Effect of intraventricularly administered low-dose recombinant tissue plasminogen activator on interleukin 1-beta and transforming growth factor beta concentrations in cerebrospinal fluid of patients with primary intracerebral hemorrhage associated with intraventricular hemorrhage: A retrospective study.

It is increasingly recognized that modulation of brain inflammation may uncover new potential therapeutic strategies for stroke. Recent studies have shifted focus from immunological implications in ischemic stroke to a more devastating form; the hemorrhagic stroke.The aim of this study was to investigate the neuroinflammatory response in cerebrospinal fluid in patients with primary intracerebral hemorrhage (ICH) associated with intraventricular hemorrhage (IVH) in the presence of low-dose recombinant tissue plasminogen activator (rt-PA).

Simultaneous appearance of cerebral venous thrombosis and subdural hematomas as rare cause of headache in puerperium following epidural analgesia: a case report.

The aim of this study is to report the first case of simultaneous appearance of cerebral venous thrombosis (CVT) and bilateral subdural hematomas (SDHs) following epidural analgesia for labor and delivery and to point out the difficulty of establishing such a diagnosis in the presence of postpartum headache. A 26-year old primigravida with a history of epilepsy received epidural analgesia for delivery. Three days after the uneventful spontaneous vaginal delivery she complained about the headache.

Intravenous thrombolysis for acute ischemic stroke--our experiences.

Intravenous (i.v.) thrombolysis with recombinant tissue plasminogen activator (rt-PA) is the only available pharmacological therapy to improve the outcome of acute ischemic stroke.

Hemodynamic changes in the posterior cerebral circulation triggered by insufficient sympathetic innervation--cause of primary intracerebral hemorrhage?

Primary intracerebral hemorrhage (ICH) is caused by hypertensive disease of small penetrating blood vessels in the basal ganglia, brain stem and cerebellum. Those regions are supplied by arteries of the so-called posterior brain circulation with insufficient sympathetic innervation. We propose the following hypothesis: due to insufficient sympathetic innervation hemodynamic changes occur in the vascular bed of the posterior brain circulation serving as a key factor for arterial rupture.