Scenes in which they fall for each other seem to build on a childhood friendship that we never see but can assume is there. Obi-Wan now always has a beard for the entire duration of the series, and Anakin Skywalker always wears black. Since these two characters are played by different actors and are the only characters in the series with such a distinction , having them look visually consistent does a great deal toward reinforcing they are the same people.
I particularly like the extra dimension it gives Yoda. This order also preserves all twists, and adds a new one or rather, makes one more effective. George Lucas knew that watching the films in Episode Order would remove the Vader and Yoda surprises, so he added the Palpatine twist to compensate - that the friendly Senator Palpatine is actually a Sith Lord and creates the Empire.
If you skip Episode I and go straight to II, all we ever see is that Count Dooku is leading a separatist movement, all on his own. This is actually a more effective twist in this context than when Obi-Wan just tells Luke in Return of the Jedi. As an added bonus, there are now about 5 hours of film between the discovery that they are siblings and the time they kissed.
After that we go back to VI, where eventually Luke confronts the Emperor. In other words, because we skipped Episode I, the parallels between Luke and Anakin are much stronger. The viewer is naturally linking the paths of these two characters together at this point, moreso than if he or she watched Episode I. Nobody else sees him do this. When watching Jedi on its own, Luke just seems a tad arrogant during these scenes. When watching Jedi immediately after watching Revenge of the Sith, the message is clear: Luke Skywalker is on the path to the Dark Side.
Why does this matter?
Because at the end of Jedi, Luke confronts the Emperor. The Emperor explains that the assault on the new Death Star is a trap and that his friends are going to die, and he keeps taunting Luke, telling him to grab his lightsaber and fight him. The film is trying to create a tension that Luke might embrace the Dark Side, but it was never really believable. Shortly after, Luke goes bananas and beats the hell out of Vader, clearly succumbing to his anger. This makes Return of the Jedi a better, more effective film. There are a few tiny issues that arise watching the films in this order.
The Kamino sequence is a little confusing. Luckily, both times he is mentioned, his relationship to the characters is restated, so it works. The weakest part of this order is when Anakin returns to Tatooine. When he has visions of his mother dying and returns, Watto says he sold her.
This definitely draws attention to the fact that one of the films was skipped. This is the one, singular thing made genuinely more confusing by skipping Episode I. Next time you break out the Blu-rays, give it a shot. Lots of people like the pod race or Darth Maul or Qui-Gon or they were born in But the thing is, do we really need to know why Anakin succumbs to the Dark Side? Armed with the new Blu-rays, we all went about watching them, and I showed them in Machete Order. IV ends with a victory that seems to have some sinister undertones, then V is dark and unresolved with a cliffhanger, II ends with victory with sinister undertones, then III is dark and unresolved with a cliffhanger again.
It works incredibly well, and when III ended everyone demanded we immediately watch VI to see how everything gets tied up. Perhaps most importantly, the flaws with Machete Order seem to not be problematic at all. How does she remember her mother? What Gets Removed? Opioids bind to the peripheral and central opioid receptors and provide analgesia without the loss of touch, proprioception, or consciousness.
They may also diminish cortical reorganization and disrupt one of the proposed mechanisms of PLP [ 4 ]. Randomized controlled trials have demonstrated the effectiveness of opioids oxycodone, methadone, morphine, and levorphanol for the treatment of neuropathic pain including PLP. Comparative trials have also shown benefit with opioids when compared with tricyclic antidepressants and gabapentin though the opioids were associated with more frequent side effects [ 48 ].
The total amount of opioid required to achieve analgesia may be less when used together with other agents, such as tricyclic antidepressants or anticonvulsants, which also have use in neuropathic pain modulation. Tramadol, a weak opioid and a mixed serotonin-noradrenalin reuptake inhibitor, has also been used in the treatment of PLP [ 4 , 49 ].
Tricyclic antidepressants are among the most commonly used medications for various neuropathic pains including PLP. The analgesic action of tricyclic antidepressant is attributed mainly to the inhibition of serotonin-norepinephrine uptake blockade, NMDA receptor antagonism, and sodium channel blockade [ 50 ].
The role of tricyclic antidepressants is well established in other neuropathic pain conditions, but the results are mixed relative to their role on PLP [ 51 ]. Nortriptyline and desipramine have been found to be equally effective and with less side effects compared to amitriptyline [ 53 ]. A small case series demonstrated the effectiveness of mirtazapine, an alpha 2 receptor antagonist with fewer side effects than tricyclic antidepressants in the treatment of PLP [ 54 ].
There are case reports relative to the efficacy of duloxetine, a NE and serotonin receptor inhibitor, in the treatment of PLP [ 55 ].
Even though there may be a role for the use of SSRI and SNRI in the treatment of neuropathic pain, the evidence is very limited and further research is needed [ 56 ]. Gabapentin has shown mixed results in the control of PLP with some studies showing positive results while others not showing efficacy [ 57 — 59 ]. Carbamazepine has been reported to reduce the brief stabbing and lancinating pain associated with PLP. Oxcarbazepine and pregabalin may also play a role in the treatment of PLP, but further studies are required [ 4 , 60 ].
