Publications by authors named "Cory Toth"

Anthropogenic noise and its effects on acoustic communication have received considerable attention in recent decades. Yet, the natural acoustic environment's influence on communication and its role in shaping acoustic signals remains unclear. We used large-scale playbacks of ocean surf in coastal areas and whitewater river noise in riparian areas to investigate how natural sounds influences song structure in six songbird species.

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Traffic noise is one of the leading causes of reductions in animal abundances near roads. Acoustic masking of conspecific signals and adventitious cues is one mechanism that likely causes animals to abandon loud areas. However, masking effects can be difficult to document in situ and the effects of infrequent noise events may be impractical to study.

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Article Synopsis
  • Human activities are causing new problems for nature, like noise and bright lights, which can confuse and stress animals.
  • Scientists are studying how these “sensory pollutants” affect animals through three main ways: masking (blocking important sounds), distracting (making it hard to focus), and misleading (giving false information).
  • Understanding these effects can help identify areas that need protection and develop ways to reduce harm to animals and their habitats.
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Background: Central neuropathic pain syndromes are a result of central nervous system injury, most commonly related to stroke, traumatic spinal cord injury, or multiple sclerosis. These syndromes are distinctly less common than peripheral neuropathic pain, and less is known regarding the underlying pathophysiology, appropriate pharmacotherapy, and long-term outcomes. The objective of this study was to determine the long-term clinical effectiveness of the management of central neuropathic pain relative to peripheral neuropathic pain at tertiary pain centers.

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Objectives: Several tools have been developed to screen for neuropathic pain. This study examined the sensitivity of the Douleur Neuropathique en 4 Questions (DN4) in screening for various neuropathic pain syndromes.

Materials And Methods: This prospective observational study was conducted in 7 Canadian academic pain centers between April 2008 and December 2011.

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Background: Painful diabetic neuropathy (PDN) is a frequent complication of diabetes mellitus. Current treatment recommendations are based on short-term trials, generally of ≤3 months' duration. Limited data are available on the long-term outcomes of this chronic disease.

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This prospective observational cohort study addressed the long-term clinical effectiveness of the management of chronic neuropathic noncancer pain at 7 Canadian tertiary pain centers. Patients were treated according to standard guidelines and were followed at 3, 6, 12, 18, and 24 months. Standard outcome measures for pain, mood, quality of life, and overall treatment satisfaction were administered, with the primary outcome measure designated as the composite of 30% reduction in average pain intensity and 1-point decrease in the mean Interference Scale Score (0-10) of the Brief Pain Inventory at 12 months relative to baseline.

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Objective: To evaluate the association between opioid dosage and ongoing therapy with physical function and disability in patients with neuropathic pain (NeP).

Design: Secondary analysis of a prospective cohort.

Setting: Multicenter clinical NeP registry.

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Although an association between diabetes mellitus (DM) and cognitive dysfunction has been recognized for a century, it is often not considered as a complication of DM and remains under-recognized. Cognitive dysfunction, usually present as mild cognitive impairment, can occur with either type 1 or type 2 DM. Both forms of DM contribute to accelerated cerebral atrophy and to the presence of heightened white matter abnormalities.

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Objectives: To study the relationship between expected pain and future outcomes along with the moderating effects of expected pain in neuropathic pain patients.

Methods: Study participants were recruited for the Canadian Neuropathic Pain Database. To examine the relationship between expected pain and 6-month pain intensity, pain-related disability, and catastrophizing, multiple regressions were performed.

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Background: Subjects with diabetes mellitus (DM) develop gait dysfunction contributing to falls, reluctance to perform activities and injuries. Neuropathic pain (NeP) related to diabetic peripheral neuropathy (DPN) is associated with increased gait variability that may contribute to gait dysfunction. We used a portable device (GaitMeter™) and related gait and balance measures to measure gait parameters in painful DPN (PDPN) subjects prior to and during analgesia.

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Introduction: The pathophysiology of neuropathic pain (NeP) in diabetic peripheral neuropathy (DPN) is unclear. A potential pathological feature associated with intraepidermal nerve fiber density (IENFD) loss in DPN is axonal swellings.

Methods: We determined the prevalence of intraepidermal axonal swellings in DPN patients with or without NeP and compared the findings with diabetes patients without DPN, patients with idiopathic neuropathy with NeP, and control subjects.

