Pub Date : 2025-04-25DOI: 10.1007/s11910-025-01419-5
Annabelle Shaffer, Helen J Kemprecos, Maxwell G Woolridge, Nicholas D Soulakis, Paul M Arnold
Purpose of review: Sport-related concussions (SRC) in high school athletes are a growing public health concern, with recent advancements in epidemiology, pathophysiology, diagnosis, management, and prevention. We concisely summarize SRC in high school athletes, emphasizing current research and clinical implications.
Recent findings: Athletes are at significant risk of SRCs, with incidence varying by sport, sex, and competitive setting. Advances in pathophysiology highlight the role of metabolic disruption, inflammation, and axonal injury. Updated diagnostic tools, such as SCAT6, aid clinical evaluation, while advanced neuroimaging and biomarkers remain investigational. Return-to-sport/learn protocols emphasize a gradual, stepwise return. Preventative measures, including policy changes, neuromuscular training, and protective equipment, have reduced SRC incidence. Comprehensive SRC management includes recognition and removal from play followed by a structured return to sport/learning. Future research directions include biomarker validation, optimized prevention strategies, and long-term outcome assessment to reduce the burden of SRC in adolescent athletes.
{"title":"Sport-Related Concussions in High School Athletes: A Comprehensive Update.","authors":"Annabelle Shaffer, Helen J Kemprecos, Maxwell G Woolridge, Nicholas D Soulakis, Paul M Arnold","doi":"10.1007/s11910-025-01419-5","DOIUrl":"https://doi.org/10.1007/s11910-025-01419-5","url":null,"abstract":"<p><strong>Purpose of review: </strong>Sport-related concussions (SRC) in high school athletes are a growing public health concern, with recent advancements in epidemiology, pathophysiology, diagnosis, management, and prevention. We concisely summarize SRC in high school athletes, emphasizing current research and clinical implications.</p><p><strong>Recent findings: </strong>Athletes are at significant risk of SRCs, with incidence varying by sport, sex, and competitive setting. Advances in pathophysiology highlight the role of metabolic disruption, inflammation, and axonal injury. Updated diagnostic tools, such as SCAT6, aid clinical evaluation, while advanced neuroimaging and biomarkers remain investigational. Return-to-sport/learn protocols emphasize a gradual, stepwise return. Preventative measures, including policy changes, neuromuscular training, and protective equipment, have reduced SRC incidence. Comprehensive SRC management includes recognition and removal from play followed by a structured return to sport/learning. Future research directions include biomarker validation, optimized prevention strategies, and long-term outcome assessment to reduce the burden of SRC in adolescent athletes.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"32"},"PeriodicalIF":4.8,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-16DOI: 10.1007/s11910-025-01420-y
Michael Lowe, Gabriele Berman, Priya Sumithran, Susan P Mollan
Purpose of review: Development of safe targeted therapies for idiopathic intracranial hypertension requires a thorough understanding of recent evidence discovering the pathophysiology of the condition. The aim is to provide a review of studies that inform on the underpinning mechanisms that have been associated with idiopathic intracranial hypertension.
Recent findings: People living with active idiopathic intracranial hypertension and obesity have been found to have with insulin resistance, hyperleptinaemia, and adverse cardiovascular outcomes. Clinically their adipose tissue is predominantly located in the truncal region and on detailed laboratory analysis the cells are primed for weight gain. There is evidence of androgen excess, altered glucocorticoid regulation and changes in pro-inflammatory cytokines. There are distinct alterations in metabolic pathways found in serum, urine and cerebrospinal fluid, that resolve following disease remission. These findings are associated with raised intracranial pressure and are likely secondary to cerebrospinal fluid hypersecretion. Idiopathic intracranial hypertension has a profile of systemic metabolic changes, endocrine dysfunction and cardiovascular risk profile distinct from that associated with obesity alone. These systemic metabolic changes are likely to contribute to dysregulation of cerebrospinal fluid dynamics, primarily hypersecretion but with a possible additional effect of reduced clearance resulting in the core feature of raised intracranial pressure.
