Search

Objective: We present our experience with surgery of jugular foramen schwannomas with special consideration of clinical presentation, surgical technique, complications, and outcomes., Methods: This retrospective study includes ten patients with jugular foramen schwannomas treated by the senior author between January 2007 and December 2012. Three patients had undergone partial tumour resection elsewhere. The initial symptom for which they sought medical help was hearing loss, dysphagia, hoarseness, and shoulder weakness. Preoperative glossopharyngeal and vagal nerve deficits were the most common signs. In our series, tumour extension was classified according to Kaye-Pellet grading system. In two cases the tumours were classified into type A and 8 patients presented with type D tumours. A retromastoid suboccipital craniotomy was performed for type A tumours and modifications of cranio-cervical approach were suitable for type D., Results: No death occurred in this series. Four patients deteriorated after surgery: in two patients preoperative cranial nerve deficits deteriorated after surgery while new cranial nerve palsy occurred in 2 other patients. In four patients, the cranial nerve dysfunction had improved at the last follow-up examination. In all other patients, the cranial nerve dysfunction remained the same. One patient experienced tumour recurrence over a follow-up period of 40 months. This patient underwent a successful second surgery without further evidence of tumour growth., Conclusions: Jugular foramen schwannomas can be radically managed with the use of skull base surgery techniques. However, the surgical treatment of jugular foramen schwannomas carries a significant risk of the lower CN deficits., (Copyright © 2014 Polish Neurological Society. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved.)

Adiponectin, an adipocyte-derived hormone, possesses anti-inflammatory properties. Its decreased levels were noted in patients with ischemic stroke (IS). Animal studies suggest that the decline of adiponectin levels in the acute IS phase is a dynamic process. The aim of the present study was to analyze the temporal expression of the adiponectin plasma levels in patients with acute IS. Thirty-one consecutive patients with first-ever IS (mean age ± SD: 69.5 ± 12.5 years; 12 women) and 26 control subjects (CS; 72.2 ± 7.6 years; 18 women) were included into the study. Plasma adiponectin levels were measured at three time points: within first 24 hours, on Days 2-4, and on Days 5-10 days after the onset of IS. Adiponectin levels were significantly lower in IS patients on admission comparing with CS (medians: 6.0 μg/ml vs. 11.3 μg/ml, respectively; P < 0.05) and continued to decline at later time points (P < 0.001).

Background and Purpose: The aim of the study is to present our experience in the surgical treatment of posterior petrous meningiomas in regard to clinical presentation, surgical anatomy, complications and long-term functional postoperative results., Material and Methods: A series of 48 consecutive patients operated on for posterior petrous meningiomas at the authors' institution between 2002 and 2011 is reported. The main symptom on first admission was hypoacusis, impairment of the fifth cranial nerve and cerebellar ataxia. The tumour was found to be attached to the premeatal dura in 46%, the inframeatal dura in 29% and the postmeatal dura in 25% of cases. Tumour resection was categorized as grade I in 16 patients, grade II in 29 patients, grade III in 1 patient and grade IV in 2 patients, according to the Simpson classification system. The petrosal approach and retrosigmoid approach were suitable for posterior petrous meningiomas., Results: Postoperative facial nerve dysfunction appeared in 8 and further deteriorated in 2 patients. Hearing function deteriorated after surgery in 8 and improved in 2 cases. Perioperative death occurred in two patients. Tumour recurrence was observed in two patients, and both underwent a second operation and postoperative stereotactic radiotherapy., Conclusions: Surgical treatment of posterior petrous meningiomas has become increasingly safe but these tumours still remain a surgical challenge because of the relatively high incidence of permanent complications associated with their removal. The site of displacement of the cranial nerves depending on the dural origin of the tumour has the most influence on the related difficulties in its removal.

The molecular mechanisms underlying the systemic response to subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms (RAs) are not fully understood. We investigated whether the analysis of gene expression in peripheral blood could provide clinically relevant information regarding the biologic consequences of SAH. Transcriptomics were performed using Illumina HumanHT-12v4 microarrays for 43 RA patients and 18 controls (C). Differentially expressed transcripts were analyzed for overrepresented functional groups and blood cell type-specific gene expression. The set of differentially expressed transcripts was validated using quantitative polymerase chain reaction in an independent group of subjects (15 RA patients and 14 C). There were 135 differentially expressed genes (false discovery rate 1%, absolute fold change 1.7): the abundant levels of 78 mRNAs increased and 57 mRNAs decreased. Among RA patients, transcripts specific to T lymphocyte subpopulations were downregulated, whereas those related to monocytes and neutrophils were upregulated. Expression profiles of a set of 16 genes and lymphocyte-to-monocyte-and-neutrophil gene expression ratios distinguished RA patients from C. These results indicate that SAH from RAs strongly influences the transcription profiles of blood cells. A specific pattern of these changes suggests suppression in lymphocyte response and enhancements in monocyte and neutrophil activities. This is probably related to the immunodepression observed in SAH.

Background: Minimal hepatic encephalopathy (MHE) is the mildest form of hepatic encephalopathy (HE). For diagnostic purposes, 2 alternative batteries of psychometric screening tests are recommended. They differ from each other in terms of the cognitive domains assessed. The research was designed to provide a profile of cognitive functioning in patients with liver cirrhosis, using an assessment that covers a wider range of cognitive functions than the usual screening battery., Material and Methods: We examined 138 persons, including 88 with liver cirrhosis and 50 healthy volunteers. The Mini Mental State Examination (MMSE) was used for screening and excluding advanced cognitive impairment. Then, to assess cognitive functions in more detail, the following tests were used: Auditory Verbal Learning Test (AVLT), Letter and Semantic Fluency Tests (LF and SF), Trail Making Test (TMT A&B), Digit Symbol Test (DST), Block Design Test (BDT), and Mental Rotation Test (MRT). The MRT task has not been used in MHE diagnosis so far. Finally, 57 patients and 48 controls took part in the entire study., Results: Patients with liver cirrhosis commit significantly more errors of intrusions in the AVLT during the delayed free recall trial. Results significantly deviating from the norm in at least 2 tests were found only in 7 cirrhosis patients., Conclusions: The results do not provide any specific profile of cognitive disturbances in MHE, but suggest that cirrhosis patients have a tendency to commit more memory errors, probably due to subtle impairments of executive function.

Background and Purpose: Recent genome-wide association studies have indicated 3 new susceptibility loci for Alzheimer disease (AD): complement receptor 1 (CR1), clusterin (CLU), and the phosphatidylinositol-binding clathrin assembly protein (PICALM). We investigated the influence of the rs6656401 single nucleotide polymorphisms (SNP) of the CR1 gene, the rs3851179 SNP of the PICALM gene, and the rs11136000 SNP of the CLU gene on risk of AD in a Polish population., Material and Methods: In 253 Caucasian AD patients and 240 controls, analyses identifying the rs6656401, rs3851179 and rs11136000 SNPs and APOE common polymorphisms were performed., Results: No significant differences were observed in the distribution of the rs6656401 of CR1, rs3851179 of PICALM and rs11136000 of CLU SNPs between AD patients and controls. The APOE ε4 common polymorphism was strongly re-lated to the risk of AD., Conclusion: Our results suggest that investigated SNPs are not associated with AD in a Polish population.

