Common treatments for<unk>  is directed towards treating the individual symptoms. Pain relief medication may be administered to temporarily reduce the discomfort in the patient. Cortisone shots have also been shown to be effective in temporarily reducing the chronic pain. Surgical removal of the damaged adipose tissue can be effective, but often the<unk>  will recur. Few convincing large studies on the treatment of<unk>  have been conducted. Most of the different treatment strategies that exist are based on case reports. Currently, there is a lack of scientific data on the use of integrative therapies for the treatment or prevention of<unk> . Not enough studies have been done to substantiate that diet and supplements could help with the<unk> . Treatment methods include the following modalities: Surgery Surgical excision of fatty tissue deposits around joints (liposuction) has been used in some cases. Liposuction may temporarily relieve symptoms although recurrences often develop. Medication Traditional analgesics The pain in<unk>  is often reported to be refractory to analgesics and to non-steroidal anti-inflammatory drugs (NSAIDs). However, this has been contradicted by the findings of Herbst et al. They reported that the pain diminished in 89% of patients (n=89) when treated with NSAIDs and in 97% of patients when treated with narcotic analgesics (n=37). The dosage required and the duration of the pain relief are not precisely stated in the article. Lidocaine An early report from 1934 showed that intralesional injections of procaine (Novocain®) relieved pain in six cases. More recently, other types of local treatment of painful sites with lidocaine patches (5%) (Lidoderm®) or lidocaine/prilocaine (25 mg/25 mg) cream (EMLA®) have shown a reduction of pain in a few cases. In the 1980s, treatment with intravenous infusions of lidocaine (Xylocaine®) in varying doses was reported in nine patients. The resulting pain relief lasted from 10 hours to 12 months. In five of the cases, the lidocaine treatment was combined with mexiletine (Mexitil®), which is a class 1B anti-arrhythmic with similar pharmacological properties as lidocaine. The mechanism by which lidocaine reduces pain in<unk>  is unclear. It may block impulse conduction in peripheral nerves, and thereby disconnect abnormal nervous impulse circuits. Nonetheless, it might also depress cerebral activity that could lead to increased pain thresholds. Iwane et al. performed an EEG during the administration of intravenous lidocaine. The EEG showed slow waves appearing 7 minutes after the start of the infusion and disappearing within 20 minutes after the end of the infusion. On the other hand, the pain relief effect was the greatest at about 20 minutes after the end of the infusion. Based on this, the authors concluded that the effect of lidocaine on peripheral nerves most likely explains why the drug has an effect on pain in<unk> . In contrast, Atkinson et al. have suggested that an effect on the central nervous system is more likely, as lidocaine can depress consciousness and decrease cerebral metabolism. In addition, Skagen et al. demonstrated that a patient with<unk>  lacked the vasoconstrictor response to arm and leg lowering, which indicated that the sympathicusmediated local veno-arteriolar reflex was absent. This could suggest increased sympathetic activity. An infusion of lidocaine increased blood flow in subcutaneous tissue and normalised the vasoconstrictor response when the limbs were lowered. The authors suggested that the pain relief was caused by a normalisation of up-regulated sympathetic activity. Methotrexate and infliximab One patient's symptoms were improved with methotrexate and infliximab. However, in another patient with<unk> , the effect of methotrexate was discreet. The mechanism of action is unclear. Previously, methotrexate has been shown to reduce neuropathic pain caused by peripheral nerve injury in a study on rats. The mechanism in the rat study case was thought to be a decrease in microglial activation subsequent to nerve injury. Furthermore, a study has shown that infliximab reduces neuropathic pain in patients with central nervous system sarcoidosis. The mechanism is thought to be mediated by tumour necrosis factor inhibition. Interferon α-2b Two patients were successfully treated with interferon α-2b. The authors speculated on whether the mechanism could be the antiviral effect of the drug, the production of endogenous substances, such as endorphins, or interference with the production of interleukin-1 and tumour necrosis factor. Interleukin-1 and tumour necrosis factor are involved in cutaneous hyperalgesia. Corticosteroids A few patients noted some improvement when treated with systemic corticosteroids (prednisolone), whereas others experienced worsening of the pain. Weinberg et al. treated two patients with juxta-articular<unk>  with intralesional injections of methylprednisolone (Depo-Medrol). The patients experienced a dramatic improvement. The mechanism for the pain-reducing ability of corticosteroids in some conditions is unknown. One theory is that they inhibit the effects of substances, such as histamine, serotonin, bradykinin, and prostaglandins. As the aetiology of<unk>  is probably not inflammatory, it is plausible that the improvement some of the patients experience when using corticosteroids is not caused by an anti-inflammatory effect. Alternative treatment CVAC sessions Cyclic Variations in Adaptive Conditioning (CVAC) is a method of touch-free cyclic hypobaric pneumatic compression for treatment of tissue edema and, therefore, edema-associated pain. As a pilot study, 10 participants with AD completed pain and quality of life questionnaires before and after 20–40 minutes of CVAC process daily for 5 days. After treatment, there was a significant decrease in pain as measured by the Pain Catastrophizing Scale and the Visual Analogue Scale, but there was no change in pain quality by the McGill Pain Questionnaire. However, there were no changes in the Pain Disability Index or Pittsburgh Sleep Quality Index. This study suggests a potential treatment role for CVAC, and the authors recommended randomized controlled clinical trials.
Dercum's disease
Freiberg disease
Butcher's wart
Martorell's ulcer
Marjolin's ulcer
Coats' disease
Swaim's Panacea
Dieulafoy's lesion