{"title":"Current Understanding of the Pathophysiology of Idiopathic Intracranial Hypertension.","authors":"Michael Lowe, Gabriele Berman, Priya Sumithran, Susan P Mollan","doi":"10.1007/s11910-025-01420-y","DOIUrl":"https://doi.org/10.1007/s11910-025-01420-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Development of safe targeted therapies for idiopathic intracranial hypertension requires a thorough understanding of recent evidence discovering the pathophysiology of the condition. The aim is to provide a review of studies that inform on the underpinning mechanisms that have been associated with idiopathic intracranial hypertension.</p><p><strong>Recent findings: </strong>People living with active idiopathic intracranial hypertension and obesity have been found to have with insulin resistance, hyperleptinaemia, and adverse cardiovascular outcomes. Clinically their adipose tissue is predominantly located in the truncal region and on detailed laboratory analysis the cells are primed for weight gain. There is evidence of androgen excess, altered glucocorticoid regulation and changes in pro-inflammatory cytokines. There are distinct alterations in metabolic pathways found in serum, urine and cerebrospinal fluid, that resolve following disease remission. These findings are associated with raised intracranial pressure and are likely secondary to cerebrospinal fluid hypersecretion. Idiopathic intracranial hypertension has a profile of systemic metabolic changes, endocrine dysfunction and cardiovascular risk profile distinct from that associated with obesity alone. These systemic metabolic changes are likely to contribute to dysregulation of cerebrospinal fluid dynamics, primarily hypersecretion but with a possible additional effect of reduced clearance resulting in the core feature of raised intracranial pressure.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"31"},"PeriodicalIF":4.8,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12003586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-11DOI: 10.1007/s11910-025-01417-7
Samuel D Browning, Julia M Costello, Hamish P Dunn, Clare L Fraser
Purpose of review: The ocular fundus reveals a wealth of pathophysiological findings which should change patient management in the emergency room (ER). Traditional fundoscopy has been technically challenging and diagnostically inaccurate, but technological advances in non-mydriatic fundus photography (NMFP) have facilitated clinically meaningful fundoscopy. This review presents an update on the literature regarding NMFP and its application to the ER, illustrating pivotal publications and recent advances within this field.
Recent findings: NMFP's application in the ER is demonstrably feasible and seamlessly integrates into emergency physicians' (EP) diagnostic workflows in a clinically meaningful and time efficient manner. The images of the ocular fundus (OF) generated by NMFP are consistently high quality, allowing a greater diagnostic accuracy to EP and ophthalmology interpreters alike. Digital NMFP images facilitate effective ophthalmology input via telemedicine to review the images in the ER. NMFP has been shown to change management decisions in the ER, improving patient and departmental outcomes. Interpretation of fundus images remains a medical education challenge, and early research highlights the potential for artificial intelligence (AI) image systems of NMFP to augment image interpretation in the ER. NMFP can change the ER approach to OF assessment, however the factors limiting its routine implementation need further consideration. There is potential for AI to contribute to NMFP image screening systems to augment EPs diagnostic accuracy.
{"title":"The Use Of Fundus Photography In The Emergency Room-A Review.","authors":"Samuel D Browning, Julia M Costello, Hamish P Dunn, Clare L Fraser","doi":"10.1007/s11910-025-01417-7","DOIUrl":"https://doi.org/10.1007/s11910-025-01417-7","url":null,"abstract":"<p><strong>Purpose of review: </strong>The ocular fundus reveals a wealth of pathophysiological findings which should change patient management in the emergency room (ER). Traditional fundoscopy has been technically challenging and diagnostically inaccurate, but technological advances in non-mydriatic fundus photography (NMFP) have facilitated clinically meaningful fundoscopy. This review presents an update on the literature regarding NMFP and its application to the ER, illustrating pivotal publications and recent advances within this field.</p><p><strong>Recent findings: </strong>NMFP's application in the ER is demonstrably feasible and seamlessly integrates into emergency physicians' (EP) diagnostic workflows in a clinically meaningful and time efficient manner. The images of the ocular fundus (OF) generated by NMFP are consistently high quality, allowing a greater diagnostic accuracy to EP and ophthalmology interpreters alike. Digital NMFP images facilitate effective ophthalmology input via telemedicine to review the images in the ER. NMFP has been shown to change management decisions in the ER, improving patient and departmental outcomes. Interpretation of fundus images remains a medical education challenge, and early research highlights the potential for artificial intelligence (AI) image systems of NMFP to augment image interpretation in the ER. NMFP can change the ER approach to OF assessment, however the factors limiting its routine implementation need further consideration. There is potential for AI to contribute to NMFP image screening systems to augment EPs diagnostic accuracy.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"30"},"PeriodicalIF":4.8,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-09DOI: 10.1007/s11910-025-01418-6
A Marengo, M Tejada, I Hancco Zirena, S Molina
Purpose of review: The effects that exercise at altitude has on the neurological system are diverse and still not well studied, and range from metabolic adaptations to modification of cerebral blood flow and neurotransmitters. In this review we summarise changes with exercise intensity, the implications of ascent, cognitive impairment, psychosis-like symptoms, the role of exercise in the development and prevention of AMS, and use of free radical scavengers to enhance sports performance and acclimatization.
