Pub Date : 2015-10-30DOI: 10.4172/2168-975X.1000191
G. D. Griffin
The diagnosis of concussion/mTBI has become a symptom only diagnosis and symptom only treatment injury over the years. This seems an inappropriate course of therapy for this common and worldwide injury. Concussion/mTBI is underestimated by not only the patients sustaining this injury, but the physicians, therapists, trainers, family members and athletes in the chain of evaluation and those self-reporting symptoms, but also every child athlete, parents of those child athletes and their ‘coaches’. The ‘coaches’ may also be parents and have an inappropriate need to see their child athlete succeed at all costs, even to the detriment of the child’s future. This urge to excel at the cost of future health and our young athletes and soldier’s future functionality and potential societal contributions needs to be muted and the right thing done for our future as well. It is fact and simple truth that when the symptoms resolve, there may still be an injured brain that has not healed. The injury is simply not visible, and must be made to be visible. Injury visibility is done by common CT and MRI for most other wounds or injuries, but it is also fact that common CT scan and MRI do NOT make concussion/ mTBI visible. CT and MRI however make other skull injuries visible, such as bleeds, fractures, and brain infrastructure injuries. When the patient with concussion/mTBI is sent back to prior to injury activity based on regular CT or MRI with symptom resolution he/she may still have an injured brain, and when back at ‘usual’ violent or athletic activity may sustain a re-injury of a partially healed prior brain injury, or a new injury on top of the older unhealed injury. This can be devastating to the patient, and doubly so for our children athletes. In concussion/mTBI, normal medical practice and standard of care seems swept aside, and the patient may be sent back to activity before objective proof of brain healing. Those patients with continued symptoms (post-concussive syndrome) are usually kept safely from activity until symptoms are resolved, but again sent to ‘action’ sans objective proof of brain healing.
{"title":"The 'Visible' Injury No One Sees","authors":"G. D. Griffin","doi":"10.4172/2168-975X.1000191","DOIUrl":"https://doi.org/10.4172/2168-975X.1000191","url":null,"abstract":"The diagnosis of concussion/mTBI has become a symptom only diagnosis and symptom only treatment injury over the years. This seems an inappropriate course of therapy for this common and worldwide injury. Concussion/mTBI is underestimated by not only the patients sustaining this injury, but the physicians, therapists, trainers, family members and athletes in the chain of evaluation and those self-reporting symptoms, but also every child athlete, parents of those child athletes and their ‘coaches’. The ‘coaches’ may also be parents and have an inappropriate need to see their child athlete succeed at all costs, even to the detriment of the child’s future. This urge to excel at the cost of future health and our young athletes and soldier’s future functionality and potential societal contributions needs to be muted and the right thing done for our future as well. It is fact and simple truth that when the symptoms resolve, there may still be an injured brain that has not healed. The injury is simply not visible, and must be made to be visible. Injury visibility is done by common CT and MRI for most other wounds or injuries, but it is also fact that common CT scan and MRI do NOT make concussion/ mTBI visible. CT and MRI however make other skull injuries visible, such as bleeds, fractures, and brain infrastructure injuries. When the patient with concussion/mTBI is sent back to prior to injury activity based on regular CT or MRI with symptom resolution he/she may still have an injured brain, and when back at ‘usual’ violent or athletic activity may sustain a re-injury of a partially healed prior brain injury, or a new injury on top of the older unhealed injury. This can be devastating to the patient, and doubly so for our children athletes. In concussion/mTBI, normal medical practice and standard of care seems swept aside, and the patient may be sent back to activity before objective proof of brain healing. Those patients with continued symptoms (post-concussive syndrome) are usually kept safely from activity until symptoms are resolved, but again sent to ‘action’ sans objective proof of brain healing.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78847647","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 : 2015-10-26DOI: 10.4172/2168-975X.1000189
F. Rachid
Background: Nicotine dependence accounts for significant mortality, morbidity, and socioeconomic burdens. Its use remains a significant public health concern since it is among the leading causes of mortality worldwide and is the leading cause of preventable death in developed countries. Despite the availability of approved medications to treat nicotine dependence along with cognitive-behavioral therapy, only 6% of the total number of smokers who report wanting to quit each year are successful in doing so for more than a month along with poor abstinence rates. Among alternative therapeutic approaches, attenuation of cue-elicited craving with neurostimulation techniques is a growing area of attention. Methods: We reviewed the literature on repetitive transcranial magnetic stimulation, intermittent theta-burst stimulation and deep transcranial magnetic stimulation in the treatment of nicotine addiction. Results: Most of these studies found that neurostimulation techniques are safe and effective in the reduction of craving to nicotine as well as in the reduction of cigarette consumption. Conclusions: Given these promising results, future controlled studies with larger samples and optimal stimulus parameters should be designed to confirm these findings.
