Pub Date : 2022-05-10DOI: 10.29328/journal.jnnd.1001062
Erdoğan Hacı Ali, Yayla Vildan, Sözer Nejla, Aydın Filiz Yıldız, Acır Ibrahim, Vural Meltem
Introduction: Fatigue is a common non-motor symptom of Idiopathic Parkinson’s Disease (IPD). The aim is to research the relationship between fatigue of IPD patients and the clinical findings, of mood disorders. Material and methods: A total of 39 patients with IPD were included in the study. The relationship between fatigue severity and demographic characteristics and the treatment was evaluated in IPD. The severity of fatigue was evaluated by Fatigue Severity Scale (FSS). Motor impairment was scored by the modified Hoehn and Yahr scale. The patients were assessed for the presence of depression and anxiety with the Hospital Anxiety and Depression Scale (HADS). Results: The mean age of the patients was 70.62 ± 8.35 years. 23 were men and 16 were women. The mean disease duration was 6.18 ± 3.35 years. The patients were assigned into two groups according to the presence of fatigue measured by FSS with less than 5 (Group I) and 5 or more (Group II). There were no statistically significant differences between the two groups with respect to mean age, mean age of onset, and mean disease duration of the patients (p > 0.05). There were no significant differences between the two groups for HADS depression, anxiety values, and terms of antiparkinsonian therapies (p > 0.05). The severity of fatigue was correlated with the HADS anxiety levels (p < 0.05). Discussion: Fatigue is an important non-motor symptom that is underestimated in clinical follow-up. We didn’t find any correlation between fatigue and age, duration of disease onset, or drug use. There was no significant correlation between the fatigue score and depression, and pain. However, the fatigue scores were higher in patients with high anxiety scores and females.
{"title":"Idiopathic parkinson’s disease and fatigue","authors":"Erdoğan Hacı Ali, Yayla Vildan, Sözer Nejla, Aydın Filiz Yıldız, Acır Ibrahim, Vural Meltem","doi":"10.29328/journal.jnnd.1001062","DOIUrl":"https://doi.org/10.29328/journal.jnnd.1001062","url":null,"abstract":"Introduction: Fatigue is a common non-motor symptom of Idiopathic Parkinson’s Disease (IPD). The aim is to research the relationship between fatigue of IPD patients and the clinical findings, of mood disorders. Material and methods: A total of 39 patients with IPD were included in the study. The relationship between fatigue severity and demographic characteristics and the treatment was evaluated in IPD. The severity of fatigue was evaluated by Fatigue Severity Scale (FSS). Motor impairment was scored by the modified Hoehn and Yahr scale. The patients were assessed for the presence of depression and anxiety with the Hospital Anxiety and Depression Scale (HADS). Results: The mean age of the patients was 70.62 ± 8.35 years. 23 were men and 16 were women. The mean disease duration was 6.18 ± 3.35 years. The patients were assigned into two groups according to the presence of fatigue measured by FSS with less than 5 (Group I) and 5 or more (Group II). There were no statistically significant differences between the two groups with respect to mean age, mean age of onset, and mean disease duration of the patients (p > 0.05). There were no significant differences between the two groups for HADS depression, anxiety values, and terms of antiparkinsonian therapies (p > 0.05). The severity of fatigue was correlated with the HADS anxiety levels (p < 0.05). Discussion: Fatigue is an important non-motor symptom that is underestimated in clinical follow-up. We didn’t find any correlation between fatigue and age, duration of disease onset, or drug use. There was no significant correlation between the fatigue score and depression, and pain. However, the fatigue scores were higher in patients with high anxiety scores and females.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"43 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134212398","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 : 2022-01-18DOI: 10.29328/journal.jnnd.1001061
Riccioni Luca, Balestrieri Antonio, D. Fuschillo, Nasi Maria Teresa, Tosatto Luigino
Intrasellar meningioma (IM) is a rare occurrence that is difficult to distinguish preoperatively from the most common non-functioning pituitary adenoma. Here we describe a case of psammomatous IM occurring in a 68-year-old woman, presented with visual defects. On magnetic resonance imaging (MRI) she was found to have an intrasellar mass with suprasellar extension that was approached with transsphenoidal surgery. Subtle radiological hints, namely dural tail sign, intralesional calcifications and a marked and homogenous early enhancement of IM on MRI after gadolinium administration, may aid clinicians in achieving an accurate pre-operative diagnosis and choosing the proper surgical approach. The clinical and neuroradiological features of IM described in the literature has been reviewed.
