By D. Grim. Salem State College. 2018.
Spinal Cord 37:235–238 Bowsher D (1999b) Central post-stroke ("thalamic syndrome") and other central pains purchase 120 mg allegra with mastercard. Am J Hosp Palliat Care 16:593–597 BowsherD(1999c)ThelifetimeoccurrenceofHerpeszosterandprevalenceofpost-herpetic neuralgia: a retrospective survey in an elderly population allegra 120mg generic. Eur J Pain 3:335–342 Bowsher D order 120 mg allegra with visa, Leijon G buy 120 mg allegra visa, Thuomas KA (1998) Central poststroke pain. Neurology 51:1352–1358 Brodal A (1947) Central course of afferent ﬁbers for pain in facialis, glossopharyngeal and vagus nerves. Arch Neurol Psychiat 57:292–306 76 References Brodal A (1981) Neurological anatomy in relation to clinical medicine, 3rd edn. Oxford University Press, New York Broman J (1994) Neurotransmitters in subcortical somatosensory pathways. Anat Embryol 189:181–214 Broman J, Anderson S, Ottersen OP (1993) Enrichment of glutamate-like immunoreactivity in primary afferent terminals throughout the spinal cord dorsal horn. Eur J Neurosci 5:1050–1061 Bromm B, Lorenz J (1998) Neurophysiological evaluation of pain. Electroencephal Clin Neurophysiol 107:227–253 BrommB,SchareinE,Vahle-HinzC(2000)Cortexareasinvolvedintheprocessingofnormal and altered pain. Springer, Berlin Heidelberg New York Brown AG, Fyffe REW (1981) Form and function of dorsal horn neurones with axons ascending the dorsal columns in cat. J Physiol 321:31–47 Brown AG, Brown PB, Fyffe REW, Pubols LM (1983) Receptive ﬁeld organization and response properties of spinal neurones with axons ascending the dorsal columns in the cat. J Physiol 377:575–588 Burstein R, Giesler GJ (1989) Retrogradely labeling of neurons in spinal cord that project directly to nucleus accumbens or the septal nuclei in the rat. Brain Res 497:149–154 Burstein R, Potrebic S (1993) Retrograde labeling of neurons in spinal cord that project directly to the amygdala or the orbital cortex in the rat. J Comp Neurol 335:469–485 Burstein R, Cliffer KD, Giesler GJ (1990a) Cells of origin of the spinohypothalamic tract in the rat. J Comp Neurol 291:329–344 Burstein R, Dado RJ, Giesler GJ (1990b) The cells of origin of the spinothalamic tract of the rat: a quantitative reexamination. Brain Res 511:329–337 Burstein R, Dado RJ, Cliffer KD, Giesler GJ (1991) Physiological characterization of spinohy- pothalamic tract neurons in the lumbar enlargement of rats. J Neurophysiol 66:261–284 Burstein R, Falkowsky O, Borsook D, Strassman A (1996) Distinct lateral and medial pro- jections of the spinohypothalamic tract of the rat. J Comp Neurol 373:549–574 Bushnell MC, Duncan GH, Hofbauer RK, Ha B, Chen JI, Carrier B (1999) Pain perception: is there a role for primary somatosensory cortex? Int Rev Neurobiol 25:39–94 Byers MR, Dong WK (1983) Autoradiographic location of sensory nerve endings in dentin of monkey teeth. Anat Rec 205:441–454 Cain DM, Wacnik PW, Turner M, Wendelschafer-Crabb G, Kennedy WR, Wilcox GL, Simone DA (2001) Functional interactions between tumor and peripheral nerve: changes in excitability and morphology of primary afferent ﬁbers in a murine model of cancer pain. J Neurosci 21:9367–9376 Calcutt NA (2002) Potential mechanisms of neuropathic pain in diabetes. Int Rev Neurobiol 50:205–228 Cameron AA, Cliffer KD, Dougherty PM, Willis WD, Carlton SM (1991) Changes in lectin, GAP-43 and neuropeptide staining in the rat superﬁcial dorsal horn following experi- mental peripheral neuropathy. Neurosci Lett 131:249–252 Cameron AA, Pover CM, Willis WD, Coggeshall RE (1992) Evidence that ﬁne primary affer- ent axons innervate a wider territory in the superﬁcial dorsal horn following peripheral axotomy. Oxford University Press, Oxford, pp 117–145 References 77 Cao YQ, Mantyh PW, Carlson EJ, Gillespie AM, Epstein CJ, Basbaum AI (1998) Primary afferenttachykininsarerequiredtoexperiencemoderatetointensepain. Nature392:334– 335 Capra NF, Dessem D (1992) Central connections of trigeminal primary afferent neurons: topographical and functional considerations. Crit Rev Oral Biol Med 4:1–52 Carlstedt T, Cullheim S, Risling M (2004) Spinal cord in relation to the peripheral nervous system. Elsevier Academic Press, Amsterdam, pp 250–263 Carlton SM, Coggeshall RE (1999) Inﬂammation-induced changes in peripheral glutamate receptor populations. Brain Res 820:63–70 Carlton SM, Hargett GL, Coggeshall RE (2001) Localization of metabotropic glutamate receptors 2/3 on primary afferent axons in the rat.
