Business model and planning case study

Table of Contents Customer Value Capabilities Connected Activities Works Cited Customer Value The firm is at a position of utilizing technology to the point of improving the quality of living all over the world. The firm invented machines that enabled the consumers to find ease especially in movement. The invention of the iBot made it easier for the consumers to move up and down stairs and even over rough surfaces. Advertising We will write a custom essay sample on Business model and planning case study specifically for you for only $16.05 $11/page Learn More Home choice dialysis machine was made in such a manner as to enable the patients with chronic renal failure move freely. It is also portable hence can be easily carried in planes or cars. There is also the intravascular stent that help patients suffering from heart problems amongst other inventions in the medical field that are reliable (Cho 319). The firm invented an alternative mode of transpo rt referred to as Segway Human Transporter. This machine offers customers and their goods convenience of moving short distances effectively. It increased the speed of movement at less amount of energy per person. The Segway HT is offered in two models the i-Series for personal and business people and the e series for transporting huge and heavy loads; it is priced like any other consumer electronic product (Cho 320). Capabilities The firms’ invention, the Segway HT, uses a design that has a smaller base with a unique stability that provides the users with safe stable and effective movement. Segway HT is provided in two unique models, the iSeries model that uses low pressure tires making it move easily over uneven grounds. The eSeries on the other hand have several capabilities which includes having an electric stand that enables it balance on its own, this provides the user the convenience of moving on and off the model when at work. The unit also provides for extra carriage capacity for luggage (Cho 319- 322). One of the capability gaps to be worked on is the weight of the design; it seems to be heavier than expected. To counter this gap the firm has plans to design a lighter version known as p-Series. The other disadvantage is that the design has no transportation laws to guard its use on the sidewalks. The firm’s capability lies on its dynamic stabilized technology that enables it to configure one of the most efficient means of personal transport. The Segway HT does not use fossil fuel which makes it convenient compared to other automobiles. This uniqueness makes it possible to be used in more congested cities where pollution is a threat. The firm has derived all of these capabilities from the combination of science, engineering and right focus (Cho 319- 322).Advertising Looking for essay on business economics? Let's see if we can help you! Get your first paper with 15% OFF Learn More In order to ensure stability the firm give s its employees the freedom to be innovative and creative, the manager encourages the staff and believes every idea from any person can always work provided it’s given the right attention (Cho 318). The Segway HT is unique in the sense that it has the ability of transporting people and goods without any space restrictions that most vehicles encounter. It does not need any fuelling for its operation and is reliable for short distance transportation. Connected Activities The company has tapped on the available knowledge and talent by recruiting creative people from different field of study. Through the engineers, the firm runs multiple small projects and encourages the outcome hence making quick development of any good idea generated (Cho 319). The firm works hand in hand with development experts from outside the company. The partners provide financial support and required technology whenever need arises. This helps the firm meet the expected deadlines during the process of dev elopment. The partners include; silicon sensing systems for integrated circuit boards and Axicon for gear manufacture (Cho 321). The firm promotes the sales of this machine through the Segway LLC which acts as marketing channel for the product. The firm has an experienced management team from other recognized companies that have helped in the development process, operations, human resource management, financial management, sales and marketing process (Cho 323). Works Cited Cho, Christopher, et al. Segway Human Transport case study. 29th March, 2010 www.dekaresearch.com/ This essay on Business model and planning case study was written and submitted by user Yadiel Hayes to help you with your own studies. You are free to use it for research and reference purposes in order to write your own paper; however, you must cite it accordingly. You can donate your paper here.

