A new method to determine the optimal orientation of Slim Modiolar cochlear implant electrode array insertion.

BACKGROUND AND PURPOSE: Our goal was to determine the optimal orientation of insertion of the Slim Modiolar electrode and develop an easy-to-use method to aid implantation surgery. In some instances, the electrode arrays cannot be inserted in their full length. This can lead to buckling, interscalar dislocation or tip fold-over. In our opinion, one of the possible reasons of tip fold-over is unfavourable orientation of the electrode array. Our goal was to determine the optimal orientation of the Slim Modiolar electrode array relative to clear surgical landmarks and present our method in one specified case. METHODS: For the measurement, we used the preoperative CT scan of one of our cochlear implant patients. These images were processed by an open source and free image visualization software: 3D Slicer. In the first step we marked the tip of the incus short process and then created the cochlear view. On this view we drew two straight lines: the first line represented the insertion guide of the cochlear implant and the second line was the orientation marker (winglet). We determined the angle enclosed by winglet and the line between the tip of the incus short process and the cross-section of previously created two lines. For the calculation we used a self-made python code. RESULTS: The result of our algorithm for the angle was 46.6055°. To validate this result, we segmented, from the CT scan, the auditory ossicles and the membranaceous labyrinth. From this segmentation we generated a 3D reconstruction. On the 3D view, we can see the position of the previous lines relative to the anatomical structures. After this we rotated the 3D model together with the lines so that the insertion guide forms a dot. In this view, the angle was measured with ImageJ and the result was 46.599°. CONCLUSION: We found that our method is easy, fast, and time-efficient. The surgery can be planned individually for each patient, based on their routine preoperative CT scan of the temporal bone, and the implantation procedure can be made safer. In the future we plan to use this method for all cochlear implantation surgeries, where the Slim Modiolar electrode is used.

Lysophosphatidic Acid Reduces Microregional Oxygen Supply/Consumption Balance after Cerebral Ischemia-Reperfusion.

BACKGROUND: Lysophosphatidic acid (LPA) is a small phospholipid-signaling molecule, which can alter responses to stress in the central nervous system. OBJECTIVE: We hypothesized that exogenous LPA would increase the size of infarct and reduce microregional O2 supply/consumption balance after cerebral ischemia-reperfusion. METHODS: This was tested in isoflurane-anesthetized rats with middle cerebral artery blockade for 1 h and reperfusion for 2 h with or without LPA (1 mg/kg, at 30, 60, and 90 min after reperfusion). Regional cerebral blood flow was determined using a C14-iodoantipyrine autoradiographic technique. Regional small-vessel (20-60 µm in diameter) arterial and venous oxygen saturations were determined microspectrophotometrically. RESULTS: There were no significant hemodynamic or arterial blood gas differences between groups. The control ischemic-reperfused cortex had a similar O2 consumption to the contralateral cortex. However, microregional O2 supply/consumption balance was significantly reduced in the ischemic-reperfused cortex with many areas of low O2 saturation (43 of 80 veins with O2 saturation below 50%). LPA did not significantly alter cerebral blood flow, but it did significantly increase O2 extraction and consumption of the ischemic-reperfused region. It also significantly increased the number of small veins with low O2 saturations in the reperfused region (76 of 80 veins with O2 saturation below 50%). This was associated with a significantly increased cortical infarct size after LPA administration (11.4 ± 0.5% control vs. 16.4 ± 0.6% LPA). CONCLUSION: This suggests that LPA reduces cell survival and that it is associated with an increase in the number of small microregions with reduced local oxygen balance after cerebral ischemia-reperfusion.

Lysophosphatidic acid increased infarct size in the early stage of cerebral ischemia-reperfusion with increased BBB permeability.

