Disease relevance of Hyperesthesia

• Inherited congenital myoclonus in Poll Hereford calves is characterized by hyperesthesia and myoclonic jerks of the skeletal musculature that occur spontaneously and in response to sensory stimuli [1].
• Toxicity occurring during chronic administration of Lonidamine at doses ranging between 45 and 275 mg/m2 twice daily, mainly consisted of somnolence, myalgias, hyperesthesia and mild hair loss [2].
• CONCLUSIONS: These data indicate that: 1) spinal NK1 and NK2 receptors do not play an important role in development and maintenance of thermal hyperesthesia evoked by paw carrageenan, and 2) the peripheral NK1 receptor may play an important role in the development of thermal hyperesthesia, but not of paw edema [3].
• We describe a 39 years-old female patient who developed hyperesthesia associated with lower limbs paresis, fourteen days after she had ingested a Dichlorvos-based insecticide [4].

High impact information on Hyperesthesia

• The data suggest that the 5HT- and PGE2-mediated increase in Na+ current may be involved in hyperesthesia in different but overlapping subpopulations of nociceptors [5].
• These effects result in hyperesthesia, increased sensitivity to light touch, and mechanical allodynia, pain evoked by normally innocuous stimulation of Abeta primary afferents [6].
• Several compounds (2, 9, 14, 22, 25) also proved to have activities superior or comparable to indomethacin in suppressing chronic as well as acute inflammation and carrageenan-induced hyperesthesia [7].
• Clonidine, but not morphine, delays the development of thermal hyperesthesia induced by sciatic nerve constriction injury in the rat [8].
• BACKGROUND: Spinally delivered alpha 2-adrenoceptor agonists and N-methyl-D-aspartate antagonists each have been shown to have actions attenuating the hyperesthesia in rat models of nerve injury pain [9].

Chemical compound and disease context of Hyperesthesia

• Intrathecal clonidine and MK-801 alone produced dose-dependent reductions of tactile hyperesthesia: ED50 9 micrograms and 10 micrograms, respectively [9].
• The effects of morphine, MK-801, an NMDA antagonist, and CP-96,345, an NK1 antagonist, on the hyperesthesia evoked by carageenan injection in the rat paw [10].
• Myalgias and hyperesthesias were markedly relieved with prednisone 5 mg twice daily [11].
• Systemic bupivacaine had no effect on the development of thermal hyperesthesia [12].
• L-Arginine itself had no effect on the development of thermal hyperesthesia [13].

Anatomical context of Hyperesthesia

• Capsaicin, which destroys most C- and some A delta-fibers in peripheral nerves, had no effect on the touch-evoked allodynia and mechanical hyperesthesia that are produced by partial sciatic nerve injury [14].

Gene context of Hyperesthesia

• CONCLUSIONS: These data indicate that (1) an NMDA receptor, but not an NK1 receptor, plays an important role in maintaining the hyperesthesia after carageenan injection; and (2) NMDA antagonism has a simple additive interaction with morphine in the carageenan model of inflammatory hyperesthesia [10].
• CONCLUSIONS: These data indicate that (1) an N-methyl-D-aspartate receptor-mediated spinal facilitation may be the common mechanism maintaining the thermal hyperesthesia evoked by the constriction injury, and (2) the effects of intrathecal morphine on this thermal hyperesthesia are time-dependent [15].
• The unique ability of the CPT exam to quantify hyperesthesia may account for its superior CTS detection sensitivity [16].
• RESULTS: The prevalence of hyperesthesia at 2,000, 250, and 5 Hz in male diabetic subjects were 14.1, 15.6, and 7.7%, respectively, and 22.2, 24.5, and 16.4% respectively in female diabetic subjects [17].

Analytical, diagnostic and therapeutic context of Hyperesthesia

• The current study investigated the effect of spinally administered morphine and clonidine, an alpha 2 agonist, on the development of thermal hyperesthesia induced by nerve constriction injury in the rat [8].

References