| 41. Stewart AG, Fernandes DJ, Tomlinson PR. The effect of glucocorticoids on proliferative of human cultured airway smooth muscle. Br J Pharmacol 1995; 116: 32193226.
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Please remember that all benefits are subject to the definitions, limitations, and exclusions in this brochure and are payable only when we determine they are medically necessary Plan dentists must provide or arrange your care. We have no deductible We cover hospitalization for dental procedures only when a non-dental physical impairment exists which makes hospitalization necessary to safeguard the health of the patient. See Section 5 c ; for inpatient hospital benefits. We do not cover the dental procedure unless it is described below. Be sure to read Section 4, Your costs for covered services, for valuable information about how cost sharing works. Also read Section 9 about coordinating benefits with other coverage, including with Medicare.
Medicaid Program Instruction MA-03-61 December 9, 2003 TO: FROM: SUBJECT: MANUALS Targeted Case Management For Mental Illness, Developmental Disabilities and Substance Abuse -1995 Revised, Behavioral Health Clinic Services -May 1, 1999 Revised, Behavioral Health Rehabilitation Services - May 1, 1999 Revised, APS Healthcare Utilization Management Guidelines - Version 2.0. PURPOSE The purpose of this Program Instruction is to disseminate national procedures codes that are replacing previous state procedure codes, and to provide a crosswalk that will assist in their replacement. BACKGROUND The Health Insurance Portability and Accountability Act of 1996 HIPAA ; requires that all state-specific health care service codes be converted to national codes. The Bureau for Medical Services has been involved in national efforts to implement these changes. POLICY PROVISION All of the changes defined in the attached chart become effective February 1, 2004. Existing state procedure codes can be used through January 31, 2004, but will not be accepted on or after February 1, 2004. The attached chart is a crosswalk that lists the current state service code and what it pays per unit of service, the name of the code, the national code that is its replacement, required modifiers where appropriate, the units definition, the applicable service limits, the rate per unit, and prior approval requirements and service descriptions. West Virginia Medicaid Program Participating Providers: Behavioral Health Clinic and Rehabilitation Providers Nancy V. Atkins, MSN, RNC, NP Commissioner National Procedure Codes for Behavioral Health Services, for instance, diazepam philippine valium.
CASE V. A 25-year-old man with lymphoblastic leukemia in nomission had been treated in the past with CNS irradiation and intrathecal methotrexate for meningeal leukemia. Two weeks before CT study, he had two seizures which began with focal motor activity involving the left extremities and generalized to grand mal. With Dilantin medication, he had no further seizures until 30 minutes after the intravenous contrast injection when a seizure occurred with focal motor activity involving the left extremities generalizing to grand mal. Because grand mal activity continued intermittently over 5 minutes, he was treated with intravenous diazepam with prompt control. CT scan showed right parietal, pons and midbrain low density lesions with no mass effect or abnormal enhancement. He died 22 days later after rapidly progressive pontine dysfunction. Pathology was that of necrosis of the pons and cerebral.
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The medical examination included a medical history, some behavioral and biological risk factors for cardiovascular disease CVD ; Leparski and N ssel, 1987 ; and an evaluation of u clinical neurological status. A dental amalgam score was calculated with the methodology proposed by Aposhian et al., 1992 ; . The examination also included blood and urine sampling for determination of: 1 ; total blood mercury B-THg ; and urine mercury U.
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High potency antipsychotic drugs are considered to be preferable as they lessen the risk of hypotension. The combination of an antipsychotic and a benzodiazepine is desirable to avoid very high antipsychotic doses when the immediate aim is sedation. Lorazepam is well absorbed via the IM route and because of its short half-life does not accumulate; it is not dependent on the liver for metabolism. Diazwpam is long-acting and may be useful, but multiple dosing can lead to toxic accumulation, delirium and respiratory depression and dilantin.