We discuss the influence of increased pressure (compression and decompression in the hyperbaric chamber) on the human body, in particular the organ of vision. An extraordinary, quite rare case of painless loss of vision connected with retinal hemorrhage, followed by scarring in the person who performed the Valsalva maneuver working inside the hyperbaric chamber. The lesion was determined with high probability as a cause of Valsalva maculopathy. At the request of the patient, the case was analyzed about six years after the onset of the disease in terms of the presence or absence of the ground for certifying it as an occupational disease of the eye.

Background and Purpose: The aim of this retrospective study was to assess the effectiveness of aneurysm clipping by computed tomography angiography (CTA) in a long-term follow-up., Material and Methods: The CTA examination was performed in 119 patients who had 143 aneurysms clipped. The examinations were performed 3 to 11 years (mean 6 years) after clipping using a GE Lightspeed PRO16 scanner., Results: In all cases but one, good quality CTA images, suitable for evaluation of the arteries around the clip site, were obtained. Complete aneurysm closure without neck remnant or regrowth was confirmed in 137 (96%) aneurysms. In 4 (3%) cases, neck remnants were detected (2 on the anterior communicating artery [AComA] and 2 on the middle cerebral artery [MCA]). A total clip slippage from the aneurysm dome was revealed in 1 case. One case of aneurysm re-rupture was noted, 11 years after clipping. The rebleeding was caused by AComA aneurysm regrowth. Among these 6 patients with unsatisfactory clipping, 2 required further treatment and 4 remain under observation. Nineteen 'de novo' aneurysms in other locations were found in 14 (12%) patients. Summing up all of the pathological findings in the study group, there were 18 (15%) patients who needed further management including close surveillance or re-treatment., Conclusions: Computed tomography angiography is a simple and reliable method of aneurysm clipping evaluation. The long- term follow-up CTA confirmed the permanent and complete obliteration of 96% of the aneurysms. The rate of unsatisfactory aneurysm closure was 4%, but only 1.4% needed re-treatment during a mean follow-up of 6 years. The annual risk of aneurysm re-rupture was 0.1%.

Background and Purpose: The results of a few studies suggest that magnetic resonance spectroscopy of the brain could allow detection of minimal hepatic encephalopathy. The goal of this study was to assess the ability of magnetic resonance spectroscopy to differentiate between cirrhotic patients with and without minimal hepatic encephalopathy., Material and Methods: Localized magnetic resonance spectroscopy was performed in the basal ganglia, occipital gray matter and frontal white matter in 46 patients with liver cirrhosis without overt encephalopathy and in 45 controls. Neurological and neuropsychological examination was performed in each participant., Results: The patients with liver cirrhosis had a decreased ratio of myoinositol to creatine in occipital gray matter and frontal white matter (mean: 0.17 ± 0.05 vs. 0.20 ± 0.04, p = 0.01 and 0.15 ± 0.05 vs. 0.19 ± 0.04, p < 0.01, respectively) and a decreased ratio of choline to creatine in occipital gray matter (mean: 0.32 ± 0.07 vs. 0.36 ± 0.08, p = 0.03). Minimal hepatic encephalopathy was diagnosed in 7 patients. Metabolite ratios did not differ significantly between patients with and without minimal hepatic encephalopathy. Metabolite ratios did not differ significantly between patients with Child-Pugh A and those with Child-Pugh B., Conclusions: Magnetic resonance spectroscopy does not allow accurate diagnosis of minimal hepatic encephalopathy. A similar profile of metabolites in the brain is observed in cirrhotic patients without cognitive impairment.

Liver cirrhosis is often accompanied by a spectrum of cognitive deficits, labelled hepatic encephalopathy (HE). The precise specification of cognitive impairment associated with HE has not been yet elucidated. The aim of this study was an attempt to examine cortical function in cirrhotic patients using EEG event-related potentials during a demanding task involving selective attention. We compared group of 30 patients with liver cirrhosis without minimal or overt HE with education-, age- and sex-matched 29 non-cirrhotic controls. Both groups performed an attentional blink (AB) task, which requires detecting and identifying two target characters in a longer series of rapidly and sequentially presented characters. EEG signals from 32 electrodes were measured and then analyzed in the paradigm of event-related potentials (ERP). Though the groups did not differ in the detection rate of the target stimuli, ERP waveforms revealed two group differences of component amplitudes. The first difference was related to the waveform amplitude within the 200-400 ms after first target in the right frontal region (frontocentral N2 component). Moreover, in patient group this amplitude positively correlated with the blood plasma level of alkaline phosphatase and gamma-glutamyl transpeptidase. The second amplitude difference was observed in the midline parieto-occipital regions within the 400-600 ms after the first target (P3b component). The AB task and ERP analysis allowed to find differences in cortical functioning in cirrhotic patients even without overt cognitive deficits. Our finding demonstrates that liver dysfunction can influence cortical processing associated with detecting and categorizing stimulus change.

Background: Beta-adrenergic blockade prevents or diminishes stress-induced hyperglycemia in different experimental models. The aim of the study was to determine if the use of beta-blockers before stroke reduces the risk of acute hyperglycemia in stroke patients., Methods: We analyzed the data of 603 consecutive patients with acute ischemic stroke and without pre-stroke diagnosis of diabetes mellitus admitted to stroke unit within 24 h after symptoms onset., Results: Plasma glucose level on admission (6.0 ± 1.4 vs 6.6 ± 1.9 mmol/L, P = 0.01) and fasting glucose on day 1 (5.2 ± 1.1 vs 5.7 ± 1.1 mmol/L, P = 0.02) were significantly lower in patients treated with beta-blockers before stroke than in those who did not receive such a treatment. On multivariate logistic analysis beta-blockers use before stroke was associated with reduced risk of glucose level on admission ≥7.8 mmol/L (OR: 0.22, 95%CI: 0.07-0.74) and fasting glucose on day 1 ≥ 7.0 mmol/L (OR: 0.21, 95%CI: 0.05-0.91). The risk of fasting hyperglycemia defined as glucose ≥6.1 mmol/L did not differ between groups., Conclusions: Beta-blockage before stroke onset may result in lower plasma glucose on admission and prevent early hyperglycemia in patients without pre-stroke diagnosis of diabetes mellitus., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Liver cirrhosis is often accompanied by cognitive deficits called minimal hepatic encephalopathy (MHE) when it is observed to a moderate extent. In the present study, brain activity and cognitive functioning were examined in patients with liver cirrhosis without MHE or overt clinical hepatic encephalopathy. A battery of neuropsychological tests and event related potentials (ERPs) were used. Moreover, an additional n-back task was administered with two difficulty levels (1- and 2-back). This task was designed to engage cognitive processes of storage and manipulation of information in working memory. The participants have to decide whether the letter shown was the same as a target (congruence condition). No significant differences were found in the performance of either the neuropsychological tests or the n-back task. However, the expected effects of decreased performance as well as a decrease in P3 amplitude with difficulty level were identified. The interaction of group x congruence condition was also observed in the P2 component time window. These results may indicate group differences manifesting in early stages of information processing in working memory. It confirms that the patients whose neuropsychological performance is within the normal range can still reveal subtle changes in CNS functioning visible in ERP research. The study confirms the usability of the ERP method in diagnosis of neurocognitive functions in patients with liver cirrhosis, which seems to be more sensitive than neuropsychological tests.

