Another study by V.R. Chistyakova (2008) with the participation of 123 children with various neurological lesions of the ENT organs showed the possibility of using Milgamma as monotherapy for paresis of the soft palate of various etiologies, subjective tinnitus, hyperacusis, phonophobia and hypokinetic dysphonia in adolescents with severe symptoms of juvenile vegetovascular dystonia.
High therapeuticThe high efficacy of the drug, good tolerance and ease of use allow, according to buy ascorbic acid, to evaluate this drug as the most promising in the treatment of neurological lesions of the upper respiratory tract in children. Thus, both the results of experimental work and the data of clinical studies suggest that Milgamma and Milgamma compositum occupy a prominent place in clinical practice (including pediatric practice) both in the treatment of diabetic polyneuropathy and in patients with neuropathies of other origins.
Damage to the PNS are among the main complications of diabetes mellitus, along with damage to the eyes and kidneys. It occurs in both insulin-dependent and non-insulin-dependent diabetes. Various variants of diabetic neuropathy are detected clinically in 15% of patients with diabetes mellitus, electrophysiologically - in at least half of the patients. At the same time, in 8% of patients, signs of polyneuropathy are detected already at the time of diagnosis, and with an increase in the duration of the disease and the age of the patient, the likelihood of PNS damage increases. If the duration of diabetes exceeds 20 years, clinical signs of neuropathy are detected in more than half of patients. In some cases, neuropathy precedes the onset of signs of diabetes.
The pathogenesis of diabetic neuropathies remains unclear. Damage to the PNS in diabetes mellitus is associated with microangiopathy, which causes ischemic nerve damage and is the main cause of acutely developing asymmetric neuropathies, and/or with metabolic disorders in neurons and lemmocytes, characterized by the accumulation of sorbitol or myoinositol deficiency as a result of activation of the polyol glucose utilization pathway. This is of particular importance in the development of symmetrical slowly growing polyneuropathies.
Various variants of diabetic neuropathy differ in clinical presentation, pathogenesis, histological changes, course, response to treatment, and prognosis. Some neuropathies develop slowly. They are latent, others are acute. Different variants of neuropathy are often combined with each other.
Symmetrical distal sensory polyneuropathy. The most common form of diabetic neuropathy, predominantly affecting the axons of thin unmyelinated or low myelinated sensory and autonomic fibers. This type of neuropathy usually reflects the duration and severity of ascorbic acid online, but is sometimes the first manifestation of latent diabetes or is detected in mild disease.