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At least 721 records · Page 40Linked to original sources
PubMed1998

Influence of urinary management on urologic complications in a cohort of spinal cord injury patients.

OBJECTIVE: To study urologic complications in patients with spinal cord injury (SCI) in relation to their bladder management. DESIGN AND SETTING: A cohort study of patients with SCI in a rehabilitation center. PARTICIPANTS: One hundred eighty-two patients were studied; demographic data, disease characteristics, and urologic history were obtained for each. INTERVENTION: Patients responding to a questionnaire were given a clinical exam. Their medical records were reviewed, with particular attention given to the following urologic complications: lithiasis, urinary infections, orchiepididymitis, urethral trauma, vesicorenal reflux, and renal failure. RESULTS: Results are reported for 123 patients. Time since SCI was 8 years. Intermittent catheterization was the main method of bladder management. Only 32 patients had changed their method of vesical voiding. Urinary complications had developed in 75% of patients. The most common complication was urinary infection. Vesicoureteral reflux occurred in 26% of patients using percussion. Trauma related to catheterization was the main problem with intermittent catheterization, responsible for a high rate of orchiepididymitis. CONCLUSION: Intermittent catheterization is the most-used method of bladder management, but with a nonnegligible rate of urethral trauma in men. Percussion and Credé maneuver appear to be acceptable techniques of bladder management if the patient is closely monitored.

Adult↗
PubMed1996

Effects of muscarinic receptor antagonism on the phosphatidylinositol bisphosphate signal transduction pathway after experimental brain injury.

Hippocampal levels of fatty acids extracted from phosphatidylinositol 4,5-bisphosphate (PIP2), free fatty acids (FFA), and lactate were measured after central fluid percussion traumatic brain injury (TBI) in rats. At 5 min after injury, there was a decrease in fatty acids extracted from PIP2 suggesting a decrease in PIP2. At the same time point, total FFA increased in saline-treated TBI rats. Levels of arachidonic acid were significantly decreased in PIP2, while at the same time arachidonic and stearic acids increased in FFA in saline-treated TBI rats. No significant alterations in PIP2-derived fatty acids or FFA were observed at 20 min after TBI. Hippocampal concentrations of lactate were significantly elevated at 5 and 20 min after injury in saline-treated rats. In general, these alterations were blunted by preinjury administration of the muscarinic antagonist, scopolamine. These results suggest that the PIP2 signal transduction pathway is activated in the hippocampus at the onset of central fluid percussion TBI and that the enhanced phospholipase C-catalyzed phosphodiestric breakdown of PIP2 is a major mechanism of liberation of FFA in these sites immediately after such injury. The blunting of PIP2 and FFA alterations in animals treated with scopolamine suggests that activation of muscarinic receptors significantly contributes to the phospholipase C (PLC) signal transduction pathophysiology in TBI. The attenuation of lactate accumulation in scopolamine-treated rats suggests that TBI-induced muscarinic receptor activation also contributes to increased glycolytic metabolism and/or ionic imbalances.

Animals↗
PubMed1997

Evaluation of learning and memory dysfunction and histological findings in rats with chronic stage contusion and diffuse axonal injury.

We previously reported a modified fluid percussion device capable of consistently producing experimental cortical contusion (CC) and diffuse axonal injury (DAI) in separate groups of rats by lateral and midline fluid percussion, respectively. The purpose of the present study was to compare the differences in learning acquisition and memory retention impairments between these two types of injured rats in the chronic stage using the Morris water maze technique. We also compared the histological differences between these two different types of traumatic brain injury. The results showed a statistically significant difference in learning acquisition impairment between the sham and CC rats and also between the sham and DAI rats. However, a significant difference in memory retention impairment was observed only between the sham and DAI rats. Histologically, the neuronal cell loss of CA3 pyramidal cells in the hippocampus was observed on the ipsilateral side in the CC and bilaterally in DAI. The neuronal cell loss was seen in bilateral entorhinal cortex layer II in DAI, but it was not seen in CC. From these results, we speculate that the marked cell loss in the hippocampus CA3 region in both CC and DAI rats was related to the impairment of spatial learning acquisition. The marked cell loss in entorhinal cortex layer II in DAI rats may be one of the important factors in the impairment of spatial memory retention.

