Aim. This study aimed to explore associations between fibrinogen and acute ischaemic stroke, neurological impairment, cerebral ischaemia, and clinical evaluation of stroke patients. Materials and methods. The study involved 153 patients categorised into two groups: patients with acute ischaemic stroke, and patients with risk factors but who had not had a stroke. Blood samples were collected to analyse the serum level of fibrinogen. The time from stroke onset to blood test was noted. The National Institutes of Health Stroke Scale was used to determine the neurological disability of the stroke patients upon hospital admission and upon discharge. Cerebral CT was performed on the same group of patients during the first 24 h after stroke onset and evidence of early ischaemic lesions was recorded. The stroke cases were divided into subgroups according to the TOAST classification. Results. Patients with ischaemic stroke had a significantly increased mean level of fibrinogen (> 4g/l). Analysis of stroke subtypes shows that patients with undetermined cause of stroke and patients with atherosclerotic stroke had a significantly higher median level of fibrinogen compared to patients with some other types of stroke. No significant connection was found between fibrinogen level and neurological deficit. A positive linear relationship was established between fibrinogen and blood sample time. A negative relation was established between the clinical evolution of ischaemic stroke patients and fibrinogen level. A significant relation between fibrinogen level and the presence of ischaemic lesions on cerebral CT was observed: patients with a fibrinogen level > 3.41g/l showed a 3.29-times increased risk of ischaemic lesions. Conclusion. Fibrinogen is a reliable biomarker that could characterise acute ischaemic stroke. Aim. This study aimed to explore associations between fibrinogen and acute ischaemic stroke, neurological impairment, cerebral ischaemia, and clinical evaluation of stroke patients. Materials and methods. The study involved 153 patients categorised into two groups: patients with acute ischaemic stroke, and patients with risk factors but who had not had a stroke. Blood samples were collected to analyse the serum level of fibrinogen. The time from stroke onset to blood test was noted. The National Institutes of Health Stroke Scale was used to determine the neurological disability of the stroke patients upon hospital admission and upon discharge. Cerebral CT was performed on the same group of patients during the first 24 h after stroke onset and evidence of early ischaemic lesions was recorded. The stroke cases were divided into subgroups according to the TOAST classification. Results. Patients with ischaemic stroke had a significantly increased mean level of fibrinogen (> 4g/l). Analysis of stroke subtypes shows that patients with undetermined cause of stroke and patients with atherosclerotic stroke had a significantly higher median level of fibrinogen compared to patients with some other types of stroke. No significant connection was found between fibrinogen level and neurological deficit. A positive linear relationship was established between fibrinogen and blood sample time. A negative relation was established between the clinical evolution of ischaemic stroke patients and fibrinogen level. A significant relation between fibrinogen level and the presence of ischaemic lesions on cerebral CT was observed: patients with a fibrinogen level > 3.41g/l showed a 3.29-times increased risk of ischaemic lesions. Conclusion. Fibrinogen is a reliable biomarker that could characterise acute ischaemic stroke.

The ultrasound fusion imaging (UFI) system is a new promising imaging modality that combines live ultrasound investigations with preregistered CT, MRI, or PET images. In this study, we want to present our initial experience with the new method that combines the transcranial color-coded sonography (TCCS) in different insonation planes and the 3T-weighted MRI cerebral images. The study validates the diagnostic capabilities of the system to detect different normal cerebral structures in healthy volunteers. In the present paper, we also discuss the advantages of US fusion imaging technology and its clinical applications in Neurology.

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Болестта на Steinert (миотонична дистрофия) е автозомно доминантно заболяване в резултат на динамични мутации в DMPK гена, локализиран в 19q13.32 хромозома. Характерна е полово-диференцирана експресия на гена. Заболяването е мултисистемно, като засяга скелетната и гладката мускулатура, очите, сърцето, ендокринната система и централната нервна система. Различават се три основни форми: конгенитална, в ранно детство и класическа с вариабилност в клиничната симптоматика. Представяме семейство, страдащо от миотонична дистрофия – жена на 57 години и трите й деца (две момичета и едно момче). Дебютът на болестта при майката е на 30-годишна възраст с класически симптоми – миотония, хипотрофия за лицева мускулатура, особенно за дъвкателни мускули, изразена хипотрофия на дисталните мускулите на ръцете и подбедриците. Налице са и типичното засягане и на други ситеми – катаракта, ендокринни смущения, пролапс на предно митрално платно с митрална регургитация при ситус инверзус тоталис. Насочена за диагностично уточняване от личния лекар, поради силно ограничение на физическите й способности. Установява се антиципация за всяко следващо дете – начало на симптомите в юношестска и детска възраст, като при второто и третото са налице катаракта и умствена ретардация. Зависими от чужда помощ. Електромиографията е типична с миотонични феномени и миогенна увреда. КФК е с повишени стоиности. Насочени за генетично изследване. Случаят е показателен за късно поставяне на диагнозата на типично протичащо наследствено заболяване (27 години след началото на симптомите) и липсата на достатъчна информираност на лекарите за възможностите за пренатална диагностика.