[Dentin hyperesthesia].
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Dentin Sensitivity↗
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[Hyperesthesia syndrome of dentin and gingiva].
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Dentin Sensitivity↗
The effect of some somatic diseases on the incidence of dental hyperesthesia.
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Adult↗
[Dentinal hyperesthesia and fluoride ionophoresis].
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Adult↗
Chronic pain and sensory changes after augmentation mammoplasty: long term effects of preincisional administration of methylprednisolone.
We studied the prevalence of chronic pain and long term sensory changes after cosmetic augmentation mammoplasty and the effects of a single i.v. preoperative dose of methylprednisolone 125 mg (n=74), parecoxib 40 mg (n=71), or placebo (n=74). A questionnaire was mailed 6 weeks and 1 year after surgery. Response rate after 1 year was 80%. At 1 year non-evoked pain was present in 13%, and evoked pain was present in 20% with no statistically significant differences between the groups. Methylprednisolone was associated with reduced odds for hyperesthesia at 1 year (OR 0.3, 95% CI 0.1-0.6), and significantly reduced the prevalence of hyperesthesia (30%) compared with placebo (56%, P<0.01) and parecoxib (51%, P<0.04). Factors associated with increased odds for pain at 1 year were intensity of pain during the first 6 days after surgery (OR 1.3, 95% CI 1.1-1.6), pain at 6 weeks (OR 18.4, 95% CI 6.9-49.3), hyperesthesia at 6 weeks (OR 2.3, 95% CI 1.1-5.1) and present hyperesthesia (OR 3.1, 95% CI 1.4-6.7). We conclude that persistent pain and sensory changes are common after augmentation mammoplasty, and that patients having pain at 6 weeks most likely will have pain also at 1 year. Acute postoperative pain, hyperesthesia at 6 weeks, and the presence of hyperesthesia increased the odds for pain at 1 year. Preoperative methylprednisolone resulted in significantly less hyperesthesia compared with both parecoxib and placebo, but did not significantly reduce the prevalence of persistent spontaneous or evoked pain.
Adult↗
Analysis of drug interaction between intrathecal clonidine and MK-801 in peripheral neuropathic pain rat model.
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. Using a fixed-dose analysis and an isobolographic paradigm, the spinal interaction between the alpha 2-adrenoceptor agonist clonidine and the N-methyl-D-aspartate antagonist MK-801 is characterized in a rat model of nerve injury-induced tactile hyperesthesia. METHODS: Male Sprague Dawley rats were anesthetized with halothane, and the left L5 and L6 spinal nerves were ligated (Chung model). After 7-10 days' recovery, a Polyethylene tubing catheter was implanted into the lumbar intrathecal space. After recovery from catheter implantations (5-7 days), intrathecal dose-response curves were established for the antihyperesthesia effects of clonidine (3, 6, 10, and 20 micrograms) and MK-801 (1, 3, 10, and 20 micrograms) alone to obtain the ED50 for each agent. In separate studies, three doses of clonidine (1, 3, and 10 micrograms) were injected mixed with one dose of MK-801 (1 microgram) for fixed-dose analysis, and three doses of the two agents (2, 6, and 20 micrograms) were injected jointly in a fraction of the dose ratio 1:1 for isobolographic analysis. Thresholds for left hind paw withdrawal to von Frey hair application were assessed. RESULTS: Rats with nerve ligation showed a reliable tactile hyperesthesia (mechanical threshold 1-3 g vs. normal > 15 g). Intrathecal clonidine and MK-801 alone produced dose-dependent reductions of tactile hyperesthesia: ED50 9 micrograms and 10 micrograms, respectively. With the fixed-dose analysis, the log dose-response curves showed a left shift that considerably exceeds the theoretical curve made by a simple sum of the effects of clonidine alone and with MK-801 (1 microgram). With the isobolographic analysis, the combination ED50 was found to be statistically less than the theoretical additive dose combination. Intrathecal atipamezole, an alpha 2 antagonist, reversed the effects of clonidine and the clonidine/MK-801 mixture but not MK-801 alone. The side effect of clonidine was sedation and urination and that of MK-801 was motor weakness at doses above 10 micrograms. These effects were considerably less severe in rats after equiactive doses in the combination group. CONCLUSIONS: The neuropathic pain is mediated by low-threshold mechanoreceptors, sympathetically dependent, and sensitive to both alpha 2 agonists and N-methyl-D-aspartate antagonists. Intrathecal clonidine may act to diminish sympathetic outflow, whereas MK-801 blocks the N-methyl-D-aspartate receptor that is associated with other spinal systems related to pain transmission mechanism. The two separate mechanisms may account for the powerful synergy observed in this study. Such combinations might be useful in neuropathic pain states to potentiate the antihyperpathic effects and to reduce the side effects of each agents.