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These include baclofen, diazepam, tizanidine and dantrolene sodium. Baclofen is commonly used in a starting dose of 1.25-2.5 mg BD orally and increased gradually upto a maximum of 3060 mg day. It is not recommended for children with seizures as it may provoke them. Diazepamm is another useful drug but excessive drowsiness that it may cause, limits its use. Recently Botulinum-A toxin BAT ; has been found to be a useful antispasticity agent. Intramuscular injections of BAT into the muscles affected by spasticity produces relaxation of the involved muscles and improves the functional status of the involved and diovan.
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Artery bypass grafting performed 10 years earlier, familial type II hyperlipidemia, angina, fibromyalgia, and osteoporosis. She also had a family history of coronary artery disease. At the time of presentation, she was taking multiple medications, including valsartan Diovan, 80 mg d ; , metoprolol succinate Toprol XL, 50 mg d ; , atorvastatin Lipitor, 40 mg d ; , ezetimibe Zetia, 10 mg d ; , clopidogrel Plavix, 75 mg d ; , aspirin 81 mg d ; , folic acid 800 g d ; , bumetanide 1 mg d ; , diazepam 1000 mg d ; , and calcium with vitamins daily. Initial laboratory tests included a complete blood cell count, blood chemistry panel, lipid panel, coagulation studies, and determination of antinuclear, antiphospholipid, and anticardiolipin antibody levels. Except for a mild increase in the leu.
A simple way to test the effectiveness of your exercise program is to find out how well it is training your heart. This is done by measuring your recovery pulse -- how much your pulse slows down in one minute after you stop exercising. A quick recovery signifies a strong heart. The stronger the heart, the more quickly it recovers from stress and the less frequently it must beat. If you are reasonably fit, you can test yourself periodically to chart your improvement. Work out as hard as you can for five minutes. Stop and immediately place one or two fingers at the side of your neck where you can feel a strong pulse. Count your pulse for six seconds, then multiply that number by 10. It is important to count for only six seconds, since your heart rate decreases very quickly once you stop exercising. Exactly one minute later, take your pulse again in the same way. Then subtract the second pulse rate from the first. The difference between the two rates is your Recovery Pulse Index. You are in good shape if the second count is at least 30 beats lower than the first, and you should be able to increase the difference as your heart gets stronger. If you think that your slow heart rate is a measure of fitness, you could be wrong. Your recovery heart rate is a far more dependable indicator. A study in Medicine and Science in Sports and Exercise July 1996 ; shows that a 20-week program of endurance training does not slow the resting heart rate, and therefore cannot be use as a measure of fitness. Hard exercise cannot hurt a healthy heart, but it can cause irregular heart beats in people who have damaged hearts and evista.
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Treatment monitoring and prognosis assessments are the two most common clinical applications for PSA determinations in men treated for prostate cancer. Local treatments include radical prostatectomy RP ; , various methods of delivery for radiation treatment RT ; and cryosurgery, whereas systemic treatments include androgen deprivation therapy ADT ; , and cytotoxic chemotherapy. Post-treatment PSA levels can provide invaluable information about the effectiveness of the therapy given and the existence of residual cancer in men treated with RP or cryosurgery. In such patients, rising PSA levels can signal cancer activity well before any clinical signs of recurrence appear. This lead-time can be further increased by months and even years when highly sensitive third-generation PSA assays are employed. In the and flomax.
