Facts Regarding The Moon And The Illusion Psychology Essay

Facts Regarding The Moon And The Illusion Psychology Essay 1. Introduction The moon rises in the east and settles in the west, following a trajectory route very similar to that of figure 2a. However, during this trajectory the appearance of the moon observed larger on the horizon compared to when it is in its elevated position in the sky is known as the moon illusion for e.g. ( Kaufman et al 1962, 2000, 2006 Reed Kuprinski 2009, Coren Aks 1990, Weizman Cohen 2003, Toskovich 2009, Nanavati 2009), see figure 1ab. This illusion is not only denoted to the moon, it can also be observed by other celestial constellations such as the sun and the stars (Ross and Plug, pg 1-2 2002) (Wade pg 377 2000). It has been found in some cases that the size of the horizon moon appeared almost 1-2 times the diameter of the elevated moon Kaufman and Rock (1962) Ross and Plug (1994). This experience persists even when one is familiar it is an illusion Weizman and Cohen (2003) and has been observed for many centuries, with Aristotle (384-322BC) making the first clear scientific account Ross and Plug, pg 1-2 (2002) Wade pg 377 (2000). However there have been many suggested theories from physics to physiology and now finally psychology as to why this illusion is experienced Wade pg377 (2000), but none has been accepted as the correct answer. The main conflicting issues involve contradictions as to whether it is a linear or angular illusion, thus a model which accounts for both linear and angular illusions providing a common unified explanation is required. Elevated Moon/ Zenith moon Horizon Moon 1a 1b Figure 1a http://facstaff.uww.edu/mccreadd/ and 1b http://www.lhup.edu/~dsimanek/3d/loony.htm (Ken Amis) what the actual illusion looks like in its two comparative positions and an illustration of what the names horizon and elevated moons infer to within this text. 2. Facts regarding the moon and the illusion This is regarded as an illusion because the increase in perception of size occurs even though the visual angle (V) subtended on the eye remains the same regardless of the trajectory position of the moon, i.e. whether the moon is on the horizon or in its elevated position-see figure 2 (For e.g. C.Reed and E. Kuprinski 2009, Kaufman et al 2000). Physically if the angular size changes then a subsequent change of the retinal image size would occur, but it remains constant and hence is regarded as a perceptual phenomenon. The value of this angle has long been accepted as a fairly constant value of 0.52 degrees regardless of elevation For e.g. (Bears, Conners and Paradiso, pg 288,3rd edition, 2006, R Casati, 2003, Ross and Plug, pg 11-14, 2002, Mccready section 1 website). Furthermore evidence can be found in photographs, where many photographers have experienced the illusion, however after photographs become developed the moon image appears small Nanavati (2009). For e.g. Ross and Plug pg 60 (2002) took multiple photos of the sun during different periods of the day and found the size of the sun to be exactly the same during each interval at the different trajectories, similar to figure 2b. Since the camera can only illustrate the linear dimensions of an object this would further enforce the suggestion the illusion is in fact a perceptual phenomenon. Another demonstration involves a simple test called Herings manoeuvre, whereby a subject holds a coin close to their eye at arms length and observes the trajectory of the moon. The result of this will always be that the moon and the coin are the same size no matter what position of trajectory of the moon The Moon Illusion, a literature thesis by Bart Borghuis, (1999), Gregory (2007). Figure 2a http://antwrp.gsfc.nasa.gov/apod/ap020130.html Credit and copyright to Shay Stephens. He picture shows the moonrise trajectory over Seattle, USA, with a snapshot taken every 2.5mins. 2a 2b Figure 2 Taken from Mccready section 1 illustrating the size of the moon does not change with the trajectory and nor does the visual angle subtended. The illusion maybe experienced in different areas of the world and the facts about the orbit of the moon around the earth can be used to explain as to why any variances in the earth-moon distance cannot play a role in the illusion. The moon travels in an orbit around the earth completing one full cycle every ~29days (1 month). The mean Earth-Moon distance is fairly constant throughout this period, however there is a degree of variance in the Earth-Moon distance caused by the elliptical shape of the orbit of travel (Nasa website). This variance causes the size of the visual angle of the horizon moon to become 2% smaller than the elevated moon and may only affect only short time viewing i.e. vieiwning the moon during separate hours in the same day Nanavati )2009), but not significant enough to cause the illusion (Mccready section 1). The distance of travel of the orbit has been monitored by NASA since the initial experimentation was carried out using retro-reflector beams/laser used in the Apollo 11 mission to the moon Faller et al (1969, 1970). The moon travels in an orbit of fairly constant mean distance of 384,000km (NASA website) from the earth and hence discounting the physical distance factor creating the illusion. The size (S) is It has been well established the physical size, distance and visual angle do not change (or not by a significant factor), however Aristotle suggested there was a physical cause that created a real magnification on the image size Nanavati (2009). It was thought this was caused by the atmospheric refraction, which had its effects greatest on the light rays on the horizon causing an increase in the moon size The Moon Illusion, a literature thesis by Bart Borghuis (1999), Ross and Plug pg57 (2002) i.e. like a stone under water where it appears to enlarge in size. However this theory was later disregarded as there was no means of measuring the actual horizon enlargement and if any it was deemed neglible, however many writers and investigators supported the idea that it could possibly play some form of secondary role Ross and Plug pg57 (2002), Gregory (2007). 3. Linear distance illusions 3.1 Size distance invariance hypothesis and Emmerts law The SDIH theory proposes the cause of the horizon moon appearing bigger is due to the extended terrain viewed in between the observer and the horizon moon, thus placing it at a perceptually further distance, for e.g. Kaufman (2000, 2006, 2007), Suzuki (2007), Gregory (2007). The SDIH assumes perceived angle (V) like the objective angle (V) is unchanged Reed and Kuprinski (2009) and implies distance is computed primarily by the visual system, while size is later inferred from this. Due to these conditions where perceived angle (V) is kept constant, only perceived distance (D) and size (S) can only change, thus suggesting a linear distance/size illusion and not an angular illusion Higashiyama (2004) Lou (2007). The SDIH can be illustrated by the formula S/D=tan V (apparent size S, apparent distance D and the physical visual angle V) Higashiyama (2006) Kaufman (2006), see figure 3. The SDIH implies the perceived size (S) is directly proportional to perceived distance (D) and this relati onship can be explained using Emmerts law. The conditions of Emmerts law are the perceived size of an object subtending a constant visual angle is directly proportional to its apparent distance Gregory (2007) Philip Servos (2006). Emmerts law in effect is the description of the size distance invariance hypothesis (SDIH) Jones et al (2009) and is one of the more researched theories within this topic. Afterimages are often used as a means to display Emmerts law since they have a constant visual angle always subtended at any distance and therefore a fixed retinal image size at all times disregarding any changes in angular size Lou (2007). Due to this retinal image size being a constant size, means any increase in the afterimage size cannot be due to any angular illusions. Since Emmerts law states size is proportional to apparent distance, then afterimages can be classed as one means of evidence for the SDIH. Figure 3 SDIH diagram taken from section 2 of http://facstaff.uww.edu/mccreadd/sectionII.html Most investigations usually conform to similar methodologies involving a form of magnitude estimation i.e. size or distance, using a reference moon to a variable moon, for e.g. (Holway and Boring 1941, Kaufman 2000, Gordon M Redding 2002, Jones Wilson 2009, Liang Lou 2007 etc). Kaufman (2000) used artificial moons to display the SDIH as a description of the moon illusion. Subjects viewed these artificial moons of constant angular size against a natural sky in horizon and zenith positions. They compared the size and distance of a reference moon to a variable moon. And altered the size of the variable moon using a keypad to achieve a match, see figure 5. In the results the horizon moon was perceived 3.2 times bigger and 4.2 times further away than the zenith. They found as they increased the distance between the reference and variable moon, the moon perceived size increased. Conversely when the distance was reduced the perceived size decreased therefore implying distance determines perceived size. Due to the availability of visual cues, the horizon moon is perceived at a distance D further than that of the zenith, causing a subsequent increase in size S Higashiyama (2006), (2007). Figure 4 illustrates the principles behind the SDIH and apparent distance theor y, where by the black circles in the inner band exemplify the moon straight above the observers head perceived as closer and hence smaller. The horizon moon in this model is perceived further away and hence bigger. Condition 2-Inside band (black circles) showing proposed SDIH condition Condition 1-Outside band (white circles) showing normal condition Horizon moon Observer Elevated moon Figure 4 (Annotated Figure 1 from Kaufman 2000) demonstrating the two conditions. Condition 1 the outer band of circles demonstrate how the moon should be perceived right from the horizon to its elevated state with no illusion. However condition 2 using this model of the illusion is represented in the second inner band of circles, suggesting the moon straight above the observers head is perceived as closer hence smaller and horizon bigger and further. Figure 5 demonstrates the apparatus used in Kaufman 2000s experiment. An IBM Think-Pad flat panel display specifically designed for this experiment was used. Virtual moons were produced as luminous disks against the natural sky. It was conducted on a hilltop on the C.W. Post campus of Long Island University in Brookville, NY. A total of four moons can be seen: one reference and one variable for both the horizon and elevated moon and subjects adjusted the variable moon using the computer accordingly. Kaufman (2006) further investigated using noise signal detection and two alternative forced choices. Luminous discs of constant visual angles were used however viewed across a virtual terrain in this case containing distance cues. Two separate experiments were conducted on size and distance, which suggested a directly proportional relationship between the two as predicted by the SDIH. Figure 6 compares the log size (y axis) versus the log depth (x axis), inferred as distance and found the slope demonstrates a linear slope of ~1. Thus these results suggest as size increases so does distance, once again supporting the SDIH. The fact the perceived size increases as a directly proportional factor to the distance perceived, indicates that the moon illusion cannot be referred to as an angular account. Figure 6 Kaufman 2006 shows the log perceived depth otherwise regarded as distance (x-axis) and log size (y-axis). A straight line is formed with a gradient of approximately 1, therefore suggesting size is proportional to distance as distance is to size. Tozawa (2006) investigated the roles of motion parallax and perspective cues on size and distance perception and the results yielded were similar and supported the SDIH. Weizman and Cohen (2003) also investigated the SDIH via a matching task using 4 different groups of subjects varying in age. Results indicated 41-88% viewed the horizon moon to be of a greater size and as a consequence supporting the SDIH. 3.2 The paradox The issue with the SDIH is it induces a paradox since many people do not experience the conditions it sets ;( the horizon moon appears both larger and further away) for e.g. (Higayshima 