The most commonly used visual aid is the slide cheap allegra 120mg with amex, either prepared before the talk or projected from a PC generic 180 mg allegra with visa. Board and coloured pens The forerunner of this technique was the blackboard and coloured chalks order allegra 120mg without prescription. Unless you really wanted to be an artist or graphic designer and have the necessary talent cheap allegra 180mg amex, do not bother to consider this as a possible medium. I have seen brilliant displays with coloured pens by anatomists as they have slowly and patiently explained the development of an organ but this is a dying art and 26 VISUAL AIDS far beyond mere mortals. Flipcharts These are best kept for those in medical management who wish to scribble two or three words on a large piece of paper before hurriedly covering it lest their illogical thinking is obvious to the audience. However, if you belong to the "I love clinical governance" minority sect you may find a flipchart helpful in confusing the audience. Overhead projector The acetate sheets needed for this visual aid must be prepared just as rigorously as slides (see below). With the introduction of PowerPoint the overhead projector has become less popular but it is still useful for a brief, 5–10 minute, presentation. Videos Videos are occasionally valuable in demonstrating a new practical technique. It is essential to obtain expert help, often from the university or medical school audio-visual department, to ensure that the video is of high quality. Do not assume that, because you can film the family barbecue on a damp Sunday in Sidcup, you are a budding Scorcese. Slides The guidelines for the preparation of slides have been well known for many years and yet basic mistakes continue to be made. If you are a novice, seek help and advice from senior colleagues who are recognised for their presentational skills. In many medical schools the audio-visual department is very willing to give practical advice and even show examples of how not to do it. Remember that visual aids are used to add to the content of the talk and should not 27 HOW TO PRESENT AT MEETINGS distract with garish colours, silly logos, and sound effects suitable for children’s television. The ready availability of computer software packages such as PowerPoint (Microsoft) means that it is easy to prepare clear slides. However, it is also possible to make a visual mess with this programme (see Chapter 5). Guidelines for slide preparation can be considered under the following headings: • general format • text • figures • tables. A problem with using programmes, such as PowerPoint, is that it is easy to present too many slides, so that the impression left with the audience may be literally that of a "moving picture show" as slides flash by. The absolute maximum number of slides is one for each minute of the talk and a more sensible rate of projection is six slides per ten minutes of talk. Avoid logos: most of the audience are not interested in where you work and know that they are attending the Third International Congress on Equine Euthanasia. Avoid frilly edges to the slide: the audience will think that you are a dress designer or worse; and avoid moving images, unless you want to ensure that the slide is not read. It is traditional to use a light colour on a dark background, such as yellow or white on a blue background and many different shades of these colours are available. The original technique was to use black lettering on white (a positive slide) and this is useful in situations in which the light in the lecture room can only be partially dimmed. Never use dark colours on a dark background – red on a dark blue background is a favourite combination and it is hopeless. Remember that the road signs in the UK are yellow on a dark green background or black on a white background because these combinations have been found to be the easiest to read. If you are unsure about the colours to use, let the Department of Transport be your guide. Standard slides are mounted in 50·8 mm (2 in) square mounts, but produce rectangular images.