Animals↗
Flap coverage for post-traumatic nerve pain in the arm.
14 patients with painful neuroma, skin hyperesthesia or neuralgic rest pain were followed up (mean 20 months) after excision of skin and scar, neurolysis and coverage with pedicled or free flaps. Painful neuroma had improved in 3 of 7 patients. Skin hyperesthesia had been eliminated in 8 of 11 patients, and had improved in 3. Neuralgic rest pain had been eliminated in 5 of 6 patients, and was partially relieved in one. It is concluded that painful neuroma in continuity is not relieved by flap coverage, whereas skin hyperesthesia and neuralgic rest pain are appropriate for this type of treatment.
Adolescent↗
Acute painful neuropathy restricted to the abdomen following rapid glycaemic control in type 2 diabetes.
A 46-year-old Japanese man with type 2 diabetes mellitus, whose only diabetic complication was simple retinopathy, developed acute painful neuropathy. This presented as paresthesia and hyperesthesia restricted to the abdomen. The patient's haemoglobin A(1c) had dropped from 12% to 7.5% within 5 months, following a rapid improvement in glycaemic control. On investigation, there were no indications of disease in the intraabdominal area. Nerve conduction studies were consistent with mild sensorimotor peripheral and autonomic neuropathy. The patient required medication (mexiletine, sulpiride and imipramine hydrochloride) to control the pain. Four months after presentation, the symptoms showed a dramatic improvement and the treatment for pain relief was discontinued without any recurrence of paresthesia or hyperesthesia in the patient's abdomen. This was a very unusual case of diabetic post-treatment painful neuropathy in which the prominent features were severe pain, paresthesia and hyperesthesia restricted to the abdomen.
Abdomen↗
Enhanced evoked excitatory transmitter release in experimental neuropathy requires descending facilitation.
Nerve injury-induced afferent discharge is thought to elicit spinal sensitization and consequent abnormal pain. Experimental neuropathic pain, however, also depends on central changes, including descending facilitation arising from the rostral ventromedial medulla (RVM) and upregulation of spinal dynorphin. A possible intersection of these influences at the spinal level was explored by measuring evoked, excitatory transmitter release in tissues taken from nerve-injured animals with or without previous manipulation of descending modulatory systems. Spinal nerve ligation (SNL) produced expected tactile and thermal hyperesthesias. Capsaicin-evoked calcitonin gene-related peptide (CGRP) release was markedly enhanced in lumbar spinal tissue from SNL rats when compared with sham-operated controls. Enhanced, evoked CGRP release from SNL rats was blocked by anti-dynorphin A(1-13) antiserum; this treatment did not alter evoked release in tissues from sham-operated rats. Dorsolateral funiculus lesion (DLF) or destruction of RVM neurons expressing mu-opioid receptors with dermorphin-saporin, blocked tactile and thermal hypersensitivity, as well as SNL-induced upregulation of spinal dynorphin. Spinal tissues from these DLF-lesioned or dermorphin-saporin-treated SNL rats did not exhibit enhanced capsaicin-evoked CGRP-IR release. These data demonstrate exaggerated release of excitatory transmitter from primary afferents after injury to peripheral nerves, supporting the likely importance of increased afferent input as a driving force of neuropathic pain. The data also show that modulatory influences of descending facilitation are required for enhanced evoked transmitter release after nerve injury. Thus, convergence of descending modulation, spinal plasticity, and afferent drive in the nerve-injured state reveals a mechanism by which some aspects of nerve injury-induced hyperesthesias may occur.
Afferent Pathways↗
Neurinoma of the trigeminal root and atypical trigeminal neuralgia: case report and review of the literature.
