeminovascular system and the parasympathetic nerve fibers
    • A defect in the central pathway of pain control and autonomic nervous system dysregulation leading to dysfunction in supraspinal control of pain and cognitive processing

Headache pattern

  • Recurrent unilateral attacks of severe pain.
    • Very intense (suicide headaches)
      • In contrast to migraine, men are more often affected than women, and extreme irritability may accompany the headache.
  • Characteristically occur at night
  • Headache cluster in time
  • Trigger unknown
  • Usually described as originating in the eye and spreading over the temporal area as the headache evolves.
  • Usually oculofrontal or oculotemporal with occasional radiation into the jaw, usually recurring on the same side of the head.
  • Ipsilateral autonomic symptoms
    • (Conjunctival injection, nasal congestion, rhinorrhea, lacrimation, facial flushing) are common.
    • Partial Horner syndrome (ptosis and miosis) sometimes occurs.
  • Temporal features
    • Headaches characteristically have no prodrome,
    • Last 30–90 minutes,
    • Recur one or more times daily,
    • Usually for 4–12 weeks,
    • Often at a similar time of day,
    • Following which there is typically a remission for an average of 12 months.

Management

  • Prophylaxis for cluster H/A is only minimally effective:
    • β-adrenergic blockers are less effective
    • Lithium:
      • Becoming drug of choice (response rate 60–80%).
      • 300mg PO TID and follow levels (desired: 0.7–1.2 mEq/L)
    • Occasionally ergotamines are used
    • Naproxen (Naprosyn®)
    • Methysergide (Sansert®)
      • 2–4mg PO TID is effective in 20–40% of cases, must cycle patient off the drug to prevent retroperitoneal fibrosis, etc. (also see below)
    • Verapamil used as prophylaxis
  • Treatment for cluster H/A:
    • Treatment is difficult because there is no prodrome and the H/A often stops after 1–2 hrs.
    • Treatment of acute attacks includes:
      • 100% O2 by face mask with patient sitting for ≤ 15min or until attack aborted
      • Ergotamine: see below
      • SQ sumatriptan: usually aborts attack within 15 minutes (see below)
      • Steroids: see below
      • Refractory cases may be considered for:
        • Percutaneous radiofrequency sphenopalatine ganglion blockade
        • Occipital nerve stimulation
        • Hypothalamic deep brain stimulation
    • Sphenopalatine ablation/stimulation