Objective: Animal studies demonstrated that protein malnutrition increases pituitary-adrenorcortical activity and leads to excessive cortisol release. The aim of our study was to determine the association between serum albumin and cortisol level in patients with acute ischemic stroke., Methods: Fifty-nine patients with first-ever ischemic stroke were included. Serum albumin level was measured within 36 h after stroke symptoms onset. Serum cortisol was measured between 36 and 72 h after stroke onset at 6 a.m., 10 a.m., 6 p.m. and 10 p.m., Results: The patients in upper tertile of serum albumin had significantly lower cortisol level measured at 6 a.m. (median with interquartiles: 549.0 [430.4-667.7] nmol/L vs 590.4 [482.8-918.7] nmol/L, P=0.047) and 10 a.m. (402.8 [344.9-510.4] nmol/L vs 634.6 [482.8-827.7] nmol/L, P<0.01) than patients in lower and middle tertiles. On logistic regression analysis adjusted for age and stroke severity, patients in lower and middle tertile of serum albumin had about 7-times higher risk of hypercortisolemia than patients in upper tertile (P<0.01)., Conclusions: Low serum albumin level in patients with ischemic stroke is associated with higher serum cortisol level and predisposes to hypercortisolemia., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Chordomas are rare tumours arising from notochordal remnants. Classical chordomas are generally extradural and, despite benign histopathology, they typically destroy the clivus and surrounding bone structures. Intradural lesions are extremely rare and less than thirty cases of intracranial, exclusively intradural chordomas have been reported so far. The intracranial, intradural but extranotochordal location of chordoma is extremely unique. The authors present a case of chordoma in intracranial location that clinically mimics lateral sphenoid wing meningioma. A previously healthy 39-year-old man was admitted to our Department because of optic disc oedema without neurological deficits. Neuroimaging studies showed a large, contrast-enhanced tumour in the right frontotemporal region that was thought to be a pterional meningioma. The patient underwent successful removal of the tumour. Histopathological study revealed a typical pattern of chordoma, confirmed by immunohistochemical findings. Because of the tumour location the differentiation between chordoma and chordoid meningioma ought to be considered. Such cases, including the present one, may lead to the conclusion that embryonic notochordal remnants may be lost in different places, even away from the neuroaxis.

Cavernous malformations (CMs) occur in approximately 0.5% of the general population and represent 5-10% of the central nervous system vascular malformations. The majority of CMs appear sporadically but genetically determined familial forms account for 10% to 15% of all cases. The aim of this study was to discuss the clinical, pathological and genetic aspects of familial cerebral cavernous malformations (CCMs). We report on five members of a family who underwent surgery due to CCMs. However, only two members were treated in our Department. The age of onset of symptoms in these cases (4 men and 1 women) ranged from 3 to 28 years. Three members of the family were asymptomatic but it turned out that they were obligatory gene carriers and in one of them the cavernous malformation was confirmed by neuroimaging study. The clinical symptoms of CCMs included seizure (three patients) and focal neurological deficit (two patients). Multiple CCMs were identified in two symptomatic patients (two lesions) and in one asymptomatic patient (three lesions). The lesions were located superficially (4), in the basal ganglia (1), in the brainstem (2) and in the cerebellar vermis (1). In two patients, the subsequent imaging studies showed a single de novo CCM formation. Only one patient with mutation of CCM2 gene was treated surgically. In patients with cavernous malformations the detailed clinical and family history of neurological events ought to be collected. This is particular important in patients with multiple changes or with de novo CCMs formation, identified in subsequent imaging studies. A well-documented family history can help to establish the final diagnosis and makes it possible to offer all members of the family proper neurological and genetic care.

Axonal loss is a major component of the pathology of multiple sclerosis (MS) and the morphological basis of permanent clinical disability. It occurs in demyelinating plaques but also in the so-called normal-appearing white matter (NAWM). However, the contribution of Wallerian degeneration to axonal pathology is not known. Here, we analyzed the extent of Wallerian degeneration and axonal pathology in periplaque white matter (PPWM) and lesions in early multiple sclerosis biopsy tissue from 63 MS patients. Wallerian degeneration was visualized using an antibody against the neuropeptide Y receptor Y1 (NPY-Y1R). The number of SMI-32-positive axons with non-phosphorylated neurofilaments was significantly higher in both PPWM and plaques compared to control white matter. APP-positive, acutely damaged axons were found in significantly higher numbers in plaques compared to PPWM. Strikingly, the number of NPY-Y1R-positive axons undergoing Wallerian degeneration was significantly higher in PPWM and plaques than in control WM. NPY-Y1R-positive axons in PPWM were strongly correlated to those in the lesions. Our results show that Wallerian degeneration is a major component of axonal pathology in the periplaque white matter in early MS. It may contribute to radiological changes observed in early MS and most likely plays a major role in the development of disability.

Background: Hyperglycemia on admission increases the risk of death in patients with acute stroke. It remains unclear whether glucose normalisation after admission is associated with improved survival. The goal of the study was to determine the relationship between postadmission glucose levels and mortality in stroke patients with and without admission hyperglycemia., Methods: 302 patients with first-ever ischemic stroke and without prior diagnosis of diabetes mellitus were enrolled. Random plasma glucose level was measured on admission and fasting glucose on day 1, 2, 3, 5 and 7. Hyperglycemia on admission was defined as glucose level > or = 7.8 mmol/L. Postadmission hyperglycemia was diagnosed if mean postadmission fasting glucose level was > or = 6.1 mmol/L., Results: After multivariable adjustment, postadmission hyperglycemia was associated with higher risk of death regardless of admission glucose levels (HR: 1.80, 95%CI: 1.39-2.86, P<0.01). Postadmission hyperglycemia increases risk of death in both patients with admission hyperglycemia (HR: 4.83, 95%CI: 1.93-12.06, P<0.01) and those with admission normoglycemia (HR: 1.64, 95%CI: 1.06-2.54, P=0.03). In patients with admission hyperglycemia glucose normalisation after admission was associated with reduced risk of death compared to those with persistent hyperglycemia (HR: 0.21, 95%CI: 0.08-0.52). The patients who were normoglycemic on day 1 and developed hyperglycemia on next days had increased risk of death compared to persistent normoglycemic patients (HR: 1.55, 95%CI: 1.01-2.39, P=0.04)., Conclusions: Postadmission, but not admission, hyperglycemia is associated with increased risk of death. Glucose normalisation after admission is associated with better survival., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)

