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None of the other specialists liked Florence and openly told me they hated to see her coming buy risperdal on line amex medicine grand rounds. I asked each one to refer her back to me if she showed up without a letter from me generic 3mg risperdal amex medicine 513. They all also agreed to hold off any new procedures for the two-month period purchase genuine risperdal on line treatment goals for depression, even if she did show up in their offices purchase risperdal once a day symptoms vertigo. The husband came from time to time with Florence, but I talked to him only a few times after our initial visit. All of this arranging took a lot of time in between visits, but to gain some understanding, I was determined to follow at least one patient who had a large number of symptoms until I had exhausted all efforts. Most patients with multiple symptoms jump from doc- tor to doctor, which gave me more motivation to follow Florence for as long as possible. The profession as a whole detested patients with many symptoms and avoided them whenever possible or dealt with them as though the organ of their specialty could be separately Florences Symptoms 71 considered. This explains the frequency with which these patients were subjected to surgical or invasive diagnostic procedures. I have often wondered how much of the national health-care bill goes for patients like Florence and the unnecessary procedures they get. Psychiatric nomenclature was no help to me, especially since it listed all such conditions as untreatable. Possible psychiatric terms included hysteria or hypochondriasis or somatizing disorder or even malingering. I decided that I would open my mind as much as possible and try to listen to what Florence might be saying with her symptoms. I had no clear formulation, except that I would avoid all labels for her until I was certain of my diagnosis. I would stay on the alert for any disease that might respond to medicines or sur- gery; I did not want to miss a treatable disease. I had decided that if I missed a disease for which there was no treatment, it would not really matter. I would listen as carefully as possible and do testing only if I se- riously suspected some disease that had not been checked before. I would rule out any likely disease that her symptoms would support (the reports from the specialists ruled out almost all such diseases I could think of). I did test for a few rare metabolic diseases that can cause diffuse and sometimes bizarre symptoms. Tese excluded, I proceeded to dissect her symptoms to the limit of my ability to ask questions. I went over and over the list to make certain that she had mentioned every conceivable symptom she was having. I asked her to get her husband to sign the list, so that he had his chance to add any symptom she had not told me about. I told her that in future visits we would simply not deal with any symptom that was not on the list. She agreed to this and spent some time going over her symptoms until she had them all listed. I was trying to pin her down, a difficult thing to do because she jumped from one subject or symptom to another. My idea with the list was to get her to come to some finality about something, even if it had to be a mere list of her symptoms. I asked what time of day it was worse, when it was better, what made it better, what made it worse, did it move around, and if so, how and in what direction. I sometimes had her draw the course of movement of the symptom on her body. Were the symptoms related to people, or places, or thoughts, or moods, or day of the week, or night or day, or travel, or the smell of anything, or the sight of anything, or the sound of something specific? I developed an endless list of questions, which I methodically applied to each of her symptoms. I wanted to know how frequently she had each one, the maximum number in a day, the longest symptom-free interval. I never asked her how she felt or how she was getting along in a more general way. I would also continue to follow the guide of Carl Rogers and be in the world of Florence. She told me early that she was absolutely convinced that she had a very rare disease that was beyond medical science. I was going 74 Symptoms of Unknown Origin to find out what was wrong with her. The use of that phrase was and still is a popular way of dealing with patients with many symptoms. I always thought it insulting to tell someone so miserable with so many symptoms that nothing is wrong. De- spite