Animals↗
PubMed1997

Histological markers of neuronal, axonal and astrocytic changes after lateral rigid impact traumatic brain injury.

The model of lateral, rigid impact traumatic brain injury is widely used but remains relatively poorly characterized by comparison with fluid percussion injury models. Thus, whilst the gross morphological changes that occur over the short- and long-term post-injury have been described, more subtle measures of neuronal injury and activation, and markers of axonal and glial reactions have not been investigated, complicating interpretation of data from this model. To address this issue, a variety of neurohistological markers were examined in adult male rats which had been subjected to open brain, lateral rigid impact injury. A piston device was unilaterally driven 3.0 mm into the somatosensory cortex at a speed of 3.2 m/s. Neuronal activation evidenced by Fos-like immunoreactivity showed a complex pattern at 3 h after injury which appeared to be related both to proximity to the impact site and cortical efferent connectivity. At 24 h after injury, acid fuchsin staining demonstrated dying neurons in the margin of the injury and in ipsilateral hippocampus and dorsal thalamus. Injured cells identified by heat-shock protein immunoreactivity showed a similar distribution. Axonal injury demonstrated with 68 kDa neurofilament immunoreactivity was more widely distributed. Less axonal damage was found with increasing distance from the injury site. At 7 days post-injury, glial fibrillary acidic protein immunoreactive astrocytes were prolific in the ipsilateral thalamus, hippocampus and striatum and throughout the injured cortex. In general, controlled, lateral rigid impact injury provides a more focused injury than is seen with lateral fluid percussion which may have implications for the behavioral deficits seen in this injury model.

Animals↗
PubMed1997

Role of impaired cAMP and calcium-sensitive K+ channel function in altered cerebral hemodynamics following brain injury.

Previous studies have shown that pial arteries constricted and responses to dilator opioids were blunted after fluid percussion injury (FPI) in newborn pigs. Membrane potential of vascular muscle is a major determinant of vascular tone and activity of K+ channels is a major regulator of membrane potential. Recent data show that opioids elicit dilation via the sequential production of cAMP and subsequent activation of calcium-sensitive K+ (K(Ca2+)) channels by this second messenger. The present study was designed to investigate the effect of FPI on cAMP and K(Ca2+) channel function. Chloralose-anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir and a metal pendulum. Brain injury of moderate severity (1.9-2.1 atm) was produced by allowing the pendulum to strike a piston on the cylinder. FPI blunted dilation to the cAMP analogs 8-Bromo cAMP and Sp 8-Bromo cAMPs (10(-8), 10(-6) M), (9 +/- 1 and 16 +/- 1 vs. 2 +/- 1 and 3 +/- 1% dilations to 8-Bromo cAMP before and after FPI, respectively, n = 8). Similarly, FPI attenuated dilation to pituitary adenylate cyclase activating peptide (PACAP), an endogenous activator of adenylate cyclase, and NS 1619, a K(Ca2+) channel agonist (9 +/- 1 and 16 +/- 1 vs. 3 +/- 1 and 5 +/- 1% for NS 1619 10(-8), 10(-6) M before and after FPI, respectively, n = 8). Moreover, FPI attenuated PACAP, methionine enkephalin, leucine enkephalin, and dynorphin induced elevations in CSF cAMP concentration (940 +/- 2, 1457 +/- 50, and 2191 +/- 53 vs. 810 +/- 17, 1033 +/- 36, and 1218 +/- 49 fmol/ml for control, PACAP 10(-8), 10(-6) M before and after FPI, respectively, n = 8). These data show that cAMP and K(Ca2+) channel function is impaired after FPI. Further these data suggest that impaired cAMP and K(Ca2+) channel function contribute to altered cerebral hemodynamics following FPI.

Animals↗
PubMed1988

Role of conventional physiotherapy in cystic fibrosis.

Because of the time and the emotional cost involved in performing daily conventional chest physiotherapy in patients with cystic fibrosis, a 3-year prospective study was undertaken to compare the long-term effects of postural drainage accompanied by percussion and the forced expiratory technique with the effects of the forced expiratory technique alone. Patients who performed the forced expiratory technique alone had mean annual rates of decline that were significantly different from zero for forced expiratory volume in 1 second (p less than 0.001), forced expiratory flow between 25% and 75% of vital capacity (p less than 0.001), and Shwachman clinical score (p less than 0.004). In the group performing conventional physiotherapy with percussion and postural drainage, only the mean annual rate of decline for forced expiratory flow between 25% and 75% of vital capacity was significantly different from zero (p less than 0.03), and it was significantly different from the mean rate of decline associated with the forces expiratory technique alone (p less than 0.04). We conclude that conventional chest physiotherapy should remain a standard component of therapy in cystic fibrosis.