{"title":"Intrasellar psammomatous meningioma: a case report and review of the literature","authors":"Riccioni Luca, Balestrieri Antonio, D. Fuschillo, Nasi Maria Teresa, Tosatto Luigino","doi":"10.29328/journal.jnnd.1001061","DOIUrl":"https://doi.org/10.29328/journal.jnnd.1001061","url":null,"abstract":"Intrasellar meningioma (IM) is a rare occurrence that is difficult to distinguish preoperatively from the most common non-functioning pituitary adenoma. Here we describe a case of psammomatous IM occurring in a 68-year-old woman, presented with visual defects. On magnetic resonance imaging (MRI) she was found to have an intrasellar mass with suprasellar extension that was approached with transsphenoidal surgery. Subtle radiological hints, namely dural tail sign, intralesional calcifications and a marked and homogenous early enhancement of IM on MRI after gadolinium administration, may aid clinicians in achieving an accurate pre-operative diagnosis and choosing the proper surgical approach. The clinical and neuroradiological features of IM described in the literature has been reviewed.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"53 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128235765","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 : 2022-01-18DOI: 10.29328/journal.jnnd.1001060
Ehsani Mojtaba, Montazeri Zeinab, Rafati Mehravar
Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are implicated in the central nervous system (CNS) diseases. The CNS has emerged as an important target for adverse health effects of exposure to air pollutants, where it can cause neurological and neurodevelopmental disorders. Air pollution includes various components of gases, particulate matter (PM), ultrafine particulate (UFPs), metals, and organic compounds. An important source of PM and UFPM in the ambient air is associated with air pollution-related trafficking, and primarily diesel exhaust particles (DEPs). Controlled animal studies and epidemiological studies show that exposure to air pollution, and in particular urban air pollution or DEPs, may lead to neurotoxicity. In specific, exposure to air pollutants as an important factor may be in neurodevelopmental disorders (eg Autism) and neurological disorders (eg.., Alzheimer’s Disease (AD)). The most noticeable effects of exposure to air pollutants in animals and humans are oxidative stress and neurodegeneration. Studies in rats exposed to DEPs showed microglial activity, increased lipid peroxidation, and neuronal accumulation in various areas of the brain, especially the olfactory bulb (OB) and the hippocampus (HI). Disorders of adult neurogenesis were also found. In most cases, the effects of DEP are more pronounced in male mice, probably due to lower antioxidant capacity due to less expression of paraoxonase 2.
{"title":"Neurotoxicity related exposure to ambient nanoparticles","authors":"Ehsani Mojtaba, Montazeri Zeinab, Rafati Mehravar","doi":"10.29328/journal.jnnd.1001060","DOIUrl":"https://doi.org/10.29328/journal.jnnd.1001060","url":null,"abstract":"Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are implicated in the central nervous system (CNS) diseases. The CNS has emerged as an important target for adverse health effects of exposure to air pollutants, where it can cause neurological and neurodevelopmental disorders. Air pollution includes various components of gases, particulate matter (PM), ultrafine particulate (UFPs), metals, and organic compounds. An important source of PM and UFPM in the ambient air is associated with air pollution-related trafficking, and primarily diesel exhaust particles (DEPs). Controlled animal studies and epidemiological studies show that exposure to air pollution, and in particular urban air pollution or DEPs, may lead to neurotoxicity. In specific, exposure to air pollutants as an important factor may be in neurodevelopmental disorders (eg Autism) and neurological disorders (eg.., Alzheimer’s Disease (AD)). The most noticeable effects of exposure to air pollutants in animals and humans are oxidative stress and neurodegeneration. Studies in rats exposed to DEPs showed microglial activity, increased lipid peroxidation, and neuronal accumulation in various areas of the brain, especially the olfactory bulb (OB) and the hippocampus (HI). Disorders of adult neurogenesis were also found. In most cases, the effects of DEP are more pronounced in male mice, probably due to lower antioxidant capacity due to less expression of paraoxonase 2.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116146532","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 : 2022-01-03DOI: 10.29328/journal.jnnd.1001059
Hatim Ghita, Chekrine Tarik, Houjami Majdouline, Boughafour Mouna, B. Zineb, B. Nadia, Jouhadi Hassan, T. Nezha, B. Abdelatif, Sahraoui Souha
