Diabetic Neuropathies

CLINICAL MANIFESTATIONS

Diabetic polyneuropathy (DPN) is one of the most common neuropathies seen in clinical practices (see Plate 6-21). It is generally length dependent, with prominent sensory symptoms, and can include both sensory loss as well as painful paresthesias. Autonomic neuropathies can occur with DPN and other forms of diabetic neuropathy, or it can occur independently and can manifest with orthostatic hypotension, sweat loss, gastrointestinal dysmotility, and erectile dysfunction, as well as other symptoms. Compression neuropathies (see Plate 6-21), such as median neuropathy at the wrist (carpal tunnel syndrome) and ulnar neuropathies at the elbow, occur frequently in diabetic patients. Diabetic radiculoplexus neuropathy (DRPN) usually manifests as severe unilateral extremity pain, often with associated weight loss, followed by weakness and sensory loss in that same extremity; over time this can become bilateral. This is usually a monophasic illness but can sometimes recur. DRPN can occur in the lower limb (lumbosacral) segment (DLRPN), the trunk (thoracic) segment (DTPN), or the upper limb (cervical) segment (DCRPN); the lower limb syndrome (DLRPN) is most common.

The presence of the clinical history of diabetes mellitus is important, as is a compelling clinical history. DPN generally occurs in long-standing diabetes mellitus, usually in patients who already have nephropathy and retinopathy associated with their diabetes. In cases with large fiber sensory involvement or weakness, nerve conduction studies and electromyography can be helpful. In DPN, nerve conduction studies usually show a length-dependent predominantly axonal peripheral neuropathy. In DLRPN, there is evidence of involvement of nerve root, plexus, and distal nerve, typically asymmetric. Electrophysiologic studies are also sensitive for evaluating for focal neuropathies and identifying common sites of compression. Autonomic reflex screen and a thermoregulatory sweat test can be helpful to assess suspected autonomic neuropathy. Other testing, such as gastrointestinal motility and urodynamic studies, can be useful in some cases. Nerve biopsies are rarely performed in diabetic neuropathies, particularly in classic DPN cases, but, where performed, show axonal loss. In cases of DLRPN, pathologic changes of microvasculitis have been found.

Overall, the best treatment strategy for diabetic neuropathies is to attempt to prevent worsening of the underlying disease through tight glucose control. Similar to cases of HMSN, good foot care is important to prevent painless injuries and ulcerations. Management of neuropathic pain is very important in these patients to improve quality of life. Supportive treatments for autonomic neuropathy can be considered depending on the specific organ in which the symptoms manifest (e.g., for orthostatic hypotension, management of fluid and salt intake, consideration of medications to increase plasma volume). In DPN, the cause of the neuropathy is related to the length and severity of the exposure to hyperglycemia. Consequently, treatment is centered on optimizing diabetic control. In DLRPN, in contrast, the putative mechanism is ischemic injury from microvasculitis. A controlled trial with intravenous methylprednisolone did show some efficacy and immunomodulatory therapy can be considered. Usually, the treatment should be a short course because the disease is most frequently monophasic.

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