{"title":"Brain Stimulation Techniques in the Treatment of Nicotine Dependence: A Review of the Literature","authors":"F. Rachid","doi":"10.4172/2168-975X.1000189","DOIUrl":"https://doi.org/10.4172/2168-975X.1000189","url":null,"abstract":"Background: Nicotine dependence accounts for significant mortality, morbidity, and socioeconomic burdens. Its use remains a significant public health concern since it is among the leading causes of mortality worldwide and is the leading cause of preventable death in developed countries. Despite the availability of approved medications to treat nicotine dependence along with cognitive-behavioral therapy, only 6% of the total number of smokers who report wanting to quit each year are successful in doing so for more than a month along with poor abstinence rates. Among alternative therapeutic approaches, attenuation of cue-elicited craving with neurostimulation techniques is a growing area of attention. \u0000Methods: We reviewed the literature on repetitive transcranial magnetic stimulation, intermittent theta-burst stimulation and deep transcranial magnetic stimulation in the treatment of nicotine addiction. \u0000Results: Most of these studies found that neurostimulation techniques are safe and effective in the reduction of craving to nicotine as well as in the reduction of cigarette consumption. \u0000Conclusions: Given these promising results, future controlled studies with larger samples and optimal stimulus parameters should be designed to confirm these findings.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78978542","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 : 2015-10-26DOI: 10.4172/2168-975X.1000190
O. Rubinsten
Developmental dyscalculia (DD) is considered a brain-based disorder usually caused by dysfunction of the parietal cortex. DD has been researched but the current available means of diagnosing and particularly of treating DD are still not clearly defined. The current review discusses the different suggested neurocognitive markers of DD subtypes and links them with suggested grounds for intervention programs.
{"title":"Developmental Dyscalculia: A Cognitive Neuroscience Perspective","authors":"O. Rubinsten","doi":"10.4172/2168-975X.1000190","DOIUrl":"https://doi.org/10.4172/2168-975X.1000190","url":null,"abstract":"Developmental dyscalculia (DD) is considered a brain-based disorder usually caused by dysfunction of the parietal cortex. DD has been researched but the current available means of diagnosing and particularly of treating DD are still not clearly defined. The current review discusses the different suggested neurocognitive markers of DD subtypes and links them with suggested grounds for intervention programs.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89667778","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 : 2015-10-20DOI: 10.4172/2168-975X.1000196
Takahiro Tokumasu, Y. Okajima, O. Takashio, Masayuki Tani, T. Izuno, D. Ikuse, Teppei Morita, Gosuke Arai, Nobuyuki Saga, K. Hori, T. Gokan, H. Matsuda, A. Iwanami
Background: Recently, voxel-based morphometry (VBM) has become a popular tool for the early diagnosis of Alzheimer’s disease (AD). The voxel-based specific regional analysis system for Alzheimer’s disease (VSRAD) is a clinically useful VBM technique that employs magnetic resonance imaging (MRI) to automatically detect the loss of Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation gray matter volume in the medial temporal lobe. Objective: To investigate the utility of VSRAD for differentiating between AD and major depressive disorder (MDD), and to identify the neuropathological differences between the two groups. Methods: The subjects included 18 patients with MDD (mean ± standard deviation: 74.8 ± 7.1 years, 4 males and 14 females) and 31 patients with AD (82.4 ± 7.3 years, 7 males and 24 females). Three-dimensional T1-weighted sagittal images, were acquired using a 1.5Tesla MRI device and analyzed using the VSRAD advance software, parahippocampal atrophy was represented as a Z-score. Neuropsychological tests consisted of the Patient Health Questionnaire 9, Hamilton Rating Scale for Depression, Global Assessment of Function and Mini-Mental State Examination (MMSE). Correlations between the Z-score and the neuropsychological test scores were statistically examined. Results: Patients with AD had significantly higher Z-scores than did patients with MDD (1.99 ± 1.27 vs. 1.11 ± 0.49, p 2 were all diagnosed as AD. In the AD group, the Z-scores were significantly correlated with the MMSE scores throughout the study period (0 weeks: p=0.015, 24 weeks: p=0.024), whereas no significant correlations between the Z-scores and MMSE were observed for the MDD group. Conclusion: Our results obtained using the VSRAD suggest that VSRAD is useful for differentiating between AD and MDD, which is important, as the these two diseases are often difficult to diagnose based solely on their symptoms. Such findings imply that VSRAD may become a useful auxiliary diagnostic tool.
