Depression and Bipolar Disorder essays

Depression and Bipolar Disorder essays Depression and bipolar disorder affects over sixteen million people in the United States today. Many people who suffer from these disorders have trouble dealing with everyday life such as school, work, and relationships. The symptoms of these diseases can range any where from anxiety, irritably, sleeplessness or insomnia, hopelessness, and loss of energy. Even though the symptoms of depression and bipolar disease are similar, they are two very different diseases and need to be treated differently. Depression can affect a persons moods, thoughts, the way they eat, sleep, and see themselves. Symptoms of depression are persistent sadness, anxiousness, hopelessness, feelings of guilt and helplessness, loss of interest in activities, decreased energy, insomnia or oversleeping, decrease in appetite or overeating, thoughts or attempts at suicide, restlessness and irritability, and can include headaches, digestive disorders, and chronic pain. When a person suffers from bipolar disease, their symptoms are split into two categories a manic stage and a depressive stage. When the person is in the depressive stage, their symptoms are the same as someone suffering from depression. The manic stage is what makes these two diseases different from one another. Symptoms of the manic stage are increased energy, an excessively high or euphoric mood, extreme irritability, racing thoughts and rapid speech, inability to concentrate, not requiring much sleep, poor judgment, denial, and intrusive or aggressive behavior. Any of these symptoms whether with depression or bipolar disease can last for a week or longer depending on the person. Depression and bipolar disease can make dealing with all aspects of life almost impossible for the person suffering. There are many treatments for depression and bipolar disease. Prescription medications and therapy are the most popular. However, the treatments are different. For depression, the medications are u...

Murder and manslaughter Essay Example | Topics and Well Written Essays - 2500 words - 1

Murder and manslaughter - Essay Example or in the event that the offender causes death in the process of carrying out an illegal act.2 According to Sir Edward Coke, murder is applied where a person of sound memory and age unlawfully kills in any country another human being under King’s peace with malice, which is premeditated as expressed by the party or implied by the law such that the wounded person dies within an year and a day out of the same. 3 To conclude that the person should be held under actus reus, there first of all has to be unlawful killing and the act of the offender must have been the established cause of death of the victim.4 The killing must be of another human being and under queen’s peace which means stipulates that killing of an enemy in war is not murder. However, the death after an year and day was removed in the law reform act of 1996.5 Under this, there is the malice afterthought. In R v Moloney (1985), the House of Lords concluded that nothing less than the intention to kill or cause bodily harm would be seen as malice afterthought. Just foreseeing the death of a victim as probable was not sufficient. There are two things to be considered under Mens Rea, first the intention to kill where murder is identified as a crime of specific intent.6 The intent in this case could be direct or oblique. In direct intent, the offender desired the death. In oblique, the death is foreseen by the offender as virtually certain, however, not desired for its own sake. Secondly, the intention to cause grievous bodily harm which was accepted under as sufficient mens rea for murder since if the offender was willing to inflict serious body harm, then he had no way of knowing certainly knowing the victim will not die. Intentional body harm is evidence that a victim could die. 7 In the case of Anthony the political activist who set up bombs in order to get attention for what he was lobbying against, genetically modified crops, a couple of considerations can be identified in this case. First, in

The Walt Disney Corporation Research Paper Example | Topics and Well Written Essays - 1000 words

The Walt Disney Corporation - Research Paper Example The dream of iestablishingthe giant corporation can be traced back in time when Alice in Wonderland short series began (Denny and Williams, 2004). A theme well developed in many of Walt’s cartoons is undying optimism, which can be related to the Vision of Dream on which the company is formed. From the time the company was incorporated to its current performance, for instance in the figures illustrated above, it is quite in order to state that the company has followed its dream. Believing in the company’s position and capacity to achieve its goals could have been the secret behind its success. Achieving what might appear impossible can only be accomplished in believing. Another character possessed by Walt Disney is that of unwavering belief in achieving anything desired of. Walt had a dream of becoming a cartoonist and the belief he had propelled him above that to be founder of animated cartoons watched all over the world. The company’s story can be said to be a successful belief, now that it even covers more than animated cartoons. Concerning a daring spirit, Walt was a good salesman from the beginning, with some fine skills that were rare to find in those times. Early in his art work, he aggressively and determinately sold his cartoons and comedies until he got into partnerships that enabled him to settle down for business. He was capable of using his salesmanship skills to successfully convince his animation team at Kansas City to relocate to California. The company’s markets its products aggressively and with a good precision to take advantage of the market better than its competitors, such that it has become a worldwide household brand Capodagli and Jackson, 2000). According to Hair et al (2008), when a market evolves to become well established, it becomes a lucrative venture that many investors would want to try. The line of business that Walt Disney deals with has