Critical Study of the Aetiology and Pathogenesis of Infantile Glaucoma The WritePass Journal

Critical Study of the Aetiology and Pathogenesis of Infantile Glaucoma Introduction Critical Study of the Aetiology and Pathogenesis of Infantile Glaucoma IntroductionEpidemiology of Primary Infantile Glaucoma Signs, Symptoms and Consequences of Primary Infantile GlaucomaPathology, Pathogeneses and Causes of Primary Infantile GlaucomaOptic Cup Asymmetry in Primary Infantile Glaucoma Secondary infantile glaucomaReferencesRelated Introduction The incidence of glaucoma in the young population is incomparable to the incidence in the adult population, as it is very rare in infants, nevertheless it can significantly affect a child’s life, as vision is vital for a young child. Signs and symptoms of infantile glaucoma can commonly be overlooked and this can cause a delay to the treatment process. The underlying causes of infantile glaucoma have been agreed upon by most authors, however the exact mechanism by which the structures in the young eye are affected are debatable. As well as primary infantile glaucoma, young children can also be affected by secondary infantile glaucoma, which again can significantly impact a young child’s life. This paper looks at the classifications, epidemiology, signs, symptoms, aetiology and pathogenesis of primary infantile glaucoma, as well as touching upon the causes of secondary infantile glaucoma. ‘Glaucoma is an Optic neuropathy with characteristic appearances of the optic disc and specific pattern of visual field defects that is associated frequently but not variably with raised intra-ocular pressure (IOP)’ (Kanski, 2003). The ciliary processes of the eye produce aqueous humor; this is then drained by the trabecular meshwork; Figure 1. A balance of this production and drainage maintains a normal IOP. The aqueous humor produced flows into the posterior chamber, then through the pupil and into the anterior chamber. The trabecular meshwork drains the aqueous humor through Schlemm’s canal. Open angle glaucoma occurs when there is a decrease in the outflow of aqueous through the trabecular meshwork, and angle closure glaucoma occurs when the iris adheres to the lens leading to a build-up of aqueous humor in the posterior chamber   (Kanski, 2003). In addition to open and closed angle glaucoma there are other types of glaucoma which are classified in Figure 2. There are several classifications of congenital and infantile glaucomas, the most accepted and simplified version is presented in figure 3. Primary infantile glaucoma is defined as ‘the result of isolated abnormal development of the anterior chamber angle structures’ (Myron Yanoff, 2009) Secondary infantile glaucomas are ‘associated with a variety of ocular and systemic syndromes and with surgical aphakia’ (Myron Yanoff, 2009). Primary congenital glaucoma is present at birth however it is not always recognised at this stage and sometimes it is diagnosed later during infancy or in early childhood. To minimise problematic visual development, recognition of primary congenital glaucoma must be as early as possible followed by respective treatment or therapy, allowing the child to lead a ‘normal’ life (A.Armstrong, 2008). Glaucoma in infants and young children is relatively rare and in some cases asymptomatic (Kanski, 2003). And so, if an increase in IOP is not detected at an early stage then there is a greater risk of blindness (Robert N. Shaffer, 1970). Some cases of glaucoma in infants are only recognised and diagnosed after several months or years at which stage sometimes significant glaucomatous damage has already occurred (Robert N. Shaffer, 1970). Most cases will present bilaterally nevertheless this does not rule out the fact that it can sometimes present unilaterally   (Robert N. Shaffer, 1970). Epidemiology of Primary Infantile Glaucoma Primary infantile glaucoma is extremely rare and occurs in one out of 10,000 births (MillerSJ, 1966). It accounts for 0.01% to 0.04% of cases of total blindness (A.Armstrong, 2008) (Vincent P Deluise, 1983) In the Irish childhood population primary open angle glaucoma is the cause of blindness for 4% of the population. (Morin JD, 1974) The majority of cases in the US and Europe present with bilateral primary infantile glaucoma; 65%-80% (Moller, 1977). It is also well-known that it occurs greater in males compared to females with a ratio of 3:2 respectively (Vincent P Deluise, 1983). This is proven by a study with 125 infants from Westerlund, 76 of whom were male i.e. nearly 61% were males (Vincent P Deluise, 1983). On the other hand in Japan, this is no longer true and the ratio is actually reversed (Vincent P Deluise, 1983). In another study based in Japan out of 46 