{"title":"Differentiating between Patients with Alzheimer's Disease and Patients with Major Depressive Disorder Using the Voxel-based Specific Regional Aanalysis System for Alzheimer's Disease","authors":"Takahiro Tokumasu, Y. Okajima, O. Takashio, Masayuki Tani, T. Izuno, D. Ikuse, Teppei Morita, Gosuke Arai, Nobuyuki Saga, K. Hori, T. Gokan, H. Matsuda, A. Iwanami","doi":"10.4172/2168-975X.1000196","DOIUrl":"https://doi.org/10.4172/2168-975X.1000196","url":null,"abstract":"Background: Recently, voxel-based morphometry (VBM) has become a popular tool for the early diagnosis of Alzheimer’s disease (AD). The voxel-based specific regional analysis system for Alzheimer’s disease (VSRAD) is a clinically useful VBM technique that employs magnetic resonance imaging (MRI) to automatically detect the loss of Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation gray matter volume in the medial temporal lobe. \u0000Objective: To investigate the utility of VSRAD for differentiating between AD and major depressive disorder (MDD), and to identify the neuropathological differences between the two groups. \u0000Methods: The subjects included 18 patients with MDD (mean ± standard deviation: 74.8 ± 7.1 years, 4 males and 14 females) and 31 patients with AD (82.4 ± 7.3 years, 7 males and 24 females). Three-dimensional T1-weighted sagittal images, were acquired using a 1.5Tesla MRI device and analyzed using the VSRAD advance software, parahippocampal atrophy was represented as a Z-score. Neuropsychological tests consisted of the Patient Health Questionnaire 9, Hamilton Rating Scale for Depression, Global Assessment of Function and Mini-Mental State Examination (MMSE). Correlations between the Z-score and the neuropsychological test scores were statistically examined. \u0000Results: Patients with AD had significantly higher Z-scores than did patients with MDD (1.99 ± 1.27 vs. 1.11 ± 0.49, p 2 were all diagnosed as AD. In the AD group, the Z-scores were significantly correlated with the MMSE scores throughout the study period (0 weeks: p=0.015, 24 weeks: p=0.024), whereas no significant correlations between the Z-scores and MMSE were observed for the MDD group. Conclusion: Our results obtained using the VSRAD suggest that VSRAD is useful for differentiating between AD and MDD, which is important, as the these two diseases are often difficult to diagnose based solely on their symptoms. Such findings imply that VSRAD may become a useful auxiliary diagnostic tool.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79490440","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 : 2015-10-20DOI: 10.4172/2168-975X.1000195
F. Zeiler
Antagonism of the upregulated NMDA receptors has been a focus of recent literature on refractory status epilepticus (RSE) and superrefractory status epilepticus (SRSE), with ketamine at the forefront. Recent systematic review of ketamine use in SE/RSE displayed 23 articles on the subject, with 110 adult and 52 pediatric patients treated with ketamine for refractory seizures [1]. The review documented a 56·5% and 63·5% seizure response (greater than 50% reduction in electrographic seizures) with ketamine administration in adult and pediatric populations respectively. Complications related to ketamine therapy were sparse. The final recommendations by the authors were an Oxford level 4, GRADE C evidence for the use of ketamine in refractory seizures, with further prospective evaluation recommended [1].