The mechanism of action of calcitonin in treatment of PLP is not clear. Studies relative to its therapeutic role have been mixed [ 61 , 62 ]. Memantine has shown some benefits in some case studies but controlled trials have shown mixed results [ 63 , 64 ]. A review concluded that memantine may be useful soon after amputation rather than for use in chronic neuropathic pain conditions [ 65 ].
The beta blocker propranolol and the calcium channel blocker nifedipine have been used for the treatment of PLP [ 60 ].
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However, their effectiveness is unclear and further studies are needed. Flupirtine, an NMDA antagonist and potassium channel agonist, has been reported to be effective when used together with opioids in cancer-related neuropathic pain but needs further studies for other etiologies [ 66 ]. Transcutaneous electrical nerve stimulation has been found to be helpful in PLP [ 40 ].
Historically, there have been multiple studies showing the effectiveness of TENS of the contralateral limb versus ipsilateral to decrease PLP [ 67 ]. Though there is no strong evidence, low-frequency and high-intensity TENS is thought to be more effective than other doses [ 68 ]. TENS devices are portable, are easy to use, and have few side effects or contraindications. Mirror therapy was first reported by Ramachandran and Rogers-Ramachandran in and is suggested to help PLP by resolving the visual-proprioceptive dissociation in the brain [ 69 , 70 ]. The patient watches the reflection of their intact limb moving in a mirror placed parasagittally between their arms or legs while simultaneously moving the phantom hand or foot in a manner similar to what they are observing so that the virtual limb replaces the phantom limb.
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Simian studies have shown the existence of mirror neurons in the brain which fire both at times when an animal performs an action or observes an action [ 71 ]. Similar homologous neurons have also been discovered in humans [ 72 ]. The presence of mirror neurons in the brain is also supported by the phenomenon of tactile sensation in the phantom limb elicited by touching the virtual image of the limb in the mirror [ 73 ]. However, a person with an amputation does not receive such null input as the limb is amputated and this results in the activation of mirror neurons which create a perception of tactile sensation.
Consequently, since the activation of these mirror neurons modulates somatosensory inputs, their activation may block protopathic pain perception in the phantom limb [ 72 , 73 ]. A randomized controlled trial of mirror therapy in patients with lower leg amputation has shown significant benefit of PLP versus the control group [ 74 ]. Another controlled trial, however, reported that the mirror condition only elicited a significantly greater number of phantom limb movements than the control condition but did not attenuate phantom limb pain and sensations any more than the control condition [ 75 ].
Although there are earlier reports suggesting temperature biofeedback to be helpful for burning sensation of PLP, there is no specific evidence to match specific types of PLP with specific biofeedback techniques [ 76 ]. There is also a case report of visual feedback helpful in reduction of phantom pain [ 74 ]. Guided imagery, relaxation techniques, and hypnosis have been employed in the treatment of different neuropathic pains and may also be useful for PLP [ 28 , 77 , 78 ].
There are case reports of the beneficial effect of acupuncture for PLP [ 79 , 80 ]. The effectiveness of cognitive behavioral therapy in neuropathic pain syndromes has been reported in a number of case studies [ 81 , 82 ]. Surgical interventions are usually employed when other treatment methods have failed. A case report relates the effectiveness of lesioning the dorsal root entry zone DREZ on upper limb phantom pain resulting from brachial plexus avulsions [ 83 ].
Another case report showed that, for selected patients, who have not obtained adequate relief with medical management, spinal cord stimulation was found to be effective [ 84 ]. Case reports of improvement of PLP with deep brain stimulation of the periventricular gray matter and thalamic nuclei have been published [ 85 ].
Motor cortex stimulation was also found to be helpful in a case of PLP [ 86 ]. A case report of positive outcome has been published even though the mechanism and role of ECT relative to PLP is not well understood [ 87 ]. PLP is a relatively common and disabling entity. We have learned much about the pathophysiology and management of PLP since it was first described about five centuries ago.
However, there is still no one unifying theory relative to the mechanism of PLP. Specific mechanism-based treatments are still evolving, and most treatments are based on recommendations for neuropathic pain. The evolution of the mechanistic hypothesis from body schema and neuropathic theories to the recently proposed role of mirror neurons in the mechanism of pain have added to our understanding of PLP. Further research is needed to elucidate the relationship between the different proposed mechanisms underlying PLP.
A synthesized hypothesis explaining the phenomenon of PLP is necessary in the future for the evolution of more specific mechanism-based treatment recommendations. National Center for Biotechnology Information , U. Journal List Pain Res Treat v. Pain Res Treat. Published online Aug Author information Article notes Copyright and License information Disclaimer. Received May 10; Accepted Jul 1.