Humanitarianism and Security Essay Example | Topics and Well Written Essays - 2250 words

Humanitarianism and Security - Essay Example This essay declares that humanitarianism operates in the best historical of emancipator ethics. It aspires to keep people alive, to expand their opportunities, and to provide them much control over their fates. It does that through various interventions, all defended on the basis that they improve the welfare and health of others who are too powerless and weak to help themselves. A variety of private and public actors contributes to humanitarian action, among them states, commercial outfits, religious bodies, philanthropies and various individuals. This paper makes a conclusion that humanitarian action they play a crucial function in saving lives across the globe. Humanitarianism as a doctrine ought to be man's duty to strive to promote the welfare of fellow mankind. In practicality, this has not been the case in many countries. Many academicians and other professional have questioned whether development and humanitarianism conventionally related. They have critic the ever increasingly involvement of government in humanitarian assistance and their motives. Humanitarian aid has been seen to be used as a political tool. However in recent years there has been hope in ‘new humanitarianism’. There exist a ‘new humanitarianism’ for the new century. ‘New humanitarianism’ is ‘principled,' ‘human rights focused and always politically sensitive. ‘New humanitarianism’ marks a break from the historical governance of humanitarian programs. It is a new concept in humanitarians a nd advocates for the system claims it can only get better with time.

How can Ebola affect us Essay Example for Free

How can Ebola affect us Essay Imagine being isolated from your own family and feeling unsure as to whether or not you will ever see them again. They do not want to come anywhere near you, for you are a threat to their health. The only visitors who come within 10 feet of you are strangers in full on protective gear. They do not want to expose the slightest bit of skin to you and you cannot see anything besides their eyes. The world fears what you are and no one wants to come close to you. You know death is near, and you are all alone. You can see the mountain of corpses outside the wiry mesh window of your facility, being burnt and thrown into mass graves, and you know that you will soon be joining them. This is the life of an Ebola victim.. In the year 1976, Ebola climbed out of its unknown hiding place, and caused the death of 280 out of the 318 people who got infected. That’s an 88% fatality rate. Fear gripped the victims, and tortured their minds. The people of Zaire waited outside clinics, churches and in their homes for a treatment of the horrible disease, but there was no cure. They were forced to watch people die, hoping that they would be saved from the violent death of the Ebola virus. From the year of 1976 till today, researchers have searched for origin and cure of the virus. Scientist have carried out numerous studies and investigations, but no one has been able to find the right explanations. There have been many others out breaks in the past but 2014/15’s outbreak has claimed more lives than all of these other outbreaks together, with a staggering 8386 death and counting. It has also spread between countries starting in Guinea then spreading across land borders to Sierra Leone calming 3,049 lives and Liberia causing 3,515 deaths and to to Nigeria causing 8 deaths. It is believed that the Ebola  virus may have initially been transmitted to humans from bats, and other forms of bush meat like monkeys ect.. fro m the jungles in central Africa, i know it must sount crazy to you to hear that some people eat monkeys but In some remote areas of Africa it is part of their culture and their way of life. In Africas Congo Basin, people eat an estimated five million tonnes of bush meat per year. The reason that bush meat is so deadly is because some animals mostly bats, can be a host to specific diseases without being harmed, were as us humans cannot carry these diseases without becoming infected. When a person contracts Ebola they will start to feel the symptoms within the next 2-21 days. The symptoms of Ebola are very distinctive and deadly. If you were to contract Ebola, your experience would be horrific you would start to get bad stomach pains, but it would just be passed off as a common bug. after that they would then start to amplify in pain until they would wake you up from your sleep, which would be followed by chronic vomiting. Anything you ate would come back up. These symptoms would continue for a few days then you would start to lose weight at an extreme rate. Chest pains would now accompany the stomach aches, by this time you would be very weak with virtually no food in your body due to the vomiting and your teeth would start to fall out while you would develop a bloody rash and you would die days later after horrific suffering. But those are just the side effects of what’s really happening in your body. Ebola attacks every organ and all of the tissue in the human body except the bones. You develop blood clots under the skin. Your organs turn to mush and the under layers of your skin die and liquefy; this is what causes the bloody bubbly rash. These things actually happen to Ebola patients every day. Ebola is a very contagious disease; this is why Ebola victims have to be kept contained in hospitals and treatment facilities. When it comes to transmission doctors take cleaning themselves after being in contact with an infected person very seriously. Ebola is transmitted through the passing of boldly fluids, which means if you get fluids from an infected person’s body onto your skin, you should be okay; but we as humans are constantly rubbing our eyes and eating with our hands so this means that we are still giving the Ebola parasite a chance to enter our body. At the moment there is no cure or vaccination for Ebola. Experiments however are taking place to find  a vaccination using antibodies of Ebola survivors. This is possible because like any other disease like small pocks and the chicken pox, one you have survived Ebola u become immune to it. Scientists are trying to figure out how to copy this into a vaccination. Most people in the uk think that they are completely safe from the disease, and at the moment yes they are. It is extremely unlikely that Ebola at the moment could reach the uk and spread like wildfire. However, every person in West Africa, Sierra Leone, Liberia ect that gets infected with Ebola provides it with an opportunity to grow and mutate, if not stopped it will eventually maybe in the next year, maybe in the next 10 years become air born. This means that even breathing near an Ebola patient will give u the disease. Once air born it will travel the world and could patiently kill a large percentage of the earth’s population. Including you. I hope now you can see why Ebola need stop be stopped. Thanks for listening