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Used mainly for the management of neuropathic pain, pregabalin is a gabapentinoid or anticonvulsant that was initially developed as an antiepileptic agent. After more than a decade of experience with pregabalin, experience and studies have shown that the adverse effect profile of pregabalin is well tolerated for the management of neuropathic pain and other conditions. Its use is associated with benign central nervous system and systemic adverse effects, and there are very limited metabolic, idiosyncratic or known teratogenic adverse effects.

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Objective: Catastrophizing may be a negative predictor of pain-related outcomes. We evaluated the impact of catastrophizing upon success of first-line pharmacotherapy in the management of neuropathic pain (NeP) due to peripheral polyneuropathy.

Methods: Patients with confirmed NeP with NeP Visual Analog Scale (VAS) pain severity score ≥4 (0-10 scale) completed the Coping Strategies Questionnaire (CSQ) catastrophizing subscale at baseline.

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Introduction: We studied the potential for motor unit number estimation (MUNE) to detect subclinical changes in motor unit numbers in children with type 1 diabetes mellitus (DM).

Methods: Blinded observers performed clinical assessment, electrophysiology, and multipoint MUNE of the extensor digitorum brevis muscle in children with DM for ≥ 5 years and age-matched healthy controls.

Results: For 51 DM subjects, the disease duration was 9.

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Background: The pathophysiology of diabetic peripheral neuropathy (DPN) is complex and uncertain. A potential comorbidity in diabetes mellitus (DM) that may contribute to greater severity of DPN is a lipid disorder, such as with elevated cholesterol, low density lipoproteins or triglycerides. Oxidized low density lipoprotein (oxLDL) is a form of cholesterol that exerts direct toxic effects and contributes to pathogenicity through ligating a receptor called lectin-like receptor (LOX-1).

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Schwann cells (SCs) are integral to peripheral nerve biology, contributing to saltatory conduction along axons, nerve and axon development, and axonal regeneration. SCs also provide a microenvironment favoring neural regeneration partially due to production of several neurotrophic factors. Dysfunction of SCs may also play an important role in the pathogenesis of peripheral nerve diseases such as diabetic peripheral neuropathy where hyperglycemia is often considered pathogenic.

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Background: The receptor for advanced glycation end-products (RAGE) is implicated in neuronal differentiation during embryogenesis and in regulation of peripheral nerve regeneration. However, the role of RAGE ligands and the signaling pathways utilized by activated RAGE in mediating axon regeneration in adult neurons remain unknown. We tested the hypothesis that RAGE signaling modulated neurotrophin-induced neurite outgrowth in cultured adult sensory neurons.

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We determined prospectively the clinical and electrophysiological progression of idiopathic, diabetic, paraproteinemic, alcoholic, and B12 deficiency neuropathy in 606 subjects over 3 years. We hypothesized that idiopathic peripheral neuropathy would demonstrate slower progression when compared with other etiologies. Laboratory assessments were used to determine the etiology of peripheral neuropathy at baseline and after 3 years.

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Aim: To analyze a large population of patients with diabetes and peripheral neuropathy (PN) to determine other meaningful comorbid etiologies for PN.

Methods: Peripheral Neuropathy is a common complication of type 1 and 2 diabetes mellitus; however, other potential causes for PN may be co-existing in patients with diabetes. A prospective cohort study was performed to assess patients with diabetes and PN.

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Type 2 diabetes (DM) is the most common cause of peripheral neuropathy in the Western world. A comorbidity, hypertension, has been speculated to contribute to initiation or worsening of diabetic peripheral neuropathy. We studied adult rat models using genetic strains with DM (Zucker Diabetic Fat rats)±hypertension (HTN (ZSF-1 rats)) to investigate the relative contributions of DM and HTN and the potential for additive effects of HTN upon existing DM for the development of peripheral neuropathy.

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Objectives: This study used a randomized withdrawal design to evaluate the efficacy of pregabalin versus placebo for pain relief in patients with painful diabetic peripheral neuropathy inadequately treated by other therapies.

Methods: A total of 665 patients received pregabalin in a 6-week single-blind phase. Two hundred ninety-four patients who achieved a ≥ 30% pain response were randomized to receive pregabalin or placebo in a double-blind phase for a further 13 weeks.

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