Background and objectives: Brainstem gliomas are tumors of the central nervous system which have varying presentations and clinical courses. This study aims to analyze the frequency, clinical and therapeutic aspects of brainstem glioma. Methods: We retrospectively analyzed the data from the record of the patients treated for brainstem glioma under the age of 20 between January 2007 and July 2020 in the Radiation Oncology department of the Ibn Rochd UHC. Results: There were fifteen patients (10 males and 5 females). The mean age of onset was 12 years (range 8 - 14 years). The duration of symptoms varied from 1 month to 2 years. Nine of the patients had intracranial hypertension due to hydrocephalus, six had cranial nerve deficits at presentation, and five patients had cerebellar signs. The lesion was pontine in 12 cases. None of the patients had a tumoral resection, nine had a ventriculo-peritoneal shunt insertion for the hydrocephalus and three had a Stereotactic biopsy that revealed one astrocytoma grade 1, one low grade glioma and one glioblastoma. The radiotherapy was indicated in all the cases but only nine patients had a 3D radiotherapy with a total dose of 54 Gy. Three patients received chemotherapy. Six patients are still alive, two are lost to follow up and seven patients are dead with a mean survival period of 8 months. Conclusion: Brainstem glioma is a devastating disease with a bad prognosis. The clinical presentation is variable and the management is multidisciplinary. Our study illustrates the importance of treatment by radiation.
{"title":"Pediatric brainstem glioma","authors":"Hatim Ghita, Chekrine Tarik, Houjami Majdouline, Boughafour Mouna, B. Zineb, B. Nadia, Jouhadi Hassan, T. Nezha, B. Abdelatif, Sahraoui Souha","doi":"10.29328/journal.jnnd.1001059","DOIUrl":"https://doi.org/10.29328/journal.jnnd.1001059","url":null,"abstract":"Background and objectives: Brainstem gliomas are tumors of the central nervous system which have varying presentations and clinical courses. This study aims to analyze the frequency, clinical and therapeutic aspects of brainstem glioma. Methods: We retrospectively analyzed the data from the record of the patients treated for brainstem glioma under the age of 20 between January 2007 and July 2020 in the Radiation Oncology department of the Ibn Rochd UHC. Results: There were fifteen patients (10 males and 5 females). The mean age of onset was 12 years (range 8 - 14 years). The duration of symptoms varied from 1 month to 2 years. Nine of the patients had intracranial hypertension due to hydrocephalus, six had cranial nerve deficits at presentation, and five patients had cerebellar signs. The lesion was pontine in 12 cases. None of the patients had a tumoral resection, nine had a ventriculo-peritoneal shunt insertion for the hydrocephalus and three had a Stereotactic biopsy that revealed one astrocytoma grade 1, one low grade glioma and one glioblastoma. The radiotherapy was indicated in all the cases but only nine patients had a 3D radiotherapy with a total dose of 54 Gy. Three patients received chemotherapy. Six patients are still alive, two are lost to follow up and seven patients are dead with a mean survival period of 8 months. Conclusion: Brainstem glioma is a devastating disease with a bad prognosis. The clinical presentation is variable and the management is multidisciplinary. Our study illustrates the importance of treatment by radiation.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"9 30","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132271780","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 : 2021-09-08DOI: 10.29328/journal.jnnd.1001057
Dave Sonya, Z. An
Repressive regulation of potassium channel genes by Polycomb group (PcG) proteins contributes to PcG protein-mediated neuroprotection against neuronal ischemic injury, as seen in an ischemic stroke. Here we asked the question whether Trithorax group (TrxG) proteins, the antagonistic partners of PcG proteins (i.e, epigenetic activators targeting the same genes) may also regulate potassium channels. Results of patch-clamp studies on cultured neuronal cells showed that inhibition of TrxG protein MLL-1 led to an increase in potassium channel activity, an unexpected effect for a presumed gene activator. In contrast, decreased sodium currents were observed with MLL-1 inhibition. Increased or decreased levels of potassium channel protein Kv2.1 or sodium channel protein Nav1.2, respectively, were seen with MLL-1 inhibition, as determined by immunocytochemistry. These results, for the first time, demonstrate an involvement of TrxG protein MLL-1 in regulating neuronal ion channels, potentially repressing potassium channel genes.
