scholarly journals Peripheral Contributions to Visceral Hyperalgesia

1999 ◽  
Vol 13 (suppl a) ◽  
pp. 37A-41A ◽  
Author(s):  
GF Gebhart
Keyword(s):  
Spinal Cord ◽  
Urinary Bladder ◽  
Tissue Injury ◽  
Mechanical Stimuli ◽  
Sensory Receptors ◽  
Visceral Hyperalgesia ◽  
Nonhuman Animals ◽  
Primary Hyperalgesia ◽  
Thermal Stimuli ◽  
Key Questions

Hyperalgesia has long been recognized clinically as a consequence of tissue injury. Primary hyperalgesia (arising from the site of injury) is generally considered to be due to sensitization of sensory receptors (eg, nociceptors) and perhaps activation of so-called ‘silent nociceptors’ by mediators released, synthesized or attracted to the site of tissue injury. Key questions associated with understanding visceral hyperalgesia relate to whether the viscera are innervated by nociceptors (ie, sensory receptors that respond selectively to noxious intensities of stimulation), whether visceral receptors and/or afferent fibres sensitize after tissue injury and whether silent nociceptors exist in the viscera. Studies in nonhuman animals have revealed that hollow organs such as the esophagus, gall bladder, stomach, urinary bladder, colon and uterus are innervated by mechanically sensitive receptors with low or high thresholds for response. Accordingly, it appears that the viscera are innervated by nociceptors, although the issue is far from settled. One characteristic of cutaneous nociceptors is their ability to be sensitized when tissue is injured. Mechanosensitive visceral receptors also sensitize when the viscera are experimentally inflamed, but both visceral receptors with low thresholds and those with high thresholds for response are sensitized. Moreover, it is often not appreciated that visceral receptors are likely polymodal rather than unimodal – that is, mechanically sensitive visceral receptors typically are also sensitive to chemical and/or thermal stimuli. In this sense, visceral receptors may be considered evolutionarily older than more highly developed, specialized cutaneous receptors. Finally, there are mechanically insensitive receptors that innervate the viscera and, when tissue is injured, develop spontaneous activity and acquire sensitivity to mechanical stimuli. In the aggregrate, visceral receptors change their behaviour in the presence of tissue injury and, along with activated mechanically insensitive receptors, increase the afferent barrage into the spinal cord, contributing to the development of visceral hyperalgesia.

Neural Processing of Pain and Itch

2021 ◽  
Author(s):  
Taylor Follansbee ◽  
Mirela Iodi Carstens ◽  
E. Carstens
Keyword(s):  
Central Sensitization ◽  
Tissue Injury ◽  
Emotional Experience ◽  
Spinal Pain ◽  
Anterior Cingulate ◽  
Mechanical Stimuli ◽  
Firing Rates ◽  
Spinal Circuitry ◽  
Ascending Pathways ◽  
Primary Hyperalgesia

Pain is defined as “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage,” while itch can be defined as “an unpleasant sensation that evokes the desire to scratch.” These sensations are normally elicited by noxious or pruritic stimuli that excite peripheral sensory neurons connected to spinal circuits and ascending pathways involved in sensory discrimination, emotional aversiveness, and respective motor responses. Specialized molecular receptors expressed by cutaneous nerve endings transduce stimuli into action potentials conducted by C- and Aδ-fiber nociceptors and pruriceptors into the outer lamina of the dorsal horn of the spinal cord. Here, neurons selectively activated by nociceptors, or by convergent input from nociceptors, pruriceptors, and often mechanoreceptors, transmit signals to ascending spinothalamic and spinoparabrachial pathways. The spinal circuitry for itch requires interneurons expressing gastrin-releasing peptide and its receptor, while spinal pain circuitry involves other excitatory neuropeptides; both itch and pain are transmitted by ascending pathways that express the receptor for substance P. Spinal itch- and pain-transmitting circuitry is segmentally modulated by inhibitory interneurons expressing dynorphin, GABA, and glycine, which mediate the antinociceptive and antipruritic effects of noxious counterstimulation. Spinal circuits are also under descending modulation from the brainstem rostral ventromedial medulla. Opioids like morphine inhibit spinal pain-transmitting circuits segmentally and via descending inhibitory pathways, while having the opposite effect on itch. The supraspinal targets of ascending pain and itch pathways exhibit extensive overlap and include the somatosensory thalamus, parabrachial nucleus, amygdala, periaqueductal gray, and somatosensory, anterior cingulate, insular, and supplementary motor cortical areas. Following tissue injury, enhanced pain is evoked near the injury (primary hyperalgesia) due to release of inflammatory mediators that sensitize nociceptors. Within a larger surrounding area of secondary hyperalgesia, innocuous mechanical stimuli elicit pain (allodynia) due to central sensitization of pain pathways. Pruriceptors can also become sensitized in pathophysiological conditions, such as dermatitis. Under chronic itch conditions, low-threshold tactile stimulation can elicit itch (alloknesis), presumably due to central sensitization of itch pathways, although this has not been extensively studied. There is considerable overlap in pain- and itch-signaling pathways and it remains unclear how these sensations are discriminated. Specificity theory states that itch and pain are separate sensations with their own distinct pathways (“labeled lines”). Selectivity theory is similar but incorporates the observation that pruriceptive neurons are also excited by algogenic stimuli that inhibit spinal itch transmission. In contrast, intensity theory states that itch is signaled by low firing rates, and pain by high firing rates, in a common sensory pathway. Finally, the spatial contrast theory proposes that itch is elicited by focal activation of a few nociceptors while activation of more nociceptors over a larger area elicits pain. There is evidence supporting each theory, and it remains to be determined how the nervous system distinguishes between pain and itch.

