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PubMed2000

Effect of systemic penicillin on pain in untreated irreversible pulpitis.

OBJECTIVE: The purpose of this prospective, randomized, double-blind study was to determine the effect of penicillin on pain in untreated teeth diagnosed with irreversible pulpitis. STUDY DESIGN: Forty emergency patients participated, and each had a clinical diagnosis of an irreversible pulpitis. Patients randomly received a 7-day oral dose (28 capsules, 500 mg each, to be taken every 6 hours) of either penicillin or a placebo control in a double-blind manner. No endodontic treatment was performed. Each patient also received ibuprofen; acetaminophen with codeine (30 mg); and a 7-day diary to record pain, percussion pain, and number and type of pain medication taken. RESULTS: The administration of penicillin did not significantly (P >.05) reduce pain, percussion pain, or the number of analgesic medications taken by patients with untreated irreversible pulpitis. The majority of patients with untreated irreversible pulpitis had significant pain and required analgesics to manage this pain. CONCLUSION: Penicillin should not be prescribed for untreated irreversible pulpitis because penicillin is ineffective for pain relief.

Adult↗

PubMed1996

Traumatic brain damage prevented by the non-N-methyl-D-aspartate antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo[f] quinoxaline.

The mechanisms of neuronal degeneration following traumatic head injury are not well understood and no adequate treatment is currently available for the prevention of traumatic brain damage in humans. Traumatic head injury leads to primary (at impact) and secondary (distant) damage to the brain. Mechanical percussion of the rat cortex mimics primary damage seen after traumatic head injury in humans; no animal model mimicking the secondary damage following traumatic head injury has yet been established. Rats subjected to percussion trauma of the cortex showed primary damage in the cortex and secondary damage in the hippocampus. Morphometric analysis demonstrated that both cortical and hippocampal damage was mitigated by pretreatment with either the N-methyl-D-aspartate (NMDA) antagonist 3-((+/-)- 2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) or the non-NMDA antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline (NBQX). Neither treatment prevented primary damage in the cortex when therapy was started after trauma. Surprisingly, delayed treatment of rats with NBQX, but not with CPP, beginning between 1 and 7 hr after trauma prevented hippocampal damage. No protection was seen when therapy with NBQX was started 10 hr after trauma. These data indicate that both NMDA- and non-NMDA-dependent mechanisms contribute to the development of primary damage in the cortex, whereas non-NMDA mechanisms are involved in the evolution of secondary damage in the hippocampus in rats subjected to traumatic head injury. The wide therapeutic time-window documented for NBQX suggests that antagonism at non-NMDA receptors may offer a novel therapeutic approach for preventing deterioration of the brain after head injury.

Animals↗

PubMed1996

Calpain inhibitor AK295 attenuates motor and cognitive deficits following experimental brain injury in the rat.

Marked increases in intracellular calcium may play a role in mediating cellular dysfunction and death following central nervous system trauma, in part through the activation of the calcium-dependent neutral protease calpain. In this study, we evaluated the effect of the calpain inhibitor AK295 [Z-Leu-aminobutyric acid-CONH(CH2)3-morpholine] on cognitive and motor deficits following lateral fluid percussion brain injury in rats. Before injury, male Sprague-Dawley rats (350-425 g) were trained to perform a beam-walking task and to learn a cognitive test using a Morris water maze paradigm. Animals were subjected to fluid percussion injury (2.2-2.4 atm; 1 atm = 101.3 kPa) and, beginning at 15 min postinjury, received a continuous intraarterial infusion of AK295 (120-140 mg/kg, n = 15) or vehicle (n= 16) for 48 hr. Sham (uninjured) animals received either drug (n = 5) or vehicle (n = 10). Animals were evaluated for neurobehavioral motor function at 48 hr and 7 days postinjury and were tested in the Morris water maze to evaluate memory retention at 7 days postinjury. At 48 hr, both vehicle- and AK295-treated injured animals showed significant neuromotor deficits (P< 0.005). At 7 days, injured animals that received vehicle continued to exhibit significant motor dysfunction (P< 0.01). However, brain-injured, AK295-treated animals showed markedly improved motor scores (P<0.02), which were not significantly different from sham (uninjured) animals. Vehicle-treated, injured animals demonstrated a profound cognitive deficit (P< 0.001), which was significantly attenuated by AK295 treatment (P< 0.05). To our knowledge, this study is the first to use a calpain inhibitor following brain trauma and suggests that calpain plays a role in the posttraumatic events underlying memory and neuromotor dysfunction.

