The Lovén reflex: the renaissance of a long-forgotten reflex involving autonomic and nociceptive pathways

Pain is not a simple phenomenon and, beyond its conscious perception, involves circuitry that allows the brain to provide an affective context for nociception, which can influence mood and memory. In the past decade, neurobiological techniques have been developed that allow investigators to elucidate the importance of particular groups of neurons in different aspects of the pain response, something that may have important translational implications for the development of novel therapies. Chemo- and optogenetics represent two of the most important technical advances of recent times for gaining understanding of physiological circuitry underlying complex behaviors. The use of these techniques for teasing out the role of neurons and glia in nociceptive pathways is a rapidly growing area of research. The major findings of studies focused on understanding circuitry involved in different aspects of nociception and pain are highlighted in this article. In addition, attention is drawn to the possibility of modification of chemo- and optogenetic techniques for use as potential therapies for treatment of chronic pain disorders in human patients.

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Opioid-free anaesthesia for the surgical correction of abnormalities associated with brachycephalic obstructive airway syndrome in five dogs

Companion Animal ◽

10.12968/coan.2020.0082 ◽

2021 ◽

Vol 26 (3) ◽

pp. 57-61

Author(s):

María Isabel Gómez Martínez ◽

Miguel Ángel Martínez Fernández

Keyword(s):

Side Effects ◽

Nerve Block ◽

Opioid Analgesic ◽

Multimodal Analgesia ◽

Human Medicine ◽

Surgical Correction ◽

Analgesic Drugs ◽

Maxillary Nerve ◽

Nociceptive Pathways ◽

Maxillary Nerve Block

Opioid-free anaesthesia is currently becoming more popular in human medicine, as it provides multimodal analgesia, affecting multiple nociceptive pathways without the use of opioids, in order to minimise opioid-related side effects. This article presents the cases of five dogs undergoing surgical correction of abnormalities associated with brachycephalic obstructive airway syndrome, all of whom received opioid-free anaesthesia for surgery. All dogs received a bilateral maxillary nerve block with bupivacaine 0.5% and a combination of non-opioid analgesic drugs. Buprenorphine was allowed during the postoperative period, based on pain assessment. Three out of five dogs received buprenorphine 6–7 hours after the nerve block was performed. Opioid-free anaesthesia provided adequate conditions for surgery and no adverse effects were reported. Prospective controlled studies comparing opioid-free anaesthesia with opioid-based techniques are required to elucidate whether or not opioid-free anaesthesia confers objective advantages.

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Motion Sickness and Migraine: Optokinetic Stimulation Increases Scalp Tenderness, Pain Sensitivity in the Fingers and Photophobia

Cephalalgia ◽

10.1046/j.1468-2982.2002.00332.x ◽

2002 ◽

Vol 22 (2) ◽

pp. 117-124 ◽

Cited By ~ 57

Author(s):

PD Drummond

Keyword(s):

Motion Sickness ◽

Pain Sensitivity ◽

Pain Perception ◽

Optokinetic Stimulation ◽

Nociceptive Pathways ◽

General Influence

The aim of this study was to determine whether scalp tenderness and photophobia, two well-recognized symptoms of migraine, develop during the motion sickness induced by optokinetic stimulation. To investigate whether motion sickness has a general influence on pain perception, pain was also assessed in the fingertips. After optokinetic stimulation, nausea increased more and headache persisted longer in 21 migraine sufferers than in 15 non-headache controls. Scalp tenderness increased during optokinetic stimulation in nauseated subjects, and pain in the fingertips increased more and photophobia persisted longer in migraine sufferers than controls. These findings suggest that the disturbance responsible for nausea also sensitizes trigeminal nociceptive neurones or releases inhibitory controls on their discharge. A low nausea threshold and a propensity for sensitization to develop rapidly in nociceptive pathways may increase susceptibility to migraine.

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Characterizing pinprick-evoked brain potentials before and after experimentally induced secondary hyperalgesia

Journal of Neurophysiology ◽

10.1152/jn.00444.2015 ◽

2015 ◽

Vol 114 (5) ◽

pp. 2672-2681 ◽

Cited By ~ 22

Author(s):

Emanuel N. van den Broeke ◽

André Mouraux ◽

Antonia H. Groneberg ◽

Doreen B. Pfau ◽

Rolf-Detlef Treede ◽

...

Keyword(s):

Event Related Potentials ◽

Stimulus Onset ◽

Secondary Hyperalgesia ◽

Brain Potentials ◽

Nociceptive Pathways ◽

Before And After ◽

Pain Ratings ◽

Related Potentials ◽

Positive Complex ◽

Stimulation Of

Secondary hyperalgesia is believed to be a key feature of “central sensitization” and is characterized by enhanced pain to mechanical nociceptive stimuli. The aim of the present study was to characterize, using EEG, the effects of pinprick stimulation intensity on the magnitude of pinprick-elicited brain potentials [event-related potentials (ERPs)] before and after secondary hyperalgesia induced by intradermal capsaicin in humans. Pinprick-elicited ERPs and pinprick-evoked pain ratings were recorded in 19 healthy volunteers, with mechanical pinprick stimuli of varying intensities (0.25-mm probe applied with a force extending between 16 and 512 mN). The recordings were performed before (T0) and 30 min after (T1) intradermal capsaicin injection. The contralateral noninjected arm served as control. ERPs elicited by stimulation of untreated skin were characterized by 1) an early-latency negative-positive complex peaking between 120 and 250 ms after stimulus onset (N120-P240) and maximal at the vertex and 2) a long-lasting positive wave peaking 400–600 ms after stimulus onset and maximal more posterior (P500), which was correlated to perceived pinprick pain. After capsaicin injection, pinprick stimuli were perceived as more intense in the area of secondary hyperalgesia and this effect was stronger for lower compared with higher stimulus intensities. In addition, there was an enhancement of the P500 elicited by stimuli of intermediate intensity, which was significant for 64 mN. The other components of the ERPs were unaffected by capsaicin. Our results suggest that the increase in P500 magnitude after capsaicin is mediated by facilitated mechanical nociceptive pathways.

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