FIGURE 8.

1
Components of a typical cut a neous nerve . There are two distinct functional
categories of axons: primary a effrents with cell bodies in the dorsal root ganglion,
and sympathetic postganglionic fibers with cell bodies in the sympathetic ganglion.
Primary a effrents include those with large-diameter myelinated (A), small-
diameter myelinated (A), and unmyelinated (C) axons. All sympathetic
postganglionic fibers are unmyelinated.

FIGURE 8-2
Events lead in go to activation, sensitization, and spread of sensitization of primary
afferent nociceptor terminals. A. Direct activation by intense pressure and
consequent cell damage. Cell damage induces lower pH (H+) and leads to release
of potassium (K+) and to synthesis of prostaglandins (PG) and bradykinin (BK).
Prostaglandins increase the sensitivity of the terminal to bradykinin and other pain-
producing substances. B. Secondary activation. Impulses generated in the
stimulated terminal propagate not only to the spinal cord but also into other
terminal branches where they induce the release of peptides, including substance P
(SP). Substance P causes vasodilation and neurogenic edema with further
accumulation of bradykinin (BK). Substance P also causes the release of histamine
(H) from mast cells and serotonin (5HT) from platelets.

FIGURE 8-3
The convergence-projection hypothesis of refferred pain. According to this
hypothesis, visceral afferent nociceptors converge on the same pain-projection
neurons as the afferents from the somatic structures in which the pain is perceived.
The brain has no way of knowing the actual source of input and mistakenly
projects the sensation to the somatic structure.

FIGURE 8-4
Pain transmission and modulatory pathways. A. Transmission system or
nociceptive messages. Noxious stimuli activate the sensitive peripheral ending of
the primary afferent nociceptor by the process of transduction. The message is then
transmitted over the peripheral nerve to the spinal cord, where it synapses with
cells of origin of the major ascending pain pathway, the spinothalamic tract. The
message is relayed in the thalamus to the anterior cingulate (C), frontal insular (F),
and somatosensory cortex (SS). B. Pain-modulation network. Inputs from frontal
cortex and hypothalamus activate cells in the midbrain that control spinal pain-
transmission cells via cells in the medulla.
FIGURE 8-5
Functional magnetic resonance imaging (FMRI) demonstrates placebo-enhanced
brain activity in anatomic regions correlating with the opioidergic descending pain
control system. Top panel: Frontal MRI image shows placebo-enhanced brain
activity in the dorsal lateral pre frontal cortex (DLPFC). Bottom panel: Sagittal
MRI images show placeboenhanced responses in the rostral anterior cingulate
cortex (rACC), the rostral ventral medullae (RVM), the periaqueductal gray (PAG)
area, and the hypothalamus. The placebo-enhanced activity in all areas was
reduced by naloxone, demonstrating the link between the descending opioidergic
system and the placebo analgesic response. (Adapted with permission from F
Eippert et al: Neuron 63:533, 2009.)

GAMBAR 8.1
Komponen yang khas memotong saraf neous. Ada dua kategori fungsional yang
berbeda dari Akson: dasar effrents dengan sel tubuh di ganglion dorsal akar, dan
simpatik serat postganglionik dengan sel tubuh di ganglion simpatik. Utama
effrents termasuk yang besar diameter neuron dimulai dan disebarkan (A),
berdiameter kecil neuron dimulai dan disebarkan (A) dan unmyelinated (C)
Akson. Semua simpatik serat postganglionik unmyelinated.

GAMBAR 8-2
Peristiwa menyebabkan dalam pergi aktivasi, sensitisasi dan penyebaran sensitisasi
Terminal utama aferen nociceptor. A. langsung aktivasi oleh tekanan dan
kerusakan sel yang konsekuen. Kerusakan sel menginduksi pH rendah (H +) dan
mengarah ke rilis kalium (K +) dan sintesis prostaglandin (PG) dan bradikinin
(BK). Prostaglandin meningkatkan sensitivitas dari terminal untuk bradikinin dan
zat lain yang menghasilkan rasa sakit. B. sekunder aktivasi. Dorongan yang
dihasilkan di terminal dirangsang menyebarkan tidak hanya ke sumsum tulang
tetapi juga ke dalam cabang-cabang terminal lain yang mana mereka mendorong
pelepasan peptida, termasuk zat P (SP). Substansi P menyebabkan vasodilatasi dan
edema neurogenik dengan lebih lanjut akumulasi bradikinin (BK). Substansi P juga
menyebabkan pelepasan histamin (H) dari sel mast dan serotonin (5HT) dari
trombosit.

GAMBAR 8-3
Hipotesis konvergensi-proyeksi satuannya sakit. Menurut hipotesis ini, mendalam
aferen nociceptors berkumpul di neuron proyeksi sakit sama sebagai afferents dari
struktur somatik di mana rasa sakit dirasakan. Otak tidak memiliki cara untuk
mengetahui sumber yang sebenarnya masukan dan keliru "proyek" sensasi somatik
struktur.

GAMBAR 8-4
Sakit transmisi dan jalur modulatory. A. sistem transmisi atau nociceptive
pesan. Berbahaya rangsangan Aktifkan perifer sensitif berakhirnya nociceptor
aferen utama oleh proses transduksi. Pesan kemudian ditransmisikan melalui saraf
tepi ke saraf tulang belakang, dimana sinaps dengan sel-sel asal utama menaik
sakit jalur, saluran spinothalamic. Pesan relay di thalamus anterior cingulate (C),
frontal picik (F) dan somatosensori korteks (SS). B. sakit-modulasi
jaringan. Masukan dari frontal korteks dan hipotalamus mengaktifkan sel-sel di
otak tengah yang mengontrol sel-sel tulang belakang sakit-transmisi melalui sel-sel
di medula.

GAMBAR 8-5
Pencitraan resonansi magnetik fungsional (FMRI) menunjukkan aktivitas otak
disempurnakan plasebo di daerah anatomi yang berhubungan dengan opioidergic
menurun sistem kontrol nyeri. Panel atas: gambar Frontal MRI menunjukkan
aktivitas otak disempurnakan plasebo dalam dorsal lateral Pra frontal korteks
(DLPFC). Panel bawah: gambar sagital MRI menunjukkan respon
placeboenhanced di korteks cingulate anterior rostral (rACC), medullae ventral
rostral (RVM), daerah abu-abu periaqueductal (PAG) dan hipotalamus. Aktivitas
disempurnakan plasebo dalam semua bidang berkurang sebesar naloxone,
menunjukkan hubungan antara sistem opioidergic menurun dan respon analgesik
plasebo. (Disesuaikan dengan izin dari F Eippert et al: Neuron 63:533, 2009.)