scholarly journals Characterization of Mouse Lumbar Splanchnic and Pelvic Nerve Urinary Bladder Mechanosensory Afferents

2008 ◽  
Vol 99 (1) ◽  
pp. 244-253 ◽  
Author(s):  
Linjing Xu ◽  
G. F. Gebhart
Keyword(s):  
Spinal Cord ◽  
Urinary Bladder ◽  
Receptive Field ◽  
Present Report ◽  
Sensory Information ◽  
Total Sample ◽  
High Threshold ◽  
Mechanical Stimuli ◽  
Afferent Fibers

Sensory information from the urinary bladder is conveyed via lumbar splanchnic (LSN) and sacral pelvic (PN) nerves to the spinal cord. In the present report we compared the mechanosensitive properties of single afferent fibers in these two pathways using an in vitro mouse bladder preparation. Mechanosensitive primary afferents were recorded from the LSN or PN and distinguished based on their response to receptive field stimulation with different mechanical stimuli: probing (160 mg to 2 g), stretch (1–25 g), and stroking of the urothelium (10–1,000 mg). Four different classes of afferent were recorded from the LSN and PN: serosal, muscular, muscular/urothielial, and urothelial. The LSN contained principally serosal and muscular afferents (97% of the total sample), whereas all four afferent classes of afferent were present in the PN (63% of which were muscular afferents). In addition, the respective proportions and receptive field distributions differed between the two pathways. Both low- and high-threshold stretch-sensitive muscular afferents were present in both pathways, and muscular afferents in the PN were shown to sensitize after exposure to an inflammatory soup cocktail. The LSN and PN pathways contain different populations of mechanosensitive afferents capable of detecting a range of mechanical stimuli and individually tuned to detect the type, magnitude, and duration of the stimulus. This knowledge broadens our understanding of the potential roles these two pathways play in conveying mechanical information from the bladder to the spinal cord.

The distribution and density of ciliary tufts on the siphons of Anodonta cygnea (Mollusca: Bivalvia)

1990 ◽  
Vol 48 (3) ◽  
pp. 518-519
Author(s):  
Wen-lung Wu
Keyword(s):  
Osmium Tetroxide ◽  
Internal Surface ◽  
Mechanical Stimuli ◽  
Type Ii ◽  
Sensory Receptors ◽  
Anodonta Cygnea ◽  
Type Iv ◽  
Sem Study ◽  
Inhalant Siphon ◽  
Type V

The mantle of bivalves has come entirely to enclose the laterally compressed body and the mantle margin has assumed a variety of functions, one of the pricipal ones being sensory. Ciliary tufts, which are probably sensory, have been reported from the mantle and siphons of several bivalves1∽4. Certain regions of the mantle margin are likely to be more or less, sensitive to certain stimuli than others. The inhalant siphon is likely to be particularly sensitive to both chemical and mechanical stimuli, whereas the exhalant siphon will be less sensitive to both. The distribution and density of putative sensory receptors on the in-and ex-halant siphon is compared in this paper.The excised siphons were fixed in glutaraldehyde and osmium tetroxide, the whole procedure of SEM study is recorded in Wu's thesis.Type II cilia cover the tips of tentacles, 6.13um. Type IV and type V cilia are found on the surface of tentacles. Type IV cilia are occasionally present at the tips of tentacles, 8 um long. They are the commonest type on the surface of tentacles. Type VI cilia occor in the internal surface of the inhalant siphon, but are not found on the surface of tentacles, 6.7-10um long.

