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        <title>BMC Neurology - Latest Articles</title>
        <link>http://www.biomedcentral.com/bmcneurol/</link>
        <description>The latest research articles published by BMC Neurology</description>
        <dc:date>2009-07-09T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2377/9/30" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/30">
        <title>Infarction in the territory of the anterior cerebral artery: clinical study of 51 patients </title>
        <description>Background:
Little is known about clinical features and prognosis of patients with ischaemic stroke caused by infarction in the territory of the anterior cerebral artery (ACA). This single centre, retrospective study was conducted with the following objectives: a) to describe the clinical characteristics and short-term outcome of stroke patients with ACA infarction as compared with that of patients with ischaemic stroke due to middle cerebral artery (MCA) and posterior cerebral artery (PCA) infarctions, and b) to identify predictors of ACA stroke.
Methods:
Fifty-one patients with ACA stroke were included in the &quot;Sagrat Cor Hospital of Barcelona Stroke Registry&quot; during a period of 19 years (1986-2004). Data from stroke patients are entered in the stroke registry following a standardized protocol with 161 items regarding demographics, risk factors, clinical features, laboratory and neuroimaging data, complications and outcome. The characteristics of these 51 patients with ACA stroke were compared with those of the 1355 patients with MCA infarctions and 232 patients with PCA infarctions included in the registry.
Results:
Infarctions of the ACA accounted for 1.3% of all cases of stroke (n = 3808) and 1.8% of cerebral infarctions (n = 2704). Stroke subtypes included cardioembolic infarction in 45.1% of patients, atherothrombotic infarction in 29.4%, lacunar infarct in 11.8%, infarct of unknown cause in 11.8% and infarction of unusual aetiology in 2%. In-hospital mortality was 7.8% (n = 4). Only 5 (9.8%) patients were symptom-free at hospital discharge. Speech disturbances (odds ratio [OR] = 0.48) and altered consciousness (OR = 0.31) were independent variables of ACA stroke in comparison with MCA infarction, whereas limb weakness (OR = 9.11), cardioembolism as stroke mechanism (OR = 2.49) and sensory deficit (OR = 0.35) were independent variables associated with ACA stroke in comparison with PCA infarction.
Conclusions:
Cardioembolism is the main cause of brain infarction in the territory of the ACA. Several clinical features are more frequent in stroke patients with ACA infarction than in patients with ischaemic stroke due to infarction in the MCA and PCA territories.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/30</link>
                <dc:creator>Adria Arboix</dc:creator>
                <dc:creator>Luis Garcia-Eroles</dc:creator>
                <dc:creator>Nuria Sellares</dc:creator>
                <dc:creator>Agnes Raga</dc:creator>
                <dc:creator>Montserrat Oliveres</dc:creator>
                <dc:creator>Joan Massons</dc:creator>
                <dc:source>BMC Neurology 2009, 9:30</dc:source>
        <dc:date>2009-07-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-30</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>30</prism:startingPage>
        <prism:publicationDate>2009-07-09T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/29">
        <title>Co-morbidities of vertiginous diseases 
</title>
        <description>Background:
Co-morbidities of vertiginous diseases have so far not been investigated systematically. Thus, it is still unclear whether the different vertigo syndromes (e.g. benign paroxysmal positional vertigo (BPPV), Meniere`s disease, vestibular migraine and phobic vertigo (PPV)) have also different spectrums of co-morbidities.
Methods:
All patients from a cohort of 131 participants were surveyed using a standardised questionnaire about the co-morbidities hypertension, diabetes mellitus, BMI (body mass index), migraine, other headache, and psychiatric diseases in general and the likelihood of a depression in particular.
Results:
We noted hypertension in 29.0% of the cohort, diabetes mellitus in 6.1%, migraine in 8.4%, other headache in 32.1%, psychiatric diseases in 16.0%, overweight and obesity in 33.6% and 13.7% respectively, as well as a clinical indication for depression in 15.9%.
