By E. Brenton. Monterey Institute of International Studies.

The pa- tients were managed surgically between January 1994 and January 2001 at the University of Texas Medical Branch at Galveston clomid 25mg online, at the University of Crete cheap clomid 50 mg amex, Heraklion generic 100 mg clomid with visa, and at the National University of Greece in Athens purchase clomid 50 mg without prescription. Fifteen patients were treated for severe neurological compromise discount clomid 50 mg visa, ranging from paraplegia to paraparesis (Fran- kel A: n=1, Frankel B,C and D: n=14) and 14 for in- tractable back pain complicating kyphoscoliotic osteo- porotic deformities. Acute burst fractures were observed in five patients and were associated with serious neuro- logical complications (Frankel B in four and Frankel A in one). Ten patients suffered from wedge compression frac- tures, two developed acute onset of symptoms, and in the remaining eight, the neurological deterioration was grad- ual. The patient failed to recover after anterior de- compression and stabilization (b) 34 Fig. This resulted from poor appli- cation of instrumentation prin- ciples in an osteoporotic spine. It was successfully revised us- ing anterior and posterior mul- tisegment fixation constructs (b) Table 1 Outcomes of surgery for spinal cord neurocompression and painful deformities Procedure Serious neurological deficita Painful deformities Combined (kyphosis/scoliosis) Total Improvement Failure Total Success Failure Total Success Failure Anterior decompression + graft 7 6/7 1/7 8 5/8 3/8 15 11/15 4/15 or cages Anterior stabilization 3 2/3 1/3b c Posterior stabilization – – – 3 3/3 0 3 3/3 0 Combined 4 4/4 0 2 2/2 0 6 6/6 0 Posterior decompression, – – – indirect reduction + stabilization Posterior decompression + 4 3/4 1/4 4 2/4 2/4 8 5/8 3/8 stabilization Morphine pump 1 0 1/1 2 1/2 1/2 3 1/3 2/3 a Serious neurological deficit indicates Frankel B–D. The patient with morphine pump deteriorated other healed in a kyphotic deformity with residual pain. Complete from Frankel D to Frankel B dislodgement of instrumentation occurred in the third patient, who b One patient with complete paraplegia never recovered was revised successfully through a combined approach. Pain im- tient with paraparesis, morphine pump was successful as a proved substantially in all patients, as well as in the pa- pain management modality; however, his neurological tients who underwent revision surgery. Two of the pa- status deteriorated and the patient died after a few months. In one patient, complete dislodgement of a cage and an anterior device occurred soon after surgery, and responded well to revision surgery (Fig. Neurological status responded successfully deformity by means of anterior and posterior instrumentation to posterior decompression and stabilization, but the treatment failed to correct the deformity and the patient remained with severe back pain Discussion With the increasing size of the elderly population (people at risk), it is expected that the rate of osteoporotic verte- bral fracture and resulting neurological complications will rise dramatically. Acute kyphotic deformity as a result of OVCF is not usually associated with neurological deficit, but may con- tinue to remain as a painful crippling condition requiring major surgical intervention (Fig. The type of OVF that can cause neurocompression results from either acute crush fracture [77, 98, 102] (Fig. The reported time period from the original injury to clinical manifestation of neurocompression varies between 1 and 18 months [8, 71, 75]. The cord is compromised ei- ther by the severity of the kyphotic deformity or by retropul- sion of a posterior wall fragment [8, 63, 71, 75, 97]. The postulated mechanisms of delayed vertebral collapse are attributed to either bone ischemia and necrosis [13, 18, Fig. Apparently, it is a combi- A,B,C signify sequential steps for each approach nation of both these factors [71, 75]. Repeated microtrau- mas have been postulated as the causative factor for pseud- arthrosis, which produces an unstable kyphotic spine ally associated with delayed vertebral collapse and pro- and severe pain. Within this context, Neurological deficit can range from acute paraplegia therefore, it is not unreasonable to entertain balloon kypho- (usually after an acute crush fracture) [98, 102] to delayed plasty, a recently introduced minimally invasive surgery, onset of insidious paralysis that gradually deteriorates to as a preventative intervention for progressive kyphotic de- severe paraplegia [69, 73]. Anterior decompression and stabilization can fracture where indirect reduction of kyphotic deformity is also be achieved through a posterior or posterolateral trans- feasible. For an experienced surgeon, anterior decom- of OVF when the spinal cord is compromised, and Table 2 37 Fig. Because screw holding grip is incomplete in osteoporotic bone, we advocate that the screw should stabilize the contralateral vertebral body cortex. Alternatively the surgeons could elect first to stabilize the spine posteriorly and, in the same sitting, proceed with an anterior decompression [119]. Anterior cord decompression can also be performed through a posterior transpedicle or posterolateral approach. In general, many surgeons who are more familiar with the posterior approach prefer this method, which also avoids the need for sectioning the diaphragm – especially advan- Fig. Through this approach, cord decompres- graft and Kaneda stabilization sion can be achieved either by: – Partial posterior vertebrectomy and bone grafting summarizes the published reports of serious neurocom- – Driving forward the retropulsed fragment by gentle di- pression complicating osteoporotic fractures. Reconstruction and fusion can be achieved either by The only technical complication reported with this ap- femoral ring bone allograft, rib struts, iliac bone, cages proach is dural tear (14%). Laminectomy, as a stand- filled with bone chips, or bioactive ceramic (we do alone procedure, should be rejected, because it does not not use methylmethacrylate as a reconstruction material deal with the anterior cord compression, and further dete- advocated by others).