children with primary infantile glaucoma 63% were actually female (Vincent P Deluise, 1983). In the majority of cases the development of primary infantile glaucoma is found to sporadic, and so it is non-familial and nonhereditary, but approximately 10% of cases are familial, transmitted to the child via autosomal recessive inheritance (Vincent P Deluise, 1983). Signs, Symptoms and Consequences of Primary Infantile Glaucoma Children are commonly referred to the Ophthalmologist due to clinical evidence of corneal oedema. Primary infantile glaucoma is commonly misdiagnosed, hence causing a delay in the correct diagnosis, as it may initially show symptoms similar to conjunctivitis such as a ‘red eye’ (Becker B, 1965). There will also be evidence of the classic triage; epiphora, blepharospasm and photophobia. (Becker B, 1965). Further examination will reveal megalocornea (enlarged corneal diameter), buphthalmos (enlarged globe), Haab’s striae (breaks in Descemet’s membrane) and optic nerve head changes (Becker B, 1965). Buphthalmos; figure 4, or ocular enlargement, occurs in primary infantile glaucoma because the globe of neonates is still distensible (Vincent P Deluise, 1983). Collagen of the cornea and scleral have not hardened enough, so expansion of the fibrils occurs due to an increase in IOP (Vincent P Deluise, 1983). This therefore causes stretching to occur in several structures of the infant eye; such as the cornea, the anterior chamber angle, the sclera, the optic nerve, scleral canal and the lamina cribrosa (Becker B, 1965). This explains why ocular enlargement due to glaucoma does not occur in adults, as the globe is no longer distensible and collagen fibres of the cornea are sclera are hardened hence expansion doesn’t occur in adults. It is agreed that delayed therapy of infants with glaucoma, will result in a poor visual outcome for the infant, which could have been prevented or at least minimised. To understand why some infants had more advanced glaucoma than others; a study with 24 infants and children was conducted (David J. Seidman MD1, 3 March 1986). Their signs and symptoms were noted. The parents of the infant were asked to indicate whether they had noticed either epiphora or photophobia and only 32% said their infant had these symptoms. A small 21% of infants presented with only signs of glaucoma, noticed by the parents but no symptoms. And finally the majority of infants, 90%, actually did have signs when presenting to the physician. It has been noted that signs of infantile glaucoma are more difficult to notice when it is bilateral, as in all 3 cases where the physicians failed several times to refer the infant to an ophthalmologist the glaucoma was in fact bilateral   (David J. Seidman MD1, 3 March 1 986). A normal value for the corneal diameter of a neonate is approximately 10mm, an increase to 12mm or greater, along with expansion of the corneal-scleral junction, is usually due to increased IOP (Kwitko, 1973). Enlargement of the cornea due to an increase in IOP is most likely to occur up to the age of three (Scheie, 1955) after which the sclera may become deformed up to age ten (Mann, 1957). Breaks occur in the endothelium and Descemet’s membrane due to the increase in IOP which also causes stretching in these layers (Vincent P Deluise, 1983).   ‘Haab’s striae form as endothelial cells lay down new basements membrane (Descemet’s membrane) and hyaline ridges develop. Breaks in Descemet’s membrane from increased IOP rarely occur after age three’ (Vincent P Deluise, 1983).   Increased IOP also causes slow expansion of the sclera of the neonate. A ‘bluish’ scleral appearance is seen due to thinning of the sclera, causing the choro id to be more apparent (Vincent P Deluise, 1983). As the neonate becomes older and growth occurs the expansion of the sclera no longer occurs due to a build-up of extracellular connective tissue (Vincent P Deluise, 1983). Even if the IOP decreases back to a value within normal the globe does not usually return to normal size (Vincent P Deluise, 1983). Studies have shown that myopia and astigmatism are the consequence of an increase in the axial length of the globe, figure 5 (Robin AL, 1979). Robin et al also found that ‘In contrast to adult eyes, the scleral canal in children apparently enlarges with high IOP. Thus, disk cup size increase in children could occur from neural tissue loss, from scleral canal enlargement, or from a combination of the two processes’ (Robin AL, 1979). ‘Myopic astigmatism and anisometropia are particularly common in cases of unilateral or asymmetric primary infantile glaucoma’ (Vincent P Deluise, 1983).   