Recently I saw a patient who had developed pain in a new location after a minor accident buy cheap allegra 180mg line. She said the pain was in her hip and that X rays showed that there was arthritis of the hip joints allegra 180 mg with amex, more on the side where she was having pain generic 180mg allegra fast delivery, and she had been told that this was the cause of her pain allegra 120 mg overnight delivery. She had proven to be highly susceptible to TMS in the past so I suggested she come in for an examination. The X rays showed a very modest amount of arthritic change in the joint in question, about what would be expected in someone of her age. She had excellent range of motion of the joint and no pain on weight bearing or movement of the leg. When I asked her to touch the exact spot where she felt the pain she identified a small area where the tendon of a muscle attaches to bone, well above the hip joint; it was tender to pressure. I told The Manifestations of TMS 11 her I thought she had TMS tendonalgia and the pain left in a few days. Hip tendonalgia is most commonly attributed to what is called trochanteric bursitis. That diagnosis was not made on this occasion because the location of pain was above the trochanter, the bony prominence that can be felt at the upper, outer aspect of the hip. TMS can manifest itself in a variety of locations and it tends to move around, particularly if something is being done to combat the disorder. It is as though the brain is unwilling to give up this convenient strategy for diverting attention away from the realm of the emotions. It is, therefore, particularly important for the patient to know where all the possible locations of pain are. My patients are routinely instructed to call me when they develop new pain so that we can determine whether it is part of TMS. In summary, TMS involves three types of tissue: muscle, nerve and tendon-ligaments. PATIENT CONCEPTS OF CAUSE AND TYPE OF ONSET When first seen most people are under the impression that they have been suffering from the long-term results of an injury, a degenerative process, a congenital abnormality or some deficiency in the strength or flexibility of their muscles. According to a survey we did a number of years ago, 40 percent of a typical group of patients reported that the pain began in association with some kind of physical incident. Lifting a heavy object or straining was another; and, of course, running, tennis, golf or basketball were often blamed. The pain began anywhere from minutes to hours or days after the incident, raising some important questions about the nature of the pain. Some of the reported incidents were trivial, such as bending over to pick up a toothbrush or twisting to reach into a cupboard, but the ensuing pain might be just as excruciating as that experienced by someone who was trying to lift a refrigerator. I recall a young man who was sitting at his office desk writing and experienced a spasm in his low back so severe and persistent that he had to be taken home by ambulance. The next forty-eight hours were agonizing; he couldnt move without setting off a new wave of spasm. How can such excruciating pain be set off by this great variety of physical incidents? In view of the different degrees of severity of the physical incidents and the great variation in when the pain begins after the incident, the conclusion is that the physical happening was not the cause of the pain but was merely a trigger. Many patients apparently dont need a trigger; the pain just comes on gradually or they awaken with it in the morning. The idea that physical incidents are triggers is reinforced by the fact that there is no way to distinguish between those pains that start gradually and those that begin dramatically in terms of subsequent severity or longevity of the attack. The physical occurrence has given the brain the opportunity to begin an attack of TMS. There is another reason to doubt the role of injury in these attacks of back pain. One of the most powerful systems that has evolved over the millions of years of life on this planet is the biologic capacity for healing, for restoration.
