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You have to do this in a way that interests readers generic aricept 10 mg without prescription medicine 50 years ago, most of whom until this moment will have lived in ignorance of the deceased cheap 5 mg aricept visa medicine doctor. You will have to avoid giving offence to grieving relatives on the one hand, while avoiding conferring an instant sainthood on the other. If the publication provides written advice, make sure that you read it carefully. Look at other obituaries in that publication, noting particularly first and final sentences, paragraphs, and style. If you are unfamiliar with the publication, make sure that you know who the target audience will be. With the best will in the world (see cliché), mistakes get through, and the greatest insult is to carry them from obituary to obituary without checking. In my experience of writing obituaries for local newspapers, surviving relatives generally find it helpful to talk about their late loved one. Your research of the publi- cation will have given you an idea of the number of paragraphs or sentences you will require. Write down three or four main areas you wish your obituary to cover: for instance, what were the form- ative influences? Write in one go, without breaking off to look at the information you have collected and thinking of your target readers (not the family of the bereaved). Revise carefully what you have written, checking the facts you have cited, and making sure that you have not left out essential details (see process of writing). Here you must make it clear that you are asking them for opinion on matters of fact only. While you owe it to the family not to cause unnecessary distress, you also owe it to your readers to paint an honest picture. The most likely source will be the family, though places of work could also help. Look for photo- graphs taken by professionals, at an award-giving ceremony, perhaps, or even better at a less formal occasion and published in a local newspaper. These are generally accurate and unlikely to give much offence, but they tend towards extremes of undue flattery or unnec- essary self-effacement. Off the record An agreement between a journalist and a source that the information given cannot be published, ever. This poses all kinds of ethical dilemmas to a conscientious journalist: 87 THE A–Z OF MEDICAL WRITING what happens if he hears it from another person, for instance? If you want to give information, but not be linked to it (for valid reasons. Be warned: there is a presumption among journalists that, as long as they have made it clear to you that they are a journalist, they will be free to report anything you tell them. The danger in scientific publications is that they become yet another means of enabling disaffected (i. Omission, sins of Many people find it extremely difficult to start writing because they fear that they are going to leave out some- thing terribly important. Yet the things we agonize about leaving out are generally matters of detail, sometimes quite trivial. Concentrate on defining the message you want to put across – and then support that message in a plausible and readable manner. The material you then need to put in should select itself (see process of writing). Ordering information Writing has a beginning and an end, so at some point in the writing process you must order the points you want to make in a linear form, by making a (preferably written) plan, noting down what you intend each paragraph to do. Before you get to this stage, however, I recommend a less rigid approach to organizing the material (see branching). It is particularly galling, then, that the advice is rather good, and is partic- ularly appropriate to writing (see process of writing). Few people complain because they have too little to read (see yellow marker test). Panic attacks It is common to have these during the process of writing; after all we shall be judged on what we are about to write. A paragraph is a unit of thought and generally each should start with a key sentence, explaining why you are moving the argument forward (see inverted triangle; yellow marker test).

