This article is dedicated to the impact of dysfunction of the basal cholinergic system on the state of cognitive functions in various diseases of the brain. domestic and foreign literature is completely reviewed. The pathogenetic mechanisms of dysfunction cholinergic system of the brain are described in myasthenia gravis. Modern approaches in the treatment of cognitive impairment with using central cholinomimetics are described.
Spinal muscle atrophy (SMA) of type 2 is an autosomal-recessive disease defined by a degenerative change in alpha-motor neurons of anterior horns. The disease is manifested in weakness of proximal muscles, pareses, respiratory disturbance and early death. Study of reinnervation process in patients with 2nd type of SMA can provide valuable information on a condition of adaptive mechanisms within the limits of neuron plasticity. According to electroneuromyography study in patients with 2nd type SMA reinnervation process is low intense. It was found out that concentration NGF (nerve growth factor) in serum of patients with 2nd type SMA is considerably higher than in control group. We studied the influence of blood serum of patients with 2 type SMA on growth neurites of sensory ganglia of 10-12 days old chicken embryos in organotypic culture. For the first time it was shown that blood serum of patients with 2nd type SMA dose-dependent inhibits of growth neurites of sensory ganglia. Apparently, neurite-inhibitory effect is caused by high concentration of neurotrophins in patient serum, due to that the reinnervation mechanisms in 2 type SMA patients are not so efficient.
Differential diagnostics of multifocal motor neuropathy (MMN) has many difficulties associated with a number of factors: rare nature of disease, polymorphic clinical forms and a phenotypic picture similar to peripheral motor neuron diseases. Such diseases also include rare nosological forms: amyotrophic lateral sclerosis, hereditary myopathies and neuropathies; their general phenotypic picture has a form of progressive flaccid paralysis, age of the disease onset and the nature of its course. However, different pathogenesis of these diseases requires a differentiated approach to therapy.
This article deals with differential diagnostics of multifocal motor neuropathy, gives examples of modern diagnostic criteria necessary for diagnosing multifocal motor neuropathy and analyzes a clinical case with an incorrect diagnosis of multifocal motor neuropathy.
Severe cognitive impairment was found in 33% of patients with DMD. The distribution of mutations in the DMD gene was not uniform, most often the mutations were found in the region from exon 43 to exon 50. Serum concentration of NGF in patients with DMD was higher than in the control group (2391 pg/ml [1587; 4136] and 553 pg / ml [314; 864], respectively (p<0.001)). In the group of patients with cognitive disorders, there was a decreased concentration of BGF (23 670 [21 700; 30 720] pg/ml (p<0.001)). In patients with BGF concentration less than 31 000 pg/ml, the chances of cognitive disorders were more than 10 times higher (p<0.001, odds ratio OR=12.0, 95% CI [1.9-76.4]). Thus, biochemical mechanisms, such as NGF overexpression and BGF deficiency, are involved in the development of cognitive disorders in patients with DMD.
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