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Abstract: Prostaglandin D2 synthase (PGDS) is the most abundant brain protein in cerebrospinal fluid (CSF) and is tied closely with inflammatory processes. This study investigated whether CSF PGDS levels in patients with acute inflammatory demyelinating polyneuropathy (AIDP) are altered. The results suggest that PGDS concentration is significantly increased in the CSF of AIDP patients compared with the control patients (p <0.05) due to a blood-CSF barrier dysfunction, whereas the intrathecal synthesis of PGDS, reflected by the CSF PGDS/albumin ratio, is significantly decreased in AIDP compared with the control group (p <0.05). The changes of CSF PGDS/albumin ratio are only observed in AIDP patients, but not in Miller Fisher Syndrome (MFS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), or multiple sclerosis (MS) patients. [Copyright &y& Elsevier]

ABSTRACT Aims Materials and Methods Results Interpretation This study aimed to identify metabolic markers for diabetic peripheral neuropathic pain (DPNP) in patients with type 2 diabetes mellitus (T2DM).Blood metabolite levels in the amino acid, biogenic amine, sphingomyelin, phosphatidylcholine (PC), carnitines, and hexose classes were analyzed in nondiabetic control (n = 27), T2DM without DPNP (n = 58), and T2DM with DPNP (n = 29) using liquid chromatography tandem mass spectrometry. Variable importance projection (VIP) evaluation by partial least squares discriminant analysis was performed on clinical parameters and metabolites.Sixteen variables with VIP > 1.0 (P < 0.05) were identified across all patient groups, and 5 variables were identified to discriminate between the two T2DM groups. DPNP patients showed elevated fasting blood glucose, glutamate, PC aa C36:1, lysoPC a C18:1, and lysoPC a C18:2, while low‐density lipoprotein cholesterol, phenylalanine, and tryptophan were reduced. Glutamate, lysoPC a C18:1, and lysoPC a C18:2 discriminated T2DM with DPNP from those without DPNP with an AUC of 0.671. The AUC was improved to 0.765 when ratios of metabolite pairs were considered.Blood metabolites include glutamate, and phospholipid‐related metabolites implicated in neuropathic pain may have the potential as biomarkers for DPNP. Further investigation is required to understand the mechanism of action of these altered metabolites in DPNP. [ABSTRACT FROM AUTHOR]

Purpose: Guillain-Barre syndrome (GBS) is an immune-mediated disease of the peripheral nerves and could be fatal and has severe neurologic complications. This study herein reports the clinical course of the first patient of GBS after SARS-CoV-2 Oxford/AstraZeneca vaccination in Taiwan., Case Report: A 38-year-old woman who presented with progressive numbness and weakness of both upper and lower limbs over 1 week. Ascending patterns was noted, and bilateral leg were more severe with diffused absence of deep tendon reflex. Clinical examination and investigation findings confirmed with the diagnosis of GBS. Deterioration of muscle power and respiratory failure had developed during the hospitalization. She had no common GBS predisposing history, but she had received her first SARS-CoV-2 Oxford/AstraZeneca vaccination intramuscularly 10 days prior to her symptoms. Clinical symptoms had much improved after double filtration plasmapheresis., Conclusion: Our case is the first case of GBS developed after AstraZeneca vaccine injection in Taiwan, presenting with atypical manifestation of early facial and bulbar involvement. The vaccination associated GBS should be closely monitored as other safety profile, since it may result in respiratory failure and severe neurologic complications. Keyword: Guillain-Barre Syndrome, SARS-CoV-2 Vaccination.

Objective: Family history is a risk factor for stroke. The objective of this study was to investigate whether stroke subtypes and gender might have a familial contribution to stroke., Methods: Detailed family history analysis was used to investigate the parents or siblings of the probands and controls who were classified into 3 groups: probands, outpatient controls, and spouse controls. The lifetime risk (LTR) of stroke was estimated using a Cox proportional hazard model., Results: The 684 probands and controls yielded 1066 parents and 3247 siblings. Compared to the parents and siblings of the controls, those of the stroke patients had a significantly higher LTR. The findings were consistent between probands with cerebral infarction (CI) or cerebral hemorrhage (CH), independent of diabetes, hypertension, and smoking. With regard to gender, family history of stroke was significant for both parents and siblings of the CH or CI patients, but not for the fathers of CI patients and sisters of CH patients. The family history of stroke was associated with an increased risk of stroke of all subtypes, except cardioembolism., Conclusions: This study supported the familial contribution to stroke in the case of both CI and CH but not cardioembolism, independent of the established risk factors for stroke. Gender differences in familial clustering of stroke subtypes were also revealed. These results warrant further molecular genetic studies.

Guillain-Barré Syndrome (GBS) is a rare autoimmune inflammatory polyneuropathy with a high risk of respiratory failure and unclear pathogenesis. Currently, there are no valid biomarkers for diagnosis of GBS. We used 2-DE and MS to analyze the protein profiles of five pairs of cerebrospinal fluid (CSF) samples of the GBS patients and the patient controls. Three proteins (orosomucoid, haptoglobin and apolipoprotein A-IV) were up-regulated, and two proteins (prostaglandin D2 synthase and transthyretin) were down-regulated in the CSF of the GBS patients. The CSF haptoglobin level, quantified by enzyme-linked immunosorbent assay, was significantly higher in the GBS patients (12.44 ± 2.70 μg/mL) compared to the chronic inflammatory demyelinating polyradiculoneuropathy (2.82 ± 0.83 μg/mL), viral meningitis (3.57 ± 0.97 μg/mL) and control patients (1.44 ± 0.35 μg/mL, p<0.05). This study indicated that protein profile analysis using a combination of 2-DE and MS provides an effective strategy for elucidating the pathogenesis and identifying potential CSF biomarkers for GBS. The raised intrathecal synthesis of haptoglobin specifically only in GBS patients, but not in patients with other neurological diseases examined, provides evidence of central nervous system involvement in GBS, and may be used as a potential diagnostic marker for GBS., (Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Inflammatory events may contribute to the pathogenesis of Parkinson's disease (PD). We conducted a case-control study in a cohort of 369 PD cases and another cohort of 326 ethnically matched controls to investigate the association of tumor necrosis factor-alpha (TNF-alpha) promoter single nucleotide polymorphisms (SNPs) with the risk of PD. The overall genotype distribution at T-1031C and C-857T sites showed significant difference between PD cases and controls (P = 0.0062 and 0.0035, respectively). However, only the more frequent -1031 CC genotype was evidently associated with PD (P = 0.0085, odds ratio: 2.96; 95% CI: 1.38-7.09). Pairwise SNP linkage disequilibrium showed -1031 and -863 sites are in strong linkage disequilibrium (D' = 0.93, Delta(2) = 0.80). Pairwise haplotype analysis among the four sites showed that -1031C-863A may act as a risk haplotype among PD cases (P = 0.0028, odds ratio: 2.18; 95% CI: 1.33-3.69)., ((c) 2006 Wiley-Liss, Inc.)

Peripheral neuropathy is usually subtle or subclinical in patients with multiple system atrophy (MSA). A 54-year-old man who initially presented with sensory polyneuropathy developed extrapyramidal and cerebellar signs and autonomic failure typical of MSA 7 years later. Sural nerve biopsy disclosed a prominent loss of large myelinated fibers, whereas the unmyelinated fibers were totally spared. These findings imply that sensory neuropathy can be part of the multiple-site degeneration in MSA, and that predominant involvement of large myelinated fibers of the sensory nerves can be a presenting feature.