BACKGROUND: We investigated whether exogenous lysophosphatidic acid (LPA), a phospholipid extracellular signaling molecule, would increase infarct size and blood-brain barrier (BBB) disruption during the early stage of cerebral ischemia-reperfusion, and whether it works through Akt-mTOR-S6K1 intracellular signaling. MATERIAL AND METHODS: Rats were given either vehicle or LPA 1 mg/kg iv three times during reperfusion after one hour of middle cerebral artery (MCA) occlusion. In another group, prior to administration of LPA, 30 mg/kg of PF-4708671, an S6K1 inhibitor, was injected. After one hour of MCA occlusion and two hours of reperfusion the transfer coefficient (Ki) of 14C-α-aminoisobutyric acid and the volume of 3H-dextran distribution were determined to measure the degree of BBB disruption. At the same time, the size of infarct was determined and western blot analysis was performed to determine the levels of phosphorylated Akt (p-Akt) and phosphorylated S6 (pS6). RESULTS: LPA increased the Ki in the ischemic-reperfused cortex (+43%) when compared with Control rats and PF-4708671 pretreatment prevented the increase of Ki by LPA. LPA increased the percentage of cortical infarct out of total cortical area (+36%) and PF-4708671 pretreatment prevented the increase of the infarct size. Exogenous LPA did not significantly change the levels of p-Akt as well as pS6 in the ischemic-reperfused cortex. CONCLUSION: Our data demonstrate that the increase in BBB disruption could be one of the reasons of the increased infarct size by LPA. S6K1 may not be the major target of LPA. A decrease of LPA during early cerebral ischemia-reperfusion might be beneficial for neuronal survival.

Improvement in Microregional Oxygen Supply/Consumption Balance and Infarct Size After Cerebral Ischemia-Reperfusion With Inhibition of p70 Ribosomal S6 Kinase (S6K1).

BACKGROUND: We tested the hypothesis that inhibition of p70 ribosomal S6 kinase (S6K1) would decrease infarct size and improve microregional O2 supply/consumption balance after cerebral ischemia-reperfusion. METHODS: This was tested in isoflurane-anesthetized rats with middle cerebral artery blockade for 1 hour and reperfusion for 2 hours with or without PF-4708671 (S6K1 inhibitor, 75 mg/kg, 15 minutes after blockade). Regional cerebral blood flow was determined using a C14-iodoantipyrine autoradiographic technique. Regional small vessel (20-60 µm diameter) arterial and venous oxygen saturations were determined microspectrophotometrically. RESULTS: There were no significant hemodynamic or arterial blood gas differences between groups. The control ischemic-reperfused cortex had a similar O2 consumption to the contralateral cortex. However, microregional O2 supply/consumption balance was significantly reduced in the ischemic-reperfused cortex with many areas of low O2 saturation (23 of 80 veins with O2 saturation below 45%). PF-4708671 did not significantly alter cerebral blood flow or O2 consumption. However, it significantly reduced the number of small veins with low O2 saturations in the reperfused region (6 of 80 veins with O2 saturation below 45%). This was associated with a significantly reduced cortical infarct size after S6K1 inhibition (12.9 ± .8% control versus 6.6 ± .3% PF-4708671). CONCLUSION: This suggests that S6K1 inhibition is important for cell survival and that it reduces the number of small microregions with reduced local oxygen balance after cerebral ischemia-reperfusion.

[Craniomandibular disorder/dysfunction. Characteristics and disorders of the masticatory organ]. / Craniomandibularis diszfunkció. A rágószerv sajátosságai és muködési zavarai.

The practising physician often meets patients with pain located in different parts of the face and facial skull, mouth opening restriction or other motion disorder of the mandible. It is not always easy to identify and explain the cause. It is not widely known among doctors that most of these problems are due to masticatory dysfunction. There is a special group of patients showing functional disorders and there are some others who present a variety of different symptoms and visit several doctors. The masticatory organ, a functional unit of the human organism has a definite and separate task and function. In the early years of life it is capable of adaptation, while later on it tends to compensation. The authors outline the functional anatomy of the masticatory organ and the characteristics of multicausal pathology, the dynamics of the process of the disease and their interdisciplinary aspects. They discuss the basic elements of craniomandibular dysfunction. Based on the diagnostic algorithm, they summarize treatment options for masticatory function disorders. They emphasize the importance that physicians should offer treatment, especially an irreversible treatment, without a diagnosis. It occurs very often that the causes are identified after the patients become symptom-free due to treatment. The aim of this report is to help the general practitioners, dentists, neurologists, ear-nose-throat specialists, rheumatologists or any other specialists in the everyday practice who have patients with different symptoms such as pain in the skull, acoustic phenomenon of the joint or craniomandibular dysfunction.

[The therapy of masticatory organ dysfunctions (CMD)]. / Rágószervi funkciózavarok (CMD) therapiája.