A study carried out by Broughton and Parks found that all of their patients with unilateral primary infantile glaucoma had anisometropia; on the affected side an average difference of 4.93D of myopia was found (Broughton WL, 1981 May). Optic nerve changes which occur in adults with glaucoma are very different to the optic nerve changes which occur in children with glaucoma. At first Becker Shaffer initially thought that cupping in primary infantile glaucoma was a process which was gradual however it was soon discovered that optic nerve changes in primary infantile glaucoma could also occur early and rapidly (Becker B, 1965). In adults with optic nerve changes which occur due to an increase in IOP the change is very unlikely to be reversible, however in infants optic nerve cupping which occurs due to an increase in IOP can be reversed once the IOP is returned back to normal (Vincent P Deluise, 1983). The most accepted and most reasonable hypothesis which aims to explain why cupping is reversible in neonates is based on the fact that the connective tissue of the lamina cribrosa is not matured (Quigley, 1977 Sep). However there are cases when even though the pressure has decreased back to normal the Optic nerve head damage does not reverse, this is due to one of two reasons. Firstly it is possible that some of the stretching is permanent ‘with remoulding of the connective tissue’   (Vincent P Deluise, 1983). Secondly it could be due to ‘a loss of glial and axons’ (Vincent P Deluise, 1983).   ‘Adult optic nerve heads with their dense connective tissue investments are more resistant to remoulding, indicating that cupping is caused by permanent loss of glia and axons’ (Vincent P Deluise, 1983). Pathology, Pathogeneses and Causes of Primary Infantile Glaucoma The explanation for the increase in IOP in primary infantile glaucoma has been described using Barkan’s membrane theory. This theory is based on the fact that the anterior chamber angle is covered by a thin and imperforate membrane, which inhibits aqueous outflow, which in turn leads to raised IOP (Vincent P Deluise, 1983). According to the theory, this raised IOP is treated by goniotomy when the surface tissue of this membrane is detached, and so â€Å"the peripheral iris falls posteriorly,† subsequently there is aqueous outflow and a decrease in IOP (Vincent P Deluise, 1983). Worst also agreed with the Barkan membrane theory, â€Å"†¦in congenital glaucoma the chamber angle is filled with a band of persistent mesodermal tissue (persistent uveal meshwork or persistent pectinate ligament). This tissue completely covers the fetal corneoscleral system, but is not the cause of the obstruction to aqueous outflow in its own right. It is the presence of an imperforate surface layer on this persistent mesodermal tissue, which is the only cause of obstructed outflow. This surface membrane, Barkans membrane, is probably an endothelial surface, which normally breaks apart, but which persists in congenital glaucoma† (Worst, April 1968). There is no well supported histopathologic evidence to support Barkan’s membrane theory, despite this Worst still believes that the theory along with its concepts are valid, he says â€Å"though histopathologic proof of this structure is almost completely lacking†¦this has little influence on the probability th at this concept is valid† (Worst, April 1968). So if Barkan’s membrane theory has insufficient evidence to explain the cause of an increase in IOP in congenital glaucoma, then what is the alternative? There is some histopathologic evidence which aims to explain in detail the anterior chamber angle and its histopathology in infants with primary infantile glaucoma see Figure 6 (Vincent P Deluise, 1983). Anderson thoroughly researched the development of the trabecular meshwork in infantile glaucoma. He said that earlier thoughts were that â€Å"the anterior chamber recess deepens by atrophy of the rarified tissue that in the earlier stage separated the trabecular meshwork and ciliary body.† He then confirmed that later thoughts highlighted the function of cleavage into the loose tissue, as there was no proof of atrophy (D.R.Anderson, 1981). These views may have seemed correct at the time however, evidence has proven that cleavage or atrophy are not the only explanations of the process of development. Both cleavage and atrophy would cause the uveal tract to become fragmented from the shell of the cornea and sclera as well as the tissue of the trabeculae (Fig 7A) (D.R.Anderson, 1981). This would result in extension of the ciliary muscle to the peripheral iris and on the posterior surface of the peripheral iris would be the ciliary processes (D.R.Anderson, 1981). However this does not actually occur, in fact the ciliary muscle and the ciliary processes continue to adhere to the envelope of the cornea and sclera although