the compelling logic against its use, it continues to be a popu- lar phrase for trying to deal with these very difficult patients. I also resisted the common course of telling such a patient that the problem was all in your head. You mean, if I just quit imagining those symptoms, they will just go away? The foremost reason was that I truly did not know what pa- tients like Florence suffered from. In fact, I began to believe that each such patient suffered from something very different from the other, that there was no one disease or even a group of diseases responsible. I came to believe that each patient suffered idiosyncratically of his or her own peculiar difficulty. How could I with any accuracy say that there was nothing wrong, or that it was just something in their head? I did not know what they had and until I did, I would tell them I did not know. Tere were at least two other prevailing strategies for dealing Florences Symptoms 75 with patients with many symptoms. The first, and the most dan- gerous, was to make a diagnostic error and assign a false diagno- sis to the patient. Tere are very few tragedies as serious as those that occur when an operation a patient did not need in the first place does permanent harm: Tus my obsession with not as- signing a diagnosis I could not prove. The other common way of dealing with these patients was to make up an innocuous diagnosis and assign it to them. Each has a counterpart dis- ease that is real but difficult to substantiate, or not too serious, or not life threatening, or trivial even when proven. Most do not have a clean lab test or procedure to prove their exis- tence or absence.

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Harris ST risperdal 3 mg visa nail treatment, Watts NB buy risperdal from india symptoms 89 nissan pickup pcv valve bad, Genant HK buy discount risperdal 2mg treatment uveitis, et EA buy risperdal 2 mg on-line medications diabetic neuropathy, Dallal GE (1997) Effect of cal- ment of osteoporosis in men and al (1999) Effects of risedronate treat- cium and vitamin D supplementation women after hip fracture. Pharma- ment on vertebral and nonvertebral on bone density in men and women cotherapy 23:190–198 fractures in women with postmeno- 65 years of age or older. Fujita T, Inoue T, Morii H, et al pausal osteoporosis: a randomized Med 337:670–676 (1999) Effect of an intermittent controlled trial. Delmas PD, Ensrud KE, Adachi JD, weekly dose of human parathyroid With Risedronate Therapy (VERT) et al (2002) Efficacy of raloxifene on hormone (1–34) on osteoporosis: a Study Group. JAMA 282:1344–1352 vertebral fracture risk reduction in randomized double-masked prospec- 41. 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Gass R (2001) the early preclinical SN, van den Kroonenberg A, Court- once-yearly increases bone mineral diagnosis of osteoporosis measuring ney A, McMahon T (1996) Etiology density – implications for osteoporo- the pure trabecular bone density. Ensrud KE, Thompson DE, Cauley hoof J, Declerck K, Raus JN (2002) fenbuttel BH (2002) Intravenous JA, et al (2000) Prevalent vertebral the relationship among history of pamidronate compared with oral alen- deformities predict mortality and hos- falls, osteoporosis, and fractures in dronate for the treatment of post- pitalization in older women with low postmenopausal women. Fracture Intervention Trial Med Rehabil 83:903–906 60:315–319 Research Group. Holzer G, Majeska RJ, Lundy MW, 48:241–249 PJ, Abou-Samra AB (1999) Charac- Hartke JR, Einhorn TA (1999) terization of an element within the rat Parathyroid hormone enhances frac- parathyroid hormone/parathyroid hor- ture healing. Nakajima A, Shimoji N, Shiomi K, C, Garcia-Ocana A, Stewart AF M, Lane JM (2003) Six minute walk et al (2002) Mechanisms for the en- (2003) Short-term, high-dose parathy- test: a new powerful predictor of hancement of fracture healing in rats roid hormone-related protein as a functional dysfunction in osteoporotic treated with intermittent low-dose hu- skeletal anabolic agent for the treat- patients with and without vertebral man parathyroid hormone (1–34). J Bone Min Res J Bone Miner Res 17:2038–2047 J Clin Endocrinol Metab 88:569–575 (in press) 73. Lindsay R, Hart DM, Forrest C, Baird et al (2001) Effect of parathyroid hor- (1997) Peripheral QCT for the diag- C (1980) Prevention of spinal osteo- mone (1–34) on fractures and bone nosis of osteoporosis. Lindsay R, Silverman SL, Cooper C, Med 344:1434–1441 intermittent administration of parathy- Hanley DA, et