Handbook of clinical neurology
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Complex multiorgan failure may require simultaneous transplantation of several organs, including heart-lung, kidney-pancreas, or multivisceral transplantation. Solid organ transplantation can also be combined with hematopoietic stem cell transplantation to modulate immunologic response to a solid organ allograft. Combined multiorgan transplantation may offer a lower rate of allograft rejection and lower immunosuppression needs. ⋯ Heart-lung allograft recipients have very similar clinical course and spectrum of neurologic complications to lung transplant recipients. At this time there are no reports of an increased risk of graft-versus-host disease with combined transplantation of solid organ allograft and hematopoietic stem cells. Chronic immunosuppression and complex toxic-metabolic disturbances after multiorgan transplantation create a permissive environment for development of a wide spectrum of neurologic complications which largely resemble complications after transplantations of individual components of complex multiorgan allografts.
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Painful diabetic neuropathy (PDN) is one of several clinical syndromes in patients with diabetic peripheral neuropathy (DPN) and presents a major challenge for optimal management. The epidemiology of PDN has not been extensively studied. On the basis of available data, the prevalence of pain ranges from 10% to 20% in patients with diabetes and from 40% to 50% in those with diabetic neuropathy. ⋯ Quantifying neuropathic pain is difficult, especially in clinical practice, but has improved recently in clinical trials with the development of neuropathic pain-specific tools, such as the Neuropathic Pain Questionnaire and the Neuropathic Pain Symptom Inventory. Hyperglycemia-induced pathways result in nerve dysfunction and damage, which lead to hyperexcitable peripheral and central pathways of pain. Glycemic control may prevent or partially reverse DPN and modulate PDN.
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Fibromyalgia is a chronic pain condition present in 2-4% of the population. Fibromyalgia consists of widespread pain with similarities to neuropathic pain in clinical findings, pathophysiology, and neuropharmacology. Pain is the predominant symptom and allodynia and hyperalgesia are common signs. ⋯ Further evidence-based trials using complementary treatments are needed. Fibromyalgia is complex and requires a multidisciplinary approach to treatment. Patient self-management is key.
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Neuropathies related to diabetes mellitus can affect 60-70% of patients with diabetes. These can include peripheral polyneuropathies, mononeuropathies, and autonomic neuropathies. ⋯ Besides control of the above listed risk factors, we do not have effective medications to treat the pathophysiologic mechanisms of diabetic neuropathies. Treatment is limited to ameliorating pain and correcting the end organ consequences of the neuropathic processes.
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Small fiber neuropathy represents a significant component of diabetic sensorimotor polyneuropathy (DSPN) which has to date been ignored in most recommendations for the diagnosis of DSPN. Small fibers predominate in the peripheral nerve, serve crucial and highly clinically relevant functions such as pain, and regulate microvascular blood flow, mediating the mechanisms underlying foot ulceration. ⋯ Because small fiber damage precedes large fiber damage, diagnostic tests for DSPN show good sensitivity but moderate specificity, because the gold standard which is used to define DSPN is large fiber-weighted. Hence new diagnostic algorithms for DSPN should acknowledge this emerging data and incorporate small fiber evaluation as a key measure in the diagnosis of DSPN, especially early neuropathy.