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Chapter 15 1. Moseley JB, O'Malley K, Petersen NJ, et al. A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2002; 347 2 ; : 81-88. 2. Small NC. Complications in arthroscopic surgery performed by experienced arthroscopists. Arthroscopy. 1988; 4 3 ; : 215221. 3. Collins JJ. Knee-joint arthroscopy--early complications. Med J Aust. 1989; 150 12 ; : 702-703. 4. National Coverage Determination NCD ; for arthroscopic lavage and arthroscopic debridement for the osteoarthritic knee. Medicare Coverage Database. CMS Pub. No. 100-3, Sec. 150.9. : cms.hhs.gov medlearn matters mmarticles 2004 MM3281 . Baltimore, MD: Center for Medicare and Medicaid Services CMS ; . June 11, 2004. 5. Pagnano MW, Clarke HD, Jacofsky DJ, Amendola A, Repicci JA. Surgical treatment of the middle-aged patient with arthritic knees. Instr Course Lect. 2005; 54: 251-259. Fond J, Rodin D, Ahmad S, Nirschl R. Arthroscopic debridement for the treatment of osteoarthritis of the knee: 2and 5-year results. Arthroscopy. 2002; 18 8 ; : 829-834. 7. Day R, Brooks P, Conaghan PG, Petersen M. A double blind, randomized, multicenter, parallel group study of the effectiveness and tolerance of intraarticular hyaluronan in osteoarthritis of the knee. J Rheumatol. 2004; 31 4 ; : 775-782. 8. Lowry V. Novel Remedies for the Aching Knees of Summer. New York Times. : nytimes 2004 06 29 health nutrition 29knee. html?pagewanted all&position . June 29, 2004. 9. Kolata G. Healing a Bad Back Is Often an Effort in Painful Futility. New York Times. : nytimes 2004 02 09 national 09BACK ? pagewanted all&position . February 9, 2004. 10. Assendelft WJ, Morton SC, Yu E, Suttorp MJ, Shekelle PG. Spinal manipulative therapy for low back pain. Cochrane Database Syst Rev. 2004; 1 ; : CD000447 and flonase.
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Volve dental therapeutic agents but occur in circumstances that are not common to dental practice. For example, a drug interaction reported after the intravenous infusion of lidocaine for treatment of cardiac arrythmias in a coronary care unit involves high blood concentration steadystate kinetics of lidocaine that is not seen after lidocaine's use for dental anesthesia. We have attempted to rate-- on the basis of quality of documentation--the reactions we will discuss in this series as established, probable, suspected, possible or unlikely.21 Additionally, because of the importance of a reaction's potential severity, three degrees of severity major, moderate and minor ; are included in the classification. The table provides definitions for both of these ratings as well as a composite score: Significance Ratings for Dental Drug Interactions. This rating.
DRUG NAME PA QLL 5.1.1 ANALGESICS $ tramadol hcl $ tramadol hcl-acetaminophen 5.1.1.1 CLASS II NARCOTICS $ fentanyl $ hydromorphone hcl $ meperidine hcl $ morphine sulfate $ oxycodone apap, -hcl $ oxycodone w acetaminophen $$ MSIR $$ OXYIR $$$$$ MS CONTIN !!!!! AVINZA !!!!! KADIAN !!!!! OXYCONTIN QLL 5.1.1.2 CLASS III NARCOTICS $ acetaminophen w codeine $ acetaminophen w hydrocodone $ hydrocodone bit-ibuprofen 5.1.1.3 CLASS IV NARCOTICS $ propoxyphene hcl $ propoxyphene hcl w acetaminophen $ propoxyphene napsylate w acetaminophen 5.1.2 DRUGS TO PREVENT AND TREAT HEADACHES $ butalbital compound $ butalbital acetaminophen caffeine $$$$ RELPAX QLL $$$$ ZOMIG, -NS, -ZMT QLL $$$$$ AXERT QLL QLL $$$$$ FROVA $$$$$ IMITREX, - INJ ; QLL $$$$$ MAXALT, -MLT QLL AMERGE QLL !!!!! 5.2.1 ANXIOLYTICS $ alprazolam $ buspirone hcl $ chlordiazepoxide hcl $ clorazepate dipotassium $ diazepam $ lorazepam 5.2.2 SEDATIVE HYPNOTIC DRUGS $ flurazepam hcl $ temazepam $ triazolam $$$ ROZEREM $$$$ AMBIEN, -PAK QLL $$$$ LUNESTA QLL $$$$ RESTORIL $$$$ SONATA QLL 5.3 ANTIMANIA DRUGS $ lithium carbonate $ lithium citrate 5.4.1 CARBAMAZEPINES $ carbamazepine.
