Abnormal brain processing of cutaneous pain in migraine patients during the attack

Tommaso, Marina de; Guido, Marco; Libro, Giuseppe; Losito, Luciana; Sciruicchio, Vittorio; Monetti, Carlo; Puca, Francomichele

doi:10.1016/s0304-3940(02)00967-9

Cited by 63 publications

(53 citation statements)

References 10 publications

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“…During migraine attacks, the area-under-the-curve of the nociceptive blink reflex R2 component is temporary increased on the affected side in comparison with the non-affected side was observed [106]. Similar results were obtained using another noxious stimulation, the radiant laser CO2: amplitude of the N2–P2 complex at the vertex was increased on the affected side compared to the non-affected side [107-109]. Interestingly, in episodic migraine LEPs did not habituate not only interictally, but also during the attacks, underscoring the different cerebral processing of noxious versus innocuous stimuli.…”

Section: Reviewmentioning

confidence: 67%

Habituation and sensitization in primary headaches

et al. 2013

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The phenomena of habituation and sensitization are considered most useful for studying the neuronal substrates of information processing in the CNS. Both were studied in primary headaches, that are functional disorders of the brain characterized by an abnormal responsivity to any kind of incoming innocuous or painful stimuli and it’s cycling pattern over time (interictal, pre-ictal, ictal). The present review summarizes available data on stimulus responsivity in primary headaches obtained with clinical neurophysiology. In migraine, the majority of electrophysiological studies between attacks have shown that, for a number of different sensory modalities, the brain is characterised by a lack of habituation of evoked responses to repeated stimuli. This abnormal processing of the incoming information reaches its maximum a few days before the beginning of an attack, and normalizes during the attack, at a time when sensitization may also manifest itself. An abnormal rhythmic activity between thalamus and cortex, namely thalamocortical dysrhythmia, may be the pathophysiological mechanism subtending abnormal information processing in migraine. In tension-type headache (TTH), only few signs of deficient habituation were observed only in subgroups of patients. By contrast, using grand-average responses indirect evidence for sensitization has been found in chronic TTH with increased nociceptive specific reflexes and evoked potentials. Generalized increased sensitivity to pain (lower thresholds and increased pain rating) and a dysfunction in supraspinal descending pain control systems may contribute to the development and/or maintenance of central sensitization in chronic TTH. Cluster headache patients are chrarcterized during the bout and on the headache side by a pronounced lack of habituation of the brainstem blink reflex and a general sensitization of pain processing. A better insight into the nature of these ictal/interictal electrophysiological dysfunctions in primary headaches paves the way for novel therapeutic targets and may allow a better understanding of the mode of action of available therapies.

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Section: Reviewmentioning

confidence: 67%

Habituation and sensitization in primary headaches

et al. 2013

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“…The concept of pre-existing frequent pain facilitating the development of chronic pain even when located elsewhere in the body is very interesting. From a pathophysiological point of view this is easily conceivable, as most chronic pain conditions are associated with central facilitation (21)(22)(23). Experimental evidence in this regard has also been provided by Sterling et al, who demonstrated a generalized sensory hypersensitivity to a variety of sensory stimuli that occurred soon after the whiplash injury and that was associated with poor recovery (24).…”

Section: Discussionmentioning

confidence: 95%

Incidence and predictors of chronic headache attributed to whiplash injury

et al. 2009

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We identified clinical, demographic and psychological predictive factors that may contribute to the development of chronic headache associated with mild to moderate whiplash injury [Quebec Task Force (QTF) ≤ II] and determined the incidence of this chronic pain state. Patients were recruited prospectively from six participating accident and emergency departments. While 4.6% of patients developed chronic headache attributed to whiplash injury according to the International Classification of Headache Disorders, 2nd edn criteria, 15.2% of patients complained about headache lasting > 42 days (QTF criteria). Predictive factors were pre-existing facial pain [odds ratio (OR) 9.7, 95% confidence interval (CI) 2.1, 10.4; P = 0.017], lack of confidence to recover completely (OR 5.5, 95% CI 2.0, 13.2; P = 0.005), sore throat (OR 5.0, 95% CI 1.5, 8.9; P = 0.013), medication overuse (OR 4.2, 95% CI 1.4, 12.3; P = 0.009), high Neck Disability Index (OR 4.0, 95% CI 1.3, 12.6; P = 0.019), hopelessness/anxiety (OR 3.8, 95% CI 1.3, 8.7; P = 0.024), and depression (OR 3.3, 95% CI 1.2, 9.4; P = 0.024). The lack of a control group limits the conclusions that can be drawn from this study. Identified predictors closely resemble those found in chronic primary headache disorders.

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“…While cephalic and extracephalic allodynia are well described, spontaneous body pain and allodynia has also been reported as preceding migraine attacks [56]. Laser evoked cutaneous pain thresholds are reduced during migraine attacks and cortical evoked potentials increased [62]. No change in heat pain thresholds are found in chronic tension-type headache, but there is pericranial tenderness [63; 80] and hyperalgesia of neck shoulder muscles [81].…”

Section: To Which Clinical Syndromes Does Central Sensitization Contrmentioning

confidence: 99%

Central sensitization: Implications for the diagnosis and treatment of pain

Woolf¹

2011

Pain

3,520

2,733

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Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and postsurgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk both of developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.

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Abnormal brain processing of cutaneous pain in migraine patients during the attack

Cited by 63 publications

References 10 publications

Habituation and sensitization in primary headaches

Habituation and sensitization in primary headaches

Incidence and predictors of chronic headache attributed to whiplash injury

Central sensitization: Implications for the diagnosis and treatment of pain

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