The authors have been dealing with disorders of the masticatory organ (CMD) for several decades and they published their experience and summarized findings that they have gained from over 2,000 cases. They gave a summary of masticatory organ dysfunction diagnostics in 3rd issue of Fogorvosi Szemle in 2011. In their current paper they discuss the treatment of masticatory organ dysfunctions (CMD) according to the logic of diagnostic algorythm and they present it to the practising dentist. They would like to emphasize that it is not allowed to indicate any treatment especially an irreversible one, without a diagnosis. The cause of the disease can very often be identified or specified after the symptom relieving treatment. After summarizing the general treatment principles depending on the functional condition of the masticatory organ, they give a detailed explanation of systematic functional therapy, i.e., symptomatic treatment or medical treatment, physiotherapy, occlusal splint therapy and the definitive treatment that follows (such as occlusal adjustment, prosthetic rehabilitation, orthodontics and surgical intervention). They classify the occlusal instruments (splint), which are often misinterpreted or not used in the proper way in practice (and bibliography), according to indications. They outline some orthodontic anomalies in connection with the masticatory organ: on the one hand when the patient who undergoes an orthodontic treatment has a latent or manifest masticatory organ dysfunction (CMD), on the other hand when the dysfunction appears during the orthodontic treatment. Among the definitive treatment principles they emphasize the gnathological aspects of prosthetic rehabilitation. They draw attention to the maintenance therapy of patients suffering from masticatory organ dysfunction.

Estimating the Nosocomial Transmission Rate of COVID-19 in Orthopaedic Surgery Patients During the Peak of the Pandemic.

Purpose: To estimate the risk of hospital-acquired COVID-19 transmission in a population of orthopaedic trauma patients during the first wave of the pandemic. Patients and Methods: This is a retrospective cohort study of 109 patients who underwent an emergent orthopedic procedure by a single orthopedic traumatologist between March 1, 2020 and May 15, 2020 during the first peak of the pandemic. After applying inclusion and exclusion criteria, a total of 82 patients (67 inpatients and 15 ambulatory) were identified for final analysis. The primary outcome measured was postoperative Coronavirus (COVID-19) status. Secondary outcome measures included length of stay and discharge disposition. Results: The mean age and length of stay in the hospital group was 59.5 years (± 21.7) and 4.3 days (± 4.6), respectively, versus 47.9 years (± 9.8) in the ambulatory group. 7.3% (6/82) of the inpatients subsequently tested or screened positive for COVID-19 at 2 weeks post-operatively, compared to 0/15 ambulatory patients (P=0.58). Of the 6 inpatients who tested positive, 4 (66.7%) were discharged to a rehabilitation center. Diabetes (P=0.05), hypertension (P=0.02), and congestive heart failure (P=0.005) were associated with transmission. Conclusion: In this analysis, there was a nosocomial transmission rate of 7% compared to zero in the ambulatory surgery center, however this was not found to be statistically significant. This data supports the use of precautions such as frequent screening, hand washing, and masks to reduce transmission when COVID-19 rates are high. There is a lower risk of nosocomial COVID-19 transmission for patients treated as an outpatient and elective surgical procedures may be safer in this setting.

[Diagnosis of masticatory organ dysfunction craniomandibular system dysfunction (CMD)]. / Rágószervi funkciózavarok diagnosztikája--craniomandibularis rendszer dysfunctiója (CMD).

A practising dentist often meets pains of different location and limited ability of mouth opening, locomotor disorder, the cause of which is difficult to identify and explain. There is a particular group of patients with functional disorder who turn to several doctors with their varied and colorful symptoms. Most of these patients suffer from cranio-mandibular disfunction (CMD). You must not indicate any treatment especially not an invasive one without a diagnosis. While relieving the patient's pains, you have to determine the cause and effect. The authors suggest discussing the issue of giving a unanimous definition of masticatory organ disfunction as an interdisciplinary diagnosis which is in accord with international bibliography. They review the algorithm of diagnosis, indication of medical examination by demonstrating some typical cases. They share their experience gained during several decades of clinical practise involving about 2,000 patients.

Inhibition of p70 ribosomal S6 kinase 1 (S6K1) by PF-4708671 decreased infarct size in early cerebral ischemia-reperfusion with decreased BBB permeability.

