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By: D. Kor-Shach, M.B.A., M.B.B.S., M.H.S.
Associate Professor, Loyola University Chicago Stritch School of Medicine
Since the first edition of this book allergy treatment elderly 25 mg promethazine otc, revisions of the nomenclature have been made by the American Psychiatric Association allergy symptoms fever buy promethazine in india. The classification of psychopathic personality was changed to that of sociopathic personality in 1958. Like most psychiatrists I continue to think of the people who are the subject of this book as psychopaths and will most often refer to them by this familiar term. Sociopath or antisocial personality will sometimes appear, used as a synonym to designate patients with this specific pattern of disorder. Although I spared no effort to make it plain that I did not have an effective therapy to offer, the earlier editions of this book led to contact with psychopaths of every type and from almost every section of the United States and Canada. The interest was desperate, however, among families, parents, wives, husbands, brothers, who had struggled long and helplessly with a major disaster for which they found not only no cure and no social, medical, or legal facility for handling, but also no full or frank recognition that a reality so obvious existed. Telephone calls from Chicago, Denver, Boston, and the West Indies and letters from Miami and Vancouver have convinced me that the psychopath is no rarity in any North American community but that his problem is, by what seems to be an almost universal conspiracy of evasion, ignored by those therapeutic forces in the human group that, reacting to what is biologically or socially morbid, have sensibly provided courts, operating rooms, tuberculosis sanatoriums, prisons, fire departments, psychiatric hospitals, police forces, and homes for the orphaned, the ill, the psychotic, and the infirm. The measures taken by the community to deal with illness, crime, failure, contagion are, one might say, often far from perfect. It cannot, however, be said, except about the problems of the psychopath, that no measure at all is taken, that nothing exists specifically designed to meet a major and obvious pathologic situation. Communications from physicians, sociologists, psychologists, students, and others from Europe, some from countries behind the Iron Curtain, and also from India, Australia, and other distant parts of the world continue to arrive. One interesting, stimulating and deeply appreciated comment came a few years ago from a physician stationed in Antarctica. These communications convince me that the psychopath presents an important and challenging enigma for which no adequate solution has yet been found. Although still in the unspectacular and perforce modest position of one who can offer neither a cure nor a well-established explanation, I am encouraged by ever increasing evidence that few medical or social problems have ever so richly deserved and urgently demanded a hearing. Although I still have no effective treatment to offer for the psychopath (antisocial personality), it has encouraged me to feel that this book has, perhaps, served a useful purpose in making clearer to the families of these patients the grave problems with which they must deal. Apparently many psychiatrists, and many other physicians, have over the years advised relatives of psychopaths to read the Mask of Sanity. The response of these relatives has given me deep satisfaction and has helped me to feel that efforts to pursue this study are not in vain. Although we may still be far from the goal of offering a cure, perhaps something has already been done to focus general interest on the problem and to promote awareness of its tremendous importance. This must be accomplished, I believe, before any organized attempt can be made by society to deal adequately, or even cogently, with the psychopath. Even now, thirty-four years after the first edition of this book was published, I often receive several letters a week from wives, parents, brothers, or other kinsmen of psychopaths. Most of these letters help me to feel that this book has at least enabled many people to see more clearly and realistically the nature of the problem with which they have had to deal blindly and in a strange and almost unique confusion. These correspondents often tell me that this book has been of great value in helping them understand better the disorder of a husband, wife, child, or sibling and plan more realistically and effectively to deal with situations heretofore entirely unpredictable and incomprehensible. The many hundreds of letters thanking me for even such a modest achievement encourage me to feel that a fifth edition may be worthwhile and that it deserves my most serious thought and concern. It is a privilege to thank friends, colleagues, and others who have given me help and encouragement in formulating my concepts and in preparing material for this book. It could not have been written without the constant assistance of my wife, Louise Cleckley, who devoted many months of her time over the years not only to the routine of typing and proofreading but to the mutual effort of shaping the essential concepts to be presented into articulate form. Her notable contributions included stimulus, encouragement, and a wisely critical presence during the conative and affective fluctuations apparently inescapable in such a task. Thigpen, my medical associate of many years, has played a major part in the development and the revision of this work. His observations and his thought, available to me during innumerable pleasant and stimulating hours of discussion, have assisted and profoundly influenced my own conclusions. My debt to him in this, and my gratitude, I can acknowledge but cannot fittingly express. Aid in clarifying several important points was given me also by John Creson and by Wayne Thigpen.