Recent findings: We discuss the impact of oxidative stress in hypobaric hypoxia and reactive oxygen species (ROS) production and its consequences, with special focus on exercise at altitude. Finally we consider how moderate intensity exercise could help prevent AMS, and the necessity of research on high intensity exercise with elevated rate of ascent, the development of specific tools of cognitive assessment, and the role of free-radical scavengers in the prevention of AMS and neurological symptoms.
{"title":"Neurological Manifestations Associated with Exercise at Altitude.","authors":"A Marengo, M Tejada, I Hancco Zirena, S Molina","doi":"10.1007/s11910-025-01418-6","DOIUrl":"https://doi.org/10.1007/s11910-025-01418-6","url":null,"abstract":"<p><strong>Purpose of review: </strong>The effects that exercise at altitude has on the neurological system are diverse and still not well studied, and range from metabolic adaptations to modification of cerebral blood flow and neurotransmitters. In this review we summarise changes with exercise intensity, the implications of ascent, cognitive impairment, psychosis-like symptoms, the role of exercise in the development and prevention of AMS, and use of free radical scavengers to enhance sports performance and acclimatization.</p><p><strong>Recent findings: </strong>We discuss the impact of oxidative stress in hypobaric hypoxia and reactive oxygen species (ROS) production and its consequences, with special focus on exercise at altitude. Finally we consider how moderate intensity exercise could help prevent AMS, and the necessity of research on high intensity exercise with elevated rate of ascent, the development of specific tools of cognitive assessment, and the role of free-radical scavengers in the prevention of AMS and neurological symptoms.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"29"},"PeriodicalIF":4.8,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-28DOI: 10.1007/s11910-025-01415-9
Barun Kumar Sen, Kausik Pan, Ambar Chakravarty
<p><strong>Purpose of review: </strong>This review highlights the causes, types and clinical staging of hepatic encephalopathy (HE). Current concepts on the probable pathogenetic mechanisms and currently practiced therapeutic options are discussed.</p><p><strong>Recent findings: </strong>HE may be covert and overt. Also known as minimal HE. Covert HE, where there are behavioral abnormalities and impairment in activities of daily living with intact sensorium. The pathophysiology of HE remains poorly understood. There is disturbance of the urea cycle due to liver disease leading to increased production of ammonia. The ammonium ion enters the astrocytes along with glutamate (converted to glutamine by ammonia) and myo-inositol, thereby increasing the osmolality of the astrocytic cytoplasm. This osmotic gradient results in accumulation of water inside the astrocytes resulting in cerebral edema and increase in brain volume. Additionally, current research has noted the role of cerebral oxidative/nitrosative stress and the synergistic effects of increased cerebral ammonia and alteration in neurotransmitters, neurometabolites, and cortical excitability due to systemic inflammation. In advanced liver disease with systemic infection or inflammation, neuroinflammatory processes play significant role in the development of HE. Inflammatory cytokines like TNF-α, IL-6, IL-17 in presence of hyperammonemia have been found to induce neurotoxicity of ammonia by passing through the blood brain barrier and causing enlarged/swollen pale astrocytes, resulting in HE. Disrupted enterohepatic circulation in end stage liver disease also causes elevation of bile acids which induces neuroinflammation. Manganese and zinc play as co-factors of enzymatic reaction. These metal deposition causes multiple psychomotor symptoms observed in HE. The gut environment has a major impact on brain function in patients with HE. Toxins such as ammonia and inflammatory cytokines produced by this impaired intestinal flora access the circulation through porto-systemic anastomoses and exacerbate or precipitate HE. Finally, as a result of recurrent cerebral edema from astrocytic dysfunction and neuroinflammation, permanent neurodegeneration occurs with cognitive decline and motor disturbances, especially parkinsonian features and gait disturbances. This is the stage of chronic hepatic encephalopathy. Currently L-ornithine L-aspartate (LOLA) is being used to lower the ammonia level by stimulating the urea cycle. HE comprises a broad spectrum of neurological and/or psychiatric abnormalities caused by hepatic insufficiency and/or portal-systemic shunting in the absence of any other causes of brain dysfunction. HE may be caused or precipitated by several factors like infections, intoxications and drugs. The encephalopathic features may be covert or overt. The pathogenetic mechanisms for HE may be different. In the presence of liver disease, HE primarily results from disturbed urea cycle with hyperammo