Conclusions:
In general, we did not detect an increased prevalence of the co-morbidities diabetes mellitus, arterial hypertension, migraine, other headache and obesity compared to the general population. There was an increased prevalence of psychiatric co-morbidity in patients with PPV.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/29</link>
                <dc:creator>Jan-Christian Warninghoff</dc:creator>
                <dc:creator>Otmar Bayer</dc:creator>
                <dc:creator>Uta Ferrari</dc:creator>
                <dc:creator>Andreas Straube</dc:creator>
                <dc:source>BMC Neurology 2009, 9:29</dc:source>
        <dc:date>2009-07-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-29</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>29</prism:startingPage>
        <prism:publicationDate>2009-07-07T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/28">
        <title>Clinical impact of B-cell depletion with the anti-CD20 antibody rituximab in chronic fatigue syndrome: a preliminary case series</title>
        <description>Background  Chronic fatigue syndrome (CFS) is a disease of unknown aetiology. A patient with CFS had unexpected, marked recovery of CFS symptoms lasting for five months during and after cytotoxic chemotherapy for Hodgkin&apos;s disease. We reasoned that the transient CFS recovery was related to methotrexate treatment, which induces immunomodulation in part through B-cell depletion.Methods  In a case series, this patient and two additional CFS patients were B-cell depleted by infusion of the monoclonal anti-CD20 antibody rituximab.Results  All three had improvement of all CFS symptoms. Patients 1 and 2 had major amelioration from 6 weeks after intervention, patient 3 slight improvement from the same time, but then improved markedly from 26 weeks after intervention. The symptomatic effect lasted until weeks 16, 18 and 44, respectively. At relapse, all were retreated with a single (patient 1) or double rituximab infusion (patients 2 and 3). Again, all three had marked symptom improvement, mimicking their first response. After new symptom recurrence, patients 1 and 2 were given weekly oral methotrexate, patient 1 having effect also from this agent. Patients 1 and 2 were again treated for a third rituximab infusion after new relapse, again with a marked clinical benefit. No unexpected toxicity was seen.Conclusion  These observations suggest that B-lymphocytes are involved in CFS pathogenesis for a subset of patients. Benefit for all CFS symptoms, the delayed symptom relief following B-cell depletion, the kinetics of relapses, and the effect also from methotrexate treatment, provide suggestive evidence that B-cells play a significant role in the ongoing clinical features, and that CFS may be amenable to therapeutic interventions aimed at modifying B-cell number and function. More systematic investigations of this therapeutic strategy, and of its biological basis, are now needed.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/28</link>
                <dc:creator>Oystein Fluge</dc:creator>
                <dc:creator>Olav Mella</dc:creator>
                <dc:source>BMC Neurology 2009, 9:28</dc:source>
        <dc:date>2009-07-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-28</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>28</prism:startingPage>
        <prism:publicationDate>2009-07-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/27">
        <title>SPEM Dysfunction and General Schizotypy as Measured by the SSQ: A Controlled Study </title>
        <description>Background:
SPEM dysfunction is a well-known phenomenon in schizophrenia. The principal aim of the present study was to examine whether SPEM dysfunction is already observable in subjects scoring high on a specific measure of schizotypy (SSQ General Schizotypy) that was selected because of its intimate relationship with schizophrenic prodromal unfolding.
Methods:
Applying ANOVAs, we determined the relationship of subjects&apos; scores on SSQ General Schizotypy and eye movements elicited by targets of different speed. We also examined whether there exists an association between our schizotypy measure and pupil size.
Results:
We found more SPEM dysfunction in subjects scoring high on SSQ General Schizotypy than in subjects scoring average on that factor, irrespective of the speed of the target. No relationship was found between baseline pupil size and General Schizotypy.