2006, Kaufman 2007, Kotaro Suzuki 2007, Kaufman 2006, Gregory 2007, Jones et al 2009). Instead (Mccready section 3) found up to 90% and Kaufman (2000) 9/10, view the larger horizon moon to be perceived as closer. Size constancy is the visual systems ability to maintain the accurate perception of real size of an object regardless of the change in retinal images size Combe Wexler (2009) Gregory (2007) i.e. when a person is walking away their physical dimensions do not appear to shrink, this relationship is maintained by size constancy regardless of the change in distance, which should create a smaller image size on the retina. One idea proposed as an answer is observers use the perceived distance to scale perceived size, as in SDIH. When enquired about distance, this scaled size and previous experience of sizes of objects from size constancy are used to determine distance. Hence due to this experience the observer makes a logical choice, thus in effect proposing there is a bias towards experiencing bigger objects to appear closer Kaufman (2000) (2007). However what is suggested in effect is there are two different routes taken to decipher size from distance and distance from size and without a ny direct evidence these ideas cannot be accepted as yet. 3.3 The apparent distance theory The apparent distance theory states the perceived distance is not only determined by the retinal image size, but factors such as visual cues within the surrounding terrain play a controlling role in judgment, for e.g. (Gregory 2008), Suzuki (2007), Kaufman (2000). There are many different types of visual cues from which the visual system can infer distance from and the amount of effect each cue has also varies. The terrain in one direction and its absence in the other play a vital role in the illusion Kaufman and Rock (1962). The role of cues plays an integral part in the SDIH, since the perceived distance determines the judged size and in effect can be described as SDIH since the findings directly support it. Pictorial representations of the illusion have been used as a methodology for investigation of depth cues, for e.g. (Coren and Aks 1990, Redding 2002, Jones et al 2009).The benefit of this being that any structural factors such as accommodation that may contribute towards the processing of size and distance are eliminated as cues and only visual cues i.e. terrain are left to investigate Redding (2002) Coren Aks (1990). The apparent distance theory would predict the horizon moon appears bigger due to distance cues placing it at a further distance and the zenith moon as closer, hence smaller, just as in SDIH. Jones and Wilson (2009) findings supported the apparent distance theory and demonstrate the level of effect of cues on the perceived distance. They used pictorial representations of of different salience as cues to depth, figure 7 displays the pictures used in increasing salience of each picture from A-D. Subjects viewed a reference moon placed on the horizon and zenith on the different scenes (figure 7 A-D) and compared this to a set of variable moon sizes on a computer, judging the match in size. A positive score (above 0) in the results from figure 8 indicated a perceived increase in size. Results show as the salience increases so does the perception of size for both moon trajectories, therefore these findings emphasize regardless of salience of cues, the mere presence of some form of cues effectively increase perceived size. However in all scenes the horizon moon is perceived bigger and significantly more so in the two scenes of high salience (figure 7 C and D). This infers proxi mity is a key factor and thus illustrates why the horizon moon is judged bigger, since it is in closer proximity to the terrain and the greater salience exaggerates this effect. Figure 7 taken from Stephanie 2009 figure 1 illustrating the different pictorial representations used as devices for the different depths of cues. A) Drawing of lowest depth cue salience B) Drawing of intermediate depth cue salience C)Drawing of high depth cue salience- Town scene D) Drawing of high depth cue salience- City scene. Figure 8 From Stephanie et al 2009 experiment number 1. The results were based on the size of error scores between the subjective responses of perceived size of the variable moon compared to the control moon size. Significant differences in size between the horizon moon and elevated moon indicated the degree of strength each cue played on that particular moon. The positive error score indicated an increase in perceived size and negative score a decrease. Redding (2002) also supported that cues in the terrain are essential for size scaling to create the impression of a bigger horizon moon, as well as the proximity to the terrain. A pictorial representation of an upright and inverted gradient, with two moons positioned like figure. The upright gradient produces fine details very close together giving the impression of a receding distance like in the horizon. However the upright gradient was more spaced out mimicking the large expanses of space surrounding the zenith moon. The apparent distance theory would predict a reverse in the illusion if the visual scene was inverted i.e. the horizon moon would now look smaller than the zenith. The results show the mean illusion, where a positive score indicates the normal moon illusion occurred and negative the reverse. These results demonstrate the prediction was correct since the horizon moon size increased in the upright direction and reversed in the inverted. Within virtual environments it has been found the size constancy mechanism is very strong when the object being viewed is surrounded by an environment, where comparisons can be made to decipher distance from, for e.g. (Kenyon et al 2007, Tanaka Fujita 2007, murgia and sharkey 2009). It has been suggested the elevated moon is perceived smaller due to the lack of surrounding visual cues for e.g. (Higashiyama 2006, Kaufman 2000, Jones et al2009). The proposed idea is the zenith moon due to no visual cues is placed at default distance related to the resting focus of approximately 1-2m regarded as empty space myopia, thus leading to its small perceived size (Da Silva 1989, Gogel Mertz, 1989, Redding 2002, Gregory 2007, Suzuki 2007). 3.4 Sky dome illusions The apparent shape of the sky was previously replicated in a drawing by King and Gruber (1962), where they made subjects project afterimages onto the sky in different directions (horizon 45. Zenith). Results had shown 81% of subjects viewed the moon bigger in the horizon sky than at 45. and 87% viewed horizon bigger than the zenith. Weizman and Cohen (2003) found the sky is perceived as an oblate profile i.e. like an inverted bowl with a flat top (see figure) and cues within this frame are used to judge the distance. It has been proposed this flattened dome top causes the zenith moon to appear closer and thus smaller. This theory implies a mental map of the shape of the sky as an oblate- bowl shape, with the flat portion directly above the observers head. This flatter area causes the perception of a shorter distance to the sky just above the observers head and thus causes the zenith moon to be perceived as smaller. This is very similar to the SDIH approach which states the same fundamental reasons, but the SDIH suggests its the absence of visual cues that place the zenith moon at a closer distance and hence smaller, not a mental map model of the sky. However Toskovich (2009) examined to test if the flattened sky caused the moon size to reduce and suggested otherwise. Subjects viewed the moon in the horizon, 45Â ° and zenith positions using head movements and were positioned at 1m, 3m and 5m from the moon. They were instructed to determine distance and size estimates from these positions. Results had shown from 1m subjects perceived distance is the same in all directions thus indicating at close distances the visual system is able to interpret very accurately. However from 3m and 5m found the distances perceived to the zenith as larger than towards the horizon and no differences in size estimations at any direction. This is opposite to the flattened sky dome approach and proposes the sky is rather perceived as elongated towards the zenith and not flat. These findings suggest the illusion is affected by head position and location. 4. Visual angle illusions To begin with Descartes, 1664 Wade 2000 pg (354-355) suggested associations with familiar objects, accommodation and convergence are all cues to distance. The apparent-distance theory is built upon the assumption the actual perceived visual angle is interpreted as the same as the physical linear visual angle Reed and Kuprinski (2009). However, alternative theories suggest the perceived visual angle may be affected by oculomotor processes unconsciously Mccready (2006) Keef and Kuprinski (2009) and size/distance then subsequently inferred from this. 4.1 The retinal representation of the moon illusion If the illusion causes the perceived visual angle to change by becoming enlarged, then subsequently the perceived retinal image size should also increase. Murray et al (2006) found illusions such as the moon illusion affect retinal representation of the image size in the primary visual cortex (V1). Using functional magnetic resonance imaging (fMRI) and a 3d scene of a hallway with walls, an image had been produced containing information to apparent depth, see figure 9a for an illustration. Two 6.5 degree sized spheres were arranged like in figure 9a and the results showed the back sphere appeared to be 17% larger in angular size than the front sphere (even when of the same physical angular size). The results in figure 9a also illustrate the peak MRI signal responses were found higher at higher eccentricities for the perceptually larger back sphere than the front and the back sphere occupied a larger area in the V1 cortex. Thus implying the perceived bigger size of the back sphere cre ated a bigger images size on the retina. Furthermore these results were compared to the responses generated by two physically different sized spheres without any illusion (6.5Â ° versus 8.125Â ° and 4.875Â ° versus 6.875Â ° sized spheres, as shown in figure 9bc). The findings demonstrate the responses generated from two physically different sized spheres yielded a response very similar to 9a. Therefore indicating the illusion created an actual change in the retinal image size and a greater eccentricity was occupied by the back sphere as a result. Thus the depth illusion causes a change in the perceived angular size on the retina and hence providing evidence towards scaling processes affecting the representation on the retina (Murray et al 2006). Since only a change in the physical visual angle or perceived visual angle may cause this change in retinal image size. Figure 9 taken from Murray et al 2006 displaying the hallway and the walls creating the illusion. the trial response graph shows the perceptual difference in angular size between the two objects. The top graph illustrates the fMRI activity for the perceived larger back object extending in eccentricity beyond that of the perceived smaller front object. The bottom row shows a similar response is triggered when two objects of physically different angular sizes are shown (with no hallway illusion placed). Therefore indicating the cause in the back object to be perceived more distant is due to an increase in angular size. 4.2 Accommodative micropsia The visual terrain contribution to the moon illusion may be mediated by the state of the oculomotor system and not via the size-distance invariance mechanism, or size constancy scaling Suzuki (2007). The perceived distance may affect the accommodation response or the converse of this may also be true i.e. the level of accommodation may affect the perceived distance of a stimulus (Edgar 2007, Suzuki 2007, Lou 2007). The micropsia phenomenon causes objects to appear smaller than usual and macropsia bigger, whereby they can be induced by changes in accommodation/ Vergence leading to underestimation/ overestimation of its apparent size Howard Rogers (2002). When viewing the zenith moon there is no depth cues and the moon is isolated in an empty space. This causes the eyes to converge onto the single object of the zenith moon, thus increasing in convergence as it does. This increase in convergence induces increase in accommodation causing the decrease in angular size and is known as micropsia, for e.g. Howard Rogers (2002) Mccready (2004) section 4, Lou (2007), Suzuki (2007). However when viewing the horizon moon in its natural settings, objects acting as depth cues in the terrain may cause the AC/V system to adjust from near to far distance thus increased divergence invoking an increase in angular size known as macropsia (Lou 2007, Mccready 2004 section 4, Tanaka Fujita 2007, Suzuki 2007). Lou (2007) used afterimages of dark circles viewed against a mobile white background on which this reference circle was projected on, see figure 10. These afterimages were projected from the various distances and subjects adjusted the variable stimulus on a computer screen when perceived a match with the reference. Results indicated subjects perceived afterimages to decrease in size at focal distances less than 1m i.e. distances at a closer range. Figure 11 displays the 30cm, 90cm and 200cm distances from where the afterimage was projected and regardless of these distances the same response of decrease in matched size. The focal distances affected the matched size and not the distance the afterimages were projected from, Lou (2007) suggested these findings are representation of accommodation micropsia. Although oculomotor cues are used as cues to distance just as visual pictorial cues are used also, they are less effective up to distances >2m Kaufman (2000). Oculomotor cues and pictorial cues play a role in judging distance, however at longer distances pictorial cues play a greater role as determinants of distance Kaufman (2000), Coren and Aks (1990). become slightly near-sighted in relative darkness (night myopia) proof is just to show accomodtaion/convergence effort changes when viewing horizon and elevated moons Figure 10 Figure 11 taken from figure 2b (Lou 2007). This figure demonstrates the 30cm, 90cm and 200cm distances from which the afterimages were viewed from and the perceived angular match to the control afterimage of size 4.25degrees. The straight angular line indicates the actual size of the afterimage (4.25 degrees). The perceived match of the angular size (y-axis) versus calculated focal distance (x-axis). All about enright and roscoedifferent eye adjustement for horizon/zenith moon measured In conclusion against oculomotor micropsia/macropsia, oculomotor cues are less effective in regards to objects being viewed at longer distances. Here the visual/ perceptual system becomes more dependent on other cues such as pictorial factors Arditi (1986) from Kaufman (2000). Kaufman et als claim is that because the moon is far away, pictorial cues dominate oculomotor cues for distance perception. Kaufman (2006) in the end argues that distance is interpreted first and then angular size. Arguing against the micropsia theory. Also , absence of these surrounding environments the size constancy changes to visual angle performance Kenyon (2007) As you look up to the sky convergence increases therefore increased accommodation occurs causing perception of closer moon distance, therefore according to SDIH a smaller perceived size. REFER TO KAUFMAN 2000 But, these micropsia and macropsia illusions cause angular size differences of less than 10%, nowhere near large enough to account for the moon illusion seen by most persons. Also, if accommodation were involved in the moon illusion, youd think that elderly people who have lost nearly all accommodation should not perceive the illusion. Yet they do. Persons with eye lens implants have no accommodation, and they do perceive the moon illusion. Covering one eye removes convergence from consideration, but that doesnt make the moon illusion go away. Pinhole astronomy 4.3 Angle of regard When looking at the horizon moon the head is positioned at eye level, where as when viewing the elevated moon the head position is further elevated by almost 45degs. It has been suggested the tilt or elevation of the head or eyes may affect the judgment of distance and thus implying the moon illusion as anisotropy (directionally dependent) for e.g. Holway and Boring (1940), Higashiyama Adachi (2006), Suzuki (2007), Toskovich (2009). Suzuki (2007) investigated the ratio of size of afterimages projected onto the horizon and zenith sky. Subjects were instructed to project the afterimages onto the horizon sky at eyelevel and then project the image again however after elevating the eye position by 60 degrees (using neck movements) onto the same area of the sky. This was also repeated for the zenith sky and the results yielded indicate the illusion is 1.09 times greater when the eyes are in an elevated position compared to eye level. These findings indicate the level of elevation of the eyes has an effect on the illusion magnitude and is consistent with previous findings. Proprioceptve descriptions suggest non visual components may contribute to judging distance using head direction, body posture, vestibular and kinetic information Toskovich (2009). Furthermore Toskovich suggested head tilt upwards could cause the perceived space to elongate. Figure 11 taken from (Roscoe and Acosta 2008)~figure 4. The number 0 would indicate a perfect size match and a positive value indicates an increase in size and negative vice versa. The x-axis displays the accommodative effort exerted by the visual system and the y-axis the interpretation of the moon size. Anisotropy End with (Perceived size and perceived distance of targets viewed from between the legs: Evidence for proprioceptive theory 2006) and how this supports direct perception model rather than the apparent distance model. (Therefore supports everything except this model) In another experiment 2 Toskovich (2009) measured size at the 3 distances and found size did not change in the three viewing directions and thus suggested the moon illusion may not be caused by a linear account, instead a more contributed input of vestibular information. (Higashiyama Adachi 2006) supported this theory and found the illusion disappeared when viewing through the legs. Thus suggesting the moon illusion is caused by the elevation of head tilt. An astronaut who views the moon above the horizon from low-earth orbit lacks terrain cues to distance. We now know that in this situation the illusion vanishes (Lu et al., 2006) from (Kayfman et al 2007). The terrestrial passage theory offers an alternative idea regarding the visual angle theories mentioned. It states the subjects learn to form an expected change in visual angle when viewing objects at different projections from past familiar experiences (Reed and Kuprinski, 2009). In a sample of 48 subjects this hypothesis was tested and the c

Physiotherapy Management of Lower Limb Tendonopathies

Physiotherapy Management of Lower Limb Tendonopathies A Systematic Review of the physiotherapy management of lower limb tendonopathies Tendonitis is a condition which is comparatively commonly seen in various clinics. The largest cohort of patients tend to have developed their condition as a result of various sports-related activities but it is acknowledged that there is a substantial cohort of RSI sufferers and occupation-related forms of tendonitis. (Kader et al 2002) In this piece we aim to review the various treatment modalities and to concentrate primarily on the eccentric muscle strengthening modalities of treatment, the rationale behind them and any evidence that they actually work. Before we can consider the direct question of eccentric loading as treatment for tendonopathies we must examine the rationale for its uses well as the basic science and theory behind the actual practice. We will do this largely by the mechanism of a literature review. Methodology In this review we shall be examining the literature for not only the methods that are currently employed in treating the various lower limb tendonopathies but also for justification for these methods and the quality of the science behind them. We shall therefore critically review the literature available and present it in a rational form. In addition to this we intend to present an overview of various factors in a wider picture that are relevant to our considerations. We shall consider the current views on the pathophysiology of tendonitis and the experimental evidence on the response of the tendon to exercise in general terms. Although it is accepted that the majority of patients currently seen in clinical practice with various forms of lower limb tendonitis are suffering from a sports related injury, we shall also look at the effects of ageing on tendon physiology as it is acknowledged that the elderly are another highly represented group with tendonitis. We conclude the preamble with a number of clinical considerations, most prominently the difficulties posed by the differences in nomenclature and terminology which renders both assessments and comparisons between clinical trials difficult. We conclude the dissertation with a review of various currently employed treatment modalities and the rationale behind them. We focus specifically on the use and place of eccentric muscle strengthening exercises in the spectrum of rational treatments.. Pathophysiology of tendonitis At the macro-anatomical level, the tendon is usually easily defined as a semi-rigid white or grey structure, generally found in close proximity to synovial joints. One of its prime functions is to transmit forces generated by muscles to the skeletal system, often inducing movement. (Huxley HE 1979). At the micro-anatomical level, it’s structure is very much more complex and requires a detailed examination before we can realistically and meaningfully consider the issues relating to the therapy of tendonitis. Tendons form part of the anatomical structures that are functionally grouped together as the extracellular matrix (ECM). The rate of turnover – both synthesis and degradation – is influenced by a number of different factors including metabolic and disease related factors, but the strongest influence on the turnover rate is mechanical stress, usually as a result of various degrees of physical activity. (Agar Pet al 2000) Tendon (and intramuscular) collagen, turns over at a rate which is about half as fast as myofibrillar protein turnover. The main physiological stimulus to turnover appears to be the multiple stimuli arising from mechanical or contractile activity.(Cuthbertson D et al2005) At the cellular level, degradation of collagen is mediated largely byte metalloprotease group of enzymes and synthesis is most strongly influenced by a number of different trophic factors which are released at the cellular level. (Algren MS. 1999) These growth factors are mainly responsible for both the transcriptional changes as well as the post-translational modifications that take place as a result of either physiological changes or disease processes. (Sand Meier et al 1997) Until comparatively recently, tendon tissue was thought to be fairly inert. Recent research work has given good supportive evidence that the internal metabolic processes, the internal vascular responses (Alstom et al 1994) and the actual catabolic turnover of the collagen protein in response to physical activity, is considerably greater than originally thought. The converse is also true, as inactivity appears to have the same inhibitory effect on tendon tissue as the better known effect of wasting in muscle tissue. (Abrahamson SO et al 1996). This effect is of particular importance in our considerations (later) when we consider that some authorities suggest that outright rest is inappropriate initial treatment for tendonitis. Collagen is a large polymer-type protein made up of many repeating subunits, (triple helices of polypeptides with a high proportion of proline and hydroxyproline). It is made by fibroblasts. In the muscle, it forms a basket-like network around the muscle fibres but then forms progressively more coherent and solid structure as it forms discrete tendon. In this way it allows the efficient transmission of forces generated by the myofibrils to the tendon – and hence to the bone. (Kjaer M 2004). Training, in the form of physical work, exercise or repetitive movements, will have a trophic effect on the tendon as a whole. Collagen turnover can be increased and there can be an overall increase in the amount of collagen protein in the tendon. (Herzog W et al 2002) Collagen, in the form in which it is found in a tendon, has enormous on-elastic tensile strength and a modest degree of ability to bend under lateral stress. As the amount of collagen in a tendon increases, the tendon’s mechanical (or more accurately, viscoelastic,) properties change. It decreases it’s stress levels for a given load, and thereby renders it more load resistant.