{"title":"Hepatic Encephalopathy: Current Thoughts on Pathophysiology and Management.","authors":"Barun Kumar Sen, Kausik Pan, Ambar Chakravarty","doi":"10.1007/s11910-025-01415-9","DOIUrl":"10.1007/s11910-025-01415-9","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review highlights the causes, types and clinical staging of hepatic encephalopathy (HE). Current concepts on the probable pathogenetic mechanisms and currently practiced therapeutic options are discussed.</p><p><strong>Recent findings: </strong>HE may be covert and overt. Also known as minimal HE. Covert HE, where there are behavioral abnormalities and impairment in activities of daily living with intact sensorium. The pathophysiology of HE remains poorly understood. There is disturbance of the urea cycle due to liver disease leading to increased production of ammonia. The ammonium ion enters the astrocytes along with glutamate (converted to glutamine by ammonia) and myo-inositol, thereby increasing the osmolality of the astrocytic cytoplasm. This osmotic gradient results in accumulation of water inside the astrocytes resulting in cerebral edema and increase in brain volume. Additionally, current research has noted the role of cerebral oxidative/nitrosative stress and the synergistic effects of increased cerebral ammonia and alteration in neurotransmitters, neurometabolites, and cortical excitability due to systemic inflammation. In advanced liver disease with systemic infection or inflammation, neuroinflammatory processes play significant role in the development of HE. Inflammatory cytokines like TNF-α, IL-6, IL-17 in presence of hyperammonemia have been found to induce neurotoxicity of ammonia by passing through the blood brain barrier and causing enlarged/swollen pale astrocytes, resulting in HE. Disrupted enterohepatic circulation in end stage liver disease also causes elevation of bile acids which induces neuroinflammation. Manganese and zinc play as co-factors of enzymatic reaction. These metal deposition causes multiple psychomotor symptoms observed in HE. The gut environment has a major impact on brain function in patients with HE. Toxins such as ammonia and inflammatory cytokines produced by this impaired intestinal flora access the circulation through porto-systemic anastomoses and exacerbate or precipitate HE. Finally, as a result of recurrent cerebral edema from astrocytic dysfunction and neuroinflammation, permanent neurodegeneration occurs with cognitive decline and motor disturbances, especially parkinsonian features and gait disturbances. This is the stage of chronic hepatic encephalopathy. Currently L-ornithine L-aspartate (LOLA) is being used to lower the ammonia level by stimulating the urea cycle. HE comprises a broad spectrum of neurological and/or psychiatric abnormalities caused by hepatic insufficiency and/or portal-systemic shunting in the absence of any other causes of brain dysfunction. HE may be caused or precipitated by several factors like infections, intoxications and drugs. The encephalopathic features may be covert or overt. The pathogenetic mechanisms for HE may be different. In the presence of liver disease, HE primarily results from disturbed urea cycle with hyperammo","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"28"},"PeriodicalIF":4.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-25DOI: 10.1007/s11910-025-01416-8
Ambar Chakravarty
Purpose of review: Primary cutaneous lymphomas (PCL) are an uncommon malignancy of the lymphocytes, primarily presenting with dermatologic lesions. Central nervous system(CNS) metastatic manifestations, are even rarer. This review focus mainly on three aspects namely early suspicion of CNS involvement, selection of cases for CNS chemo-prophylaxis and lastly, the rare occurrence from skin straight to brain without other organ involvement.