al (2002) Risk of new 74. Neuner JM, Zimmer JK, Hamel MB roid hormone on fracture healing in vertebral fracture in the year follow- (2003) Diagnosis and treatment of os- ovariectomized rats. JAMA 17:285:320–323 teoporosis in patients with vertebral 23:1089–1094 62. Jalava T, Sarna S, Pylkkanen L, et al G, Braunstein E, Johnston CC (1997) Soc 51:483–491 (2003) Association between vertebral Effect of osteoarthritis in the lumbar 75. Nordin BE, Morris HA (1989) the fracture and increased mortality in os- spine and hip on bone mineral density calcium deficiency model for osteo- teoporotic patients. Jordan KM, Cooper C (2002) Epi- 7:564–569 Richards HK, Compston JE (2003) A demiology of osteoporosis Best Pract 63. Lofman O, Larsson L, Toss G (2000) prospective study of discordance in Res Clin Rheumatol 16:795–806 Bone mineral density in diagnosis of diagnosis of osteoporosis using spine 50. 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Melton LJ 3rd, Chrischilles EA, Bone regeneration in critical size de- line induces heterotopic and ortho- Cooper C, Lane AW, Riggs BL fects by cell-mediated BMP-2 gene topic bone formation in rodents. How many transfer: a comparison of adenoviral thop Res 16:330–339 women have osteoporosis? Liberman UA, Weiss SR, Broll J, et Miner Res 7:1005–1010 10:1089–1098 al (1995) Effect of oral alendronate 69. Osteoporos Int 10:214–221 an osteoblastic osteosarcoma (UMR III Osteoporosis Treatment Study 70. Miller PD (2001) New possibilities 106–01) cell line results in growth in- Group. N Engl J Med 333:1437–1443 for diagnosis and treatment of osteo- hibition. Peter CP, Cook WO, Nunamaker ER, Lane JM (2003) Fracture evalua- 46:215–221 DM, Provost MT, Seedor JG, Rodan tion and clinical complications. Moro M, Hecker AT, Bouxsein ML, GA (1996) Effect of alendronate on Favus MJ (ed) Primer on the meta- Myers ER (1995) Failure load of tho- fracture healing and bone remodeling bolic bone diseases and disorders of racic vertebrae correlates with lumbar in dogs. Tinetti ME, Baker DI, Garrett PA, Morphometric X-ray absorptiometry role of vitamin D and calcium-vita- Gottschalk M, Koch ML, Horwitz RI and morphometric radiography of the min D deficiency, vitamin D insuffi- (1993) Yale FICSIT: risk factor spine: a comparison of prevalent ver- ciency, and vitamin D sufficiency. J Bone Age Ageing 29:301–304 J Am Geriatr Soc 41:315–320 Miner Res 15:564–574 92. Rea JA, Chen MB, Li J, et al (2001) JL, Black DM, Harper KD (2002) DF, Williams MB, Helm GA (2002) Vertebral morphometry: a comparison Relationships between bone mineral CT and radionuclide study of BMP-2 of long-term precision of morphomet- density and incident vertebral fracture gene therapy-induced bone formation. 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Maturation of Ia connections during Walking development the spinal stretch reflex can produce a mechani- It has been reported that cheap risperdal 4mg with visa treatment 7th feb bournemouth, in the normal newborn cally effective contraction and provides a pathway baby generic risperdal 2mg without prescription treatment 2015,atendontapmayelicitshort-latencyheterony- through which rapid automatic load compensation mous excitatory responses in antagonistic muscle to an unexpected disturbance can be generated cheap risperdal 2mg online medicine 2410. However purchase risperdal 2 mg line symptoms panic attack, it gered by unexpected ankle joint displacement, con- would be prudent to retain reservations about these tribute significant stabilisation of the supporting conclusions (see p. Motor tasks and physiological implications Perturbations of upright stance Muscle stretch elicits a reflex response from the Perturbationsoftheuprightstanceinsubjectsstand- corresponding motoneurone pool, and this has at ing on a rotating platform produce an early spinal least two separate components: the classical short- stretch reflex response (M1), which is prominent in latency spinal reflex (M1), the latency of which is soleus. After loss of large-diameter muscle spindle compatible with monosynaptic Ia excitation, and a afferents, M1 is absent but posture is quite stable, medium-latency component (M2) of more complex suggesting that M1 is not essential for equilibrium origin. The short-latency spinal stretch reflex during Spinal and transcortical stretch reflexes natural motor tasks the medium-latency (M2) response to stretch fol- the spinal stretch reflex utilises the simplest reflex lowing the early spinal (M1) response has a different pathway and interacts