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Clinical, radiographic and histological characteristics of secondary retention of permanent molars.

Secondary retention refers to the cessation of eruption of a tooth after emergence neither due to a physical barrier in the path of eruption nor as a result of an abnormal position. In this study, the clinical and radiographic features of 81 secondary retained permanent molars in a group of 53 patients were evaluated. Retained molars removed for therapeutic reasons (n = 38) were examined histologically to detect any areas of ankylosis. The first molars in the mandible and maxilla were most frequently affected. The mean infraocclusion at the patients' first visit was 4.3 +/- 1.9 mm. After 6 months, infraocclusion increased in adolescents but was stable in adults. Tilting of the adjacent teeth was observed in 39 cases. A sharp, solid percussion sound and a partial absence of the periodontal ligament space on radiographs were noted in less than one-fifth of the affected molars, while histological evaluation revealed that local areas of ankylosis were present in all cases. From the data relating to the 38 molars removed for therapeutic reasons, the sensitivity of the percussion test and radiographic evaluation was found to be 29 and 21 per cent respectively. During a period of 4 years, six new cases of secondary retention were observed in the same population. From this study it is concluded that secondary retention of permanent molars seems to be associated with focal ankylosis and that percussion tests and radiographs are not sufficiently reliable to exclude the presence of ankylotic areas. The presence of ankylotic areas and tendency of infraocclusion to increase in adolescents but to be stable in adults have major implications for therapy.

Adolescent↗

Nefiracetam improves Morris water maze performance following traumatic brain injury in rats.

Nefiracetam, a pyrrolidone derivative, is a nootropic agent that has facilitated cognitive function in a wide variety of animal models of cognitive dysfunction. The purpose of this study was to investigate the efficacy of the chronic postinjury administration of nefiracetam (DM-9384) in improving cognitive performance following central fluid percussion brain injury in rats. Twenty-four hours following surgical preparation, a sham injury or a moderate fluid percussive injury (2.1 atm) was delivered. Nefiracetam was administered chronically (0 or 9 mg/kg, po, for sham animals and 0, 3, or 9 mg/kg for injured animals) on postinjury days 1-15. Cognitive performance was assessed using the Morris water maze (MWM) on postinjury days 11-15. Chronic administration of 3 and 9 mg/kg nefiracetam attenuated MWM deficits produced by central fluid percussive brain injury. Importantly, the MWM performance of the injured animals treated with 9 mg/kg did not significantly differ from uninjured, sham animals. The 9-mg/kg dose of nefiracetam did not have a positive or negative effect on MWM performance of uninjured animals. The results of the present experiment suggest that a nootropic such as nefiracetam may be an appropriate treatment for trauma-induced cognitive dysfunction.

Animals↗

Hypothermia attenuates the loss of hippocampal microtubule-associated protein 2 (MAP2) following traumatic brain injury.

Traumatic brain injury (TBI) produces a tissue-specific decrease in protein levels of microtubule-associated protein 2 (MAP2), an important cross-linking component of the neuronal cytoskeleton. Because moderate brain hypothermia (30 degrees C) reduces certain neurobehavioral deficits produced by TBI, we examined the efficacy of moderate hypothermia (30 degrees C) in reversing the TBI-induced loss of MAP2 protein. Naive, sham-injured, and moderate (2.1 atm) fluid percussion-injured rats were assessed for MAP2 protein content 3 h post injury using quantitative immunoreactivity measurements. Parallel groups of sham-injured and fluid percussion-injured animals were maintained in moderate hypothermia (30 degrees C), as measured by temporalis muscle temperature, for MAP2 quantitation 3 h post injury. No difference in MAP2 levels was observed between naive and sham-injured normothermic animals. Hypothermia alone had no effect on soluble MAP2 levels in sham-injured animals compared with normothermic sham-injured controls (88.0 +/- 7.3%; p > 0.10). Fluid percussion injury dramatically reduced MAP2 levels in the normothermic group (44.3 +/- 5.9%; p < 0.0005) compared with normothermic sham-injured controls. No significant reduction of MAP2 was seen in the hypothermic injured group (95.2 +/- 4.6%; compared with hypothermic sham-injured controls, p > 0.20). Although it is premature to infer any causal link, the data suggest that the attenuation of injury-induced MAP2 loss by hypothermia may contribute to its overall neuroprotective action.