在缺血性中风中，Polycomb group (PcG)蛋白对钾通道基因的抑制调控有助于PcG蛋白介导的神经保护，防止神经元缺血性损伤。在这里，我们提出了Trithorax group (TrxG)蛋白，PcG蛋白的拮抗伙伴(即针对相同基因的表观遗传激活因子)是否也可能调节钾通道的问题。膜片钳对培养的神经细胞的研究结果表明，抑制TrxG蛋白MLL-1导致钾通道活性增加，这是一种意想不到的基因激活剂。相比之下，MLL-1抑制可降低钠电流。通过免疫细胞化学测定，MLL-1抑制分别导致钾通道蛋白Kv2.1或钠通道蛋白Nav1.2水平升高或降低。这些结果首次证明了TrxG蛋白MLL-1参与调节神经元离子通道，潜在地抑制钾通道基因。
{"title":"Differential roles of trithorax protein MLL-1 in regulating neuronal Ion channels","authors":"Dave Sonya, Z. An","doi":"10.29328/journal.jnnd.1001057","DOIUrl":"https://doi.org/10.29328/journal.jnnd.1001057","url":null,"abstract":"Repressive regulation of potassium channel genes by Polycomb group (PcG) proteins contributes to PcG protein-mediated neuroprotection against neuronal ischemic injury, as seen in an ischemic stroke. Here we asked the question whether Trithorax group (TrxG) proteins, the antagonistic partners of PcG proteins (i.e, epigenetic activators targeting the same genes) may also regulate potassium channels. Results of patch-clamp studies on cultured neuronal cells showed that inhibition of TrxG protein MLL-1 led to an increase in potassium channel activity, an unexpected effect for a presumed gene activator. In contrast, decreased sodium currents were observed with MLL-1 inhibition. Increased or decreased levels of potassium channel protein Kv2.1 or sodium channel protein Nav1.2, respectively, were seen with MLL-1 inhibition, as determined by immunocytochemistry. These results, for the first time, demonstrate an involvement of TrxG protein MLL-1 in regulating neuronal ion channels, potentially repressing potassium channel genes.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"65 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124527967","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 : 2021-07-27DOI: 10.29328/journal.jnnd.1001055
Castro Frank Phillip
Single-level Anterior Cervical Decompression and Fusion (ACDF) was initially performed using Iliac Crest Bone Graft (ICBG) [1]. Fusion rates improved when a surgical technique change, the addition of anterior plate ixation, was incorporated decades later [2,3]. Single level ACDFs with a machined allograft and plate ixation technique eventually became the industry standard as it demonstrated equivalent fusion rates with fewer complications than single level ACDFs with ICBG. This surgical technique was extended for use in patients with contiguous disk herniations. Multilevel ACDFs performed with machined allografts or interbody spacers and a two-level plate offered shorter operative times, less blood loss, better restoration of lordosis, and less immediate pain [4]. Successful multi-level ACDFs were strongly in luenced by the bone graft source [5], the smoking addiction [6], and the construct stability [7]. Placement of two additional ixation screws in the central vertebral body, another improvement in the surgical technique, increased the construct strength compared to constructs with screws only placed into the end vertebral bodies [8]. Using allografts for multilevel ACDFs was a device disadvantage as they often resulted in high nonunion rates [9,10].