Animals↗

PubMed2006

Middle-finger reflex.

A new reflex is described: middle-finger extensor reflex elicited by percussion of tendon insertion of musculus extensor digitorum communis in forearm. Following percussion using a reflex hammer, two EMG responses from the belly of the muscle were recorded: a short latency monosynaptic reflex with a latency of 31.4 +/- 1.5 ms (M1), and a long-latency middle-finger reflex with a mean latency of 64.8 +/- 6.31 ms (M2), the former being a monosynaptic extensor reflex, and the latter belonging to a spino-cortico-spinal reflex circuitry. It was suggested that the middle-finger extensor reflex elicited by radial nerve afferents and efferents (C7-C8) would be of clinical and theoretical importance.

Afferent Pathways↗

PubMed2002

Comparing suprapubic urine aspiration under real-time ultrasound guidance with conventional blind aspiration.

UNLABELLED: To determine the optimal method of suprapubic aspiration (SPA), the success rates of real-time ultrasound-guided SPA were compared with those of conventional SPA, and factors associated with success were studied. Thirty infants were randomly allocated to group A (for real-time ultrasound-guided SPA) and 30 infants to group B (for blind SPA with a prehydration protocol). The results showed that the overall success rates for all attempts were similar (26/30 or 87% in group A vs 24/30 or 80% in group B, p > 0.05). The first attempts in both groups were equally successful (both 18/30 or 60%). In comparison with failed attempts, successful ultrasound SPA attempts were associated with a greater bladder depth (mean +/- SD: 28 +/- 11 vs 21 +/- 5 mm, p < 0.01), length (32 +/- 12 vs 23 +/- 9 mm, p < 0.05) and volume (17 +/- 13 vs 8 +/- 6 ml, p < 0.01), but similar width (33 +/- 9 vs 29 +/- 5 mm, p > 0.05). In blind SPA, successful attempts were associated with the presence of bladder dullness on percussion (odds ratio 29). CONCLUSION: This study confirms that ultrasound-guided SPA has a high success rate. Blind SPA could also be equally successful with appropriate preparation. Ultrasound-guided SPA is recommended when the bladder depth exceeds 3 cm, or the bladder length exceeds 3.7 cm. If an ultrasound machine is not available, blind SPA may be an alternative, with attention being paid to prehydration and the demonstration of bladder dullness by percussion.

Computer Systems↗

PubMed2001

Inferring handedness from lithic evidence.

Until recently research into the origins of human handedness has been hampered by the lack of valid techniques for inferring handedness in pre-modern populations. A method developed by Toth for inferring handedness from lithic evidence, based on orientation of the cortex on lithic flakes, has produced promising results. However, this method is limited in applicability and has a variable signal to noise ratio. The authors describe a separate method, based on the orientation of the cone of percussion in lithic flakes, for inferring handedness from the lithic evidence. This method complements the cortex method. Some preliminary experimental evidence is presented which indicates that handedness can be inferred from lithic evidence using the cone of percussion method. Suggestions for further research are made.

Journal Article↗

PubMed2001

Neurobehavioral assessment of outcome following traumatic brain injury in rats: an evaluation of selected measures.

Neurobehavioral assessment of outcome has played an integral part in traumatic brain injury (TBI) research. Given the fundamental role of neurobehavioral measurement, it is critical that the tasks used are of the highest psychometric quality. The purpose of this paper is to evaluate several, commonly used neurobehavioral measures along the dimensions of reliability, sensitivity, and validity. Using both the midline and lateral fluid-percussion injury models, nine neurobehavioral measures were evaluated that assessed three different neurobehavioral constructs. Reflex suppression was measured by the duration of the suppression of the pinna, corneal, and righting reflexes. Vestibulomotor function was assessed with the beam-balance, beam-walking, and rotorod tasks. Cognitive function was evaluated by three measures of Morris water maze performance (goal latency, path length, cumulative distance). The evaluation of the reliability of the nine neurobehavioral measures found that all had acceptably high reliability coefficients (0.79 or higher). The analysis of each measure's sensitivity to injury found that all measures were capable of detecting injury-induced impairments. However, there were some substantial differences in the sensitivity of the measures of vestibulomotor and maze performance: the rotorod was the most sensitive vestibulomotor measure and goal latency and path length were equally sensitive measures of maze performance. In the assessment of validity, the results of a factor analysis supported the convergent and discriminative validity of the measures. And in cases in which the preclinical and clinical research have assessed the same construct, the animal model neurobehavioral measures had predictive (or external) validity. Thus, according to the psychometric standards by which measurement instruments are evaluated, the results indicated that these measures provide a valid assessment of neurobehavioral function after fluid percussion TBI.

