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. Do đó, tác giả đã đề nghị rằng thuật ngữ "đau thần kinh cấp tính kiểm soát đường huyết nhanh chóng" được sử dụng để mô tả điều kiện này (48). Lịch sử tự nhiên của neuropathies đau cấp tính là một sự cải tiến gần như được đảm bảo (49) trái ngược với bệnh thần kinh mãn tính đối xứng xa | Clinical Features of Diabetic Polyneuropathy 251 is no evidence. The author has therefore recommended that the term acute painful neuropathy of rapid glycemic control be used to describe this condition 48 . The natural history of acute painful neuropathies is an almost guaranteed improvement 49 in contrast to chronic distal symmetrical neuropathy 36 . The patient presents with burning pain paraesthesiae allodynia often with a nocturnal exacerbation of symptoms and depression may be a feature. There is no associated weight loss unlike acute painful neuropathy of poor glycemic control. Sensory loss is often mild or absent and there are no motor signs. There is little or no abnormality on nerve conduction studies but there is impaired exercise induced conduction velocity increment 48 50 . There is usually complete resolution of symptoms within 12 months. On sural nerve biopsy typical morphometric changes of chronic distal symmetrical neuropathy but with active regeneration were observed 49 . In contrast degeneration of both myelinated and unmyelinated fibres was found in acute painful neuropathy of poor glycemic control 44 . A recent study looking into the epineurial vessels of sural nerves in patients with acute painful neuropathy of rapid glycemic control demonstrated marked arterio venous abnormality including the presence of proliferating new vessels similar to those found in the retina 48 . The study suggested that the presence of this fine network of epineural vessels may lead to a steal effect rendering the endoneurium ischaemic and the authors also suggested that this process may be important in the genesis of neuropathic pain 48 . These findings were also supported by studies in experimental diabetes which demonstrated that insulin administration led to acute endoneurial hypoxia by increasing nerve arterio-venous flow and reducing the nutritive flow of normal nerves 51 . Further work needs to address whether these observed sural nerve vessel changes resolve .