{"title":"NMDA Receptor Antagonism in Refractory Status Epilepticus: Right Idea, Wrong Target?","authors":"F. Zeiler","doi":"10.4172/2168-975X.1000195","DOIUrl":"https://doi.org/10.4172/2168-975X.1000195","url":null,"abstract":"Antagonism of the upregulated NMDA receptors has been a focus of recent literature on refractory status epilepticus (RSE) and superrefractory status epilepticus (SRSE), with ketamine at the forefront. Recent systematic review of ketamine use in SE/RSE displayed 23 articles on the subject, with 110 adult and 52 pediatric patients treated with ketamine for refractory seizures [1]. The review documented a 56·5% and 63·5% seizure response (greater than 50% reduction in electrographic seizures) with ketamine administration in adult and pediatric populations respectively. Complications related to ketamine therapy were sparse. The final recommendations by the authors were an Oxford level 4, GRADE C evidence for the use of ketamine in refractory seizures, with further prospective evaluation recommended [1].","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85519807","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 : 2015-10-20DOI: 10.4172/2168-975X.1000197
Tzipi Horowitz-Kraus
Reading is defined as the ability to extract semantically meaningful, verbal information from written language. This is one of the most important cognitive academic abilities and has been found to be related to scores on the American College Test [1]. However, reading is not as intuitive as we may think. The neuroimaging era provides insights into the neural circuits involved in reading, and it appears that this cognitive ability relies not only on neural circuits related to language processing [2,3] but also those related to visual processing [3] and higher-level cognitive abilities, such as executive functions [4,5]. A fascinating orchestra of synchronized activation between the superior temporal gyrus and inferior frontal gyrus (i.e., language processing, see [2] the fusiform gyrus, cuneus and precuneus (i.e., visual processing, see ref. [3]), and the anterior cingulate cortex in particular and the cinguloopercular and fronto-parietal cognitive control networks in general [46] all are needed for fluent reading. Given this involvement of multiple neural circuits and cognitive abilities, it is not surprising that reading difficulties may result from a variety of impairments or an altered activation in any of the aforementioned neural circuits. Alternatively, reading difficulties can result from a lack of synchronization between the activation of these neural circuits (i.e., altered functional connectivity). Children with dyslexia [3] attention deficit hyperactivity disorder (ADHD) [7], psychiatric disorders [8] epilepsy [9] autism [10], or mental retardation [11] all suffer from reading difficulties. However, these types of reading challenges are only the tip of the iceberg, as this is what a teacher notices in the classroom. Neuroimaging data provide us with insight into the underlying causes and pathway “flosses” (the bottom of the iceberg) that are the basis for these reading challenges. Children with dyslexia show an under activation of the fusiform gyrus compared to typical readers during reading [3], but also have decreased functional connectivity between visualand executive functionsrelated regions (fusiform gyrus and anterior cingulate cortex) during reading [12] and the cingulo-opercular cognitive-control network (related to executive functions), even during rest [13]. Conversely, children with both ADHD and dyslexia, who showed much more severe reading difficulties than those with dyslexia alone, demonstrated greater activation in neural circuits related to executive functions (i.e., dorsolateral prefrontal cortex) compared to children with dyslexia during word reading (unpublished data). In the field of psychiatry, children with mood disorders demonstrated more severe reading and phonological-processing difficulties compared to those with behavioral disorders, as well as decreased white-matter diffusivity (fractional anisotropy) in white-matter tracks related to language processing (left arcuate fasciculus, which crosses the frontal a
{"title":"All Roads Lead to Rome? Distinct Neural Circuits in Different Developmental Disorders are Related to Reading Difficulties in Children","authors":"Tzipi Horowitz-Kraus","doi":"10.4172/2168-975X.1000197","DOIUrl":"https://doi.org/10.4172/2168-975X.1000197","url":null,"abstract":"Reading is defined as the ability to extract semantically meaningful, verbal information from written language. This is one of the most important cognitive academic abilities and has been found to be related to scores on the American College Test [1]. However, reading is not as intuitive as we may think. The neuroimaging era provides insights into the neural circuits involved in reading, and it appears that this cognitive ability relies not only on neural circuits related to language processing [2,3] but also those related to visual processing [3] and higher-level cognitive abilities, such as executive functions [4,5]. A fascinating orchestra of synchronized activation between the superior temporal gyrus and inferior frontal gyrus (i.e., language processing, see [2] the fusiform gyrus, cuneus and precuneus (i.e., visual processing, see ref. [3]), and the anterior cingulate cortex in particular and the cinguloopercular and fronto-parietal cognitive control networks in general [46] all are needed for fluent reading. Given this involvement of multiple neural circuits and cognitive abilities, it is not surprising that reading difficulties may result from a variety of impairments or an altered activation in any of the aforementioned neural circuits. Alternatively, reading difficulties can result from a lack of synchronization between the activation of these neural circuits (i.e., altered functional connectivity). Children