It is not clear whether inhibition of p70 ribosomal S6 kinase 1 (S6K1) is neuroprotective in cerebral ischemia-reperfusion. Decreasing blood-brain barrier (BBB) disruption has been associated with a better neuronal outcome in cerebral ischemia. We hypothesized that inhibition of S6K1 would decrease BBB disruption and infarct size in the early stage of cerebral ischemia-reperfusion. Middle cerebral artery occlusion (MCAO) was performed in rats under isoflurane anesthesia with controlled ventilation. 75 mg/kg of PF-4708671, an S6K1 inhibitor, was administered intraperitoneally 15 min after MCAO. After 1 h of MCAO and 2 h of reperfusion, the transfer coefficient (Ki) of 14C-α-aminoisobutyric acid and the volume of 3H-dextran distribution were determined to assess the degree of BBB disruption. At the same time point, phosphorylated Rictor (pT1135) and the infarct size were measured to evaluate S6K1 activity. In the PF-4708671 treated rats, the Ki of the ischemic-reperfused cortex was lower than the untreated rats (-22%, P < 0.05) and the volume of dextran distribution was significantly lower in most brain regions. With PF-4708671, a significant decrease in pT1135 Rictor was observed and the percentage of cortical infarct out of total cortical area was decreased (11.6 ±â€¯2.0% vs 7.2 ±â€¯1.1%, P < 0.0001). Our data demonstrate that PF-4708671 decreased the size of the cortical infarct in the ischemic-reperfused cortex with a decrease in BBB disruption suggesting that inhibition of S6K1 may induce neuronal survival in early cerebral ischemia-reperfusion and that a decrease of BBB disruption could be one of the contributing factors.

Effectiveness of P6 Stimulation for Reduction of Nausea and Vomiting During Caesarean Section Under Combined Spinal-Epidural Anaesthesia: A Randomised Controlled Trial.

OBJECTIVE: Obstetric patients who receive combined spinal-epidural (CSE) anaesthesia for elective caesarean section (CS) frequently experience intraoperative nausea and vomiting (N&V). Prophylactic therapy with antiemetic agents can have multiple adverse effects to the mother and baby. We designed a randomised clinical trial to evaluate the efficacy of electrical P6 stimulation for prophylactic N&V treatment for scheduled elective CS performed under CSE anaesthesia. METHODS: Following the Institutional Review Board approval and informed consent, a total of 180 patients were randomly allocated into three groups: (1) P6 stimulation (via a peripheral nerve stimulator), (2) intravenous (IV) antiemetics (metoclopramide and ondansetron), and (3) control (no IV antiemetic medications and no P6 stimulation), with 60 parturients in each group. RESULTS: Significantly fewer patients experienced intraoperative N&V in the P6 group (nausea 36.7% and vomiting 13.3%) and IV antiemetic group (nausea 23.3% and vomiting 16.7%) than those in the control group (nausea 73.3% and vomiting 45%; p<0.001). In addition, significantly fewer patients required rescue antiemetic medications in the P6 group (35%) and the IV antiemetic group (31.7%) than those in the control group (73.3%; p<0.001). There was no significant difference in the overall anaesthetic care satisfaction reported between the three study groups. CONCLUSION: Our data suggest that P6 stimulation is as simple and as effective as our routine prophylactic IV antiemetic treatment for prevention of N&V during CS performed under CSE anaesthesia that could be of great interest to patients and obstetric anaesthesiologists who prefer treatments with fewer potential side effects.

Sphenopalatine Ganglion Block Successfully Treats Migraines in a Type 1 Arnold Chiari Malformation Pregnant Patient: A Case Report.

A 32-year-old woman at 36 weeks gestation with a medical history of corrected Type 1 Arnold Chiari malformation presented with an intractable headache. When methylprednisolone and morphine treatment provided no relief, we performed 2 topical transnasal sphenopalatine ganglion blocks by applying 4% lidocaine drops into each nostril via a cotton-tipped applicator. The patient's symptoms significantly improved, and she was discharged home the same day. She has been without relapse of headaches during the 6 months of follow-up by our pain service.

Spinal Cord Neuromodulation Therapy for Levofloxacin-Reinduced Complex Regional Pain Syndrome and Neurotoxicity: A Case Report.