with pre-programmed and origininvariousmuscles:intheflexorpollicislongus other reflex mechanisms to compensate for distur- (and intrinsic muscles of the hand) the long latency bances during natural motor tasks. There is con- is due to a transcortical pathway fed by Ia afferents, siderable literature about the contribution of the whereas in foot and leg muscles the stretch response short-latencystretchreflexoftricepssuraetovarious is mediated through a spinal pathway fed by slowly natural movements, but few data for other muscles. Bothtranscorticaland spinal group II pathways could contribute to the M2 response in proximal upper limb muscles, such as Running, hopping and landing the biceps brachii. Duringthestancephaseofrunningandhoppingand after the impact of landing, the short-latency spinal Heteronymous monosynaptic Ia excitation stretch reflex of the triceps surae is superimposed on pre-programmed activity and contributes to the There are little experimental data on the functional musclecontractionresponsibleforthepushingoffof role of heteronymous Ia connections. However, the Resume´ ´ 105 different organisation of these connections in the and tibialis anterior when leaning backward). On cat and baboon hindlimb and the human lower theotherhand,diffuseIaconnectionscouldbecome limb suggests that the connections are functionally functionally inconvenient, because the activation of important, having adapted to provide the particular Ia afferentsfromacontractingmusclemightresultin reflex assistance required in each species. Suppressionofunwantedheterony- mousIadischargescanbeachievedthroughfocused Weak connections between ankle extensors corticospinal control of presynaptic inhibition of the weakness of the connections between ankle Ia terminals and of recurrent inhibition. The need extensors in human subjects may be related to the for this control suggests that the heteronymous Ia role of triceps surae in walking: it resists and brakes discharge does play a functional role, because it the passive ankle dorsiflexion produced by extrinsic must be suppressed in tasks for which it is not forces (kinetic force and gravity), but must be over- required. It would then be undesirable to have exces- Upper limb sive activity from the triceps surae stretch reflex, and weak Ia connections between the different heads of the diffuse distribution of the Ia projections from the muscle would help ensure this. Some of these connec- Studies in patients and tions are weak, but their strength has been under- clinical implications estimated in experimental studies and, in any case, this would not prevent them from modulating the In practice, assessing Ia connectivity involves meas- excitability of motoneurones that are already depo- urements of the H reflex. During the stance phase of running, hop- advantages of doing so during voluntary contrac- ping and landing, all extensors undergo a lengthen- tions (see above). Modulation of the on-going EMG ingcontractionthatevokesastrongIadischarge,and by a heteronymous volley may allow access to a it is probable that the extensive Ia connections link- motoneuronepoolbyafferentinputsthatdonottra- ing muscles across joints modulate the role played verse the same nerve or nerve root as homonymous by the different muscles in load compensation. Projections onto antagonists operating Peripheral neuropathies, mononeuropathies at another joint and nerve lesions Theseprojectionsaredesirablefunctionallybecause These may be accompanied by a decrease in the of the versatile synergisms required to accomplish amplitude and an increase in the latency of the the various tasks of the human lower limb. Reflex depression usually results from an co-contraction of quadriceps and gastrocnemius- afferent abnormality and will occur when there is soleus in running and hopping, but of quadriceps either a loss of conducting afferents or dispersion of 106 Monosynaptic Ia excitation the afferent volley. Tests of reflex function provide a sion is markedly attenuated, probably because the tooltodistinguishbetweenisolatedperipheralnerve enhanced Ia firing during voluntary contraction lesions and lesions involving roots or plexus. Spasticity the ratio Hmax/Mmax is, on average, increased in soleus but not, or hardly so, in FCR in hemiplegics. Post-activation depression in spastic patients Whether measured as the depression induced by passive stretch of the test muscle or by high stimu- Post-activation depression at the lus rate, post-activation depression is significantly Ia-motoneurone synapse decreased in spastic patients due to spinal cord injury and multiple sclerosis, and on the affected Background from animal experiments side of patients with hemiplegia. This reduction is It has long been known that the size of the mono- probably a consequence of the disuse due to motor synaptic reflex decreases when it is repeatedly impairment, and may be an important spinal mech- elicited. The results from a variety of preparations indicate the presence of an early facili- REFERENCES tationofrelativelyshortdurationsuperimposedona depression of much longer duration. 