Emotietheorieën

Emotietheorieën zien veelal cognitieve of non-cognitieve elementen als essentieel voor emoties. In dit essay wordt, door een commentaar op William James en Jesse Prinz, beargumenteerd dat een theorie over emoties zowel cognitieve als non-cognitieve elementen moet bevatten. Daarnaast wordt aangetoond dat een dergelijke theorie compatibel is met empirisch onderzoek op het gebied van emotie

Guillain-Barré syndrome: a century of progress

In 1916, Guillain, Barré and Strohl reported on two cases of acute flaccid paralysis with high cerebrospinal fluid protein levels and normal cell counts — novel findings that identified the disease we now know as Guillain–Barré syndrome (GBS). 100 years on, we have made great progress with the clinical and pathological characterization of GBS. Early clinicopathological and animal studies indicated that GBS was an immune-mediated demyelinating disorder, and that severe GBS could result in secondary axonal injury; the current treatments of plasma exchange and intravenous immunoglobulin, which were developed in the 1980s, are based on this premise. Subsequent work has, however, shown that primary axonal injury can be the underlying disease. The association of Campylobacter jejuni strains has led to confirmation that anti-ganglioside antibodies are pathogenic and that axonal GBS involves an antibody and complement-mediated disruption of nodes of Ranvier, neuromuscular junctions and other neuronal and glial membranes. Now, ongoing clinical trials of the complement inhibitor eculizumab are the first targeted immunotherapy in GBS

Patients Enrolled in Large Randomized Clinical Trials of Antiplatelet Treatment for Prevention After Transient Ischemic Attack or Ischemic Stroke Are Not Representative of Patients in Clinical Practice: the Netherlands Stroke Survey

Background and Purpose—Many randomized clinical trials have evaluated the benefit of long-term use of antiplatelet drugs in reducing the risk of new vascular events in patients with a recent transient ischemic attack or ischemic stroke. Evidence from these trials forms the basis for national and international guidelines for the management of nearly all such patients in clinical practice. However, abundant and strict enrollment criteria may limit the validity and the applicability of results of randomized clinical trials to clinical practice. We estimated the eligibility for participation in landmark trials of antiplatelet drugs of an unselected group of patients with stroke or transient ischemic attack from a national stroke survey. Methods—Nine hundred seventy-two patients with transient ischemic at

Soluble Beta-Amyloid Precursor Protein Is Related to Disease Progression in Amyotrophic Lateral Sclerosis

Background: Biomarkers of disease progression in amyotrophic lateral sclerosis (ALS) could support the identification of beneficial drugs in clinical trials. We aimed to test whether soluble fragments of beta-amyloid precursor protein (sAPPa and sAPPß) correlated with clinical subtypes of ALS and were of prognostic value. Methodology/Principal Findings: In a cross-sectional study including patients with ALS (N = 68) with clinical follow-up data over 6 months, Parkinson’s disease (PD, N = 20), and age-matched controls (N = 40), cerebrospinal fluid (CSF) levels of sAPPa a, sAPPß and neurofilaments (NfH SMI35) were measured by multiplex assay, Progranulin by ELISA. CSF sAPPa and sAPPß levels were lower in ALS with a rapidly-progressive disease course (p = 0.03, and p = 0.02) and with longer disease duration (p = 0.01 and p = 0.01, respectively). CSF NfH SMI35 was elevated in ALS compared to PD and controls, with highest concentrations found in patients with rapid disease progression (p,0.01). High CSF NfH SMI3 was linked to low CSF sAPPa and sAPPß (p = 0.001, and p = 0.007, respectively). The ratios CSF NfH SMI35 /CSF sAPPa,-ß were elevated in patients with fast progression of disease (p = 0.002 each). CSF Progranulin decreased with ongoing disease (p = 0.04). Conclusions: This study provides new CSF candidate markers associated with progression of disease in ALS. The data suggest that a deficiency of cellular neuroprotective mechanisms (decrease of sAPP) is linked to progressive neuro-axona

Guillain-Barré syndrome without sensory loss (acute motor neuropathy):A subgroup with specific clinical, electrodiagnostic and laboratory features

We analysed data obtained from 27 out of a group of 147 patients with Guillain-Barré syndrome, who did not have sensory loss during a follow-up period of 6 months (motor Guillain-Barré syndrome). These patients had a distinctive clinical pattern compared with the other 120 Guillain-Barré syndrome patients. The clinical course was marked by a more rapid onset of weakness (3.9 versus 6.1 days, P = 0.002), an earlier nadir (6.3 versus 9.1 days, P &lt; 0.001), an initially predominant distal weakness (67% versus 27%, P &lt; 0.001), sparing of the cranial nerves (26% versus 68%, P &lt; 0.001) and the disease was more often preceded by a gastro-intestinal illness (41% versus 13%, P = 0.001) often caused by a Campylobacter jejuni infection (67% versus 28% in the other Guillain-Barré syndrome patients, P &lt; 0.001). High titres of anti-GM1 antibodies were also significantly more common in motor Guillain-Barré syndrome patients (42% versus 5%, P &lt; 0.001). Electromyographic data of the motor Guillain-Barré syndrome patients at nadir revealed little or no evidence for demyelination. Abundant denervation activity was present in half of the patients. The response to immune globulin treatment was good but with plasma exchange significantly fewer motor Guillain-Barré syndrome patients reached the stage of independent locomotion after a follow-up period of 6 months especially if the acute motor neuropathy occurred after a C.jejuni infection.</p