Spasticity Following Stroke: a Literature Review

Spasticity Following Stroke: a Literature Review ABBREVIATIONS UMN: UPPER MOTOR NEURON SPASM: SUPPORT PROGRAMME FOR ASSEMBLY OF DATABASE FOR SPASTICITY MEASUREMENT CNS: CENTRAL NERVOUS SYSTEM PMS: PASSIVE MUSCLE STRETCHING TS: TRICEPS SURAE TA: TIBIALIS ANTERIOR ROM: RANGE OF MOTION INTRODUCTION: Spasticity is a major disabling symptom that most commonly arises after stroke, multiple sclerosis, spinal cord injury, some traumatic brain injuries and other central nervous system (CNS) lesion (Dietz and Sinkjaer 2007). Lesion of the cortico-fugal pathway along with the pyramidal tracts, at any level, like cortex, brainstem, internal capsule or spinal cord results in spasticity (Carr et al. 1995). The term spasticity was derived from the Greek word ‘spasticus’ meaning ‘to pull or to tug’ (Ghai et al. 2013). The definition of spasticity that has been formerly cited is that of Lance in 1980: ‘Spasticity is motor disorder characterised by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex, as one component of the upper motor neurone (UMN) syndrome.’(Brown 1994). Though this definition is useful for diagnosis, yet for the purpose of understan ding and managing the effects of inappropriate muscle actions after stroke, it is too restrictive (Bhakta 2000). Recently SPASM (Support Programme for Assembly of database for Spasticity Measurement) redefined spasticity as â€Å"disordered sensori-motor control, resulting from an UMN lesion, presenting as intermittent or sustained involuntary activation of muscles† (Mirbagheri et al. 2009). For the purpose of study the clinicians have divided the UMN syndrome into ‘positive’ and ‘negative’ effects. The characteristics of the negative features are loss of dexterity, weakness and easy fatigability on the other hand spasticity, increased tendon reflexes, extensor and flexor spasm, clonus etc are the features of positive UMN syndrome. The later definition of spasticity includes all the characteristics of positive UMN syndrome excluding its negative features and the biomechanical changes in the joints and soft tissues (Mirbagheri et al. 2009). The negati ve features of UMN syndrome are regarded to be more disabling than the positive features (Carr et al. 1995) but recent studies have showed that spasticity adds on to the impairment of function and to limitation of activity for the affected person (Bovend’Eerdt et al. 2008). The core feature of spasticity is increase in stretch reflex, manifested as hypertonus. Muscle tone is defined as the tension of a muscle due to involuntary contractions of its motor units; it is determined both by the passive elasticity of muscular tissues, the viscoelastic properties of the fibrillary proteins contained within each muscle fibre and by the active (though not continuous) contraction of muscle in response to the reaction of the nervous system (Grabowski and Tortora, 2003). Alternately active and inactive motor units help in maintaining normal tone in a muscle. Any imbalance in the input from central motor pathways like the cortico-reticulo-spinal and other descending pathways to the inter-neuronal circuit of spinal cord results in alteration in the involuntary contraction in a muscle. The main tract restricting the spinal reflex activity is the dorsal reticulospinal tract that runs along the lateral spino thalamic tract. It arises from the ventero medial reticular for mation which has less facilitatorty control over the cortical motor areas, thereby augmenting the inhibitory drive. The main excitatory pathway also arising in the brainstem is the medial reticulo spinal tract. Damage to these tracts give rise to a net loss of inhibitory control leading to increased alpha motor neurone excitability at the segmental cord level and subsequent increase in muscle tone. Several studies also claim that peripheral neural changes also contribute to the increased muscle tone. Muscle tone has two components, neural involving CNS and musculoskeletal, where muscles are involved (Barnes, M. P. et al. 2003). Both the components help in maintaining normal muscle tone. Normal tone is the slight amount of constant tension in the healthy muscles offering small resistance to displacement (Barnes, Michael P. and Johnson 2008). There is change in mechanical, visco-elastic properties of muscle fibres as a result of paresis and immobilisation after an UMN lesion. Activation of actin and myosin cross bridges also increases muscle tone (Lee et al, 2005). CNS and neural pathways maintain tone by overlapping actin and myosin filaments on muscle contraction. Insufficient contraction results in decreased muscle tone due to insufficient development of tension (Grabowski and Tortora 2003). Through the phasic and tonic stretch reflexes the muscle spindle plays an important role in regulating