Objective: Glioma cells can produce anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta) which inhibit T cell and monocyte function. It is unknown if production of these cytokines is limited to the site of tumor or these molecules are also released to cerebrospinal fluid and blood. The goal of our study was to determine if patients with astrocytoma have increased levels of IL-10 and TGF-beta 2 in cerebrospinal fluid (CSF) and serum., Methods: CSF and serum samples were taken from 16 patients with astrocytoma of grade III or grade IV according to the WHO classification and from 28 age- and gender-matched controls (patients with normal pressure hydrocephalus or with lumbar disk herniation). Cytokine concentrations were measured using ELISA methods., Results and Discussion: There was no difference in serum levels of IL-10 and TGF-beta 2 between groups. Patients with astrocytoma had decreased levels of IL-10 (0.9 +/- 1.2 versus 3.5 +/- 9.2 pg/ml, p=0.01) and TGF-beta 2 (0.0 +/- 0.0 versus 5.4 +/- 9.4 pg/ml, p=0.05) in CSF compared to controls. Because serum IL-10 and TGF-beta 2 levels are similar in patients with astrocytoma and in controls, these cytokines are probably not directly involved in peripheral monocyte and T cell deactivation.

Acute cerebral ischemia triggers interleukin-6 (IL-6) release into cerebrospinal fluid and blood. IL-6 induces synthesis of the acute phase proteins (APPs) in the liver. Higher blood IL-6 level in stroke patients is associated with larger infarct size, greater neurological deficit on admission, early neurological worsening, and increased risk of death or poor functional outcome. The level of C-reactive protein (CRP), the major APP in man, rises in blood during acute stroke reaching maximal values between 5 and 7 day after stroke onset. Elevated CRP level in acute ischemic stroke predicts unfavorable outcome and is associated with increased risk of recurrent stroke or other cardiovascular events. Increased level of fibrinogen, another APP, is associated with worse outcome in patients with ischemic stroke. The acute phase reaction accompanies also intracerebral hemorrhage. Serum IL-6 and CRP level increases in the first days after intracerebral hemorrhage. Plasma IL-6 is independently associated with hematoma enlargement and fibrinogen level predicts early neurological deterioration and outcome in patients with intracerebral hemorrhage.

Background: Oxidative stress plays an important role in vascular pathology and contributes to the pathophysiology of primary intracerebral hemorrhage (PICH). Glutathione peroxidase 1 (GPX1) is a key enzyme of the antioxidant system. Here, we investigated whether a functional C593T polymorphism of GPX1 gene is associated with PICH in a Polish population., Methods: Genotyping was performed in 192 PICH patients and 197 unrelated controls matched for age and sex. All were of Caucasian origin. The C593T GPX1 polymorphism was investigated using the polymerase chain reaction/restriction fragment length polymorphism method., Results: Multivariable logistic regression analysis revealed a significant association between genotypes containing the T allele and the entire PICH group (OR = 1.53; 95% CI = 1.02-2.29) and lobar PICH (OR = 2.36; 95% CI = 1.31-4.26) but not nonlobar PICH (OR = 1.19; 95% CI = 0.75-1.89)., Conclusions: We found a positive association between the studied GPX1 polymorphism and lobar PICH in a Polish population., ((c) 2008 S. Karger AG, Basel.)

Background and Purpose: Previous epidemiological studies of stroke in Poland completed more than 10 years ago reported moderate incidence rates but very high case fatality rates due to stroke. We used the data of the Krakow Stroke Registry to calculate the attack rates as well as short- and long-term case fatality rates from stroke in hospitalized inhabitants of Krakow, Poland., Material and Methods: We prospectively recorded all cases of stroke (defined according to the ICD-10) in adult permanent residents of Krakow, who were admitted to hospitals in that city. The registration took one year (between 1 July 1999 and 30 June 2000). The vital status of participants was established on days 30, 90 and 180 and at one year after their stroke., Results: 1096 strokes occurred in a population of 589,820. Attack rate standardized for the European population was 180.0 per 100,000 (218.3 in men and 151.9 in women). Ischaemic stroke was diagnosed in 532 (48.6%), stroke not specified as haemorrhagic or ischaemic in 406 subjects (37.0%), intracerebral haemorrhage in 86 (7.8%), and subarachnoid haemorrhage in 72 (6.6%). The 30-day, 90-day, 180-day and one-year case fatality rates for all strokes were 17.8%, 28.1%, 30.8% and 39.7%, respectively. Case fatality rates for ischaemic stroke were 9.8%, 19.0%, 21.6% and 31.2%, respectively and for intracerebral haemorrhage 44.2%, 55.8%, 55.8% and 60.5%, respectively., Conclusions: The attack rates of stroke in urban areas of Poland are similar to the average European rates. Short- and long-term case fatality rates are much lower than previously reported.

The angiotensin-converting enzyme (ACE) catalyzes the formation of angiotensin II and the breakdown of bradykinin into inactive products. The insertion/deletion (I/D) polymorphism affects the activity of the enzyme, with the DD genotype being responsible for the highest activity of the enzyme. Meta-analysis of 11 studies including white persons showed that the DD genotype was a risk factor for ischemic stroke. No such correlation was found in an Asian population. Studies on different etiologies or intermediate phenotypes of ischemic stroke did not bring univocal results. There are still no convincing data on whether the I/D polymorphism of the ACE gene is a risk factor for spontaneous intracerebral hemorrhage and intracranial aneurysms, ruptured or unruptured. Several pharmacogenetic studies analyzed the influence of the ACE I/D polymorphism on the response to acute stroke therapy (thrombolysis) or prevention strategies (lifestyle modification and treatment of vascular risk factors). Presently, however, there is no consensus on whether the efficacy of these therapies is affected by the ACE gene I/D polymorphism.

Objectives: Beta-blockers reduce mortality in patients after myocardial infarction. Experimental studies suggest that beta-blockers have also neuroprotective properties. The aim of this study was to assess if use of beta-blockers is associated with reduced risk of early death in ischemic stroke patients., Materials and Methods: Retrospective data analysis of 841 consecutive patients with acute ischemic stroke admitted to the stroke unit within 24 h after stroke onset., Results: 10.6% of patients received beta-blockers during hospitalization. Thirty-day case fatality was significantly lower in patients treated with beta-blockers than in those not treated with beta-blockers (6.8% versus 19.0%, P < 0.01). After adjustment for other prognostic factors, the use of beta-blockers was associated with reduced risk of early death (relative hazard 0.37, 95% confidence interval 0.16-0.84) independently of age, stroke severity, fasting glucose, total cholesterol level and pneumonia. When patients who died of cardiovascular causes were excluded from the analysis, the use of beta-blocker was no longer significantly associated with risk of death (P = 0.12)., Conclusion: In a retrospective series the use of beta-blockers was associated with reduced risk of early death in patients with ischemic stroke.