Bioelectrodes for Neural Prostheses

1985 ◽  
Vol 55 ◽  
Author(s):  
F. Terry Hambrecht
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Urinary Bladder ◽  
Cochlear Implants ◽  
Neural Prostheses ◽  
The Future ◽  
Spinal Cord Disorders ◽  
The Central Nervous System ◽  
Auditory Prostheses

ABSTRACTNeural prostheses which are commercially available include cochlear implants for treating certain forms of deafness and urinary bladder evacuation prostheses for individuals with spinal cord disorders. In the future we can anticipate improvements in bioelectrodes and biomaterials which should permit more sophisticated devices such as visual prostheses for the blind and auditory prostheses for the deaf based on microstimulation of the central nervous system.

Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury

1982 ◽  
Vol 60 (11) ◽  
pp. 1415-1424 ◽  
Author(s):  
H. B. Demopoulos ◽  
E. S. Flamm ◽  
M. L. Seligman ◽  
D. D. Pietronigro ◽  
J. Tomasula ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Tissue Injury ◽  
Functional Restoration ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Cord Injury

The hypothesis that pathologic free-radical reactions are initiated and catalyzed in the major central nervous system (CNS) disorders has been further supported by the current acute spinal cord injury work that has demonstrated the appearance of specific, cholesterol free-radical oxidation products. The significance of these products is suggested by the fact that: (i) they increase with time after injury; (ii) their production is curtailed with a steroidal antioxidant; (iii) high antioxidant doses of the steroidal antioxidant which curtail the development of free-radical product prevent tissue degeneration and permit functional restoration. The role of pathologic free-radical reactions is also inferred from the loss of ascorbic acid, a principal CNS antioxidant, and of extractable cholesterol. These losses are also prevented by the steroidal antioxidant. This model system is among others in the CNS which offer distinctive opportunities to study, in vivo, the onset and progression of membrane damaging free-radical reactions within well-defined parameters of time, extent of tissue injury, correlation with changes in membrane enzymes, and correlation with readily measurable in vivo functions.

Histopathology of experimental hematomyelia

1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher
Keyword(s):  
Spinal Cord ◽  
Tissue Injury ◽  
Central Canal ◽  
Microglial Cells ◽  
Neurological Deficits ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Cellular Debris ◽  
Dorsal Columns

✓ The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 µl blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.

THE MOTILITY AND REACTIVITY OF THE OESTROGENIZED RABBIT UTERUS IN VIVO; WITH COMPARATIVE OBSERVATIONS ON MILK EJECTION

1958 ◽  
Vol 16 (3) ◽  
pp. 237-260 ◽  
Author(s):  
B. A. CROSS
Keyword(s):  
Spinal Cord ◽  
Mammary Gland ◽  
Spinal Anaesthesia ◽  
Dose Range ◽  
Abdominal Muscles ◽  
Mechanical Stimuli ◽  
Milk Ejection ◽  
Thoracic Spinal ◽  
Spontaneous Motility ◽  
Stimulation Of