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In Handbook of Physiology, sec- when the stimulus rate is decreased, and disappears tion I, the Nervous System,vol. Bethesda,USA:AmericanPhysiological contraction of the test muscle, the reflex depres- Society. Projections of group Ia affer- postural reactions to a sudden body displacement in man. Experimental In Spinal and Supraspinal Mechanisms of Voluntary Motor Brain Research, 76, 223–8. JournalofPhysiology(London), afferents from forearm muscles to motoneurones supply- 405, 1–37. Pattern of projec-´ different motoneuronal pools of the lower limb in man. Synaptic connections from tendon taps and electrical stimulation of tibial nerve. Elec- largeafferentsofwristflexorandextensormusclestosyner- troencephalographyandClinicalNeurophysiology,54,469– gistic motoneurones in man. Monosynaptic and oligosynaptic contributions to bution of heteronymous Ia facilitation and recurrent inhi- humananklejerkandH-reflex. Methodologicalimplicationsofthe tary contraction on the H reflex of various muscles. Vestibular and proprioceptive influences on the mental Brain Research, 56, 126–34. Sacralcordconduc- Thesignificanceofproprioceptiononposturalstabilization tion time of the soleus H-reflex. Motorcortexreflexesassociatedwithlearned activity of leg muscles in running. Body oscillations post-synaptic potentials and changes in firing probability inbalancingduetosegmentalstretchreflexactivity. Auto- between pre-activity and stretch reflex in human triceps genetic inhibition of motoneurones by impulses in group brachii during landing from forward falls. H-reflexes of different sizes guished from pre-programmed muscle activations follow- exhibit differential sensitivity to low frequency depression. Evidence for interneuronally mediated Ia excita- gence of monosynaptic excitatory afferents onto many dif- tory effects to human quadriceps motoneurones. 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Green  2004 John Wiley & Sons, Ltd ISBN: 0-471-98787-5 13 D entistry and axillo-facial MAY C. LO Dental Public Health, Faculty of Dentistry, the University of Hong Kong, Hong Kong INTRODUCTION Aside from oral diseases there are a number of conditions or disorders of the oral cavity that SCOPE OF THE CHAPTER are of concern. Malalignment and malocclusion of teeth (crooked teeth) is prevalent and severe Dentistry is concerned with the prevention and in many countries and most report a growing treatment of diseases and disorders of the teeth, demand for orthodontic treatment to correct the gums (periodontium) and oral cavity. In the US, it is estimated that most common oral diseases are dental caries around half of the population are in need of some (tooth decay) and periodontal (gum) diseases. Removable prosthesis (dentures or false adults in most countries throughout the world teeth) and fixed prosthesis (bridges) as well as have been affected by dental caries. In addition, implants (screw in teeth) have been used to findings from epidemiological surveys throughout address these problems. The prevalence First, the disease aetiology and measurements of oral cancer varies from country to country, in of dental caries and periodontal disease will most countries it accounts for less than 1% of be presented. Second, clinical trials methods the total cancer incidence whereas in the Indian used in dentistry will then be outlined and subcontinent it can account for 30–50% of the illustrated with examples. Green  2004 John Wiley & Sons, Ltd ISBN: 0-471-98787-5 194 TEXTBOOK OF CLINICAL TRIALS caries, oral rehabilitation, periodontal disease clinical signs. Fourth, the tal disease, usually the depth of the periodontal current issues of evidence-based dentistry and pocket and/or the attachment loss are measured hierarchical data analysis will also be discussed. Last, the impact of clinical trials on dental Following the developments in medical re- practice will be summarised.