Background: Oxidative stress plays a role in atherosclerosis. Human paraoxonase (PON) gene products exhibit antioxidant properties. We studied the significance of the Q192R and M55L polymorphisms of the PON1 gene and the C311S polymorphism of the PON2 gene in different etiologies of ischemic stroke., Methods: One hundred and thirty-six patients with large vessel disease (LVD) stroke, 140 with small vessel disease stroke, 272 with cardioembolic stroke, and their age- and sex-matched controls were included. PON genotypes were evaluated by PCR-RFLP analyses., Results: The distribution of PON1 polymorphisms was similar in each stroke group and in the respective controls. Genotypes with the C allele of the PON2 gene C311S polymorphism were overrepresented in LVD stroke patients as compared with their controls, both in univariate and multivariate (dominant model: OR = 1.58, 95% CI: 1.006-2.48) analyses., Conclusion: The genotype with the C allele of the PON2 gene is a risk factor for LVD stroke in a Polish population., (Copyright 2007 S. Karger AG, Basel.)

Inflammation plays an important role in the pathogenesis of Alzheimer's disease. This article reviews the results of prospective studies demonstrating that the level of systemic inflammation markers, particularly C-reactive protein and interleukin-6, can predict cognitive decline or dementia. The potential mechanisms linking systemic inflammatory molecules to cognitive decline are also discussed.

Background and Purpose: Increased plasma fibrinogen is a risk factor for vascular diseases related to atherosclerosis. Its long-term predictive value in stroke survivors is not established. We conducted this study to establish the significance of hyperfibrinogenemia as the possible predictor of 30-day and one-year mortality in patients with acute ischemic stroke., Methods: We studied 900 unselected patients with ischemic stroke admitted to the hospital within 24 h after onset of symptoms. We noted demographic data, risk factors for stroke, neurological deficit and disturbances of consciousness on admission. We measured plasma concentration of fibrinogen and the body temperature on day 1 and registered vital status at 1, 3, 6 and 12 months after stroke., Results: Mean concentration of plasma fibrinogen was 2.9 g/L and 25.2% of patients had increased plasma concentration of fibrinogen (i.e. > or = 3.5 g/L) on day 1. Patients with hyperfibrinogenemia were more likely to die after 1, 3, 6 and 12 months than those with normal plasma fibrinogen (21.1% vs. 15.6%, 36.4% vs. 24.6%, 42.6% vs. 27.3%, 45.7% vs. 31.2%, respectively; P < 0.001 for the last three differences). Hyperfibrinogenemia did not predict short-term case-fatality, but increased concentration of plasma fibrinogen was an independent predictor of one-year case-fatality (P = 0.013; OR: 1.69 (95% CI 1.12-2.55)). Other independent predictors of one-year case-fatality were: neurological deficit on admission, age, white blood cell count, and body temperature on day 1., Conclusions: Increased concentration of plasma fibrinogen shortly after ischemic stroke independently increases risk of death within one year after stroke.

Background: To prevent the recurrence of primary intracerebral hemorrhage (PIH) it is important to identify patients with underlying structural vascular abnormalities (VA). According to previous study data-- the site of hemorrhage, the patient's age and pre-existing hypertension affect the likelihood of finding VA. However, the indications for angiography, the gold standard for the diagnosis of VA, still remain controversial., Purpose: To assess the frequency of VA and to determine features that might increase the probability of finding VA in patients with PIH., Material and Methods: 100 patients with PIH, without a history of trauma, coagulopathy, or known pre-existing brain abnormality, who were admitted to the Stroke Unit of the Department of Neurology, Jagiellonian University, between January 1999 and November 2000 entered this prospectively designed study. In the group of 96 patients, 53 persons underwent conventional angiography within 14 days of stroke onset (in 4 cases we found bleeding into the tumor and these patients were not included in further analysis)., Results: Vascular abnormalities were found in 14 of 53 patients (26.4%); ruptured aneurysms in 9 patients (17.0%), arteriovenous malformations (AVM) in 3 patients (5.7%), venous angioma in 1 patient (1.8%) and cavernous angioma in 1 patient (1.9%). Vascular malformations were found in 12 of 25 patients with lobar hemorrhage, in 1 of 8 patients with hemorrhage originating in the thalamus and in 1 of 2 patients with hemorrhage originating in the pons. Angiographic findings were negative in 8 patients with hemorrhage in the periventricular white matter, in 8 with hemorrhage originating in the basal ganglia and in 2 patients with hemorrhage in the cerebellum. Patients with VA were significantly younger than patients without VA (49.9 +/- 11.7 years and 58.7 +/- 13.3 years respectively, p = 0.03) and they had a history of hypertension significantly less often (50.0% and 89.7%, p = 0.001). Intraventricular hemorrhage and subarachnoid bleeding occurred in a similar percentage of patients with ICH, independent of whether or not they had VA (28.6% and 38.5%; 21.4% and 10.3% respectively, p = n.s.)., Conclusions: (1) A vascular abnormality is the cause of about 26% of ICH, with a higher likelihood in younger patients and with lobar hemorrhage. (2) A history of hypertension does not exclude the presence of VA. (3) Intraventricular hemorrhage or subarachnoid bleeding does not predict the presence of VA.

Dementia affects up to 30% of stroke survivors 3 months after stroke. The goal of this study was to determine the risk factors of poststroke dementia (PSD) in a cohort of consecutive stroke patients in Poland. A standard stroke evaluation was conducted on admission in 220 consecutive patients with ischemic/hemorrhagic stroke after excluding 30 (12%) patients with prestroke dementia. After 3 months, the survivors completed a comprehensive neuropsychological examination. The DSM-IV definition was used for diagnosis of dementia. Dementia was diagnosed in 44 (22.6%) patients 3 months after stroke. In logistic regression analysis, age (OR 1.08, 95% CI 1.04-1.14, p < 0.001), diabetes mellitus (OR 2.67, 95% CI 1.06-6.57, p = 0.03) and neurological deficit on admission (OR 0.92, 95% CI 0.89-0.96, p < 0.001) were independently associated with PSD in the Polish hospital-based population., (Copyright (c) 2006 S. Karger AG, Basel.)

Background and Purpose: Alpha-1-antichymotrypsin (ACT) is an acute phase protein involved in inflammatory reaction, promoting the assembly of beta amyloid protein into filaments and contributing to its resistance to proteolytic digestion. The aim of our study was to determine ACT signal peptide polymorphism (A/T) as a possible risk factor for post-stroke dementia (PSD)., Methods: 142 consecutive ischemic stroke patients and 188 controls were included in this study. Pre-stroke dementia (PRESD) was evaluated using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). The diagnosis of the post-stroke dementia (PSD) was established according to DSM-IV criteria. The ACT gene (A/T) polymorphism was determined by PCR-RFLR., Results: Both ACT-TT genotype and T-allele were significantly more prevalent in patients with PSD than in non-demented stroke patients, controls or patients with PRESD. After adjustment for age, gender, and vascular risk factors, both the ACT-TT genotype and T-allele remained independently associated with PSD., Conclusion: Our findings suggest that ACT polymorphism (A/T) is a risk factor for PSD.