(Fowls JL et al. 2000). Again this facts of great relevance to our clinical considerations later in this piece. The stiffness, or resistance to lateral stress, is a function of the cross-linking of sulphur bonds across the parallel bands of protein. In general terms, the more cross-links, the stiffer the tendon. The degree of cross-linking is a result of a complex interaction between a number of enzyme systems in the matrix of the tendon. (Hamill OP et al.2001) Polyglycans are an important feature of this enzyme cascade and become an increasingly important functional component as age increases. Older or ageing collagen will tend to exhibit glycolated cross links in addition to the sulphur links of youth. This is part of the reason why older tendons are less flexible (and possibly more prone to injury). (Inglemark BE 1948). The functional significance of these links is that they render the tendon even stiffer and less able to bend.(Davidson PF 1989).Understanding these processes is fundamental to the prescribing of a rational treatment regime for tendon injuries and other pathologies. It is also important to have a complete understanding of both the vascular and neurologically mediated adaptation processes that are present in the my-tendon complex. These work on a far more rapid and immediate time frame than the processes that we have just described, and are primarily responses to rapid changes in the mechanical loading stresses. As muscle tissue develops physiologically, there is a symbiotic relationship between the muscle and the extracellular matrix. The various physiological mechanisms that stimulate muscle growth and hypertrophy appear to have a similar effect on the extracellular matrix. (MacLean et al 1991) But in the latter case, they are less well understood. We know that that significant and repeated mechanical loading will trigger off, or initiate a process, which starts with the activation of trophic gene in a cellular nucleus, (Banes AJ et al.1999), it progresses through the complex processes of protein synthesis and functionally ends with the deposition of collagen in the tendon tissue.(Yasuda et al 2000) Responses of the tendon to exercise There would appear to be some form of integration between the muscular and the extracellular matrix signalling pathways, which optimises the co-ordinated activity of the trophic processes in response to the stimuli (which can be both loading and tensile in nature), which produce the response in the first place. (Viidik A.1993). This co-ordination mechanism must exist, as it is a well-recognised phenomenon that a tendon hypertrophies to accommodate the increased mechanical stress that its associated hypertrophied muscle produces. (Derwin et al 1999) Considerable research effort has been expended in trying to delineate the mechanism, but to date, the results have not increased our understanding of the situation significantly. (Vierck J et al 2000) Specific studies in this area have been able to show a clear correlation between collagen response and an increase in physical training. (Langberg et al 2001). The response was detectable after a 4week training programme and was maximal at 11 weeks. When we consider the pathophysiology of RSI (repetitive strain injury) or even chronic overload syndrome, the stimuli that can produce muscle hypertrophy or increase muscle fibrosis can also produce fundamental changes in the tendon structure. (Birk DE et al 1990) These changes can include changes in both the chemistry and the functionality of cross bonding of the collagen fibres, (Barnard K et al1987), changes in the size of the collagen fibrils, areas of locally increased blood flow (known as hyper vascularisation zones), and an increase in the catabolic processes which can result in either (or both) collagen being synthesised and laid down, or increase in fibroblastic activity which increases the fibrous component of the tendon. (Greenfield EM et al 1999) It is a fundamental recognition of the fact that these processes require â€Å"adjusted loading† rather than an enforced absence of loading(immobilisation) to reverse the physiological processes, that underpins most of the thrust of this review.( Howell JN et al 1993), (Jà ¤rvinenTAH et al 2002) The experimental evidence to support this view comes from the classic set of investigations by Gibson (et al 1987) who compared the rate of collagen synthesis and turnover in an immobilising long-cast leg with the rate of turnover in the unaffected leg. The rate of collagen synthesis dropped by half over a seven week period in the immobilised leg. The investigators also found an adaptive (and compensatory)reduction in the rate of collagen degradation which had the overall effect of reducing the protein loss in the tendons. In the overall context of our investigation it is also important to note that the authors also found that minimal electrical stimulation of the muscle (5% of maximum voluntary contraction for 1 hr. per day),increased protein synthesis to such an extent that there was no net protein loss over the same seven week period of the trial. (Gibson etal 1989) In a study that was remarkable for its invasiveness (the authors took repeated biopsies of human patella tendon after periods of exercise), Miller (et al 2004) demonstrated that tendon collagen synthesis showed a 30% rise within 6hrs of exercise and up to a 50%rise within a 24 hr. period. This was found to exactly follow the pattern of protein synthesis in skeletal muscle. This finding is strongly supportive of the assertions made earlier in this essay, that there would appear to be a mechanical or humeral mechanism that links the trophic effects that are apparent in both tendon and skeletal muscle. Various authors have postulated different mechanisms (it has to be said with scant evidence), including integrin’s, (Levenhagen et al2002), growth factors including transforming growth factor beta (TGFB) (Moore et al.2005), or mechano growth factor (MGF) (Rennie et al 2004),which they suggest may be responsible for the co-ordination of the trophic effects of perimysium collagen, tendon collagen and the myofibrils. More concrete evidence exists (and is arguably of greater relevance to our investigation here), for the fact that dietary protein alone can produce a trophic stimulus for tendon collagen. (Jefferson Kimball 2001). It is postulated that there is some form of amino acid sensor that is responsive to the availability of amino acids. This haste effect of changing the availability of various protein kinases in the extracellular matrix generally and a subsequent enzymatic cascade which results in an increase in various anabolic signalling molecules which are, in turn, responsible for the activation of mRNA. This is then responsible for the increased synthesis of collagen (and other related proteins), in tendon and other extracellular matrix tissues. This series of very elegant experiments was done in carefully controlled conditions which removed the possibility of other anabolic factors being relevant as the only variable was the availability of amino acids. (Cuthbertson et al 2005) There is further evidence of the effect of exercise on tendon structure in the form of the set of experiments by Rennie and disco-workers. Looking specifically at the metabolism of collagen Rennie found that after strenuous exercise, the rate of incorporation of a marker into tendon collagen followed a specific pattern (Rennie Tipton 2000). There was a latent period of about 90 mines after exercise where there was no change in metabolic rate. It was then noticed that there was a dramatic increase to about 5 times normal rates of synthesis, which peaked at about 12 hrs., was maintained for about 12hrs, and then declined over the next 48 hrs. In line with the findings of Cuthbertson (above) the investigators noted that the rise in levels of synthesis is greatest if associated with an amino acid load just pre- or post-exercise, and this effect can be further enhanced by the administration of insulin secretagogues(such as glucose). There is therefore little doubt that feeding helps the post exercise response. (Atherton P et al 2005) The effects of ageing on tendon pathophysiology We have already commented, in passing, on the physiological effects of ageing in relation to the polyglycan cross bonding in tendons. There are a number of other changes which will naturally occur in relation to advancing years, which are of direct relevance to our considerations here. It is clearly a matter of observation that muscles, bones and tendons deteriorate as age increases. This deterioration leads to physical symptoms such as loss of strength, mobility and suppleness together with an increase in fatigability and a general reduction in proprioception. This condition is sometimes called â€Å"sarcopenia†.(Forbes 1987) Epidemiological studies (Dorrens et al 2003), provide good evidence to support the popularly held view that an active lifestyle into old age is more likely to support a higher level of bone density, muscle bulk and tendon flexibility, than a sedentary one. One can postulate that the trophic mechanisms referred to above, stay active for longer when constantly stimulated by mechanical activity. One effect of ageing that has been experimentally demonstrated, is that the trophic effects of available amino acids in the bloodstream are not as great in the elderly as in the young. The elderly appear to have an ability to develop resistance to the trophic effects of amino acids, which was not present when they were younger. (Cuthbertson et al 2005) Another physiological change that can be demonstrated in the elderly, is a reduced RNA : DNA ratio in tendon tissue, which is a marker of a reduced ability to manufacture protein. This, together with reduction in the amount of detectable anabolic signalling proteins, seems to be central in the failure of the muscle and tendon synthesising mechanisms. (Smack et al.2001). If we add these findings to other work of Smack (et al 2001) and Leverhagen (et al 2002) which shows that the elderly can show responsiveness in terms of trophic changes in the collagen content of tendons by manipulation of the diet. Both studies showed that maximising the protein : energy ratio of ingested food is a reasonable strategy. It should also be noted that they also demonstrated that one has to be careful to keep the energy content of the food low in order to minimise unwanted weight gain. The elderly could reasonably be assisted to maximise the benefit they get from training (resistance training in these particular studies), by integrating it with feeding concentrated in the immediate pre- or post-exercise period. This appears to have the effect of increasing the positive synergistic relationship between exercise and amino acid delivery.