A compar- vices for inhaled asthma medication Clinical ison of three different exercise tests purchase clomid 25 mg with mastercard. Med Sci Sports Exercise (1982) 14: tis and pulmonary parenchymal diseases order 50mg clomid amex. Amsterdam: agreement buy generic clomid 100mg on line, and physiologic correlates of two new Elsevier Science (1993) 261–89 discount clomid 25 mg otc. Am J Respir Crit Care Med (1995) 152: development and final revision of a health status 838–60 discount clomid 25 mg mastercard. The MOS ceptor agonists: a new perspective in the treatment short-form general health survey. Points to consider on clinical investi- PJ, Grunstein MM, Leff AR, Woolcock AJ, eds. Philadelphia: Lippincott-Raven (1997) patients with chronic obstructive pulmonary dis- 1647–66. The pressurized metered dose (pMDI) inhaler in asth- cost of acute asthma: how much is preventable? Systemic re- therapeutic ratio with application to studies in views and meta-analyses on treatment of asthma: respiratory diseases. Index Note: page numbers in italics refer to figures and tables and boxes α-blockers 179 GM-CSF 145 reporting acetylcholinesterase (AChE) induction regimens 144–5 in Chinese medicine inhibitors 244 Kaplan–Meier survival curves 71, 73 acne 213–14 146 in gastrointestinal cancer disability index 214 length of remission 145–6 trials 132 outcome measures 219 maintenance regimens 144–5 age limit, upper for trials 56 treatment 214 molecular characterisation 142 air pollution 361 acupuncture 80–1 older patients 143–4, 146 airway cohort studies 81 outcome measures 145–6 diseases 359–73 humoral theory 81 overall survival 146 narrowing 360 neurological theory 81 post-remission therapy 142, upper, function tests 366–7 pain control 68 143, 144, 145 airway resistance 365 placebo 80–1 QoL 146 measurement 366–7 acute lymphoblastic leukaemia response rate 145 albuterol (salbutamol) 393 (ALL) statistical issues in allergic disease childhood 103, 104, 112–13 design/analysis of trials atopic dermatitis 214 translational research 105 144–6 respiratory 360 acute myeloid leukaemia (AML) subtypes 142 rhinitis 361, 370–1 141–6 treatment failure 142 allocation to treatment 24–5 competing risks 146 treatment phases 144 cognitive behavioural therapy complete response (CR) rate acute progranulocytic leukaemia 287, 288 144, 145 (APL) 142–3 contraception trials 327 cure models 146 adaptive design of trials 95–7 depression 300 cytogenetic characterisation adolescents 50 dynamic procedure 25 142 cancer trials 103 gynaecology 350 disease-free survival 145, 146 adverse events concealment 351 drug-resistant 142, 143 herbal medicine 70–1, 72–3, infertility 341, 350 event-free survival 145, 146 73–4 concealment 351 factorial design of trials monitoring in paediatric clinical random 14 144–5 trials 49–50 alopecia androgenetica 226 Textbook of Clinical Trials. He then worked for the broadsheets and the BBC and was education correspondent of the New Statesman. Rampant hypochondriasis steered him into medical journalism, and he was executive editor of World Medicine and editor of BMA News Review. Since 1990 he has run his own training company, delivering hundreds of courses on writing to doctors and other health profes- sionals. THE A-Z OF MEDICAL WRITING Tim Albert Tim Albert Training, Surrey, UK BMJ Books © BMJ Books 2000 BMJ Books is an imprint of the BMJ Publishing Group All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording and/or otherwise, without the prior written permission of the publishers. First published in 2000 by BMJ Books, BMA House, Tavistock Square, London WC1H 9JR www. I have written it for a completely different purpose, which has come from my experiences over the past 10 years working with doctors and other health profes- sionals to sort out a wide range of writing problems. It is clear that they face several difficulties when it comes to writing. They are torn between the pressure to communicate with patients on the one hand, and meet the expectations of their peers for horrendously prolix prose on the other. Although they will have had no formal training on writing since they were 16, they will be expected to publish in high status journals if they are to advance in their careers. Writing cultures have grown up that are, frankly, destructive of effective communication and individual talent. And of course, as trained doctors rather than trained writers, they have more useful things to do anyway. So this is not another reference book laying down rules on grammar, style, or journalology, or the presentation of statistics or the ethics of publication, even though I stray into these areas from time to time. What this book sets out to