N. Matsutomo, Mitsuha Fukami, Kuninori Kobayashi, Yuta Endo, S. Kuhara, Tomoaki Yamamoto
The purpose of this study was to evaluate the impact of eyes‐closed resting and eyes‐open conditions on the measurement of cerebral blood flow (CBF) using arterial spin labeling magnetic resonance imaging (ASL MRI).
{"title":"Effects of eyes‐closed resting and eyes‐open conditions on cerebral blood flow measurement using arterial spin labeling magnetic resonance imaging","authors":"N. Matsutomo, Mitsuha Fukami, Kuninori Kobayashi, Yuta Endo, S. Kuhara, Tomoaki Yamamoto","doi":"10.1111/ncn3.12674","DOIUrl":"https://doi.org/10.1111/ncn3.12674","url":null,"abstract":"The purpose of this study was to evaluate the impact of eyes‐closed resting and eyes‐open conditions on the measurement of cerebral blood flow (CBF) using arterial spin labeling magnetic resonance imaging (ASL MRI).","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"11 1","pages":"10 - 16"},"PeriodicalIF":0.4,"publicationDate":"2022-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42422614","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}
We describe a middle‐aged patient with breast implants presenting with chronic headaches. We obtained a detailed clinical history from the patient about the temporal course of her headaches to her breast implant placement. We tried to rule out another potential differential diagnosis. Chronic headaches started 6 months after the patient underwent bilateral breast augmentation with saline breast implants, and they resolved soon after the implant was removed. We were able to rule out other possible causes of headaches clinically. Several well‐powered studies have shown a strong association between breast implant illness and neurological conditions. However, this may be easily overlooked if we do not have a solid clinical suspicion based on history. In an appropriate clinical setting, breast implant illness should be considered in patients presenting with new‐onset persistent headaches.
{"title":"A case of breast implant illness presenting as chronic headaches: A case report","authors":"Chetan S. Nayak, M. Sivaraman","doi":"10.1111/ncn3.12673","DOIUrl":"https://doi.org/10.1111/ncn3.12673","url":null,"abstract":"We describe a middle‐aged patient with breast implants presenting with chronic headaches. We obtained a detailed clinical history from the patient about the temporal course of her headaches to her breast implant placement. We tried to rule out another potential differential diagnosis. Chronic headaches started 6 months after the patient underwent bilateral breast augmentation with saline breast implants, and they resolved soon after the implant was removed. We were able to rule out other possible causes of headaches clinically. Several well‐powered studies have shown a strong association between breast implant illness and neurological conditions. However, this may be easily overlooked if we do not have a solid clinical suspicion based on history. In an appropriate clinical setting, breast implant illness should be considered in patients presenting with new‐onset persistent headaches.","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"11 1","pages":"41 - 42"},"PeriodicalIF":0.4,"publicationDate":"2022-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45869329","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}
Armando Cardosa‐Aguilar, Luis E. Martínez‐Bravo, Juan de Dios Garza‐Rivera, Diego A. Hidalgo‐Díaz
We report a 23‐year‐old‐female with MELAS (Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, Stroke‐like episodes) syndrome with uncontrolled epilepsy due to massive gastric dilatation, immediate decompression and medical treatment was initiated; after it, she improved remarkably and has remained seizure free following hospitalization. This case illustrates massive gastric dilatation, an uncommon and underdiagnosed presentation of intestinal pseudo‐obstruction, as a potential cause of uncontrolled epilepsy in patients with MELAS syndrome.
