Cerebral vasomotor reactivity in neurodegenerative diseases

Small-caliber cerebral vessels change their diameters in response to alterations of key metabolite concentrations such as carbon dioxide or oxygen. This phenomenon, termed the cerebral vasomotor reactivity (CVMR), is the basis for blood flow regulation in the brain in accordance with its metabolic status. Typically, CVMR is determined as the amount of change in cerebral blood flow in response to a vasodilating stimulus, which can be measured by various neuroimaging methods or by transcranial Doppler. It has been shown that CVMR is impaired in cerebrovascular diseases, but there is also evidence of a similar dysfunction in neurodegenerative disorders. Here, we review studies that have investigated CVMR in the common neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and multiple sclerosis. Moreover, we discuss potential neurodegenerative mechanisms responsible for the impairment of CVMR

Metody profilaktyki żylnej choroby zakrzepowo-zatorowej u chorych w ostrej fazie udaru mózgu – aktualny stan wiedzy

Deep venous thrombosis (DVT) and its sequel, pulmonary embolism (PE), are serious complications of stroke. There are pharmacological and physical methods to prevent these complications. The authors review the literature and present the current state of knowledge regarding the effectiveness of each of the DVT and PE prevention methods in stroke patients and cite current Polish, European and American recommendations regarding this issue. Heparins are the method of choice for the prevention of venous thromboembolism in both ischaemic and haemorrhagic stroke patients.Zakrzepica żył głębokich kończyn i jej konsekwencja – zatorowość płucna, są poważnymi powikłaniami udaru mózgu. Istnieją farmakologiczne i fizyczne metody zapobiegania tym powikłaniom. Autorzy dokonują przeglądu piśmiennictwa i prezentują aktualny stan wiedzy na temat skuteczności każdej z metod stosowanych w profilaktyce zakrzepicy żył głębokich kończyn i zatorowości płucnej u chorych po udarze mózgu, a także cytują aktualne zalecenia polskie, europejskie i amerykańskie. Stosowanie heparyn jest metodą z wyboru w zapobieganiu powikłaniom zakrzepowo-zatorowym u unieruchomionych chorych z udarem mózgu, zarówno niedokrwiennym, jak i krwotocznym

Ostra dystonia ogniskowa wywołana trójpierścieniowym lekiem przeciwdepresyjnym u pacjenta z chorobą Wilsona – opis przypadku

The authors present the case of a 19-year-old patient with Wilson disease (WD) who developed symptoms of acute focal dystonia of the left hand (a ‘starfish’ hand presentation) shortly after treatment with the tricyclic antidepressant clomipramine. The diagnosis of WD was made 8 months earlier based on abnormal copper metabolism parameters and was confirmed by genetic testing. Initially, the patient presented with akathisia, sialorrhea, oromandibular dystonia (occasionally grimacing) and slight dysarthria. The patient's symptoms diminished after treatment with d-penicillamine was initiated. No further deterioration was observed after copper-chelating therapy was started. The authors diagnosed acute focal dystonia induced by clomipramine. Botulinum toxin and intensive rehabilitation was initiated; complete regression of hand dystonia was observed. Based on the case, the authors suggest that care should be exercised with regard to starting medications that could potentially impact the extrapyramidal system in WD patients.W pracy przedstawiono przypadek 19-letniego pacjenta z chorobą Wilsona, u którego po włączeniu trójpierścienio-wego leku przeciwdepresyjnego – klomipraminy – wystąpiły objawy ostrej dystonii ogniskowej w postaci ręki „rozgwiazdy”. Chorobę Wilsona rozpoznano u pacjenta 8 miesięcy wcześniej na podstawie nieprawidłowego metabolizmu miedzi i badań genetycznych. Początkowo chory prezentował dyskretne objawy neurologiczne: akatyzję, ślinotok, dystonię ustno-żuchwową oraz dyzartrię. Po włączeniu leczenia d-penicylaminą nie obserwowano pogorszenia stanu neurologicznego, a początkowe objawy w trakcie leczenia chelatującego znacznie się zmniejszyły, dlatego rozpoznano u pacjenta ostrą dystonię ogniskową indukowaną klomipraminą. Pacjenta leczono toksyną botulinową oraz rehabilitowano z dobrym efektem, objawy dystonii ogniskowej całkowicie ustąpiły w ciągu roku. Autorzy proponują zachowanie szczególnej ostrożności w stosowaniu leków potencjalnie wpływających na układ pozapiramidowy u pacjentów z chorobą Wilsona

Infections and Ischemic Stroke Outcome

Background. Infections increase the risk of ischemic stroke (IS) and may worsen IS prognosis. Adverse effects of in-hospital infections on stroke outcome were also reported. We aimed to study the prevalence of pre- and poststroke infections and their impact on IS outcome. Methods. We analysed clinical data of 2066 IS patients to assess the effect of pre-stroke and post-stroke infections on IS severity, as well as short-term (up to 30 days) and long-term (90 days) outcome. The independent impact of infections on poor outcome (death, death/dependency) was investigated by use of logistic regression analysis. The effect of antibiotic therapy during hospitalization on the outcome was also assessed. Results. Pre-stroke infections independently predicted worse short-term outcome. In-hospital infections were associated with worse short-term and long-term IS prognosis. Antibacterial treatment during hospitalization did not improve patients' outcome. Conclusions. Prevention of infections may improve IS prognosis. The role of antibiotic therapy after IS requires further investigations

Severe disease exacerbations in patients with multiple sclerosis after discontinuing fingolimod

Discontinuation of fingolimod in patients with multiple sclerosis (MS) can lead to disease reactivation. In this review, we describe cases of severe exacerbations in patients with MS following discontinuation of fingolimod, including three cases from our center. We consider potential mechanisms of disease reactivation after cessation of fingolimod, and the evidence supporting this rebound effect. We conclude that discontinuation of fingolimod results in the return of disease activity, which then leads to severe exacerbations (i.e., rebounds) in a clinically significant proportion of patients. Lastly, we consider disease-modifying treatment options for patients who discontinue fingolimod