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THE CAPSAICIN MODEL TO EXPLORE PAIN SENSORY PROFILES AND FUNCTIONAL CONNECTIVITY IN HUMANS. A COMBINED PSYCHOPHYSICAL AND fMRI STUDY IN NORMAL CONTROLS.
No full textIl dolore neuropatico viene definito dall' International Association for the Study of Pain (IASP) come diretta conseguenza di una lesione o di una malattia che colpisce il sistema somatosensoriale. Questa tipologia di dolore spesso include nella sintomatologia fenomeni come l' allodinia e l' iperalgesia.
I modelli animali offrono una grande quantità di dati sperimentali che tuttavia sono difficili da riprodurre in ambito clinico.
Al contrario, i meccanismi neurofisiologici che sottendono il dolore neuropatico negli esseri umani non sono ancora ben compresi e inoltre i relativi farmaci sono spesso inefficaci.
Data tale difficoltà, è essenziale poter disporre di un efficace modello sperimentale di dolore neuropatico nell'uomo.
Inoltre è risaputo che vi è una elevata variabilità nella percezione del dolore negli esseri umani e questo può spiegare gran parte della variabilità riscontrata nella risposta ai farmaci. E di questo aspetto se ne deve tener conto anche nello sviluppo di nuove sostanze analgesiche.
Il modello sperimentale che si basa sulla capsaicina, una sostanza che deriva dal peperoncino, viene utilizzato per esplorare i profili sensoriali nell'uomo.
La capsaicina permette lo studio sia dei sintomi che prevedono un incremento di funzione come l'iperalgesia e l'allodinia sia fenomeni legati a perdita di funzione come l'ipoalgesia.
Il bersaglio della capsaicina è il recettore TRPV1, che è espresso nelle fibre C e Aδ.
In questo studio, abbiamo testato soggetti umani sani nei quali è stato indotto sperimentalmente un dolore cutaneo acuto mediante l'applicazione topica di un cerotto ad alta concentrazione di capsaicina (8%). Altri studi hanno già utilizzato la capsaicini tuttavia a concentrazioni più basse (0,025-3%).
Il primo obiettivo di questo studio è stato quello di indagare la variabilità della percezione del dolorein soggeti sani, studiando i profili somatosensoriali prima e durante una condizione sperimentale di dolore (capsaicina 8%) utilizzando il Quantitative Sensory Testing (QST).
Un altro obiettivo è stato quello di indagare le varizioni e la connettività tra i resting-state Networks utilizzando la risonanza magnetica funzionale prima e durante una condizione sperimentale di dolore (cerotto alla capsaicina, 8%) in soggetti sani.
Abbiamo combinato l'uso di un test psicofisico applicato perifericamente sulla pelle nel sito di stimolazione (avambraccio destro) con un metodo di imaging del sistema nervoso centrale per esplorare la "via del dolore" dai recettori periferici fino ai networks cerebrali.
Nella prima parte dello studio è stato eseguito un protocollo standardizato di QST in un gruppo di 32 volontari sani prima (T0) e dopo l'applicazione di capsaicina topica (3x3 cm, 30 ') sull'avambraccio destro (a T1: per esplorare l'iperalgesia e l'allodinia primaria e secondaria; e a T2 dopo 24 ore: per esplorare l'ipoalgesia tardiva).
Nel secondo studio, 18 volontari sani sono stati sottoposti ad un protocollo di resting-state fMRI prima e durante l'applicazione di capsaicina topica sull'avambraccio destro per esplorare i resting-state Networks e la connettività funzionale, utilizzando i software FSL e CONN per l'elaborazione dei dati.
I risultati del primo esperimento indicano che la capsaicina influenza sia le soglie termiche e meccaniche del QST con un pattern complessivo di incremento di funzione (iperalgesia termica e meccanica e allodinia meccanica dinamica).
I risultati hanno anche mostrato diversi pattern di variabilità inter-individuale dei parametri del QST; alcuni parametri appaiono più stabili di altri.
Per quanto riguarda il secondo esperimento, abbiamo trovato, durante l'applicazione di capsaicina,
una maggiore connettività funzionale che coinvolge diverse aree cerebrali. Abbiamo anche dimostrato una ridotta connettività funzionale che riguarda una coppia di regioni.