BACKGROUND: Neurinomas of the trigeminal nerve are a rare entity: those located in the posterior fossa account for 20% of all cases. In the majority of cases, the clinical presentation begins with fifth cranial nerve involvement producing a constant pain associated with other cranial nerve palsy and cerebellar signs. METHODS: We report the clinical features, neuroradiological imagings, and management of a case of trigeminal neurinoma located in the cerebellopontine angle, arising from the Vth cranial nerve root, presenting with an atypical trigeminal neuralgia; moreover, we analyze similar cases reported in the literature and we discuss whether pain can be produced by a neurinoma that arises central to the ganglion. RESULTS: The tumor presented with an atypical trigeminal neuralgia characterized by constant trigeminal pain with paroxystical burns, hyperesthesia and hyperactive autonomic dysfunction. Neuroradiological examinations provided the best preoperative localization of this lesion, allowing better planning of the surgical approach, considering the large size of this tumor. A retromastoid incision and posterior fossa craniectomy approach was used, with complete excision of the tumor. The paraxysmal sharp pain and hyperesthesia disappeared completely, but the constant burning pain persisted although it was less intense. At an 8-month follow-up examination, the patient showed a progressive improvement of clinical symptoms and control magnetic resonance imaging (MRI) showed the complete removal of the neoplasm and the absence of residuals or recurrences. CONCLUSION: Although in a high percentage of cases of atypical trigeminal neuralgia a neurovascular conflict might be suspected, the review of the present case suggests that the hypothesis of a trigeminal neurinoma must be investigated both with adequate neuroradiological procedures and/or microsurgical exploration of the trigeminal root.
Cranial Fossa, Posterior↗
The majority of unmyelinated afferent axons in human ventral roots probably conduct pain.
Three patients with intractable chest pain had undergone dorsal rhizotomy. None had obtained relief, but all three had developed dysesthesia and hyperesthesia, in addition to the original pain persisting in the supposedly deafferented area. Dorsal ganglionectomy was performed for these 3 patients in 1976 and they were followed for 3 years. Following ganglionectomy two of the three developed total anesthesia, including loss of dysesthesia, hyperesthesia, and the original pain. Light and electron microscopical examination of the ventral roots removed at the time of ganglionectomy showed that unmyelinated axons constituted approximately 25% of the total fiber count. Two ventral roots from one patient who previously had serendipitous removal of dorsal ganglia showed a marked reduction in the population of unmyelinated axons. The observations support Coggeshall's contention that the majority of unmyelinated axons in the ventral roots are sensory and probably conduct pain.
Adult↗
Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists.
Intrathecal administration of glycine (strychnine) or GABA (bicuculline) but not opioid (naloxone), adrenergic (phentolamine) or serotonin (methysergide) receptor antagonists resulted in a dose-dependent organized agitation response to light tactile stimulation. This effect was maximally evoked by oscillating but not continuous stimulation applied to a dermatome corresponding to the levels of spinal cord acted upon by the intrathecal antagonist. Similar results were observed in chloralose-urethane anesthetized rats in which tactile stimulation evoked hypertensive responses following local tactile stimuli. The effects were only mildly depressed by even high doses of spinal morphine or DADL and not at all by ST-91 or baclofen. In contrast, intrathecal injections of glutamate receptor antagonists resulted in a dose-dependent depression of the strychnine evoked hyperesthesia with the ordering of activity being MK-801, AP-5, kynurenic acid, SKF10047 and ketamine. At doses below those which produced motor dysfunction, however, these agents had no effects on the hot-plate response latency. These data emphasize that low threshold afferent input is likely subject to an ongoing modulation, the loss of which results in a miscoding of the afferent stimulus yielding a pain relevant message. The lack of effect of agents having a powerful effect on somatic pain stimuli and the converse effects of glutamate receptor antagonists on the strychnine hyperesthesia at doses which do not affect the somatic pain response indicate discriminable processing systems, the characteristics of which resemble the clinical phenomenon observed in patients suffering from sensory dysesthesia following central and peripheral horn injury.
Analgesics↗
Effects of sympathectomy in a model of causalgiform pain produced by partial sciatic nerve injury in rats.
