The progression of electrophysiologic abnormalities during epileptogenesis after experimental traumatic brain injury.

OBJECTIVE: Posttraumatic epilepsy (PTE) accounts for 20% of acquired epilepsies. Experimental models are important for studying epileptogenesis. We previously reported that repetitive high-frequency oscillations with spikes (rHFOSs) occur early after lateral fluid percussion injury (FPI) and may be a biomarker for PTE. The objective of this study was to use multiple electrodes in rat hippocampal and neocortical regions to describe the long-term electroencephalographic and behavioral evolution of rHFOSs and epileptic seizures after traumatic brain injury (TBI). METHODS: Adult male rats underwent mild, moderate, or severe FPI or sham injury followed by video-electroencephalography (EEG) recordings with a combination of 16 neocortical and hippocampal electrodes at an early, intermediate, or late time-point after injury, up to 52 weeks. Recordings were analyzed for the presence of rHFOSs and seizures. RESULTS: Analysis was done on 28 rats with FPI and 7 shams. Perilesional rHFOSs were recorded in significantly more rats after severe (70.3%) than mild (20%) injury or shams (14.3%). Frequency of occurrence was significantly highest in the early (10.8/h) versus late group (3.2/h). Late focal seizures originating from the same electrodes were recorded in significantly more rats in the late (87.5%) versus early period (22.2%), occurring almost exclusively in injured rats. Seizure duration increased significantly over time, averaging 19 s at the beginning of the early period and 27 s at the end of the late period. Seizure frequency also increased significantly over time, from 4.4 per week in the early group to 26.4 per week in the late group. Rarely, rats displayed early seizures or generalized seizures. SIGNIFICANCE: FPI results in early rHFOSs and later spontaneous focal seizures arising from peri-lesional neocortex, supporting its use as a model for PTE. Epilepsy severity increased over time and was related to injury severity. The association between early rHFOSs and later focal seizures suggests that rHFOSs may be a potential noninvasive biomarker of PTE.

Pathologic electrographic changes after experimental traumatic brain injury.

OBJECTIVE: To investigate possible electroencephalography (EEG) correlates of epileptogenesis after traumatic brain injury (TBI) using the fluid percussion model. METHODS: Experiments were conducted on adult 2- to 4-month-old male Sprague-Dawley rats. Two groups of animals were studied: (1) the TBI group with depth and screw electrodes implanted immediately after the fluid percussion injury (FPI) procedure, and (2) a naive age-matched control group with the same electrode implantation montage. Pairs of tungsten microelectrodes (50 µm outer diameter) and screw electrodes were implanted in neocortex inside the TBI core, areas adjacent to TBI, and remote areas. EEG activity, recorded on the day of FPI, and continuously for 2 weeks, was analyzed for possible electrographic biomarkers of epileptogenesis. Video-EEG monitoring was also performed continuously in the TBI group to capture electrographic and behavioral seizures until the caps came off (28-189 days), and for 1 week, at 2, 3, and 6 months of age, in the control group. RESULTS: Pathologic high-frequency oscillations (pHFOs) with a central frequency between 100 and 600 Hz, were recorded from microelectrodes, beginning during the first two post-FPI weeks, in 7 of 12 animals in the TBI group (58%) and never in the controls. pHFOs only occurred in cortical areas within or adjacent to the TBI core. These were associated with synchronous multiunit discharges and popSpikes, duration 15-40 msec. Repetitive pHFOs and EEG spikes (rHFOSs) formed paroxysmal activity, with a unique arcuate pattern, in the frequency band 10-16 Hz in the same areas as isolated pHFOs, and these events were also recorded by screw electrodes. Although loss of caps prevented long-term recordings from all rats, pHFOs and rHFOSs occurred during the first 2 weeks in all four animals that later developed seizures, and none of the rats without these events developed late seizures. SIGNIFICANCE: pHFOs, similar to those associated with epileptogenesis in the status rat model of epilepsy, may also reflect epileptogenesis after FPI. rHFOSs could be noninvasive biomarkers of epileptogenesis.

Clinical relevance of midline fluid percussion brain injury: Acute deficits, chronic morbidities and the utility of biomarkers.