The veloc- ity of a ball falling a distance d is given by the equation v 5 (2 g d)1/2 in which v is the speed of the spherical ball and d is the distance of the fall allegra 120mg without a prescription. Thus we obtain the following equation for the power produced by gravity: P 5 mg [2 g (h 2 y)]1/2 in which y is the height of the falling ball at time t and h is the height from which it is falling generic allegra 180mg online. Note that the power produced by gravity is not constant but increases with the falling distance order allegra 120mg without a prescription. The power exerted by gravity is negative when a ball moves upward in the opposite direction of the gravitational acceleration allegra 120mg generic. Next consider the power produced by the ground reaction force acting on a spherical ball rolling without slip down an inclined plane (see Fig. Because the ball does not slip, the velocity of the point of applica- tion of the ground force (point A) is zero. The power of external forces and couples acting on a rigid body is given by the following equation: P 5S(F? Let us express the velocity of the point of application of F in terms of the velocity of the center of mass and the angular velocity of the body: v 5 vc 1 v 3 r Using this expression in Eqn. Energy Transfers in which SF denotes the resultant force and (SMc) is the resultant mo- ment about the center of mass. According to Newton’s laws of motion, the resultant external force acting on an object is equal to the product of the mass and the acceleration of the center of mass of the object: (SF)? Using the principle of conservation of angular momentum, we can express the resultant external moment in terms of the angular accel- eration and angular velocity. For the planar motion studied in Chapter 4: SMc 5 Ic a in which Ic is the mass moment of inertia with respect to an axis that passes through the center of mass. Although we have derived this equation for a rigid body whose plane of motion is parallel to a plane of symmetry of the body, it can be shown that even in the most general three-dimensional motion, mechanical power of ex- ternal moment acting on a rigid object is equal to the time derivative of the part of the kinetic energy associated with rotation around the cen- ter of mass. Integrating this equation with respect to time, we arrive at the following relation: T2 5 T1 1 W1-2 (8. A sphere of radius a is released from rest and rolls without sliding down an inclined plane (see Fig. Thus, the in- crease in kinetic energy must be equal to the work done on the ball by the gravitational force: T 5 (1/ ) m (v)2 1 (1/ ) (2/5) ma2 (v/a)2 5 0. In this equation, the vector v represents the velocity of the point of application of force F. The position vector connecting the origin O of the inertial reference frame E to the point of application of the force F is termed r and is represented in terms of its projections to the axes of the coordinate system as follows: r 5 x1 e1 1 x2 e2 1 x3 e3 In the following, we present expressions for the work done by various types of forces that are commonly associated with human movement and motion. Work Done by the Gravitational Force The gravitational force acting on a body with mass m is equal to 2mg e2. Gravity does positive work when the body moves downward and negative work when the body moves upward. In the case of conservative forces, the work is expressible in terms of a scalar function V that is called the potential energy: W1-2 5 V(t1) 2 V(t2) (8. The work done by the gravitational force can be expressed as the difference in potential energy between time points t1 and t2: W1-2 52Vg2 1 Vg1 (8. For example, when a ball rolls on a planar surface, the normal force acting on the ball creates no work and therefore does not affect the kinetic energy of the rigid body. If there is no relative movement between the interacting surfaces, the displace- ment is zero, and hence there is no work done by the frictional force. This is important because the frictional forces that enable us to walk or run do zero work during these activities because they act on a point of zero ve- locity. If, however, one body moves relative to the other at the point of contact, friction contributes to the work done by external forces. Work Done by the Spring Forces Consider a spring with spring constant k and force-free length Lo. Let xj denote the dis- placement of the end of the spring marked with symbol A along the di- rection of the unit vector e at time tj. Then the force exerted by the spring on the mass m at time tj can be written as Fj 52kxj e (8. On the other hand, the spring force is in the direction of e at time t2 because x2 , 0.