Object: Data concerning an association between the ENG gene intronic insertion polymorphism and intracrahial aneurysms (IAs) remain inconsistent. In this study the authors investigated whether this polymorphism is associated with a subarachnoid hemorrhage (SAH) caused by a ruptured IA in a Polish population., Methods: One hundred nineteen patients with aneurysmal SAH and 119 sex-matched healthy volunteers were studied. The insertion ENG gene polymorphism in intron 7 was identified using polymerase chain reaction-single-strand chain polymorphism method. The distribution of the insertion allele did not differ between the SAH (13%) and control (16%) cases (p = 0.36). The homozygous insertion/insertion genotype frequencies in these cases were 3.4 and 0.8%, respectively (p = 0.18)., Conclusions: The authors failed to find an association between the intronic insertion polymorphism of the ENG gene and aneurysmal SAH in a Polish population.

Background and Purpose: The member 3 of clade A of serine proteinase inhibitors (SERPINA3), known previously as the alpha1-antichymotrypsin, is an acute phase protein, the levels of which increase in acute and chronic inflammation. The A/T polymorphism of the SERPINA3 gene influences expression of SERPINA3 protein. SERPINA3 can be related to aneurysmal subarachnoid hemorrhage (SAH) by influencing inflammation or by regulating cathepsin G activity. We studied the significance of SERPINA3 A/T polymorphism in patients with aneurysmal SAH compared with healthy controls., Methods: A total of 180 patients with aneurysmal SAH and 263 healthy controls were genotyped for the SERPINA3 A/T polymorphism. Aneurysmal SAH was diagnosed by cranial computed tomography or lumbar puncture and digital subtraction angiography. SERPINA3 polymorphism was detected by polymerase chain reaction amplification and restriction enzyme digestion., Results: The SERPINA3 genotype distribution in patients with aneurysmal SAH (AA-29 16.1%; AT-108 60.0%; TT-43 23.9%) differed significantly from controls (AA-70 26.6%; AT-123 46.8%; TT-70 26.6%; P=0.009). A logistic regression model showed that the presence of genotype with T allele (AT+TT; odds ratio [OR], 2.01; 95% CI, 1.19 to 3.38; P=0.009) or AA genotype (OR, 0.49; 95% CI, 0.30 to 0.84; P=0.009) of the SERPINA3 influences the risk for aneurysmal SAH independently from smoking, excessive alcohol consumption, and hypertension., Conclusions: The A/T polymorphism of SERPINA3 gene is associated with the risk factor for aneurysmal SAH.

Background: Interleukin 1 (IL-1) is a proinflammatory cytokine involved in atherogenesis and thrombosis. The aim of this study was to investigate the association between the IL-1beta gene polymorphism (-511) and the risk of large vessel disease (LVD) stroke, small vessel disease (SVD) stroke and cardioembolic (CE) stroke., Methods: We genotyped 115 patients with LVD stroke and 194 matched controls, 122 patients with SVD stroke and 227 controls and 221 patients with CE stroke and 219 controls. The IL-1beta polymorphism was analyzed by a polymerase chain reaction followed by a restriction enzyme digestion., Results: The allele T distribution did not change significantly between patients with LVD stroke and their controls nor between patients with CE stroke and their controls. The frequency of the T allele was higher in patients with SVD stroke than in the control group (37.7 vs. 30.4%, p = 0.05). After adjustment for vascular risk factor, the TT genotype was an independent risk factor for SVD stroke (OR: 2.40, 95% CI: 1.17-4.94)., Conclusions: The TT genotype of the IL-1beta gene may be associated with an increased risk of SVD stroke., (Copyright 2005 S. Karger AG, Basel.)

Background and Purpose: Factor (F) XIII is a transglutaminase which stabilizes fibrin clots by forming cross-links between chains of fibrin. A common Val34Leu polymorphism of FXIII is correlated with the level of activated plasma FXIII. The homozygous 34Val genotype may be associated with an increased risk for thrombosis by forming fibrin fibers more resistant to fibrinolysis. The aim of the study was to investigate the association between the FXIII Val34Leu polymorphism and the risk of ischemic stroke due to small vessel disease (SVD) or the risk of primary intracerebral hemorrhage (PICH)., Methods: 66 patients with SVD stroke and 135 age- and sex-matched controls as well as 64 patients with PICH and their 127 controls were included. The FXIII Val34Leu polymorphism was genotyped using the polymerase chain reaction and restriction enzyme digestion methods., Results: The homozygous 34Val genotype was found significantly more often in patients with SVD stroke than in their controls (62 vs. 42%). On multivariate analysis, the Val/Val genotype was associated with an increased risk of SVD stroke (odds ratio: 2.1, 95% confidence interval: 1.1-3.9). The genotype distribution did not differ significantly between PICH patients and their controls (50 vs. 43%)., Conclusion: Our results suggest that the Val/Val genotype of FXIII could be associated with an increased risk of SVD stroke., (Copyright 2005 S. Karger AG, Basel)

Of brain-injured patients admitted to intensive care units, a significant number acquires nosocomial infections. Increased susceptibility to infectious agents could, at least partly, be due to transient immunodepression triggered by brain damage. Immune deficiency in patients with severe brain injury primarily involves T cell dysfunction. However, humoral and phagocytic deficiencies are also detectable. Activation of the hypothalamo-pituitary-adrenal axis and the sympathetic nervous system plays a crucial role in brain-mediated immunodepression. In this review we discuss the role of immunodepression in the development of nosocomial infections and clinical trials on immunomodulation in brain-injured patients with hospital-acquired infections.

Background and Purpose: Evidence exists in support of a role of genetic factors in susceptibility to aneurysmal subarachnoid hemorrhage (SAH) in humans. Meta-analysis of 2 previous studies showed that the I allele of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism was a weak, but significant, risk factor for aneurysmal SAH. Moreover, a recent study has shown that the local renin-angiotensin system (RAS) is involved in the development of intracranial aneurysm. The aim of this study was to investigate the association between ACE I/D polymorphism and a risk for aneurysmal SAH in a Polish population., Methods: Ninety patients with aneurysmal SAH (mean age: 48.9+/-14.0 years) and 128 healthy controls matched for age and sex were genotyped for the ACE I/D polymorphism. Aneurysmal SAH was diagnosed by cranial computed tomography and/or lumbar puncture and digital subtraction angiography. ACE gene polymorphism was detected by polymerase chain reaction amplification of the intron 16-specific I/D fragments, 490-bp and 190-bp, respectively., Results: The ACE genotype distribution in patients with aneurysmal SAH (II, 52.2%; ID, 15.6%; DD, 32.2%) differed significantly from controls (II, 23.4%; ID, 50.8%; DD, 25.8%) (P<0.001). A logistic regression model showed that the II genotype of ACE gene was independent from female sex and smoking as a risk factor for aneurysmal SAH (OR, 4.57; 95% CI, 2.35 to 8.90)., Conclusions: Here we report that II genotype of ACE gene is a risk factor for aneurysmal SAH.