compared to their earlier position they do become depressed (Fig 7B) (D.R.Anderson, 1981). Anderson found that there is an overlay of the ciliary muscle in particular the ciliary processes over the trabecular meshwork; however they are subsequently depressed behind the scleral spur (D.R.Anderson, 1981). He found that â€Å"This repositioning can be explained only by a posterior sliding of the uveal tissues in relation to the cornea and sclera, presumably due to a differential growth rate of the various tissue elements† (D.R.Anderson, 1981). He concluded that this course of repositioning was not simply due to the â€Å"sliding of the uveal tract along the inner side of the sclera. There is also a repositioning of the various layers within the uveal tract in relation to one another: initially the innermost muscle fibers have a position relatively more anterior than the outermost fibers† (D.R.Anderson, 1981) Anderson also found that compared to the ciliary muscle the ciliary processes are at first a lot more frontward, as time passes both become level behind the scleral spur and meshwork (D.R.Anderson, 1981). So, far it has been established that primary infantile glaucoma occurs because the anterior chamber does not develop normally. At what stage of development do these changes or lack of changes occur? It has been noted that at week twelve of development â€Å"a wedge shaped mass of mesenchyme can be identified at the anterior chamber angle i.e. at the junction of the papillary membrane and the lateral margins of the cornea. Within this wedge shaped portion of the tissue there is a row of small capillaries, which are lined with mesoderm-derived vascular endothelial cells† (A.Armstrong, 2008). At the beginning of the fifth month â€Å"early trabeculae are apparent separated by intervening spaces† (A.Armstrong, 2008) subsequently the capillaries fuse to form the canal of Schlemm, this is continuous with the collector channels as well as the scleral vessels (A.Armstrong, 2008). â€Å"The meshwork becomes specialised into inner uveal trabeculae, numerous intermediate layers of lamellar corneoscleral trabeculae, and a more loosely organised cribriform meshwork† (A.Armstrong, 2008). The inner surface of the meshwork is lined with cuboidal cells, perforations of these cells occur onwards from 15 weeks (A.Armstrong, 2008). Communication between the meshwork and the anterior chamber occur via these cuboidal cells (A.Armstrong, 2008). Between the sixth and ninth month development of the anterior chamber occurs (A.Armstrong, 2008). It presents â€Å"as a chink in the mesoderm between the iris root and the developing trabeculum. If the mesoderm does not entirely regres s in this region, an impervious layer may remain bridging the angle between the iris and the cornea and which impedes access of aqueous to the trabecular meshwork† (A.Armstrong, 2008). Figure 8: Comparision of optic cup asymmetry in normal infants with unilateral glaucoma infants. Taken from (Richardson, April 1968) Optic Cup Asymmetry in Primary Infantile Glaucoma It has been established that chronic open angle glaucoma is found to be bilateral and symmetrical to a certain extent, however some meticulous studies may find that there is somewhat of asymmetry in the cupping of the optic discs (Richardson, April 1968). Nevertheless the asymmetry of the discs can be used to diagnose early signs of glaucoma (Richardson, April 1968). Although optic disc cupping is assessed in infantile glaucoma it is not used as prominently compared to chronic open angle glaucoma (Richardson, April 1968). One of the reasons for this is due to the obvious fact that it is not as easy to conduct ophthalmoscopy in infants especially with added factors such as hazy corneas, miotic pupils (Richardson KT, 1966). It is also a common misconception that cupping in the optic nerve occurs at a very late stage and so it is no longer relevant to aid diagnosis (Richardson, April 1968). The opposite is actually true, as changes to the optic disc in infantile glaucoma occur relatively early on, hence valuable factor to aid prognosis (Shaffer.RN, 1967). To emphasise the importance of asymmetry of optic discs in infantile glaucoma compared to chronic glaucoma, the following study was conducted by Kenneth Richardson. Normal newborn infants, 96 hours old or less, were randomly chosen and their optic discs were assessed. Out of 468 it was found that only 11 infants had optic cup asymmetry, 2.3%; figure 8 (Richardson, April 1968). Similarly Snydacker found that out a random 500 adults only 15 had any sign of asymmetry, 3% (SyndackerD, 1964). Going back to the infants it was found that only 3 out of the 11 actually had marked asymmetry between their optic cups i.e. only 0.6%; figure 8 (Richardson, April 1968). A very different but much predicted result was found when Shaffer conducted a slightly different study (Shaffer.RN, 1967). 