Animals↗

Vibratory massage and short-term recovery from muscular fatigue.

Percussive vibratory massage has long been purported to offset the negative effects of muscular exercise. The purpose of this experiment was to determine the effect of this type of massage on recovery from repeated submaximal contractions. Twelve male subjects performed repeated, static contractions of the quadriceps at 70% maximal voluntary contraction (MVC), with periodic MVCs performed after every fourth one. This pattern continued until the subject could no longer produce the required 70% (Tlim). The entire procedure was repeated three times with rest periods between each series. The rate of fatigue (ROF) was calculated from a regression line fit to the decline of the periodic MVCs. We studied the ROF during static exercise alone, as well as during static exercise following cycling for 30 min at 75% VO2max. In the control conditions, the subjects rested for 5 min between each of the three series of contractions. In the experimental conditions the subjects received 4 min of percussive vibratory massage and 1 min of rest. The results showed that there was no significant difference in ROF in either static or following dynamic exercise between the control and vibrated conditions. Although ROF was the same in all experimental conditions. Tlim occurred sooner following dynamic exercise because the initial MVC was significantly lower than static (p less than .008). We have therefore concluded that short-term recovery from intense muscular activity is not augmented by percussive vibratory massage.

Adult↗

Continuing axonal and vascular change following experimental brain trauma.

The course of axonal and vascular change following trauma was investigated in an animal model of fluid-percussion brain injury. To assess axonal change, the anterograde transport of horseradish peroxidase in selected cerebral and cerebellar efferents was studied in cats that had sustained minor to moderate injuries and had survived the traumatic episode for periods ranging from several hours to several months. To assess vascular change, cats were equipped with cranial windows, which allowed for both the direct functional study of the pial vasculature following injury and the postmortem harvesting of the studied vessels for morphologic analyses. Following fluid-percussion brain injury, a subtle focal perturbation of the axon occurred, and over a 12 to 24 hour period, this perturbation became progressively severe, with the result that the axon swelled, separated from its distal segment, and thereby formed an enlarged reactive swelling. With continued survival, some swellings persisted intact, others degenerated, and others demonstrated a dramatic regenerative response. This regenerative response, characterized by regenerative sprouting and growth conelike outgrowths, persisted through all survival periods considered. Immediately following the induction of the fluid-percussion injury, the pial arterioles dilated, manifested morphologic change, and displayed functional abnormalities. These vascular abnormalities appeared mediated by an accelerated metabolism of arachidonate via cyclooxygenase, which results in the generation of oxygen radicals. Radicals, such as the superoxide anion, continue to be produced within the first hour following injury and thus, similar to the observed axonal responses, continue to contribute to the brain's response to trauma. Although these axonal and vascular changes do not appear to be causally related, they both appear as a continuum of the initial insult and may become interlinked should a secondary insult ensue.

Animals↗

Increased plasma PGE2, 6-keto-PGF1 alpha, and 12-HETE levels following experimental concussive brain injury.

Previous investigations have shown that brain prostaglandin levels are transiently elevated following experimental fluid percussion brain injury. Associated with these increased prostaglandin levels there is free radical production and abnormalities in cerebral arteriolar function. The purpose of this study was to determine whether experimental fluid percussion brain injury in cats is associated with increased systemic levels of prostaglandins and the lipoxygenase product, 12-HETE. Blood samples were collected before and at various periods of time after 2.7 atm of fluid percussion brain injury was produced in adult cats. Prostaglandin and 12-HETE analysis was performed by radioimmunoassay after extraction of the plasma samples. The control levels for 6-keto-PGF1 alpha, PGE2, and 12-HETE were 477 +/- 42, 2,372 +/- 431, and 13,328 +/- 1,769 pg/ml, respectively. Following injury all three eicosanoids reached peak plasma levels by 1-5 min after injury. The percentile increases for all eicosanoids were similar and increased from 70 to 110%. The increases were sustained at up to 30 min postinjury and by 1 h after injury were at control levels. As in previous studies, hypertension following injury was maximal by 1 min postinjury and blood pressure had returned to near normal levels by 5 min postinjury. These studies demonstrate prolonged systemic increases in eicosanoids following injury. Since free radical production and vascular damage occur concomitantly with eicosanoid production, the prolonged increases in these products suggest that there is an attainable therapeutic window following injury during which administration of free radical scavengers may decrease radical damage and reduce the consequences of injury.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Traumatic brain injury creates biphasic systemic hemodynamic and organ blood flow responses in rats.