In a previous report we presented a novel behavioral model of neuropathic pain disorders, produced in rat by a unilateral ligation of about half of the sciatic nerve. The model is characterized by rapid onset of behaviors suggesting spontaneous pain and disordered responses to non-noxious and noxious stimuli. These include reduced withdrawal thresholds to repetitive touch in the partially deafferented skin ('touched-evoked hyperesthesia'), touch-evoked allodynia, reduced withdrawal thresholds to noxious thermal stimuli and exaggerated responses to noxious heat and mechanical stimuli ('thermal hyperalgesia'). Some of these disorders are seen at mirror image sites on the hind limb opposite the lesion. These disorder start within hours after partial nerve injury, last many months and are very similar to causalgia in humans following partial nerve injury. Since sympathetic efferent activity is known to aggravate causalgia in humans and sympathectomy is known to relieve it, we studied the effect of changing sympathetic outflow in the rat model. Reversible sympathectomy was carried out using guanethidine injected intraperitoneally in 3 experiments, each at a different time in relation to the partial nerve injury. We found that: (1) sympathectomy performed several months postoperatively alleviated the sensory disorders bilaterally; (2) sympathectomy prior to nerve injury partially prevented the appearance of thermal hyperalgesia but did not affect hyperesthesia to repetitive touch; and (3) sympathectomy at the time of nerve injury aggravated the sensory disorders during the first few days. As maintenance and production of the sensory disorders in this animal model depended on sympathetic nervous outflow, we conclude that the rats were suffering from a syndrome analogous to sympathetically maintained causalgia in man.
Animals↗
Sudden death due presumably to internal use of methamphetamine.
A 26-year-old male was found naked and excited in the backyard of his neighbor's house. He was carried to a nearby hospital, and returned home with his family, but took a sudden turn for the worse and died. In a judicial autopsy, the ethanol concentration of blood was found to be 0.58 milligrams, and methamphetamine (MA) was detected in his blood by thin-layer chromatography. The concentration of MA in his blood was 4.38 mumol/dl, higher than the fatal level. The amount of MA in his stomach was 5.8 mg (34.58 mumol/100 g), indicating that he ingested MA by internal use. Among the autopsy cases of acute MA poisoning reported in Japan, hyperesthesia is known to last 1-3 h before death, whether the administration is by intravenous injection or orally. But the present case is quite unusual, as the death followed 6 h or more of hyperesthesia. This was attributed to the patient's combined intake of alcohol with MA, as it is known to decrease the mortality in mice.
Adult↗
Postherpes simplex type 1 neuralgia simulating postherpetic neuralgia.
Patients with prodromal neuralgia associated with recurrent herpes simplex type 1 (HST1) infection and chronic facial pain following years of relapsing HST1 have been described. Chronic neuralgia following a single clinical HST1 infection and simulating postherpetic neuralgia has not been previously reported. Such a case is described: A 49-yr-old woman with a 2-mo history of oral-facial dyskinesia developed burning pain and hypersensitivity of the left side of the tongue, lower gum, and inner cheek, followed 1 day later by a vesicular rash in the same painful distribution. Viral cultures of the lesions identified HST1 but not herpes zoster. Cerebrospinal fluid analyses during the vesicular lesion stage and 1 mo later were normal with no viral growth. Oral and facial lesions resolved after 10 days; acyclovir was given for 3 wk. Brain and brainstem magnetic resonance imaging (MRI), electroencephalogram, and brainstem evoked potential studies were normal. Hyperesthesias, allodynia, and burning pain persisted despite nonsteroidal antiinflammatory agents, codeine and hydrocodone. Oral opioids were administered until sedation occurred, with no relief of pain. The burning pain and hyperesthesia resolved after the 16th day of amitriptyline use, 75 mg/day. A trial off amitriptyline 6 mo later resulted in recurrence of pain, and amitriptyline was restarted with good pain control. Post-HST1 neuralgia may simulate postherpetic neuralgia clinically, and painful symptoms may respond to amitriptyline.
Amitriptyline↗
Fibrocartilaginous embolism.