The imaginary line dividing nasal and temporal fibers passes through the center of fovea allergy testing yahoo 25mg promethazine amex. All temporal fibers lying lateral to the line do not cross allergy and immunology salary discount promethazine online visa, while the nasal fibers cross to the opposite optic tract in the chiasma. Because of this orderly arrangement, the superior visual field is projected onto inferior retina, the nasal field onto temporal retina, the inferior visual field onto superior retina and the temporal field onto nasal retina. Owing to this inverted relationship, lesions of the retina cause defects in the corresponding opposite visual field. Lesions of the Optic Nerve Involvement of both the optic nerves causes complete blindness with the absence of pupillary. If only one optic nerve is damaged, it results in ipsilateral blindness with loss of ipsilateral direct and contralateral consensual pupillary reactions. The lesion of the proximal part of optic nerve results in ipsilateral blindness and contralateral superotemporal field defect (Traquair junctional scotoma) due to looping of crossed fibers in the optic nerve of opposite side. Lesions of the Optic Chiasma the nasal fibers, which constitute about 60% of the total fibers, cross in the chiasma to the opposite optic tract. The fibers from the lower and nasal quadrants of the retina bend medially into the anterior portion of chiasma. After crossing, the anterior fibers in the chiasma loop into the optic nerve of opposite side. The chiasmal fibers, because of their closeness to pituitary gland, are liable to be compressed by enlargement of the gland resulting in optic atrophy. As one side is usually compressed before the other, the earliest defect is a unilateral scotoma. An intra-sellar or extra-sellar tumor produces pressure upon the chiasma and causes early loss in the upper half of field, while supra-sellar tumors cause early loss in the lower half of visual field, and later bitemporal hemianopia may develop. When there is loss of the temporal half of one field of binocular vision and the nasal half of the other field the condition is called as homonymous hemianopia. Lesions of the Visual Pathway 327 pretectal area in the midbrain where they synapse. The association of hemianopia with contralateral third cranial nerve palsy and ipsilateral hemiplegia indicates an optic tract lesion. Syphilitic and tuberculous meningitis, tumors of optic thalamus, tentorial meningioma and aneurysm of the superior cerebellar and posterior cerebral arteries cause optic tract lesions. Lesions of the Optic Tract the optic tract carries uncrossed temporal fibers of the same side and crossed nasal fibers of the opposite side, therefore, a lesion of the tract results in homonymous hemianopia. As the arrangement of the nerve fibers in the tract is not regular, lesions of the tract give incongruous (two sides not exactly equal) homonymous hemianopia. The afferent pupillary fibers (20%) accompany the visual fibers in the optic tract and reach the Lesions of the Optic Radiations the visual fibers running between the lateral geniculate bodies and the occipital lobe constitute the optic radiations. The fibers from the temporal upper quadrant of the ipsilateral and the nasal upper quadrant of the contralateral retina are present in the upper half of the radiation, while the lower half of the radiation represents the lower quadrants of the corresponding retina. As the nerve fibers in the optic radiations are regularly arranged, the lesions of the optic radiations (brain abscess, tumors and vascular lesions) give congruous homonymous hemianopia. More superiorly, the visual fibers travel posteriorly through the parietal lobe of brain. The lesion of the temporal lobe causes complete superior homonymous quadrantanopia. The macular fibers are spared owing to their widespread but segregated course in the optic radiations and their dual representation. Lesions of the Visual Cortex the visual cortex is an area above and below the calcarine fissure which extends into the floor of the fissure as well as to the posterior pole of the occipital cortex. The lesions of the visual cortex classically produce homonymous hemianopic field defects. The visual cortex is affected by injury, especially a fall on the back of the head or gunshot injury, cerebral tumors and cerebrovascular accidents. When the cortical lesion is situated near the angular gyrus, wordblindness is observed.