Animals↗

PubMed2001

Talampanel, a novel noncompetitive AMPA antagonist, is neuroprotective after traumatic brain injury in rats.

Talampanel [(R)-7-acetyl-5-(4-aminophenyl)-8,9-dihydro-8-methyl-7H-1,3-dioxolo[4,5-h][2,3] benzodiazepine] is an orally active noncompetitive antagonist of the AMPA subtype of glutamate excitatory amino acid receptors. The purpose of this study was to determine whether treatment with talampanel would protect in a rat model of traumatic brain injury (TBI). Twenty-four hours prior to TBI, a fluid-percussion interface was positioned parasagittally over the right cerebral cortex. On the following day, fasted rats were anesthetized with 3% halothane, 70% nitrous oxide, and a balance of oxygen; mechanically ventilated and physiologically regulated; and subjected to right parieto-occipital parasagittal fluid-percussion injury (1.5-2.0 atm). The agent (talampanel, bolus infusion of 4 mg/kg followed by infusion of 4 mg/kg/h over 72 h) or vehicle was administered i.v. starting at either 30 min or 3 h after trauma. Seven days after TBI, brains were perfusion-fixed, coronal sections at various levels were digitized, and contusion areas were measured. Treatment with talampanel, when instituted 30 min after trauma, significantly reduced total contusion area compared to vehicle-treated rats (0.54 +/- 0.25 vs. 1.79 +/- 0.42 mm2, respectively). When talampanel treatment was begun at 3 h, the neuroprotective effect of the drug was lost. In addition, treatment with talampanel starting at 30 min significantly attenuated neuronal damage in all three subsectors of the hippocampal CA1 sector compared to vehicle-treated rats (normal-neuron counts, right (ipsilateral) medial CA1: 80.3 +/- 2.0 [talampanel] vs. 66.3 +/- 2.1 [vehicle] (mean +/- SEM); middle CA1: 71.5 +/- 2.0 vs. 60.3 +/- 2.2; lateral CA1: 74.5 +/- 3.0 vs. 63.0 +/- 3.2, respectively). By contrast, when talampanel treatment was begun at 3 h, normal pyramidal-neuron counts were almost identical in both groups. Our findings document that talampanel therapy instituted 30 min after trauma significantly reduces histological damage.

Animals↗

PubMed2002

Genes preferentially induced by depolarization after concussive brain injury: effects of age and injury severity.

Fluid percussion (FP) brain injury leads to immediate indiscriminate depolarization and massive potassium efflux from neurons. Using Northern blotting, we examined the post-FP expression of primary response/immediate early genes previously described as induced by depolarization in brain. RNA from ipsilateral and contralateral hippocampus was harvested from immature and adult rats 1 h following mild, moderate, or severe lateral fluid percussion injury and compared against age-matched sham animals. C-fos gene expression was used as a positive control and showed marked induction in both pups (6-25-fold with increasing severity) and adults (9.7-17.1-fold). Kinase-induced-by-depolarization-1 (KID-1) and salt-inducible kinase (SIK) gene expression was increased in adult (KID-1 1.5-1.6-fold; SIK 1.3-3.9-fold) but not developing rats. NGFI-b RNA was elevated after injury in both ages (pups 1.8-6.1-fold; adults 3.5-5-fold), in a pattern similar to that seen for c-fos. Secretogranin I (sec I) demonstrated no significant changes. Synaptotagmin IV (syt IV) was induced only following severe injury in the immature rats (1.4-fold). Our results reveal specific severity- and age-dependent patterns of hippocampal immediate early gene expression for these depolarization-induced genes following traumatic brain injury. Differential expression of these genes may be an important determinant of the distinct molecular responses of the brain to varying severities of trauma experienced at different ages.

Age Factors↗

PubMed2003

The glutamate AMPA receptor antagonist, YM872, attenuates cortical tissue loss, regional cerebral edema, and neurological motor deficits after experimental brain injury in rats.