Recent findings: Primary extranodal large B-cell lymphomas are very heterogeneous. Recent molecular data have thrown some light on such divergent clinical behaviour. The peculiar, stage-independent risk of CNS spread in testicular, breast, uterine, and possibly Primary Cutaneous Diffuse Large B Cell Lymphoma Leg type (PCDBLCL-LT), may be related to prevalent MCD (MYD88/CD79B-mutated) genomic subtype in these lymphomas. It remains to be seen how this genotype might facilitate invasion of the CNS parenchyma, and whether therapies targeting the B-cell receptor or NF-κB signalling pathways could lower the risk. Some sites of extranodal involvement, almost always indicate disseminated disease with a high propensity to invade the bone marrow and leptomeningeal compartments, particularly in double-hit lymphoma. Conversely, unifocal bone, craniofacial, thyroid, or gastric DLBCL show a relatively favourable prognosis with standard immunochemotherapy. Their risk of CNS recurrence might be largely driven by potential local invasion due to anatomic proximity when epidural, orbital, or skull involvement is present, thus requiring a case-by-case approach to prophylaxis. Future studies can help clarify the relationship between extranodal DLBCLs and their indolent MALT counterparts, and whether the favorable behavior of some ABC-like lymphomas (Activated B-cell-like (ABC) diffuse large B-cell lymphomas (e.g. in the stomach or craniofacial sites) might be explained by less aggressive genotypes (e.g. BCL6/NOTCH2 subtype). MALT lymphoma is a type of non-Hodgkin lymphoma (NHL) that starts in the mucosa lining some body organs and cavities. It is a type of NHL called marginal zone lymphoma. PCL can be defined as non-Hodgkin lymphomas that initially present in the skin without any extra cutaneous manifestations at the time of diagnosis. The skin is the second most common site of occurrence of non-Hodgkin lymphomas, second only to the lymphatic system. PCL can be broadly divided into two types-T cell lymphomas and B cell lymphomas.Major subtypes of T cell lymphomas include mycosis fungoides (MF) and its variants, Sezary syndrome, CD30 + lymphoproliferative disorders, and other more rare entities like subcutaneous panniculitis- like T-cell lymphoma, extranodal NK/T cell lymphoma nasal type, primary cutaneous peripheral T-cell lymphoma not otherwise specified, and adult T-cell leukemia/lymphoma. Cutaneous B-cell lymphomas comprise approximately 25% of all cutaneous lymphomas. There are three mai
{"title":"Central Nervous System Manifestations of Cutaneous Lymphomas.","authors":"Ambar Chakravarty","doi":"10.1007/s11910-025-01416-8","DOIUrl":"10.1007/s11910-025-01416-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>Primary cutaneous lymphomas (PCL) are an uncommon malignancy of the lymphocytes, primarily presenting with dermatologic lesions. Central nervous system(CNS) metastatic manifestations, are even rarer. This review focus mainly on three aspects namely early suspicion of CNS involvement, selection of cases for CNS chemo-prophylaxis and lastly, the rare occurrence from skin straight to brain without other organ involvement.</p><p><strong>Recent findings: </strong>Primary extranodal large B-cell lymphomas are very heterogeneous. Recent molecular data have thrown some light on such divergent clinical behaviour. The peculiar, stage-independent risk of CNS spread in testicular, breast, uterine, and possibly Primary Cutaneous Diffuse Large B Cell Lymphoma Leg type (PCDBLCL-LT), may be related to prevalent MCD (MYD88/CD79B-mutated) genomic subtype in these lymphomas. It remains to be seen how this genotype might facilitate invasion of the CNS parenchyma, and whether therapies targeting the B-cell receptor or NF-κB signalling pathways could lower the risk. Some sites of extranodal involvement, almost always indicate disseminated disease with a high propensity to invade the bone marrow and leptomeningeal compartments, particularly in double-hit lymphoma. Conversely, unifocal bone, craniofacial, thyroid, or gastric DLBCL show a relatively favourable prognosis with standard immunochemotherapy. Their risk of CNS recurrence might be largely driven by potential local invasion due to anatomic proximity when epidural, orbital, or skull involvement is present, thus requiring a case-by-case approach to prophylaxis. Future studies can help clarify the relationship between extranodal DLBCLs and their indolent MALT counterparts, and whether the favorable behavior of some ABC-like lymphomas (Activated B-cell-like (ABC) diffuse large B-cell lymphomas (e.g. in the stomach or craniofacial sites) might be explained by less aggressive genotypes (e.g. BCL6/NOTCH2 subtype). MALT lymphoma is a type of non-Hodgkin lymphoma (NHL) that starts in the mucosa lining some body organs and cavities. It is a type of NHL called marginal zone lymphoma. PCL can be defined as non-Hodgkin lymphomas that initially present in the skin without any extra cutaneous manifestations at the time of diagnosis. The skin is the second most common site of occurrence of non-Hodgkin lymphomas, second only to the lymphatic system. PCL can be broadly divided into two types-T cell lymphomas and B cell lymphomas.Major subtypes of T cell lymphomas include mycosis fungoides (MF) and its variants, Sezary syndrome, CD30 + lymphoproliferative disorders, and other more rare entities like subcutaneous panniculitis- like T-cell lymphoma, extranodal NK/T cell lymphoma nasal type, primary cutaneous peripheral T-cell lymphoma not otherwise specified, and adult T-cell leukemia/lymphoma. Cutaneous B-cell lymphomas comprise approximately 25% of all cutaneous lymphomas. There are three mai","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"27"},"PeriodicalIF":4.