Page 529 - Motor Disorders Third Edition
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CHAPTER 28
Diabetic Neuropathy
David S. Younger
Diabetes mellitus (DM) is a chronic disease character- a patient with clinical and pathological evidence of a painful
ized by persistent hyperglycemia. Patients with insulin distal leg weakness. Charcot (2) coined the term “diabetic
dependent DM (IDDM) demonstrate relatively little insu- paraplegia” to describe a patient with ataxia resembling
lin secretion by pancreatic beta cells, whereas those with tabes dorsalis with profound leg weakness. Pryce (3) later
non-IDDM (NIDDM) have normal or increased insulin suggested separation of the diabetic neuropathic syndromes
secretion related to peripheral tissue receptor resistance. A into motor or paralytic, and sensory or ataxic types. Bruns
clinically significant neuropathy manifested by weakness (4), and later Garland and Taverner (5), described a painful,
and sensory changes occurs in about 10% of all patients predominantly motor disorder of asymmetrical weakness
with diabetes and is one of the most common neuropathies and wasting, with Babinski signs, without sensory changes,
worldwide. Although the pathogenesis of diabetic periph- so-termed “diabetic myelopathy.” Garland (6) termed the
eral neuropathy is unknown, it is generally ascribed to a same disorder “diabetic amyotrophy” in consideration of
complex interaction of genetic, metabolic, microvascular, the presumed clinical spinal cord and anterior horn cell
and autoimmune factors related to chronic hyperglycemia. and root involvement. Early investigations of diabetic neu-
The result is a spectrum of distinct neuropathy types, with ropathy utilized nerve trunks obtained from diseased limbs
variable motor and sensory involvement, including distal obtained at surgical amputation and postmortem examina-
symmetrical polyneuropathy (DSPN), diabetic lumbosa- tion (7–9). However, such patients had long-standing diabe-
cral radiculoplexus neuropathy (DLSRPN), mononeuropa- tes that tended to increase the likelihood of arteriosclerosis,
thy multiplex (MNM), and diabetic autonomic neuropathy. and Renaut corpuscles, a feature of peripheral neuropathy,
Cranial and entrapment neuropathies, as well as chronic were probably misinterpreted as infarcts.
inflammatory demyelinating polyradiculoneuropathy
(CIDP), all occur in DM with increased frequency com- Decades later, investigations of peripheral nerve
pared to the general population. microvessels stained by periodic acid Schiff (PAS) showed
thickening of the walls of endoneurial blood vessels (10)
This chapter reviews the historical aspects, epidemiol- that was subsequently found to be reduplication of the
ogy, clinical presentation, laboratory diagnosis, pathology, basal lamina, a change also common to retinopathy and
etiopathogenesis, and treatment of diabetic peripheral neu- nephropathy. Other investigators (11–14) were unable to
ropathy with an emphasis on the motor sequela. validate the correlation between so-called microangiopa-
thy and neuropathy, and attention focused on metabolic
HISTORICAL ASPECTS AND BACKGROUND alterations in nerve elements (15). A variety of inter-
changeable descriptive terms evolved to emphasize the
The earliest reported patients with diabetic neuropathy had often proximal nature of the illness, including ischemic
prominent motor involvement in association with variable mononeuropathy multiplex, diabetic proximal amyotro-
pain and sensory involvement. In 1887, Pryce (1) described phy, subacute proximal diabetic neuropathy, painful lum-
bosacral plexopathy, proximal diabetic neuropathy, and
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