( Williams et al. 2002) Clinical considerations Differential diagnosis The first and possibly most fundamental issue that we have to consider when looking at the issues of the treatment of tendonitis, is the issue of correct diagnosis. This, sadly, is compounded by the fact that there appear to be several different terminology vocabularies in common clinical use. It therefore can be difficult to directly compare treatment studies of â€Å"tendonitis â€Å" unless one has direct and clear diagnostic criteria. (Saxena 1995) Tendonitis may be taken in some medical circles to include all those conditions which come under the broad heading of â€Å"painful overuse tendon conditions† (Khan et al 1999). This is generally accepted by the uncritical, as meaning that this equates with a painful inflammatory reaction in the tendon tissue. Histological investigation of the typical chronically painful tendon, generally shows an absence of the polymorphonuclear and other associated inflammatory cells. In some literature we can see the emergence and replacement of the term tendonitis with tendinitis. This latter term tends to be defined as pertaining to areas of collagen degeneration, increased ground substance and neo-vascularisation. (Purdue et al 1996) To both illustrate and clarify the point, let us consider thevarious clinical entities that may either present like, or may be diagnosed as, â€Å"tendonitis†. For ease of classification and clarity, in this section we shall consider the term â€Å"tendonitis† in specific relation to the Achilles tendon. Williams (1986) produced the (arguably) most commonly currently accepted definitions of Achilles tendon pathologies. He classified them into:- Rupture, Focal degeneration, Tendinitis, Per tendonitis (peritendonosis), Mixed lesions, Origin/insertion lesions, Other cases such as metabolic/rheumatic causes. In common clinical parlance, any of them can be referred to, with reasonable accuracy, as â€Å"tendonitis†. (Galloway et al 1999) The aetiologies can vary (and this may well have a bearing on treatment), from trauma, reduced flexibility, abnormal or changed biomechanical considerations (such as excessive pronation, supination or limb length inequalities) to name but a few. (Saxena, A 1998) It should be noted that the anatomy of the Achilles tendon is unusual and certainly different from any other in the lower limb. It does not have a true synovial sheath but a petition which extends from its origin in the muscle to its insertion in the calcaneus. Peritendonosisis therefore a commonly misdiagnosed as Achilles tendonitis. It is also clinically significant that there is a region of decreased vascularity in the tendon, which is typically about 6 comes above its insertion (Hume 1994). The clinical difference between these two conditions is that true Achilles tendonitis may, if chronic, be characterised by fucoid, or fatty focal degenerative, changes in the tendon itself, where asperitendonitis will not involve the Achilles tendon at all. (Kvist1994). These degenerative changes may be extremely resistant to non-surgical forms of treatment. In practice, the two conditions may well be presenting the same individual. (Killer et al 1998) The differentiating signs are, however, fairly easy to detect and the two conditions can be separately distinguished in most cases. Per tendonitis is the inflammation of the petition and can usually be clinically distinguished by the presence of clinical crepitus as the Achilles tendon tries to glide back and forth along the inflamed petition. This sign together with pain, generally tends to increase with activity and the tenderness is normally felt along the whole length of the tendon. Achilles tendonitis on the other hand classically gets better with movement and is at its worst after a period of rest. The discomfort tends to be more localised into discrete areas and is more commonly found in cases where there has been either a partial or even a complete rupture in the past. (Clement et al 1994) Other pathologies can arise associated with the Achilles tendon, and for the sake of completeness we should briefly consider them as they could be potentially confounding factors in any trial which aims to consider tendonitis. Tendocalcinosis is an inflammatory process which involves the Achilles tendon but only at the point of insertion to the calcaneal bone. It typically will result in calcification and therefore should be considered a different entity to Achilles tendonitis as such. It is characterised by localised pain, and prominence of the calcaneal insertion of the tendon which may well be associated with a retro-tendon bursitis. (Williams 1986) If we apply the same rationale to the patella tendon, we are again faced with a bewildering array of terminology and conditions which tend to get lumped together as â€Å"tendonitis† and may also therefore be confounding factors in any study. We shall therefore spend a few paragraphs delineating them. Some authors point to the fact that conditions that had been previously referred to as tendonitis, when examined at a histological level, are found to be the result of collagen breakdown rather than inflammation (Khan et al 1996), and therefore suggest the title oftendinosis is more appropriate. (Cook et al 2000) (I) The whole issue of the role of the inflammatory process in the tendonopathies appears to be far from clear. An examination of the literature can point to work (such as that by Khan – above), who demonstrated that the prime histological changes were non-inflammatory and were more typical of fucoid, hyaline or fibrous degeneration with occasional calcific processes being identified. Other investigators however, point to the clinical picture which commonly includes the classic inflammatory triad of dolour, rub our and tumour (pain, redness and swelling)(Almekinders et al 1998). This, associated with the evidence of the relieving effect of NSAIA’s or corticosteroids(Friedberg 1997) leads to an ambiguous picture. The pathophysiology of this condition is most commonly thought tube related to jumping and landing activity which is the mechanism which appears to cause the rupture of the collagen filaments and hence the histological appearances. The characteristics of this type of condition are that it tends to be focal, and often in the region of the lower pole of the patella. Initially it tends to be self healing but as the chronicity increases, the pain levels can increase to the point where pain is experienced even at rest (Cook et al 2000) (II) This type of condition must clearly be differentiated from there-patella bursitis (Housemaid’s knee) which is often mistakenly diagnosed as a patella tendonitis. (Halaby et al 1999) Factors which appear to predispose to tendonopathy Many authors identify chronic overuse as being one of the major factors in tendonopathy generally. (Kist 1994) (King et al 2000). This applies equally to the occupational tendonopathy as much as the sports-related conditions. (Jon stone 2000) (Kraushaar et al 1999). We should acknowledge that the term overuse can refer equally to overuse in terms of repetitive action just as much as it can refer to overloading. The two factors being independent (but often related). Some of the current literature points to the fact that there can be differentiation in the spectrum of overuse injuries between those conditions that arise from some form of biochemical change in the structure of the tendon itself (Joss et al 1997), those that are associated with biomechanical changes (such as change in function or previous injury) (Alstom 1998) and those that arise as a result of ageing or other degenerative changes (Alstom et al 1995). These factors can arise as a result of, or independently from, other factors such as the fact that the anatomical path of a tendon can take it over (or in close proximity to) friction-inducing structures such as a bony prominence – as in the case of the tibias posterior tendon, (Benjamin et al 1998) or factors relating to the site of insertion of the tendon into the bone – as in the case of theAchilles-calcaneum interface.(Benjamin et al 1995) We can point to evidence that extraneous factors can also predispose to tendonopathy. There are genetic factors (Singer et al 1986), and a relationship to blood type (Joss et al 1989). The presence of certain concomitant chronic or debilitating illnesses can certainly be associated with tendonopathies (Kannur et al 1991) as can the chronic use of certain medications – most notably the fluoroquinolone group.(Huston 1994)(Ribard et al 1992). The mechanism in the latter case appears to be associated with an increase in the amount of MMP and its associated activity which seems to be associated with an increase in the rate of degradation of protein (especially collagen) in certain tissues. (Williams et al 2000). Other authors have identified biomechanical factors as being significant (rather than necessarily causal), in the development oftendonopathies, but we shall discuss this in specific relation to treatment, and so will not discuss it further here The spectrum of currently available treatment Before beginning any rational consideration of the various forms of treatment available, one must appreciate a common truth in medicine, and that is that different treatments and different patients will respond differently to a specific treatment modality, and one of the factors that will influence this phenomenon is the skill and experience of the practitioner concerned. For example, a surgeon may well find that he gets good results from tenotomise but poor results from eccentric exercises and therefore will recommend surgery. Physiotherapist may find the converse. It is therefore important to be critical of such factors in any appreciation and appraisal of different techniques for the treatment of the lower-limb tendonopathies. In this section we shall examine the available literature to try to obtain an overview of the various treatment modalities that are currently being prescribed and examine the rationale behind their use and efficacy Most authors seem to agree that, before considering the specific conditions, a general approach of conservative measures (such as load reduction, strengthening exercises, and massage) should be tried before other modalities such as medication and physical interventions(ultrasound etc.), and that surgery should only realistically be considered as a last resort. The only obvious exception to that approach would be when complete (or sometimes perhaps partial ) rupture of the tendon has occurred, and then surgery may well be considered the prime intervention. (Cook et al 2000) (I) Let us consider the various options in turn. In this section we will begin (again, for the sake of clarity), by specifically considering the options available for patella tendonitis. We accept that there will, of course, be overlap between the treatments for the various tendonopathies, but it makes for a rational approach to consider each in turn. The first comment that we must make is that, after examination of the literature it is noticeable that there are only a comparatively few well constructed, placebo controlled randomised trials in this area.(Almekinders et al 1998). Those that we can examine appear to suggest that the traditional treatments aimed at minimising the inflammatory processes in the condition are largely ineffective. The authors (Cooked al 2000) (II) suggest that this may well be because of the findings we have quoted earlier (Khan et al 1996) that histologically, the prime pathology is not inflammatory. Relative Rest Cook (et al 2000) (I) points to the fact that many strategies can rationally involve load reduction and the (now outmoded) instruction to â€Å"Stop everything and rest† is positively contraindicated. The rationale for this relates to the mechanisms that we have examined earlier in this piece. Immobilisation of a tendon is actually harmful as we can point to evidence (above) that shows that tensile stress and mechanical action not only stimulates collagen production, it also is vital in tendon to ensure it’s optimal fibre alignment. Rational treatment suggests that a programme of â€Å"Relative rest† may be beneficial. By that, the authors (Cook et al 2000)(I) suggest that activity should continue as long as the prime traumas of jumping, landing or sprinting can be avoided and reintroduced in a carefully graded fashion. Biomechanical Correction Because patella tendonitis is primarily related to jumping and sprinting sports ( in numbers that present clinically), we will consider treatment in relation to them. The forces that are generated in the patella tendon on landing after a jump are considerably greater than those that produced the jump in the first place. (Richards et al1996). It logically follows that if biomechanical methods can be employed to more efficiently minimise the forces, they would be best employed on landing strategies than jumping ones. One should appreciate that the energy-absorbing capacity of the limbs dependant, not only on the patella tendon, but factors at the hip and ankle as well. Studies show that the ankle and calf are the prime sites of absorbing the initial landing load (Richards et al 1996) and, if these structures are not biomechanically sound, then this will increase the forces transmitted to the knee. Prilutskii and his co-workers (et al 1993) completed a series of studies which showed that up to 40% of the energy absorbed on landing is transmitted proximally from the ankle/calf mechanism. It follows that it must be biomechanically sound if it is to absorb the 60% bulk of the load which otherwise would be transmitted upwards to the knee mechanism. Another set of studies (Prapavessis et al 1999) concluded that when flat-foot and fore-foot landings were compared, the latter generated less forces throughout the lower limb and that the forces could be reduced further (up to another 25%) by increasing the range of both hip and knee flexion on landing. There are a number of other potential biomechanical deficiencies that can be amenable to