Clinical and Experimental Evidence of Hypoglycemic Neuropathy
When compared with the extensive research on hypoglycemic impacts on Central
Nervous System and cardiovascular system, the effects of hypoglycemia on
the Peripheral Nervous System have not been investigated as thoroughly.
Epidemiologic data and risk factors for hypoglycemic neuropathy are still lacking.
Interestingly, hyperglycemia mainly results in the damage of sensory and autonomic nerve fibers,
whereas hypoglycemia predominantly leads to the development of motor neuropathy.
Most clinical features are concluded from patients with insulinoma, and neuropathology
has shown axonal degeneration in large myelinated fibers. Experimental animal models
support the clinical and histopathological findings.
The exact pathophysiological mechanisms of hypoglycemic neuropathy remain elusive. The
influence of hypoglycemia on peripheral nervous system warrants further investigations.
Hypoglycemia is a condition primarily affecting diabetic patients treated under excessive medication, such as insulin or other hypoglycemic agents.1-3Other causes of hypoglycemia
include insulinoma, poor intake, infections, liver, and kidney diseases.
The incidence of hypoglycemia varies considerably among studies by means of using different biochemical criteria to define an event.4,5 The symptoms of hypoglycemia vary
between individuals. Neurogenic (autonomic) symptoms include tremor, palpitations, hunger,
and cold sweating. Neuroglycopenic symptoms often include behavioral changes, confusion,
seizure, coma, and death.4Compared to the abundant and extensive data on hypoglycemia effects on the Central Nervous System (CNS) and cardiovascular system, there is little evidence
in humans and experimental animal studies toward hypoglycemic effects on the Peripheral
When looking at the rats, pathological changes of hypoglycemic neuropathy at the nerve trunk level are much more
obvious than at the spinal root level, including ventral horn and
dorsal root ganglion.26-31 This discovery is again compatible with
cerebrospinal fluid and pathologic results in human beings.
Diabetes Res Open J. 2015; 1(5): 131-135. doi: 10.17140/DROJ-1-121