{"title":"Five-year follow up on the single level corpectomy","authors":"Castro Frank Phillip","doi":"10.29328/journal.jnnd.1001055","DOIUrl":"https://doi.org/10.29328/journal.jnnd.1001055","url":null,"abstract":"Single-level Anterior Cervical Decompression and Fusion (ACDF) was initially performed using Iliac Crest Bone Graft (ICBG) [1]. Fusion rates improved when a surgical technique change, the addition of anterior plate ixation, was incorporated decades later [2,3]. Single level ACDFs with a machined allograft and plate ixation technique eventually became the industry standard as it demonstrated equivalent fusion rates with fewer complications than single level ACDFs with ICBG. This surgical technique was extended for use in patients with contiguous disk herniations. Multilevel ACDFs performed with machined allografts or interbody spacers and a two-level plate offered shorter operative times, less blood loss, better restoration of lordosis, and less immediate pain [4]. Successful multi-level ACDFs were strongly in luenced by the bone graft source [5], the smoking addiction [6], and the construct stability [7]. Placement of two additional ixation screws in the central vertebral body, another improvement in the surgical technique, increased the construct strength compared to constructs with screws only placed into the end vertebral bodies [8]. Using allografts for multilevel ACDFs was a device disadvantage as they often resulted in high nonunion rates [9,10].","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"141 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126997679","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 : 2021-07-15DOI: 10.29328/JOURNAL.JNND.1001053
R. Juntas-Morales, E. D. L. Cruz, F. Esselin, N. Pageot, G. Taieb, W. Camu
Objectives: To describe a patient with facial-onset sensory-motor neuronopathy (FOSMN) that later developed Huntington’s disease (HD). Case report: A 62-year-old woman complained of progressive dysphagia 8 years before referral. At initial evaluation, there was excessive salivation, dysphagia, and sensory-motor trigeminal impairment. Denervation was noted on the upper limbs and the tongue. Blink reflexes were abolished. Genetic study of amyotrophic lateral sclerosis (ALS)-related genes was normal. She was diagnosed with FOSMN syndrome. Her clinical state progressively worsened with corneal anesthesia, severe denutrition, right arm and axial weakness. Seven years after referral, she was unable walk and developed generalized chorea. Abnormal huntingtin gene repeat expansion confirmed the diagnosis of HD. She died 16 years after onset of dysphagia. Conclusion: Cases with both HD and ALS have already been reported but not FOSMN and HD, to our knowledge. Some FOSMN cases have been linked to ALS-related gene mutations and HD phenocopies have been associated with C9ORF72 repeat expansions. Recently, huntingtin repeat expansions were described in the ALS population. Although a chance association cannot be excluded, data from the literature are in favor of a pathogenic relationship between FOSMN and HD in this particular case. We suggest that huntingtin gene be more systematically studied in patients with FOSMN.
{"title":"Facial-onset sensory-motor neuronopathy, a rare variant of Huntington’s disease or chance association?","authors":"R. Juntas-Morales, E. D. L. Cruz, F. Esselin, N. Pageot, G. Taieb, W. Camu","doi":"10.29328/JOURNAL.JNND.1001053","DOIUrl":"https://doi.org/10.29328/JOURNAL.JNND.1001053","url":null,"abstract":"Objectives: To describe a patient with facial-onset sensory-motor neuronopathy (FOSMN) that later developed Huntington’s disease (HD). Case report: A 62-year-old woman complained of progressive dysphagia 8 years before referral. At initial evaluation, there was excessive salivation, dysphagia, and sensory-motor trigeminal impairment. Denervation was noted on the upper limbs and the tongue. Blink reflexes were abolished. Genetic study of amyotrophic lateral sclerosis (ALS)-related genes was normal. She was diagnosed with FOSMN syndrome. Her clinical state progressively worsened with corneal anesthesia, severe denutrition, right arm and axial weakness. Seven years after referral, she was unable walk and developed generalized chorea. Abnormal huntingtin gene repeat expansion confirmed the diagnosis of HD. She died 16 years after onset of dysphagia. Conclusion: Cases with both HD and ALS have already been reported but not FOSMN and HD, to our knowledge. Some FOSMN cases have been linked to ALS-related gene mutations and HD phenocopies have been associated with C9ORF72 repeat expansions. Recently, huntingtin repeat expansions were described in the ALS population. Although a chance association cannot be excluded, data from the literature are in favor of a pathogenic relationship between FOSMN and HD in this particular case. We suggest that huntingtin gene be more systematically studied in patients with FOSMN.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114306906","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 : 2021-07-15DOI: 10.29328/JOURNAL.JNND.1001054
Dutta Rajib
Huntington’s disease (HD) is an incurable neurodegenerative disease that causes involuntary movements, emotional lability, and cognitive dysfunction. HD symptoms usually develop between ages 30 and 50, but can appear as early as 2 or as late as 80 years. Currently no neuroprotective and neurorestorative interventions are available. Early multimodal intervention in HD is only possible if the genetic diagnosis is made early. Early intervention in HD is only possible if genetic diagnosis is made at the disease onset or when mild symptoms manifest. Growing evidence and understanding of HD pathomechanism has led researchers to new therapeutic targets. Here, in this article we will talk about the multimodal treatment strategies and recent advances made in this field which can be used to target the HD pathogenesis at its most proximal level.