27 infants with unilateral glaucoma were assessed and it was found that 89% or 24 out of 27 had marked asymmetry; figure 8 (Shaffer.RN, 1967). In other infantile glaucoma studies Schaffer also found that 61% (52/85) patients had optic cups with a disc diameter greater than 1/3 in comparison to 2.6%(26/936) normal newborns who had optic cups with a disc diameter greater than 1/3 (Shaffer.RN, 1967). The above data provides vital evidence supporting the views that optic disc assessment in newborn infants is extremely important and any asymmetry in optic cupping is very significant as ‘normal’ infants are expected and likely to have symmetrical optic cups. Hence any asymmetry of cupping could be indicative of congenital glaucoma. Also it can be said that optic cupping assessment is of more importance in congenital glaucomas â€Å"since these cases are prone to follow a more asymmetrical course than adult glaucomas† (Richardson, April 1968). In order chronic glaucoma in order to be able to determine whether cupping is physiological or pathological the disc appearance must be tracked over many years. Whereas in newborns the cupping is expected to be symmetrical at birth therefore any asymmetry should be and can be picked up at birth (Richardson, April 1968). Secondary infantile glaucoma There are several causes of secondary infantile glaucoma, the most important is ocular trauma and this is due to the fact that ocular trauma is common in young infants. Blunt trauma to the eye causes compression of the globe which in turn leads to a temporary increase in IOP. When a blunt object hits the eye its cause indentation of the cornea, this then forces the aqueous humor â€Å"laterally against the anterior chambers angle structures and backwards against the iris and lens† (Robert N. Shaffer, 1970). Thereafter â€Å"in the anterior segment the iris sphincter ruptures† (Robert N. Shaffer, 1970) the ciliary body could become separated from the scleral spur or it may just be split or torn (Robert N. Shaffer, 1970). Likewise the trabecular meshwork may become ruptured, consequently leading to glaucoma (Robert N. Shaffer, 1970). Traumatic iritis is another cause of secondary glaucoma. Blunt ocular trauma can cause inflammatory cells and increase in proteins in the aqueous humor, in the early stages. These cells along with the protein molecules then cause obstruction of the trabecular meshwork. (Robert N. Shaffer, 1970) Oedema of the trabecular meshwork will also lead to resistance in the outflow of the aqueous. Even though there is an increase in the resistance of outflow, the IOP will remain within a normal range and in some cases it may actually be lower than normal because the blow will have caused depression of the ciliary body along with hyposecretion (Robert N. Shaffer, 1970). Anterior chamber haemorrhage (hyphema) occurs due to trauma or injury to the eye. Small haemorrhages are unlikely to clot, however large haemorrhages may fill the anterior chamber and cause compression of the meshwork which in turn leads to an acute increase in IOP (Robert N. Shaffer, 1970). Another cause of secondary glaucoma is recession of the anterior chamber angle. â€Å"A significant percentage of traumatic hyphemas results from a longitudinal cleavage of the ciliary body† (Robert N. Shaffer, 1970). A chain of damage reactions which occur to the trabecular meshwork following this will decrease the outflow and lead to glaucoma. Contusion cataract can be caused by blunt trauma. â€Å"If the cataract intumesces, a phacogenic pupillary block glaucoma may result. If the cataract becomes hypermature the lens cortex which is liquefied may leak into the anterior chamber†¦Ã¢â‚¬ , (Robert N. Shaffer, 1970) a macrophage response occurs and these cells then cause an increase in IOP as they block access of the aqueous to the trabecular meshwork. (Robert N. Shaffer, 1970) This is known as phacolytic glaucoma. Dislocation of the lens most likely occurs due to trauma, and if the lens after dislocation ends up in the anterior chamber then pupillary block glaucoma is l ikely (Robert N. Shaffer, 1970). Secondary glaucoma is usually the result of a laceration to the globe. A blunt blow, by a child’s fist, is often very serious as the smaller size of the fist does not allow the orbit to provide protection and the blow lands straight on the eye (Robert N. Shaffer, 1970). Intra-ocular foreign bodies can also cause glaucoma; particles which contain iron will oxidise and can be toxic to structures within the eye such as the trabecular meshwork (Robert N. Shaffer, 1970). Severe iritis can lead to glaucoma, and transient or chronic glaucoma can result from inflammation of the trabecular meshwork with increased resistance to outflow (Robert N. Shaffer, 1970).   