the muscle tone (Cameron-Tucker 1983). These muscle spindles can be adjusted in terms of their response to stretching. Spasticity is generated due to the over activity of the alpha motor neurons. Over activity occurs when the monosynaptic input via Ia afferent fibres and polysynaptic afferent input via the Golgi tendon organs and cutaneous receptors loose descending inhibition from the cerebral cortex and basal ganglia, which is relayed through the dorsal and medial reticulospinal and vestibulospinal tracts. Spinal inter-neurons are responsible for presynaptic and reciprocal inhibition of Ia fibres. Due to the loss of this inhibition inappropriate muscle co-contraction occur disabling voluntary limb movement (Bhakta 2000). The course of development of both cerebral and spinal spasticity after an insult is slow in humans, except for the cases of high brain stem lesion like traumatic brain injury where the increase in the tone is immediate (Carr et al. 1995). The time gap between the injury and appearance of spasticity may vary from days to months, depending upon the level of lesion (Ghai et al. 2013). The effect of spasticity ranges from mild muscle stiffness to severe, very painful and uncontrollable muscle spasm. If left untreated spasticity gives rise to many problems like pain, spasm, contracture and deformity leading to a loss of mobility and dexterity, problem in self hygiene, inability to wear orthotics hence resulting in decreased functioning, participation and low self esteem (Ghai et al. 2013). A multidisciplinary approach is required for the effective management of spasticity taking into consideration other variables that might affect treatment outcome. Aim of treatment should include prevention of abnormal limb or trunk posture and facilitation of movement in the context of functional activities (Bhakta 2000). Secondary to the neural changes there are dramatic changes of the structural and mechanical properties of the spastic muscle. A review conducted by Jared et al. concluded that the following changes occur in a spastic muscle: a) alteration of the size of muscle fibre and the type of fibre distribution; b) morphologically and biomechanically measured there is proliferation of extracellular matrix material; c) increased stiffness in the spastic cell muscle; d) compared to the normal muscle there is inferior mechanical properties of extra cellular matrix in the spastic muscle (Foran et al. 2005). As a management of spasticity the researchers have tried to alter the motor neuron excitability by many interventions like electrical stimulation (Bajd et al. 1985), pressure (Leone and Kukulka 1988), muscle tapping (Belanger et al. 1989), vibration (Gillies et al. 1969), cooling (Bell and Lehmann 1987), massage (Sullivan et al. 1991) and stretch (Kunkel et al. 1993, Avela et al. 1999). Among all of these, stretching has been intensively used as it is safe, economical and convenient (Tsai, KUEN-HORNG et al. 2001). Stretching is the process of applying tension to the soft tissue structures like muscle, tendon, and vascular, dermal, connective, neural tissues for elongation. Stretching can be applied mechanically (example- with dynamometer or an intelligent feedback control device) offering well controlled intervention and manually, which is difficult to standardise but represents clinical practice better. Stretching changes the viscoelastic, structural and excitatory property of the muscle. (Nielsen et al. 2007). However many neural as well as non neural property of stretching remains unclear. Stretching aims on decreasing muscle tone, maintain or increase soft tissue extensibility leading to improvement in function (Barnes, Michael P. and Johnson 2008). Lots of variation can be done while implementing stretching as an intervention. The amount of tension, the duration of the stretch, the velocity of stretch, the number of repetition can all be varied. LITERATURE REVIEW: A study was done by Harvey et al. in the year 2000 on the â€Å"Effects Of Four Weeks Of Daily Stretching On Ankle Mobility In Patients With Spinal Cord Injuries†. 14 recently injured subjects with paraplegia and quadriplegia were taken from two spinal injury units in Sydney, Australia. Their ankle was stretched into dorsiflexion, continuously for 30 minutes with a torque of 7.5 Nm for every weekday, for 4 consecutive weeks. The main outcome measure was measuring the torque angle in knee flexed and extended position. Measurements were taken pre-test and post test. Post test measurements were also taken thrice I,e, during the study (2nd week), just after the study (4th week) and one week after the study (5th week). Intervention was given by a custom made stretching device that is able to give ankle stretch. The baselines of all the subjects were same. The result showed that even after stretching for a longer time than usual there was no significant difference in the post test value in any of the three parameters from pre test. Hence the study concluded that there is no significant change in ankle mobility after 30 minutes of stretching for 4 weeks in SCI patients. The strength of the study is good, with random allocation, blinding of assessor, similar baseline of all the subjects but the intervention device needed to be more standardised. The study has a score of 8 on PEDro scale of assessment. A study by Tsai et al. 2001 examined the effect of a single session of prolonged muscle stretch (PMS) on the spastic muscle. 