correction and should therefore be sought outspans planes may be an obvious anatomical problem detectable at an initial examination (Kaufman et al 1999), but there are other types of functional abnormality (such as excessively rapid pronation on landing) (McCrery et al 1999), that may require far more sophisticated evaluation. Outhouses inside shoes may go a long way to help these problems Some authors, (McCrery et al 1999), regard a reduced range of movement in the sub-taller joints as an aggravating factor which places and undue stress on the Achilles tendon and that manual mobilisation of the joint is indicated in these cases. Cry therapy In the light of the histological findings mentioned earlier,cryotherapy has a rational place in treatment. It is thought th Physiotherapy Management of Lower Limb Tendonopathies Physiotherapy Management of Lower Limb Tendonopathies A Systematic Review of the physiotherapy management of lower limb tendonopathies Tendonitis is a condition which is comparatively commonly seen in various clinics. The largest cohort of patients tend to have developed their condition as a result of various sports-related activities but it is acknowledged that there is a substantial cohort of RSI sufferers and occupation-related forms of tendonitis. (Kader et al 2002) In this piece we aim to review the various treatment modalities and to concentrate primarily on the eccentric muscle strengthening modalities of treatment, the rationale behind them and any evidence that they actually work. Before we can consider the direct question of eccentric loading as treatment for tendonopathies we must examine the rationale for its uses well as the basic science and theory behind the actual practice. We will do this largely by the mechanism of a literature review. Methodology In this review we shall be examining the literature for not only the methods that are currently employed in treating the various lower limb tendonopathies but also for justification for these methods and the quality of the science behind them. We shall therefore critically review the literature available and present it in a rational form. In addition to this we intend to present an overview of various factors in a wider picture that are relevant to our considerations. We shall consider the current views on the pathophysiology of tendonitis and the experimental evidence on the response of the tendon to exercise in general terms. Although it is accepted that the majority of patients currently seen in clinical practice with various forms of lower limb tendonitis are suffering from a sports related injury, we shall also look at the effects of ageing on tendon physiology as it is acknowledged that the elderly are another highly represented group with tendonitis. We conclude the preamble with a number of clinical considerations, most prominently the difficulties posed by the differences in nomenclature and terminology which renders both assessments and comparisons between clinical trials difficult. We conclude the dissertation with a review of various currently employed treatment modalities and the rationale behind them. We focus specifically on the use and place of eccentric muscle strengthening exercises in the spectrum of rational treatments.. Pathophysiology of tendonitis At the macro-anatomical level, the tendon is usually easily defined as a semi-rigid white or grey structure, generally found in close proximity to synovial joints. One of its prime functions is to transmit forces generated by muscles to the skeletal system, often inducing movement. (Huxley HE 1979). At the micro-anatomical level, it’s structure is very much more complex and requires a detailed examination before we can realistically and meaningfully consider the issues relating to the therapy of tendonitis. Tendons form part of the anatomical structures that are functionally grouped together as the extracellular matrix (ECM). The rate of turnover – both synthesis and degradation – is influenced by a number of different factors including metabolic and disease related factors, but the strongest influence on the turnover rate is mechanical stress, usually as a result of various degrees of physical activity. (Agar Pet al 2000) Tendon (and intramuscular) collagen, turns over at a rate which is about half as fast as myofibrillar protein turnover. The main physiological stimulus to turnover appears to be the multiple stimuli arising from mechanical or contractile activity.(Cuthbertson D et al2005) At the cellular level, degradation of collagen is mediated largely byte metalloprotease group of enzymes and synthesis is most strongly influenced by a number of different trophic factors which are released at the cellular level. (Algren MS. 1999) These growth factors are mainly responsible for both the transcriptional changes as well as the post-translational modifications that take place as a result of either physiological changes or disease processes. (Sand Meier et al 1997) Until comparatively recently, tendon tissue was thought to be fairly inert. Recent research work has given good supportive evidence that the internal metabolic processes, the internal vascular responses (Alstom et al 1994) and the actual catabolic turnover of the collagen protein in response to physical activity, is considerably greater than originally thought. The converse is also true, as inactivity appears to have the same inhibitory effect on tendon tissue as the better known effect of wasting in muscle tissue. (Abrahamson SO et al 1996). This effect is of particular importance in our considerations (later) when we consider that some authorities suggest that outright rest is inappropriate initial treatment for tendonitis. Collagen is a large polymer-type protein made up of many repeating subunits, (triple helices of polypeptides with a high proportion of proline and hydroxyproline). It is made by fibroblasts. In the muscle, it forms a basket-like network around the muscle fibres but then forms progressively more coherent and solid structure as it forms discrete tendon. In this way it allows the efficient transmission of forces generated by the myofibrils to the tendon – and hence to the bone. (Kjaer M 2004). Training, in the form of physical work, exercise or repetitive movements, will have a trophic effect on the tendon as a whole. Collagen turnover can be increased and there can be an overall increase in the amount of collagen protein in the tendon. (Herzog W et al 2002) Collagen, in the form in which it is found in a tendon, has enormous on-elastic tensile strength and a modest degree of ability to bend under lateral stress. As the amount of collagen in a tendon increases, the tendon’s mechanical (or more accurately, viscoelastic,) properties change. It decreases it’s stress levels for a given load, and thereby renders it more load resistant.(Fowls JL et al. 2000). Again this facts of great relevance to our clinical considerations later in this piece. The stiffness, or resistance to lateral stress, is a function of the cross-linking of sulphur bonds across the parallel bands of protein. In general terms, the more cross-links, the stiffer the tendon. The degree of cross-linking is a result of a complex interaction between a number of enzyme systems in the matrix of the tendon. (Hamill OP et al.2001) Polyglycans are an important feature of this enzyme cascade and become an increasingly important functional component as age increases. Older or ageing collagen will tend to exhibit glycolated cross links in addition to the sulphur links of youth. This is part of the reason why older tendons are less flexible (and possibly more prone to injury). (Inglemark BE 1948). The functional significance of these links is that they render the tendon even stiffer and less able to bend.(Davidson PF 1989).Understanding these processes is fundamental to the prescribing of a rational treatment regime for tendon injuries and other pathologies. It is also important to have a complete understanding of both the vascular and neurologically mediated adaptation processes that are present in the my-tendon complex. These work on a far more rapid and immediate time frame than the processes that we have just described, and are primarily responses to rapid changes in the mechanical loading stresses. As muscle tissue develops physiologically, there is a symbiotic relationship between the muscle and the extracellular matrix. The various physiological mechanisms that stimulate muscle growth and hypertrophy appear to have a similar effect on the extracellular matrix. (MacLean et al 1991) But in the latter case, they are less well understood. We know that that significant and repeated mechanical loading will trigger off, or initiate a process, which starts with the activation of trophic gene in a cellular nucleus, (Banes AJ et al.1999), it progresses through the complex processes of protein synthesis and functionally ends with the deposition of collagen in the tendon tissue.(Yasuda et al 2000) Responses of the tendon to exercise There would appear to be some form of integration between the muscular and the extracellular matrix signalling pathways, which optimises the co-ordinated activity of the trophic processes in response to the stimuli (which can be both loading and tensile in nature), which produce the response in the first place. (Viidik A.1993). This co-ordination mechanism must exist, as it is a well-recognised phenomenon that a tendon hypertrophies to accommodate the increased mechanical stress that its associated hypertrophied muscle produces. (Derwin et al 1999) Considerable research effort has been expended in trying to delineate the mechanism, but to date, the results have not increased our understanding of the situation significantly. (Vierck J et al 2000) Specific studies in this area have been able to show a clear correlation between collagen response and an increase in physical training. (Langberg et al 2001). The response was detectable after a 4week training programme and was maximal at 11 weeks. When we consider the pathophysiology of RSI (repetitive strain injury) or even chronic overload syndrome, the stimuli that can produce muscle hypertrophy or increase muscle fibrosis can also produce fundamental changes in the tendon structure. (Birk DE et al 1990) These changes can include changes in both the chemistry and the functionality of cross bonding of the collagen fibres, (Barnard K et al1987), changes in the size of the collagen fibrils, areas of locally increased blood flow (known as hyper vascularisation zones), and an increase in the catabolic processes which can result in either (or both) collagen being synthesised and laid down, or increase in fibroblastic activity which increases the fibrous component of the tendon. (Greenfield EM et al 1999) It is a fundamental recognition of the fact that these processes require â€Å"adjusted loading† rather than an enforced absence of loading(immobilisation) to reverse the physiological processes, that underpins most of the thrust of this review.