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Retinal hemorrhages can occur in a wide variety of conditions such as trauma allergy testing geelong buy promethazine american express, hypertensive and diabetic retinopathies allergy medicine best purchase promethazine with mastercard, occlusion of central or branch retinal vein and blood dyscrasias. It is characterized by telangiectatic blood vessels, multiple small aneurysms and varying amount of yellowishwhite exudates and hemorrhages near or temporal to the fovea. The lesion is usually raised and may cause exudative detachment of retina, cataract and glaucoma. Retinal Hemorrhages the retinal hemorrhages are either intraretinal (within the tissue) or preretinal. The hemorrhages assume a characteristic appearance according to their location, conforming to the anatomical peculiarities of the layer in which they lie. The superficial hemorrhages lie in the nerve fiber layer and assume striate or flame-shaped appearance. Initially they are large and round, but soon become hemispherical due to the sedimentation of erythrocytes. The oxygenation causes obliteration of premature retinal blood vessels followed by fibrovascular proliferation. Besides exposure to excessive concentration of oxygen, low birth weight and prematurity increase the risk of developing the disease. Stage 1: A thin irregular grayish-white demarcation line is seen separating the avascular peripheral retina from the vascular posterior retina. Stage 3: the ridge is associated with extraretinal fibrovascular proliferation and hemorrhages in the retina and the vitreous. Retinopathy of prematurity is differentiated from retinoblastoma by a positive history of prematurity, low weight at birth and oxygen therapy. At least 2 detailed dilated fundus examinations using an indirect ophthalmoscope are recommended for all infants with a birth weight of less than 1500 grams or with a gestational age. The child should be followed up every 1 to 2 weeks until the retina gets fully vascularized. Central Retinal Artery Occlusion Etiology the central retinal artery is occluded almost always at the lamina cribrosa due to its narrowing. The obstruction in young people may be due to the spasm of vessels seen in toxemia of pregnancy and quinine toxicity, while in advanced age group it is associated with arteriosclerosis and hypertension. Occasionally, the occlusion may occur due to increased intraocular pressure as seen in acute angle-closure glaucoma or excessive pressure on the globe during retinal reattachment surgery or neurosurgical procedures. The retinal arteries appear thread-like, while there is no change in the caliber of retinal veins. There occurs a striking cherry-red spot at the macula as the choriocapillaris shine against the ischemic white background of macular edema. If the occlusion is incomplete, a slight pressure on the globe may present a cattle-truck phenomenon, the segmented blood column moves in a jerky way in the veins sometimes in the normal direction of blood flow and sometimes in the opposite. When the central retinal artery blockage remains for more than 90 minutes, the retina undergoes atrophic changes with serious visual loss. Later the edema clears up, the retina regains its transparency and near normal sheen mostly owing to the viability of its outer layers which get their nourishment from the choroid. The eye loses useful vision due to optic atrophy, and the direct pupillary reaction to light becomes absent. Rubeosis iridis may develop in a small percentage of eyes with obstruction of the central retinal artery that may be complicated by neovascular glaucoma. It occurs sooner after arterial occlusion (mean period of 4-5 weeks) than venous occlusion. The emboli can be from carotid arteries containing cholesterol (Hollenhorst plaques), arteriosclerotic vessels consisting of platelet-fibrin, or cardiac valvular diseases comprising calcium. Other causes include fat emboli from fractures of long bones, septic emboli form infective endocarditis and talc emboli in drug abusers. Sickle-cell anemia, coagulation disorders, trauma, migraine, and oral contraceptives may also cause branch retinal arterial occlusion. If the patient reports early, attempts should be made to restore the retinal circulation by massaging the globe intermittently for at least 15 minutes.