with dyslexia [3] attention deficit hyperactivity disorder (ADHD) [7], psychiatric disorders [8] epilepsy [9] autism [10], or mental retardation [11] all suffer from reading difficulties. However, these types of reading challenges are only the tip of the iceberg, as this is what a teacher notices in the classroom. Neuroimaging data provide us with insight into the underlying causes and pathway “flosses” (the bottom of the iceberg) that are the basis for these reading challenges. Children with dyslexia show an under activation of the fusiform gyrus compared to typical readers during reading [3], but also have decreased functional connectivity between visualand executive functionsrelated regions (fusiform gyrus and anterior cingulate cortex) during reading [12] and the cingulo-opercular cognitive-control network (related to executive functions), even during rest [13]. Conversely, children with both ADHD and dyslexia, who showed much more severe reading difficulties than those with dyslexia alone, demonstrated greater activation in neural circuits related to executive functions (i.e., dorsolateral prefrontal cortex) compared to children with dyslexia during word reading (unpublished data). In the field of psychiatry, children with mood disorders demonstrated more severe reading and phonological-processing difficulties compared to those with behavioral disorders, as well as decreased white-matter diffusivity (fractional anisotropy) in white-matter tracks related to language processing (left arcuate fasciculus, which crosses the frontal a","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91458543","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 : 2015-10-05DOI: 10.4172/2168-975X.S1.005
Lu ShengYu Lee ShiouLan Chen, YunHsuan Chang
L dose memantine might possess anti-inflammatory and neuroprotective effects mechanistically remote from the NMDA receptor. We investigated whether using valproic acid (VPA) add-on memantine (5 mg/day) to treat bipolar II disorder (BP-II) is more effective than using VPA alone. In this randomized, double-blind, controlled 12 week study, BP-II patients were randomly assigned to a group: VPA+Memantine or VPA+Placebo (Pbo). The Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS) were used to evaluate clinical response, alone with plasma levels of tumor necrosis factor (TNF-α), interleukin 6 (IL-6), IL-8, and IL-1and metabolic profiles during week 0, 1, 2, 4, 8 and 12.After 12 weeks, there was a significant increase of high-density lipoprotein cholesterol (HDL-C) (p<0.009) in the memantine group compared with the Pbo group. The TNF-α were significantly decreased in the memantine group than in the Pbo group (P=0.013).The changes in HDRS score were significantly associated with changes in IL-6 (P=0.012) and IL-1(P=0.005) levels; changes in YMRS score associated with changes with TNF-α(P=0.005) level changes.The association between BDNF Val66Met polymorphism with treatment response was evaluated. After stratified by BDNF Val66Met genotypes, significantly greater decreases in HDRS scores were found in the VPA+memantine group in patients with the Val/Met genotype (p=0.004). We conclude that memantine might benefit treatment of BP-II via decreasing cytokines and increasing HDL-C. The BDNF Val66Met polymorphism influences responses to add-on memantine by decreasing depressive symptoms in BP-II.
{"title":"Anti-inflammation and neuroprotective drugs benefit the treatment of bipolar II disorder patients","authors":"Lu ShengYu Lee ShiouLan Chen, YunHsuan Chang","doi":"10.4172/2168-975X.S1.005","DOIUrl":"https://doi.org/10.4172/2168-975X.S1.005","url":null,"abstract":"L dose memantine might possess anti-inflammatory and neuroprotective effects mechanistically remote from the NMDA receptor. We investigated whether using valproic acid (VPA) add-on memantine (5 mg/day) to treat bipolar II disorder (BP-II) is more effective than using VPA alone. In this randomized, double-blind, controlled 12 week study, BP-II patients were randomly assigned to a group: VPA+Memantine or VPA+Placebo (Pbo). The Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS) were used to evaluate clinical response, alone with plasma levels of tumor necrosis factor (TNF-α), interleukin 6 (IL-6), IL-8, and IL-1and metabolic profiles during week 0, 1, 2, 4, 8 and 12.After 12 weeks, there was a significant increase of high-density lipoprotein cholesterol (HDL-C) (p<0.009) in the memantine group compared with the Pbo group. The TNF-α were significantly decreased in the memantine group than in the Pbo group (P=0.013).The changes in HDRS score were significantly associated with changes in IL-6 (P=0.012) and IL-1(P=0.005) levels; changes in YMRS score associated with changes with TNF-α(P=0.005) level changes.The association between BDNF Val66Met polymorphism with treatment response was evaluated. After stratified by BDNF Val66Met genotypes, significantly greater decreases in HDRS scores were found in the VPA+memantine group in patients with the Val/Met genotype (p=0.004). We conclude that memantine might benefit treatment of BP-II via decreasing cytokines and increasing HDL-C. The BDNF Val66Met polymorphism influences responses to add-on memantine by decreasing depressive symptoms in BP-II.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74957563","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 : 2015-10-05DOI: 10.4172/2168-975X.S1.006
Reeta Jaya Philip Sneha Mareen Varghese B S Premalatha, Anita Reddy
Objective: Patients with BP-II have a higher prevalence rate of metabolic disturbance and obesity than do the general population. Genetic variants of the methylene tetrahydrofolate reductase (MTHFR) gene have been regarded as predictors of weight gain in schizophrenia. In the present study, we investigated whether the MTHFR C677T polymorphism may predict changes in metabolic indices after 12 weeks of treatment in patients with BP-II.
