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By P. Lisk. Salem College.

With the expansion of Islam Galen’s works contain many errors buy fucidin 10 gm on-line, primarily because of through the Middle East and North Africa during the eighth his desire to draw definitive conclusions regarding human body century buy discount fucidin 10 gm online, the surviving manuscripts from Alexandria were taken functions on the basis of data obtained largely from animals back to the Arab countries cheap fucidin 10gm free shipping, where they were translated from such as monkeys, pigs, and dogs. He proved to be an experimentalist, demon- Church attempted to stifle any scholarship or worldly knowledge strating that the heart of a pig would continue to beat when that was not acceptable within Christian dogma. The study of spinal nerves were transected so that nerve impulses could not the human body was considered heretical, and the Church reach the heart. He showed that the squealing of a pig stopped banned all writings on anatomical subjects. Without the Islamic when the recurrent laryngeal nerves that innervated its vocal repository of the writings of Aristotle, Hippocrates, Galen, and cords were cut. Galen also tied off the ureter in a sheep to prove others, the progress of centuries in anatomy and medicine would that urine was produced in the kidney, not in the urinary blad- have been lost. It wasn’t until the thirteenth century that the der as had been falsely assumed. In addition, he proved that the Arabic translations were returned to Europe and, in turn, trans- arteries contained blood rather than pneuma. During the translation process, any Arabic termi- Galen compiled a list of many medicinal plants and used nology that had been introduced was systematically removed, so medications extensively to treat illnesses. Although he fre- that today we find few anatomical terms of Arabic origin. He accumulated a wide variety of medical instruments and suggested their use as forceps, retractors, scissors, and splints (fig. He was also a strong advocate of helping nature heal through good epidemic: Gk. History of Anatomy © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 Chapter 1 History of Anatomy 13 Renaissance The period known as the Renaissance was characterized by a re- birth of science. It lasted roughly from the fourteenth through the sixteenth centuries and was a transitional period from the Middle Ages to the modern age of science. The Renaissance was ushered in by the great European universities established in Bologna, Salerno, Padua, Montpel- lier, and Paris. The first recorded human dissections at these newly established centers of learning were the workof the sur- geon William of Saliceto (1215–80) from the University of Bologna. The study of anatomy quickly spread to other universi- ties, and by the year 1300 human dissections had become an in- tegral part of the medical curriculum. However, the Galenic dogma that normal human anatomy was sufficiently understood persisted, so interest at this time centered on methods and tech- niques of dissection rather than on furthering knowledge of the human body. The development of movable type in about 1450 revolu- tionized the production of books. Celsus, whose De re medicina was “rediscovered” during the Renaissance, was the first medical author to be published in this manner. Among the first anatomy books to be printed in movable type was that of Jacopo Beren- gario of Carpi, a professor of surgery at Bologna. He described many anatomical structures, including the appendix, thymus, FIGURE 1. The most influential text of the period was written ciculus Medicinae by Johannes de Ketham. The anatomy professor by Mondino de’ Luzzi, also of the University of Bologna, in 1316. The dissections were performed by hired First published in 1487, it was more a dissection guide than a assistants. One of them, the ostensor, pointed to the internal struc- study of gross anatomy, and in spite of its numerous Galenic er- tures with a wand as the professor lectured. Because of the rapid putrefaction of an unembalmed corpse, the anatomy textbooks of the early Renaissance were orga- Leonardo nized so that the more perishable portions of the body were consid- ered first. Dissections began with the abdominal cavity, then the The great Renaissance Italian Leonardo da Vinci (1452–1519) is chest, followed by the head, and finally the appendages. He displayed genius as a painter, sculptor, ar- With the increased interest in anatomy during the Renais- chitect, musician, and anatomist—although his anatomical sance, obtaining cadavers for dissection became a serious prob- drawings were not published until the end of the nineteenth cen- lem. As a young man, Leonardo regularly participated in cadaver finally an official decree was issued that permitted the bodies of dissections and intended to publish a textbook on anatomy with executed criminals to be used as specimens. When Corpses were embalmed to prevent deterioration, but this Leonardo died, his notes and sketches were lost and were not dis- was not especially effective, and the stench from cadavers was apparently a persistent problem. The advancement of anatomy from a thronelike chair at some distance from the immediate area would have been accelerated by many years if Leonardo’s note- (fig.