Background and Purpose: Glycoprotein IIIa (GpIIIa) is a platelet membrane receptor for fibrinogen and von Willebrand factor. It plays a key role in platelet aggregation. Previous studies in stroke patients, without analysis based on specific subtypes of stroke cause, have not shown any link between GpIIIa A1/A2 polymorphism and stroke risk. We studied the significance of the GpIIIa gene A1/A2 polymorphism in stroke patients with different stroke causes., Methods: We genotyped 92 patients with stroke caused by large-vessel disease (LVD stroke) and 184 matched controls; 103 patients with stroke caused by small-vessel disease (SVD stroke) and 206 controls; and 182 patients with cardioembolic stroke (CE stroke) and 182 controls (TOAST criteria). The GpIIIa A1/A2 polymorphism was analyzed by polymerase chain reaction followed by restriction enzyme digestion and electrophoresis., Results: The genotype distribution of the GpIIIa gene in patients with LVD stroke (A1/A1, 63%; A1/A2, 34.8%; A2/A2, 2.2%) differed significantly from their controls (A1A1, 79.3%; A1/A2, 20.1%; A2/A2, 0.6%). The distribution of the GpIIIa A1/A2 polymorphism in patients with SVD stroke and CE stroke was similar to that of their controls. In contrast to females with LVD stroke, we found that males with LVD stroke presented with an overrepresentation of at least 1 A2 allele of the GpIIIa gene when compared with their controls (39.7% versus 23.0%; P=0.003). Conditional logistic regression analysis showed that possession of at least 1 A2 allele of the GpIIIa gene was an independent risk factor for LVD stroke in males (OR, 2.51; 95% CI, 1.21 to 5.20)., Conclusions: A2 allele of the GpIIIa gene is an independent risk factor for LVD stroke in males.

Background and Purpose: A previous study showed that low triglyceride concentration predicts higher mortality after stroke. The aim of our study was to determine whether serum triglyceride level is associated with stroke severity on admission., Methods: 863 consecutive patients with acute ischemic stroke were included. Serum triglyceride level was measured within 36 hours after stroke onset. Stroke severity on admission was assessed using Scandinavian Stroke Scale (SSS). The patients were divided into 2 groups: those with severe stroke (SSS < or =25) and those with mild/moderate stroke (SSS >25)., Results: Patients with severe stroke had significantly lower serum triglyceride level than patients with mild/moderate stroke (1.4+/-0.6 versus 1.7+/-1.3 mmol/L). After adjusting for age, sex, atrial fibrillation, diabetes mellitus, obesity, and ischemic heart disease, patients with triglyceride >2.3 mmol/L had lower risk of severe stroke than those with triglyceride < or =2.3 mmol/L (OR: 0.58; 95% CI: 0.35 to 0.95)., Conclusions: Our results suggest that lower level of triglyceride is associated with the more severe stroke.

Background and Purpose: Animal studies showed that human albumin therapy is strongly neuroprotective in focal ischemia. The aim of our study was to determine if relatively high serum albumin level is associated with decreased risk of poor outcome in ischemic stroke patients., Methods: Seven hundred fifty-nine consecutive patients with acute ischemic stroke were included. Functional outcome was measured 3 months after stroke using modified Rankin Scale (mRS). Poor outcome was defined as mRS >3 or death. Serum albumin level was measured within 36 hours after stroke onset., Results: Patients with poor outcome had significantly lower serum albumin level than patients with nonpoor outcome (34.1+/-7.4 versus 36.8+/-6.7 g/L). On logistic regression analysis, serum albumin level remained independent predictor of poor outcome (odds ratio [OR]: 0.43; 95% confidence interval [CI]: 0.26 to 0.70)., Conclusions: Relatively high serum albumin level in acute stroke patients decreases the risk of poor outcome.

Background: Many stroke patients who fulfilled diagnostic criteria for dementia three months after stroke had a mental deterioration before stroke, implying an underlying neurodegenerative process. The goal of this study was to determine the factors associated with pre-stroke dementia in hospitalised-based population., Subjects and Methods: Pre-stroke cognitive decline was evaluated in 250 stroke patients using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Patients with IQCODE score > or=104 were classified as having pre-stroke dementia. Clinical, radiological, and biochemical data of patients with and without pre-stroke dementia were compared., Results: Pre-stroke dementia was found in 12% of 250 stroke patients. Patients with pre-stroke dementia were older, suffered more frequently from ischemic heart disease and diabetes, and had more frequently prior cerebrovascular disease. These patients had significantly more brain atrophy and number of old infarcts on CT than patients without pre-stroke dementia. Serum gamma-globulins levels at admission were significantly higher in patients with pre-stroke dementia. In logistic regression analysis female gender (OR 3.47, CI 95% 1.25-9.64), history of previous stroke (OR 3.46, CI 95 % 1.26-9.51), the number of old infarcts on CT (OR 1.58, CI 95 % 1.08-2.33) and serum gamma-globulins level (OR 1.19, CI 95 % 1.02-1.40) were independently associated with pre-stroke dementia., Conclusions: Female gender and previous ischemic stroke are the most important determinants of pre-stroke cognitive decline.

Background and Purpose: Several studies show a link between microalbuminuria and markers of inflammation. Increased urine albumin excretion accompanies acute ischaemic stroke. The mechanisms responsible for microalbuminuria in acute stroke patients remain unclear. The goal of this study was to determine if there is a relationship between urine albumin excretion and interleukin-6, a key mediator of acute phase reaction., Methods: Nineteen acute ischaemic stroke patients and 13 controls matched for age, sex and cardiovascular risk factors were included. Serum interleukin-6 level was measured on the 2nd day of stroke at 06:00 am, 10:00 am, 06:00 pm and 10:00 pm using ELISA method. Urine albumin excretion was determined using immunonephelometric method., Results: Interleukin-6 level and urine albumin excretion were significantly higher in stroke patients than in controls. There was a significant correlation between interleukin-6 level and urine albumin excretion in stroke patients (R = -0.60 at 06:00 am; R = -0.49 at 10:00 am; R = -0.64 at 06:00 pm; R = -0.54 at 10:00 pm) but not in controls., Conclusions: Urine albumin excretion in acute ischaemic stroke is related to serum interleukin-6.

Cerebral ischemia triggers interleukin-6 (IL-6) release into blood. IL-6 is a key mediator of acute phase reaction. Markers of acute phase reaction (C-reactive protein, fibrinogen, fever) have been linked to poor prognosis in stroke patients. Interleukin-6 soluble receptor (sIL-6R) can potentiate IL-6 pro-inflammatory activity. The aim of this study was to investigate the relationship between IL-6 and sIL-6R in stroke patients. Serum cytokine levels were measured in 18 stroke patients and 13 controls using the ELISA method. On the second day of stroke, IL-6 levels were significantly higher in stroke patients than in controls; sIL-6R levels did not differ significantly between groups. Three months after stroke, IL-6 levels did not differ significantly between groups; sIL-6R levels were significantly decreased in stroke patients when compared with that in controls and with levels in acute phase of stroke. Decreased sIL-6R early after stroke might reflect a regulatory mechanism attenuating inflammatory response.