A massive increase in extracellular glutamate is thought to contribute to brain damage after traumatic brain injury. We examined the neuroprotective effect of the AMPA receptor antagonist YM872 in a rat head injury model using the fluid-percussion procedure. Male Sprague-Dawley rats were subjected to right lateral (parasagittal) fluid-percussion brain injury or sham injury. At 15 min postinjury, they received either YM872 (20 mg/kg/h, 20 mg/3 mL) or normal saline (vehicle) intravenously for 4 h. The administration of YM872 significantly improved the composite neuroscore at 1 and 2 weeks postinjury (p < 0.05), and markedly reduced the volume of tissue loss in the injured cortex (p < 0.05). It also significantly reduced cerebral edema in the ipsilateral parietal cortex at 48 h postinjury (p < 0.01). These results indicate that the posttraumatic administration of YM872 may be neuroprotective by ameliorating cortical tissue loss and regional cerebral edema, and suggest the importance of AMPA receptors in traumatic brain damage involving secondary injury processes.

Animals↗

PubMed2003

Neuronal and glial cell number in the hippocampus after experimental traumatic brain injury: analysis by stereological estimation.

Fluid percussion (FP) brain injury causes spatial memory dysfunction in rats regardless of injury location (midline vs. lateral). Standard histological analysis of the injured brains shows hippocampal neuronal loss after lateral, but not midline FP injury. We have used the optical volume fractionator (OVF) stereological procedure to quantify neuronal loss and glial proliferation within specific subregions of the hippocampus after midline or lateral FP injury. The OVF method is a design-based cell counting procedure, which combines cellular numerical density estimates (from the optical disector) with volume estimates (generated by point counting and the fractionator stereology method) to produce an estimate of the absolute cell number. Fifteen adult male Sprague-Dawley rats were randomly divided into 3 groups (n = 5/group): midline injury, lateral injury and naive. A single fluid percussion pulse was delivered to anesthetized rats in the injured groups. At 14 days post-injury, strict morphological criteria enabled the estimation of neurons, astrocytes, oligodendrocytes, and microglia in defined hippocampal subregions. The results confirm that hippocampal neurons are selectively vulnerable to brain injury, particularly observed as a significant loss in the hilus following both types of injury and in area CA3 after lateral injury. In contrast, the number of astrocytes and oligodendrocytes remains unaffected by brain injury, regardless of subregion. However, the significant increase in microglia number (bilaterally after midline and ipsilateral following lateral injury) suggests that underlying cellular processes continue weeks following injury. The implications of the observed cell population changes are discussed in relation to the reported cognitive deficits associated with both lateral and midline FP brain injury.

Animals↗

PubMed1999

A clinical study on the effects of pulsed Nd:YAG laser irradiation at root canals immediately after pulpectomy and shaping.

OBJECTIVE: The effects of pulsed Nd:YAG laser irradiation for the treatment of root canals immediately after pulpectomy and shaping with regard to improvement of symptoms were evaluated clinically. SUMMARY BACKGROUND DATA: The effects of pulsed Nd:YAG laser irradiation for the treatment of root canals were experimentally investigated using an animal model, but not under clinical conditions. MATERIALS AND METHODS: Thirty-eight teeth from 29 patients were diagnosed as normal or irreversible pulpitis were used. After extirpation of pulp and shaping using a step-back technique and cleansing with 5% sodium hypochlorite (NaOCl) and 3% hydrogen peroxide (H2O2), laser irradiation was applied at 1 W and 15 pps for 1 second in 23 teeth (laser-treated group). Root canals were then obturated with gutta-percha points and sealer by the lateral condensation method. The condition of the obturations was confirmed radiographically. The control teeth were treated in the same way, but without laser irradiation. Occurrence of spontaneous pain was recorded 1 day after treatment and occurrence of percussion pain was recorded 1, 2, and 3 weeks after treatment. RESULTS: Effective ratio, which was the ratio of the number of "none" teeth to total teeth number in the laser-treated group, was higher than that in the control group, but there was no significant difference between 2 groups with regard to spontaneous and percussion pain (p > 0.05). CONCLUSION: These results suggest that the clinical application of pulsed Nd:YAG laser might be advantageous for the one-visit treatment of root canals immediately after pulpectomy shaping and to reduce postoperative pain.

Adolescent↗

PubMed1988

Regional rates of glucose utilization in the cat following concussive head injury.

Injections of [14C]-deoxyglucose ([14C]DG) were used to study rates of local cerebral glucose utilization (LCGU) in control cats and cats subjected to concussive brain injury produced by a fluid-percussion device. Studies in separate groups of animals demonstrated that the injury level selected produced transient behavioral suppression probably associated with traumatic disturbances of consciousness. LCGU was sampled near the site of fluid-percussion injury and more caudally in pontine regions. Histopathologic studies examined the possibility of hemorrhage, contusion, or breakdown of the blood-brain barrier in regions within which LCGU was calculated. These studies yielded analyses indicating that (1) the [14C]DG technique can be applied usefully to infer changes in regional levels of brain activity after concussion, (2) concussive injury produces changes in brain function that differ reliably across various regions of the central nervous system and may include both depression and focal activation of specific brain sites. Data are discussed that suggest that changes in brain activity in specific regions indicated by changes in LCGU could contribute to acute neurologic disturbances after concussion including unconsciousness.

