Pub Date : 2017-01-01Epub Date: 2017-03-21DOI: 10.23937/2378-3001/4/1/1066
Stephanie L McManimen, Leonard A Jason
Post-exertional malaise (PEM) is a cardinal symptom of myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS), which often distinguishes patients with this illness from healthy controls or individuals with exclusionary illnesses such as depression. However, occurrence rates for PEM fluctuate from subject to how the symptom is operationalized. One commonly utilized method is exercise testing, maximal or submaximal. Many patients with ME and CFS experience PEM after participating in these tests, and often show abnormal results. However, some patients still exhibit normal results after participating in the exercise testing. This study examined the differences between two patient groups with ME and CFS, those with normal results and those with abnormal results, on several PEM-related symptoms and illness characteristics. The results suggest those that displayed abnormal results following testing have more frequent and severe PEM, worse overall functioning, and are more likely to be bedbound than those that displayed normal results.
{"title":"Differences in ME and CFS Symptomology in Patients with Normal and Abnormal Exercise Test Results.","authors":"Stephanie L McManimen, Leonard A Jason","doi":"10.23937/2378-3001/4/1/1066","DOIUrl":"https://doi.org/10.23937/2378-3001/4/1/1066","url":null,"abstract":"<p><p>Post-exertional malaise (PEM) is a cardinal symptom of myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS), which often distinguishes patients with this illness from healthy controls or individuals with exclusionary illnesses such as depression. However, occurrence rates for PEM fluctuate from subject to how the symptom is operationalized. One commonly utilized method is exercise testing, maximal or submaximal. Many patients with ME and CFS experience PEM after participating in these tests, and often show abnormal results. However, some patients still exhibit normal results after participating in the exercise testing. This study examined the differences between two patient groups with ME and CFS, those with normal results and those with abnormal results, on several PEM-related symptoms and illness characteristics. The results suggest those that displayed abnormal results following testing have more frequent and severe PEM, worse overall functioning, and are more likely to be bedbound than those that displayed normal results.</p>","PeriodicalId":14172,"journal":{"name":"International Journal of Neurology and Neurotherapy","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510614/pdf/nihms873019.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35173709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-09-30DOI: 10.23937/2378-3001/2/2/1032
S. Gruber, Kelly A Sagar, M. Dahlgren, A. Gonenç, Nina Conn, J. Winer, D. Penetar, S. Lukas
Objective Citicoline is an endogenous nucleotide that has historically been used to treat stroke, traumatic brain injury, and cognitive dysfunction. Research has also shown that citicoline treatment is associated with improved cognitive performance in substance-abusing populations. We hypothesized that marijuana (MJ) smokers who received citicoline would demonstrate improvement in cognitive performance as well as increased neural efficiency during tasks of cognitive control relative to those who received placebo. Method The current study tested this hypothesis by examining the effects of citicoline in treatment-seeking chronic MJ smokers. In an 8-week double-blind, placebo-controlled study, 19 MJ smokers were randomly assigned via a double-blind procedure to the citicoline (8 Males, 2 Females) or placebo group (9 Males, 0 Females). All participants completed fMRI scanning at baseline and after 8 weeks of treatment during two cognitive measures of inhibitory processing, the Multi Source Interference Test (MSIT) and Stroop Color Word Test, and also completed the Barratt Impulsiveness Scale (BIS-11), a self-report measure of impulsivity. Results Following the 8 week trial, MJ smokers treated with citicoline demonstrated significantly lower levels of behavioral impulsivity, improved task accuracy on both the MSIT and Stroop tasks, and exhibited significantly different patterns of brain activation relative to baseline levels and relative to those who received placebo. Conclusions Findings suggest that citicoline may facilitate the treatment of MJ use disorders by improving the cognitive skills necessary to fully engage in comprehensive treatment programs.
{"title":"Citicoline Treatment Improves Measures of Impulsivity and Task Performance in Chronic Marijuana Smokers: A Pilot BOLD fMRI Study","authors":"S. Gruber, Kelly A Sagar, M. Dahlgren, A. Gonenç, Nina Conn, J. Winer, D. Penetar, S. Lukas","doi":"10.23937/2378-3001/2/2/1032","DOIUrl":"https://doi.org/10.23937/2378-3001/2/2/1032","url":null,"abstract":"Objective Citicoline is an endogenous nucleotide that has historically been used to treat stroke, traumatic brain injury, and cognitive dysfunction. Research has also shown that citicoline treatment is associated with improved cognitive performance in substance-abusing populations. We hypothesized that marijuana (MJ) smokers who received citicoline would demonstrate improvement in cognitive performance as well as increased neural efficiency during tasks of cognitive control relative to those who received placebo. Method The current study tested this hypothesis by examining the effects of citicoline in treatment-seeking chronic MJ smokers. In an 8-week double-blind, placebo-controlled study, 19 MJ smokers were randomly assigned via a double-blind procedure to the citicoline (8 Males, 2 Females) or placebo group (9 Males, 0 Females). All participants completed fMRI scanning at baseline and after 8 weeks of treatment during two cognitive measures of inhibitory processing, the Multi Source Interference Test (MSIT) and Stroop Color Word Test, and also completed the Barratt Impulsiveness Scale (BIS-11), a self-report measure of impulsivity. Results Following the 8 week trial, MJ smokers treated with citicoline demonstrated significantly lower levels of behavioral impulsivity, improved task accuracy on both the MSIT and Stroop tasks, and exhibited significantly different patterns of brain activation relative to baseline levels and relative to those who received placebo. Conclusions Findings suggest that citicoline may facilitate the treatment of MJ use disorders by improving the cognitive skills necessary to fully engage in comprehensive treatment programs.","PeriodicalId":14172,"journal":{"name":"International Journal of Neurology and Neurotherapy","volume":"36 1","pages":"1 - 8"},"PeriodicalIF":0.0,"publicationDate":"2015-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90526066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-08-28DOI: 10.23937/2378-3001/2/2/1031
T. Rohn
The presence of corpora amylacea (CA) in the CNS is associated with both normal aging and neurodegenerative conditions including Alzheimer’s disease (AD) and vascular dementia (VaD). CA are spherical bodies ranging in diameter (10–50 μm) and whose origin has been documented to be derived from both neural and glial sources. CA are reported to be primarily composed of glucose polymers, but approximately 4% of the total weight of CA is consistently composed of protein. CA are typically localized in the subpial, periventricular and perivascular regions within the CNS. The presence of CA in VaD has recently been documented and of interest was the localization of CA within the hippocampus proper. Despite numerous efforts, the precise role of CA in normal aging or disease is not known. The purpose of this mini review is to highlight the potential function of CA in various neurodegenerative disorders with an emphasis on the potential role if any these structures may play in the etiology of these diseases.