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Medical Care in Turner Syndrome: USA: 2000-2004. Eileen D Lange * 1, Bakalov K Vladimir1, Carolyn A Bondy1. 1Devel Endocrinol Br, NICHD, NIH, Bethesda, MD. Purpose of Study: To assess adherence to current medical recommendations for individuals with Turner Syndrome TS ; in the United States. Background: TS is due to complete or partial monosomy for the X chromosome and affects 1 2500 live female births. Current medical recommendations for the care of women with TS include: renal and cardiac ultrasounds US ; and audiological evaluation at diagnosis with repeat cardiac and audiological evaluations at 5 year intervals, or more often if clinically indicated.1 Methods: 120 women 19-60 years ; and 46 girls 8-18 years ; enrolled in an NIH natural history study were surveyed about past medical history of renal and cardiac imaging and audiological testing. Requirements for enrolling in the study included the prior, karyotype-based diagnosis of TS with 70% of cells 45, X. Results: Among adults with TS, we found that only 50% of these women ever had a renal US, 65% ever had a cardiac US, and 80% ever had audiology testing. Of those who had a least one prior cardiac US, only 38% had been studied within 5 years, and of those who had prior audiological testing, 43% had been retested within 5 years. These data are summarized in the Table. The minimum age of this group was 19 years, the maximum age was 60 years old and the mean age was 36.6 years.[table1]In the pediatric population, we found that 80% 37 46 ; had a renal ultrasound, 85% 39 46 ; had a cardiac US, and 85% 39 46 ; had audiology testing. The pediatric age range was 8 18 years and the mean age was 13.5 years. Summary: These findings demonstrate that 35% of women and 15% of children with a clear diagnosis of TS have never had cardiac evaluation; 20% of adults and 15% of girls have never had audiological testing. The rate of follow-up testing for heart and hearing among adults was only 50%. These observations show a serious gap between actual practice and current guidelines for the care of women with TS in the United States. Implications: The results indicate the need for greater education of healthcare providers regarding the standards of medical care for girls and women with TS. 1. Saenger P, Wikland KA, Conway GS, et al.: Recommendations for the diagnosis and management of Turner syndrome. J Clin Endocrinol Metab 2001; 86 7 ; : 3061-9. Supported by NICHD DIR CLINICAL - Endocrine Nursing: Progress in Patient Care 6: 30 - 8: Presentation Date: 6 4 2005 Time: 12: 00: 00 Location: Ballroom C and diflucan.
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Hormone proponents had previously attempted to neutralize HERS by arguing that the arteries of women with cardiac disease were too damaged to respond to estrogen. This argument led to the recommendation to start hormones during the years prior to cardiac compromise, early in menopause. The WHI, a primary prevention trial, was designed to assess the effect of treatPerspectives in Biology and Medicine.
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Table 2. Seizure duration and need for restimulation Audit 1 Audit 2 n 165 n 169 No need for restimulation 16 seconds or more ; Need for restimulation 15 seconds or less ; 130 35 148 seizure threshold, this might be expected to increase the rates of brief seizures. TCA use has diminished, as reported in an earlier audit Tresize, 1998 ; , but the effects of TCAs and selective serotonin reuptake inhibitors, which both reduce the seizure threshold, are complex and probably vary between members of each drug group Royal College of Psychiatrists, 1995 ; . Therefore, the change in prescription of antidepressants may not be relevant. It is noteworthy that benzodiazepine use has not changed. The clinic updated its machine to the Ectron Series 5A after audit one. This allowed greater dosing flexibility, with an output range of 25-700 mC compared with the older machine which had a maximum output of 400 mC. It is interesting that in audit one, 34 of the brief seizures occurred in one patient, a 65-year-old female on a low dose of diazepam, despite using 400 mC in most of the treatments. In audit two, 19% of the brief seizures occurred in one patient, a 51-year-old male who required diiazepam in very high doses. He received increasing doses up to 700 mC ; with a concomitant increase in seizure duration. He would probably have had much shorter seizures with the older, less powerful machine. It is also possible that improved operator training had an effect, particularly the greater recognition of the importance of increasing the dose throughout a course of ECT if seizure duration decreases Robertson et al, 1995; Royal College of Psychiatrists, 1995 ; . Improved documentation and communication between the ECT clinic and ward teams facilitated dose increases. The second major finding is the disappointingly low `success' rate of restimulation. Trainees followed guidelines in the event of a brief seizure more often in audit two but the induction of an adequate seizure only occurred in 25% of cases. Many factors might contribute to this but it may be that the patient is restimulated too quickly without allowing the raised, post-ECT seizure threshold to drop. In a study of multiple ECT in open session, the period between stimulations was 3 minutes Roemer et al, 1990 ; , a much longer period than that used in routine practice.