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-21DOI: 10.1007/s11910-025-01411-z
Jigisha P Thakkar, Diego D Luy, Andrew Pickles, Tamer Refaat, Vikram C Prabhu
Purpose of review: Chronic complications of brain tumors and brain tumor treatments can lead to impairment of health-related quality of life and decreased functionality. These largely include cognitive decline, fatigue, headache, seizures, and secondary malignancies. Outpatient neurologists are an integral part of the multidisciplinary neuro-oncology team who help diagnose and manage chronic complications in this complex patient population. Timely diagnosis and treatment of these complications in outpatient neurology and neuro-oncology clinics helps improve quality of life and survival of brain tumor patients.
Recent findings: We discuss updated information and management regarding various chronic neurologic complications among neuro-oncology patients. Understanding of chronic neurologic complications associated with central nervous system tumors and with common contemporary cancer treatments will facilitate neurologists management of these patient populations. While there are aspects analogous to the diagnosis and management in the non-oncologic population, a number of unique features discussed in this review should be considered.
{"title":"Chronic Neurological Complications of Brain Tumors and Brain Tumor Treatments.","authors":"Jigisha P Thakkar, Diego D Luy, Andrew Pickles, Tamer Refaat, Vikram C Prabhu","doi":"10.1007/s11910-025-01411-z","DOIUrl":"10.1007/s11910-025-01411-z","url":null,"abstract":"<p><strong>Purpose of review: </strong>Chronic complications of brain tumors and brain tumor treatments can lead to impairment of health-related quality of life and decreased functionality. These largely include cognitive decline, fatigue, headache, seizures, and secondary malignancies. Outpatient neurologists are an integral part of the multidisciplinary neuro-oncology team who help diagnose and manage chronic complications in this complex patient population. Timely diagnosis and treatment of these complications in outpatient neurology and neuro-oncology clinics helps improve quality of life and survival of brain tumor patients.</p><p><strong>Recent findings: </strong>We discuss updated information and management regarding various chronic neurologic complications among neuro-oncology patients. Understanding of chronic neurologic complications associated with central nervous system tumors and with common contemporary cancer treatments will facilitate neurologists management of these patient populations. While there are aspects analogous to the diagnosis and management in the non-oncologic population, a number of unique features discussed in this review should be considered.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"26"},"PeriodicalIF":4.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18DOI: 10.1007/s11910-025-01412-y
Ugur Sener, Jessica A Wilcox, Adrienne A Boire
Purpose of review: Leptomeningeal disease (LMD), or spread of cancer cells into the pia and arachnoid membranes encasing the brain and spinal cord, is associated with high symptom burden and poor survival at 2 to 5 months. Conventional treatments including photon-based radiation therapy, systemic chemotherapy, and intrathecal chemotherapy demonstrate limited efficacy. Despite significant successes for a range of solid tumors, immunotherapy has not yet demonstrated significant efficacy in management of LMD. Advances in understanding of LMD pathophysiology, improved diagnostics, and novel therapeutics are shifting this paradigm. In this article, we review diagnostic and treatment challenges associated with LMD.
Recent findings: We discuss the use of novel cerebrospinal fluid (CSF) analysis techniques such as circulating tumor cell and CSF cell-free DNA assessment to overcome limitations of conventional diagnostic modalities. We then review advances in treatment including clinical trial data demonstrating efficacy of proton craniospinal radiation to treat the entire neuroaxis. We discuss emerging data regarding targeted therapeutics conferring durable survival benefit. Novel therapeutics and combinatorial treatment approaches will likely further improve outcomes for patients with LMD.
