Expression of stromal‐cell‐derived factor‐1 (SDF‐1): a predictor of ischaemic stroke?

Background and purpose: Platelet stromal‐cell‐derived factor‐1 (SDF‐1) plays a pivotal role in angiogenesis and the regeneration of ischaemic tissue through the regulation of haematopoietic progenitor cells and is upregulated at the sites of vascular injury and platelet activation. Thus, SDF‐1 has recently been discussed as a predictor in ischaemic diseases such as acute myocardial infarction. However, no clinical data pertinent to the investigation of the platelet SDF‐1 expression in patients with stroke are available. Methods: We consecutively evaluated 196 patients who were admitted to the stroke unit with symptoms suspected for stroke. Surface expression of the platelet activation markers (P‐selectin and GPIb) and the expression of platelet‐bound SDF‐1 were determined by two‐colour whole blood flow cytometry. Results: Patients with transient ischaemic attack (TIA) as well as with ischaemic stroke showed similar levels of SDF‐1 expression on hospital admission compared with patients with non‐ischaemic (NI) events and with 30 healthy controls (TIA (mean fluorescence intensity ± SD): 31.5 ± 18.2 vs. NI: 26.4 ± 15.7; P = 0.361; stroke: 28.7 ± 19.8 vs. NI; P = 0.943; control: 26.1 ± 11.3; P > 0.05 compared with all). Platelet SDF‐1 expression showed a trend with the severity of stroke according to National Institute of Health Stroke Scale score (r = 0.125; P = 0.085), but significantly correlated with the peak levels of C‐reactive protein (r = 0.218; P = 0.002) and with the levels of platelet activation (P‐selectin: r = 0.389; P = 0.001). Multifactorial analysis of covariance revealed a significant influence on platelet SDF‐1 expression by smoking (P = 0.019). Conclusions: Platelet SDF‐1 surface expression did not show any significant difference in patients with TIA and ischaemic stroke compared with patients with NI events. Thus, single biomarker evaluation of platelet SDF‐1 surface expression is not helpful to predict ischaemic stroke.     

Perception of first‐ and second‐order motion: Separable neurological mechanisms?

An unresolved issue in visual motion perception is how distinct are the processes underlying “first‐order” and “second‐order” motion. The former is defined by spatiotemporal variations of luminance and the latter by spatiotemporal variations in other image attributes, such as contrast or depth. Here we describe two neurological patients with focal unilateral lesions whose contrasting perceptual deficits on psychophysical tasks of “first‐order” and “second‐order” motion are related to the maps of the human brain established by functional neuroimaging and gross anatomical features. We used a relatively fine‐grained neocortical parcellation method applied to high‐resolution MRI scans of the patients' brains to illustrate a subtle, yet highly specific dissociation in the visual motion system in humans. Our results suggest that the two motion systems are mediated by regionally separate mechanisms from an early stage of cortical processing. Hum. Brain Mapping. 7:67–77, 1999. © 1999 Wiley‐Liss, Inc.     

Lack of progression of brain atrophy in Aicardi-Goutières syndrome

Aicardi-Goutières syndrome is a severe and progressive familial encephalopathy that is characterized by acquired microcephaly, intracranial calcification (mainly of the basal ganglia), signs of white matter disease, and chronic lymphocytosis with elevated levels of interferon-alpha in the cerebrospinal fluid in the absence of other evidence of infection. Although the degree of calcification and the severity of brain atrophy are variable, typically the brain lesions appear to progress on successive examinations. In this article a 4-year-old male patient with Aicardi-Goutières syndrome who manifested the typical neurologic signs of the disease was re-evaluated. The evaluation revealed, on successive cranial computed tomography and magnetic resonance imaging scans, increasing calcification with remarkable reduction of brain atrophy. To the best of our knowledge, there is only one previously mentioned study of a 4-year-old female patient with progressive features of Aicardi-Goutières syndrome, including intracranial calcification, who displayed a lack of progression of brain atrophy at MRI scan.     

Olivopontocerebellar atrophy: paraneoplastic syndrome of brain tumour?

We describe a patient who, three years after the onset of an olivopontocerebellar atrophy, developed a right cerebral tumour. The cerebellar symptomatology also included, as in other cerebellar patients previously described, a peripheral dysgraphia. Because this deficit of writing is generally reported in patients with right cerebral lesion, the authors hypothesized that functional alterations of supratentorial structures preceding the tumour by years may be able to damage the neural substrates connecting cerebral and cerebellar structures and to produce cerebellar atrophy.     

What features improve the accuracy of the clinical diagnosis of progressive supranuclear palsy‐parkinsonism (PSP‐P)?

Progressive supranuclear palsy‐parkinsonism (PSP‐P) is a primary tauopathy characterised by neurofibrillary degeneration, which is frequently mistaken for Parkinson's disease (PD), multiple system atrophy (MSA), and vascular parkinsonism (VP) at presentation. The aim of this study was to identify particular clinical features (green flags) that may be helpful in differentiating PSP‐P from these other disorders. We identified 37 patients with PSP‐P from 726 patients archived at the Queen Square Brain Bank. Using a retrospective case notes review the clinical features were compared between the PSP‐P group and Lewy body associated parkinsonism (PD, n = 444 and dementia with Lewy bodies (DLB), n = 46), MSA (n = 90), and VP (n = 19), using the χ²‐test for proportions for a two‐by‐two contingency table. The sensitivity, specificity, and positive predictive values (PPV) and negative predictive values (NPV) were calculated for individual clinical features. A specificity of >0.85 or a PPV of >0.85 were considered reliable discriminators. No clinical features were predictive of PSP‐P, but late drug induced dyskinesias (specificity 0.92, PPV 0.99), late autonomic dysfunction (specificity 0.94, PPV 0.99) and any visual hallucinations (specificity 0.94, PPV 0.99) were better in distinguishing PD and PSP‐P than predicted using operational diagnostic criteria for PD. PSP‐P shares many clinical features with PD and DLB, MSA and VP, but visual hallucinations, drug induced dyskinesias and autonomic dysfunction are very uncommon and may be helpful exclusion criteria. © 2010 Movement Disorder Society