The concomitant use of LOIOFTand alcchol in depressed pccr, ts u at advised. Patientsshould be told that while no adverse ntactiOfl of 1OhOFTwith cc rheo, nter 10Th drug products is known to Occur, the potenhal for interaction exists. Thus, the oseof any OT prodoc she'd ha noted rc'csly crcn'&ng to the direobonn of use given for the OTCproduct. Pahentsshould be cd d chfy cr phjo u.c : f hey buome p'eg": t or intend to becomepnegnantduring shercpy. Patren should be adviced tu onfy hu.r ph, f c, -e h'eaofeedng en : nfcrt Loboratory Tests: None. Drug letiractions: Potential Effects of Coadministration of Drugs Highly Round to Plasma Proteins - Beccusesertnc!ioeis tightly buond to piusiric prore-- he dnrstr n- of ZOLOFTrct'c'-e dorhlo. tide ; to a paherl taking coother drug which is nightly bund to roreiu e.g., vto r `oAr .cy uci C O f iOO' centrations petentiolly resulting in an cdverse effect. Cco.eruu!, deroe uffu.o ru, ust f-o dopocerrent a' protern-hound 7010Ff by other tightly bound drugs. In a study comparing prothrombn toe 0U 0 120 hi ; fsllawng doting with warfcrin 10.75 mg kgl before and after 21 days of dosingwith either ?OIOFT 50-200 ng, doyl or placebo, there was a mean increase in pnothsombintime of 8# to baseline far 1OhOFT relahve compcredto a 1: decreosefor placebo lp'-O.02 ; Thenormalization of prothrombin Omefor the ZOLOFT group was delayed comparedto the placebo group. Theolnual srgnifiocnoeof this change is unknown. Accordingly, prethrombintime shouldbe carefullymonitored when 1OIOFTtherapy o otiared or stopped Cimetidiee In c sxudyassessingdisposition af 1OhOFT 100 mgI on the scusrd of 8 dcyu o' rmudmno cdutrction `ff00 mg doi!yl. them were increasesin ZOIOFTmecn AUT ISO' ; , mux 124' and hcf!fe 26 compeed to he placebogroup ThenIrool sig'nfiaanceof these changes is unknown. CNS Active Dregs - in c study cr-pang re d opos'cn of inrrcwccoly administered diazepam before and oftet 21 days of dosing with either 1OLOFT150 to 200 mg day ersolcrng dssel cr plccebe, there wooa 32# c decreaserelative to baseline in diazepcm cleorcncefor the ZOLOFT group corpoed o o 19 decreasere1ctiveto bcseline fox the placebo group p OO3l Therewas a 23# ircreoue in Trnroe des-rrerhyldczepc' in the 7OIOFTgroup comparedto a for 20ci decreasein the placebogroup p0.03 ; . Theo.iosi ugnificcr a cf husu uugu: u kn; un. In c ptnrcbscout'nlled in normal volunteers, the odmnstnction of Fuo dosesof LOhOFTdd nut rr; ifuuntl1 o!tu otcodyrtcra th: un lev&r or tu mnc! clearanceof lithium. Nonetheless, at this time, it is rcuornmendcdthat plasma lith.urr eels be monitored following iritictior; of ZOLOFT therapy with appropriate adjustments to the lithium dose. Therisk of using ZOIOFTin combination with other INS ootive drugs has net been systematically evaluated. Consequently, caution is advised if the concomitant administration of LOLOFT and suchdrugs is required. Thereis