{"title":"Massive gastric dilatation associated with uncontrolled epilepsy in MELAS syndrome","authors":"Armando Cardosa‐Aguilar, Luis E. Martínez‐Bravo, Juan de Dios Garza‐Rivera, Diego A. Hidalgo‐Díaz","doi":"10.1111/ncn3.12671","DOIUrl":"https://doi.org/10.1111/ncn3.12671","url":null,"abstract":"We report a 23‐year‐old‐female with MELAS (Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, Stroke‐like episodes) syndrome with uncontrolled epilepsy due to massive gastric dilatation, immediate decompression and medical treatment was initiated; after it, she improved remarkably and has remained seizure free following hospitalization. This case illustrates massive gastric dilatation, an uncommon and underdiagnosed presentation of intestinal pseudo‐obstruction, as a potential cause of uncontrolled epilepsy in patients with MELAS syndrome.","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"10 1","pages":"331 - 333"},"PeriodicalIF":0.4,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43370995","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}
Parkinson's disease (PD) is a hypokinetic movement disorder with degeneration of dopaminergic and other neurons, whereas dystonia is a hyperkinetic movement disorder caused by various pathogenesis, that is, sporadic, genetic, stroke, brain injury, and other diseases, such as PD. Dopamine receptor 1 (D1R) antagonist and dopamine receptor 2 (D2R) antagonist induce dystonic symptom in monkey. Consistently, D1R antagonist and D2R antagonist decrease locomotion in mice. Moreover, D1R knock‐out (KO) mice and D2R KO mice show motor deficits. In humans, dopa‐responsive dystonia (DRD) is caused by genetically defective dopamine (DA) synthesis. DYT1 dystonia and genetic mouse models show decreased striatal D1R and D2R. Therefore, PD, pharmacological dystonia models, DRD and DYT1 dystonia, have defective DA pathways. Firing of globus pallidus internus (GPi) neurons is increased in PD and dystonia with local anesthesia. However, the ordinary firing loop model cannot explain how defective DA pathways induce dystonia. PD shows thalamic neurodegeneration, whereas PD with dystonia has relatively intact thalamic neurons. Since thalamic GABAergic interneurons are innervated by GPi GABAergic neurons, here I propose to add thalamic GABAergic interneurons between GPi GABAergic neurons and thalamic glutamatergic neurons as thalamic inverse pathway for healthy condition and dystonia, whereas thalamic ordinary pathway due to degeneration of thalamic GABAergic interneurons is suitable to PD. On the contrary, PD with dystonia has both thalamic ordinary and inverse pathways. Although precise thalamic circuits have not been elucidated, discrepancy in the ordinary firing loop model for dystonia seems to be solved by the thalamic switch from dystonia to PD.
{"title":"Reconsideration of the firing loop models for dystonia and Parkinson's disease","authors":"F. Yokoi","doi":"10.1111/ncn3.12670","DOIUrl":"https://doi.org/10.1111/ncn3.12670","url":null,"abstract":"Parkinson's disease (PD) is a hypokinetic movement disorder with degeneration of dopaminergic and other neurons, whereas dystonia is a hyperkinetic movement disorder caused by various pathogenesis, that is, sporadic, genetic, stroke, brain injury, and other diseases, such as PD. Dopamine receptor 1 (D1R) antagonist and dopamine receptor 2 (D2R) antagonist induce dystonic symptom in monkey. Consistently, D1R antagonist and D2R antagonist decrease locomotion in mice. Moreover, D1R knock‐out (KO) mice and D2R KO mice show motor deficits. In humans, dopa‐responsive dystonia (DRD) is caused by genetically defective dopamine (DA) synthesis. DYT1 dystonia and genetic mouse models show decreased striatal D1R and D2R. Therefore, PD, pharmacological dystonia models, DRD and DYT1 dystonia, have defective DA pathways. Firing of globus pallidus internus (GPi) neurons is increased in PD and dystonia with local anesthesia. However, the ordinary firing loop model cannot explain how defective DA pathways induce dystonia. PD shows thalamic neurodegeneration, whereas PD with dystonia has relatively intact thalamic neurons. Since thalamic GABAergic interneurons are innervated by GPi GABAergic neurons, here I propose to add thalamic GABAergic interneurons between GPi GABAergic neurons and thalamic glutamatergic neurons as thalamic inverse pathway for healthy condition and dystonia, whereas thalamic ordinary pathway due to degeneration of thalamic GABAergic interneurons is suitable to PD. On the contrary, PD with dystonia has both thalamic ordinary and inverse pathways. Although precise thalamic circuits have not been elucidated, discrepancy in the ordinary firing loop model for dystonia seems to be solved by the thalamic switch from dystonia to PD.","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"11 1","pages":"3 - 9"},"PeriodicalIF":0.4,"publicationDate":"2022-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45107122","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}
COVID-19 disease can be associated with several health-related consequences that are directly or indirectly related to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Acute psychiatric illnesses in the setting of COVID-19 infection are one of the reported consequences. In this case report, we discuss acute onset of psychosis in a young patient that we believe was related to post-COVID-19 infection. Some findings in the EEG in this patient, we believe, were related to use of antipsychotic medications and that caused challenges in the diagnosis. It is important to be aware of post-COVID-19 psychosis and challenges that may be encountered in the workup.
