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Accurate etiology diagnosis in patients with stroke and atrial fibrillation: A role for brain natriuretic peptide

Atrial fibrillation (AF) is the leading cause of cardioembolic stroke (CES), and patients with stroke and AF are frequently assumed to have CES. However, strokes presumably due to atherosclerotic pathophysiologies in large or small vessels can also occur in patients with AF. The aims of the present study were to clarify the prevalence of and factors related to a non-cardioembolic etiology in acute stroke patients with AF. from Journal of the Neurological Sciences https://ift.tt/2JRn7wV

Induction of apoptosis in CD4(+) T-cells is linked with optimal treatment response in patients with relapsing-remitting multiple sclerosis treated with Glatiramer acetate

Induction of T-cell apoptosis constitutes a mechanism of action for Glatiramer Acetate (GA). We investigated whether activation of apoptotic T-cell death may be indicative of optimal treatment response in patients with relapsing-remitting Multiple Sclerosis (RRMS), with respect to radiological activity. from Journal of the Neurological Sciences https://ift.tt/2Ud8TdO

A unique Japanese CPEO family with a novel homozygous m.14819 T > G (p. S25A) substitution

Chronic progressive external ophthalmoplegia (CPEO), which is an inherited mitochondrial disease associated with the mutation or deletion of mitochondrial DNA (mtDNA), is induced by nuclear DNA mutations in the DNA polymerase gamma (POLG) gene [1], but is rarely induced by mtDNA mutations. Here we report a unique Japanese CPEO family with a novel homozygous m.14819 T > G (p. S25A) substitution accompanied by an mtDNA deletion (m.8483₋13,459, del 4977), showing bilateral ptosis and muscle weakness in the proband and the proband's mother, but not in the brother. from Journal of the Neurological Sciences https://ift.tt/2JRn3gF

Absence of gut microbiota during early life affects anxiolytic Behaviors and monoamine neurotransmitters system in the hippocampal of mice

The gut microbiome is composed of an enormous number of microorganisms, generally regarded as commensal bacteria. Resident gut bacteria are an important contributor to health and significant evidence suggests that the presence of healthy and diverse gut microbiota is important for normal cognitive and emotional processing. Here we measured the expression of monoamine neurotransmitter-related genes in the hippocampus of germ-free (GF) mice and specific-pathogen-free (SPF) mice to explore the effect of gut microbiota on hippocampal monoamine functioning. from Journal of the Neurological Sciences https://ift.tt/2JLVFAC

The Sub-Saharan Africa Conference on Stroke (SSACS): An idea whose time has come

Stroke is a leading cause of global morbidity and mortality. Sub-Saharan Africa (SSA), where an unprecedented rise in stroke burden is currently raging, has the highest age-standardized stroke incidence, stroke prevalence, and stroke mortality rates. This is in sharp contrast to the relative decline in stroke incidence in high-income countries over the past four decades through better awareness and control of vascular risk factors. Compared to other groups, Africans tend to have a higher risk of stroke, higher percentage of the hemorrhagic type and much poorer outcomes. from Journal of the Neurological Sciences https://ift.tt/2Ui2Bth

Hyperglycemia induces mechanical hyperalgesia and depolarization of the resting membrane potential of primary nociceptive neurons: Role of ATP-sensitive potassium channels

Cumulating data suggests that ion channel alterations in nociceptive neurons might be involved in the development of diabetic painful neuropathy. In the present study we investigated the involvement of ATP-sensitive potassium (K+ATP) channels in the acute effect of high glucose solution in vitro and in vivo. High glucose concentrations depolarized cultured nociceptive neurons and depolarization was blocked by the K+ATP opener, diazoxide or by insulin. Glucose injection at the rat dorsal root ganglia (L5) resulted in acute mechanical hyperalgesia that was blocked by diazoxide. from Journal of the Neurological Sciences https://ift.tt/2FzghqE

Motor neuron disease as a treatment responsive paraneoplastic neurological syndrome in patient with small cell lung cancer, anti-Hu antibodies and limbic encephalitis

Non-classical paraneoplastic neurological syndrome (PNS) may be identified and classified as “definite” and “probable” according to the antineuronal antibodies status and the presence or absence of an associated cancer [1]. Paraneoplastic motor neuron disease (PMND) is a rare, potentially treatable, non-classical PNS that may be undistinguishable from sporadic motor neuron disease (MND) [2]. from Journal of the Neurological Sciences https://ift.tt/2YwuugK

Differences in the intra-cerebellar connections and graph theoretical measures between Parkinson's disease and multiple system atrophy

Parkinson's disease (PD) does not present with motor symptoms until dopaminergic neuronal loss exceeds 50%. This might indicate that a network-level compensatory mechanism involving surviving regions in PD acts to reduce brain abnormalities. In contrast, there is no evidence of a compensatory mechanism in multiple system atrophy (MSA). We hypothesized that a comparison of these two diseases would help to identify compensatory effects in PD. from Journal of the Neurological Sciences https://ift.tt/2HTcfvO