BACKGROUND: After 30 years of characterisation and implementation, fluid percussion injury (FPI) is firmly recognised as one of the best-characterised reproducible and clinically relevant models of TBI, encompassing concussion through diffuse axonal injury (DAI). Depending on the specific injury parameters (e.g. injury site, mechanical force), FPI can model diffuse TBI with or without a focal component and may be designated as mild-to-severe according to the chosen mechanical forces and resulting acute neurological responses. Among FPI models, midline FPI may best represent clinical diffuse TBI, because of the acute behavioural deficits, the transition to late-onset behavioural morbidities and the absence of gross histopathology. REVIEW: The goal here was to review acute and chronic physiological and behavioural deficits and morbidities associated with diffuse TBI induced by midline FPI. In the absence of neurodegenerative sequelae associated with focal injury, there is a need for biomarkers in the diagnostic, prognostic, predictive and therapeutic approaches to evaluate outcomes from TBI. CONCLUSIONS: The current literature suggests that midline FPI offers a clinically-relevant, validated model of diffuse TBI to investigators wishing to evaluate novel therapeutic strategies in the treatment of TBI and the utility of biomarkers in the delivery of healthcare to patients with brain injury.

Distinct effect of impact rise times on immediate and early neuropathology after brain injury in juvenile rats.

Traumatic brain injury (TBI) can occur from physical trauma from a wide spectrum of insults ranging from explosions to falls. The biomechanics of the trauma can vary in key features, including the rate and magnitude of the insult. Although the effect of peak injury pressure on neurological outcome has been examined in the fluid percussion injury (FPI) model, it is unknown whether differences in rate of rise of the injury waveform modify cellular and physiological changes after TBI. Using a programmable FPI device, we examined juvenile rats subjected to a constant peak pressure at two rates of injury: a standard FPI rate of rise and a faster rate of rise to the same peak pressure. Immediate postinjury assessment identified fewer seizures and relatively brief loss of consciousness after fast-rise injuries than after standard-rise injuries at similar peak pressures. Compared with rats injured at standard rise, fewer silver-stained injured neuronal profiles and degenerating hilar neurons were observed 4-6 hr after fast-rise FPI. However, 1 week postinjury, both fast- and standard-rise FPI resulted in hilar cell loss and enhanced perforant path-evoked granule cell field excitability compared with sham controls. Notably, the extent of neuronal loss and increase in dentate excitability were not different between rats injured at fast and standard rates of rise to peak pressure. Our data indicate that reduced cellular damage and improved immediate neurological outcome after fast rising primary concussive injuries mask the severity of the subsequent cellular and neurophysiological pathology and may be unreliable as a predictor of prognosis.

Behavioral deficits after mild traumatic brain injury by fluid percussion in rats.

Mild traumatic brain injury (TBI) can lead to various disorders, encompassing cognitive and psychiatric complications. While pre-clinical studies have long investigated behavioral alterations, the fluid percussion injury (FPI) model still lacks a comprehensive behavioral battery that includes psychiatric-like disorders. To address this gap, we conducted multiple behavioral tasks over two months in adult male Wistar rats, focusing on mild FPI. Statistical analyses revealed that both naive and sham animals exhibited an increase in sweet liquid consumption over time. In contrast, the TBI group did not show any temporal changes, although mild FPI did induce a statistically significant decrease in sucrose consumption compared to control groups during the chronic phase. Additionally, social interaction tasks indicated reduced contact time in TBI animals. The elevated plus maze task demonstrated an increase in open-arm exploration following fluid percussion. Nonetheless, no significant differences were observed in the acute and chronic phases for the forced swim and light-dark box tasks. Evaluation of three distinct memory tasks in the chronic phase revealed that mild FPI led to long-term memory deficits, as assessed by the object recognition task, while the surgical procedure itself resulted in short-term spatial memory deficits, as evaluated by the Y-maze task. Conversely, working memory remained unaffected in the water maze task. Collectively, these findings provide a nuanced characterization of behavioral deficits induced by mild FPI.

Lateral fluid percussion injury: A rat model of experimental traumatic brain injury.