do is to give support, encour- agement, and informed advice, so that people who have found writing hard will somehow find it less hard. Acting on the experience of training courses, I have chosen a large number of topics, which are arranged alphabetically, from abbreviations to zzzzz. Tim Albert vii How to use this book I expect this book to be used in two ways. The first is as an old- fashioned companion, to be kept by a bedside or on a desk, so that you can dip into it during an otherwise idle moment and find the odd entry that will interest, amuse, stimulate or annoy. The second is to use it for advice and encouragement when you have a specific writing problem. In such cases, you should turn to the specific entry, which in turn should guide you to other related entries, and in some cases to details of books that I have on my book- shelf and find useful. This book, as the title makes clear, is a personal choice, and I am sure that many topics could have been dealt with differently, and that some important ones have been left out altogether. I hope that this book will evolve, and that we shall be able to make regular updates, both in the paper version and in electronic form.

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Evidenceforincreasedpresynapticinhi- heel strike clomid 25mg without a prescription, there is indirect evidence for a decrease bitionwaslaterdemonstrated purchase 100 mg clomid overnight delivery,anditwasshownthat in presynaptic inhibition of homonymous Ia termi- the modulation of presynaptic inhibition through- nals on quadriceps motoneurones 50 mg clomid with mastercard. Later clomid 25mg line, presynap- out a stride parallels that of the H reflex (Faist generic 100 mg clomid amex, Dietz tic inhibition of quadriceps Ia terminals increases & Pierrot-Deseilligny, 1996; see p. It has been progressively to become greater than during stand- argued that the phase-dependent presynaptic inhi- ing at the moment of the yield of the knee (see bition of the soleus H reflex results from proprio- p. Group II excitation However, investigations limiting knee joint move- ments during walking have demonstrated that the Homonymous group II excitatory discharges pro- reflex inhibition is of central origin (Garrett, Kerr & duced by the lengthening contraction of the 546 Spinal pathways in different motor tasks triceps surae during the stance phase contribute sig- peroneusbrevis[seep. On the other hand, transmission cussed above the modulation of reciprocal Ia inhi- of heteronymous group II excitation from pretibial bition is less marked than during voluntary move- flexors to quadriceps motoneurones is facilitated in ments,andthiscouldalsoreflecttheneedtostabilise early stance with respect to voluntary contraction in the ankle. However, here again depolarisation of the of the ankle comes from the large stretch responses, relevant propriospinal neurones by group I afferents spinal or transcortical, produced in both the might play a crucial role by potentiating the group II soleus and tibialis anterior during the stance phase excitation. Non-reciprocal group I inhibition Prevention of excessive reflex activity Non-reciprocalgroupIinhibitionfrompretibialflex- in triceps surae orstobicepsfemoris,seenduringvoluntarycontrac- tions when standing or at the end of the swing phase Because the homonymous group II excitation of of walking, is reversed to oligosynaptic group I exci- the triceps surae contributes to the excitation of tation in early stance (see pp. The lengthening contrac- Recurrent inhibition tion of triceps surae also evokes a strong Ia dis- Heteronymous recurrent inhibition from soleus to charge, but Ia spinal pathways are not responsible quadriceps is suppressed during the stance phase for the decrease in soleus EMG activity when the when there is a simultaneous contraction of soleus muscle is unexpectedly unloaded (see above). The role of this reflex is to help resist and thereby slow ModulationofreciprocalIainhibitionbetweenankle the passive ankle dorsiflexion produced by extrin- muscles during the walking cycle helps ensure that sic mechanisms, such as kinetic and gravitational antagonistic motoneurones are not activated inap- forces. How- excessive reflex activity in triceps surae should be ever, the modulation is less marked than during vol- minimised or a stiff gait would appear, much as untary movements (see pp. Sev- eral mechanisms help to limit the reflex activation Mechanisms operating at ankle level of triceps surae motoneurones: (i) the absence in humans of heteronymous Ia connections from gas- Stabilisation of the ankle trocnemius medialis to soleus, and their weakness The appearance in humans