What Is Diabetic Neuropathy?
Diabetic neuropathy is the most common complication of diabetes mellitus. It is estimated to affect more than 50% of people with long-standing diabetes and is one of the principal causes of chronic neuropathic pain and functional impairment.
It is a form of peripheral nerve injury that develops gradually as a result of chronic hyperglycaemia, meaning persistently elevated blood glucose levels.
The clinical presentation varies. The most common form is symmetrical peripheral polyneuropathy, which causes burning, prickling or tingling sensations in the extremities, particularly the feet, together with reduced sensation that increases the risk of injuries going unnoticed because pain is not felt.
Other forms affect the autonomic nerves, known as autonomic neuropathy, or individual nerves, known as mononeuropathy. Diabetic neuropathy also plays a significant role in the development of diabetic foot complications.
Pathophysiology of Diabetic Neuropathy
The pathophysiology of diabetic neuropathy is multifactorial. Chronic hyperglycaemia damages the vasa nervorum, the microscopic blood vessels that supply the nerves, resulting in chronic ischaemia and hypoxia of nervous tissue.
At the same time, the accumulation of toxic metabolites, including sorbitol and advanced glycation end products, directly impairs the function of neurons and Schwann cells, which produce myelin.
It is important to emphasize that although neuropathy is closely associated with diabetes, it does not necessarily improve through blood glucose control alone, particularly once nerve injury has become established. Treatment must therefore address not only glycaemic control but also the underlying neural ischaemia.
Scientific Studies
Studies evaluating the use of hyperbaric oxygen therapy in patients with diabetic neuropathy have reported improvements in nerve conduction, as measured by nerve conduction studies, reductions in neuropathic pain and improved sensory function.
The documented mechanism of action focuses on restoring oxygenation to the vasa nervorum and stimulating neurotrophic factors that support the function and structural integrity of nerve fibres.
In addition, the antioxidant effects of hyperbaric oxygen therapy reduce oxidative stress, one of the principal mechanisms of neuronal injury in diabetes. In this way, the treatment directly addresses one of the key pathophysiological drivers of diabetic neuropathy.
The Role of Hyperbaric Oxygen Therapy
In diabetic neuropathy, hyperbaric oxygen therapy is used as an adjunctive intervention that addresses neural ischaemia, a key pathological mechanism that antidiabetic medication cannot directly correct.
Increasing the amount of oxygen dissolved in the plasma allows oxygen to reach nerve fibres even when the vasa nervorum have sustained severe vascular injury.
Improved neuronal energy metabolism may support more effective nerve conduction, reduce neuropathic pain and partially restore sensory function. The accompanying antioxidant effects may also help protect against further progression of nerve injury.
A typical treatment course consists of 30 to 40 sessions and is planned in collaboration with the diabetologist and neurologist, with progress monitored through nerve conduction studies and clinical assessment.