Questo modello potrebbe essere utile per sviluppare nuovi farmaci analgesici, potendoli testare in un numero più limitato ma selezionato di soggetti.Neuropathic pain is defined by the International Association for the Study of Pain as pain arising as a direct consequence of a lesion or disease affecting the somatosensory system and it frequently may include allodynia and hyperalgesia. Animal models offer a large amount of experimental data, which are difficult to translate in the clinical setting. In contrast, the neurophysiological mechanisms underlying neuropathic pain in humans are not yet well understood and drugs are often ineffective. Given the pitfalls in translating animal data to humans, it is essential to have an experimental model of neuropathic pain in humans.
Moreover there is a high variability in pain perception in humans and this may account for much of the variability in response to neuropathic pain drugs.
The capsaicin model is used to explore sensory profiles in humans. Capsaicin is the pungent ingredient of chili peppers. Capsaicin allows the study of both gain-of-function (hyperalgesia and allodynia: similar to the chronic sensory symptoms of a patient with neuropathic pain) and loss-of-function (hypalgesia) phenomena. Capsaicin target is the transient receptor potential vanilloid 1 channel (TRPV1) which is expressed in the polymodal C and Aδ nociceptive fibers and it is a key molecolar component of the pain pathway.
In the present study, we tested healthy human subjects in whom acute cutaneous pain is induced experimentally by topical application of high-concentration capsaicin (8%, patch) unlike other studies that used lower concentrations (0,025-3%).
The first aim of this study was to investigate the variability of experimental pain perception in normal controls by studying somatosensory profiles before and during an experimental pain condition (8% capsaicin patch) using quantitative sensory testing (QST).
Another aim was to investigate the changes and the connectivity in the resting state networks using BOLD functional magnetic resonance imaging before and during an experimental pain condition (8% capsaicin patch) in healthy subjects.
We have combined the use of a psychophysical test applied peripherally in the skin stimulation site with a method of central nervous system imaging to explore the “pain pathway” from the peripheral receptors up to brain connections.
In the first part of the study a standardized QST protocol was performed in a group of 32 normal volunteers prior to (T0) and after topical capsaicin application (3 x 3 cm, 30’) on the forearm (T1: early primary and secondary hyperalgesia/allodynia; T2: late hypalgesia).
In the second experimental design, 18 healthy volunteers were submitted to a resting state fMRI protocol before and after capsacin path application to explore the Resting State Networks and functional connectivity, using FSL and CONN to process the data.
Results of first experiment indicate that capsaicin affect both thermal and mechanical QST thresholds resulting in a pattern of “gain of function” with heat and pinprick hyperalgesia and dynamic mechanical allodynia. Results also showed different patterns of inter-individual variability with some more stable parameters than others.
Regarding the second experiment we found greater and positive resting-state functional connectivity involving different brain areas in capsaicin condition compared to pre-capsaicin condition. We also found a reduced connectivity only for a couple of regions.
This model might be useful to profiling novel analgesic agents in more limited numbers of subjects than required in patient efficacy studies
Central sensitization and sensory symptoms spread in carpal tunnel syndrome: A response to Ginanneschi and Rossi's letter on the relationship between central plastic changes and sensory symptoms in peripheral entrapment neuropathies.
No full textno abstract availabl
Central sensitization in carpal tunnel syndrome with extraterritorial spread of sensory symptoms.
No full textExtraterritorial spread of sensory symptoms is frequent in carpal tunnel syndrome (CTS). Animal models suggest that this phenomenon may depend on central sensitization. We sought to obtain psychophysical evidence of sensitization in CTS with extraterritorial symptoms spread. We recruited 100 unilateral CTS patients. After selection to rule out concomitant upper-limb causes of pain, 48 patients were included. The hand symptoms distribution was graded with a diagram into median and extramedian pattern. Patients were asked on proximal pain. Quantitative sensory testing (QST) was performed in the territory of injured median nerve and in extramedian territories to document signs of sensitization (hyperalgesia, allodynia, wind-up). Extramedian pattern and proximal pain were found in 33.3% and 37.5% of patients, respectively. The QST profile associated with extramedian pattern includes: (1) thermal and mechanic hyperalgesia in the territory of the injured median nerve and in those of the uninjured ulnar and radial nerves and (2) enhanced wind-up. No signs of sensitization were found in patients with the median distribution and those with proximal symptoms. Different mechanisms may underlie hand extramedian and proximal spread of symptoms, respectively. Extramedian spread of symptoms in the hand may be secondary to spinal sensitization but peripheral and supraspinal mechanisms may contribute. Proximal spread may represent referred pain. Central sensitization may be secondary to abnormal activity in the median nerve afferents or the consequence of a predisposing trait. Our data may explain the persistence of sensory symptoms after median nerve surgical release and the presence of non-anatomical sensory patterns in neuropathic pain
Pain and motor function in carpal tunnel syndrome : A clinical, neurophysiological and psychophysical study.