{"title":"Multimodal treatment strategies in Huntington’s disease","authors":"Dutta Rajib","doi":"10.29328/JOURNAL.JNND.1001054","DOIUrl":"https://doi.org/10.29328/JOURNAL.JNND.1001054","url":null,"abstract":"Huntington’s disease (HD) is an incurable neurodegenerative disease that causes involuntary movements, emotional lability, and cognitive dysfunction. HD symptoms usually develop between ages 30 and 50, but can appear as early as 2 or as late as 80 years. Currently no neuroprotective and neurorestorative interventions are available. Early multimodal intervention in HD is only possible if the genetic diagnosis is made early. Early intervention in HD is only possible if genetic diagnosis is made at the disease onset or when mild symptoms manifest. Growing evidence and understanding of HD pathomechanism has led researchers to new therapeutic targets. Here, in this article we will talk about the multimodal treatment strategies and recent advances made in this field which can be used to target the HD pathogenesis at its most proximal level.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"17 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116396603","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 : 2021-07-06DOI: 10.29328/JOURNAL.JNND.1001052
Dutta Rajib
Parkinson’s disease (PD) is thought to be the most common neurodegenerative disease with movement disorder. The key motor symptoms are rigidity, tremor, akinesis/hypokinesia/bradykinesia, and postural instability. However, in our day-to-day clinical practice we tend to see several other symptoms which may be motor or non-motor. Non-motor symptoms (NMS) are quite common and debilitating. The pathological hallmarks of PD are loss of dopaminergic neurons in the substantia nigra pars compacta (SNPc) and accumulation of unfolded or misfolded alpha-synuclein. Diagnosis of PD is difficult in the pre-motor stage. Late diagnosis renders a substantial loss of dopaminergic neurons in SNPc and spread of disease in other parts of the brain. This may manifest as either full blown symptoms requiring multiple medications or may even lead to life threatening condition due to lack of early diagnostic tools and techniques. Biomarkers are required to diagnose PD at a very early stage when prevention is possible. Hence, we see a lot of interest among researchers involved in finding a biomarker specific to the disease. Biomarkers may be clinical, image based, genetic, and biochemical. Cerebrospinal fluid (CSF) and serum markers which may correlate with disease pathophysiology are of great significance. One such molecule which recently gained a lot of attention is neuron-specific enolase (NSE). The main aim of this paper is to highlight the role of NSE in predicting neurodegeneration and neuroinflammation ultimately reflecting damage of brain cells in PD.
