Diabetic polyneuropathy is a disorder of the peripheral nervous system caused by diabetes mellitus.
Diabetic polyneuropathy (DPN) is the most common, yet still insufficiently understood, complication of diabetes mellitus. It is believed that more than 80% of people with diabetes develop this complication, and according to some authors, 9 out of 10 patients develop neuropathy.
Globally, diabetic neuropathy affects approximately 132 million people as of 2010 (1.9% of the population).
Diabetes is the leading known cause of neuropathy in developed countries, and neuropathy is the most common complication and the major contributor to morbidity and mortality among people with diabetes. Diabetic neuropathy is involved in 50-75% of non-traumatic amputations.
Although diabetic neuropathy may develop despite good glycaemic control, prolonged hyperglycaemia remains one of its most important risk factors, it affects both sexes equally, and it occurs more often in the elderly, and is present in a small percentage of children with diabetes, approximately 2%.
The exact cause of diabetic neuropathy remains unknown, and opinions vary.
Complications of high blood glucose that contribute to nerve damage include any of the following:
– Impaired circulation leading to damage of the small blood vessels supplying the nerves;
– Accumulation of lipids in the cells forming the nerve sheath, disrupting their normal function;
– Metabolic disturbances that impair the transport of proteins, neurotransmitters, and other nutrients to the distal (terminal) parts of the nerves.
Risk factors for diabetic neuropathy include duration of diabetes, age, cigarette smoking, hypertension, and hyperlipidaemia.
How does the disease manifest itself?
Neuropathy is usually asymptomatic in its early stages. At this stage, when the patient is asymptomatic, the neurologist may detect diminished reflex responses during the examination of deep tendon reflexes, as well as sensory impairment.
The symptomatic stage develops gradually, although it may occasionally have a sudden onset.
The most common symptoms include burning, tingling, pins-and-needles sensation in the feet, especially on the soles, together with intermittent or persistent numbness and the sensation of wearing socks or boots even when barefoot.
Patients may also experience a persistent burning sensation accompanied by severe pain. Walking is often painful and is frequently described as walking on “hot coals”.
Some patients may experience sudden, intense shooting pain in the feet or legs.
Diabetic neuropathy most commonly presents as distal symmetrical sensorimotor polyneuropathy.
The earliest symptoms usually appear in the feet as tingling, pins-and-needles sensations and burning, most often during the night.
Muscle cramps affecting the calves and feet are also common, while cramps in the hands occur less frequently.
These symptoms are often followed by muscle atrophy (muscle wasting), most commonly affecting the small muscles of the feet.
As the disease progresses, deep tendon reflexes become diminished or absent, and numbness of the feet develops and gradually spreads to the lower legs, hands, and trunk. Trophic skin changes may occur on the feet, including dry, thin skin that cracks easily and ulcers. Patients often experience reduced sensitivity to touch, temperature, and pain, which increases the risk of injuries and burns.
Neuropathic pain is also part of the clinical spectrum of diabetic polyneuropathy.
There are positive and negative symptoms of neuropathic pain.
Positive symptoms of neuropathic pain
- Spontaneous pain – a painful sensation that occurs without the presence of an appropriate stimulus
- Allodynia – pain caused by a stimulus that does not normally provoke pain (touch, pressure, mild heat or cold)
- Hyperalgesia – an intensified painful sensation of a stimulus that is normally painful (cold, heat, pinprick)
- Dysaesthesia – an unpleasant abnormal sensation, either spontaneous or evoked (pins and needles sensations)
- Paraesthesia – an abnormal sensation that is not unpleasant, either spontaneous or induced (tingling, vibration, etc.)
Negative symptoms of neuropathic pain
- Hypoaesthesia – decreased sensitivity to light touch or gentle pressure.
- Hypoalgesia – reduced sensation of pain to a stimulus that normally causes pain
- Analgesia – complete absence of pain perception in response to a stimulus that would normally be painful.
Neuropathic pain can be intermittent (paroxysmal), that is, episodic in nature, or continuous. Paroxysmal Neuropathic pain is usually characterized by sensations that patients describe as stabbing or electric shock-like. Common qualities of neuropathic pain include sensations of burning or coldness, “pins and needles,” numbness, and itching.
Polyneuropathy may lead to difficulty walking (paresis), but in severe cases walking is impossible (paralysis).
How is diabetic polyneuropathy diagnosed?
The diagnosis of diabetic neuropathy is based on a thorough medical history, providing a clear picture of the onset and progression of symptoms in a patient with diabetes mellitus. Other possible causes of polyneuropathy should also be considered and ruled out. In addition to a comprehensive neurological examination, the diagnosis is confirmed with neurophysiological tests, primarily by measuring nerve conduction velocity (electromyoneurography, EMNG).
As previously mentioned, the disease develops insidiously, and patients may remain free of subjective symptoms for a prolonged period despite already having nerve damage. Therefore, every patient diagnosed with diabetes should be referred to a neurologist for neurological and neurophysiological evaluation in order to implement preventive measures against diabetic polyneuropathy or, if neuropathy is already present, to prevent its progression.
How is diabetic polyneuropathy treated?
When it comes to treating diabetic polyneuropathy, it should be emphasized that the most important thing is prevention, which consists of optimal regulation of blood glucose levels.
To prevent the occurrence of neuropathy, and even when it exists, it is necessary to strictly maintain maintain good glycaemic control, reduce body weight, control serum lipid levels, stop smoking and excessive alcohol consumption, and follow a healthy diet.
Although blood glucose levels are not always directly associated with the development of complications, more severe forms of polyneuropathy have been observed in patients with poorly controlled diabetes.
The first years of the diagnosis of diabetes are considered critical for the development of neuropathy: if the patient does not get it at that time or has it in a milder form, then there is a good chance that the neuropathy will not progress later if it is treated regularly.
Therapeutic strategies for the management of neuropathic pain include a wide range of methods, from physical therapy, acupuncture, cognitive and behavioural therapy, relaxation and occupational therapy, and pharmacological measures. Pharmacological therapy is certainly the gold standard in the treatment of neuropathic pain, and includes the use of tricyclic antidepressants, serotonin and noradrenaline reuptake inhibitors, antiepileptics that block calcium and sodium ion channels, local anaesthetics, lidocaine, and capsaicin.
Important in the treatment of diabetic polyneuropathy are also vitamins of group B (B1, B6 and B12). Their deficiency contributes to neuropathies and more difficult healing of the nervous system. Conversely, their use in that case can contribute to pain control and to the regeneration of the nervous system.
The treatment of the most common form of diabetic polyneuropathy is based on antioxidant treatment, using antioxidant preparations, medical treatment of neuropathic pain, drugs that improve peripheral circulation, B group vitamins (B1, B6 and B12), and physical therapy using a variety of therapeutic modalities.
Given the pathophysiological complexity of diabetic polyneuropathy, its treatment requires a multidisciplinary approach and collaboration between an endocrinologist, neurologist, physical medicine and rehabilitation specialist, and psychologist.