The disease caused by the SARS-CoV-2 virus is multi-organ and involves almost all organs and systems. Myalgias and arthralgias and, in particular, back pain are common symptoms of COVID-19 and can be observed both at the onset of the disease and in the postcovid period. The causes of muscle and joint damage include both systemic inflammation and direct viral injury. Traditionally, musculoskeletal pain is treated with non-steroidal anti-inflammatory drugs. However, using this drug class in patients with COVID-19 requires caution due to the presence of comorbid diseases and possible complications of viral infection. The review discusses clinical variants and pathophysiological mechanisms of joints and muscles damage in patients with COVID-19 and treatment tactics for patients with musculoskeletal pain.
Diabetic polyneuropathy (DPN) is the most common chronic complication of diabetes mellitus and can develop just at the prediabetes stage. As DPN progresses and, in the absence of its adequate treatment, leads to worse quality of life and its shorter expectancy in patients. The paper discusses current clinical guidelines for the examination and management of patients with DPN, diagnostic methods, and pathogenetic treatment of this disease.
Low back pain (lumbodynia) is a most common reason for seeking medical care and a most common of disability. The review presents current clinical guidelines for the management of patients with acute nonspecific lumbodynia. The diagnosis of acute nonspecific lumbodynia is based on clinical findings and, in most cases, requires no instrumental studies. Nonsteroidal anti-inflammatory drugs are most effective in reducing pain. Additional therapies, such as therapeutic exercises, manual therapy, massage, acupuncture, etc., are discussed. There are data on the use of B vitamins, Milgamma® in particular, in acute non-specific lumbalgia.
Polyneuropathies are a heterogeneous group of diseases that can be caused both by a primary lesion of peripheral nerves, and secondarily, against the background of various somatic diseases. The most common cause of chronic polyneuropathy is distal symmetrical diabetic polyneuropathy. In clinical practice, it is important to be aware of dysimmune polyneuropathy, such as Guillain Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and paraproteinemic polyneuropathy, which lead to severe motor impairment and disability in patients. Identification of the cause of polyneuropathy requires real art, which includes knowledge of the clinical, electrophysiological picture and variants of the course of the disease, as well as a wide range of conditions leading to their development. Timely diagnosis of polyneuropathies and early assignment of etiological and pathogenetic therapy reduce the risk of developing irreversible changes in peripheral nerves caused by axonal degeneration. In the treatment of polyneuropathy of various origins, a special place is occupied by B vitamins, which have a neurotropic effect. Cyanocobalamin is a pathogenetic therapy in patients with diabetes who take metformin for a long time and who developed polyneuropathy due to vitamin B12 deficiency. In one patient, a combination of several variants of polyneuropathies is possible. The article presents a clinical case of a patient with type 1 diabetes mellitus (DM) who developed dysimmune chronic inflammatory demyelinating polyneuropathy (CIDP) associated with DM on the background of distal symmetrical painless diabetic polyneuropathy after a COVID- 19 infection. A feature of the development of CIDP was the acute onset of the disease. Variants of the clinical picture, ENMG criteria, as well as features of treatment, the effectiveness of therapy and the prognosis of CIDP in patients with DM are discussed.
Hereditary neuropathy with liability to pressure palsies (HNPP) is a rare hereditary disorder characterized by recurrent episodes of nerve compression. The first attack usually occurs in the second or third decade of life. In the majority of cases, HNPP is associated with a mutation at chromosome 17 p11.2-12 comprising the gene encoding peripheral myelin protein 22 (PMP22). Here we present a case report of a 43-year-old male with HNPP confirmed by DNA testing. The patient complained of recurrent episodes of bilateral foot extensor muscles weakness and/or hyperesthesia on the outer surface of the hands and forearms, which started after a prolonged posture maintaining and without evident precipitating factors. We also describe typical clinical, electrophysiological, and nerve ultrasound characteristics of the disease.
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