Altered hypothalamo-pituitary-adrenal axis was reported in stroke patients; however, mechanisms responsible for this phenomenon are barely understood. Acute cerebral ischemia triggers interleukin-6 (IL-6) release into blood. Circulating IL-6 can stimulate hypothalamo-pituitary-adrenal axis. The goal of our study was to assess a relationship between serum IL-6 and cortisol in acute ischemic stroke. Twenty two patients with ischemic stroke and 17 controls were included. Serum samples were collected on the 2nd day of stroke at 6:00, 10:00 18:00, 22:00 h and at the same time points in control group. Cytokines and cortisol levels were measured using ELISA method. Serum IL-6 and cortisol levels were higher in stroke patients than in controls. Cortisol displayed diurnal variations in both stroke patients and controls. In contrast with control subjects, serum IL-6 levels did not display diurnal variations in stroke patients. In stroke patients, but not in controls, IL-6 level correlated significantly with cortisol level and morning serum IL-6 level independently predicted evening/night cortisol level. In conclusion, brain ischemia could stimulate IL-6 release in blood and in this way modulate hypothalamo-pituitary-adrenal axis.

The brain modulates the immune system in an asymmetrical way. Intracerebral hemorrhage triggers IL-6 and IL-10 release into blood. We measured (using ELISA method) serum IL-6 and IL-10 in acute phase of intracerebral hemorrhage in 11 patients with right hemisphere's hematoma and 15 patients with left hemisphere's hematoma. These patients did not differ significantly with respect to their age, size, and location of hematoma. IL-6 level was comparable in patients with left hematoma and patients with right hematoma, but patients with left hematoma had significantly higher level of IL-10 than patients with right hematoma. These results suggest that left and right hemisphere could modulate IL-10 release in different way.

Objectives: Mannitol, a drug widely used to decrease intracranial pressure, can cause renal failure. The goal of this study is to determine the renal safety of mannitol therapy in patients with intraparenchymal hemorrhages., Material and Methods: 51 patients with intracerebral hemorrhages were treated with mannitol according to guideline of American Heart Association. Serum urea and creatinine levels were measured before mannitol administration and on the 2nd, 5th and 14th day., Results: Transient elevation of urea and creatinine concentration was noticed, however, none of patients developed anuria or oliguria., Conclusions: Our study points out safety of mannitol therapy under control of osmolality, although control of urea and creatinine concentrations in special group of patients (persons with history of renal failure or diabetes) should be considered.

Inflammatory mechanisms are involved in the pathogenesis of Alzheimer's disease (AD). It is postulated that cytokine synthesis is altered in AD patients compared with nondemented subjects. Glucocorticoids play an important role in cytokine synthesis. We assessed the release of tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10) and interleukin-12 (IL-12) and its regulation by dexamethasone in AD patients in vitro. Cytokine levels were measured using the ELISA method in unstimulated, LPS-stimulated or whole-blood samples incubated with LPS and dexamethasone from 18 AD patients and 12 controls. The cytokine levels spontaneously produced by blood cells after incubation with LPS or LPS and dexamethasone did not differ significantly between groups. Dexamathasone inhibited TNF-alpha synthesis by LPS-stimulated blood cells more effectively in AD patients than in controls. These results suggest that cytokine synthesis in AD patients could be regulated by glucocorticoids in a different way than in nondemented subjects., (Copyright 2003 S. Karger AG, Basel)

Background and Purpose: Acute brain insult can cause systemic anti-inflammatory response, including anti-inflammatory cytokine release. The goal of this study was to determine the serum level of interleukin-6, interleukin-10, and interleukin-13 in patients with intracerebral hemorrhage and to correlate cytokine concentrations with stroke severity., Methods: Thirty patients with intraparenchymal hemorrhage and 16 control subjects were included. Serum samples were collected on the second day of hemorrhagic stroke. Cytokine level was measured with the enzyme-linked immunosorbent assay method., Results: Increased serum levels of interleukin-6 and interleukin-10 were detected in stroke patients. Interleukin-6 and interleukin-10 levels were significantly correlated with Glasgow Coma Scale score. In addition, interleukin-6 level correlated with blood volume and mass effect., Conclusions: Intracerebral hemorrhage is associated with systemic release of anti-inflammatory cytokines.

Biliverdin is required for Xenopus laevis embryo dorsal axis formation. When the tetrapyrrole is inactivated by phototransforming it with ultraviolet light prior to the first division, the embryo fails to synthesize dorsal mRNAs, such as goosecoid or chordin, yet forms increased amounts of ventral transcripts, such as Vent 1, and, consequently, develops ventralized morphology. Here we describe the metabolism of biliverdin during oogenesis and early embryogenesis. Estrogen induces frog hepatocytes to synthesize biliverdin and vitelogenin. The two molecules form a complex that is secreted into and transported in the plasma to be taken up by the oocyte as it matures through its six stages of oogenesis. In the oocyte, the biliverdin-vitellogenin complex is processed and stored in the yolk platelets. In these organelles, biliverdin is associated entirely with the lipovitellin domain of the processed vitellogenin. Once the egg is fertilized, its biliverdin content decreases over a 5-6 h period to participate in the chemical machinery required for dorsal axis formation. This participation must be initiated during the period encompassing the first embryonic mitosis. The results describe the pathway that generates, transports, and stores biliverdin as part of oogenesis, define the time course for its utilization after fertilization, and link biliverdin to the metabolism of the phosphoglycolipometalloprotein, vitellogenin.

Hypercortisolemia is thought to be a marker of the stress response following stroke. The aim of this study was to investigate the prevalence and prognostic significance of hypercortisolemia. The circadian variation of cortisol level and the relationship between serum cortisol levels and other stress, inflammatory, and haemostatic markers were also investigated. Seventy consecutive patients with their first ischemic stroke and 24 age- and sex-matched controls were included in the study. Serum cortisol levels (at 6:00 AM, 10:00 AM, 6:00 PM, and 10:00 PM), 24-h urine catecholamine excretion, beta-thromboglobulin levels, and other standard biochemical and haematological parameters were measured on the first day of hospitalisation and in control subjects. Outcome measures used the Barthel Index at Day 30, as well as 30- and 90-day mortality rates. Hypercortisolemia, defined as at least two of the four measurements above the normal range of serum cortisol levels (i.e. >618 nmol/l from the morning samples and >460 nmol/l from the evening samples) was found in 25 (35.7%) of the acute stroke patients and in 3 (12.5%) of the controls (p<0.05). Hypercortisolemia was associated with older age, greater severity of neurological deficit, larger ischemic lesions on CT, and worse prognoses (p<0.05). The study did not find a correlation between serum cortisol levels and other markers of the stress response such as catecholamines excretion and glucose levels. A significant correlation between serum cortisol levels and some markers of the inflammatory response, such as fever, fibrinogen level, white blood cell (WBC) count, and beta-thromboglobulin level, was established in stroke patients. Prognostic significance of hypercortisolemia in acute stroke patients seems to be related to the inflammatory response rather than to the stress response.