Conclusion:
The present study provides additional evidence that SPEM dysfunction is associated with schizotypic features that precede the onset of schizophrenia and is already observable in general population subjects that show these features.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/27</link>
                <dc:creator>Dirk van Kampen</dc:creator>
                <dc:creator>Jan Berend Deijen</dc:creator>
                <dc:source>BMC Neurology 2009, 9:27</dc:source>
        <dc:date>2009-06-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-27</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>27</prism:startingPage>
        <prism:publicationDate>2009-06-29T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/26">
        <title>Role of the H1 haplotype of microtubule-associated protein tau (MAPT) gene in Greek patients with Parkinson&apos;s disease</title>
        <description>Background:
The extended tau haplotype (H1) that covers the entire human microtubule-associated protein tau (MAPT) gene has been implicated in Parkinson&apos;s disease (PD). Nevertheless, controversial results, such as two studies in Greek populations with opposite effects, have been reported. Therefore, we set out to determine whether the H1 haplotype and additional single nucleotide polymorphisms (SNPs) included in H1 are associated with PD in a sample of Greek patients.
Methods:
We analysed MAPT haplotypes in cohorts of 122 patients and 123 controls of Greek origin, respectively. SNP genotyping was performed with Taqman assays and genotyping results were confirmed by sequencing.
Results:
The presence of the H1 haplotype was significantly associated with PD (odds ratio for H1H1 vs. H1H2 and H2H2: 1.566; 95% CI: 1.137-2.157; P = 0.006) and remained so after adjustment for sex. Further analysis of H1 sub-haplotypes with three single nucleotide polymorphisms (rs242562, rs2435207 and rs3785883) demonstrated no significant association with PD.
Conclusion:
Our data support the overall genetic role of MAPT and the H1 haplotype for PD susceptibility in Greek patients. However, the previously supported association of H1 sub-haplotypes with PD could not be confirmed in our study.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/26</link>
                <dc:creator>Nikolaos Refenes</dc:creator>
                <dc:creator>Juliane Bolbrinker</dc:creator>
                <dc:creator>Georgios Tagaris</dc:creator>
                <dc:creator>Antonio Orlacchio</dc:creator>
                <dc:creator>Nikolaos Drakoulis</dc:creator>
                <dc:creator>Reinhold Kreutz</dc:creator>
                <dc:source>BMC Neurology 2009, 9:26</dc:source>
        <dc:date>2009-06-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-26</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>26</prism:startingPage>
        <prism:publicationDate>2009-06-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/25">
        <title>Pontine infarction with pure motor hemiparesis or hemiplegia: A prospective study</title>
        <description>Background:
The study aimed to prospectively observe the clinical and neuroimaging features of pontine infarction with pure motor hemiparesis (PMH) or hemiplegia at early stage.
Methods:
In 118 consecutive selected patients with the first-ever ischemic stroke within 6 hours after onset, fifty of them presented with PMH or hemiplegia and had negative acute computed tomography (CT) scans, then magnetic resonance imaging (MRI) confirmed the corresponding infarcts in pons or cerebrum. The clinical and neuroimaging features of the pontine infarctions were compared with those of cerebral infarctions.
Results:
The pontine infarction with PMH or hemiplegia accounted for 10.2% (12/118) of all first-ever ischemic stroke patients and 24% (12/50) of the patients with both PMH or hemiplegia and acute negative CT scans. Compared to the patients with cerebral infarction, the patients with pontine infarction had more frequency of diabetes mellitus (50.0% vs 5.3%, P = 0.001), nonvertiginous dizziness at onset (58.3% vs 21.1%, P = 0.036) and a progressive course (33.3% vs 2.6%, P = 0.011).