{"title":"Leptomeningeal Disease: Current Approaches and Future Directions.","authors":"Ugur Sener, Jessica A Wilcox, Adrienne A Boire","doi":"10.1007/s11910-025-01412-y","DOIUrl":"10.1007/s11910-025-01412-y","url":null,"abstract":"<p><strong>Purpose of review: </strong>Leptomeningeal disease (LMD), or spread of cancer cells into the pia and arachnoid membranes encasing the brain and spinal cord, is associated with high symptom burden and poor survival at 2 to 5 months. Conventional treatments including photon-based radiation therapy, systemic chemotherapy, and intrathecal chemotherapy demonstrate limited efficacy. Despite significant successes for a range of solid tumors, immunotherapy has not yet demonstrated significant efficacy in management of LMD. Advances in understanding of LMD pathophysiology, improved diagnostics, and novel therapeutics are shifting this paradigm. In this article, we review diagnostic and treatment challenges associated with LMD.</p><p><strong>Recent findings: </strong>We discuss the use of novel cerebrospinal fluid (CSF) analysis techniques such as circulating tumor cell and CSF cell-free DNA assessment to overcome limitations of conventional diagnostic modalities. We then review advances in treatment including clinical trial data demonstrating efficacy of proton craniospinal radiation to treat the entire neuroaxis. We discuss emerging data regarding targeted therapeutics conferring durable survival benefit. Novel therapeutics and combinatorial treatment approaches will likely further improve outcomes for patients with LMD.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"25"},"PeriodicalIF":4.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-17DOI: 10.1007/s11910-025-01414-w
Elisabetta Indelicato, Michael Zech, Anna Eberl, Sylvia Boesch
Purpose of review: Large-scale studies using hypothesis-free exome sequencing have revealed the strong heritability of neurodevelopmental disorders (NDDs) and their molecular overlap with later-onset, progressive, movement disorders phenotypes. In this review, we focus on the shared genetic landscape of NDDs and movement disorders.
Recent findings: Cumulative research has shown that up to 30% of cases labelled as "cerebral palsy" have a monogenic etiology. Causal pathogenic variants are particularly enriched in genes previously associated with adult-onset progressive movement disorders, such as spastic paraplegias, dystonias, and cerebellar ataxias. Biological pathways that have emerged as common culprits are transcriptional regulation, neuritogenesis, and synaptic function. Defects in the same genes can cause neurological dysfunction both during early development and later in life. We highlight the implications of the increasing number of NDD gene etiologies for genetic testing in movement disorders. Finally, we discuss gaps and opportunities in the translation of this knowledge to the bedside.
{"title":"Insights on the Shared Genetic Landscape of Neurodevelopmental and Movement Disorders.","authors":"Elisabetta Indelicato, Michael Zech, Anna Eberl, Sylvia Boesch","doi":"10.1007/s11910-025-01414-w","DOIUrl":"10.1007/s11910-025-01414-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Large-scale studies using hypothesis-free exome sequencing have revealed the strong heritability of neurodevelopmental disorders (NDDs) and their molecular overlap with later-onset, progressive, movement disorders phenotypes. In this review, we focus on the shared genetic landscape of NDDs and movement disorders.</p><p><strong>Recent findings: </strong>Cumulative research has shown that up to 30% of cases labelled as \"cerebral palsy\" have a monogenic etiology. Causal pathogenic variants are particularly enriched in genes previously associated with adult-onset progressive movement disorders, such as spastic paraplegias, dystonias, and cerebellar ataxias. Biological pathways that have emerged as common culprits are transcriptional regulation, neuritogenesis, and synaptic function. Defects in the same genes can cause neurological dysfunction both during early development and later in life. We highlight the implications of the increasing number of NDD gene etiologies for genetic testing in movement disorders. Finally, we discuss gaps and opportunities in the translation of this knowledge to the bedside.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"24"},"PeriodicalIF":4.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-15DOI: 10.1007/s11910-025-01410-0
Derek Lin, Andrea Howard, Ahmed S Raihane, Mario Di Napoli, Eder Cáceres, Michael Ortiz, Justin Davis, Allae N Abdelrahman, Afshin A Divani
Purpose of review: A deeper understanding of the communication network between the gut microbiome and the central nervous system, termed the gut-brain axis (GBA), has revealed new potential targets for intervention to prevent the development of neurodegenerative disease associated with tramatic brain injury (TBI). This review aims to comprehensively examine the role of GBA post-traumatic brain injury (TBI).