17 spastic hemiplegic patients were selected for the study and as an intervention PMS was given on the triceps surae (TS) muscles by standing on the tilt table with feet dorsiflexed for 30 minutes. Here the outcome measures were Modified Ashworth scale of the TS, the H/M ratio of TS and the F/M ratio of tibialis anterior (TA) and passive range of motion (ROM) of ankle dorsiflexion,. The measurements were taken pre test, post test and 45 minutes after the test. ROM was measured with a goniometer and electromiograph was used to perform nerve stimulation and reflex recording. The results showed non-significant difference in the Modified Ashworth scale, significant change in the ROM of ankle dorsiflexion, F/M ratio and H/M ratio. There was increase in the passive ROM of the ankle dorsiflexion post treatment compared to pre treatment, additionally PMS reduced motor neuron excitability of the TS and increased that of TA in the post treatment. There was no significant difference of result with in immediate post test and 45 minutes after post test. The study was well written but the sample size was too small. The age of the effected patients varied from 33 till 79 years which is a very wide range and the acuteness of the patients varied from 4.5 months post attack to 79.6 months post attack. These factors may cause a problem while generalising the results and the amount of stiffness may vary with the duration of illness. Bressel and McNair (2002) did a study to compare prolonged static stretch with cyclic stretching on ankle joint stiffness, torque relaxation and gait in stroke patients. 10 community dwelling people were randomly allocated into two groups; one of the groups received single session of static stretch and the other cyclic stretch of the calf muscle for 30 minutes. There was a washout period for one week and then the group interventions were exchanged. The interventions were given by an isokinetic dynamometer that measured the torques and the angles also. Before and after treatment the time taken to walk 10 m was taken and stiffness of the ankle joint was calculated from the slope of the torque and angle curves before and immediately after the treatments. Over the 30 minutes stretch the percentage of the decrease in peak passive torque was the torque relaxation achieved. Results showed that there was significant decrease in ankle stiffness in both the intervention but there was not much significant difference between the post test values of the two interventions. The amount of torque relaxation was 53% greater in static stretching than that of cyclic stretching. And the 10 m walk duration did not have any significant difference pre and post test. The sample size of the study was very small to generalise the results and the wash over period between the two sessions were of just one week. Since the prolonged effect of the stretching is unknown hence it can’t be commented that whether there was any residual effect of the previous session that may have affected the results of the second session. Nowhere in the study blinding was done hence there may be a chance of being bias from the assessor. The baselines of both the groups were not similar. A study by Yeh et al. (2005) compared the effectiveness of constant-torque prolonged muscle stretching (PMS) treatment in subjects with ankle hypertonia. The study design was a pre and post test analysis. 30 subjects suffering from hemiplegia and calf muscle hypertonia were given stretching device using a motor driven stretching device for 30 minutes in constant torque or constant angle mode. The main outcome measures were Modified Ashworth scale, passive range of motion and viscoelastic property of the planter flexors were measured pre and post treatment. Result showed significant improvement in all the measures, but the in the viscoelastic component the constant torque showed more evident changes compared to the constant angle measure. This study proved that there is significant reduction in spasticity after a single session of PMS. The methodology of the study was appropriate and the analysis of the data leading to the result was done well. the study also mention about the future scope of study by changing the mode of stretch from constant to intermittent. Neither the subjects, nor the assessor was blinded in the study, so the question of bias remains. A systemic review done by Bovend’Eerdt et al. (2008) was the first review done on the effects of stretching in spasticity. Studies were taken from databases like Medline, Cochrane library, CINHAL, Web of Science, PEDro and Alied and Complementary medicine for review. 