{"title":"Acute psychosis post-COVID-19 pneumonia.","authors":"Odai Abdalla, Emma Oskar, Shahram Izadyar","doi":"10.1111/ncn3.12668","DOIUrl":"10.1111/ncn3.12668","url":null,"abstract":"<p><p>COVID-19 disease can be associated with several health-related consequences that are directly or indirectly related to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Acute psychiatric illnesses in the setting of COVID-19 infection are one of the reported consequences. In this case report, we discuss acute onset of psychosis in a young patient that we believe was related to post-COVID-19 infection. Some findings in the EEG in this patient, we believe, were related to use of antipsychotic medications and that caused challenges in the diagnosis. It is important to be aware of post-COVID-19 psychosis and challenges that may be encountered in the workup.</p>","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":" ","pages":""},"PeriodicalIF":0.4,"publicationDate":"2022-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9537979/pdf/NCN3-9999-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33515210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sangharsha Thapa, Sangam Shah, Aastha Subedi, Sara Bagherieh, Swati Chand, O. Mirmosayyeb, S. Eckert
One the disease modifying therapies (DMTs) that has been reported to be beneficial in multiple sclerosis (MS) is ponesimod, and as it holds true for all other autoimmune diseases, attempts to design immunosuppressive agents to help control the progression of MS while causing minimal side effects play a pivotal role in helping individuals suffering from the disease. Consequently, we have designed this review to comprehensively look into the safety and efficacy of ponesimod in persons with MS. A systematic database search was performed in March 2021. Double‐blinded RCTs on patients with MS with Ponesimod as their experimental medication were included. Annualized relapse rate (ARR), disability accumulation rate (DAR), the score of Fatigue Symptom and Impact Questionnaire–Relapsing Multiple Sclerosis (FSIQ–RMS), and adverse reactions were interpreted as efficacy and safety measurements, respectively. Ninety‐Five papers were retrieved in the literature search. After duplicate elimination, 92 studies remained. Finally, the review included two studies that met the criteria and used varied study designs. Ponesimod reduced ARR by 30.5% (p value = 0.001), DRA by 58% (p value = 0.29), and FSIQ‐RMS mean score by 3.57 (p value = 0.002). Meanwhile, the drugs have few side effects which were mild or moderate in intensity but has less cardiovascular side effects comparing to other S1P drugs like fingolimod. The advantageous properties of ponesimod in terms of its favorable risk: benefit and convenience profile, ponesimod has been regarded recently as a potential SIP‐1 drug for treating MS.
{"title":"Efficacy and Safety of Ponesimod in Relapsing Multiple Sclerosis: A Systematic Review","authors":"Sangharsha Thapa, Sangam Shah, Aastha Subedi, Sara Bagherieh, Swati Chand, O. Mirmosayyeb, S. Eckert","doi":"10.1111/ncn3.12669","DOIUrl":"https://doi.org/10.1111/ncn3.12669","url":null,"abstract":"One the disease modifying therapies (DMTs) that has been reported to be beneficial in multiple sclerosis (MS) is ponesimod, and as it holds true for all other autoimmune diseases, attempts to design immunosuppressive agents to help control the progression of MS while causing minimal side effects play a pivotal role in helping individuals suffering from the disease. Consequently, we have designed this review to comprehensively look into the safety and efficacy of ponesimod in persons with MS. A systematic database search was performed in March 2021. Double‐blinded RCTs on patients with MS with Ponesimod as their experimental medication were included. Annualized relapse rate (ARR), disability accumulation rate (DAR), the score of Fatigue Symptom and Impact Questionnaire–Relapsing Multiple Sclerosis (FSIQ–RMS), and adverse reactions were interpreted as efficacy and safety measurements, respectively. Ninety‐Five papers were retrieved in the literature search. After duplicate elimination, 92 studies remained. Finally, the review included two studies that met the criteria and used varied study designs. Ponesimod reduced ARR by 30.5% (p value = 0.001), DRA by 58% (p value = 0.29), and FSIQ‐RMS mean score by 3.57 (p value = 0.002). Meanwhile, the drugs have few side effects which were mild or moderate in intensity but has less cardiovascular side effects comparing to other S1P drugs like fingolimod. The advantageous properties of ponesimod in terms of its favorable risk: benefit and convenience profile, ponesimod has been regarded recently as a potential SIP‐1 drug for treating MS.","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"10 1","pages":"305 - 314"},"PeriodicalIF":0.4,"publicationDate":"2022-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46492775","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}
Y. Nakano, Yuki Taira, Ryo Sasaki, Koh Tadokoro, Taijun Yunoki, Emi Nomura, Y. Fukui, M. Takemoto, R. Morihara, N. Shimozawa, T. Yamashita
We report a case of a symptomatic female carrier of X‐linked adrenoleukodystrophy (ALD) with a novel ABCD1 gene mutation. She has developed slowly progressive gait disturbance since age 40, and her father and sister had similar symptoms. When admitted to our hospital at age 66, blood analysis showed slight increase of very long‐chain fatty acids (VLCFA), and DNA analysis of ABCD1 gene revealed a novel heterozygous missense mutation (c.1700 A>C, p.Gln567Pro). The genetic testing for ABCD1 gene can be considered in female patients over middle age presenting spastic gait, because female ALD carriers tend to be symptomatic beyond age 60.
