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The article presents the results of ultrasound studies inpatients with hereditary motor and sensory neuropathy, orCharcot-Marie-Tooth disease (CMT). Based on standardelectroneuromiography, the patients were divided into two groupswith demyelinating (n=25) or axonal (n=31) process, CMT1 andCMT2 respectively. Demyelinating forms were characterized byspecific prolonged sonographic changes with uniform thickeningof all studied nerves and abnormalities of their cable structure.In axonal forms the character of structural changes was not assevere and specific as in CMT1, but symmetrical prolongationof the nerve structure was seen in this type of CMT as well. Thedescription of genetically confirmed familial cases of HMSN type1X in male relatives is presented, which demonstrates modernpotential of unltrasound studies in diagnosing the involvementof peripheral nerves in patients from a heterogeneous group ofhereditary neuropahies.

Cerebrovascular diseases are the major cause of morbidity and mortalityamong adults. The extensive development of various diagnosticmethods and their introduction into routine practice increasedthe detection of previously underappreciated and unknown neurologicaldiseases. Comorbidity, i.e. the joining of various other disordersof nervous system (neurodegenerative or demyelinating) tocerebrovascular disease, often leads to a layering of additionalsymptoms which contribute to a significant decline of the quality oflife and increase the costs of treatment. In this clinical analysis casehistories of patients with combined disorders of the nervous systemare reviewed. Approaches to the diagnostic strategy and the need forpersonalized treatment based on the identified comorbidity are discussed.

We present results of clinical and electrophysological analysis of34 patients with recurrent facial neuropathy (rFN). Its frequency(10.9%) among all forms of facial neuropathies was determined,and clinical and EMG characteristics, as well as possiblerisk factors, were described. A separate group of familial rFN wasidentified, and these patients exhibited high percentage of subclinicalperipheral nerve involvement. Positive family history,presence of relapses and electroneurographic features allowed tosuspect hereditary neuropathy with liability to pressure palsy inthese patients. However, molecular analysis of the РМР22 genefailed to reveal a typical gene deletion. These results leave openthe question about etiology and pathophysiologic mechanismsof rFN and warrant further studies of genetic defect underlyinga familial form of rFN.