Thus generic aricept 5 mg with visa symptoms zollinger ellison syndrome,specificationofthedirectionand Motor learning probably speed of the movement would be elabo- rated by supraspinal motor structures trusted 10mg aricept symptoms 6 weeks, especially the The motor performance of deafferented patients motor cortex (the higher level). This contribution of showsthatreflexsupportisnotindispensabletoper- themotorcortextotheinitiationofreachingispartly forming or grading a contraction, at least in labo- channelled through the spinal propriospinal system ratory tasks. The required co-ordinated motions afferent feedback and the resulting activity in spinal of the shoulder, elbow and wrist are then assisted by circuitry are important in refining the motor output the divergent projections of propriospinal neurones (see pp. Whenlearningamotortask,movementsareslowand often involve co-contraction of antagonists to brace thejoint. Suchcontractionswouldbeassociatedwith State-dependent modulation of an effective increase in drive to the contracting sensory feedback muscles(seebelow). Thefeedbackfromspindleend- ings would be important, not only for smoothing The spinal cord contains the substrate for many the movement trajectory but also for providing the complex motor actions (e. This holds for both homonymous and rones involved in generating these complex move- heteronymous -driven spindle discharges. This internalisation of learnt programmes, and perfec- requires a dynamic regrouping of interneurones to tion of the movement depends on trial and error. As would learning progresses, a motor programme is shaped beexpectedfromthisconceptualframework,experi- which is subsequently available to command the mentsonreflexcontrolofmuscleactivityduringvar- movement (see Windhorst et al. Co-activation of information regarding the different spinal pathways antagonistic finger and wrist muscles is used in the (see Lundberg, Malmgren & Schomburg, 1987). Co-contractions information is essential for calling up the coor- of antagonists also occur in many voluntary tasks, dinated synergies that characterise the movement such as when unpredictable perturbations may be when the motor programming has been learnt. Smith, 1981; Akazawa, Milner & Stein, 1983; Llewellyn, Yang & Prochazka, 1990). Efference copy C3–C4 propriospinal neurones in the cat have ascending collaterals to the lateral reticular nucleus Control of spinal pathways during (LRN). Via these ascending collaterals, the LRN, co-contraction of antagonists which projects to the cerebellum, receives mirror information of the action that reaches motoneu- Hinge joints rones via the propriospinal neurones, and this con- stitutes a perfect efference copy. This may allow the AcomprehensivereviewoftheextensiveworkbyJens cerebellum to take corrective measures with a mini- Nielsenonco-contractionattheanklejointhasbeen mal delay, for which purpose it has at its disposal the published in a thesis (1998). Internal feedback of this type may regu- late a forthcoming movement at its onset. Feed- Reciprocal Ia inhibition between antagonistic ankle back inhibitory interneurones also have ascend- muscles is almost completely suppressed when dor- ing projections to the LRN, indicating that correc- siflexors and plantar flexors are voluntarily activated tion of the movement takes into account the out- simultaneously (see pp. The suppression is put from propriospinal neurones and the input greater than expected from the sum of the effects that they receive from feedback inhibitory interneu- of separate dorsiflexion and plantar flexion contrac- rones. Such copies of the propriospinally medi- tions, and results from a suppressive central control ated input to motoneurones and of their feed- specific to co-contraction (see below). Reciprocal Ia back inhibition could play a crucial role when inhibition is depressed maximally even at low co- using trial and error in motor learning. Evidence contraction levels, and there is no modulation as the for similar ascending projections of the cervical strength of co-contraction increases. Because of the descend- Co-contractions of antagonists at ing inhibition of Renshaw cells during separate the same joint strong contractions of soleus (cf. Increased recurrent inhibition during the animal has to co-contract antagonistic muscles co-contraction is greater than expected from the (Hulliger et al. However, suppression of contractions to suppress reciprocal Ia inhibition, the descending control cannot account for all of but the more active the recurrent inhibition the the features of the increased recurrent inhibition smallerthegainofthemotoneuronepool(seep. This probably explains inhibition has two effects: (i) reduction of the gain of why, at hinge joints, less voluntary EMG is pro- the motor output (see p. Presynaptic inhibition of Ia terminals Ball joints Presynaptic inhibition on Ia terminals on motoneu- Non-reciprocal group I inhibition rones of soleus and tibialis anterior is increased Radial-induced non-reciprocal group I inhibition of during voluntary co-contraction of the two mus- FCR motoneurones is moderately reduced during cles. This increased presynaptic inhibition is largely theco-contractionofantagonisticwristmuscles. The due to a descending control that could be specific inhibition was greater than the sum of the inhibi- for co-contraction (see p. Increased presynap- tions during separate ECR and FCR voluntary con- tic inhibition also has two effects: (i) suppression tractions in the two subjects investigated by Nielsen of the monosynaptic Ia excitation of the involved &Kagamihara (1992) during a power grip, but of motoneurone pools (see p. It is likely that more forearm and hand muscles would have been active in the former task than the latter.