of Ia connections, not from soleus to gastrocnemius medialis or from gas- matchedbyequivalentprojectionsofrecurrentinhi- trocnemius medialis to gastrocnemius lateralis, as bition, between ankle muscles that are not syner- compared with the cat (see p. Vibration of the rectus this phase of gait, several spinal mechanisms help femoris produces an earlier onset time of the swing the quadriceps contraction (see above): (i) trans- phase (Verschueren et al. Although this effect mission to quadriceps motoneurones of the strong was modest, it suggests the involvement of Ia affer- group I–group II excitation due to the lengthen- ents from thigh muscles in triggering the transition ing contraction of the tibialis anterior is facilitated; from the stance phase to swing in humans. Ib inhibition from pretibial flexors to biceps motoneurones is reversed to facilitation in early stance. Thus, at this time of the gait cycle, the muscle Reactions to external perturbations afferent discharge elicited by the lengthening con- traction of ankle dorsiflexors facilitates both quadri- Unexpected perturbations may occur during ceps (see above) and biceps motoneurones. Facilita- walking: the foot may slip, the ground may give tion of the antagonists operating at knee level con- way under the weight of the body, or the swinging tributes to their co-contraction, and helps ensure leg or foot may hit an obstacle. In all these cases, maximal stability of the knee joint when the leg is compensatory reactions signalled by changes in about to carry the body weight. However, it is possible that the widespread heteronymous monosynaptic Ia connections between ankle and Stretch-induced responses kneemusclesalsocontributetothediffusionofthese Ia spinal stretch reflexes monosynaptic responses (see p. These responses are consistently observed in triceps surae, provided the velocity of the perturbation is Medium-latency responses high enough. Incontrast,M2stretch-inducedresponsesin nals on soleus motoneurones during walking, and tibialis anterior are smaller when it is active during the concordant absence of involvement of Ia affer- the swing phase than during voluntary contractions ents in the unloading-induced decrease in on-going (see p. Studies of stretch-induced group II- soleus EMG activity (see above), the existence of a mediated medium-latency responses in the tibialis significantstretchreflexmayseemsurprising. Infact, anterior during the stance phase have yielded dis- presynaptic inhibition on Ia terminals does not have cordant results: the absence of the M2 response to a the same effect on a reflex response to an abrupt vertical displacement (Christensen et al. Ia spinal stretch-induced responses the subjects were walking (Berger, Dietz & Quintern, appear in the soleus only during the stance phase, 1984;pp. In fact, contrary to a vertical dis- and in particular in early stance (10–20% of the step placement that is limited to the ankle, deceleration cycle), when the torque resulting from the soleus of a treadmill results in a large postural disturbance, stretch reflex is greatest. This timing suggests that which favours group II-mediated medium-latency these responses play a role in the stabilisation of responses to stretch (see p. Only small variable stretch-induced Long-latency responses responses appear at monosynaptic Ia latency in the Long-latency stretch responses (M3) in soleus are tibialis anterior, when it is active in the swing phase elicited rarely during voluntary plantar flexion, but (see p. The latency of these long- latency responses is compatible with a transcorti- Stumbling over an obstacle cal pathway, and this is supported by the finding Monosynaptic responses occur simultaneously in that they are not seen in patients with corticospinal ankle and knee flexors and extensors when stum- lesions(Sinkjæretal. Duringthestancephase bling over an obstacle during the swing phase of of walking, despite the inhibition of tibialis ante- walking. These responses have been attributed to rior motoneurones due to reciprocal Ia inhibition transmission through the limb of the sudden jar (seep. These long-latency responses to stretch are opposite effects on the on-going EMG of tibialis not present in patients with corticospinal lesions anterior: suppression by peroneal but facilitation by (Christensen et al. There are also cutaneous responses in that they result from increased excitability of tibialis the contralateral muscles during walking and run- anterior-coupled cortical neurones (Capaday et al. They are the only significant responses in tibialis anterior after ver- Functional implications tical displacement of the ankle in the stance phase.

