Does Occipital Nerve Stimulation Alter Pain Response as Measured by Quantitative Sensory Testing in Patients With Chronic Migraine or Cluster Headache

Headache is one of the most common neurological problems accounting for 4% of primary care consultations and up to 30% of neurology appointments. Even though considerable advances in the understanding of the pathogenesis of migraine, new pharmacologic treatments and the emergence of new innovative interventions for difficult cases, in many patients with migraine remain intractable to medical therapy.

The trigeminocervical complex (TCC) has a crucial role in the pathophysiology of migraines. The TCC is a common convergent pathway by which both trigeminal (dural) and cervical (mainly via the greater occipital nerve) afferent inputs project into higher centres in the thalamus and cortex. This afferent pathway is further influenced by the conditioned pain modulation (CPM) pathway originating from the brainstem structures including periaqueductal grey matter, nucleus raphe magnus, and the rostroventral medulla. There is some evidence to suggest that increased peripheral sensitization of the afferent inputs of the TCC, generalized central sensitization of the trigemino-spinal or the second order trigeminal neurons and impaired descending pain inhibitory pathway, may all contribute to the development of the chronic intractable or treatment resistant primary headache disorder Neurostimulation techniques for treating intractable headache range from invasive deep brain stimulation to less invasive peripheral implantation and stimulation. In 1999 Weiner and Reed described the beneficial effects of subcutaneous Occipital nerve stimulation (ONS) in patients with medically intractable, highly disabling chronic headache disorders Open-label studies have suggested that this treatment modality is effective and safe (Lambru and Matharu 2012). Although the exact mechanism of action is poorly understood, ONS is thought to act by stimulating the distal branches of C1, C2 and C3 in turn influencing the TCC favourably by inhibiting the nociceptive process, resulting in an improvement of symptoms. Previous work has demonstrated a consistent and sustained improvement in conditioned pain modulation (CPM) following ONS as confirmed with quantitative sensory testing (QST) (Wodehouse et al, 2014). QST has the particular advantage of being a functional test that provides a quantitative pain stimulus and assesses the subject's individual response to the stimulus. QST also provides a reliable assessment of changes in pain thresholds and the benefit of ONS. However general anaesthetic has also been demonstrated to cause changes/improvements in pain thresholds, peripheral and central sensitisation and this effect can be long lasting and may account for changes/improvements as measured by QST in subjects having ONS that the anaesthetic provides relief as opposed to the ONS intervention.

Quantitative sensory testing (QST) QST is a term used to describe different forms of psychophysical testing of skin, mucosa, or muscle tissue that assess sensory and pain perception pathways. Nociception inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitisation in turn manifesting as pain hypersensitivity, particularly dynamic tactile allodynia, and secondary punctate or pressure hyperalgesia and enhanced temporal summation.

QST has been used for measuring thresholds for different sensations in neuropathic pain reflecting the possible nerve fibres that may be implicated in the pathogenesis. Heat sensation threshold reflects the unmyelinated C-fiber function, cold sensation threshold reflects the thinly myelinated A-fiber function and vibration threshold reflects the thickly myelinated AB- fiber function.

QST tests can be classified into the following: