Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of electrical stimulation of the cervical vagus nerve were determined in cervical or lumbar spinal neurons in 27 rats anesthetized with pentobarbital. Ipsilateral cervical vagus stimulation (ICVS) increased activity of 44 neurons in the C1 segment. At the same stimulation parameters, contralateral cervical vagus stimulation (CCVS) either increased, decreased or did not affect activity of C1 neurons that were excited by ICVS. For C1 cells excited by both ICVS and CCVS, the mean latency for activation was significantly longer for CCVS than for ICVS, and ICVS produced a greater degree of excitation than CCVS. In segments C2-C6, 16 of 18 neurons were excited by ICVS and 2 were inhibited. However, CCVS did not excite the C2-C6 neurons but either inhibited or did not affect activity. In 6 cervical cells, a CCVS conditioning stimulus reduced the level of excitation by ICVS (test stimulus). Transection of the C2 or C3 dorsal roots did not significantly affect the excitatory vagal input to C1 cells. Excitatory somatic receptive fields were classified for 60 cervical spinal cells that responded to vagal stimulation. Most (87%) cells were excited by noxious pinch; 29 were wide dynamic range (WDR) cells and 21 were high threshold cells. In contrast to upper cervical neurons, spinothalamic tract (STT) and spinal cells in lumbar segments were not excited by ICVS or CCVS at the stimulation parameters used in this study, but were primarily inhibited by vagal stimulation. Results of this study showed that a group of cells in upper cervical segments were excited by vagal afferents. This excitatory vagal input reaches the C1 segment primarily via an ipsilateral, supraspinal route.
Pain 1992 Oct
PMID:Vagal afferent fibers excite upper cervical neurons and inhibit activity of lumbar spinal cord neurons in the rat. 145 10

A 33-year-old male developed stiffness of the left neck and pain of the left shoulder two years previously. Six months prior to admission, he noticed tingling sensation of the left 2nd, 3rd and 4th fingers and motor weakness of the left hand, both of which gradually progressed. On admission, positive neurological findings were neck pain on dorsal extension, left hemiparesis more advanced in the upper limb, diffuse muscle atrophy of the left upper limb, hyperreflexia of the left upper and lower limbs with positive Babinski sign and dysesthesia corresponding to the left C3-T5 sensory dermatomes. Enhanced CT and Metrizamide CT myelography showed a large extra- and intra-dural mass from the C1 segment to the medulla oblongata on the left. Angiography disclosed a fusiform aneurysm of the left vertebral artery. Proximal ligation of the left vertebral artery was performed. Postoperatively, clinical signs were markedly improved and shrinkage of the aneurysm was demonstrated on postoperative Metrizamide CT myelogram. Pathogenesis of diffuse muscle atrophy of the left upper limb was undetermined, but was probably not due to disturbance of the anterior spinal artery because of good visualization of the artery on the angiogram. Indication of the proximal ligation of the vertebral artery with an aneurysm was discussed.
 ...
PMID:[Fusiform aneurysm of the vertebral artery presenting with foramen magnum syndrome: a case report]. 356 84

The capacity of opioids to alleviate inflammatory pain is negatively regulated by the glutamate-binding N-methyl-D-aspartate receptor (NMDAR). Increased activity of this receptor complicates the clinical use of opioids to treat persistent neuropathic pain. Immunohistochemical and ultrastructural studies have demonstrated the coexistence of both receptors within single neurons of the CNS, including those in the mesencephalic periaqueductal gray (PAG), a region that is implicated in the opioid control of nociception. We now report that mu-opioid receptors (MOR) and NMDAR NR1 subunits associate in the postsynaptic structures of PAG neurons. Morphine disrupts this complex by protein kinase-C (PKC)-mediated phosphorylation of the NR1 C1 segment and potentiates the NMDAR-CaMKII, pathway that is implicated in morphine tolerance. Inhibition of PKC, but not PKA or GRK2, restored the MOR-NR1 association and rescued the analgesic effect of morphine as well. The administration of N-methyl-D-aspartic acid separated the MOR-NR1 complex, increased MOR Ser phosphorylation, reduced the association of the MOR with G-proteins, and diminished the antinociceptive capacity of morphine. Inhibition of PKA, but not PKC, CaMKII, or GRK2, blocked these effects and preserved morphine antinociception. Thus, the opposing activities of the MOR and NMDAR in pain control affect their relation within neurons of structures such as the PAG. This finding could be exploited in developing bifunctional drugs that would act exclusively on those NMDARs associated with MORs.
 ...
PMID:The mu-opioid receptor and the NMDA receptor associate in PAG neurons: implications in pain control. 2215 45

A 44-year old male patient was admitted to the First Affiliated Hospital, Zhejiang University School of Medicine with left ptosis and pain on the left head and neck for 20 days.Brain MRI showed subacute cerebral infarction on left parietal lobe and intramural hematoma on left internal carotid artery. CT angiography showed stenosis line on the C1 segment of left internal carotid artery. Digital subtraction angiography showed dissection on the C1 segment of left internal carotid artery.The condition of patients was improved after anticoagulant therapy.
 ...
PMID:[Carotid artery dissection with Horner syndrome as main manifestation: a case report]. 2603 45