10 RCTs and 11 clinical trials were assessed. Randomised control trails were assessed on PEDro scale for methodologic quality and the other clinical trials were assessed using data extraction form containing 13 items from CASP guidelines and CONSORT statement. The methodological qualities of the RCTs were low and there was a huge diversity on the methodology, intervention, population etc. Both manual and mechanical stretching was given. The review concludes as there is not much evidence on the basis of which the review can say if stretching on spasticity has its clinical benefit. A recent study by Gao et al. (2011) aims to investigate the changes occurring in biomechanical properties of the calf muscle–tendon unit after controlled ankle stretching in stroke survivors. Comparison was done between 10 stroke patients with ankle spasticity/contracture in one group and ten healthy subjects in the control group. 60 minute ankle stretching was given as an intervention to both the groups. Joint biomechanical properties like resistance torque, index of hysteresis and stiffness were evaluated pre- and post-intervention. Length of Achilles tendon was measured with ultrasonography. The force output of the triceps surae muscles was given in torque–angle relationship, by stimulating the calf muscles at a definite intensity across different ankle positions. The device used for intervention was an ankle stretching device with intelligent control (the velocity of stretching was inversely proportional to the joint resistance torque) was used. Pre test the stroke survivors showed significantly higher resistance torques and joint stiffness, which were to a large extent reduced after the stretching intervention, especially in dorsiflexion. Stretching also significantly improved the force production of the impaired calf muscles in stroke population under matched stimulations, along with the ankle ROM. The study interpreted that at the joint level, repeated stretching leads to increased passive ROM and decreased joint stiffness; at the muscle–tendon level, calf muscle force output improved. The study provided evidence of improvement in muscle tendon properties through stretching intervention. Apart from the small sample size the study was well written and the methodology was well described. DISCUSSION: Spasticity is a disabling and often painful condition that occur secondary to the UMN lesion that leads to hypertonicity, exaggerated reflexes, weakness of muscle and loss of dexterity. Spasticity has both neural and non neural components. Stretching is a very commonly used intervention used in clinical physiotherapy. But stretching and spasticity together is a very complicated concept. From the articles reviewed one can conclude that stretching does have a positive effect on spasticity, but its effect on the neural component of spasticity alone is yet not proved. In this study the stretching that has been described are mechanical stretches, but there are various other form of stretches given through splinting, plaster cast, weights which could not be discussed because of their low level of evidence. Many studies could not be included because there stretching was combined with strengthening, stimulation, passive motion etc. Even among the articles taken in this study there is heterog eneity in methodology of stretching, its duration, the type of stretch and even the outcome measures used. Inspite of being a component in the definition none of the articles investigated spasticity by using different velocities of displacement. Due to so much of diversity it is tough to comment on which mode of stretching is most beneficial for spasticity. To come down to a conclusion, future studies are needed to be done to find a standardised protocol of stretching for spasticity. In the future studies the outcome measure should be chosen carefully and intervention should be planed keeping the aim of the study in mind. CONCLUSION: The studies taken in this review shows a great diversity in respect to methodology, intervention, population and outcome measures. Though from the reviewed articles it can be said that stretching is effective for spasticity but there is need of good quality of studies to decide on a stretching protocol, its long term and short term effects and to come down to a conclusion as to which type of stretching is most effective in spasticity . TOTAL WORD COUNT IS 2978.