Traumatic brain injury (TBI) represents one of the leading causes of disability and death worldwide. The annual economic impact of TBI-including direct and indirect costs-is high, particularly impacting low- and middle-income countries. Despite extensive research, a comprehensive understanding of the primary and secondary TBI pathophysiology, followed by the development of promising therapeutic approaches, remains limited. These fundamental caveats in knowledge have motivated the development of various experimental models to explore the molecular mechanisms underpinning the pathogenesis of TBI. In this context, the Lateral Fluid Percussion Injury (LFPI) model produces a brain injury that mimics most of the neurological and systemic aspects observed in human TBI. Moreover, its high reproducibility makes the LFPI model one of the most widely used rodent-based TBI models. In this chapter, we provide a detailed surgical protocol of the LFPI model used to induce TBI in adult Wistar rats. We further highlight the neuroscore test as a valuable tool for the evaluation of TBI-induced sensorimotor consequences and their severity in rats. Lastly, we briefly summarize the current knowledge on the pathological aspects and functional outcomes observed in the LFPI-induced TBI model in rodents.

Can structural or functional changes following traumatic brain injury in the rat predict epileptic outcome?

PURPOSE: Posttraumatic epilepsy (PTE) occurs in a proportion of traumatic brain injury (TBI) cases, significantly compounding the disability, and risk of injury and death for sufferers. To date, predictive biomarkers for PTE have not been identified. This study used the lateral fluid percussion injury (LFPI) rat model of TBI to investigate whether structural, functional, and behavioral changes post-TBI relate to the later development of PTE. METHODS: Adult male Wistar rats underwent LFPI or sham injury. Serial magnetic resonance (MR) and positron emission tomography (PET) imaging, and behavioral analyses were performed over 6 months postinjury. Rats were then implanted with recording electrodes and monitored for two consecutive weeks using video-electroencephalography (EEG) to assess for PTE. Of the LFPI rats, 52% (n = 12) displayed spontaneous recurring seizures and/or epileptic discharges on the video-EEG recordings. KEY FINDINGS: MRI volumetric and signal analysis of changes in cortex, hippocampus, thalamus, and amygdala, (18) F-fluorodeoxyglucose (FDG)-PET analysis of metabolic function, and behavioral analysis of cognitive and emotional changes, at 1 week, and 1, 3, and 6 months post-LFPI, all failed to identify significant differences on univariate analysis between the epileptic and nonepileptic groups. However, hippocampal surface shape analysis using large-deformation high-dimensional mapping identified significant changes in the ipsilateral hippocampus at 1 week postinjury relative to baseline that differed between rats that would go onto become epileptic versus those who did not. Furthermore, a multivariate logistic regression model that incorporated the 1 week, and 1 and 3 month (18) F-FDG PET parameters from the ipsilateral hippocampus was able to correctly predict the epileptic outcome in all of the LFPI cases. As such, these subtle changes in the ipsilateral hippocampus at acute phases after LFPI may be related to PTE and require further examination. SIGNIFICANCE: These findings suggest that PTE may be independent of major structural, functional, and behavioral changes induced by TBI, and suggest that more subtle abnormalities are likely involved. However, there are limitations associated with studying acquired epilepsies in animal models that must be considered when interpreting these results, in particular the failure to detect differences between the groups may be related to the limitations of properly identifying/separating the epileptic and nonepileptic animals into the correct group.

Adiponectin and traumatic brain injury.

Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke therapy; however, little is known about the effects of adiponectin on traumatic brain injury. The present study examined the immunoactivity of adiponectin.Adult male Sprague-Dawley rats were subjected to lateral fluid percussion injury using the Dragonfly device. Immuno-histochemical studies showed that the adiponectin expression was increased in the cerebral cortex at 24 h after injury and in the hippocampus at 72 h after injury. Our findings suggest that adiponectin might participate in the pathophysiological process occurring after traumatic brain injury.

Is decompressive craniectomy a risk factor for ventriculomegaly?

OBJECTIVE: Decompressive craniectomy (DC) is an established therapeutic option following severe traumatic brain injury (TBI). However, several delayed complications of DC have been reported, including ventriculomegaly, which can lead to poor patient outcomes. Nevertheless, ventriculomegaly can occur after TBI even without DC. The aim of the present study was to investigate the influence of DC on ventriculomegaly. MATERIAL AND METHODS: Adult male Sprague-Dawley rats (300-400 g) were subjected to lateral fluid percussion injury using a fluid percussion device. Rats were randomly divided into four groups: sham, craniectomized without trauma (D group), traumatized without DC (FPI group), and craniectomized immediately after trauma (FPI + D group). On day 28 of recovery, ventricular volumes were measured by image analysis. RESULTS: There was no significant difference in ventricular size between the sham group and the D group animals or between the FPI group and the FPI + D group animals. CONCLUSION: These data suggest that DC may not be a risk factor for ventriculomegaly after TBI.