This finding is reminiscent of the Ia connections without recurrent inhibition found between flex- Comparison with the pattern of monosynaptic ors of the digits in the cat (Hamm discount aricept 10mg otc medicine 003, 1990) order aricept 5mg with visa symptoms 8dpo, and sug- Ia excitation geststhatthepatternofrecurrentinhibitionisdeter- Overlap between recurrent and Ia projections mined by function during locomotion rather than The grey cells in Table 4. Recurrent inhibition without Ia excitation Functional implications The overlap in the expression of Ia excitation and It has been assumed that, in the cat, the recurrent recurrent inhibition in different motoneurone pools pathway has a focusing action, which helps limit is not total: recurrent connections from gastrocne- the extent of Ia excitation (Hultborn, Jankowska & mius medialis to soleus and peroneus brevis are Lindstrom,¨ 1971b). Similarly, it will be suggested on notparalleledbycorrespondingIaprojections(hori- pp. The functional synergism between two heads of the triceps surae (gastrocnemius medialis Heteronymous recurrent projections to and soleus) is obvious. The absence of Ia input from motoneurones in the upper limb gastrocnemius medialis to soleus may be related to a particular requirement of plantigrade gait Pattern of distribution (cf. The pattern of heteronymous recurrent inhibition in Ia excitation without recurrent inhibition the cat forelimb differs from that in the hindlimb: Ia excitatory connections without their recurrent more extended transjoint connections, and projec- counterpart (vertically hatched cells) also exist tions from proximal to distal muscles (see Illert & between some muscles acting on the ankle. In contrast, transjoint connections Organisation and pattern of connections 171 are more restricted in the upper than in the lower Recurrent inhibition of interneurones limb of human subjects (Creange´ et al. The deltoid motor nucleus, supply- ing the most proximal muscle investigated, receives Evidence for recurrent inhibition of Ia the largest number of recurrent heteronymous pro- inhibitory interneurones jectionsfromdistalmuscles,butsomeofthem(from muscles supplied by the median nerve) are not Reciprocal inhibition produced by an electrical vol- matched by equivalent Ia connections. An interest- ley to the triceps brachii nerve and assessed with ing finding, also described in the cat (Illert & Wietel- the biceps tendon jerk was conditioned by a pre- mann, 1989), is that ECR-coupled Renshaw cells ceding tendon reflex discharge in the triceps (Katz, inhibit FCR motoneurones and vice versa (Aymard Penicaud´ & Rossi, 1991;Fig. This is in keeping with the finding ceps motor discharge strongly depressed recipro- that Renshaw cells activated by FCR or ECR motor cal Ia inhibition, with a short central delay and discharges do not inhibit reciprocal inhibition a long duration, i. Renshaw cells (D), although it would have produced similar post-activation depression at the synapse of the Ia fibre and the Ia interneurone. It is there- Functional implications fore likely to be due to recurrent inhibition and not Thedistributionofrecurrentinhibitioninthehuman to the tap-induced afferent volley. A similar sup- upperlimbismorerestrictedthaninthecatforelimb, pression was observed in the opposite direction, adifferencethatistheoppositeofthatforthehuman from biceps brachii to triceps, indicating that Ren- lower limb and the cat hindlimb. Heteronymous Ia shaw cells coupled to elbow motor nuclei project projectionsfromdistaltoproximalmusclespresum- to Ia interneurones mediating reciprocal Ia inhibi- ably provide support to the hand during manipu- tion between elbow muscles. However, from soleus similarly depresses reciprocal Ia inhibi- the motor repertoire of the upper limb is much tionfromsoleustotibialisanterior(Baretetal. Recurrent inhibition evoked which the assistance of Ia excitatory projections is byaflexor or extensor motor discharge has no effect not critical. Recurrent inhibition of reciprocal Ia inhibition and cortical depression of recurrent inhibition. The dashed arrow indicates the conditioning volley eliciting reciprocal Ia inhibition. Reciprocal Ia inhibition was conditioned by a Tri tendon jerk, and the resulting amount of reciprocal inhibition (●, expressed as a percentage of the unconditioned value of reciprocal inhibition) is plotted against the ISI between this tendon tap and the test stimulus. Reflexes (expressed as a percentage of their control value) are plotted against the