STIR imaging produces fat suppression and these necrotic or cystic areas show no enhancement order fucidin 10 gm line. This technique fluid show high signal intensity trusted 10gm fucidin, well-defined margins generic fucidin 10 gm with visa, and increases lesion conspicuity [14, 15], but typically has a homogeneous signal intensity, and is particularly important lower signal-to-noise ratio than does spin-echo imaging; it when guiding biopsy to areas that harbor diagnostic tissue. Lesions are generally well seen on standard imaging, and Magnetic Resonance Diagnosis STIR imaging tends to reduce the variations in signal in- tensities identified on conventional spin-echo MRI, which Despite the superiority of MRI in delineating soft-tissue is most helpful in tissue characterization. Murphey terize them, with most lesions demonstrating prolonged T1 study has suggested that MR can differentiate benign from and T2 relaxation times. The majority of lesions remain malignant masses in greater than 90% of cases based on nonspecific, with a correct histologic diagnosis reached on the morphology of the lesion. Criteria used for benign the basis of imaging studies alone in only approximately lesions included smooth, well-defined margins, small size, 25-35% of cases [22-24]. There are instances, however, in and homogeneous signal intensity, particularly on T2- which a specific diagnosis may be made or strongly sus- weighted images. Other studies, however, note that malig- pected on the basis of MRI features (Table 1). This is usu- nant lesions may appear as smoothly marginated, homoge- ally done on the basis of lesion signal intensity, pattern of neous masses and MR cannot reliably distinguish benign growth, location and associated “signs” and findings. This discrepancy MRI appearance of these lesions has been well reported likely reflects differences within the studied populations. More commonly, MRI may re- When the MR images of a lesion are not sufficiently veal a nonspecific appearance. In such cases, it is often not characteristic to suggest a specific diagnosis, a conserva- possible to establish a meaningful differential diagnosis or tive approach is warranted. Malignancies, by virtue of reliably determine whether a lesion is benign or malignant. Consequently, the larger a mass is, of MR in many cases, the issue of whether it can reliably and the greater its heterogeneity, the greater is the concern distinguish benign from malignant is much less clear. Only 5% of benign soft-tissue tumors ex- ceed 5 cm in diameter [25, 26]. In addition, most malig- nancies are deep lesions, whereas only about 1% of all be- Table 1. Specific diagnoses that may be made or suspected on the basis of magnetic resonance imaging nign soft-tissue tumors are deep [25, 26] Although these figures are based on surgical, not imaging, series, these Vascular lesions Hemangioma trends likely remain valid for radiologists. Hemangiomatosis (angiomatosis) When sarcomas are superficial, they generally have a less Arteriovenous hemangioma (arteriovenous malformation) aggressive biologic behavior than do deep lesions. As a Lymphangioma rule, most malignancies grow as deep space-occupying le- Lymphangiomatosis sions, enlarging in a centripetal fashion, pushing, rather Bone and cartilage Myositis ossificans than infiltrating adjacent structures (although clearly there forming lesions Panniculitis ossificans are exceptions to this general rule). As sarcomas enlarge, a Fibrous lesions Elastofibroma pseudocapsule of fibrous connective tissue is formed around Fibrous hamartoma of infancy them by compression and layering of normal tissue, associ- Musculoaponeurotic fibromatosis ated inflammatory reaction, and vascularization. Superficial fibromatosis (plantar fibromatosis/Dupuytren contracture) Generally, they respect fascial borders and remain within Lipomatous lesions Lipoma anatomic compartments until late in their course. It is this Lipomatosis pattern of growth which gives most sarcomas relatively Hibernoma well-defined margins, in distinction to the general concepts Intramuscular lipoma of margins used in the evaluation of osseous tumors. Neural fibrolipoma Increased signal intensity in the skeletal muscle sur- Lipoblastoma Lipoblastomatosis rounding a musculoskeletal mass on T2-weighted SE MR Liposarcoma images or other fluid-sensitive sequences (i. These results are based on studies in which both lesions MPNST (malignant peripheral nerve bone and soft-tissue lesions were evaluated. Although sheath tumors) this increased signal intensity may be seen with malig- Synovial lesions