Sudden death after fatal percussion of the cervical neurovascular bundle.

Background: Atypical compression of the neck may be classified as asphyxia in which the external compression on the cervical anatomical structures occurs in a peculiar manner. In such cases, death occurs due to the combination of several pathophysiological phenomena, such as respiratory, vascular, and nervous. When the mechanical action on the neck is violent and rapid, it is more correct to use the word percussion rather than compression. Usually there are no skin lesions of special significance in this type of neck percussion, unlike the cases of choking, strangulation, and hanging, and the diagnosis is challenging. It is important to carefully evaluate the body during the autopsy to identify which pathophysiological mechanism caused the death. Case report: A young woman died immediately after being struck by a concrete beam at the level of her neck. The woman was on vacation with her boyfriend and decided to hang from a concrete beam suspended between two columns to take a souvenir photo when the beam suddenly broke and fell on her. The autopsy revealed multiple abrasions, swelling, and lacerations to the face, neck, and chest. Internal examination revealed primarily the presence of hemorrhagic infiltration in the anterior cervical compartments and lacerations of various organs, including the trachea. Conclusion: Based on all the obtained data, including toxicological and histological, the cause of death was atypical ab extrinsic percussion of the neck, directed particularly at the right cervical neurovascular bundle.

Maintenance of a Lateral Fluid Percussion Injury Device.

Traumatic brain injury (TBI) accounts for roughly 2.5 million emergency room visits and hospitalizations annually and is a leading cause of death and disability in children and young adults. TBI is caused by a sudden force applied to the head and, to better understand human TBI and its underlying mechanisms, experimental injury models are necessary. Lateral fluid percussion injury (LFPI) is a commonly used injury model due to similarities in the pathological changes found in human TBI compared to LFPI, including hemorrhages, vascular disruption, neurological deficits, and neuron loss. LFPI employs a pendulum and a fluid-filled cylinder, the latter having a moveable piston at one end, and a Luer lock connection to stiff, fluid-filled tubing at the other end. Preparation of the animal involves performing a craniectomy and attaching a Luer hub over the site. The next day, the tubing from the injury device is connected to the Luer hub on the animal's skull and the pendulum is raised to a specified height and released. The impact of the pendulum with the piston generates a pressure pulse which is transmitted to the intact dura mater of the animal via the tubing and produces the experimental TBI. Proper care and maintenance are essential for the LFPI device to function reliably, as the character and severity of the injury can vary greatly depending on the condition of the device. Here, we demonstrate how to properly clean, fill, and assemble the LFPI device, and ensure that it is adequately maintained for optimal results.

Lens subluxation after use of a percussion massage gun: A case report.

RATIONALE: To report the first case of lens dislocation and secondary acute angle-closure glaucoma (AACG) following use of a percussion massage gun (PMG) around the eye. PATIENT CONCERNS: A 69-year-old Chinese man had been using a PMG around his right eye for 2 months in order to relieve headache. After eye pain and blurred vision for 5 days, he went to the ophthalmological emergency department. His best-corrected visual acuity at distance was counting fingers. DIAGNOSIS: The patient was diagnosed with lens subluxation, secondary AACG and pterygium in the right eye. Cataracts were diagnosed in both eyes. INTERVENTIONS: The patient underwent phacoemulsification and anterior vitrectomy. After surgery, the patient was given eye drops containing tobramycin, dexamethasone, 0.1% bromfenac sodium hydrate ophthalmic solution and Mydrin-P for 1 month. OUTCOMES: At 3-month follow-up, uncorrected visual acuity in the right eye was counting fingers. The outcome of optometry in the right eye was +11.50 DS/-0.50 DC * 110°, with corrected-distance visual acuity of 4/20. IOP was 20.7 mm Hg in the right eye and 15.7 mm Hg in the left. Endothelium in the right cornea showed endothelial damage. Nevertheless, the patient reported no right eye pain anymore, and he indicated that he was satisfied with his situation. LESSONS: Caregivers, sports professionals and the general public should be aware of the dangers of PMGs and the need to use them appropriately and safely, for example during self-massage and rehabilitation therapy. In particular, we recommend not using PMGs above the neck, which should be clearly indicated in instruction manuals.