Adolescent↗
PubMed1998

The effect of occlusal reduction on pain after endodontic instrumentation.

One hundred seventeen patients with posterior teeth requiring endodontic treatment were studied. Specific clinical findings were recorded, including pulp, vitality, preoperative pain, sensitivity to percussion, and the presence of a periradicular radiolucency. Excluded from the study were teeth with restorations to be maintained, greater than class I mobility, pocket depths > 5 mm, endodontic retreatments, and patients taking pain altering medications. Teeth were randomly assigned to 1 of 3 groups: (i) total occlusal reduction, (ii) simulated occlusal reduction (nonfunctional cusp reduction), or (iii) control (occlusion untouched). After canal instrumentation, a questionnaire was used by patients to record pain responses over a 48-h post-operative period. Responses were tabulated using a chi(2) test (p = < 0.05), and a statistically valid profile of patients most likely to benefit from occlusal reduction was developed. Occlusal reduction should prevent postoperative pain in those patients whose teeth initially exhibit pulp vitality, percussion sensitivity, preoperative pain, and/or the absence of a periradicular radiolucency.

Chi-Square Distribution↗
PubMed2000

A comparative study on the disintegration of filamentous fungi.

Different methods for cell disintegration were tested for their efficacy on filamentous fungi, including percussion grinding, homogenization using an Ultra-Turrax, chemical treatment and lyophylization. The release of protein from Ganoderma applanatum and Pycnoporus cinnabarinus and the activity of cytoplasmatic glucose-6-phosphate dehydrogenase in the crude extracts were monitored to determine the efficiency of each disintegration technique used. Fungal cells proved to be particularly resistant towards some disintegration methods commonly used for yeasts and bacteria. Best results were obtained using a percussion grinder, if necessary, in combination with an Ultra-Turrax pretreatment.

Basidiomycota↗
PubMed1998

Expression of trkB mRNA is altered in rat hippocampus after experimental brain trauma.

Recent investigations have shown that expression of mRNAs for the neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) is differentially altered in the hippocampus following traumatic brain injury. In the present study, modulation of neurotrophin receptor expression was examined in the hippocampus in a rat model of traumatic brain injury using in situ hybridization. Messenger RNA for trkB, the high-affinity receptor for BDNF and neurotrophin-4 (NT-4), was increased between 3 and 6 h bilaterally in the dentate gyrus following a lateral fluid-percussion brain injury of moderate severity (2.0-2.1 atm). No time-dependent alterations were observed for trkB mRNA in hippocampal subfields CA1 and CA3. Levels of mRNA for trkC, the high-affinity receptor for NT-3, did not change in any region of the hippocampus. These data demonstrate that lateral fluid-percussion injury modulates expression of trkB mRNA in the hippocampus and support a role for BDNF/trkB signalling mechanisms in secondary events associated with traumatic brain injury.

Animals↗
PubMed1998

Cognitive dysfunction and histological findings in rats with chronic-stage contusion and diffuse axonal injury.

The Morris water maze (MWM) technique is well known as a prominent method of evaluating learning acquisition and memory retention impairments in rats. We previously reported on a modified fluid percussion device that is able to consistently produce experimental cortical contusion (CC) and diffuse axonal injury (DAI) in separate groups of rats. The purpose of the present protocol is to evaluate the differences in learning acquisition and memory retention impairments between these two types of injured rats in the chronic stage using the MWM technique. CC and DAI rats are respectively induced by lateral and midline fluid percussion. We also compare the histological differences between these two different types of traumatic brain injury. The results show statistically significant differences in learning acquisition impairment between the sham and CC rats and between the sham and DAI rats. However, a difference in memory retention impairment was expected to be seen only between the sham and DAI rats. Histologically, the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the CC and bilaterally in DAI. Neuronal cell loss was observed in bilaterally in layer II of the entorhinal cortex in DAI, but not in CC.

Animals↗
PubMed1989

Effects of traumatic brain injury on regional cerebral blood flow in rats as measured with radiolabeled microspheres.