limited controlled experienceregarding the optimol Timingof switching from other anridepressanrs to ?OIOFT recod prudent rrrediccljudgment should be euercisedwher uwiruhng, pcrticulorly run longcrng ogerto Thedunion of en appropriate vuuhcr pecod whiuh ulould intervuiu, befuiu sw: tulii.g ru uu ue!uu'e ucr rorake br SSPII to cnattrcr hon not bear eotcbshcd. Dregs Metaboliaed by P450 2D6 - f'a urdepressun e g . SSRls, . inc sennnalinc, mast rnieyolicnhpressonts inhibitthe buhemua uutiviryof the diu retobozng uu: , cod a , ovhrurne P450 2Db Idebnisoqule hydeoeylaoe ; , nd, thus, tray increasethe plaorrraconcentrations curudnroiservd drugs thct crc metobolizedby P450 a of 2D6. ThedtugsfoewhiehthisWteehol interactiveisofgreatest concernore dronemenboli: ed primarilyby 2D6 andwhichhavea narrow therapeuticindex, e.g., the enieyelic anhdepeessonts endthe Theextent to which this intenoehee animpvntantclinicalpeoblem is dependson theeetenrof the irihbbo of P450 206 by tc crhdeprcsocnt and ftc thercpeuhc index of the ooodmnistereddrug. Thereis vorobilty amuirgthe uiitideprussunrs the cvtvnt of duaI!y impcrtort 2D6 inhibition, cod iii in foetsereralineat lowerdoseshasa lessprominentinhibitoryvffet on 206 boo cornru orfie's in fcc class. 5ucrtheIess, evenoertroline has the peeenhalfor clinically important 2D6 inhibihon. Consequently, conuuin'ort se of o drug meralized by P450 2D6 with LOIOFT may require lowerdosesthenusuallyprescribed the other drug. Fuinhurnora, whenever1OIOFTiswithdrawnfrom os-themfor Pt, an imxreosed oseof the co-administered moybe required Hype lycemic Dre!s In c plcrebo-enorrolledtriol in normal d dru volunteers, administration of ZOLOFT 22 days ioc!dng 200 n; dc u c for 3 oy .u: ud a u'3turu, ugnif cot 16# . decreasefrom baseline in the clearanceof ohutcmde foiov. ig .r. uccus COCg uuuc LOIDTI udo'strctior did not noticeably changeeither the plasmapmoteobinding or thu cppurcnt volue u' dtr5utir a' olbutorrde, ouggesringthat the d&teaoed clearancewas due Toa change in the metobobsmof he drug. The cli'co signfiocrcc of this decease o rotburomide clearanceis unknown. Ate.alai - 1OIOFT 1100 mgI when cdmnuured to TOh: lry "c'e rber'r hod ro effect on the heroadrenergtoblacking abilityofatenolol. Digoxin - In o plooobu-ooorrol!edrc - nc-nc' o'oee-r, ado'- ru': o' ?OIOFTfo' I 1 days including 200 mg day for the last 10 daysl did not chongeserumdgce cue'; u digcvrn renc iiccrcre. Microsomal Enzyme Induction - Preolincal studies hoou shown Z0[OFT u -o: e epat.u - urn-nrc!ezyTer. In loudi rrudies 1OIOFTwas shown to inducehepatic enzymes minimc7y cc duterrnrinedby a rocl 5 but stotisticclly signifiocnr decreasein anhpyrine halfife following odminisnnananof 200 mg day for 21 dcys. Thissorcil change in cntipyrine half-life reflects a clinically insignificant change in hepahc metabolism. Electroconvulsive Therapy - Therecc on oliniccl studiesesrcblishing the.