Na-K-Cl cotransporter-1 in the mechanism of cell swelling in cultured astrocytes after fluid percussion injury.

Brain edema and associated increased intracranial pressure are major consequences of traumatic brain injury (TBI). An important early component of the edema associated with TBI is astrocyte swelling (cytotoxic edema). Mechanisms for such swelling, however, are poorly understood. Ion channels/transporters/exchangers play a major role in cell volume regulation, and a disturbance in one or more of these systems may result in cell swelling. To examine potential mechanisms in TBI-mediated brain edema, we employed a fluid percussion model of in vitro barotrauma and examined the role of the ion transporter Na(+)-K(+)-2Cl(-)-cotransporter 1 (NKCC1) in trauma-induced astrocyte swelling as this transporter has been strongly implicated in the mechanism of cell swelling in various neurological conditions. Cultures exposed to trauma (3, 4, 5 atm pressure) caused a significant increase in NKCC1 activity (21%, 42%, 110%, respectively) at 3 h. At 5 atm pressure, trauma significantly increased NKCC1 activity at 1 h and it remained increased for up to 3 h. Trauma also increased the phosphorylation (activation) of NKCC1 at 1 and 3 h. Inhibition of MAPKs and oxidative/nitrosative stress diminished the trauma-induced NKCC1 phosphorylation as well as its activity. Bumetanide, an inhibitor of NKCC1, significantly reduced the trauma-induced astrocyte swelling (61%). Silencing NKCC1 with siRNA led to a reduction in trauma-induced NKCC1 activity as well as in cell swelling. These findings demonstrate the critical involvement of NKCC1 in the astrocyte swelling following in vitro trauma, and suggest that blocking NKCC1 activity may represent a useful therapeutic strategy for the cytotoxic brain edema associated with the early phase of TBI.

Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats.

BACKGROUND: Traumatic brain injury (TBI) evokes a systemic immune response including leukocyte migration into the brain and release of pro-inflammatory cytokines; however, the mechanisms underlying TBI pathogenesis and protection are poorly understood. Due to the high incidence of head trauma in the sports field, battlefield and automobile accidents identification of the molecular signals involved in TBI progression is critical for the development of novel therapeutics. METHODS: In this report, we used a rat lateral fluid percussion impact (LFPI) model of TBI to characterize neurodegeneration, apoptosis and alterations in pro-inflammatory mediators at two time points within the secondary injury phase. Brain histopathology was evaluated by fluoro-jade (FJ) staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay, polymerase chain reaction (qRT PCR), enzyme linked immunosorbent assay (ELISA) and immunohistochemistry were employed to evaluate the CCL20 gene expression in different tissues. RESULTS: Histological analysis of neurodegeneration by FJ staining showed mild injury in the cerebral cortex, hippocampus and thalamus. TUNEL staining confirmed the presence of apoptotic cells and CD11b+ microglia indicated initiation of an inflammatory reaction leading to secondary damage in these areas. Analysis of spleen mRNA by PCR microarray of an inflammation panel led to the identification of CCL20 as an important pro-inflammatory signal upregulated 24 h after TBI. Although, CCL20 expression was observed in spleen and thymus after 24 h of TBI, it was not expressed in degenerating cortex or hippocampal neurons until 48 h after insult. Splenectomy partially but significantly decreased the CCL20 expression in brain tissues. CONCLUSION: These results demonstrate that the systemic inflammatory reaction to TBI starts earlier than the local brain response and suggest that spleen- and/ or thymus-derived CCL20 might play a role in promoting neuronal injury and central nervous system inflammation in response to mild TBI.

Low-pressure fluid percussion minimally adds to the sham craniectomy-induced neurobehavioral changes: Implication for experimental traumatic brain injury model.