Fluoroquinolones are a class of popular outpatient antimicrobial agents with a wide spectrum of therapeutic indications for respiratory and genitourinary infections. Though the most common side effects are gastrointestinal, fluoroquinolones have been increasingly associated with neurotoxicity including peripheral neuropathy and seizures. We present here a case of a 43-year-old woman with previously resolved type I complex regional pain syndrome (CRPS) who presented with symptoms of CRPS and neurotoxicity in the setting of levofloxacin administration. Our aim is to advocate for increased caution in prescribing to patients with a history of neuropathology including CRPS.

Topical Sphenopalatine Ganglion Block Compared With Epidural Blood Patch for Postdural Puncture Headache Management in Postpartum Patients: A Retrospective Review.

BACKGROUND AND OBJECTIVES: Postdural puncture headache (PDPH) is a severe and debilitating complication of unintentional dural puncture. The criterion-standard treatment for PDPH has been epidural blood patch (EBP), but it is an invasive intervention with the potential for severe complications, such as meningitis and paralysis. We believe this is the first ever 17-year retrospective chart review in which we compare the effectiveness of sphenopalatine ganglion block (SPGB) to EBP for PDPH treatment in postpartum patients. METHODS: We conducted a chart review of the first authors' obstetric patients who experienced PDPH from an unintentional dural puncture from a 17-gauge Tuohy needle for labor epidural from January 1997 to July 2014. Demographic characteristics, headache severity, and associated symptoms were collected prior to treatment. Forty-two patients who received SPGB and 39 patients who received EBP were identified. Residual headache, recovery from associated symptoms, and new treatment complications were compared between the 2 groups at 30 minutes, 1 hour, 24 hours, 48 hours, and 1 week posttreatment. RESULTS: A greater number of patients showed significant relief in their PDPH and associated symptoms at 30 and 60 minutes after treatment with SPGB than after treatment with EBP (P < 0.01). Only the EBP patients complained of posttreatment complications, which all resolved in 48 hours. CONCLUSIONS: A greater number of patients experienced a quicker onset of headache relief, without any new complications, from treatment with SPGB versus EBP. We believe that SPGB is a safe, inexpensive, and well-tolerated treatment. We hope that clinical trials will be conducted in the future that will confirm our findings and allow us to recommend SPGB for PDPH treatment prior to offering patients EBP.

Akt activation improves microregional oxygen supply/consumption balance after cerebral ischemia-reperfusion.

There have been reports that activation of Akt may provide neuroprotection after cerebral ischemia-reperfusion. We tested the hypothesis that activation of Akt would decrease infarct size and improve microregional O2 supply/consumption balance after cerebral ischemia-reperfusion. This hypothesis was tested in isoflurane-anesthetized rats with middle cerebral artery blockade for 1 h and reperfusion for 2 h with or without SC-79 (Akt activator, 0.05 mg/kg, three doses). Regional cerebral blood flow was determined using a C14-iodoantipyrine autoradiographic technique. Regional small vessel (20-60 µm diameter) arterial and venous oxygen saturations were determined microspectrophotometrically. Akt phosphorylation was determined by Western blot. There were no significant hemodynamic or blood gas differences between groups. The control ischemic-reperfused cortex had a similar O2 consumption, but lower blood flow and higher O2 extraction compared to the contralateral cortex. However, microregional O2 supply/consumption balance was significantly reduced in the ischemic-reperfused cortex with many areas of low O2 saturation (42 of 80 veins with O2 saturation below 50%). SC-79 did not significantly affect cerebral O2 consumption, but significantly improved O2 supply/consumption balance in the reperfused area (18 of 80 veins with O2 saturation below 50%). This was associated with a reduced cortical infarct size (13.3 ±â€¯0.5% control vs 6.7 ±â€¯0.3% SC-79). In control, Akt phosphorylation was elevated at 2 h after ischemia. With SC-79, Akt was activated at 15 min but not at 2 h in the ischemic reperfused area. These results suggest that early Akt activation is important for not only cell survival, but also for the control of local oxygen balance after cerebral ischemia-reperfusion.

Activation of Akt by SC79 decreased cerebral infarct in early cerebral ischemia-reperfusion despite increased BBB disruption.

