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).This retrospective study included 88 adults with primary ICH associated with IVH. Patients were divided into 2 groups: rt-PA group and non-rt-PA group, which received normal standard of care for this diagnosis. The rt-PA group was treated via catheter-based clot lysis using low-dose rt-PA injected through the external ventricular drain (EVD) system, and the non-rt-PA group was treated with saline applied to EVD system in equivalent volume. Cerebrospinal fluid samples from rt-PA were obtained from the EVD system at 4 time points: once before the drug administration, and then on day 1, 3, and 7. No attempt at randomization was made. The decision to inject rt-PA was based on the preference of the primary attending neurologist and the ability to obtain consent. Temporal interleukin-1 beta and transforming growth factor beta concentration changes were analyzed and compared between the 2 groups.The concentration of interleukin-1 beta was significantly lower in the rt-PA group than in the non-rt-PA group on day 7. In addition, the concentration of transforming growth factor beta was significantly higher in the rt-PA group than in the non-rt-PA group on day 1. There was a significant difference in interleukin-1 beta concentration between days 0 and 1 in comparison to day 3 in the rt-PA group, and between day 0 in comparison to day 3 and 7 in the non-rt-PA group. We also observed a significant difference in transforming growth factor beta concentration between days 0 and 1 and between days 3 and 7.The different pattern of pro- and anti-inflammatory cytokines in patients with ICH associated with IVH suggest distinct characteristics of secondary brain injury depending on the treatment modality.

Chemical meningitis is a very rare but potentially devastating complication of spinal anaesthesia and analgesia.It can be provoked by intrathecal application of substances, such as local anaesthetics, or may occur as a result of the anaesthesia technique used.We describe, until now published, a case of 20-year-old primipara who received spinal analgesia with levobupivacaine for labor and delivery and developed generalized epileptic seizures and high fever.Laboratory tests showed an increased white blood cell count, elevated neutrophil granulocytes, and elevated C-reactive protein; the cerebrospinal fluid (CSF) analysis showed increased levels of proteins, lactate, leukocytes, and erythrocytes.A brain computed tomography (CT) and CT angiography scan did not reveal any pathological alteration.Microbiological analysis of CSF and blood cultures did not show any pathogen growth, and the patient was treated with antibiotics and corticosteroids.The patient later fully recovered and was discharged from the hospital.

The cyclophosphamide as a predisposing factor for Posterior Reversible Encephalopathy Syndrome (PRES) and therapeutic option for systemic lupus erythematosus (SLE) is still confusing. The first and only case of PRES, probably induced by cyclophosphamide, in Croatia followed by the findings of 36 SLE patients diagnosed with PRES after treatment with cyclophosphamide worldwide are described. An 18-year-old Caucasian female patient with a 1-year history of SLE was admitted to the hospital due to lupus nephritis and acute arthritis. After the second dose of cyclophosphamide was administered, according to the Euro-lupus protocol, the patient presented with a grand mal status epilepticus. The differential diagnosis of neurolupus, cerebrovascular insult, and infection were excluded. The MRI findings showed brain changes in corresponding to PRES. The treatment consisted of antihypertensives, antiepileptics, antiedema therapy, mechanical ventilation, and avoiding further cyclophosphamide use. A Naranjo Adverse Drug Reaction Probability Scale total score of five and a probable reaction related to drug therapy (cyclophosphamide, PRES) was confirmed. In this systematic review, along with cyclophosphamide use, the main predisposing factors involved in PRES occurrence in SLE patients were active SLE and renal involvement. Due to the high number of simultaneously involved predisposing factors (max. six) and their overlapping effect, it is still not possible to clearly establish the role of every factor on PRES onset. The use of cyclophosphamide, as a contributing factor for PRES onset, should be carefully assessed, based on clinicians' experience and knowledge, in the setting of active SLE.

Increasing research evidence suggests that basal ganglia are an important part of frontal-subcortical circuit which is involved not only in motor control but also in affective, cognitive and executive functions. In this article, we describe the ability of facial emotion recognition and cognitive functioning in a patient with left basal ganglia and insula damage. The patient's ability to recognise facial emotional expressions was intact in spite of unilateral injury of the left insula and basal ganglia. He showed preserved intellectual function in general, but experienced difficulties on subsets of the executive functions: set-shifting and ability to activate or generate cognitive strategies, commonly found in patients with caudate lesions. This case contributes to evidence that striatal structures are important for executive functions.

Subarachnoid hemorrhage is a neurologic emergency and a detrimental cerebrovascular event with a high rate of death and complications. Recommendations have been developed and based on literature search, evaluation of the results of large international clinical trials, collective experience of the authors, and endorsed by the Croatian Society of Neurovascular Disorders, Croatian Society of Neurology including Section for Neurocritical Care, Croatian Neurosurgical Society, Croatian Society for Difficult Airway Management and Croatian Medical Association. The aim of these guidelines is to provide current and comprehensive recommendations and to assist physicians in making appropriate decisions in the management of subarachnoid hemorrhage. Evidence based information on the epidemiology, risk factors and prognosis, as well as recommendations on diagnostic work up, monitoring and management are provided, with regard to treatment possibilities in Croatia.

