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onicity of the gastrointestinal tract (gastroparesis) and bladder dilation, sexual impotence, and postural hypotension The most striking examples in our experience have included severe abdominal and limb pain, reminiscent of tabetic crises The basis of this type of involvement is not well understood Duchen and associates, who studied the sympathetic ganglia in diabetic patients with autonomic symptoms, described vacuoles and granular deposits in sympathetic neurons and little if any neuronal degeneration; there was also a loss of myelinated nerve bers in the vagus and splanchnic nerves and the rami communicantes, as well as changes in neurons of the intermediolateral columns of the spinal cord Pathology and Pathophysiology In the mundane symmetrical distal diabetic polyneuropathy, a loss of myelinated nerve bers is the most prominent nding according to Thomas and Tomlinson In addition, segmental demyelination and remyelination of remaining axons are apparent in teased nerve ber preparations The latter ndings are probably too severe and widespread to be simply a re ection of axonal degeneration Occasionally, repeated demyelination and remyelination leads to onion-bulb formations of Schwann cells and broblasts, as it does in the relapsing in ammatory neuropathies Unmyelinated bers are also reduced in number in most specimens Similar lesions are found in the posterior roots and posterior columns of the spinal cord and in the rami communicantes and sympathetic ganglia Under the electron microscope, the basement membranes of intraneural capillaries are seen to be thickened and duplicated There are changes in the microvasculature of the nerves as well, similar to what is seen in other organs and in the skin as noted later However, substantial uncertainties persist about the pathogenesis of the diabetic neuropathies Both the cranial (diabetic ophthalmoplegia) and peripheral mononeuropathies as well as the painful, asymmetrical, predominantly proximal neuropathy of sudden onset have been considered by most neuropathologists to be ischemic in origin, secondary to a vasculopathy of the vasa nervorum that is a property of the diabetic state Obliterative microvascular lesions were well illustrated by Raff and coworkers, and corresponding multiple small infarcts were found in the nerve trunks The observations of Dyck and of Johnson and their associates have suggested that all forms of diabetic neuropathy could have the same microvascular basis These authors described multiple foci of ber loss throughout the length of the peripheral nerves, beginning in the proximal segments and becoming more frequent and severe in the distal segments This pattern of change differs from that observed in diffuse metabolic disease of Schwann cells and in the dying-back type of neuropathy; ie, the ndings suggest an ischemic etiology Fagerberg had earlier noted that the fascicular capillaries and epineural arterioles have thickened and hyalinized basement membranes, similar to the microvascular changes seen in the retina, kidney, and other organs But occlusion of vessels and frank infarction of nerve has not been observed in most cases of polyneuropathy for which reason a vascular pathogenesis remains unsettled in the minds of some pathologists In the past several years an alternative view has been offered, based largely on the work of PJB Dyck and colleagues and of Said and coworkers They have found areas of perivascular in ammation and a suggestion of adjacent damage to nerve fascicles in the proximal asymmetric radicular plexus lesions In Said s report, this necrotizing vasculitis was observed in 6 of 22 patients and a degree of perivascular in ammation in 21, changes not seen in the typical.

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distal sensory-motor polyneuropathy of diabetics These ndings, if valid, have implications for treatment, particularly since corticosteroids have been suggested with potential for worsening hyperglycemia In ammatory-vascular changes in diabetic nerves have not been as impressive in our material The several biochemical ndings implicated in diabetic polyneuropathy and their interpretations have been reviewed by Thomas and Tomlinson and by Brown and Greene The latter authors advance the idea that persistent hyperglycemia inhibits sodium-dependent myoinositol transport Low levels of intraneural myoinositol reduce phosphoinositide metabolism and sodiumpotassium ATPase activity Others have emphasized a de ciency of aldose reductase and an elevation of polyols (particularly sorbitol) as being causally important In reviewing these articles, one can only conclude that a convincing biochemical pathogenesis has yet to be formulated Another group of novel ndings holds that there is a reduction in various trophic factors within diabetic nerves (NGF, VEGF, erythropoietin, etc) and in diabetic animals, partial reversal of the polyneuropathy can be obtained by replacement of these factors through gene therapy The work is provocative but its clinical meaning is not yet clear Trials addressing this mode of treatment are noted later Treatment The only preventive treatment is the maintenance of the blood glucose concentration at a close to normal range, since the prevailing view, derived from prolonged human studies, is that there is some relationship between peripheral nerve damage and inadequate regulation of the diabetes This notion is supported by the ndings of the National Diabetic Complications Trial, in which 715 patients with type 1 diabetes were followed for 6 to 10 years There was a clear relation between strict glucose control, by means of an intravenous insulin infusion system, and a reduction or delay in the occurrence of painful neuropathic symptoms, retinopathy, and nephropathy However, this came at the price of a threefold increase in hypoglycemic reactions (see also Samanta and Burden) Whether similar protective effects apply to type 2 diabetes is not known, but for most patients this degree of control is not practical A number of small trials have been conducted with aldose reductase inhibitors based on theoretical considerations of the abovementioned metabolic changes (see Thomas and Tomlinson) Some recent interest has also been directed at the therapeutic use of gangliosides, which are normal components of neuronal membranes and can be administered exogenously The authors have had no experience with either of these agents and neither one has entered routine practice The approach to treatment using gene therapy has been pursued in our laboratories founded by the late Dr Jeffrey Isner In experimental models of diabetic neuropathy the intramuscular administration of vascular endothelial growth factor (VEGF) has had a bene cial effect on several measures of nerve conduction and on the histologic changes of diabetic nerve damage in the treated limb Whether this is mediated by a trophic in uence on nerves and Schwann cells, or is the result of angiogenesis, is not known Two trials of nerve growth factor (NGF) injections in almost 500 patients conducted by Apfel and colleagues gave equivocal results, the rst being positive and the follow-up study not showing improvement We are conducting a trial of VEGF in humans In the long term, the distressing paresthesias of the distal extremities are best managed with amitriptyline or one of the newer generation of antidepressants, such as sertraline or uoxetine,.

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