( Howell JN et al 1993), (Jà ¤rvinenTAH et al 2002) The experimental evidence to support this view comes from the classic set of investigations by Gibson (et al 1987) who compared the rate of collagen synthesis and turnover in an immobilising long-cast leg with the rate of turnover in the unaffected leg. The rate of collagen synthesis dropped by half over a seven week period in the immobilised leg. The investigators also found an adaptive (and compensatory)reduction in the rate of collagen degradation which had the overall effect of reducing the protein loss in the tendons. In the overall context of our investigation it is also important to note that the authors also found that minimal electrical stimulation of the muscle (5% of maximum voluntary contraction for 1 hr. per day),increased protein synthesis to such an extent that there was no net protein loss over the same seven week period of the trial. (Gibson etal 1989) In a study that was remarkable for its invasiveness (the authors took repeated biopsies of human patella tendon after periods of exercise), Miller (et al 2004) demonstrated that tendon collagen synthesis showed a 30% rise within 6hrs of exercise and up to a 50%rise within a 24 hr. period. This was found to exactly follow the pattern of protein synthesis in skeletal muscle. This finding is strongly supportive of the assertions made earlier in this essay, that there would appear to be a mechanical or humeral mechanism that links the trophic effects that are apparent in both tendon and skeletal muscle. Various authors have postulated different mechanisms (it has to be said with scant evidence), including integrin’s, (Levenhagen et al2002), growth factors including transforming growth factor beta (TGFB) (Moore et al.2005), or mechano growth factor (MGF) (Rennie et al 2004),which they suggest may be responsible for the co-ordination of the trophic effects of perimysium collagen, tendon collagen and the myofibrils. More concrete evidence exists (and is arguably of greater relevance to our investigation here), for the fact that dietary protein alone can produce a trophic stimulus for tendon collagen. (Jefferson Kimball 2001). It is postulated that there is some form of amino acid sensor that is responsive to the availability of amino acids. This haste effect of changing the availability of various protein kinases in the extracellular matrix generally and a subsequent enzymatic cascade which results in an increase in various anabolic signalling molecules which are, in turn, responsible for the activation of mRNA. This is then responsible for the increased synthesis of collagen (and other related proteins), in tendon and other extracellular matrix tissues. This series of very elegant experiments was done in carefully controlled conditions which removed the possibility of other anabolic factors being relevant as the only variable was the availability of amino acids. (Cuthbertson et al 2005) There is further evidence of the effect of exercise on tendon structure in the form of the set of experiments by Rennie and disco-workers. Looking specifically at the metabolism of collagen Rennie found that after strenuous exercise, the rate of incorporation of a marker into tendon collagen followed a specific pattern (Rennie Tipton 2000). There was a latent period of about 90 mines after exercise where there was no change in metabolic rate. It was then noticed that there was a dramatic increase to about 5 times normal rates of synthesis, which peaked at about 12 hrs., was maintained for about 12hrs, and then declined over the next 48 hrs. In line with the findings of Cuthbertson (above) the investigators noted that the rise in levels of synthesis is greatest if associated with an amino acid load just pre- or post-exercise, and this effect can be further enhanced by the administration of insulin secretagogues(such as glucose). There is therefore little doubt that feeding helps the post exercise response. (Atherton P et al 2005) The effects of ageing on tendon pathophysiology We have already commented, in passing, on the physiological effects of ageing in relation to the polyglycan cross bonding in tendons. There are a number of other changes which will naturally occur in relation to advancing years, which are of direct relevance to our considerations here. It is clearly a matter of observation that muscles, bones and tendons deteriorate as age increases. This deterioration leads to physical symptoms such as loss of strength, mobility and suppleness together with an increase in fatigability and a general reduction in proprioception. This condition is sometimes called â€Å"sarcopenia†.(Forbes 1987) Epidemiological studies (Dorrens et al 2003), provide good evidence to support the popularly held view that an active lifestyle into old age is more likely to support a higher level of bone density, muscle bulk and tendon flexibility, than a sedentary one. One can postulate that the trophic mechanisms referred to above, stay active for longer when constantly stimulated by mechanical activity. One effect of ageing that has been experimentally demonstrated, is that the trophic effects of available amino acids in the bloodstream are not as great in the elderly as in the young. The elderly appear to have an ability to develop resistance to the trophic effects of amino acids, which was not present when they were younger. (Cuthbertson et al 2005) Another physiological change that can be demonstrated in the elderly, is a reduced RNA : DNA ratio in tendon tissue, which is a marker of a reduced ability to manufacture protein. This, together with reduction in the amount of detectable anabolic signalling proteins, seems to be central in the failure of the muscle and tendon synthesising mechanisms. (Smack et al.2001). If we add these findings to other work of Smack (et al 2001) and Leverhagen (et al 2002) which shows that the elderly can show responsiveness in terms of trophic changes in the collagen content of tendons by manipulation of the diet. Both studies showed that maximising the protein : energy ratio of ingested food is a reasonable strategy. It should also be noted that they also demonstrated that one has to be careful to keep the energy content of the food low in order to minimise unwanted weight gain. The elderly could reasonably be assisted to maximise the benefit they get from training (resistance training in these particular studies), by integrating it with feeding concentrated in the immediate pre- or post-exercise period. This appears to have the effect of increasing the positive synergistic relationship between exercise and amino acid delivery.( Williams et al. 2002) Clinical considerations Differential diagnosis The first and possibly most fundamental issue that we have to consider when looking at the issues of the treatment of tendonitis, is the issue of correct diagnosis. This, sadly, is compounded by the fact that there appear to be several different terminology vocabularies in common clinical use. It therefore can be difficult to directly compare treatment studies of â€Å"tendonitis â€Å" unless one has direct and clear diagnostic criteria. (Saxena 1995) Tendonitis may be taken in some medical circles to include all those conditions which come under the broad heading of â€Å"painful overuse tendon conditions† (Khan et al 1999). This is generally accepted by the uncritical, as meaning that this equates with a painful inflammatory reaction in the tendon tissue. Histological investigation of the typical chronically painful tendon, generally shows an absence of the polymorphonuclear and other associated inflammatory cells. In some literature we can see the emergence and replacement of the term tendonitis with tendinitis. This latter term tends to be defined as pertaining to areas of collagen degeneration, increased ground substance and neo-vascularisation. (Purdue et al 1996) To both illustrate and clarify the point, let us consider thevarious clinical entities that may either present like, or may be diagnosed as, â€Å"tendonitis†. For ease of classification and clarity, in this section we shall consider the term â€Å"tendonitis† in specific relation to the Achilles tendon. Williams (1986) produced the (arguably) most commonly currently accepted definitions of Achilles tendon pathologies. He classified them into:- Rupture, Focal degeneration, Tendinitis, Per tendonitis (peritendonosis), Mixed lesions, Origin/insertion lesions, Other cases such as metabolic/rheumatic causes. In common clinical parlance, any of them can be referred to, with reasonable accuracy, as â€Å"tendonitis†. (Galloway et al 1999) The aetiologies can vary (and this may well have a bearing on treatment), from trauma, reduced flexibility, abnormal or changed biomechanical considerations (such as excessive pronation, supination or limb length inequalities) to name but a few. (Saxena, A 1998) It should be noted that the anatomy of the Achilles tendon is unusual and certainly different from any other in the lower limb. It does not have a true synovial sheath but a petition which extends from its origin in the muscle to its insertion in the calcaneus. Peritendonosisis therefore a commonly misdiagnosed as Achilles tendonitis. It is also clinically significant that there is a region of decreased vascularity in the tendon, which is typically about 6 comes above its insertion (Hume 1994). The clinical difference between these two conditions is that true Achilles tendonitis may, if chronic, be characterised by fucoid, or fatty focal degenerative, changes in the tendon itself, where asperitendonitis will not involve the Achilles tendon at all. (Kvist1994). These degenerative changes may be extremely resistant to non-surgical forms of treatment. In practice, the two conditions may well be presenting the same individual. (Killer et al 1998) The differentiating signs are, however, fairly easy to detect and the two conditions can be separately distinguished in most cases. Per tendonitis is the inflammation of the petition and can usually be clinically distinguished by the presence of clinical crepitus as the Achilles tendon tries to glide back and forth along the inflamed petition. This sign together with pain, generally tends to increase with activity and the tenderness is normally felt along the whole length of the tendon. Achilles tendonitis on the other hand classically gets better with movement and is at its worst after a period of rest. The discomfort tends to be more localised into discrete areas and is more commonly found in cases where there has been either a partial or even a complete rupture in the past. (Clement et al 1994) Other pathologies can arise associated with the Achilles tendon, and for the sake of completeness we should briefly consider them as they could be potentially confounding factors in any trial which aims to consider tendonitis. Tendocalcinosis is an inflammatory process which involves the Achilles tendon but only at the point of insertion to the calcaneal bone. It typically will result in calcification and therefore should be considered a different entity to Achilles tendonitis as such. It is characterised by localised pain, and prominence of the calcaneal insertion of the tendon which may well be associated with a retro-tendon bursitis. (Williams 1986) If we apply the same rationale to the patella tendon, we are again faced with a bewildering array of terminology and conditions which tend to get lumped together as â€Å"tendonitis† and may also therefore be confounding factors in any study. We shall therefore spend a few paragraphs delineating them. Some authors point to the fact that conditions that had been previously referred to as tendonitis, when examined at a histological level, are found to be the result of collagen breakdown rather than inflammation (Khan et al 1996), and therefore suggest the title oftendinosis is more appropriate. (Cook et al 2000) (I) The whole issue of the role of the inflammatory process in the tendonopathies appears to be far from clear. An examination of the literature can point to work (such as that by Khan – above), who demonstrated that the prime histological changes were non-inflammatory and were more typical of fucoid, hyaline or fibrous degeneration with occasional calcific processes being identified. Other investigators however, point to the clinical picture which commonly includes the classic inflammatory triad of dolour, rub our and tumour (pain, redness and swelling)(Almekinders et al 1998). This, associated with the evidence of the relieving effect of NSAIA’s or corticosteroids(Friedberg 1997) leads to an ambiguous picture. The pathophysiology of this condition is most commonly thought tube related to jumping and landing activity which is the mechanism which appears to cause the rupture of the collagen filaments and hence the histological appearances. The characteristics of this type of condition are that it tends to be focal, and often in the region of the lower pole of the patella. Initially it tends to be self healing but as the chronicity increases, the pain levels can increase to the point where pain is experienced even at rest (Cook et al 2000) (II) This type of condition must clearly be differentiated from there-patella bursitis (Housemaid’s knee) which is often mistakenly diagnosed as a patella tendonitis. (Halaby et al 1999) Factors which appear to predispose to tendonopathy Many authors identify chronic overuse as being one of the major factors in tendonopathy generally. (Kist 1994) (King et al 2000). This applies equally to the occupational tendonopathy as much as the sports-related conditions. (Jon stone 2000) (Kraushaar et al 1999). We should acknowledge that the term overuse can refer equally to overuse in terms of repetitive action just as much as it can refer to overloading. The two factors being independent (but often related). Some of the current literature points to the fact that there can be differentiation in the spectrum of overuse injuries between those conditions that arise from some form of biochemical change in the structure of the tendon itself (Joss et al 1997), those that are associated with biomechanical changes (such as change in function or previous injury) (Alstom 1998) and those that arise as a result of ageing or other degenerative changes (Alstom et al 1995). These factors can arise as a result of, or independently from, other factors such as the fact that the anatomical path of a tendon can take it over (or in close proximity to) friction-inducing structures such as a bony prominence – as in the case of the tibias posterior tendon, (Benjamin et al 1998) or factors relating to the site of insertion of the tendon into the bone – as in the case of theAchilles-calcaneum interface.