Conclusion:
The pontine infarction may present as PMH or hemiplegia with more frequency of nonvertiginous dizziness, a progressive course and diabetes mellitus. MRI can confirm the infarct location in the basal pons at early stage after stroke onset.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/25</link>
                <dc:creator>Li Ling</dc:creator>
                <dc:creator>Liangfu Zhu</dc:creator>
                <dc:creator>Jinsheng Zeng</dc:creator>
                <dc:creator>Songjie Liao</dc:creator>
                <dc:creator>Suping Zhang</dc:creator>
                <dc:creator>Jian Yu</dc:creator>
                <dc:creator>Zhiyun Yang</dc:creator>
                <dc:source>BMC Neurology 2009, 9:25</dc:source>
        <dc:date>2009-06-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-25</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>25</prism:startingPage>
        <prism:publicationDate>2009-06-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/24">
        <title>Psychosocial Outcomes in StrokE: the POISE observational stroke study protocol</title>
        <description>Background:
Each year, approximately 12,000 Australians of working age survive a stroke. As a group, younger stroke survivors have less physical impairment and lower mortality after stroke compared with older survivors; however, the psychosocial and economic consequences are potentially substantial. Most of these younger stroke survivors have responsibility for generating an income or providing family care and indicate that their primary objective is to return to work. However, effective vocational rehabilitation strategies to increase the proportion of younger stroke survivors able to return to work, and information on the key target areas for those strategies, are currently lacking.Methods/DesignThis multi-centre, three year cohort study will recruit a representative sample of younger (&lt; 65 years) stroke survivors to determine the modifiable predictors of subsequent return to work. Participants will be recruited from the New South Wales Stroke Services (SSNSW) network, the only well established and cohesively operating and managed, network of acute stroke units in Australia. It is based within the Greater Metropolitan area of Sydney including Wollongong and Newcastle, and extends to rural areas including Wagga Wagga. The study registration number is ACTRN12608000459325.DiscussionThe study is designed to identify targets for rehabilitation-, social- and medical-intervention strategies that promote and maintain healthy ageing in people with cardiovascular and mental health conditions, two of the seven Australian national health priority areas. This will rectify the paucity of information internationally around optimal clinical practice and social policy in this area.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/24</link>
                <dc:creator>Maree Hackett</dc:creator>
                <dc:creator>Nick Glozier</dc:creator>
                <dc:creator>Stephen Jan</dc:creator>
                <dc:creator>Richard Lindley</dc:creator>
                <dc:source>BMC Neurology 2009, 9:24</dc:source>
        <dc:date>2009-06-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-24</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>24</prism:startingPage>
        <prism:publicationDate>2009-06-12T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/23">
        <title>Dopamine Agonists and their risk to induce psychotic episodes in Parkinson&apos;s disease: a case-control study</title>
        <description>Background:
Psychosis is rare in untreated patients with Parkinson&apos;s disease (PD) but the prevalence rises to 40% during dopaminergic treatment. So far, no systematic comparison of the psychogenic potential of different dopaminergic drugs had been performed.
Methods:
Eighty PD patients with psychotic episodes were compared to an age-matched control group of PD patients without psychotic episodes (n = 120) in a cross-sectional retrospective study.
Results:
We found a positive correlation between psychotic episodes and dementia, number of concomitant medication, and pergolide intake. Odds ratio calculation confirmed the association with dementia. With respect to dopaminergic treatment, pergolide showed the highest odds ratio, levodopa the lowest. An adjusted logistic regression model confirmed the strong association with psychotic episodes and pergolide and no association with levodopa (adjusted odds ratio 2.01 and 0.11, respectively).
Conclusion:
The analysis indicates that dementia and concomitant medication are factors in PD associated with psychotic symptoms. Furthermore, different dopaminergic drugs showed markedly different associations with psychotic symptoms</description>
        <link>http://www.biomedcentral.com/1471-2377/9/23</link>
                <dc:creator>Daniel Ecker</dc:creator>
                <dc:creator>Alexander Unrath</dc:creator>
                <dc:creator>Jan Kassubek</dc:creator>
                <dc:creator>Michael Sabolek</dc:creator>
                <dc:source>BMC Neurology 2009, 9:23</dc:source>
        <dc:date>2009-06-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-23</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>23</prism:startingPage>
        <prism:publicationDate>2009-06-10T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/22">
        <title>Correlates of degree of nerve involvement in early Bell&apos;s palsy</title>
        <description>Background:
This study aimed to evaluate the still unknown factors correlating with the degree of nerve involvement in early Bell&apos;s palsy.
Methods:
This retrospective chart review study of newly diagnosed cases of Bell&apos;s palsy was conducted over a three-year period. Information on age, sex, day of onset, comorbidities, corticosteroid use, and electroneurographic test results were collected. The electroneurographic quotient (amplitude of compound muscle action potential on the affected side divided by that on the healthy side and expressed in percent) was used as an index of nerve involvement, with lower quotient indicating more severe disease.