Traumatic brain injury affects systemic circulation as well as directly damages the brain. The present study examined the effects of fluid percussion brain injury on systemic hemodynamics and organ arterial blood flow in rats. Rats were prepared for fluid percussion injury under anesthesia. Twenty-four hours later, rats were anesthetized (1.0% halothane in N2O:O2) and prepared for radioactive microsphere measurement of cardiac output and organ blood flow. After baseline blood flow and physiological measurements were established, the rats were injured (2.47 +/- 0.02 atm, n = 17) or not injured (n = 20). Additional blood flow determinations were made at two of the following four time (T) points: 5, 15, 30, and 60 min after the injury or sham injury. Fluid percussion brain injury produced an immediate systemic hypertension followed by a hypotension and low cardiac output. Organ blood flows remained constant or increased for 30 min and then declined. Decreased blood flow was most pronounced in the kidneys and the spleen and was less severe in the liver. The reduced cardiac output was redistributed to favor blood flow through the heart and pancreas. These data suggest that traumatic brain injury creates a hyperdynamic period followed by a hypodynamic state with a heterogeneous hypoperfusion among organs.

Animals↗

The rotarod test: an evaluation of its effectiveness in assessing motor deficits following traumatic brain injury.

The purpose of the present experiment was to examine the effectiveness of a modified rotarod test in detecting motor deficits following mild and moderate central fluid percussion brain injury. In addition, this investigation compared the performance of the rotarod task with two other commonly used measures of motor function after brain injury (beam-balance and beam-walking latencies). Rats were either injured with a mild (n = 14) or moderate (n = 8) level of fluid percussion injury or were surgically prepared but not injured (n = 8). All rats were assessed on all tasks for 5 days following their respective treatments. Results revealed that both the mild and moderate injury levels produced significant deficits in the ability of the animals to perform the rotarod task. Performance on the beam-balance and beam-walking tasks were not significantly impaired at the mild injury level. It was only at the moderate injury level that the beam-balance and beam-walking tasks detected deficits in motor performance. This result demonstrated that the rotarod task was a sensitive index of injury-induced motor dysfunction following even mild fluid percussion injury. A power analysis of the three tasks indicated that statistically significant group differences could be obtained with the rotarod task with much smaller sample sizes than with the beam-balance and beam-walking tasks. Performance on the rotarod, beam-walk, and beam-balance tasks were compared and evaluated by a multivariate stepdown analysis (multiple analysis of variance followed by univariate analyses of covariance). This analysis indicated that the rotarod task measures aspects of motor impairment that are not assessed by either the beam-balance or beam-walking latency. These findings suggest that compared to the beam-balance and beam-walking tasks, the rotarod task is a more sensitive and efficient index for assessing motor impairment produced by brain injury.

Animals↗

Effects of traumatic brain injury on the cholinergic system in the rat.

Rats subjected to a mild to moderate fluid percussion injury exhibit memory deficits that are similar to rats that have received lesions of the septohippocampal system. Because the cholinergic system plays a major role in septohippocampal function, we studied the kinetics of the synthetic enzyme for acetylcholine, choline acetyltransferase (ChAT), at 1 h, 24 h, or 5 days after a fluid percussion injury. Decreases in ChAT activity were found in the dorsal hippocampus (25%), frontal (32%), and temporal (23%) cortices 1 h after injury. In the parietal cortex, a greater than 50% increase in ChAT activity was observed at all time intervals assessed. At 5 days after TBI, there was an 18% increase in ChAT activity in the medial septal area. These data provide evidence that a mild to moderate fluid percussion injury produces changes in the cholinergic system in brain areas related to memory.

Analysis of Variance↗

Metabotropic glutamate receptor protein alterations after traumatic brain injury in rats.