SUMMARY The spontaneous motility of the intact uterus of spayed oestrogenized rabbits under sodium pentobarbitone anaesthesia has been recorded. Both uteri of each animal behaved similarly, and contractions often appeared to be synchronous. Small changes of load affected the amplitude of contractions, but did not alter uterine responsiveness to neurohypophysial or adrenomedullary hormones. Mid-thoracic section of the spinal cord obliterated spontaneous motility of the uterus; spinal anaesthesia did not. Spontaneous motility persisted for as long as 7 hr after decerebration and removal of the pituitary gland. The threshold dose of oxytocin for activating the oestrogenized uterus was the same as that for the lactating mammary gland, i.e. 1–5 mu. Doses up to 50 mu. usually gave an increase in frequency and amplitude of contractions. In the same dose range vasopressin either had little effect or inhibited spontaneous uterine motility, although milk ejection was stimulated. Slow infusion of oxytocin at rates of 1·5–48 mu./min produced graded increases in the rate and depth of uterine contractions and, at the same time, in similarly treated, lactating animals, rhythmic milk-ejection responses which at the higher rates of infusion merged to give a tetanic (plateau) type of milk ejection. Adrenaline or noradrenaline in doses of 1–5 μg produced diphasic uterine responses, initial contractions being followed by inhibition of spontaneous motility. They also inhibited the uterine, as well as the milk-ejection response to oxytocin injected 10–30 sec later. The inhibitory effect of adrenaline on both organs was about twice that of noradrenaline. The above-mentioned responses to adrenaline and oxytocin could also be elicited by electrical stimulation of the hypothalamus. Stimuli in the dorsal, lateral, perifornical and posterior hypothalamic areas produced effects equivalent to those of 1–5 μg adrenaline on both the uterus and mammary gland. These responses were abolished by mid-thoracic section of the spinal cord or by spinal anaesthesia. In such preparations responses typical of those produced by oxytocin were seen in both organs after stimulation of the paraventricular nuclei, supraoptic nuclei and the hypothalamo-hypophysial nerve pathways of the tuber cinereum and neural stalk. Dilatation of the vagina (or rectum) gave rise to a uterine response similar to that resulting from adrenaline or noradrenaline. The response was abolished by spinal anaesthesia, but not by mid-thoracic spinal section or decerebration. The same stimuli also produced 'bearing down' contractions of the abdominal muscles. Contractions of the uterus could also be elicited by mechanical stimuli, in the absence of functional spinal connexions.

scholarly journals A Simple Radiological Technique for Demonstration of Incorrect Positioning of a Foley Catheter with Balloon Inflated in the Urethra of a Male Spinal Cord Injury Patient

2006 ◽  
Vol 6 ◽  
pp. 2445-2449 ◽  
Author(s):  
Subramanian Vaidyanathan ◽  
Peter L. Hughes ◽  
Bakul M. Soni
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Urinary Bladder ◽  
Contrast Medium ◽  
Foley Catheter ◽  
Autonomic Dysreflexia ◽  
X Ray ◽  
Malpractice Claims ◽  
Cord Injury ◽  
Radiological Technique

In a male patient with cervical spinal cord injury, the urinary bladder may go into spasm when a urethral catheter is removed and a new Foley catheter is inserted. Before the balloon is inflated, the spastic bladder may push the Foley catheter out or the catheter may slip out of a small-capacity bladder. An inexperienced health professional may inflate the balloon of a Foley catheter in the urethra without realizing that the balloon segment of the catheter is lying in the urethra instead of the urinary bladder. When a Foley balloon is inflated in the urethra, a tetraplegic patient is likely to develop autonomic dysreflexia. This is a medical emergency and requires urgent treatment. Before the incorrectly placed Foley catheter is removed, it is important to document whether the balloon has been inflated in the urinary bladder or not. The clinician should first use the always available tools of observation and palpation at the bedside without delays of transportation. A misplaced balloon will often be evident by a long catheter sign, indicating excessive catheter remaining outside the patient. Radiological diagnosis is not frequently required and, when needed, should employ the technique most readily available, which might be a body and pelvic CT without intravenous contrast. An alternative radiological technique to demonstrate the position of the balloon of the Foley catheter is described. Three milliliters of nonionic X-ray contrast medium, Ioversol (OPTIRAY 300), is injected through the side channel of the Foley catheter, which is used for inflating the balloon. Then, with a catheter-tip syringe, 30 ml of sterile Ioversol is injected through the main lumen of the Foley catheter. Immediately thereafter, an X-ray of the pelvis (including perineum) is taken. By this technique, both the urinary bladder and balloon of the Foley catheter are visualized by the X-ray contrast medium. When a Foley catheter has been inserted correctly, the balloon of the Foley catheter should be located within the urinary bladder, but when the Foley catheter is misplaced with the balloon inflated in the urethra, a round opaque shadow of the Foley balloon is seen separately below the urinary bladder. This radiological study takes only a few minutes to perform, can be carried out bedside with a mobile X-ray machine, and does not require special expertise or preparations, unlike transrectal ultrasonography. When a Foley balloon is inflated in the urethra, abdominal ultrasonography will show an absence of the Foley balloon within the bladder. The technique described above aids in positive demonstration of a Foley balloon lying outside the urinary bladder. Such documentation proves valuable in planning future treatment, education of health professionals, and settlement of malpractice claims.

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