Animals↗

PubMed1988

The effects of scopolamine and traumatic brain injury on central cholinergic neurons.

This study examined the effects of scopolamine and fluid percussion traumatic brain injury (TBI) on the activity of cholinergic neurons in specific areas of the rat brain 12 min, 4 h, and 24 h after injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using gas chromatography-mass fragmentography. Scopolamine pretreatment prevented significant increases in dorsal pontine ACh turnover at 12 min and 4 h after TBI, suggesting that the drug's protective actions against the neurologic deficits following TBI may involve blockade of cholinergic neuronal activation as well as postsynaptic muscarinic blockade. The responses of thalamic, hippocampal, and amygdaloid cholinergic neurons to TBI did not differ substantially in scopolamine-pretreated rats from those studied previously in untreated fluid-percussion-injured rats. However, cholinergic neurons in the cingulate-frontal cortex of rats receiving TBI did respond in a different manner to scopolamine than those of rats receiving sham injury, suggesting a disruption of regulation of cortical cholinergic neurons following this model of TBI.

Acetylcholine↗

PubMed1988

The effects of traumatic brain injury on regional cerebral blood flow in rats.

Alterations in cerebral blood flow (CBF) are among the most important secondary pathophysiologic consequences of traumatic brain injury. The present study compared CBF in control rats (n = 20) and in rats that received a calibrated experimental traumatic brain injury (n = 17). The traumatized rats were anesthetized with ketamine (25 mg/kg) and xylazine (10 mg/kg), and prepared for fluid percussion injury (FPI). Twenty-four hours later, the rats were anesthetized with 1% halothane in nitrous oxide-oxygen (70:30) and the left atrium was catheterized via a thoroacotomy. The atrial cannula was used to inject 15 microns radiolabeled microspheres to measure CBF. Following surgery, the concentration of halothane was reduced to 0.5% and the rats were paralyzed with pancuronium bromide (0.1 mg/kg). Thirty minutes later, baseline microsphere determinations were made, and the rats were injured (2.47 +/- 0.08 atm). Each rat received additional injections of microspheres at two of the following four times (T): 5, 15, 30, and 60 min after the brain injury. The procedures for the control group rats were the same as described above except that the rats were not subjected to the craniotomy and the FPI. The traumatized group exhibited heterogeneous decreases in CBF following trauma. Global CBF in this group was 78% (p less than 0.01), 64% (p less than 0.05), 52% (p less than 0.001) of those in the control group at T5, 15, 30, and 60, respectively. In rats, the most prominent cerebral circulatory changes following fluid percussion injury were early reductions of CBF and an increasingly heterogeneous CBF pattern. Hemorrhage, edema, and elevated prostagandin levels are mechanisms that may contribute to these changes.

Animals↗

PubMed1988

Experimental traumatic brain injury elevates brain prostaglandin E2 and thromboxane B2 levels in rats.

Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) levels were measured in rats following experimental traumatic brain injury. Rats (n = 36) were prepared for fluid percussion brain injury under pentobarbital anesthesia. Twenty-four hours later, rats were lightly anesthetized using methoxyflurane, injured (2.3 atm), and killed 5 or 15 min later. Twelve of the rats died before and are not included in the analyses. The following groups were used for data analysis: group I (n = 6) were sham-injured rats prepared for injury but not injured: group II (n = 6) were injured and killed 5 min later; group III (n = 12) were injured and killed 15 min posttrauma. Thirty seconds prior to sacrifice by decapitation into liquid nitrogen, all rats were injected with indomethacin (3 mg/kg, intravenously [IV]) to prevent postmortem PG synthesis. After sacrifice, brains were removed, weighed, and homogenized in a small quantity of phosphate buffer with indomethacin (50 micrograms/ml). PGE2 and TxB2 levels were determined using double-label radioimmunoassays. Posttraumatic convulsions were observed in 5 of 12 rats in group III and these rats were analyzed separately. PGE2 and TxB2 levels increased significantly (p less than 0.05) in both hemisphere and brainstem 5 min posttrauma. Fifteen minutes after injury, both PGE2 and TxB2 levels remained elevated but the levels were lower than at 5 min in the rats that did not exhibit posttraumatic seizures. This decrease in PG levels at 15 min was not observed in the rats that had seizures after injury and both PGE2 and TxB2 levels remained high in hemispheres and brainstem. Thus, fluid percussion brain injury results in substantial elevations in PGE2 and TxB2 levels and posttraumatic seizures exacerbate the observed increases.