Glutamate toxicity, mediated via ion channel-linked receptors, plays a key role in traumatic brain injury (TBI) pathophysiology. Excessive glutamate release after TBI also activates protein G-linked metabotropic glutamate receptors (mGluRs). We performed Western blot and immunohistochemical analysis with antibodies for group 1 and 2 mGluRs in hippocampal and cortex tissue at 7 and 15 days after lateral fluid-percussion TBI in rats. Protein homogenates of brain tissue were separated on 7.5% sodium dodecyl sulfate (SDS)-polyacrylamide gels, transferred to nitrocellulose, and incubated with either antibodies recognizing both mGluR2 and mGluR3 or antibodies against mGluR5. Equivalent protein loading of lanes was confirmed by using beta-actin antibody. Immunoreactive proteins were revealed with enhanced chemiluminescence and relative optical density of Western blots quantified by computerized image analysis. At 7 days after TBI, mGluR2/3 immunobinding ipsilateral to the fluid-percussion injury was reduced by 28% in hippocampus and 25% in cortex in comparison with the contralateral hemisphere (p < .05). mGluR5 immunobinding ipsilateral to the fluid-percussion injury was reduced by 20% in hippocampus and 27% in cortex (p < .05). At 15 days after TBI, the decreases in immunobinding were no longer significant. Immunohistochemical staining with the same antibodies revealed density changes congruent with the Western blot results. These data suggest that TBI produces an alteration in receptor protein expression that spontaneously recovers by 15 days after injury.

Animals↗

Influence of polyethylene glycol superoxide dismutase/catalase on altered opioid-induced pial artery dilation after brain injury.

BACKGROUND: The current study was designed to investigate the influence of pretreatment with the oxygen radical scavengers polyethylene glycol superoxide dismutase and catalase (SODCAT) on altered opioid-induced pial artery dilation after fluid percussion brain injury (FPI) in the newborn pig. It has been observed previously that brain injury produces pial artery vasoconstriction in the piglet associated with elevated cerebrospinal fluid opioid levels. Furthermore, opioid-induced vasodilation and cyclic guanosine monophosphate production are attenuated following brain injury. Finally, oxygen free radicals have been implicated in the pathogenesis of brain injury. METHODS: Anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. Fluid percussion brain injury of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Superoxide dismutase-inhibited nitroblue tetrazolium reduction was determined as an index of superoxide generation. RESULTS: Superoxide dismutase- inhibited tetrazolium was increased markedly after FPI and these increases were blunted by SODCAT (1,000 U/kg and 10,000 U/kg, respectively) treatment 30 min before FPI (1 +/- 1 vs. 14 +/- 2 vs. 1 +/- 1 pmol/mm(2) for control, FPI, and FPI pretreated with SODCAT, respectively). Methionine enkephalin, an endogenous mu opioid agonist, produced vasodilation that was attenuated by FPI and partially restored by SODCAT pretreatment (17 +/- 1, 8 +/- 1, and 14 +/- 1% for methionine enkephalin 10(-6)m during control conditions, after FPI and after FPI pretreated with SODCAT, respectively). Methionine enkephalin-induced dilation was associated with increased cerebrospinal fluid cycle guanosine monophosphate and these biochemical changes were likewise blunted by FPI and partially restored by SODCAT (342 +/- 12 and 640 +/- 13 vs. 267 +/- 6 and 321 +/- 17 vs. 301 +/- 9 and 504 +/- 43 fmol/ml for resting conditions and 10 (-6)M methionine enkephalin during control, after FPI, and after FPI pretreated with SODCAT, respectively). Leucine enkephalin, an endogenous delta agonist, induced pial dilation and associated changes incerebrospinal fluid cyclic guanosine monophosphate, which were similarly altered by FPI and partially restored by SODCAT. Dynorphin, an endogenous kappa agonist, which has been shown to revert from a dilator to a constrictor after FPI, was restored to a vasodilator by SODCAT (18 +/- 1, -11 +/- 4, and 17 +/-5% for dynorphin 10(-6)m during control conditions, after FPI, and after FPI pretreated with SODCAT, respectively). Dynorphin-induced vasodilation was associated with a large increase in cerebrospinal fluid cyclic guanosine monophosphate, which was blunted by FPI and partially restored by SODCAT. CONCLUSIONS: These data show that superoxide anion is produced after brain injury and that opioid-induced vasodilation and cyclic guanosine monophosphate production are partially restored after brain injury in the presence of SODCAT. (Key words: Brain injury: newborn. Circulation: cerebral. Free radicals: oxygen. Gases: nitric oxide. Nucleotides cyclic.

Animals↗

Posttraumatic hypothermia is neuroprotective in a model of traumatic brain injury complicated by a secondary hypoxic insult.