{"title":"Novel ABCD1 mutation detected in a symptomatic female carrier of adrenoleukodystrophy","authors":"Y. Nakano, Yuki Taira, Ryo Sasaki, Koh Tadokoro, Taijun Yunoki, Emi Nomura, Y. Fukui, M. Takemoto, R. Morihara, N. Shimozawa, T. Yamashita","doi":"10.1111/ncn3.12667","DOIUrl":"https://doi.org/10.1111/ncn3.12667","url":null,"abstract":"We report a case of a symptomatic female carrier of X‐linked adrenoleukodystrophy (ALD) with a novel ABCD1 gene mutation. She has developed slowly progressive gait disturbance since age 40, and her father and sister had similar symptoms. When admitted to our hospital at age 66, blood analysis showed slight increase of very long‐chain fatty acids (VLCFA), and DNA analysis of ABCD1 gene revealed a novel heterozygous missense mutation (c.1700 A>C, p.Gln567Pro). The genetic testing for ABCD1 gene can be considered in female patients over middle age presenting spastic gait, because female ALD carriers tend to be symptomatic beyond age 60.","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"11 1","pages":"58 - 60"},"PeriodicalIF":0.4,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48325777","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}
Daiki Fukunaga, J. Fujinami, T. Kishitani, Naoki Tokuda, Soichiro Numa, Y. Nagakane
We describe an 83‐year‐old woman who presented with an acute onset of hemifacial droop. The patient's neurological examination showed peripheral‐type facial palsy with dysgeusia of the right anterior two‐thirds of her tongue. However, MRI revealed an anterior inferior cerebellar artery lesion, diagnosed as brain stem infarction. Peripheral‐type facial palsy has been reported in some stroke cases, with these cases not presenting with dysgeusia. Thus, this finding usually helps differentiate facial nerve palsy from peripheral‐type facial palsy caused by brain stem lesions. Despite the cerebral infarction, our patient presented with peripheral facial nerve palsy with taste disorder. This is because the lesion not only involved the pons but also the middle cerebellar peduncle. Therefore, patients with multiple vascular risk factors need to be carefully diagnosed.
{"title":"A case of peripheral‐type facial palsy with dysgeusia due to pontine infarction: A case report","authors":"Daiki Fukunaga, J. Fujinami, T. Kishitani, Naoki Tokuda, Soichiro Numa, Y. Nagakane","doi":"10.1111/ncn3.12666","DOIUrl":"https://doi.org/10.1111/ncn3.12666","url":null,"abstract":"We describe an 83‐year‐old woman who presented with an acute onset of hemifacial droop. The patient's neurological examination showed peripheral‐type facial palsy with dysgeusia of the right anterior two‐thirds of her tongue. However, MRI revealed an anterior inferior cerebellar artery lesion, diagnosed as brain stem infarction. Peripheral‐type facial palsy has been reported in some stroke cases, with these cases not presenting with dysgeusia. Thus, this finding usually helps differentiate facial nerve palsy from peripheral‐type facial palsy caused by brain stem lesions. Despite the cerebral infarction, our patient presented with peripheral facial nerve palsy with taste disorder. This is because the lesion not only involved the pons but also the middle cerebellar peduncle. Therefore, patients with multiple vascular risk factors need to be carefully diagnosed.","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"10 1","pages":"325 - 327"},"PeriodicalIF":0.4,"publicationDate":"2022-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49175082","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}
Adithya Chandregowda, Joseph R Duffy, Mary M Machulda, Val J Lowe, Jennifer L Whitwell, Keith A Josephs
A 57-year-old man presented with dynamic aphasia with evolving agrammatism and anomia. Additionally, he exhibited emerging atypical parkinsonism and features of behavioral variant frontotemporal dementia. Insights pertinent to this complex clinical presentation are discussed.
{"title":"Dynamic aphasia with emerging agrammatism, anomia, and aberrant frontal behaviors in a case of atypical parkinsonism.","authors":"Adithya Chandregowda, Joseph R Duffy, Mary M Machulda, Val J Lowe, Jennifer L Whitwell, Keith A Josephs","doi":"10.1111/ncn3.12658","DOIUrl":"https://doi.org/10.1111/ncn3.12658","url":null,"abstract":"<p><p>A 57-year-old man presented with dynamic aphasia with evolving agrammatism and anomia. Additionally, he exhibited emerging atypical parkinsonism and features of behavioral variant frontotemporal dementia. Insights pertinent to this complex clinical presentation are discussed.</p>","PeriodicalId":19154,"journal":{"name":"Neurology and Clinical Neuroscience","volume":"10 5","pages":"262-265"},"PeriodicalIF":0.4,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9642987/pdf/nihms-1825224.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10133463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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