Recent findings: The GBA functions through neural, metabolic, immune, and endocrine systems, creating bidirectional signaling pathways that modulate brain and gastrointestinal (GI) tract physiology. TBI perturbs these signaling pathways, producing pathophysiological feedback loops in the GBA leading to dysbiosis (i.e., a perturbed gut microbiome, impaired brain-blood barrier, impaired intestinal epithelial barrier (i.e., "leaky gut"), and a maladaptive, systemic inflammatory response. Damage to the CNS associated with TBI leads to GI dysmotility, which promotes small intestinal bacterial overgrowth (SIBO). SIBO has been associated with the early stages of neurodegenerative conditions such as Parkinson's and Alzheimer's disease. Many of the bacteria associated with this overgrowth promote inflammation and, in rodent models, have been shown to compromise the structural integrity of the intestinal mucosal barrier, causing malabsorption of essential nutrients and further exacerbating dysbiosis. TBI-induced pathophysiology is strongly associated with an increased risk of neurodegenerative diseases, including Parkinson's and Alzheimer's diseases, which represents a significant public health burden and challenge for patients and their families. A healthy gut microbiome has been shown to promote improved recovery from TBI and prevent the development of neurodegenerative disease, as well as other chronic complications. The role of the gut microbiome in brain health post-TBI demonstrates the potential for microbiome-targeted interventions to mitigate TBI-associated comorbidities. Promising new evidence on prebiotics, probiotics, diet, and fecal microbiota transplantation may lead to new therapeutic options for improving the quality of life for patients with TBI. Still, many of these preliminary findings must be explored further in clinical settings. This review covers the current understanding of the GBA in the setting of TBI and how the gut microbiome may provide a novel therapeutic target for treatment in this patient population.
{"title":"Traumatic Brain Injury and Gut Microbiome: The Role of the Gut-Brain Axis in Neurodegenerative Processes.","authors":"Derek Lin, Andrea Howard, Ahmed S Raihane, Mario Di Napoli, Eder Cáceres, Michael Ortiz, Justin Davis, Allae N Abdelrahman, Afshin A Divani","doi":"10.1007/s11910-025-01410-0","DOIUrl":"10.1007/s11910-025-01410-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>A deeper understanding of the communication network between the gut microbiome and the central nervous system, termed the gut-brain axis (GBA), has revealed new potential targets for intervention to prevent the development of neurodegenerative disease associated with tramatic brain injury (TBI). This review aims to comprehensively examine the role of GBA post-traumatic brain injury (TBI).</p><p><strong>Recent findings: </strong>The GBA functions through neural, metabolic, immune, and endocrine systems, creating bidirectional signaling pathways that modulate brain and gastrointestinal (GI) tract physiology. TBI perturbs these signaling pathways, producing pathophysiological feedback loops in the GBA leading to dysbiosis (i.e., a perturbed gut microbiome, impaired brain-blood barrier, impaired intestinal epithelial barrier (i.e., \"leaky gut\"), and a maladaptive, systemic inflammatory response. Damage to the CNS associated with TBI leads to GI dysmotility, which promotes small intestinal bacterial overgrowth (SIBO). SIBO has been associated with the early stages of neurodegenerative conditions such as Parkinson's and Alzheimer's disease. Many of the bacteria associated with this overgrowth promote inflammation and, in rodent models, have been shown to compromise the structural integrity of the intestinal mucosal barrier, causing malabsorption of essential nutrients and further exacerbating dysbiosis. TBI-induced pathophysiology is strongly associated with an increased risk of neurodegenerative diseases, including Parkinson's and Alzheimer's diseases, which represents a significant public health burden and challenge for patients and their families. A healthy gut microbiome has been shown to promote improved recovery from TBI and prevent the development of neurodegenerative disease, as well as other chronic complications. The role of the gut microbiome in brain health post-TBI demonstrates the potential for microbiome-targeted interventions to mitigate TBI-associated comorbidities. Promising new evidence on prebiotics, probiotics, diet, and fecal microbiota transplantation may lead to new therapeutic options for improving the quality of life for patients with TBI. Still, many of these preliminary findings must be explored further in clinical settings. This review covers the current understanding of the GBA in the setting of TBI and how the gut microbiome may provide a novel therapeutic target for treatment in this patient population.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"25 1","pages":"23"},"PeriodicalIF":4.8,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}