{"title":"Corpora Amylacea in Neurodegenerative Diseases: Cause or Effect?","authors":"T. Rohn","doi":"10.23937/2378-3001/2/2/1031","DOIUrl":"https://doi.org/10.23937/2378-3001/2/2/1031","url":null,"abstract":"The presence of corpora amylacea (CA) in the CNS is associated with both normal aging and neurodegenerative conditions including Alzheimer’s disease (AD) and vascular dementia (VaD). CA are spherical bodies ranging in diameter (10–50 μm) and whose origin has been documented to be derived from both neural and glial sources. CA are reported to be primarily composed of glucose polymers, but approximately 4% of the total weight of CA is consistently composed of protein. CA are typically localized in the subpial, periventricular and perivascular regions within the CNS. The presence of CA in VaD has recently been documented and of interest was the localization of CA within the hippocampus proper. Despite numerous efforts, the precise role of CA in normal aging or disease is not known. The purpose of this mini review is to highlight the potential function of CA in various neurodegenerative disorders with an emphasis on the potential role if any these structures may play in the etiology of these diseases.","PeriodicalId":14172,"journal":{"name":"International Journal of Neurology and Neurotherapy","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80072619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-01-15DOI: 10.23937/2378-3001/2/1/1014
Troy T Rohn
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by an array of symptoms affecting memory and cognition. Some common symptoms of AD include memory loss that disrupts daily life, challenges in planning or solving problems, confusion with time or place, and changes in mood and personality [1]. Central dogma to the etiology of AD is the beta-amyloid cascade, which stipulates that beta-amyloid in oligomeric forms represents the earliest step in a cascade eventually leading to the formation of senile plaques and neurofibrillary tangles (NFTs) and neurodegeneration [2]. For many years the connection between plaques and tangles was unknown, however, in 2002 we reported that caspase activation and the cleavage of tau might link these two molecular entities in AD [3]. Our evidence was based on the synthesis and application of a caspase-cleavage site directed antibody to a known caspase-cleavage site within tau located at the amino-terminus (position 25). Figure 1 depicts the first experiment ever performed with affinity-purified tau caspase-cleavage antibody that revealed widespread labeling predominantly within NFTs, neuropil threads, and dystrophic neurites (Figure 1A) that was absent in age-matched control sections (Figure 1B).
{"title":"Caspase Cleaved Tau in Alzheimer's Disease: A Therapeutic Target Realized.","authors":"Troy T Rohn","doi":"10.23937/2378-3001/2/1/1014","DOIUrl":"https://doi.org/10.23937/2378-3001/2/1/1014","url":null,"abstract":"Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by an array of symptoms affecting memory and cognition. Some common symptoms of AD include memory loss that disrupts daily life, challenges in planning or solving problems, confusion with time or place, and changes in mood and personality [1]. Central dogma to the etiology of AD is the beta-amyloid cascade, which stipulates that beta-amyloid in oligomeric forms represents the earliest step in a cascade eventually leading to the formation of senile plaques and neurofibrillary tangles (NFTs) and neurodegeneration [2]. For many years the connection between plaques and tangles was unknown, however, in 2002 we reported that caspase activation and the cleavage of tau might link these two molecular entities in AD [3]. Our evidence was based on the synthesis and application of a caspase-cleavage site directed antibody to a known caspase-cleavage site within tau located at the amino-terminus (position 25). Figure 1 depicts the first experiment ever performed with affinity-purified tau caspase-cleavage antibody that revealed widespread labeling predominantly within NFTs, neuropil threads, and dystrophic neurites (Figure 1A) that was absent in age-matched control sections (Figure 1B).","PeriodicalId":14172,"journal":{"name":"International Journal of Neurology and Neurotherapy","volume":"2 1","pages":"014"},"PeriodicalIF":0.0,"publicationDate":"2015-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4308811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33348871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1900-01-01DOI: 10.23937/2378-3001/1410109
Robbins Lawrence
{"title":"CGRP Monoclonal Antibodies for Prevention of Migraine: There are Many Adverse Effects","authors":"Robbins Lawrence","doi":"10.23937/2378-3001/1410109","DOIUrl":"https://doi.org/10.23937/2378-3001/1410109","url":null,"abstract":"","PeriodicalId":14172,"journal":{"name":"International Journal of Neurology and Neurotherapy","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89248702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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