To clarify the effect of experimental brain injury on regional CBF (rCBF), repeated rCBF measurements were performed using radiolabeled microspheres in rats subjected to fluid-percussion traumatic brain injury. Three consecutive microsphere injections in six uninjured control rats substantiated that the procedure induces no significant changes in hemodynamic variables or rCBF. Animals were subjected to left parietal fluid-percussion brain injury of moderate severity (2.1-2.4 atm) and rCBF values were determined (a) prior to injury and 15 min and 1 h following injury (n = 7); and (b) prior to injury and 30 min and 2 h following injury (n = 7). At 15 min post injury, there was a profound reduction of rCBF in all brain regions studied (p less than 0.01). Although rCBF in the hindbrain had recovered to near-normal by 30 min post injury, rCBF in both injured and contralateral (uninjured) forebrain areas remained significantly suppressed up to 1 h post injury. At 2 h post injury, recovery of rCBF to near-normal values was observed in all brain regions except the focal area of injury (left parietal cortex) where rCBF remained significantly depressed (p less than 0.01). This prolonged focal oligemia at the injury site was associated with the development of reproducible cystic necrosis in the left parietotemporal cortex at 4 weeks post injury. Our results demonstrate that acute changes in rCBF occur following experimental traumatic brain injury in rats and that rCBF remains significantly depressed up to 2 h post injury in the area circumscribing the trauma site.

Animals↗
PubMed1997

The determination of vasoactive substances during autonomic dysreflexia.

Urinary bladder percussion induced autonomic dysreflexia (AD) was observed in spinal cord injured patients with a complete neurological lesion, the upper level being above T5. To document the pathology and study the etiology of autonomic dysreflexia to further investigate its mechanism, this paper presents some clinical data on the determination of vasoactive substances such as norepinephrine (NE), epinephrine (E), renin (R), angiotensin II (AII) and atrial natriuretic polypeptide (ANP) before and during bladder percussion in 30 patients with a thoracolumbar or cervical spine and spinal cord injury. It is demonstrated that tapping the urinary bladder of such patients can cause AD. Changes of some of the vasoactive substances in the plasma were also observed, which might indicate that autonomic dysreflexia result from excitation of the sympathetic nervous system. Overactivity of the sympathetic nervous system was antagonized by excitation of the vegetative nerve system. There was no correlation between changes of blood pressure and adrenal function as well as the change of R-A II system; during autonomic dysreflexia, the inclement of ANP secretion played an important role in recovering homeostasis.

Adult↗
PubMed2004

Microbiological examination of infected dental root canals.

OBJECTIVES: The aim of this study was to investigate the root canal microbiota of primary and secondary root-infected canals and the association of constituent species with specific endodontic signs and symptoms. METHODS: Microbial samples were taken from 60 root canals, 41 with necrotic pulp tissues (primary infection) and 19 with failed endodontic treatment (secondary infection). Strict anaerobic techniques were used for serial dilution, plating, incubation and identification. RESULTS: A total of 224 cultivable isolates were recovered belonging to 56 different bacterial species. Individual root canals yielded a maximum of 10 bacterial species. Of the bacterial isolates, 70% were either strict anaerobes or microphilic. The anaerobes most frequently isolated were: Peptostreptococcus micros (35%), Fusobacterium necrophorum (23.3%), Fusobacterium nucleatum (11.7%), Prevotella intermedia/nigrescens (16.7%), Porphyromonas gingivalis (6.7%) and Porphyromonas endodontalis (5%). The root canal microflora of untreated teeth with apical periodontitis was found to be mixed, comprising gram-negative and gram-positive and mostly anaerobic microorganisms and usually containing more than 3 species per canal. On the other hand, facultative anaerobic and gram-positive bacteria predominated in canals with failed endodontic treatment, which harbored 1-2 species per canal. Suggested relationships were found between anaerobes, especially gram-negatives, and the presence or history of pain, tenderness to percussion and swelling (P<0.05). In particular, associations were found between: a) pain (n=29) and P. micros (P<0.01), P. intermedia/nigrescens and Eubacterium spp. (both P<0.05); b) history of pain (n=31) and P. micros (P<0.01) Porphyromonas and Fusobacterium spp. (P<0.05); c) tenderness to percussion (n=29) and Porphyromonas spp. (P<0.01), Peptostreptococcus and Fusobacterium spp. (P<0.001); d) swelling (n=20) and Peptostreptococcus spp. (P<0.01), Porphyromonas and Enterococcus spp. (P<0.05); e) wet canals (n=33) and Porphyromonas and Fusobacterium spp. (P<0.05); f) purulent exudate (n=20) and Porphyromonas, Peptostreptococcus and Fusobacterium spp. (P<0.05); previous endodontic treatment and Enterococcus faecalis, Streptococcus spp., P. micros, F. necrophorum (P<0.05). CONCLUSIONS: Our findings indicate potential complex interactions of species resulting in characteristic clinical pictures which cannot be achieved by individual species alone. They also indicate that the microbiota of primary infected canals with apical periodontitis differs in number and in species from the secondary infected canals by using the culture technique.

