SUMMARY Observations have been made on nine cases of painful diabetic neuropathy of acute onset. All cases were male and all were associated with and preceded by precipitous and severe weight loss. The When diabetic neuropathy was first adequately defined during the latter part of the last century, it was recognised that it could be manifested either by patchy and predominantly motor involvement or as a more diffuse and mainly sensory disorder.' The latter was subdivided into a painful or "hyperalgesic" form and an ataxic or "pseudotabetic" variety,' 2 foreshadowing the separation into small and large fibre types advocated in recent years by Brown et al.3 The features of the pain in the hyperalgesic form were documented by Pavy4 who noted that it was of burning and unremitting quality. He emphasised the characteristic exaggeration at night. It was also commented that affected individuals often complained of a sensation in the feet when walking that was likened to treading barefoot on pebbles. Focal and multifocal neuropathies such as isolated lesions of cranial or limb nerves, or diabetic amyotrophy, may also be painful.

Summary.Peripheral blood flow is known to be qualitatively increased in diabetic patients with neuropathy. We have measured the actual blood flow in the feet of diabetic patients with neuropathy using non-invasive mercury strain gauge plethysmography and Doppler sonogram techniques and shown that it is increased on average five times above normal at an ambient temperature of 20 ~ -22 ~ Moreover, reduction of this high flow by sympathetic arousal stimuli proved possible in those with severe painful neuropathy contrasting strongly with failure to reverse it in those with severe non-painful sensory neuropathy. Reduction of blood flow was associated with reduction in neuropathic pain. We studied 22 diabetic patients with severe sensory neuropathy and eight with painful neuropathy. High resting foot blood flows were demonstrated in both groups with neuropathy. The big toe flow in those with severe sensory neuropathy was 29.3 + 9.2 ml. rain-1. 100m1-1 (mean+-SD) and in the painful neuropathy group, 25.9+_7.5, compared with 5.2+2.4ml.min -1. 100m1-1 in the non-diabetic control subjects (p<0.001). High foot skin temperatures were also recorded in the groups with neuropathy, reflecting the high blood flow. The subjects with painful neuropathy retained the ability to constrict peripheral blood vessels in response to arousal stimuli, and reduce peripheral flow on average by 32% compared with the patients with sensory neuropathy who responded on average by only 10%. The demonstration of a peripheral sympathetic defect, responsible for the high blood flow and the potential reversal of such flow in painful neuropathy may be important in our further understanding of the aetiology of such pain and its treatment.Key words: Diabetes mellitus, peripheral blood flow, sensory neuropathy, painful neuropathy, peripheral sympathetic neuropathy.During the nineteenth century, the feet of diabetic patients with peripheral neuropathy were observed to be hot and erythematous [1] and the blood flow in such feet was considered to be increased. This increase is now thought to be due to the dilation of denervated arteriovenous shunts [2-9] normally controlled by sympathetic nerves.Measurement of actual blood flow in diabetic neuropathic feet has only been undertaken in one previous study [10]. Blood flow was not found to be increased in neuropathic subjects probably because the studies were conducted by waterbath plethysmography at 32~ causing vasodilatation and increased flow in the control subjects.The aim of this study was to measure the magnitude of resting foot blood flow in a group of diabetic patients with severe sensory neuropathy and to discover whether the hot, burning foot, so characteristic of distal painful neuropathy, also has a high resting flow resulting from a peripheral sympathetic defect. In addition, the sympathetic responses of both types of neuropathy were tested to discover whether either retained the ability to reduce peripheral flow by vasoconstriction, and whether any benefits might result from this. Subjects and metho...

The possibility that digital gangrene in patients with diabetic nephropathy might be due to abnormalities of peripheral blood flow secondary to vascular calcification has been investigated. Twenty patients with renal failure due to diabetic nephropathy were studied. Peripheral blood flow was measured using venous occlusion plethysmography, together with an assessment of medial arterial calcification on plain radiographs of the hands and feet, and transcutaneous oxygen tension (TcPO2). Hallux blood flow was markedly raised (median 22.5, range 11.5-56.5, ml min-1 100-ml-1) compared with non-diabetic control subjects (4.7, 1.1-10.5, ml min-1 100-ml-1; p less than 0.01) and similar to that in diabetic patients with autonomic neuropathy (29.5, 16.7-49.6, ml min-1 100-ml-1). Although vascular calcification was common and extensive in the patients with diabetic nephropathy, TcPO2 measurements in the supine foot were normal and did not indicate tissue ischaemia. We conclude that despite extensive vascular calcification high peripheral blood flow occurs in the feet of these patients at rest together with normal transcutaneous oxygen tension.

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SUMMARY1. Intravenous injection of 2 mg naloxone produced a rapid and pronounced rise of blood flow (63 + 5-0 to 670 +151 ml min-1 100 ml-1) and skin temperature (28&3 + 3-0 to 32-4 + 1-2 'C) in the finger and hand of seven of ten normal volunteers. In the other three there was only a small response. Skin temperature did not change in either the face or the foot. Three responding subjects who were retested with 0 4 mg naloxone showed a smaller and briefer response.2. To exclude a local effect of naloxone on skin blood flow due to release of histamine, responders and non-responders were tested with naloxone and morphine pricked into the skin of the hand and forearm. All showed a weal and flare reaction to morphine which was not abolished by mixture with naloxone; none showed any reaction to naloxone alone.3. These results suggest that, in some subjects at least, skin blood flow in the hand may be under endogenous opioid control and they raise the possibility that opioid antagonists might have value in the treatment of disorders of skin blood flow such as Raynaud's disease.