ISI between cortical and test stimulation (TMS given at time zero). The intensity of TMS was set to produce no significant effect on the reference H reflex. Adapted from Katz, Penicaud & Rossi (´ 1991)(b), Mazzocchio, Rossi & Rothwell (1994)(d ), Barbeau et al. However, as seen above, the suppres- sion of recurrent inhibition begins some millisec- Corticospinal suppression of onds later than the facilitation of the corresponding recurrent inhibition motoneurones. Thus,thefemoral-inducedrecurrent inhibition of the earliest motoneurones discharging Corticospinal depression of homonymous intheMEPisnotdepressedbythecorticospinalinhi- recurrent inhibition bitionofRenshawcells,whereasrecurrentinhibition Changes in recurrent inhibition of FCR and soleus of motoneurones discharged by later corticospinal motoneurones, assessed with the paired H reflex volleys is depressed by the action of the fastest technique, have been investigated after cortical sti- cortical volley on Renshaw cells. TMS produced significant facilitation of the H test reflex in the FCR at an intensity that produced no facil- Motor tasks and physiological itation of the reference H reflex (Fig. A change in the AHP was eliminated, rent inhibition during various motor tasks in human and these findings presumably reflect corticospinal subjects suggests that recurrent inhibition might depression of Renshaw cells, as has been observed serve several functions, that are not exclusive. How- in the cat after stimulation of the pericruciate cortex ever, functional interpretations must be made with (MacLean & Leffman, 1967)orthe internal capsule care because: (i) it cannot be taken for granted that (see Koehler et al. Because the the response of Renshaw cells to a tonic input is the corticospinal inhibition of Renshaw cells has a lower same as the response to the phasic inputs explored threshold than the cortical facilitation of motoneu- in the experiments below, and (ii) experiments deal- rones, Mazzocchio, Rossi & Rothwell (1994)argued ingwithhomonymousrecurrentinhibitionwereper- that TMS might also act by corticospinal suppres- formed using the paired H reflex technique, and sion of a tonic excitatory drive from the reticular would be affected by changes in the motoneuronal formation (specifically, the nucleus raphe magnus; AHP (see p. Regardless,thecorticaleffectsonrecur- Recurrent inhibition of motoneurones of a rent inhibition occur 3–4 ms later than the effects on muscle involved in selective contractions motoneurones.

Pooled 15% reduction in vertebral height quality aricept 5mg medicine 4 times a day, including worsening of results of two studies with risedronate in 184 men receiv- pre-existing fractures discount aricept 5 mg on line treatment jiggers, to 20% reduction in vertebral height ing chronic steroid therapy showed a significant reduction and more than 4 mm. Therefore, an expected finding in the risk of vertebral fracture over 1 year of treatment would be that the most stringent definition will result in. As is the case in women, calcium and vitamin D de- fewer fractures being detected than the looser one, inde- ficiency have been prevented by systematic calcium sub- pendently of the antifracture efficacy of the drug. There- Glucocorticosteroid-induced osteoporosis fore, an expected finding would be that the studies includ- ing highest-risk patients would show a greater fracture in- Glucocorticosteroid-induced osteoporosis (GIO) is by far cidence, including in the control group. However, these the most frequent cause of secondary osteoporosis [4, 89], studies may fail to be representative of the patients in and fracture incidence under corticosteroids may be as which the drug will be used later in daily practice. The pathogenesis of GIO is complex: calculated NNTs should therefore be interpreted in this proposed mechanisms include decreased osteoblast prolif- light, considering that in some cases less efficacious drugs eration and biosynthetic activity as well as increased bone have the best NNTs. However, osteoporosis is a chronic, slowly debilitat- first months under glucocorticoid treatment, and remains ing disease, and European CPMP and US American FDA elevated over the entire duration of therapy. Our results are in line with those corticosteroids may be deleterious to bone [87, 94]. Secondly, we ex- density of several therapeutic agents for the management cluded all studies reporting fracture rates only, and con- of GIO has been recently determined using meta-regres- sidered only studies reporting