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Titolo:
Brain processing of capsaicin-induced secondary hyperalgesia - A functional MRI study
Autore:
Baron, R; Baron, Y; Disbrow, E; Roberts, TPL;
Indirizzi:
Univ Kiel, Neurol Klin, D-24105 Kiel, Germany Univ Kiel Kiel Germany D-24105 Kiel, Neurol Klin, D-24105 Kiel, Germany Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Stadt Krankenhaus Kiel, Radiol Abt, Kiel, Germany Stadt Krankenhaus Kiel Kiel Germany aus Kiel, Radiol Abt, Kiel, Germany
Titolo Testata:
NEUROLOGY
fascicolo: 3, volume: 53, anno: 1999,
pagine: 548 - 557
SICI:
0028-3878(19990811)53:3<548:BPOCSH>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSITRON-EMISSION-TOMOGRAPHY; NOXIOUS THERMAL-STIMULATION; ANTERIOR CINGULATE CORTEX; HUMAN CEREBRAL-CORTEX; SOMATOSENSORY CORTEX; PREFRONTAL CORTEX; PERIPHERAL MONONEUROPATHY; INTRADERMAL INJECTION; EPISODIC MEMORY; HEAT STIMULI;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Baron, R Univ Kiel, Neurol Klin, Niemannsweg 147, D-24105 Kiel, Germany Univ Kiel Niemannsweg 147 Kiel Germany D-24105 105 Kiel, Germany
Citazione:
R. Baron et al., "Brain processing of capsaicin-induced secondary hyperalgesia - A functional MRI study", NEUROLOGY, 53(3), 1999, pp. 548-557

Abstract

Objective: To investigate, using functional MRI (fMRI), the neural networkthat is activated by the pain component of capsaicin-induced secondary mechanical hyperalgesia. Background: Mechanical hyperalgesia(i.e., pain to innocuous tactile stimuli) is a distressing symptom of neuropathic pain syndromes. Animal experiments suggest that alterations in central pain processingoccur that render tactile stimuli capable of activating central pain-signaling neurons. A similar central sensitization can be produced experimentally with capsaicin. Methods: In nine healthy individuals the cerebral activation pattern resulting from cutaneous nonpainful mechanical stimulation at the dominant forearm was imaged using fMRI. Capsaicin was injected adjacent to the stimulation site to induce secondary mechanical hyperalgesia. The identical mechanical stimulation was then perceived as painful without changing the stimulus intensity and location. Both activation patterns were compared to isolate the specific pain-related component of mechanical hyperalgesia from the tactile component. Results: The pattern during nonpainful mechanical stimulation included contralateral primary sensory cortex (SI) and bilateral secondary sensory cortex (SII) activity. During hyperalgesia, significantly higher activation was found in the contralateral prefrontal cortex: the middle (Brodmann areas [BAs] 6, 8, and 9) and inferior frontal gyrus (BAs 44 and 45). No change was present within SI, SII, and the anterior cingulate cortex. Conclusions: Prefrontal activation is interpreted as a consequence of attention, cognitive evaluation, and planning of motor behavior in response to pain. The lack of activation of the anterior cingulate contrasts with physiologic pain after C-nociceptor stimulation. It might indicatedifferences in the processing of hyperalgesia and C-nociceptor pain or it might be due to habituation of affective sensations during hyperalgesia compared with acute capsaicin pain.

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Documento generato il 02/04/20 alle ore 12:45:08