Subedi and G. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Abstract The vast amount of research over the past decades has significantly added to our knowledge of phantom limb pain. Introduction The concept of phantom limb pain PLP as being the pain perceived by the region of the body no longer present was first described by Ambrose Pare, a sixteenth century French military surgeon [ 1 ].
Table 1 Risk factors for phantom limb pain. Female sex Upper extremity amputation Presence of preamputation pain Residual pain in remaining limb Time after amputation. Open in a separate window. Mechanisms PLP was once thought to be primarily a psychiatric illness. Table 2 Proposed theoretical mechanisms to explain phantom limb pain. Peripheral Mechanism During amputation, peripheral nerves are severed. Central Neural Mechanisms 2. Changes at the Level of Spinal Cord The axonal sprouts at the proximal section of the amputated peripheral nerve form connections with the neurons in the receptive field of the spinal cord.
Changes at the Level of the Brain Cortical reorganization is perhaps the most cited reason for the cause of PLP in recent years.
Phantom Limb Pain: Mechanisms and Treatment Approaches
Psychogenic Mechanism The assumption that PLP is of psychogenic origin has not been supported in the recent literature even though stress, anxiety, exhaustion, and depression are believed to exacerbate PLP [ 38 ]. Treatment A number of different therapies relying on different principles have been proposed for the management of PLP as shown in Table 3. Table 3 Treatments for phantom limb pain. Pharmacological Approaches 3. PreEmptive Analgesia and Anesthesia Preemptive use of analgesics and anesthetics during the preoperative period is believed to prevent the noxious stimulus from the amputated site from triggering hyperplastic changes and central neural sensitization which may prevent the amplification of future impulses from the amputation site [ 42 ].
Opioids Opioids bind to the peripheral and central opioid receptors and provide analgesia without the loss of touch, proprioception, or consciousness. Antidepressants Tricyclic antidepressants are among the most commonly used medications for various neuropathic pains including PLP. Anticonvulsants Gabapentin has shown mixed results in the control of PLP with some studies showing positive results while others not showing efficacy [ 57 — 59 ]. Calcitonin The mechanism of action of calcitonin in treatment of PLP is not clear.
Other Medications The beta blocker propranolol and the calcium channel blocker nifedipine have been used for the treatment of PLP [ 60 ]. Nonpharmacological Treatment 3. Mirror Therapy Mirror therapy was first reported by Ramachandran and Rogers-Ramachandran in and is suggested to help PLP by resolving the visual-proprioceptive dissociation in the brain [ 69 , 70 ]. Biofeedback, Integrative, and Behavioral Methods Although there are earlier reports suggesting temperature biofeedback to be helpful for burning sensation of PLP, there is no specific evidence to match specific types of PLP with specific biofeedback techniques [ 76 ].
Surgical Intervention Surgical interventions are usually employed when other treatment methods have failed. Electroconvulsive Therapy A case report of positive outcome has been published even though the mechanism and role of ECT relative to PLP is not well understood [ 87 ]. Conclusion PLP is a relatively common and disabling entity. References 1. Weinstein SM.
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Phantom limb pain: a case of maladaptive CNS plasticity? Nature Reviews Neuroscience. Maldynia: pathophysiology and management of neuropathic and maladaptive pain—a report of the AMA council on science and public health. Pain Medicine. Optimized perioperative analgesia reduces chronic phantom limb pain intensity, prevalence, and frequency: a prospective, randomized, clinical trial.
The use of prolonged peripheral neural blockade after lower extremity amputation: the effect on symptoms associated with phantom limb syndrome. Anesthesia and Analgesia. Baron R. Mechanisms of disease: neuropathic pain—a clinical perspective. Nature Clinical Practice Neurology. Descending facilitation from the brainstem determines behavioural and neuronal hypersensitivity following nerve injury and efficacy of pregabalin.
Neuropathic pain: a maladaptive response of the nervous system to damage. Annual Review of Neuroscience. Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment. The Lancet Neurology. Dynamic reorganization of referred sensations by movements of phantom limbs. Cortical reorganization in primary somatosensory cortex in patients with unilateral chronic pain. Phantom limb pain, cortical reorganization and the therapeutic effect of mental imagery.
Spring J. Neural plasticity and the progress of phantom pain research mind matters. The Wesleyan Journal of Psychology. Chronic motor cortex stimulation for phantom limb pain: a functional magnetic resonance imaging study: technical case report.
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Head H, Holmes G. Sensory disturbances from cerebral lesions. The Lancet. Central mechanisms in phantom limb perception: the past, present and future. Brain Research Reviews. Melzack R. Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture. Iannetti GD, Mouraux A. From the neuromatrix to the pain matrix and back Experimental Brain Research. Mechanisms underlying embodiment, disembodiment and loss of embodiment. Neuroscience and Biobehavioral Reviews. Mirrored, imagined and executed movements differentially activate sensorimotor cortex in amputees with and without phantom limb pain.
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