Elec- device defibrillates best clomid 100 mg, for example order clomid 25mg with visa, how can it trophysiologic testing was not used to identify be withheld from someone with known life- high-risk patients cheap 25 mg clomid fast delivery. This was faced was lower in this study than in the prior study generic clomid 25 mg fast delivery, in the AVID trial clomid 25 mg visa. Here too, there was a significant death from other causes, plus adverse events such reduction in mortality in the defibrillator group. If the patients are at truly very ment of Congestive Heart Failure (REMATCH), high risk of arrhythmic death, even though which was conducted from 1997 to 2001. This optimal medical therapy is being used, then it trial compared use of a left ventricular assist might be inappropriate to randomise them to device versus medical therapy in 129 patients medical therapy if a possibly useful device or with end-stage heart failure who were not can- surgical procedure exists. The one-year that were done showed that in moderately high- survival was 52% in the group receiving the left risk patients, the use of the defibrillator saved ventricular assist device and 25% in the medical lives with an acceptable number of adverse therapy group, a highly significant difference. If the risk level is less, however, as might two years, the rates of survival were 23% and 8%. It was known Trials have looked at various ways of identi- that the device was mechanically sound, and fying patients at sufficiently high risk to see if worked in the short-term as a bridge to trans- defibrillators are beneficial, but not at so high plantation. The justification for the trial was that risk that it would be unethical to randomise. The long-term benefit, either for survival or quality Multicentre Automatic Defibrillator Implantation of life, was unknown. Occasionally, however, this can be made by one manufacturer will be better than done. One such trial was Mode Selection Trial others, blurring the outcome of the trial. Batteries and other components may need to be replaced, but unless there are device, but in those randomised to single- problems, they last for years. This is generally a chamber pacing, only one lead was activated, strength of such trials. There is less problem with therefore mode of pacing was randomised rather compliance to protocol and long-term follow- than type of device. The patients were blinded regarding whether the several coronary artery bypass graft surgery trials patient was in the dual- or single-chamber arm; assessed outcome 10, and in some cases more cross-over at the last follow-up was 31. This was in from the drug, simply stopping administration contrast to another study that inserted only single- is usually sufficient. But what if the device or chamber devices in those randomised to that surgery trial turns out not to show benefit? What group and dual-chamber devices only in those is the obligation of the investigator, especially if randomised to the dual-chamber group. Here the the device or procedure is shown by the trial to cross-over rate was 2. The Coronary Artery Bypass Graft not blinded, but cross-over from single- to dual- (CABG) Patch trial42 compared transthoracic chamber pacing would have required another implantation of cardioverter defibrillators against procedure, accounting for the low cross-over rate. As with many drug trials, trials of devices At the end of an average 32 months follow- can look at either single devices (or upgrades up, there was no significant mortality difference of these devices as they become available) or between the groups. The AVID26 trial compared results of the trial and subsequent therapy was the use of advanced-generation units with tiered individualised. All patients were urged to have therapy capable of antitachycardia pacing, car- electrophysiologic testing to see if they were at dioversion and defibrillation, as well as brady- high risk of serious arrhythmia, and thus possibly cardia pacing, made by more than one company, in need of the defibrillator in the future. About against any of several drugs (though primarily 40% of the patients in the intervention group amiodarone), thus testing whether the strategy of elected to have the device turned off or removed using implantable defibrillators was preferable to [J. This kind of trial is more likely to be done by public organ- isations, such as the National Institutes of Health, TRIALS OF BEHAVIOUR CHANGE than by industry. They include trials aimed at CARDIOVASCULAR 185 smoking prevention or cessation; diet change and pressure can affect the trials in major ways. The interventions are ones vention are the Dietary Approaches to Stop that many can either implement on their own Hypertension (DASH) trial43 and a subsequent or stop because they are difficult to maintain. Implantation of devices or under 160 mm Hg and diastolic pressure 80 to surgical procedures require major efforts by the 95 mm Hg. Participants were randomly allocated investigator or surgeon, but usually only on a one- to one of three groups: a diet rich in fruits and time basis. At the consequence of the first two factors, the study end of eight weeks, both of the intervention diets duration is often much shorter than with other reduced blood pressure, with a greater reduction types of trials.

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