Assessing anxiety- and depression-like behaviour in preprodynorphin knockout mice Alexandra Stefanescu The dynorphins are a group of endogenous opioid peptides, together with the enkephalins and the endorphins. They are generally thought to be the major ligands of the Gi-protein coupled -opioid receptors. Recent studies on the dynorphin system implicate its involvement in pharmacologically important states as addiction, chronic pain, fibromyalgia and stress- related behaviours. Previous studies have demonstrated a lack of function of the anxiolytic drug diazepam in mice given -opioid receptor antagonists and this has raised the question of a possible function of the dynophins in anxiety-related behaviours. In this study, mice lacking a functional preprodynorphin gene were compared to wildtype C-57Bl 6J mice in behavioural paradigms such as the open-field, light-dark box test, elevated plus-maze and forced swim test for assessing their locomotor activity and anxiety- and depression-like behaviours. The results obtained show a higher level of anxiety-like behaviours in the knockout mice, while no differences between the groups were observed in the forced swim test. The results of the open-field test showed a slight decrease in locomotor activity of the knockout mice as compared to the wildtypes, which in this case was interpreted as an anxiety-like response to the testing conditions. These results suggest an important function of the preprodynorphin gene products in brain pathways involved in regulation of anxiety. Keywords: preprodynorphin knockout mice; anxiety; depression; locomotor activity.
REM SLEEP DEPRIVATION DISRUPTS PREPULSE INHIBITION OF THE ACOUSTIC STARTLE REFLEX Roberto Frau1, Marco Orr1, Raimondo Spissu1, Monica Puligheddu2, Paola Devoto1, Francesco Marrosu2, Giampaolo Mereu3, Marco Bortolato1, Gian Luigi Gessa1 1 Bernard B. Brodie Department of Neuroscience, University of Cagliari; 2Institute of Cardiovascular and Neurological Sciences, University of Cagliari; 3Bernardo Loddo Department of Experimental Biology, University of Cagliari. Prolonged sleep deprivation SD ; is known to induce perceptual impairments, ranging from perceptual distortion to hallucinatory states. Although the phenomenon has been extensively described in literature, its neurobiological underpinnings are still elusive. Animal research has shown that SD induces a series of behavioral patterns that might be reflective of psychosis and mania, such as hyperlocomotion and sensitization to psychotogenic drugs. Notably, such changes are accompanied by transitory alterations of dopaminergic signaling. Based on the hypothesis that both psychotic and manic disorders are underlain by alterations in sensorymotor gating, the present study was aimed at the assessment of the impact of SD on the behavioral model of prepulse inhibition of the startle PPI ; , a reliable paradigm for the study of informational filtering. Rats subjected to SD 24, 48, 72h ; exhibited a dramatic deficit in PPI in a time-dependent fashion, and recovered PPI 24 hour after termination of the SD period. Interestingly, this alteration was efficiently prevented by haloperidol 0.1 mg kg, i.p. ; clozapine 5 mg kg, i.p. ; and risperidone 1 mg kg, i.p. ; . Furthermore, nicotine 0.10.2 mg kg i.p. ; dose-dependently attenuated PPI disruption. Conversely, neither the anxiolytic diazepam 5 mg kg, i.p. ; nor the antidepressant citalopram 5 mg Kg i.p ; affected the PPI disruption mediated by SD. Our data suggest that SD induces gating deficits that might be relevant to the hallucinatory phenomena observed in humans, and provide a novel reliable animal model where such relationship can be studied. ANTIPSYCHOTIC-LIKE PROPERTIES OF 5-ALPHA-REDUCTASE INHIBITORS Roberto Frau1, Marco Orr1, Monica Puligheddu2, Antonella Tuveri2, Paola Devoto1, Francesco Marrosu2, Giampaolo Mereu3, Gian Luigi Gessa1 1 Bernard B odie Department of Neuroscience, University of Cagliari; 2Institute of Cardiovascular and Neurological Sciences, University of Cagliari; 3Bernardo Loddo Department of Experimental Biology, University of Cagliari. Background: Recent evidence indicates that neuroactive steroids may participate in the pathogenesis of schizophrenia-spectrum disorders, yet the mechanisms of this involvement are elusive. Methods: Since 5-alpha-reductase 5AR ; is the