(Benjamin et al 1995) We can point to evidence that extraneous factors can also predispose to tendonopathy. There are genetic factors (Singer et al 1986), and a relationship to blood type (Joss et al 1989). The presence of certain concomitant chronic or debilitating illnesses can certainly be associated with tendonopathies (Kannur et al 1991) as can the chronic use of certain medications – most notably the fluoroquinolone group.(Huston 1994)(Ribard et al 1992). The mechanism in the latter case appears to be associated with an increase in the amount of MMP and its associated activity which seems to be associated with an increase in the rate of degradation of protein (especially collagen) in certain tissues. (Williams et al 2000). Other authors have identified biomechanical factors as being significant (rather than necessarily causal), in the development oftendonopathies, but we shall discuss this in specific relation to treatment, and so will not discuss it further here The spectrum of currently available treatment Before beginning any rational consideration of the various forms of treatment available, one must appreciate a common truth in medicine, and that is that different treatments and different patients will respond differently to a specific treatment modality, and one of the factors that will influence this phenomenon is the skill and experience of the practitioner concerned. For example, a surgeon may well find that he gets good results from tenotomise but poor results from eccentric exercises and therefore will recommend surgery. Physiotherapist may find the converse. It is therefore important to be critical of such factors in any appreciation and appraisal of different techniques for the treatment of the lower-limb tendonopathies. In this section we shall examine the available literature to try to obtain an overview of the various treatment modalities that are currently being prescribed and examine the rationale behind their use and efficacy Most authors seem to agree that, before considering the specific conditions, a general approach of conservative measures (such as load reduction, strengthening exercises, and massage) should be tried before other modalities such as medication and physical interventions(ultrasound etc.), and that surgery should only realistically be considered as a last resort. The only obvious exception to that approach would be when complete (or sometimes perhaps partial ) rupture of the tendon has occurred, and then surgery may well be considered the prime intervention. (Cook et al 2000) (I) Let us consider the various options in turn. In this section we will begin (again, for the sake of clarity), by specifically considering the options available for patella tendonitis. We accept that there will, of course, be overlap between the treatments for the various tendonopathies, but it makes for a rational approach to consider each in turn. The first comment that we must make is that, after examination of the literature it is noticeable that there are only a comparatively few well constructed, placebo controlled randomised trials in this area.(Almekinders et al 1998). Those that we can examine appear to suggest that the traditional treatments aimed at minimising the inflammatory processes in the condition are largely ineffective. The authors (Cooked al 2000) (II) suggest that this may well be because of the findings we have quoted earlier (Khan et al 1996) that histologically, the prime pathology is not inflammatory. Relative Rest Cook (et al 2000) (I) points to the fact that many strategies can rationally involve load reduction and the (now outmoded) instruction to â€Å"Stop everything and rest† is positively contraindicated. The rationale for this relates to the mechanisms that we have examined earlier in this piece. Immobilisation of a tendon is actually harmful as we can point to evidence (above) that shows that tensile stress and mechanical action not only stimulates collagen production, it also is vital in tendon to ensure it’s optimal fibre alignment. Rational treatment suggests that a programme of â€Å"Relative rest† may be beneficial. By that, the authors (Cook et al 2000)(I) suggest that activity should continue as long as the prime traumas of jumping, landing or sprinting can be avoided and reintroduced in a carefully graded fashion. Biomechanical Correction Because patella tendonitis is primarily related to jumping and sprinting sports ( in numbers that present clinically), we will consider treatment in relation to them. The forces that are generated in the patella tendon on landing after a jump are considerably greater than those that produced the jump in the first place. (Richards et al1996). It logically follows that if biomechanical methods can be employed to more efficiently minimise the forces, they would be best employed on landing strategies than jumping ones. One should appreciate that the energy-absorbing capacity of the limbs dependant, not only on the patella tendon, but factors at the hip and ankle as well. Studies show that the ankle and calf are the prime sites of absorbing the initial landing load (Richards et al 1996) and, if these structures are not biomechanically sound, then this will increase the forces transmitted to the knee. Prilutskii and his co-workers (et al 1993) completed a series of studies which showed that up to 40% of the energy absorbed on landing is transmitted proximally from the ankle/calf mechanism. It follows that it must be biomechanically sound if it is to absorb the 60% bulk of the load which otherwise would be transmitted upwards to the knee mechanism. Another set of studies (Prapavessis et al 1999) concluded that when flat-foot and fore-foot landings were compared, the latter generated less forces throughout the lower limb and that the forces could be reduced further (up to another 25%) by increasing the range of both hip and knee flexion on landing. There are a number of other potential biomechanical deficiencies that can be amenable to correction and should therefore be sought outspans planes may be an obvious anatomical problem detectable at an initial examination (Kaufman et al 1999), but there are other types of functional abnormality (such as excessively rapid pronation on landing) (McCrery et al 1999), that may require far more sophisticated evaluation. Outhouses inside shoes may go a long way to help these problems Some authors, (McCrery et al 1999), regard a reduced range of movement in the sub-taller joints as an aggravating factor which places and undue stress on the Achilles tendon and that manual mobilisation of the joint is indicated in these cases. Cry therapy In the light of the histological findings mentioned earlier,cryotherapy has a rational place in treatment. It is thought th

Ellis Island :: essays research papers fc

Ellis Island In the 1600's, Ellis Island was known as Gull Island by the Mohegan tribe and was simply two to three acres. During high tide, the island could barely have been seen above the rising waters. After being discovered for its rich oyster beds in 1628, Dutch settlers renamed it Oyster Island. And then in 1765, which was the hanging of Anderson the Pirate, the island was again renamed the Gibbet Island, after the instrument used to hang him. Finally on January 20, 1785, Samuel Ellis purchased the property and gave it his name, which is still the name of the island today, Ellis Island After passing through a few generations of Ellis's descendents, the island was bought by the state of New York, and then sold to the federal government in 1808 for ten thousand dollars. During the years of 1812 to 1814, the United States Army erected Fort Gibson, which was eventually taken apart by the government in 1861. In 1876, the United States Navy used Ellis Island as a weapons warehouse, storing 260,000 pounds of powder. However, complaints from nearby New Jersey residents lead to the removal of the storage area in 1890. The original station, Castle Garden at the Battery in lower Manhattan, could not handle all of the immigrants coming in. To have room for the immigrants, the island grew to 3.3 acres. In the next two years, Ellis was enlarged to fourteen acres in order to hold all of the immigrants and support buildings. By January 1, 1892, Ellis's first immigration station, a two story high structure of Georgia pine, was open ready for business The most impressive room in the building was the registry room. It measured 200 feet by 100 feet, and had an impressive fifty-six foot arched ceiling. Twelve narrow aisles, divided by iron bars, channeled new arrivals to be examined by doctors at the front of the room. The officials who worked at the island, however, were not impressed by the architecture. In fact, they constantly complained of leaky roofs, and other problems within the building. After long and heated arguments between experts, it was decided that the Superintendent of Construction was extremely inexperienced, and that there was "recklessness in the handling of public money," on the part of the Treasury Department and the Immigration Bureau of Officials. The entire building, excluding the hospitals, had been built shoddily. After news of the problems with the building had been in the media, a lot of people involved with the construction of the building resigned their positions.

Willa Cathers Death Comes for the Archbishop :: Willa Cather Death Comes for the Archbishop

Willa Cather's Death Comes for the Archbishop - A Powerful Non-Novel Responding to the criticism that Death Comes for the Archbishop is not a novel, Willa Cather proposed that the work was a narrative. Her choice of the word narrative signifies that the structure of Death Comes for the Archbishop is closer to that of a biography. A narrative is a type of composition used to recount events over a period of time and can incorporate description as well plot, but it does not necessarily have to. Death Comes for the Archbishop follows the guidelines of a narrative in that it recounts the events of Father Latour's life, beginning when he is appointed to New Mexico and ending with his death. Cather incorporates description into her narration, but does not offer dramatic plot structure. A novel utilizes the elements of narration, specifically including description and plot. Novels also incorporate a climax to the story along with denouement. Plot is unfolded by the actions, speech and thoughts of a character. It is these actions that lead to the climax and the resolution of the story. Based upon the guidelines used to classify a novel, Death Comes for the Archbishop does not meet the requirements and is therefore not a novel. Her work tells a story, but does not offer plot, climax or resolution. The events that are recounted in Cather's work do not build upon each other in order to offer a climax. Each event is no more significant than the one before it; for example, Cather places just as much emphasis on Latour's relationship with Olivares as he does with helping Sade pray (p 175, 213). While the events themselves do not add up to create the dramatic plot structure necessary to call Death Comes for the Archbishop a novel, each individual event experienced by Latour, is in itself a story that includes both climax and resolution. An example of this is Father Latour's death. It begins with him getting sick and living his last days, building up to his final moments and culminating in his death. The resolution to this individual event is the bell tolling and Latour being placed in the church he built. Each event in Latour's life does have plot and resolution, creating difficulty in not calling it a novel. However, if the work is examined as a whole piece, from beginning to end, it is evident that while it fits the boundaries of narration, it does not meet the qualifications of a novel.