OBJECTIVE: Human traumatic brain injury frequently results in secondary complications, including hypoxia. In previous studies, we have reported that posttraumatic hypothermia is neuroprotective and that secondary hypoxia exacerbates histopathologic outcome after fluid-percussion brain injury. The purpose of this study was to assess the therapeutic effects of mild (33 degrees C) hypothermia after fluid-percussion injury combined with secondary hypoxia. In addition, the importance of the rewarming period on histopathologic outcome was investigated. DESIGN: Prospective experimental study in rats. SETTING: Experimental laboratory in a university teaching hospital. INTERVENTION: Intubated, anesthetized rats underwent normothermic parasagittal fluid-percussion brain injury (1.8-2.1 atmospheres) followed by either 30 mins of normoxia (n = 6) or hypoxic (n = 6) gas levels and by 4 hrs of normothermia (37 degrees C). In hypothermic rats, brain temperature was reduced immediately after the 30-min hypoxic insult and maintained for 4 hrs. After hypothermia, brain temperature was either rapidly (n = 6) or slowly (n = 5) increased to normothermic levels. Rats were killed 3 days after traumatic brain injury, and contusion volumes were quantitatively assessed. MEASUREMENTS AND MAIN RESULTS: As previously shown, posttraumatic hypoxia significantly increased contusion volume compared with traumatic brain injury-normoxic animals (p <.02). Importantly, although posttraumatic hypothermia followed by rapid rewarming (15 mins) failed to decrease contusion volume, those animals undergoing a slow rewarming period (120 mins) demonstrated significantly (p <.03) reduced contusion volumes, compared with hypoxic normothermic rats. CONCLUSIONS: These data emphasize the beneficial effects of posttraumatic hypothermia in a traumatic brain injury model complicated by secondary hypoxia and stress the importance of the rewarming period in this therapeutic intervention.

Analysis of Variance↗

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

The purpose of this prospective, randomized, blinded study was to determine the effect of apical trephination on postoperative pain and swelling in symptomatic necrotic teeth. 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 an apical trephination or mock trephination procedure. The trephination procedure used a Stabident perforator to provide an initial opening in the cortical bone that was enlarged with files (#25 through #120) and an endodontic spoon. Postoperatively, 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 demonstrated the use of an apical trephination procedure did not significantly (p > 0.05) reduce pain, percussion pain, swelling, or number of ibuprofen tablets taken in symptomatic necrotic teeth with periapical radiolucencies. The trephination procedure did significantly (p < 0.05) reduce the use of acetaminophen with codeine overall for the 7 days. In conclusion, because there was not a significant reduction in pain, percussion pain, or swelling we cannot recommend the routine use of an apical trephination procedure, as used in this study, in symptomatic necrotic teeth with radiolucencies.

Acetaminophen↗

Can one predict when ultrasound will be useful with percutaneous liver biopsy?

OBJECTIVE: We previously showed that ultrasound altered position of biopsy in 15% of cases by demonstrating intervening structures. This study was designed to test whether one could predict in which cases ultrasound would be useful. METHODS: A standard percussion technique was used. The site chosen was marked. Criteria were established to indicate whether a move might be predicted to be likely. If 10 or more points were assigned, then it was predicted that ultrasound would change position. A difficult percussion was assigned 10 points; obesity, 5 points; and chest deformity, 5 points. The ultrasound was then applied to the marked spot in every case. If an intervening structure was present within 6 cm, the biopsy site was moved. Otherwise, the biopsy was taken from the marked site. RESULTS: One hundred seventeen consecutive liver biopsies were included between January 1999 and January 2000. The criteria predicted the desirability of nine moves. No moves were made, however, in these cases. In 17 cases (14.5%), moves were made because of intervening structures. None of the cases were predicted. A move was made in 1 of 23 obese patients. There was no statistical difference in moves made between obese and nonobese patients. CONCLUSIONS: Using criteria of difficult percussion, obesity, and unusual chest shape, we could not predict when ultrasound would be useful. This is in contrast to the belief that ultrasound can be applied to selected liver biopsies considered in advance to be more difficult, as in the obese patients, and instead suggests that to avoid intervening structures, one should apply ultrasound to all cases.

Biopsy, Needle↗

Treatment of replacement resorption by intentional replantation, resection of the ankylosed sites, and Emdogain--results of a 6-year survey.

