Vol 3-2 Mini Review

Neuroimaging in Cerebral Small Vessel Disease

Wolf-Dieter Heiss, MD

1Max Planck Institute for Metabolism Research, Cologne, Germany

The diagnosis of cerebral small vessel disease (SVD) is difficult because there is no consensus on clinical criteria and therefore, imaging is important for diagnosis. Most patients undergo brain imaging by computed tomography (CT), which is able to detect ischemic strokes, hemorrhages and brain atrophy and may also indicate white matter changes. Magnetic resonance imaging (MRI) remains the key neuroimaging modality and is preferred to CT in vascular cognitive impairment (VCI) because it has higher sensitivity and specificity for detecting pathological changes. These modalities for imaging morphology permit to detect vascular lesions traditionally attributed to VCI in subcortical areas of the brain, single infarction or lacunes in strategic areas (thalamus or angular gyrus), or large cortical-subcortical lesions reaching a critical threshold of tissue loss. In SVD multiple punctuate or confluent lesions can be seen in the white matter by MRI and were called leukoaraiosis. Another major neuroimaging finding of small vessel disease in VCI are microhemorrhages. However, while CT and MRI are able to detect morphologic lesions, these modalities cannot determine functional consequences of the underlying pathological changes.

Positron emission tomography (PET) can support the clinical diagnosis by visualizing cerebral functions in typically affected brain regions. In SVD, Fluor-Deoxy-Glucose (FDG)-PET can clearly differentiate scattered areas of focal cortical and subcortical hypometabolism that differ from the typical metabolic pattern seen in Alzheimer Dementia (AD) with marked hypometabolism affecting the association areas. Additional PET tracers can further support the diagnosis of a type of dementia and also yield information on the underlying pathophysiology.

DOI: 10.29245/2572.942X/2018/2.1171 View / Download Pdf
Vol 3-2 Case Report

Yersinia enterocolitica and Chlamydia pneumoniae possible triggering agents of Guillain-Barre syndrome: a case report

Septimiu Tudor Bucurescu

Neurology at Vital-Klinik, Bad Driburg, Germany

In this paper we describe the case of a Guillain-Barré syndrome patient who was diagnosed with an active yersiniosis and past chlamydiosis. We also discuss the diagnosis, therapy and recovery prognosis of patients with Guillain-Barré syndrome.

DOI: 10.29245/2572.942X/2018/2.1156 View / Download Pdf
Vol 3-2 Commentary

Retinal changes in Alzheimer's disease: Disease Mechanisms to Evaluation perspectives.

M Mirzaei1,2,3 *, V B Gupta4, V K Gupta2

1Department of Molecular Sciences, Macquarie University, Sydney, NSW, Australia

2Department of Clinical Medicine, Macquarie University, Sydney, NSW, Australia

3Australian Proteome Analysis Facility, Macquarie University, Sydney, NSW, Australia

4School of Medical Sciences, Edith Cowan University, Joondalup, WA, Australia

DOI: 10.29245/2572.942X/2018/2.1173 View / Download Pdf
Vol 3-2 Commentary

Cognitive Stimulation in Dementia: Time to Go into Detail. A Commentary.

Elke Kalbe1*, Ann-Kristin Folkerts1

1 Medical Psychology | Neuropsychology and Gender Studies & Center for Neuropsychological Diagnostics and Intervention (CeNDI), University Hospital Cologne, Kerpenerstraße 62, 50937 Cologne, Germany

While it is undeniable that cognitive stimulation (CS) is effective in patients with dementia, there is still a lack of understanding of the underlying mechanisms of the effects, and questions like “Who benefits?” or “Which factors determine the benefits?” are not yet answered. Therefore, this commentary gives an overview of different aspects (e.g., sociodemographic factors, disease characteristics, living setting) that need to be considered while doing research on CS to understand their impact on CS effects. It is also necessary to examine the effects of CS in real-life settings (e.g., geriatric hospitals) with mixed samples (e.g., patients with different severity of dementia). Additionally, important factors for future studies on CS in dementia (e.g., reporting according to the CONSORT guidelines, more health-economics studies) are outlined.

DOI: 10.29245/2572.942X/2018/2.1175 View / Download Pdf
Vol 3-2 Research

Adverse effects of Gulf War Illness (GWI) serum on neural cultures and their prevention by healthy serum

Apostolos P. Georgopoulos1,2*, Effie-Photini C. Tsilibary1,2, Eric P. Souto1, Lisa M. James1,2, Brian E. Engdahl1,2, Angeliki Georgopoulos3

1Brain Sciences Center, Department of Veterans Affairs Health Care System, Minneapolis, Minnesota

2Department of Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota

3Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota

Gulf War Illness (GWI) is a chronic debilitating disease of unknown etiology that affects the brain and has afflicted many veterans of the 1990-91 Gulf War (GW). Here we tested the hypothesis that brain damage may be caused by circulating harmful substances to which GW veterans were exposed but which could not be eliminated due to lack of specific immunity. We assessed the effects of serum from GWI patients on function and morphology of brain cultures in vitro, including cultures of embryonic mouse brain and neuroblastoma N2A line. Blood serum from GWI and healthy GW veterans was added, alone and in combination, to the culture and its effects on the function and morphology of the culture assessed. Neural network function was assessed using electrophysiological recordings from multielectrode arrays in mouse brain cultures, whereas morphological assessments (neural growth and cell apoptosis) were done in neuroblastoma cultures. In contrast to healthy serum, the addition of GWI serum disrupted neural network communication and caused reduced cell growth and increased apoptosis. All of these detrimental effects were prevented or ameliorated by the concomitant addition of serum from healthy GW veterans. These findings indicate that GWI serum contains neuropathogenic factors that can be neutralized by healthy serum. We hypothesize that these factors are persistent antigens circulating in GWI blood that can be neutralized, possibly by specific antibodies present in the healthy serum, as proposed earlier1.

DOI: 10.29245/2572.942X/2018/2.1177 View / Download Pdf