rate-limiting enzyme of one of the two major metabolic pathways in brain steroidogenesis, we investigated the effects of its blockade in several rat models of psychotic-like behavior. Results: The 5AR inhibitor finasteride FIN, 36-100 mg kg, intraperitoneal, i.p. ; dose- and time-dependently antagonized prepulse inhibition PPI ; deficits induced by apomorphine APO, 0.25 mg kg, s.c. ; and d-amphetamine AMPH, 5 mg kg, s.c. ; , but not dizocilpine DIZ, 0.1-1 mg kg, s.c. ; , in a manner analogous to haloperidol HAL, 0.1 mg kg, i.p. ; . Similar results were observed with the other 5AR inhibitors dutasteride DUT, 20-40 mg kg, i.p. ; and SKF 105, 111 30 mg kg, i.p. ; . FIN 60-100 mg kg, i.p. ; also reduced hyperlocomotion induced by AMPH 3 mg kg ; and attenuated stereotyped behaviors induced by APO 0.25 mg kg, s.c. ; . However, unlike HAL 1 mg kg, i.p. ; , FIN 60-100 mg kg, i.p. ; induced no catalepsy in either the bar test or the paw test. Conclusions: Our results suggest that 5AR inhibitors elicit antipsychotic-like effects in animals and may be proposed as a putative novel target in the management of psychotic disorders.
Department of Health Sciences, University of York, York YO10 5DD Simon Coulton senior research fellow Christine Godfrey professor J Martin Bland professor Section of Addictive Behaviour, Division of Mental Health, St George's Hospital Medical School, University of London, London SW17 0RE Colin Drummond professor Department of Clinical Psychology Training, Whitchurch Hospital, Cardiff CF14 7XB Darren James trainee clinical psychologist Centre for Health Economics, Alcuin College, University of York Steve Parrott research fellow Department of Biochemistry, King's College, University of London, London WC2R 2LS Timothy Peters professor Correspondence to: S Coulton sc21 york.ac.
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Benzodiazepines clorazepate, diazepam, estazolam, flurazepam midazolam, triazolam ; toxicity may be increased; concurrent use of midazolam and triazolam is specifically contraindicated.
Scared many physicians away from the field of pain management"; "probably persuaded other physicians not to enter this specialty, thus worsening the already widespread problem of patients being undertreated or untreated for chronic pain." He also found that conclusions drawn by the DEA from these data were "significantly flawed." Among his other major points are: "The DEA's criteria for `OxyContinrelated deaths' are problematic." Fiftyeight analgesic drugs contain oxycodone. Because "there is no chemical test to distinguish OxyContin from other oxycodone drugs, it is difficult to see how the DEA" could positively claim "that a death attributable to oxycodone is due to OxyContin and not other short-acting oxycodone drugs." However, "the DEA counts as an `OxyContin-related death'" any fatality "in which oxycodone was detected without the presence of aspirin or [acetaminophen]." "If an OxyContin tablet is found in the gastrointestinal tract of a deceased person, the DEA labels it an `OxyContinverified death, ' regardless of other circumstances. Even more problematic, if investigators find OxyContin pills or prescriptions at a crime scene, or a family member or witness merely mentions the presence of OxyContin, the death is also confirmed as `OxyContin-verified.'" Victims of overdose often had multiple drugs in their systems. Autopsy reports of OxyContin-related deaths showed: In approximately 40%, diazepam-like drugs were present; In another 40%, a second opiate eg, hydrocodone bitartrate and acetaminophen combination ; plus oxycodone was found; 30% showed an antidepressant such as fluoxetine hydrochloride; 14% had over-the-counter antihistamines or cold medications present; 15% had cocaine present. "Deaths like those could be the result of any of the drugs present, drugs working in combination, or one or more drugs plus effects of other conditions, such as illness or disease." Dr Libby reported that the March 2003 issue of the Journal of Analytical ToxGoldstein Editor's Message!
Accepted for publication September 22, 1998. Address correspondence to Clifford Schmeising, MD, Department of Anesthesia, Stanford University School of Medicine, 300 Pasteur Dr., Stanford, CA 94305. Address e-mail to gerancher stanford.
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