Pigmented villonodular synovitis nancy, in our experience this finding is quite nonspecif- Giant cell tumor of tendon sheath Synovial chondromatosis ic. In fact, prominent high signal intensity surrounding a Synovial cyst soft-tissue mass more commonly suggests an inflamma- Synovial sarcoma tory processes, abscesses, myositis ossificans, local trau- Tumor-like lesions Aneurysm ma, hemorrhage, biopsy or radiation therapy rather than Abscess a primary soft-tissue neoplasm. These researchers found that malignancy Hematoma was predicted with the highest sensitivity when lesions Myxoma had a high signal intensity on T2-weighted images, were Pseudoaneurysm larger than 33 mm in diameter, and had an heterogeneous Table 2. Distribution of common malignant soft-tissue tumors by anatomic location and patient age: part I. MFH, malignant fibrous histiocytoma; DFSP, dermatofibrosarcoma protu- berans; MPNST, malignant peripheral nerve sheath tumor a Based on an analysis of 12,370 cases seen in consultation by the Department of Soft Tissue Pathology, AFIP, over 10 years (modified from AJR 1995;164:129-134) b 5(45) indicates there were 5 fibrosarcomas in the hand and wrist of patients 0-5 years, and this represents 45% of all malignant tumors in this location and age group Table 3. Distribution of common malignant soft-tissue tumors by anatomic location and age: part II.

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Psychosocial Issues in Conditions of the Eye and Blindness 137 The most common mobility aid is the with visual impairment (Vance proven fucidin 10gm, 2000) purchase fucidin 10gm fast delivery. An viewed as malingerers by their families orientation and mobility specialist pre- and acquaintances because they can see scribes the cane according to the individ- some things but not others discount fucidin 10gm. The ed of denying their condition by those individual moves the cane rhythmically in who expect individuals with visual impair- an arc in front of the body to ensure a safe ments to be dependent and isolated. Although this pro- Adjustment to vision loss is not necessar- vides some protection, it does not account ily correlated with the degree of remain- for objects above the waist that are in the ing vision. In an attempt to com- do not have fewer adjustment issues than pensate for this type of obstacle, some those who are totally blind, and in fact canes have tone-emitting radar units that may have more adaptation difficulties be- give a differential pitch for the direction cause their partial sight presents an am- and height of obstacles in front of the biguous situation for others. Some individuals prefer col- individuals with partial sight may exhib- lapsible, folding, or telescopic canes, it high levels of anxiety because they may which are less obtrusive and can be col- be unsure about whether or when they lapsed and slipped into a purse or under will lose more of their residual vision. Even when individuals with severe Electronic travel aids may also be used. When the light beam or ultrasound activities for which they are more depend- wave hits an object in the individual’s ent on assistance from others. In other instances individu- Partially Sighted als, in an attempt to demonstrate self- reliance and independence, may reject Individuals with low vision or who are help from family and friends, causing partially sighted do not quite fit into the alienation and social isolation. Counseling category of either the blind or sighted pop- individuals to understand sighted people’s ulation. Consequently, they often have reactions may facilitate social interactions special needs that are overlooked. The and enhance the development of con- social community often lacks understand- structive and realistic interactions. At ing of the true nature of vision impair- times, individuals with visual impair- ment, so that individuals with low vision ment may find it helpful to share their are ridiculed in public for appearing to see experiences and problems with others more than would be expected by a person who also have low vision. Because of their lack of visual expe- avoid potential rejection or avoidance by riences in their environment, such as the others. They may deny their disability observation of others’ tasks or behaviors, altogether and associate only with sight- concepts that sighted individuals often ed persons in an attempt to be accepted take for granted must be learned by oth- by the mainstream of society. This adaptive learning of tasks make excuses for awkward behavior or then becomes a natural part of their devel- attempt