patients with at least one sion models. However, the drawback of the loss of of the evaluated agents, whereas calcitonin and vitamin D data of isolated studies was outweighed by far by the im- were more effective than no therapy or calcium. Promis- proved quality of the remaining data, especially as the ing data with respect to BMD have furthermore been ob- present review focused on vertebral fractures. In fact, for tained with PTH, which had not yet been included in that statistical analysis, the basic assumption is that all events meta-analysis of 2002. However, for all mentioned can be regarded as independent; a second event in the same therapeutic strategies in GIO, fracture data are scarce, since patient being as likely as a first event in this or in another many of the trials had a preventive design and were of patient. The combined results of two parallel 12-months tri- tifracture effect in that combined study was reached for all als (one conducted in the US, one in 15 other countries) patients together and for postmenopausal women, only. Again they showed Although more effective than calcium alone in main- no significant difference in overall incidence between the taining lumbar BMD, calcitonin failed to reduce frac- bisphosphonate and placebo groups (P=0. Although patients had a relatively low Management of acute and chronic pain background prevalence of vertebral fractures (12–15%) the reduction in the incidence of vertebral fractures under Most osteoporotic vertebral fractures are asymptomatic. However, even placebo group and 1/143 patients in the alendronate group asymptomatic fractures lead to spine deformity with chronic experienced new morphometric fractures over 2 years, back pain and progressive disability. A recent comparative 2-years trial between chronic back pain relies on analgesics (paracetamol), non calcitriol, vitamin D plus calcium and alendronate plus steroidal anti-inflammatory drugs (NSAIDs), and, more calcium in 195 subjects (134 women, 61 men) commenc- recently, on selective COX-II inhibitors (coxibs), which ing or already taking glucocorticoids showed that alen- have demonstrated equal efficacy in pain relief and an im- dronate was superior to the other two treatment regimens proved gastrointestinal safety profile as compared to for glucocorticoid-induced bone loss, especially in the NSAIDs [13, 57]. Six of 66 subjects treated with calcitriol, 1 of or intranasally, has demonstrated excellent analgesic effi- 61 treated with ergocalciferol, and 0 of 64 treated with al- cacy in some patients. Additional non-pharmacologic endronate sustained new vertebral fractures. That study was interventions include physiotherapy, physical activity and not powered for a fracture endpoint; however, it is inter- fall prevention programs. The efficacy of risedronate was evaluated in two 1-year Conclusion studies for prevention and treatment. The pre- vention trial included 224 men and women who had be- The selection of the appropriate drug for treatment of ver- gun to take glucocorticoids within the previous 3 months. When data from these two risk is an important criterion for decision-making, drugs studies were combined, risedronate led to a 70% (P=0. Adinoff AD, Hollister JR (1983) (1997) Intermittent etidronate therapy (2001) Two-year effects of alendronate Steroid-induced fractures and bone loss to prevent corticosteroid-induced os- on bone mineral density and vertebral in patients with asthma. N Engl J Med 337:382–387 fracture in patients receiving glucocor- Med 309:265–268 ticoids. Dursun N, Dursun E, Yalcin S (2001) C (1999) Monofluorophosphate com- et al (1994) Vertebral deformities as Comparison of alendronate, calcitonin bined with hormone replacement ther- predictors of non-vertebral fractures. Canalis E (2003) Mechanisms of glu- 55:505–509 tion and resorption in postmenopausal cocorticoid-induced osteoporosis. J Clin Opin Rheumatol 15:454–457 Knickerbocker RK, et al (1999) Reduc- Endocrinol Metab 84:3013–3020 19. Cauley JA, Black DM, Barrett-Connor tion of vertebral fracture risk in post- 6. Alexandersen P, Toussaint A, Chris- E, Harris F, et al (2001) Effects of hor- menopausal women with osteoporosis tiansen C, Devogelaer P, et al (2001) mone replacement therapy on clinical treated with raloxifene: results from a Ipriflavone in the treatment of post- fractures and height loss: the Heart and 3-year randomized clinical trial. JAMA menopausal osteoporosis: a random- Estrogen/Progestin Replacement Study 282:637–645 ized controlled trial.