{"title":"Role of neuron specific enolase as a biomarker in Parkinson’s disease","authors":"Dutta Rajib","doi":"10.29328/JOURNAL.JNND.1001052","DOIUrl":"https://doi.org/10.29328/JOURNAL.JNND.1001052","url":null,"abstract":"Parkinson’s disease (PD) is thought to be the most common neurodegenerative disease with movement disorder. The key motor symptoms are rigidity, tremor, akinesis/hypokinesia/bradykinesia, and postural instability. However, in our day-to-day clinical practice we tend to see several other symptoms which may be motor or non-motor. Non-motor symptoms (NMS) are quite common and debilitating. The pathological hallmarks of PD are loss of dopaminergic neurons in the substantia nigra pars compacta (SNPc) and accumulation of unfolded or misfolded alpha-synuclein. Diagnosis of PD is difficult in the pre-motor stage. Late diagnosis renders a substantial loss of dopaminergic neurons in SNPc and spread of disease in other parts of the brain. This may manifest as either full blown symptoms requiring multiple medications or may even lead to life threatening condition due to lack of early diagnostic tools and techniques. Biomarkers are required to diagnose PD at a very early stage when prevention is possible. Hence, we see a lot of interest among researchers involved in finding a biomarker specific to the disease. Biomarkers may be clinical, image based, genetic, and biochemical. Cerebrospinal fluid (CSF) and serum markers which may correlate with disease pathophysiology are of great significance. One such molecule which recently gained a lot of attention is neuron-specific enolase (NSE). The main aim of this paper is to highlight the role of NSE in predicting neurodegeneration and neuroinflammation ultimately reflecting damage of brain cells in PD.","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126921999","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 : 2021-06-29DOI: 10.29328/JOURNAL.JNND.1001051
Cirio Juan J, Ciardi Celina, Lopez Matias, Scrivano Esteban V, Lundquist Javier, Lylyk Ivan, Perez Nicolas, Lylyk Pedro
The association between intracranial large vessel occlusion (LVO) and concurrent steno-occlusive lesion of an ipsilateral extracranial internal carotid artery (ICA) is considered a tandem occlusion (TO) [1]. In approximately half of TO, the irst clinical manifestation are acute occlusions of the extracranial ICA associated with occlusion of the middle cerebral artery (MCA), with additional occlusion of the intracranial ICA in up to 25% of these cases.[2] This particular lesion subset is technically challenging for endovascular treatment (EVT) and is also characterized by lower success rates of intravenous thrombolysis [3], worse prognosis compared to intracranial occlusions alone, and higher rates of symptomatic intracranial hemorrhage [4]. The optimal approach regarding EVT of TO remains controversial, and reports in this regard are scarce. There are two proposed strategies according to the selection of the irst lesion to be treated. The proximal approach comprises stenting of the proximal cervical ICA followed by mechanical thrombectomy (MT) of the intracranial vessel, whereas the distal approach involves MT followed by stenting of the cervical ICA [3–14].
{"title":"Endovascular management of tandem occlusions in stroke: Treatment strategies in a real-world scenario","authors":"Cirio Juan J, Ciardi Celina, Lopez Matias, Scrivano Esteban V, Lundquist Javier, Lylyk Ivan, Perez Nicolas, Lylyk Pedro","doi":"10.29328/JOURNAL.JNND.1001051","DOIUrl":"https://doi.org/10.29328/JOURNAL.JNND.1001051","url":null,"abstract":"The association between intracranial large vessel occlusion (LVO) and concurrent steno-occlusive lesion of an ipsilateral extracranial internal carotid artery (ICA) is considered a tandem occlusion (TO) [1]. In approximately half of TO, the irst clinical manifestation are acute occlusions of the extracranial ICA associated with occlusion of the middle cerebral artery (MCA), with additional occlusion of the intracranial ICA in up to 25% of these cases.[2] This particular lesion subset is technically challenging for endovascular treatment (EVT) and is also characterized by lower success rates of intravenous thrombolysis [3], worse prognosis compared to intracranial occlusions alone, and higher rates of symptomatic intracranial hemorrhage [4]. The optimal approach regarding EVT of TO remains controversial, and reports in this regard are scarce. There are two proposed strategies according to the selection of the irst lesion to be treated. The proximal approach comprises stenting of the proximal cervical ICA followed by mechanical thrombectomy (MT) of the intracranial vessel, whereas the distal approach involves MT followed by stenting of the cervical ICA [3–14].","PeriodicalId":382788,"journal":{"name":"Journal of Neuroscience and Neurological Disorders","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131721375","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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