in other ways to conceal the fact opment, so that adjustment to visual lim- that they have low vision. They may itations is incorporated into their self- refuse to use low-vision aids, such as a perception and daily activities as a normal cane, for mobility or reject suitable orien- part of growing up. In extreme Individuals with loss of vision later in cases they may engage in dangerous life have the advantage of being able to activities such as illegal driving. People draw on visual experiences in the environ- often view the ability to drive as very ment as a frame of reference for physical important to the maintenance of inde- concepts, but they may find it more dif- pendence. This makes it extremely diffi- ficult to accept blindness than those who cult for individuals who are losing their have never had vision. Further- lose vision later in life must modify their more, by its very nature, the gradual loss self-perception as a result of physical of vision creates a time period in which changes and the subsequent need to re- the decision to stop driving is particular- structure daily activities. The emphasis on self-care and are newly blind may experience grief and independence for individuals with partial despair over their loss of visual function. Some may become reluctant to interact in social sit- Psychological Issues in Conditions of uations because they want to avoid the the Eye and Blindness awkwardness of initial attempts at social interactions. Loss of control over standard Vision loss often precipitates a sense of methods of initiating conversations (e. Visual impairments may be of sighted persons, and often prolonged present at birth, or they may develop sud- gaps in conversations may lead newly denly or slowly at any time in an individ- blind individuals to believe that they are ual’s life. Individuals with a on many factors, including the degree of visual loss must adjust their self-concept loss and the age at which the individual and personal goals to take into account becomes visually impaired. Activities eye, or chemical burn) may have to cope such as bathing, combing the hair, shav- not only with sudden loss of vision but ing, applying makeup, and dressing in a also with insurance company representa- coordinated fashion can all be performed tives, attorneys, and other legal and independently through skills training and bureaucratic aspects surrounding the cir- systematic organization and labeling of cumstance of their disability. Some individ- Vision is crucial for many activities of uals have difficulty adjusting to this loss daily living. In other instances, documents vision must learn new techniques for car- or forms must be translated into Braille or rying out routine activities of self-care and read to the individual, perhaps reducing mobility.

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The role of the A1 receptor cheap fucidin 10gm mastercard, more concentrated on GABA/SP neurons and linked to D1 receptors order 10 gm fucidin with mastercard, is even less clear although there is evidence that these two adenosine receptors have reciprocal effects buy cheap fucidin 10 gm online. Whether A1 activation would result in 318 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION reduced activity of the Dir Path and possibly alleviate levodopa-induced dyskinesias remains to be seen, but it does counteract D1-driven GABA release in that pathway. Summary of therapy Apart from dopamine many NTs such as glutamate, GABA, various peptides, adenosine and ACh are all involved in striatal function but their wide distribution in the CNS makes it difficult to restrict any manipulation of their activity to the striatum after systemic drug administration. By contrast, the unique loss of DA in PD and its relative restriction to the striatum makes it more amenable to manipulation and augmenting dopamine function is currently the only realistic and effective therapy for PD. Nevertheless, increasing knowledge of basal ganglia circuitry and modifying other NTs involved could lead to some improvement in overall therapy while DA-based therapy itself could be improved. The swings in response to levodopa might be avoided by using DA agonists that are not simply the most potent and specific for D2 receptors, as this may overcompensate for DA loss, while if levodopa-induced dyskinesias depend on D1 receptor stimulation then using levodopa with a D1 antagonist or partial agonist might overcome them. Foetal mesencephalic tissue has been implanted in the striatum of PD patients and it survives sufficiently for axons to extend, branch