Activation of Akt has been suggested to produce neuronal protection in cerebral ischemia. Decreasing blood-brain barrier (BBB) disruption has been associated with a better neuronal outcome in cerebral ischemia. We hypothesized that activation of Akt would decrease BBB disruption and contribute to decreasing the size of infarct in the early stage of cerebral ischemia-reperfusion within the therapeutic window. Transient middle cerebral artery occlusion (MCAO) was performed in rats under isoflurane anesthesia with controlled ventilation. Rats were treated with SC79 (a selective Akt activator which is cell and BBB permeable) 0.05 mg/kg × 3 i.p. or vehicle i.p. perioperatively. After one hour of MCAO and two hours of reperfusion, the transfer coefficient (Ki) of 14C-α-aminoisobutyric acid (14C-AIB, molecular weight 104 Da) and the volume of 3H-dextran (molecular weight 70,000 Da) distribution were determined to measure the degree of BBB disruption. At the same time point, the size of infarction was determined using tetrazolium staining. In an additional group of rats, a higher dose of SC79 (0.5 mg/kg × 3) was administered to determine the size of infarct. Administration of SC79 increased the Ki in the ischemic-reperfused cortex (IR-C, +32%, p < 0.05) as well as in the contralateral cortex (CC, +35%, p < 0.05) when compared with the untreated animals with MCAO/reperfusion. The volume of dextran distribution was not significantly changed by SC79. SC79 treatment significantly produced a decrease in the percentage of cortical infarct out of total cortical area (12.7 ±â€¯1.7% vs 6.9 ±â€¯0.9%, p < 0.001). Increasing the dose of SC79 by ten times did not significantly affect the size of cortical infarct. Contrary to our hypothesis, our data demonstrated that SC79 decreased the size of the infarct in the ischemic-reperfused cortex despite an increase in BBB disruption. Our data suggest the importance of activation of Akt for neuronal survival in the early stage of cerebral ischemia-reperfusion within the therapeutic window and that the mechanism of neuroprotection may not be related to the BBB effects of SC79.

An Unusual Cause of Failure to Ventilate.

We report an unusual case of endotracheal tube failure. It was due to a manufacturing defect in the internal white plastic piece that is normally depressed by the luer-lock syringe within the blue pilot balloon. Prior to use, the endotracheal tube was tested and functioned normally. A 64-year-old patient in the intensive care unit with a history of hypertension was being mechanically ventilated after uneventful abdominal surgery. After several hours in the intensive care unit, he was noted to be suddenly no longer receiving adequate tidal volumes from the ventilator. It was found that the cuff on the endotracheal tube was not retaining air when it was filled with air from a syringe. This lead to a large "leak" around the endotracheal tube such that the intended tidal volumes set on the ventilator were not delivered to the patient. The patient was uneventfully reintubated and did well. Subsequent investigation revealed the cause to be a manufacturing defect in the internal white plastic piece that is normally depressed by the luer-lock syringe within the blue pilot balloon. Other mechanisms of cuff failure are reviewed in this case report. This case is an unusual reason for cuff failure. Illustrations supplied alert the reader how to identify the appearance of this manufacturing defect in a pilot balloon. This case illustrates the potential device malfunctions that can develop during a procedure, even when the equipment has been tested and previously functioned well. Even small defects developing in well-engineered products can lead to critical patient care emergencies.

Near-fatal kinking of mammary graft due to emphysematous lung disease.

Left internal mammary artery grafting is commonly used in elective coronary artery bypass graft surgery. We report a near-fatal case with graft kinking upon sternal closure due to distended, emphysematous lungs impinging on the mammary graft. After the sternum was closed, the patient suffered a severe hemodynamic deterioration. Surgical examination revealed kinking of his left internal mammary artery upon sternal closure due to distended, emphysematous lungs impinging on the mammary graft. Using an off-bypass technique, the kink in the mammary graft to the left anterior descending artery was removed by moving the origin of the left internal mammary artery to a hooded graft of a saphenous vein graft instead. In this position, the graft no longer was impinged upon by the distended emphysematous lungs. Subsequently, the patient's sternum was closed without hemodynamic impingement. Although chronic obstructive pulmonary disease is well described to increase complications in coronary artery bypass graft surgery, it has not been previously associated with the kinking of a left internal mammary artery. This report highlights another contribution that chronic obstructive pulmonary disease can make to increased morbidity following coronary artery bypass graft surgery and alerts readers to watch for this complication in susceptible patients.