Results:
Data were collected on 563 patients. The mean electroneurographic quotient varied inversely with age (p &lt; 0.001) and was higher in patients who used corticosteroids than those who did not (47.1% vs. 40.3%; p = 0.002). There was no correlation between the degree of nerve involvement and sex, season of onset, hypertension, or diabetes.
Conclusion:
The degree of nerve involvement in early Bell&apos;s palsy correlates positively with age and negatively with corticosteroid use.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/22</link>
                <dc:creator>Ru-Lan Hsieh</dc:creator>
                <dc:creator>Chia-Wei Wu</dc:creator>
                <dc:creator>Ling-Yi Wang</dc:creator>
                <dc:creator>Wen-Chung Lee</dc:creator>
                <dc:source>BMC Neurology 2009, 9:22</dc:source>
        <dc:date>2009-06-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-22</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>22</prism:startingPage>
        <prism:publicationDate>2009-06-07T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2377/9/21">
        <title>Markers of cerebral damage during delirium 
in elderly patients with hip fracture
</title>
        <description>Background:
S100B protein and Neuron Specific Enolase (NSE) can increase due to brain cell damage and/or increased permeability of the blood-brain-barrier. Elevation of these proteins has been shown after various neurological diseases with cognitive dysfunction. Delirium is characterized by temporal cognitive deficits and is an important risk factor for dementia. The aim of this study was to compare the level of S100B and NSE of patients before, during and after delirium with patients without delirium and investigate the possible associations with different subtypes of delirium.
Methods:
The study population were patients aged 65 years or more acutely admitted after hip fracture. Delirium was diagnosed by the Confusion Assessment Method and the subtype by Delirium Symptom interview. In maximal four serum samples per patient S100B and NSE levels were determined by electrochemiluminescence immunoassay.
Results:
Of 120 included patients with mean age 83.9 years, 62 experienced delirium. Delirious patients had more frequently pre-existing cognitive impairment (67% vs. 18%, p &lt; 0.001). Comparing the first samples during delirium to samples of non-delirious patients, a difference was observed in S100B (median 0.16 versus 0.10 &#956;g/L, p = &lt; 0.001), but not in NSE (median 11.7 versus 11.7 ng/L, p = 0.97). Delirious state (before, during, after) (p &lt; 0.001), day of blood withdrawal (p &lt; 0.001), pre- or postoperative status (p = 0.001) and type of fracture (p = 0.036) were all associated with S100B level. The highest S100B levels were found &apos;during&apos; delirium. S100B levels &apos;before&apos; and &apos;after&apos; delirium were still higher than those from &apos;non-delirious&apos; patients. No significant difference in S100B (p = 0.43) or NSE levels (p = 0.41) was seen between the hyperactive, hypoactive and mixed subtype of delirium.
Conclusion:
Delirium was associated with increased level of S100B which could indicate cerebral damage either due to delirium or leading to delirium. The possible association between higher levels of S100B during delirium and the higher risk of developing dementia after delirium is an interesting field for future research. More studies are needed to elucidate the role of S100B proteins in the pathophysiological pathway leading to delirium and to investigate its possibility as biomarker for delirium.</description>
        <link>http://www.biomedcentral.com/1471-2377/9/21</link>
                <dc:creator>Barbara van Munster</dc:creator>
                <dc:creator>Catharina Korse</dc:creator>
                <dc:creator>Sophia de Rooij</dc:creator>
                <dc:creator>Johannes Bonfrer</dc:creator>
                <dc:creator>Aeilko Zwinderman</dc:creator>
                <dc:creator>Johanna Korevaar</dc:creator>
                <dc:source>BMC Neurology 2009, 9:21</dc:source>
        <dc:date>2009-05-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2377-9-21</dc:identifier>
        <prism:publicationName>BMC Neurology</prism:publicationName>
        <prism:issn>1471-2377</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>21</prism:startingPage>
        <prism:publicationDate>2009-05-27T00:00:00Z</prism:publicationDate>
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