What is the role of trigeminal and parasympathetic neuropeptides in the pathophysiology of chronic paroxysmal hemicrania (CPH)?

Updated: Jun 12, 2019
  • Author: Monica Saini, MD, MBBS; more...
  • Print
Answer

The release of trigeminal and parasympathetic neuropeptides during headache has been described. [7] Activation of the ipsilateral trigeminovascular system may explain sudden, unilateral headache and may lead to miosis, increased intraocular pressure (IOP), and other autonomic abnormalities.

Increased sweating and decreased salivation during attacks and the ability of an alpha-blocking agent or a stellate ganglion blockade to inhibit an increase in IOP suggest sympathetic involvement.

Increased tearing, nasal secretion, and miosis may be due to parasympathetic stimulation. Trigeminoparasympathetic activation during CPH attacks has been suggested; increases in the vasoactive intestinal peptide (ie, parasympathetic peptide) level have been reported. levels of calcitonin gene-related peptide also are reported to be high during CPH attacks.

Pain and pressure threshold, nociceptive flexion reflex, and blink and corneal reflexes have been studied in patients with CPH. The corneal reflex thresholds have been found to be decreased bilaterally during CPH attacks. Increases in corneal temperature on the symptomatic side also have been reported; this finding may be due to increased ocular blood flow.

The effectiveness of indomethacin in CPH may be due partly to reduction of intracranial blood flow (via a nonprostaglandin mechanism) and partly to the drug’s anti-inflammatory effects.

These findings may indicate a primary central mechanism and a secondary involvement of peripheral factors, affecting the sympathetic and parasympathetic systems.


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!