Fibrocartilaginous embolism (FCE) is an acute myelopathy that affects primarily dogs and human beings, and occasionally other mammalian species. It is frequently associated with trauma or vigorous exercise; in dogs it tends to affect mature non-chondrodystrophoid and giant breeds. Signs are acute and frequently indicate a very lateralized or focal lesion within the spinal cord, with resultant disparities in sensory and motor function. Lower motor neuron disease is common and hyperesthesia is unusual. The primary differential diagnoses are concussive trauma and intervertebral disc herniation, but the acute onset of strongly lateralizing spinal cord deficits without hyperesthesia in a breed at risk is strongly suggestive of the FCE syndrome. Attention must be given to other systemic diseases that might also give rise to emboli in the absence of FCE. Diagnosis is based on history, clinical signs, and elimination of other differential diagnoses. Treatment is largely supportive, although high doses of methylprednisolone may be beneficial early in the course of the disease. Affected patients may make a functional recovery if deep pain sensation is preserved and there are not complete lower motor neuron signs in affected limbs or sphincters.
Animals↗
A novel model of primary and secondary hyperalgesia after mild thermal injury in the rat.
Secondary hyperesthesia was investigated in a rat thermal injury model. After a mild focal thermal injury (52 degrees C/45 s) to the rat heel, the response latency for a thermal stimulus directed at the injured site was reduced (10 --> 6 s; e.g. primary thermal hyperalgesia) but no change was seen at the distal site. Conversely, tactile threshold at the distal site was significantly reduced (15 --> 5 g; e.g. secondary tactile allodynia) but much less so at the injured site. Magnitude of the secondary tactile allodynia paralleled the severity of the primary injury. Accordingly, this model has the same characteristics seen in human post-tissue-injury hyperesthetic states and provides a tool for the study of mechanisms underlying primary and secondary hyperesthesia.
Animals↗
Comparison of effects of lidocaine hydrochloride, buffered lidocaine, diphenhydramine, and normal saline after intradermal injection.
STUDY OBJECTIVE: To evaluate pain and the spread of analgesia when local anesthetics are given as an intradermal injection into the dorsal aspect of the hand. DESIGN: Randomized, double-blinded, placebo-controlled study. SETTING: University medical center. PATIENTS: 40 consenting adult volunteers. INTERVENTIONS: Volunteers were randomly assigned to receive a 0.25-mL injection of either lidocaine hydrochloride (1%), buffered lidocaine, diphenhydramine (1%), or placebo (0.9% sodium chloride solution) into the dorsal aspect of both hands. MEASUREMENTS: The volunteers used a visual analog scale to compare the pain of needle insertion and solution injection. Then at 1, 2, 5, 10, 20, and 30 minutes after intradermal injection, the extent of the analgesic area was marked on a strip of tape placed horizontally across the hand. Then at 32 minutes after intradermal injection, the extent of the analgesic area was marked on a strip of tape placed vertically across the hand. The volunteers were called each day and asked the duration of their numbness or hyperesthesia until their hands were no longer numb or sore. MAIN RESULTS: Buffered lidocaine during intradermal infiltration was found to be significantly (p < 0.05) less painful than either lidocaine hydrochloride or diphenhydramine and equivalent to placebo. Diphenhydramine and lidocaine hydrochloride during intradermal infiltration induced significantly (p < 0.05) more pain than buffered lidocaine or placebo. Lidocaine hydrochloride displayed a significantly (p < 0.05) larger diameter of analgesia than placebo by 1 minute after the injection, buffered lidocaine by 2 minutes after injection, and diphenhydramine by 5 minutes after injection. By 20 minutes after injection, diphenhydramine diameter of analgesia was significantly (p < 0.05) larger than placebo but significantly less than buffered lidocaine. By 30 minutes after injection, diphenhydramine diameter of analgesia was equivalent to placebo whereas buffered lidocaine and lidocaine diameters were still significantly (p < 0.05) larger than placebo. Diphenhydramine injection resulted in numbness that lasted significantly (p < 0.05) longer than other study solutions whereas buffered lidocaine and lidocaine injections resulted in numbness that lasted significantly longer than placebo. Diphenhydramine injection resulted in hyperesthesia that lasted for 2 or more days in 12 of the volunteers. CONCLUSION: There is a reduction of infiltration pain using buffered lidocaine as opposed to lidocaine and diphenhydramine. Although lidocaine injection resulted in a slightly faster spread of analgesic diameter, buffered lidocaine was equivalent to lidocaine from minute 2 until minute 30. Therefore, to obtain optimal anesthetic conditions, we recommend that buffered lidocaine be given 2 minutes before performing catheterization, whereas diphenhydramine should be given 5 minutes before catheterization, but only when buffered lidocaine cannot be used.
Adult↗