Animals↗

PubMed1988

The effect of traumatic brain injury on the visual system: a morphologic characterization of reactive axonal change.

Reactive axonal changes following fluid-percussion brain injury were studied in the highly organized afferent pathways of the cat visual system. The visual system offers several features advantageous to the study of traumatic brain injury. Specifically, as the retinal cells of origin of the optic nerve and tract are isolated from the employed fluid-percussion injury, concomitant traumatically induced somatic change is not a confounding variable. Additionally, the existence of axons of varying diameters and topographic localization within the visual pathways allows the relationship between both fiber size and distribution and their predilection for traumatically induced change to be considered. Since the visual pathway is a highly organized sensory pathway, data obtained in this system can be compared with similar studies previously conducted in motor systems. In these experiments, 20 adult cats were subjected to brain injury and killed at posttraumatic survival periods ranging from 2 to 60 days. Six cats received intravitreous injections of horseradish peroxidase (HRP) to aid in the recognition of axonal change. At the designated survival time, all animals were perfused with aldehydes. The visual system from optic chiasm to lateral geniculate was sectioned and prepared for routine light (LM) and electron microscopic (TEM) study. Animals injected with HRP were processed for the LM and TEM visualization of HRP reaction products. By the second posttraumatic day, reactive axonal swellings were observed in the optic tracts as they entered the medial intralaminar nuclei of the lateral geniculate bodies. Proximal segments of the reactive axons showed enlargement and lobulation, whereas the distal segments underwent wallerian degeneration. Over a 2 week posttraumatic course, some axonal swelling persisted unchanged, some degenerated, and others initiated regenerative sprouting. with continued survival, however, all the reactive swellings manifested only progressive degenerative change. These reactive axonal changes appeared to constitute a primary response to the traumatic episode and occurred without concomitant damage to either the related brain parenchyma or its intrinsic vasculature. Although these findings replicate many of those previously described in motor pathways, new conceptual information has been provided. These studies preclude concomitant somal damage as a confounding variable and suggest that large-caliber axons are susceptible to the shear and tensile forces of traumatic brain injury.

Animals↗

PubMed1989

Experimental models of brain injury.

General categories of experimental brain injury models are reviewed regarding their clinical significance, and two new models are presented that use different methodology to produce injury. This report describes and characterizes the pathophysiologic changes produced by a novel fluid percussion (FP) method and a controlled cortical impact (CI) technique, both developed at the General Motors Research Laboratories (GMRL). The new models are compared to prior experimental brain injury techniques in relation to ongoing physical and analytical modeling used in automotive safety research by GMRL. Experimental results from our laboratory indicate that although the FP technique, currently the most widely used method for producing brain injury, is useful for producing graded injury responses systemically and centrally, it is not well-suited for detailed biomechanical analyses. This conclusion is based on high-speed cineradiographic studies where the physiologic saline in the FP cannula was substituted with a radiopaque contrast medium (Conray 1:1 dilution/saline). High speed x-ray movies (1000 fps) were taken of the fluid percussion pulse (1.5-3.4 atm/20 msec) in sagittal, dorsal, and frontal planes of orientation. When viewed together, the cineradiography revealed a complex, dynamic interaction between the injected fluid and the skull/cranial contents. Rapid lateral and anterior/posterior epidural fluid flow suggest that the pathology and dysfunction following FP brain injury reflects diffuse mechanical loading of the brain. Because fluid is used to transfer mechanical energy to brain tissue, and because fluid flow characteristics (i.e., direction, velocity, and displacement) are dependent on the brain geometry and species used, accurate analytical and biomechanical analyses of the resultant injury would be difficult at best. In contrast, the cortical impact model of experimental brain injury uses a known impact interface and a measurable, controllable impact velocity and cortical compression. These controlled variables enable the amount of deformation and the change in deformation over time to be accurately determined. In addition, the CI model produces graded, reproducible cortical contusion, prolonged functional coma, and extensive axonal injury, unlike the FP technique. The quantifiable nature of the single mechanical input used to produce the injury allows correlations to be made between the amount of deformation and the resultant pathology and functional changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