A syndrome of thoracoabdominal radiculopathy characterized by severe pain and dysesthesia is also well described (Sun et al). Almost always the diabetes has been of long standing (Kikta et al). The pain is distributed over one or several adjacent segments of the chest or abdomen; it may be unilateral, or less often bilateral, and, as with the lumbar radiculoplexopathy, sometimes follows a period of recent weight loss. Superficial sensory loss can be detected over the involved area in most patients. The pathology of this state is not known, but it is presumed to be an ischemic radiculopathy. The EMG changes consist of fibrillations of the paraspinal and abdominal muscles in one or more adjacent myotomes, corresponding to the painful area. With control of the diabetes, or perhaps spontaneously, recovery eventually occurs but it may be protracted. The differential diagnosis includes preeruptive herpes zoster, sarcoid infiltration of nerve roots, and thoracic disc rupture.
In all forms of diabetic polyneuropathy the CSF protein may be elevated from 50 to 150 mg/dL and sometimes higher. The protein concentration is usually normal in cases of diabetic mononeuropathy. Whether a slight elevation of CSF protein, discovered incidentally, can be attributed to diabetes in the absence of a polyneuropathy is uncertain.
Symptoms of autonomic involvement include any combination of pupillary and lacrimal dysfunction, impairment of sweating and vascular reflexes, nocturnal diarrhea, atonicity of the gastrointestinal tract (gastroparesis) and bladder dilation, erectile dysfunction, and postural hypotension. The most striking examples in our experience include severe abdominal and limb pain in young type 1 diabetics, symptoms comparable to the crises of tabes dorsalis that required narcotics to control.
The basis of this type of autonomic 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 fibers 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 of the Diabetic Neuropathies
In the typical symmetrical diabetic distal sensory polyneuropathy, loss of myelinated nerve fibers is the most prominent finding. In addition, segmental demyelination and remyelination of remaining axons are apparent in teased nerve fiber preparations. The latter findings are probably too severe and widespread to be simply a reflection of axonal degeneration. Occasionally, repeated demyelination and remyelination lead to onion-bulb formations of Schwann cells and fibroblasts, as it does in the relapsing inflammatory neuropathies. Unmyelinated fibers are also reduced in number in most specimens. Similar scattered 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 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 of diabetics.