Death And Corruption In Hamlet Essay -- Corruption in Hamlet

Harold Blume said it best when he said, â€Å"Hamlet is deaths ambassador to us.† Throughout Hamlet, we have the images of death, decay, rottenness, and corruption pressed upon us. The imagery corresponds with the plot of the play perfectly, all culminating with the gravedigger scene. The corruption images illuminate the actions of the people in Claudius’ court, beginning with Claudius’ own actions. The beginning of the play lets us know that it is winter with Fransisco’s statement that it is â€Å"bitter cold† (1.1.6) This may be an allusion to death in itself – things are dead in winter. The guards speak of the ghost and we know right away that we have a supernatural theme, as well as a theme of death. In act 1 scene 2 we get the impression that King Hamlet has been gone for a while. Gertrude is already re-married and is happily out of mourning clothes. Gertrude even tells Hamlet, who is in full black mourning clothes, to cheer up. Good Hamlet, cast thy nightly colour off, And let thine eye look like a friend on Denmark. Do not for ever with thy vailed lids Seek for thy noble father in the dust: Thou know'st 'tis common; all that lives must die, Passing through nature to eternity.   Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  (1.2.68-73) Hamlet does not feel that it is time for him to shed his wretchedness just yet. The impression given is that it has been a long time scince the death of the old king and only Hamlet still clings to his memories and grief. After everyone leaves, however, we find out all the sordid details about the new King and Hamlet’s mother. Hamlet begins the rottenness imagery right away when he compares the world to â€Å"an unweeded garden that grows to seed; things rank and gross in nature posses it merely.† (1.2.135-6) He is utterly despondent and blames his mother and uncle for not feeling the way he does. He is the one who points out that the old King, his father, has not been dead long at all – only a month in fact. He rails over the fact that his mother could be so fickle, marrying again so soon. The affront is ground even more sharply into his frail sensibilities when she marries his father’s brother, his uncle. The fact that the two of them could be so jolly s o soon after the death of his father just staggers him. He predicts t... ...ferences to death are true references and not just imagery.   Ã‚  Ã‚  Ã‚  Ã‚  Alexander died, Alexander was buried, Alexander returneth into dust; the dust is earth; of earth we make loam; and why of that loam, whereto he was converted, might they not stop a beer-barrel? Imperious Caesar, dead and turn'd to clay, Might stop a hole to keep the wind away:   Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  (5.1.192-7) Hamlet is coming to terms with his own mortality and realizing the true physical destiny. He finds irony in the fact that a king could become a meal for a peasant, a seal for a beer-barrel, or a patch to keep wind out of a dwelling. Hamlet shows us that life is to be viewed without prejudice. It does no good to go about life with only your own interests in mind. He saw the rottenness and corruption that comes of that and it broke him. He loved his father and to see him so maligned was heartbreaking, especially coming from those who should have loved him most. That revelation shattered Hamlets ideal view of the world.