Bacteria, Anaerobic↗
PubMed1998

Evidence for the involvement of corticotrophin-releasing hormone in the pathogenesis of traumatic brain injury.

The aim of this study was to investigate the role of the neuropeptide corticotrophin-releasing hormone (CRH) in neurodegeneration induced by traumatic brain injury, using a well characterized model of lateral fluid percussion injury in male, Sprague-Dawley rats. In the first series of experiments, CRH gene expression was assessed by in situ hybridization after traumatic brain injury. A bilateral increase in CRH mRNA in the paraventricular nucleus was observed in rats subjected to traumatic brain injury compared with sham-operated controls. A maximal (40%) increase in hybridization signal was detected 2 h after trauma compared with control rat brains. In addition, marked induction of CRH transcripts was found in the ipsilateral amygdala after trauma, but no increase was detected in the ipsilateral cortex around the area of damage. In a separate experiment, the effects of the CRH antagonist, D-Phe CRH(12-41) (25 microg total dose), or appropriate vehicle injected intracerebroventricularly, was tested on infarct volume caused by brain injury. Repeated intracerebroventricular injection of D-Phe CRH(12-41) significantly reduced, by 45%, the volume of cortical damage in injured rats compared with vehicle-treated, trauma animals. The rapid upregulation of CRH gene expression in the paraventricular nucleus and amygdala following lateral fluid percussion injury and the marked neuroprotection achieved by inhibiting CRH action suggest that CRH is involved directly in the pathogenesis of traumatic brain injury. This observation may have important implications for the development of novel therapeutic strategies for treating the neurological consequences of brain trauma and related conditions.

Animals↗
PubMed1994

Alterations in regional brain catecholamine concentrations after experimental brain injury in the rat.

Although activation of brain catecholaminergic systems has been implicated in the cerebrovascular and metabolic changes during subarachnoid hemorrhage, cerebral ischemia, cortical ablation, and cortical freeze lesions, little is known of the response of regional brain catecholamine systems to traumatic brain injury. The present study was designed to characterize the temporal changes in concentrations of norepinephrine (NE), dopamine (DA), and epinephrine (E) in discrete brain regions following experimental fluid-percussion traumatic brain injury in rats. Anesthetized rats were subjected to fluid-percussion brain injury of moderate severity (2.2-2.3 atm) and killed at 1 h, 6 h, 24 h, 1 week, and 2 weeks postinjury (n = 6 per timepoint). Control animals (surgery and anesthesia without injury) were killed at identical timepoints (n = 6 per timepoint). Tissue concentrations of NE, DA, and E were evaluated using HPLC. Following brain injury, an acute decrease was observed in DA concentrations in the injured cortex (p < 0.05) at 1 h postinjury, which persisted up to 2 weeks postinjury. Striatal concentrations of DA were significantly increased (p < 0.05) only at 6 h postinjury. Hypothalamic concentrations of DA and NE increased significantly beginning at 1 h postinjury (p < 0.05 and p < 0.05, respectively) and persisted up to 24 h for DA (p < 0.05) and 1 week (p < 0.05) for NE. These data suggest that acute alterations occur in regional concentrations of brain catecholamines following brain trauma, which may persist for prolonged periods postinjury.

Animals↗
PubMed1995

The sodium channel blocker and glutamate release inhibitor BW1003C87 and magnesium attenuate regional cerebral edema following experimental brain injury in the rat.