Varicella Pneumonia: Case Report and Review of a Potentially Lethal Complication of a Common Disease.

Varicella zoster virus causes varicella (chickenpox). It can be reactivated endogenously many years later to cause herpes zoster (shingles). Although varicella is usually a benign disease in healthy children, it resulted in over 11 000 hospitalizations and over 100 deaths every year, in all ages, in the United States. Morbidity was considerably worse in older teenagers and adults. Between 5% and 15% of cases of adult chickenpox will produce some form of pulmonary illness. Progression to pneumonia risk factors include pregnancy, age, smoking, chronic obstructive pulmonary disease, and immunosuppression. Typically, pulmonary symptoms occur 1 to 6 days after varicella zoster infection. They often include cough, fever, and dyspnea. Treatment is a 7-day course of intravenous acyclovir for varicella pneumonia. Early intervention may modify the course of this complication. This review illustrates practical features with a case of a 34-year-old female with severe varicella pneumonia. Despite the lack of significant past medical history and absence of immunosuppression, her pneumonia worsened and by using continuous positive airway pressure mask, intubation was avoided. More important, the radiographic progression of severe varicella pneumonia is shown. This highlights how a common disease of varicella can progress in an adult and manifest with significant organ malfunction.

[Determination and practical application of articulator related individual functional parameters. New method of measurement: virtual articulator and face-bow]. / Artikulátorra vonatkoztatott egyéni funkciós ertékek meghatározása es gyakorlati alkalmazása. Uj módszer: virtuális artikulátor es arcív.

The aim of each occlusal surface reconstruction is to take the functionally developed biomorphologic aspects into consideration while restoring occlusal conditions. In order to fulfil these conditions, it is necessary to represent individual mandible movement as accurately as possible. In addition to physiological knowledge, it is indispensable for us to be able to simulate spatial mandible movement and determine individual parameters in an utmost precise way. By correcting projecting mistakes, the articulator should reproduce static and dynamic occlusal conditions according to reality. This is a difficult task. The advance of technology, spreading of computers and the idea of 'virtual articulator' have all helped to fulfil all these conditions by quick digital data processing instead of complicated and slow mechanical gadgets. The aim of our publication is to present the programming possibilities of the articulator of individual value belonging to the system and the advantages of the method.

Blood -brain barrier disruption was less under isoflurane than pentobarbital anesthesia via a PI3K/Akt pathway in early cerebral ischemia.

One of the important factors altering the degree of blood-brain barrier (BBB) disruption in cerebral ischemia is the anesthetic used. The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway has been reported to be involved in modulating BBB permeability and in isoflurane induced neuroprotection. This study was performed to compare the degree of BBB disruption in focal cerebral ischemia under isoflurane vs pentobarbital anesthesia and to determine whether inhibition of PI3K/Akt would affect the disruption in the early stage of focal cerebral ischemia. Permanent middle cerebral artery (MCA) occlusion was performed in rats under 1.4% isoflurane or pentobarbital (50mg/kg i.p.) anesthesia with controlled ventilation. In half of each group LY294002, which is a PI3K/Akt inhibitor, was applied on the ischemic cortex immediately after MCA occlusion. After one hour of MCA occlusion, the transfer coefficient (Ki) of 14C-α-aminoisobutyric acid (14C-AIB) was determined to quantify the degree of BBB disruption. MCA occlusion increased the Ki both in the isoflurane and pentobarbital anesthetized rats. However, the value of Ki was lower under isoflurane (11.5±6.0µL/g/min) than under pentobarbital (18.3±7.1µL/g/min) anesthesia. The Ki of the contralateral cortex of the pentobarbital group was higher (+74%) than that of the isoflurane group. Application of LY294002 on the ischemic cortex increased the Ki (+99%) only in the isoflurane group. The degree of BBB disruption by MCA occlusion was significantly lower under isoflurane than pentobarbital anesthesia in the early stage of cerebral ischemia. Our data demonstrated the importance of choice of anesthetics and suggest that PI3K/Akt signaling pathway plays a significant role in altering BBB disruption in cerebral ischemia during isoflurane but not during pentobarbital anesthesia.