and innervate neurons. Experimental studies show DA is formed and in patients PET scans show increased fluorodopa uptake, some function is restored and the dose of levodopa can be reduced. Although DA release cannot be measured directly in patients, there is in fact indirect evidence for it from studies in one transplant patient (Piccini et al. These showed that 10 years after a graft into one putamen the number of D2 receptors there as measured by PET scans of the binding of the specific D antagonist (11C) raclopride was normal but upregulated (by 44%) in the non-grafted 2 putamen. Since postsynaptic DA receptors are known to increase in number if DA release is reduced this was taken to indicate that DA release was still reduced on the untreated side but restored to normal on the graft side. Also amphetamine, which releases DA to compete with and reduce raclopride binding, did this more effectively on the grafted side Ð another indication of greater DA release. Unfortunately transplants require 6±7 foetal brains to obtain enough transplantable material for one patient, which itself raises ethical considerations, and as the tissue cannot diffuse its influence is restricted, even with multiple injection sites, and only a fraction (approx. Also without knowledge of the cause of PD the transplant could meet the same fate as the original neurons. The concept, however, demands perseverance and a number of variants are being tried. Some ethical and practical concerns may be overcome by the use of porcine rather than human foetal cells and their potential is on trial. Certainly xenotransplants can survive in the human brain partly because it does not show the same immunoreactivity as the rest of the body but recipients will still require some immunosuppressant drugs. Attempts are also being made, with some success, to expand mesencephalic dopamine DISEASES OF THE BASAL GANGLIA 319 neurons in vitro by the use of nerve growth factors, and so produce large numbers for transplant. Non-neuronal transplants such as adrenal chromaffin cells have been tried but do not survive although some L-dopa-producing cell lines (e. PC12) or glomus cells of the carotid body do produce DA in vivo and may provide the equivalent of a continuous infusion of dopa (and DA) directly into the brain. Expression of tyrosine hydroxylase to promote dopa and DA synthesis in striatal cells by direct gene transfer in vivo or in cultures for subsequent transplanting, may also be possible. The same effect could be achieved quite specifically and permanently by lesioning the SThN or GP. Surprisingly, stimulation of SThN and GP through chronically implanted electrodes is also effective but since this required high-frequency stimulation (100 Hz) it is possible that this is blocking rather than initiating impulse flow and is like a temporary lesion. AETIOLOGY AND PREVENTION If the symptoms of PD arise when nigra cell loss results in a particular depletion of striatal DA (e. Fortunately this is not the case as many people can reach 90 or 100 years without developing PD. In fact, PM studies show that in normal subjects nigra DA cell loss proceeds at 4±5% per 10 years but in PD sufferers it occurs at almost ten times this level (Fearnley and Lees 1991). Thus either the gradual loss of nigral cells and striatal DA is accelerated for some reason in certain people, so that these markers fall to below 50% of normal around 55± 60 years, or some people experience a specific event (or events) during life which acutely reduces DA concentration. This could be to a level which is not enough to produce PD at the time but ensures that when a natural ageing loss of DA is superimposed on it the critical low level will be reached and PD emerge before natural death. The first possibility is likely to have a genetic basis but although examples of familial PD are rare there is typically an increased incidence (2±14) of the disease in the family of a PD patient and initial PET studies show a much higher (53%) loss of DA neuron labelling in the monozygotic than the dizygotic twin of a PD sufferer even if the disorder is not clinically apparent. While a number of gene markers have been identified in different families there is no consistent mutation although parkin on chromosome 6 and a synuclein on 4 have aroused most interest. Mutations of the gene encoding the latter, such as threonine replacing alanine on amino acid 53 (A53T) or phenylalanine for alanine on 30 (A30P) have certainly been established in particular families with inherited PD.

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