Neurology International

688 KiB

Open AccessCase Report

Does Intravenous Administration of Recombinant Tissue Plasminogen Activator for Ischemic Stroke can Cause Inferior Myocardial Infarction?

by Mostafa Almasi, Saeed Razmeh, Amir Hassan Habibi and Amir Hassan Rezaee

Neurol. Int. 2016, 8(2), 6617; https://doi.org/10.4081/ni.2016.6617 - 29 Jun 2016

Cited by 5 | Viewed by 321

Abstract

Recombinant tissue plasminogen activator (rTPA) is one of the main portions of acute ischemic stroke management, but unfortunately has some complications. Myocardial infarction (MI) is a hazardous complication of administration of intravenous rTPA that has been reported recently. A 78-year-old lady was admitted for elective coronary artery bypass graft surgery. On the second day of admission, she developed acute left hemiparesis and intravenous rTPA was administered within 120 minutes. Three hours later, she has had chest pain. Rescue percutaneous coronary intervention was performed on right coronary artery due to diagnosis of inferior MI, and the symptoms were resolved. Full article

534 KiB

Open AccessEditorial

Frontotemporal Dementia in Amyotrophic Lateral Sclerosis: From Rarity to Reality?

by Marco Orsini, Ana Carolina Andorinho de Freitas Ferreira, Osvaldo J.M. Nascimento, Jano Alves de Souza, Thaís Nascimento Magalhães, Anna Carolina Damm de Assis, Larissa Kozow Westin, Bruno L. Pessoa, Acary Bulle Oliveira, Rossano Fiorelli, Marcos R.G. de Freitas, Juliana Bittencourt, Stenio Fiorelli, Maria Fernanda Freitas Ferreira Moreira and Pedro Ribeiro

Neurol. Int. 2016, 8(2), 6534; https://doi.org/10.4081/ni.2016.6534 - 29 Jun 2016

Cited by 1 | Viewed by 306

Abstract

^{Amyotrophic lateral sclerosis (ALS) was initially described in 1869 by Jean-Martin Charcot [...]} Full article

531 KiB

Open AccessReview

Neuropathic Pain Treatment: Still a Challenge

by Osvaldo J.M. Nascimento, Bruno L. Pessoa, Marco Orsini, Pedro Ribeiro, Eduardo Davidovich, Camila Pupe, Pedro Moreira Filho, Ricardo Menezes Dornas, Lucas Masiero, Juliana Bittencourt and Victor Hugo Bastos

Neurol. Int. 2016, 8(2), 6322; https://doi.org/10.4081/ni.2016.6322 - 29 Jun 2016

Cited by 17 | Viewed by 509

Abstract

Neuropathic pain (NP) is the result of a series of conditions caused by diseases or lesions to the somatosensory system. Due to the better understanding of NP pathophysiology previously unexplored therapies have been used with encouraging results. In this group, acetyl-L-carnitine, alpha-lipoic-acid, cannabinoids, clonidine, EMA401, botulinum toxin type A and new voltage-gated sodium channel blockers, can be included. Besides, changing paradigms may occur with the advent of optogenetics and a better understanding of epigenetic regulation. We reviewed the published literature on the pharmacological treatment of NP. Despite the interesting results, randomized controlled trials are demanded the majority of the therapies previously mentioned. In spite of several studies for the relief of NP, pain control continues being a challenge. Full article

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Open AccessCase Report

Ataxia and Hypogonadotropic Hypogonadism with Intrafamilial Variability Caused by RNF216 Mutation

by Mohammed Alqwaifly and Saeed Bohlega

Neurol. Int. 2016, 8(2), 6444; https://doi.org/10.4081/ni.2016.6444 - 15 Jun 2016

Cited by 28 | Viewed by 456

Abstract

Gordon Holmes syndrome (GHS) is a distinct phenotype of autosomal recessive cerebellar ataxia, characterized by ataxia, dementia, reproductive defects and hypogonadism; it has been recently found to be associated with RNF216 mutation. We performed whole-exome sequencing and filtered the resulting novel variants by the coordinates of the shared autozygome. We identified a novel splicing variant in RNF216 that is likely to abolish the canonical splice site at the junction of exon/intron 13 (NM_207111.3:c.2061G>A). We herein report two patients with GHS caused by a novel RNF216 mutation as the first follow up report on RNF216-related GHS, and show interfamilial variability of phenotype supporting the previously reported RNF216-related cases. Full article

570 KiB

Open AccessArticle

Diagnostic Value of D-dimer’s Serum Level in Iranian Patients with Cerebral Venous Thrombosis

by Leila Hashami, Vahid Rakhshan, Hoda Karimian and Mehdi Moghaddasi

Neurol. Int. 2016, 8(2), 6310; https://doi.org/10.4081/ni.2016.6310 - 15 Jun 2016

Cited by 2 | Viewed by 518

Abstract

Cerebral venous thrombosis (CVT) is a longterm debilitating vascular brain disease with high morbidity and mortality. It may be associated with rise in D-dimer level. The aim of this study was to examine this potential association and identify the critical D-dimer cut-off level corresponding to increase the risk of CVT. This case-control study was conducted on two groups of patients with and without CVT attending the Rasool Akram Hospital (Iran) during 2014 and 2015. D-dimer levels were measured by the rapid sensitive D-dimer assay. Data were analyzed by Spearman’s correlation coefficient test, independent-samples t-test, backward-selection multiple linear regression and multiple binary logistic regression analyses. Sensitivity-specificity tests were used to detect D-dimer cut-off for CVT. Differences between the D-dimer levels of the case and control groups were significant (P<0.001). It showed that each level of increase in the number of symptoms could increase the risk of thrombosis occurrence for about 3.5 times. All symptom types except for headache were associated with D-dimer level, while headache has negative association with D-dimer level. D-dimer cut-off point for CVT diagnosis was estimated at 350 ng/mg. We concluded that D-dimer serum level significantly rises in CVT patients. A rounded cut-off point of 350 ng/mg can be used as a diagnostic criterion for CVT prediction. Full article

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Neurol. Int., Volume 8, Issue 2 (June 2016) – 5 articles

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