The anterior part of the capsule is formed by the tendon of the quadriceps femoris muscle food allergy treatment 2013 buy 25 mg promethazine fast delivery, which also supports the patella allergy shots child promethazine 25 mg discount. Intracapsular structures include two cruciate ligaments that cross each other, extending from the intercondylar notch of the femur to the intercondylar eminence of the tibia. The superior surface of the tibia, showing the semilunar cartilages and the cruciate ligaments. Semilunar cartilages or menisci are incomplete discs of white fibrocartilage lying on top of the articular condyles of the tibia. They prevent lateral displacement of the bones, and cushion the moving joint by shifting within the joint space according to the relative positions of the articulating bones. They prevent friction between a bone and a ligament or tendon and between the skin and the patella. The menisci are not covered with synovial membrane because they are weight bearing. External ligaments of the joint provide further support, making it a hard joint to dislocate. The main ligaments are the patellar ligament, an extension of the quadriceps tendon, the popliteal ligaments at the back of the knee and the collateral ligaments to each side. When the joint is locked, it is possible to stand upright for long periods of time without tiring the knee extensors. The main muscles extending the knee are the quadriceps femoris, and the principal flexors are the gastrocnemius and hamstrings. There are four important ligaments strengthening this joint: the deltoid and the anterior, posterior, medial and lateral ligaments. Movements are produced by muscles in the leg with long tendons that cross the ankle joint, and by muscles of the foot. The tendons crossing the ankle joint are encased in synovial sheaths and are held close to the bones by strong transverse ligaments. In addition to moving the joints of the foot, these muscles support the arches of the foot and help to maintain body balance. Muscle tissue Learning outcomes After studying this section you should be able to: identify the main characteristics of skeletal muscle relate the structure of skeletal muscle fibres to their contractile activity describe the nature of muscle tone and fatigue discuss the factors that affect the performance of skeletal muscle. Three types of muscle tissue are identified: smooth, cardiac and skeletal, each differing in structure, location and physiological function. Smooth muscle Smooth (involuntary or non-striated) muscle is not under conscious control. Unlike skeletal and cardiac muscle, smooth muscle cells do not have a striped appearance under the microscope. Smooth muscle forms sheets in the walls of hollow organs and tubular structures to regulate diameter and propel substances through tracts. Some smooth muscle units have the ability to initiate their own contraction independently of nerve stimulation (automaticity); cardiac muscle has this property too. In addition some hormones and local metabolites may influence contraction; for example, adrenaline (epinephrine) from the adrenal medulla dilates the airways. Cardiac muscle Cardiac muscle is found exclusively in the wall of the heart (see also p. Skeletal muscle this type of muscle is also called voluntary muscle because there is conscious control over it; these muscles are attached to bone via tendons, and are used to move the skeleton. It is also referred to as striped or striated muscle because of the characteristic banded pattern of the cells seen under the microscope. Within the muscle, the cells are collected into separate bundles called fascicles, and each fascicle is covered in its own connective tissue sheath called the perimysium. Within the fascicles are the individual muscle cells, each wrapped in a fine connective tissue layer called the endomysium. They bind the fibres into a highly organised structure, and blend together at each end of the muscle to form the tendon, which secures the muscle to the bone. Often the tendon is rope-like, but sometimes it takes the form of a broad sheet called an aponeurosis. The multiple connective tissue layers throughout the muscle are important for transmitting the force of contraction from each individual muscle cell to its points of attachment to the skeleton. The fleshy part of the muscle is called the belly, and when the muscle contracts it bulges and becomes shorter.