Susac's syndrome (SS) is an infrequent neurological disorder characterized by the clinical triad of encephalopathy, branch retinal artery occlusion and hearing loss due to an autoimmune endotheliopathy associated with anti-endothelial cell antibodies. At the onset of the disease SS rarely appears with the complete clinical triad. The most important diagnostic procedures involved in the diagnosis of SS are brain MRI, audiometric testing and retinal fluorescein angiography. Presence of at least two components of the SS clinical triad accompanied by specific brain MRI findings is highly suggestive of SS. We report a case of a young pregnant woman with a history of encephalopathy, hearing loss and walking impairment. Brain MRI revealed a spectrum of findings previously described in patients with SS. We induced labor at 37 weeks' gestation to start with immunosuppressive treatment and avoid possible fetal toxicity. To the best of our knowledge this is the first report of SS in Croatia.

These are evidence based guidelines for the management of medical complications in patients following aneurysmal subarachnoid hemorrhage, developed and endorsed by the Croatian Society of Neurovascular Disorders, Croatian Society of Neurology including Section for Neurocritical Care, Croatian Neurosurgical Society, Croatian Society for Difficult Airway Management and Croatian Medical Association. They consist of recommendations for best monitoring, medical treatment and interventions based on the literature, evaluation of the results of large international clinical trials, and collective experience of the authors.

Aim: Carotid artery stenosis is a progressive constriction in the process of atherosclerosis, which, as well as the attendant risks, is being considered as one of the reasons for reduction of cognitive capabilities. In this study we examined the connection between cognitive disorders and stenotic change of carotid artery supplying dominant brain hemisphere (left inner carotid artery in right handed persons and right carotid artery in left handed persons) being responsible for the primary irrigation of brain hemisphere. Methods: The study included 67 patients (36 women and 31 men), who according to their medical history did not suffer a stroke, transient ischemic attack and no carotid trombendarterectomy was performed on them, but they have an asymptomatic high level of stenosis of the dominant inner carotid artery. The control group of 30 patients consisted of patients without stenotic processes of extracranial parts of the carotid, age and sex approximately equally represented. Cognitive disorder was monitored by modified mental scale and BDI-MC test (blessed-dementia information- memory concentration test). Results: We found that there was no statistically significant difference in cognitive disorder between groups. Conclusion: Cognitive disorder is not connected to a high level of stenotic processes of the carotid arteries supplying dominant brain hemispheres.

With its onset and symptoms the acute brain stroke causes relatively clear and recognizable clinical features. However, there are chronic, single and/or diffuse ischemic brain lesions which are clinically asymptomatic and which take longer to recognize. The term ”silent brain infarct” is frequently used to describe the brain infarct which is determined with the autopsy by chance or which could be determined with computerized tomography. Such brain infarct could also be determined using the brain magnetic resonance imaging on people who never before had clinical symptoms transient ischemic attack or brain stroke in their lives. For the most of the time this is about small infarct in deep sub-cortical brain regions. It is morphologically similar to symptomatic lacunar infarct. Lacunar ischemic brain lesion is the consequence of the deep, perforating artery occlusion. Its base is mainly the hypertensive brain microangiopathy. The silent brain infarct is given great attention in the last decade because the studies show the silent brain infarct presence doubles the symptomatic brain stroke and dementia risk. In this review we show the epidemiology, the pathophysiologic attributes, the risk factors and possible silent brain infarct consequences.

neurodegenerative diseases, namely Alzheimer disease, Parkinson’s disease, progressive supranuclear palsy, frontotemporal dementia, corticobasal degeneration, Huntington disease, prion disease, amiotrophic lateral sclerosis and spinocerebelar ataxias are storage diseases. Their pathophysiology can be linked to abnormal proteins which settle down in central nervous system causing a slow and progressive breakdown of nervous tissue and cause typical manifestations of the disease. Autoimmune demyelinating disease as multiple sclerosis is as well thought to be a neurodegenerative disease, which in difference to other diseases, occurs in younger population. Neurodegenerative diseases mostly occur as a consequence of genetic, epigenetic, and environmental factors and we think of them as multifactorial diseases; even though cases of monogenetic inheritance have been postulated. The contribution of genes as risk factors has been postulated not only in genetically inherited forms but also in sporadic forms. Many genes have been thought to be of importance for the development of disease, and some have been thought to contribute to a number of neurodegenerative diseases. Many genes have still not been discovered, and in a number of described genes no explanation was given of their function in disease development. Although gene therapy was postulated in some diseases, as in Parkinson’s disease, the modification of risk genes has still not taken its turn in. Future investigations should enlighten new genetic markers and epistatic and epidgenetic interactions which have an important role in complex predisposition for neurodegenerative diseases