The present clinical study investigated the outcome of intentional replantation using resection of the ankylosed sites of the root, extraoral endodontic treatment using titanium posts and Emdogain for periodontal healing following trauma-related ankylosis. During an evaluation period of 6 years, 16 ankylosed teeth affected by replacement resorption were treated as described. Evaluation parameters before treatment and during the follow-up period included Periotest scores, percussion sound and periapical radiographs. All findings were compared to those of the adjacent teeth. In a second accident, one tooth was lost after 7 months and was excluded as a dropout. Ankylosis did not recur in seven replanted teeth, which were observed for an average of 52.3 months (range: 24-68 months). Ankylosis recurred in eight teeth after an average period of 12 months (range: 4-26 months). An infraocclusion, normal or only slightly reduced Periotest scores and normal percussion sound were preoperatively found in six of seven successfully replanted teeth, which corresponded to a relatively small area of ankylosis. The majority of the teeth showing recurrent ankylosis preoperatively presented with normal position, negative Periotest scores and a high percussion sound which corresponded to an extended area of ankylosis. Statistically significant relationship between preoperative findings and the treatment outcome (P = 0.031) have become apparent. The results indicate that the treatment of minor areas of ankylosis by intentional replantation, resection of the ankylosed sites and Emdogain appeared to prevent or delay the recurrence of ankylosis in 7 of 15 teeth.

Adolescent↗

Commercial slaughter methods used on Atlantic salmon: determination of the onset of brain failure by electroencephalography.

This study investigated the effect of exsanguination without prior stunning, or carbon dioxide narcosis followed by exsanguination, or percussive stunning or spiking the brain, on the time taken to abolish the visual evoked responses (VERS) of farmed Atlantic salmon. Only percussive stunning and spiking killed the fish immediately and the other two methods resulted in aversive reactions by the fish. The VERS were lost between 148 and 440 seconds after exsanguination without stunning, and between 300 and 554 seconds after carbon dioxide narcosis followed by exsanguination. During both these procedures the fish showed strong aversive behaviour. In contrast, percussive stunning and spiking the brain could result in the immediate loss of VERS and no aversive reactions from the fish if the stun was applied correctly.

Abattoirs↗

Effects of hydration and physical therapy on tracheal transport velocity.

A new tracer method for quantitative measurement of tracheal transport velocity (mm per min) in dogs has been described. Using the same technique, the effects of dehydration, rehydration, postural drainage, and chest percussion on tracheal transport velocity were studied. Mean tracheal transport velocity decreased significantly (14.1 +/- 1.4) after dehydration (P less than 0.05) and reverted to normal (19.0 +/- 1.3) with rehydration in 10 dogs. After postural drainage in 7 dogs, mean tracheal transport velocity increased 39.7 +/- 1.78 (SE) per cent (P less than 0.01). After chest percussion in 6 dogs, mean tracheal transport velocity increased 50.9 +/- 1.22 (SE) per cent. With combined postural drainage and chest percussion, mean tracheal transport velocity increased 50.0 +/- 0.32 (SE) per cent. Although maximal improvement occurred after the combined therapy, the changes were not significantly different from those observed with each therapy alone. These therapeutic measures have been used empirically in the past. The present study gives some objective evidence for their beneficial effects in anesthetized dogs.

Animals↗

[A study on local cerebral glucose utilization in the acute phase of experimental head injury in rat].

The changes in local cerebral glucose utilization (LCGU) following a fluid-percussion injury were studied in 23 rats using the 2-deoxyglucose (2-DG) technique in order to determine the critical period for neuronal damage. Three rats were used as controls. All the rats received a moderate impact of 4.8-5.6 atm from a fluid-percussion device using the University of California, San Francisco, method. LCGU was studied at 15, 30, 45, 60, and 120 min and 24 hours after injury. The optical density on autoradiographs was measured at the site of the brain contusion, in the rim around the contused brain, and in the bilateral cerebral cortex, hippocampus, and thalamus. Decreased 2-DG uptake was observed in the contused brain. However, increased 2-DG uptake was seen in the rim around the contused brain from 15-60 min after injury. The changes in 2-DG uptake noted in this study were very similar to those caused by permanent focal ischemia in a previous study, which suggests that the pathophysiologic phenomena occurring after fluid-percussion injury in the rat brain are based on ischemic changes.

Acute Disease↗