Inflammation of the cornea can also cause secondary glaucoma, due to further inflammation of the meshwork leading to obstruction of the aqueous outflow (Robert N. Shaffer, 1970). It is well-known that glaucoma can be induced by steroids. An increase in IOP can be induced by prolonged use of topical steroids, in susceptible individuals. Ocular tumours uncommon in children, however if one is present it can sometimes lead to secondary glaucoma (Robert N. Shaffer, 1970). Retinoblastoma, a well-known and common tumour found in the young can also cause glaucoma. The tumour will invade the anterior chamber angle structures; iris and trabecular meshwork. There is a very strong link between prenatal rubella infection and glaucoma and it is now well agreed upon that prenatal rubella can in fact cause glaucoma. It is estimated that rubella infantile glaucoma occurs in 2-4% of children with congenital rubella syndrome (Robert N. Shaffer, 1970). It usually presents in the first six months of life and the symptoms are identical to those of primary congenital glaucoma; an enlarged oedematous cornea which is cloudy, a deep anterior chamber and the classic high IOP (Robert N. Shaffer, 1970). Clinically it is found to be almost impossible to distinguish rubella infantile glaucoma from primary congenital glaucoma (Robert N. Shaffer, 1970). In conclusion, it has been determined that although rare conditions both primary and secondary infantile glaucoma can significantly affect the life of a child. Hence examination of the optic discs at birth is vital to ensure that any asymmetry of optic cups is detected and the possibility of the newborn developing glaucoma is known immediately, as it has been proven that infants with glaucoma are significantly more likely to show asymmetry of optic cupping compared to ‘normal’ infants. If the glaucoma is not detected at birth it is vital that healthcare professionals are able to recognise the signs and symptoms of infantile glaucoma so it can be treated before any significant damage has occurred, as it has been proven that the majority of children present with all or some of the signs and symptoms of glaucoma yet they are either overlooked by the parents or misdiagnosed by clinicians. In relation to the pathogenesis of infantile glaucoma significant evidence or lack of has proven that Worst along with Barkan’s Membrane theory are no longer valid. Vital histopathologic evidence undermines the theory; in fact Anderson has provided substantial evidence to prove that repositioning, sliding, cleavage and atrophy play a significant role in the development of primary infantile glaucoma. Along with the histopathologic evidence it can be concluded that Anderson’s findings can be accepted. References A. Edward Maumenee, M. (1962). Further observations on the pathogenesis of congenital glaucoma. TR. AM. OPHTH J. SOC, VOl. 60, 140-162. A.Armstrong, R. (2008, December 12th). Congenital Glaucoma; The genetics of primary congenital glaucoma. Optometry Today, pp. 40-43. Becker B, S. R. (1965). Diagnosis and Therapy of the Glaucomas. St Louis: CV Mosby. Broughton WL, P. M. (1981 May). An analysis of treatment of congenital glaucoma by goniotomy. Am J Ophthalmol. , 91(5):566-72. Ching Lin Ho, F. a. (September/October 2004). Primary Congenital Glaucoma: 2004 Update. Journal of Pediatric Ophthalmology and Strabismus , Vol. 41:271-288. D.R.Anderson. (1981). The development of the trabecular meshwork and its abnormality in primary infantile glaucoma. Trans Am Ophthalmol Soc, 79:458-85. David J. Seidman MD1, L. B. (3 March 1986). Signs and Symptoms in the Presentation of Primary Infantile Glaucoma. PEDIATRICS , Vol. 77 No. pp. 399-404. Harley, R. D. (1983). Pediatric Ophthalmology. Saunders. John S Crawford, J. D. (1983). The Eye in Childhood. New York: Grune and Stratton. Kanski, J. J. (2003). Clinical Ophthalmology A Systematic Approach. Butterworth Heinemann. Kwitko, M. (1973). Glaucoma in Infants and Children (ed 2). New York: Appleton-Century-Crofts. Mann, I. (1957). Developmental Abnormalities of the Eye. Philadelphia: JB Lippincott. MillerSJ. (1966). Genetic aspects of glaucoma. Trans Ophthalmol Soc U K., 86:425-34. Moller, P. (1977). Goniotomy and congenital glaucoma. Acta Ophthal, pp. 55: 436-442. Morin JD, M. S. (1974). Primary congenital glaucoma: a survey. Can J Ophthal, pp. 9:17-28. Myron Yanoff, J. S. (2009). Ophthalmology. Mosby Elsevier. NEI. (1968-date). Glaucoma. Retrieved February 2011, from National Eye Institue: nei.nih.gov/health/glaucoma/glaucoma_facts.asp Quigley, H. (1977 Sep). The pathogenesis of reversible