Excitatory amino acid (EAA) neurotransmitters may play a role in the pathophysiology of traumatic injury to the CNS. Although NMDA receptor antagonists have been reported to have therapeutic efficacy in animal models of brain injury, these compounds may have unacceptable toxicity for clinical use. One alternative approach is to inhibit the release of EAAs following traumatic injury. The present study examined the effects of administration of a novel sodium channel blocker and EAA release inhibitor, BW1003C87, or the NMDA receptor-associated ion channel blocker magnesium chloride on cerebral edema formation following experimental brain injury in the rat. Animals (n = 33) were subjected to fluid percussion brain injury of moderate severity (2.3 atm) over the left parietal cortex. Fifteen minutes after injury, the animals received a constant infusion of BW1003C87 (10 mg/kg, i.v.), magnesium chloride (300 mumol/kg, i.v.), or saline over 15 min (2.75 ml/kg/15 min). In all animals, regional tissue water content in brain was assessed at 48 h after injury, using the wet weight/dry weight technique. In saline-treated control animals, fluid percussion brain injury produced significant regional brain edema in injured left parietal cortex (p < 0.001), the cortical area adjacent to the site of maximal injury (p < 0.001), left hippocampus (p < 0.001), and left thalamus (p = 0.02) at 48 h after brain injury. Administration of BW1003C87 15 min postinjury significantly reduced focal brain edema in the cortical area adjacent to the site of maximal injury (p < 0.02) and left hippocampus (p < 0.01), whereas magnesium chloride attenuated edema in left hippocampus (p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Temporal patterns of poly(ADP-ribose) polymerase activation in the cortex following experimental brain injury in the rat.

The activation of poly(ADP-ribose) polymerase, a DNA base excision repair enzyme, is indicative of DNA damage. This enzyme also undergoes site-specific proteolysis during apoptosis. Because both DNA fragmentation and apoptosis are known to occur following experimental brain injury, we investigated the effect of lateral fluid percussion brain injury on poly(ADP-ribose) polymerase activity and cleavage. Male Sprague-Dawley rats (n = 52) were anesthetized, subjected to fluid percussion brain injury of moderate severity (2.5-2.8 atm), and killed at 30 min, 2 h, 6 h, 24 h, 3 days, or 7 days postinjury. Genomic DNA from injured cortex at 24 h, but not at 30 min, was both fragmented and able to stimulate exogenous poly(ADP-ribose) polymerase. Endogenous poly(ADP-ribose) polymerase activity, however, was enhanced in the injured cortex at 30 min but subsequently returned to baseline levels. Slight fragmentation of poly(ADP-ribose) polymerase was detected in the injured cortex in the first 3 days following injury, but significant cleavage was detected at 7 days postinjury. Taken together, these data suggest that poly(ADP-ribose) polymerase-mediated DNA repair is initiated in the acute posttraumatic period but that subsequent poly(ADP-ribose) polymerase activation does not occur, possibly owing to delayed apoptosis-associated proteolysis, which may impair the repair of damaged DNA.

Animals↗
PubMed2000

Effect of trephination on postoperative pain and swelling in symptomatic necrotic teeth.

OBJECTIVE: The purpose of this prospective, randomized, blinded study was to determine the effect of trephination on postoperative pain and swelling in symptomatic necrotic teeth. STUDY DESIGN: Fifty emergency patients participated, and each had a clinical diagnosis of a symptomatic necrotic tooth with associated periapical radiolucency. After endodontic treatment, patients randomly received either a trephination or mock trephination procedure. The trephination procedure used an intraosseous perforator to provide an initial opening in the cortical bone that was enlarged with files (No. 25 through No. 70) and an endodontic spoon. After surgery, each patient received ibuprofen; acetaminophen with codeine (30 mg); and a 7-day diary to record pain, percussion pain, swelling, and number and type of pain medication taken. RESULTS: The majority of patients with symptomatic necrotic teeth had significant postoperative pain and required analgesics to manage this pain. The use of a trephination procedure with an intraosseous perforator, files, and a spoon excavator did not significantly reduce pain, percussion pain, swelling, or the number of analgesic medications taken in symptomatic necrotic teeth with periapical radiolucencies (P >.05). CONCLUSION: We cannot recommend the routine use of a trephination procedure, as used in this study, for relief of pain in symptomatic necrotic teeth with radiolucencies.

Adult↗