Diabetic neuropathy can be broadly categorized into either generalised or focal neuropathies. Generalised neuropathies include sensorimotor polyneuropathy and diabetic autonomic neuropathy. They are common, usually chronic and often progressive. The focal neuropathies are less common, usually acute in onset and often self-limited. The focal forms of diabetic neuropathy reflect damage to various single (mononeuropathy) or multiple peripheral nerves (mononeuropathy multiplex) as well as cranial nerves. A number of biochemical mechanisms, including non-enzymatic glycosylation, increases in oxidative stress, neuroinflammation and activation of the polyol and protein kinase-C (PKC) pathways have been found to be involved in the development of diabetic neuropathy. Other molecular pathways and systems include an increased flux through the hexosamine pathway, cellular damage caused by disposal of excess glucose and advanced glycation products induced pathological changes. The current treatment options are mostly involved with providing symptomatic benefits and rarely impede and alleviate the underlying processes of disease
Diabetic neuropathy can be broadly categorized into either generalised or focal neuropathies. Generalised neuropathies include sensorimotor polyneuropathy and diabetic autonomic neuropathy. They are common, usually chronic and often progressive. The focal neuropathies are less common, usually acute in onset and often self-limited. The focal forms of diabetic neuropathy reflect damage to various single (mononeuropathy) or multiple peripheral nerves (mononeuropathy multiplex) as well as cranial nerves. A number of biochemical mechanisms, including non-enzymatic glycosylation, increases in oxidative stress, neuroinflammation and activation of the polyol and protein kinase-C (PKC) pathways have been found to be involved in the development of diabetic neuropathy. Other molecular pathways and systems include an increased flux through the hexosamine pathway, cellular damage caused by disposal of excess glucose and advanced glycation products induced pathological changes. The current treatment options are mostly involved with providing symptomatic benefits and rarely impede and alleviate the underlying processes of disease