cupping in congenital glaucoma. Am J Ophthalmol., 84(3):358-70. Richardson KT, S. R. (1966). Optic nerve cupping in congenital glaucoma. Am J. Ophth., 62: 507. Richardson, K. T. (April 1968). Optic Cup symmetry in normal newborn infants. Investigative Ophthalmology, 137-140. Robert N. Shaffer, D. I. (1970). Congenital and Pediatric Glaucomas. USA: The C. V. Mosby Company. Robin AL, Q. H. (1979). An analysis of visual acuity, visual fields, and disk cupping in childhood glaucoma. Am J Ophthal , 88(5):847-58. Scheie, H. (1955). Symposiumon congenital glaucoma: Diagnosis, clinical course and treatment other than goniotomy (ed 2). Trans Am Acad Ophthalmol Otolaryngol 59, pp. 309–321. Shaffer.RN. (1967). New concepts in infantile glaucoma. Canad J. Ophth, 2: 243. SyndackerD. (1964). The normal optic disc. Ophthalmoscopic and photographic studies. Arch Ophthal, 58:958. Vincent P Deluise, D. R. (1983). Primary Infantile Glaucoma (Congenital Glaucoma). 28(1). Worst, J. G. (April 1968). Congenital glaucoma Remarks on the aspect of chamber angle: Ontogenic and pathogenic background and mode action of goniotomy. Investigative Ophthalmology, 7:127-134.

Perception Dependence Argument Essay Example | Topics and Well Written Essays - 1000 words

Perception Dependence Argument - Essay Example For instance, by stating that X=Y and Y=Z, it implies that X=Z. This is an example of logical arguments. However, there are arguments that are based on incorrect principles of logics, leading to logical fallacies and false or illogical conclusions. One type of argument that has attracted a lot of debates and controversy with regards to the truth about its premises and inferences/conclusions is perception-dependent argument. This paper thus evaluates whether the premises of the perception-Dependent Argument are true. In addition, the paper explores whether the argument’s inference are good. Perception Dependent Arguments The awareness or apprehension of one’s environment through senses such as sight, touch, hearing, smell, taste is referred to as perception, a study area that has continued to intrigue not only philosophers but also other scholars since historical times2. One reason perception-dependent arguments have always been considered fallacious is the problem creat ed by the association of perception with hallucinations and illusions. Both hallucination and illusion refer to situations in which a person perceives objects in ways that in which they do not exist. Thus, the possibilities of errors occasioned by illusions and hallucinations make the true nature of arguments based on perception questionable. Because of illusion- and hallucination-related errors, arguments, their premises and inferences, always based on perception, lead to questions on whether perceptions are intuitively what they appear to be. Perceptions could therefore not be directly linked to reality and neither are they necessarily the immediate access to reality. The possibility of hallucination and illusion errors in perception dependent arguments therefore challenges the logical nature of arguments based on perceptions. Illusion refers to a situation in which an object or subject is perceived to appear in way other than it really is. For instance, using a yellow light in a house with white walls make the walls appear have yellow color. Another example of illusion is the sour taste of a sweet drink if consumed immediately after consuming a sweeter drink. It should however be noted that illusion does not imply there is deception since one is not deceived into believing that objects are not what they are. In other words, there is a possibility that one may actually be aware that he/she is experiencing an illusion. From the illusion and hallucination errors that perception dependent arguments are prone to, it is imperative that the obvious truth of peoples’ experiences and the perception-related errors in arguments are reconciled. The perceptual experiences otherwise referred to as openness to the world, which lead to true premises and good inferences in arguments, have been consistently challenged by the existence of illusions and hallucinations. From its definition, it is apparent that basing one’s arguments on illusion will most likely re sult in false premises and bad conclusions/inferences. Arguments based on perceptions (illusions and hallucinations) always occur through certain steps. When one is under illusion, an object appears to have some characteristic or quality F. In reality, the object under view, feel, taste, or touch does not always have the perceived quality. Interestingly, another object encountered or experienced somewhere by the person under illusion possesses the quality/feature F perceived by the person. In