Abstract
Although motor deficits in humans with diabetic neuropathy have been extensively researched, its effect on the motor system is thought to be lesser than that on the sensory system. Therefore, motor deficits are considered to be only due to sensory and muscle impairment. However, recent clinical and experimental studies have revealed that the brain and spinal cord, which are involved in the motor control of voluntary movement, are also affected by diabetes. This review focuses on the most important systems for voluntary motor control, mainly the cortico-muscular pathways, such as corticospinal tract and spinal motor neuron abnormalities. Specifically, axonal damage characterized by the proximodistal phenotype occurs in the corticospinal tract and motor neurons with long axons, and the transmission of motor commands from the brain to the muscles is impaired. These findings provide a new perspective to explain motor deficits in humans with diabetes. Finally, pharmacological and non-pharmacological treatment strategies for these disorders are presented.
Highlights
Diabetic neuropathy (DN) affects both somatic and autonomic nerves in a distal, symmetrical form that progresses following a fiber-length-dependent pattern
This review addresses the effects of diabetes on the cortico-muscular pathway, which includes the primary motor cortex (M1); the corticospinal tract (CST), which conducts motor commands generated in the brain directly to the spinal cord; and motor neurons (MNs), which transmit these commands from the spinal cord to skeletal muscles [31,33,34]
We reported the morphological alteration of MNs in STZ-induced diabetic rats using retrograde labeling techniques (3kD dextran was used as a retrograde tracer agent) at 12 and 22 weeks STZ rats, which suggested that γ-MNs are more likely to be affected by diabetes compared to α-MNs [48,49]
Summary
Diabetic neuropathy (DN) affects both somatic and autonomic nerves in a distal, symmetrical form that progresses following a fiber-length-dependent pattern. More direct data reveal changes in motor representations in the motor cortex and impaired conduction of the corticospinal tract (CST) in rodents with type 1 diabetes induced by streptozotocin (STZ) administration [28,29] Given this context, CNS involvement cannot be further ignored when trying to understand the mechanisms of diabetes-related movement disorders. There is a need to know the motor commands generated by the interaction between several brain regions and their modulation as well as the effects of diabetes on the flow of motor commands from the brain to the spinal cord and from the spinal cord to the muscles; both elements play an essential role in voluntary movement [30,31] For the former, there is a recent and valuable review that comprehensively summarizes changes in various parts of the brain related to motor control in humans with diabetes and models of diabetes [32].
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