No full textOBJECTIVE : Patients with carpal tunnel syndrome (CTS) complain of motor symptoms. The study is aimed to understand which features are associated with the presence of motor symptoms in CTS. METHODS : We recruited 282 consecutive CTS patients. After selection, 129 patients (203 hands) were included. Patients were asked about the presence and severity of hand weakness (HW) and hand clumsiness (HC). They underwent a self-administered questionnaire on symptoms, clinical evaluation and neurographic study. Quantitative sensory testing (QST) was performed on the patients with unilateral right CTS. RESULTS : HW and HC may be found in 56 \% and 48 \% of CTS hands, respectively. HW was related to the severity of sensory symptoms (pain, numbness and tingling) but not to clinical-neurographic measures of median nerve involvement. HC was related to the severity of sensory symptoms and to the clinical-neurographic signs of motor but not sensory nerve damage. Motor symptoms were significantly more frequent in right hands. QST showed a relationship between the presence and severity of HW and HC and the warm threshold. CONCLUSIONS : Motor symptoms may be found in approximately half of CTS hands. Clinical and neurographic signs of median nerve motor damage appear to be poorly correlated to motor symptoms. The factor that can help reconcile the discrepancy between motor symptoms and motor signs is pain. Pain modulation on motor function may take place at various anatomical levels in CTS. Nociceptive C-fibers may be involved in pain-motor interactions finally leading to motor symptoms.Objective: Patients with carpal tunnel syndrome (CTS) complain of motor symptoms. The study is aimed to understand which features are associated with the presence of motor symptoms in CTS. Methods: We recruited 282 consecutive CTS patients. After selection, 129 patients (203 hands) were included. Patients were asked about the presence and severity of hand weakness (HW) and hand clumsiness (HC). They underwent a self-administered questionnaire on symptoms, clinical evaluation and neurographic study. Quantitative sensory testing (QST) was performed on the patients with unilateral right CTS. Results: HW and HC may be found in 56 % and 48 % of CTS hands, respectively. HW was related to the severity of sensory symptoms (pain, numbness and tingling) but not to clinical-neurographic measures of median nerve involvement. HC was related to the severity of sensory symptoms and to the clinical-neurographic signs of motor but not sensory nerve damage. Motor symptoms were significantly more frequent in right hands. QST showed a relationship between the presence and severity of HW and HC and the warm threshold. Conclusions: Motor symptoms may be found in approximately half of CTS hands. Clinical and neurographic signs of median nerve motor damage appear to be poorly correlated to motor symptoms. The factor that can help reconcile the discrepancy between motor symptoms and motor signs is pain. Pain modulation on motor function may take place at various anatomical levels in CTS. Nociceptive C-fibers may be involved in pain-motor interactions finally leading to motor symptoms. © 2008 Springer
Theta-burst stimulation may modulate myoclonus in cortico-basal degeneration. A case report
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Brachial artery blood flow during submaximal isometric contraction of the biceps brachii and triceps brachii in humans: A preliminary observation.
No full textThe purpose of this study was to evaluate brachial artery blood flow changes during submaximal isometric contraction of the biceps and triceps brachii, in order to clarify the influence of the upper arm muscles activity on the local arterial flow. The brachial artery blood flow velocity and diameter were evaluated in twenty healthy men (mean age 29.6 years) at baseline (resting position) and during submaximal isometric contraction of the biceps and triceps brachii by means of ultrasonography (B-MODE and Doppler ultrasound methods). The brachial artery blood flow velocity was significantly higher than resting position during submaximal isometric contraction of the biceps (P < 0.001) and triceps brachii (P = 0.019). As to the brachial artery diameter, no significant change was observed during submaximal isometric contractions of the biceps and triceps brachii. Our preliminary findings suggest that the brachial artery blood flow velocity similarly increases during submaximal isometric contraction of the biceps and triceps brachii
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