This increased excitability can be blocked by glutamate antagonists (Woolf and Thomp- son 1991; Liu and Sandkühler 1995) generic 120mg allegra free shipping, supporting release of glutamate by these ﬁbers and a primary role for glutamatergic transmission in hypersensitivity (Willis 2001 order allegra 120mg on-line, 2002) buy allegra 180mg fast delivery. Thus buy allegra 180mg cheap, better understanding of the mechanisms of hypersensitivity may be gained by studying the effects of peripheral injury on glutamate and its receptors. Glutamate receptors in the SC are down-regulated bilaterally following unilateral inﬂammation of the paw in rats, possibly as a result of indirect effects of the lesion (Pellegrini-Giampietro et al. On the other hand, immuno- cytochemical evidence suggests ipsilateral up-regulation of AMPA receptors in superﬁcial laminae of the DH following chronic nerve ligation (Harris et al. While these apparent discrepancies may be explained on the basis of differences in the experimental models, none of these studies provides direct evidence that changes in glutamate receptors occur at synapses of PA terminals. Recent advances in postembedding immunocytochemistry made it possible to address this question at the ﬁrst brain synapse (Phend et al. ThepresentstudyisfocusedonthelaminaII,because this is the region where the basic mechanisms responsible for the processing of no- ciceptivestimuliresideandwhereperipheralﬁbersinvolvedincentralsensitization after injury terminate (Woolf and Doubell 1994). Section of a peripheral nerve was chosen as the experimental model, because this procedure is known to result in hy- perexcitability of DH cells, perhaps triggered by ectopic discharge at the neuroma or in SG (Devor 1994), and because it is highly reproducible from animal to animal. A portion of this band, corresponding to the representation of the sciatic nerve, was attenuated or absent on the lesioned side. In contrast to this prominent effect, only modest changes were seen in immunoreactivity for GluR2/3 on the two sides using con- ventional confocal microscopy. These included weakly increased staining intensity for somata, dendrites and poorly deﬁned neuropil on the lesioned side. The mean intensity of immunoﬂuorescence over lamina II on the lesioned side (as measured in ten 25-µm-thick sections from two rats) was only 7% greater than that on the control side. However, more detailed image analysis revealed signiﬁcant changes in staining, especially a substantial increase in the number of very bright pixels on the lesioned side (Popratiloff et al. Though consistent with an up-regulation of glutamate receptor protein, it was not possible from LM data to establish whether the increase was primarily in somata (perhaps reﬂecting increased biosynthesis), dendrites (reﬂecting increased transport), or at the postsynaptic membrane (re- ﬂecting functional glutamate receptors). At the EM, structural details were clearly visible even in the absence of osmium, allowing identiﬁcation of glomerular ter- minals at the end of PA ﬁbers. Myelin whorls and glycogen particles were observed on the lesioned side, but not on the control side (Kapadia and LaMotte 1987; Zhang X et al. Another change apparent on the lesioned side involved glomerular terminals that in control material have dark axoplasm, few mitochondria and clear vesicles of irregular size. After periph- eral nerve lesion, these terminals can no longer be identiﬁed (Castro-Lopes et al. Other glomerular terminals in superﬁcial DH with clear axoplasm, numer- ous mitochondria, and clear vesicles of regular size, corresponding to the central element of type C2 glomeruli (Figs. Quantitative analy- sis was performed on these terminals, since they were recognizable on the operated side as easily as on the control side. A larger number of particles coding for AMPA receptor subunits was evident at glomerular synapses on the lesioned (Fig. To verify these qualitative observations, we counted gold particles at synapses made by C2 terminals on the two sides in the three animals used for EM. In each of the animals, labeling at synapses of C2 terminals was signiﬁcantly increased on the injured side, with ratios ranging from 1. A slight (7%–8%) increase in the length of the synaptic active zone may have contributed to this increase, but most of the increased labeling could be attributed to increased receptor density, as indicated by the density of gold particles per micrometer of synaptic contact. Nonparametric analysis conﬁrmed that receptor density was signiﬁcantly elevated on the injured side (p≤0. These data established AMPA receptor up-regulation at synapses of PAs ipsilateral to the lesion in each of the animals studied. To address this issue, we further analyzed the data Central Changes Consequent to Peripheral Nerve Injury 55 with a paired t-test, comparing the mean number of gold particles/synapse on the lesioned and unlesioned sides for the three animals. Notwithstanding inevitable variations in tissue processing, the mean labeling on lesioned and control sides for each animal was very consistent in our material, thus making it possible to reject the null hypothesis that the observed effect might arise from random variations among animals (p>0. We took advantage of the characteristic morphology of different types of synapses in superﬁcial laminae to address whether changes in glutamate receptors after peripheral injury are conﬁned to synapses of PAs. Besides glomerular ter- minals, superﬁcial laminae contain nonglomerular, dome-shaped terminals ﬁlled with clear, round vesicles, and making single asymmetric synaptic contacts. Most of these are glutamatergic terminals originating from interneurons or descending ﬁbers (Rustioni and Weinberg 1989).