Modeling experimental traumatic brain injury (TBI) in rodents is necessarily required to understand the pathophysiological and neurobehavioral consequences of neurotrauma. Numerous models have been developed to study experimental TBI. Fluid percussion injury (FPI) is the most extensively used model to represent clinical phenotypes. Nevertheless, the surgical 'sham' procedure (craniectomy), a prerequisite of FPI, is the impeding factor in experimental TBI. We hypothesized that if craniectomy causes substantial structural and functional changes in the brain, it might mimic the mild FPI-induced neurobehavioral dysfunctions. To understand the hypothesis, C57BL/6 mice were exposed to lateral FPI at 1.2 atm pressure and changes in the neuronal architecture, hippocampal neurogenesis, neuroinflammation, and behavioral functions were compared to the sham (craniectomy) and control mice at day 7 post-FPI. We observed that both the craniectomy and FPI significantly augmented the ipsilateral hippocampal neurogenesis as evaluated by DCX and Beta-III tubulin immunoreactivity. Similarly, a significant increase in GFAP and TMEM immunoreactivity in CA1 and CA3 regions showed that craniectomy mimics FPI-induced neuroinflammation. The additive damaging effect of craniectomy with FPI was also reported in the term of axonal and dendritic fragmentation, swelling and neuronal death using silver staining, Fluoro-jade, and MAP-2 immunoreactivity. Sham-exposed mice showed a significant functional decrease in grip strength. Our results indicate that sham craniectomy itself is enough to cause TBI like characteristics, and thus fluid percussion at mild pressure is minimally additive with craniectomy. Considering the method as a mixed (focal & diffused) injury model, the 'net neurotrauma severity' should be compared with naïve control instead of the sham as it is an outcome of cumulative damage due to fluid pressure and craniectomy. Nevertheless, to understand the long term consequences of neurotrauma, the extent of recovery in surgical sham may separately be quantified.

Effect of mechanical percussion combined with patient position change on the elimination of upper urinary stones/fragments: a systematic review and meta-analysis.

The objective of this study is to explore the efficacy and safety of mechanical percussion combined with changed patient position (MPPP) on elimination of residual stones/fragments in the upper urinary tract. The study was a systematic review and meta-analysis. A systematic literature review using Pubmed, Embase, Medline, and Cochrane Library was conducted to obtain randomized-controlled trials (RCTs) evaluating the efficacy and safety of MPPP treatment of patients with residual stones/fragments in the upper urinary tract. The retrieval of data ended in October 2018. Statistical analysis was carried out using summarized unadjusted risk ratios (RRs) with 95% confidence intervals (CIs). Seven RCTs comprising 1132 patients were included. Compared with patients in the control group, patients treated with MPPP had higher stone-free rates (SFRs) with RR 1.55 (CI 1.11-2.18; p = 0.01) and lower complication rates with RR 0.48 (CI 0.25-0.94, p = 0.03). In subgroup analysis based on stone location, the SFR for the lower calyx was significantly higher in the intervention group than in the control group: RR 1.80 (CI 1.47-2.21, p < 0.00001). In subgroup analysis based on complication type, compared with the control patients, the intervention patients had lower hematuria rate with RR 0.46 (CI 0.28-0.74, p = 0.001) and lower leucocyturia rate with RR 0.33 (CI 0.12-0.89, p = 0.03). MPPP is a worthwhile non-invasive method for elimination of residual stones/fragments in the upper urinary tract. Furthermore, we recommend MPPP for patients with residual stones or fragments located in the lower calyces.

Effect of mechanical chest percussion on intracranial pressure: a pilot study.

BACKGROUND: Treatment of brain injury is often focused on minimizing intracranial pressure, which, when elevated, can lead to secondary brain injury. Chest percussion is a common practice used to treat and prevent pneumonia. Conflicting and limited anecdotal evidence indicates that physical stimulation increases intracranial pressure and should be avoided in patients at risk of intracranial hypertension. OBJECTIVES: To explore the safety of performing chest percussion for patients at high risk for intracranial hypertension. METHODS: A total of 28 patients with at least 1 documented episode of intracranial hypertension who were having intracranial pressure monitored were studied in a prospective randomized control trial. Patients were randomly assigned to either the control group (no chest percussion) or the intervention group (10 minutes of chest percussion at noon). Intracranial pressure was recorded once a minute before, during, and after the intervention. RESULTS: Mean intracranial pressures for the control group before, during, and after the study period (14.4, 15.0, and 15.9 mm Hg, respectively) did not differ significantly from pressures in the intervention group (13.6, 13.7, and 14.2 mm Hg, respectively). CONCLUSIONS: Mechanical chest percussion may be a safe intervention for nurses to use on neurologically injured patients who are at risk for intracranial hypertension.

Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury.

The lateral fluid percussion injury (FPI) model is well established and has been used to study TBI and post-traumatic epilepsy (PTE). However, considerable variability has been reported for the specific parameters used in different studies that have employed this model, making it difficult to harmonize and interpret the results between laboratories. For example, variability has been reported regarding the size and location of the craniectomy, how the Luer lock hub is placed relative to the craniectomy, the atmospheric pressure applied to the dura and the duration of the pressure pulse. Each of these parameters can impact injury severity, which directly correlates with the incidence of PTE. This has been manifested as a wide range of mortality rates, righting reflex times and incidence of convulsive seizures reported. Here we provide a detailed protocol for the method we have used to help facilitate harmonization between studies. We used FPI in combination with a wireless EEG telemetry system to continuously monitor for electrographic changes and detect seizure activity.  FPI is induced by creating a 5 mm craniectomy over the left hemisphere, between the Bregma and Lambda and adjacent to the lateral ridge. A Luer lock hub is secured onto the skull over the craniectomy. This hub is connected to the FPI device, and a 20-millisecond pressure pulse is delivered directly to the intact dura through pressure tubing connected to the hub via a twist lock connector. Following recovery, rats are re-anesthetized to remove the hub. Five 0.5 mm, stainless steel EEG electrode screws are placed in contact with the dura through the skull and serve as four recording electrodes and one reference electrode. The electrode wires are collected into a pedestal connector which is secured into place with bone cement. Continuous video/EEG recordings are collected for up to 4 weeks post TBI.

Benign paroxysmal vertigo secondary to placement of maxillary implants using the alveolar expansion technique with osteotomes: a study of 4 cases.

The osteotome method is an often-used technique of great utility in certain patients with maxillary bone atrophy. However, it has been associated with the provocation of benign paroxysmal positional vertigo (BPPV), which has been described as a consequence of working the implant bed with osteotomes. During the placement of maxillary dental implants using the osteotome technique, the trauma induced by percussion with the surgical hammer, along with hyperextension of the neck during the operation, can displace otoliths and induce BPPV. Four cases of BPPV occurring after the preparation of maxillary implant beds are presented. Treatment consists fundamentally of maneuvers to move the calcium carbonate crystals from their anomalous location in the semicircular canal to their correct place in the utricle.

Implication of surgical procedure in the induction of headache and generalized painful sensation in a fluid percussion injury model in rats.

BACKGROUND: This study demonstrated the effects of traumatic brain injury (TBI) and each step of the surgical procedure for a fluid percussion injury (FPI) model on periorbital allodynia. NEW METHOD: Adult male Wistar rats were divided in naive, incision, scraping, sham-TBI and TBI groups. Periorbital allodynia was evaluated using von Frey filaments, and heat hyperalgesia of the hindpaws was evaluated by a Plantar Test Apparatus. RESULTS: The statistical analyses revealed that the surgical procedure decreased von Frey filaments thresholds twenty-four hours after the surgery in all groups when compared to the naive group (p < 0.0001). Scraping, sham-TBI and TBI groups showed a decrease in the periorbital mechanical threshold for 35 days compared with the naive and incision groups (p < 0.0001). Only the TBI group demonstrated a significant difference in periorbital allodynia at 45 and 60 days after the injury (p < 0.01). A significant decrease in the thermal withdrawal latency of the hindpaw contralateral to the lesion was observed in the TBI group compared with the naive group at 7 days and 28 days after the lesion (p < 0.05). COMPARISON WITH EXISTING METHODS: This study presented in detail the effects of each stage of the surgical procedure for a FPI model on periorbital allodynia over time and characterized the TBI model for this evaluation. CONCLUSION: The FPI model is relevant for the study of headache and generalized pain in both acute and chronic phases after an injury.