Muscle at the junction: Where next generation sequencing is sending us

Skeletal muscle membrane stability is dependent on the actions of sodium, calcium, and chloride channels to appropriately gate ion activity. The sodium channel Na v 1.4 in particular has been recognized as having a critical role in the gating of ion current in skeletal muscle. 1 Mutations in Na v 1.4 due to variants in the SCN4A gene result in a variety of phenotypes including hyperkalemic and hypokalemic periodic paralysis, paramyotonia congenita, and congenital myasthenic syndrome with mixed dominant and recessive inheritance. Dominantly inherited disorders such as hypokalemic periodic paralysis result in leaky sodium channels that in turn results in transient episodic weakness that often presents early in childhood. 2 Eventually, many of these patients develop myopathic features including fixed proximal weakness. Dominant mutations in SCN4A that result in increased sodium influx cause hyperkalemic periodic paralysis and paramyotonia congenita phenotypes. 3 In contrast, loss-of-

Does reducing blood pressure and cholesterol provide any HOPE for preventing cognitive decline and dementia?

Dementia is a rapidly increasing global clinical and public health issue in aging populations, and insights from observation and clinical assessment aided by pathology consistently suggest that modifying cardiovascular risk factors may prevent cognitive decline. 1 Such an approach was tested in the third Health Outcomes Prevention Evaluation (HOPE-3) trial, 2 as reported in this issue of Neurology ®, in which an assessment of cognitive outcomes was included in an older subgroup (age ≥70 years) of 12,705 participants who had intermediate cardiovascular risk but had no prior cardiovascular events who were randomized to blood pressure (BP) lowering with a combination of candesartan and hydrochlorothiazide and cholesterol lowering with rosuvastatin. Of the initial 3,086 (24%) participants eligible for the cognitive substudy by age, 2,361 (77%) agreed to participate, and 1,626 (69%) were able to complete a series of tests emphasizing various aspects of cognitive function at baseline and a

High serum neurofilament light chain predicts a worse fate in early parkinsonism

People with motor symptoms, such as involuntary tremor, slowness of movement, and gait difficulty, often first present for evaluation and diagnosis in general neurology offices. Although the first sign in Parkinson disease (PD) at an early stage varies, the diagnosis of PD is often the correct one, simply by taking account of its prevalence. However, confirmation of that diagnosis takes time and serial examinations, and it is increasingly recognized that a fraction of those diagnosed with PD actually have another movement disorder and will therefore have a different neurodegenerative disease at autopsy. 1 In particular, the atypical parkinsonism disorders (APDs), such as multiple system atrophy (MSA), progressive supranuclear palsy, and corticobasal syndrome, as well as vascular parkinsonism, can mimic PD at early stages of the clinical disease. These misdiagnoses are not isolated to the general neurology practice; in fact, when the presentation is unusual or early enough, even moveme

Managing treatment fluctuations in Parkinson disease: "On" again-, "off" again

The first truly effective medical therapy for Parkinson disease (PD), levodopa, was introduced in the 1960s. Patients had to take huge doses of levodopa, with treatment limited by peripheral decarboxylation of levodopa to dopamine by dopa decarboxylase (DDC), resulting in substantial peripheral side effects. 1 Benserazide and carbidopa were developed as dopa decarboxylase inhibitors (DDCIs); because they do not cross the blood-brain barrier, they effectively block the peripheral decarboxylation of levodopa to dopamine. The combination of carbidopa and levodopa (Sinemet; Merck, Whitehouse Station, NJ) was marketed in 1975. This allowed for levodopa dose reduction due to increased (brain) bioavailability and a marked reduction of peripheral side effects. 2 The total daily dose of carbidopa needed to effectively block peripheral decarboxylation of levodopa has been 75 to 100 mg, although some patients require supplemental higher doses of carbidopa (Lodosyn; Aton Pharma, Lawrenceville, N

Teaching neurology: Guided walk in the park or solo free-climb?

In this issue of Neurology ®, Safdieh et al. 1 present an update of the original Neurology Clerkship Core Curriculum previously prepared by a consortium of neurology educators and originally published in this journal in 2002. 2 Safdieh et al. do a comprehensive job by including core concepts fundamental for a required clinical neurology experience. In many ways, this updated iteration of the "essence of a neurology clinical experience" feels like the result of a Darwinian process. Several changes in the structure of clinical neurology experiences, as well as national requirements, have occurred since the original 2002 article, requiring curricula goal and objective updates. For example, in 2014, the Association of American Medical College's annual Graduation Questionnaire began including questions about direct observation of history-taking and physical examination skills in the neurology clerkship, essentially requiring directors to include such components as part of th

Core curriculum guidelines for a required clinical neurology experience

Physicians in most specialties frequently encounter patients with neurologic conditions. For most non-neurologists, postgraduate neurologic education is variable and often limited, so every medical school's curriculum must include clinical learning experiences to ensure that all graduating medical students have the basic knowledge and skills required to care for patients with common neurologic symptoms and neurologic emergencies. In the nearly 20 years that have elapsed since the development of the initial American Academy of Neurology (AAN)–endorsed core curriculum for neurology clerkships, many medical school curricula have evolved to include self-directed learning, shortened foundational coursework, earlier clinical experiences, and increased utilization of longitudinal clerkships. A workgroup of both the Undergraduate Education Subcommittee and Consortium of Neurology Clerkship Directors of the AAN was formed to update the prior curriculum to ensure that the content is current