Centeral pain control and inhibitory pain pathways pharmacology

سال انتشار: 1397
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 355

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شناسه ملی سند علمی:

APAMED08_015

تاریخ نمایه سازی: 23 آذر 1397

چکیده مقاله:

Nociceptives sends mechanical, thermal, and chemical noxious stimuli. Pain is transmitted to the spinal cord, relayed there, and then to brainstem integration sites. spinothalamic pathways carry discriminative pain-related informations. axons of lamina I STT neurons cross the midline and ascend in the lateral spinal cord white matter on the opposite side. descending input to the spinal cord modulates either facilitate or inhibit the sensory signal. Descending pathways modulate pain include axons originating in the pontine locus coeruleus and medullary reticular formation.Centers for higher processing have an impact on the awareness, motivational responses and regulation of autonomic, emotional, and motor responses to pain. Aβ afferents, large, myelinated, fast-conducting , are activated by low-intensity mechanical stimuli. Aδ fibers, smaller, myelinated, fast-conducting , respond to thermal or mechanical, low / high-threshold stimuli. C fibers, small unmyelinated, very slowly conducting, are activated by thermal or mechanical stimuli .With ongoing small afferent input, there is a spinal sensitization that reflects acute increases in neuronal responsiveness mediated by NMDA receptors and longer term by kinases. Bulbospinal serotonergic act excitatory 5-HT3 receptors to enhance the firing of lamina V neurons display a facilitated state called wind-up. following peripheral nerve injury, ongoing pain represent ectopic activity in the neuroma and the DRG, a phenomena reflecting upregulation of sodium channels.The enhanced response to low threshold stimulation may reflect loss of intrinsic GABA and glycinergic inhibition and activation of non-neuronal cells.

نویسندگان

Kambiz Sadegi

MD, Anesthesiologist, pain fellowship