Primary headaches and trigeminal neuralgia: neuropathic pain yes or not? Evidences from neurophysiological procedures

Abstract

Despite the fact that neurophysiological evaluation is not useful for primary headache diagnosis, the nociceptive system exploration through reflexes and evoked potentials procedures may give an aid in understanding the pathophysiological mechanism subtending pain. Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system, which is supported by clinical evaluation and instrumental assessment by trigeminal and nociceptive reflexes and laser evoked potentials. The same methods, applied to migraine and cluster headache, together with evidences coming from structural and functional neuroimaging, excluded the neuropathic origin of pain, which is attaining to symptomatic and idiopathic trigeminal neuralgia, but confirmed a complex dysfunction of pain processing. Tension-type headache fits with a model of non-nociceptive and non-neuropathic pain, subtended by a complex interaction of peripheral muscular and central neuronal factors. The presence of altered modulation of pain concurs with migraine and tension-type headache, and should be taken into account for the choice of the best therapeutic approach.

Keywords::

• cluster headache
• migraine
• neuropathic pain
• neurophysiological procedures
• tension-type headache
• trigeminal neuralgia

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• • The definition of nociceptive pain arising from actual or threatened damage to non-neural tissue and due to the activation of nociceptors, neuropathic pain as caused by a lesion or disease of the somatosensory nervous system, and syndromes where neither damage to non-neural tissue nor lesion of somatosensory system is demonstrable as non-organic or ‘psychogenic’ pain, are only partly adapted to describe primary headaches.

• • In migraine, the anatomical integrity of pain pathways and the occurrence of sterile neurogenic inflammation may account for nociceptive trigeminal pain, activated and perpetuated by complex neuronal phenomena associated with persistent dysfunction of modulation systems.

• • The model of ‘psychogenic non-organic pain’ with consequent muscle contraction and tenderness seems the most adapt to describe tension-type headache, although it does not account for the complex dysfunction of pain modulation and peripheral muscle factors involvement shown by the application of neurophysiological methods.

• • In cluster headache, the anatomical and functional integrity of pain pathways and the occurrence of sterile neurogenic inflammation may account for nociceptive trigeminal pain arising from neuronal abnormality in the hypothalamus and trigeminal system facilitation. The dysfunction of pain modulating descending systems and the occurrence of enhanced phenomena of central sensitization is actually not fully supported.

• • Clinical and neurophysiological evidence support the neuropathic origin of pain in trigeminal neuralgia, either in symptomatic or in idiopathic forms.