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  • The classification of diabetic neuropathy, according to which its description is presented, is given below.
  • It should be noted that clinically similar to diabetic neuropathy is also observed in pathological conditions other than diabetes, in particular alcoholic and inflammatory neuropathy.
  • As a result, diabetic neuropathy is diagnosed by exclusion. Atypical manifestations of doxazosin sensory neuropathy include rapid progression, foot drop, back or neck pain, asymmetric lesions, weight loss, and family history of neuropathy.
  • To date, there are no methods of direct treatment of developed neuropathy, and only its prevention is most effective. In particular, maintaining glycemia within the target values by 60% reduces the incidence and progression of neuropathy.
Thioctic (alpha-lipoic) acid has both direct antioxidant activity (direct removal of free radicals) and indirect (participates in the recycling of other antioxidants, such as glutathione levels and vitamins C and E). It has been established that thioctic acid prevents lipid peroxidation and increases the activity of antioxidant enzymes - catalase and superoxide dismutase.

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May 25th, 2023

By reducing oxidative stress, thioctic acid normalizes impaired endoneural blood flow, as well as impaired impulse conduction velocity. A number of studies have established its neuroregenerative and neuroprotective effects. In connection with the above, it can be used to treat any type of doxazosin neuropathy. Distal symmetric sensorimotor polyneuropathy. Distal symmetric polyneuropathy is the most common form of diabetic polyneuropathy, observed in 33% of diabetic patients.

Sensory symptoms and signs (sensory neuropathy) usually dominate motor lesions and depend on the involvement of a certain class of nerve fibers. Damage to large fibers is manifested by a decrease in the sensitivity of the proprioceptive and light touch, which results in an unsteady ataxic gait and weakness of the deep muscles of the arms and legs. The defeat of small fibers is accompanied by a decrease in pain and temperature sensitivity, which leads to increased injuries, especially of the feet and hands (burns, for example).

In the case of severe lesions, it can be found invertical streaks of sensory deficit in the chest or abdomen when shorter nerve endings in the trunk are involved. Sometimes patients complain of high hypersensitivity to light touch, superficial burning or sharp or deep dull or tearing pain, which most often disturbs at night. In some cases, neuropathic pain becomes unbearable, incapacitating the patient, especially when small fibers are affected. To reduce night pains, patients get out of bed, walk around, immerse their feet in cold water - this is the difference between such pains and ischemic pains, which are exacerbated by physical activity.

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Both neuropathic pain and paresthesias are the result of spontaneous depolarization of newly formed nerve fibers. When examining a patient, special attention should be paid to the condition of the foot - ulcers, deformities, Charcot's joint. Dry skin indicates associated sympathetic dysfunction (autonomic neuropathy). With long-term sensorimotor neuropathy, small muscle atrophy is observed. The most basic neurological examination should include a pressure sensitivity assessment (10-gram monofilament) plus one of the following.

All these tests must be carried out on both sides, and after examining the patient's shoes, the patient's gait must also buy doxazosin online. Patients with severe sensory impairment often have an unsteady gait during normal walking due to loss of proprioceptive sensitivity. Decreased or absent deep tendon reflexes, especially Achilles tendon reflexes, and loss of the ability to sense the 10-gram monofilament may be early manifestations of otherwise asymptomatic neuropathy.

Bilateral painless proximal motor weakness is observed in genetically determined myopathies, motor neuronal disorders and lesions of neuromuscular endings. In these cases, characteristic changes are detected on the electromyogram. For the differential diagnosis of monoclonal benign myopathy, chronic inflammatory demyelinating polyneuropathy, vasculitis and paraneoplastic syndrome, a detailed electromyographic examination is necessary, as well as a study of antibodies to nerve structures and paraneoplastic antibodies in the blood.

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