{"title":"The MTHFR gene predict weight change in drug-naive patients with bipolar II disorder","authors":"Reeta Jaya Philip Sneha Mareen Varghese B S Premalatha, Anita Reddy","doi":"10.4172/2168-975X.S1.006","DOIUrl":"https://doi.org/10.4172/2168-975X.S1.006","url":null,"abstract":"Objective: Patients with BP-II have a higher prevalence rate of metabolic disturbance and obesity than do the general population. Genetic variants of the methylene tetrahydrofolate reductase (MTHFR) gene have been regarded as predictors of weight gain in schizophrenia. In the present study, we investigated whether the MTHFR C677T polymorphism may predict changes in metabolic indices after 12 weeks of treatment in patients with BP-II.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85122976","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 : 2015-10-05DOI: 10.4172/2168-975X.S1.004
N. Rasgon
Workshop Details: Session 1 (required for session 2) Education: We will examine the following aspects of Neuroplasticity: • how zombie systems (unconscious mental processing) are created • the three primary levels of zombie systems • how we can recreate our environments to foster positive zombie systems at all levels Training: Practical application of what we’ve learned • Experience Foundational Cognition Targeted Neuroplastic Training (TNT) proven effective at improving performance of 100% of over 3500 people in military, business, education and brain trauma recovery • The only program of its kind in the world, vetted and approved by US Special Operations Command, used by Navy SEALs, Pilots, Snipers and Marines • Vetted and approved by Rush Hospital’s Road Home program as an effective accelerator of brain trauma recovery • You will keep the neuroplastic training tools to use on your own after the workshop to continue to experience the benefits of improved focus and intuition and better, faster decision making especially under stress
{"title":"3D dilemma of this century","authors":"N. Rasgon","doi":"10.4172/2168-975X.S1.004","DOIUrl":"https://doi.org/10.4172/2168-975X.S1.004","url":null,"abstract":"Workshop Details: Session 1 (required for session 2) Education: We will examine the following aspects of Neuroplasticity: • how zombie systems (unconscious mental processing) are created • the three primary levels of zombie systems • how we can recreate our environments to foster positive zombie systems at all levels Training: Practical application of what we’ve learned • Experience Foundational Cognition Targeted Neuroplastic Training (TNT) proven effective at improving performance of 100% of over 3500 people in military, business, education and brain trauma recovery • The only program of its kind in the world, vetted and approved by US Special Operations Command, used by Navy SEALs, Pilots, Snipers and Marines • Vetted and approved by Rush Hospital’s Road Home program as an effective accelerator of brain trauma recovery • You will keep the neuroplastic training tools to use on your own after the workshop to continue to experience the benefits of improved focus and intuition and better, faster decision making especially under stress","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81217389","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 : 2015-10-02DOI: 10.4172/2168-975X.1000188
E. Wang, Chenguang Du
We know remarkably little about deficits in memory impairment calculation. This study reports the neurophysiological and behavioral correlates of digital memory encoding features in Chinese individuals with and without dyscalculia. The results showed that individuals with dyscalculia exhibit impaired digital memory encoding and deficits in psychological resource allocation.
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