Imran Sarker, R. K. Khan, A. Haque, M. Hannan, R. Islam, A. N. Rizvi, A. Habib, S. Biswas
Background: Alzheimer’s disease is one of the common causes of dementia in our country. The growth of the elderly population, together with the rising incidence of dementia requires immediate attention. There is very limited data regarding how CSF Tau protein correlates with this group of people’s cognitive function. Objectives: To evaluate association of CSF Tau protein in different types of dementia patients (AD and non-AD) and to find out the correlation of CSF Tau with severity of dementia and duration of disease. Methods: This cross sectional analytical study was conducted in dementia clinic (OPD) and inpatient department of Neurology, BSMMU from March’2013 to September’2015. 48 both male and female adult subjects were included in this study. Then they were divided into 3 groups: Alzheimer’s disease (AD) group (n=15), non-AD other dementias (OD) group (n=18) and subjects having neither AD and/or OD were included as control (n=15). CSF Tau protein was measured and compared between 3 groups. Results: Mean age of dementia in AD group was 68.2±9.33 years and in OD group was 67.72±12.74 years. Mean MMSE score in AD group was 13.47± 4.72, in OD group 15.83±3.31 and in control group 28.60±1.12. This study showed that CSF Tau protein was highly elevated in AD group (315.30±279.68 pg/ml) than in OD (57.08±27.41pg/ml) and control (39.23±12.21) groups. Conclusion: The study found that CSF Tau levels are elevated in AD patients in comparison to non AD other dementias. So, CSF Tau protein can be an early biomarker of Alzheimer’s disease.
{"title":"Association of Cerebrospinal Fluid Tau Protein in Patients with Alzheimer’s and Non Alzheimer’s Dementias in a Tertiary Level Hospital in Bangladesh","authors":"Imran Sarker, R. K. Khan, A. Haque, M. Hannan, R. Islam, A. N. Rizvi, A. Habib, S. Biswas","doi":"10.12691/ijcen-5-1-4","DOIUrl":"https://doi.org/10.12691/ijcen-5-1-4","url":null,"abstract":"Background: Alzheimer’s disease is one of the common causes of dementia in our country. The growth of the elderly population, together with the rising incidence of dementia requires immediate attention. There is very limited data regarding how CSF Tau protein correlates with this group of people’s cognitive function. Objectives: To evaluate association of CSF Tau protein in different types of dementia patients (AD and non-AD) and to find out the correlation of CSF Tau with severity of dementia and duration of disease. Methods: This cross sectional analytical study was conducted in dementia clinic (OPD) and inpatient department of Neurology, BSMMU from March’2013 to September’2015. 48 both male and female adult subjects were included in this study. Then they were divided into 3 groups: Alzheimer’s disease (AD) group (n=15), non-AD other dementias (OD) group (n=18) and subjects having neither AD and/or OD were included as control (n=15). CSF Tau protein was measured and compared between 3 groups. Results: Mean age of dementia in AD group was 68.2±9.33 years and in OD group was 67.72±12.74 years. Mean MMSE score in AD group was 13.47± 4.72, in OD group 15.83±3.31 and in control group 28.60±1.12. This study showed that CSF Tau protein was highly elevated in AD group (315.30±279.68 pg/ml) than in OD (57.08±27.41pg/ml) and control (39.23±12.21) groups. Conclusion: The study found that CSF Tau levels are elevated in AD patients in comparison to non AD other dementias. So, CSF Tau protein can be an early biomarker of Alzheimer’s disease.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"5 1","pages":"11-17"},"PeriodicalIF":0.0,"publicationDate":"2017-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42226653","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}
S. Chaudhuri, Deep Das, S. Bhattacharya, S. Chakraborty, Kingshuk Bhattacharjee
Cerebral venous sinus thrombosis (CVST) is a neuromuscular disorder with protean manifestation requiring a high index of suspicion. Early diagnosis is sometimes lifesaving. It is particularly challenging is to establish an accurate etiology as it guides the clinician for long term thrombo-prophylaxis. We report a young female with no conventional risk factors for CVST, who presented with headache, generalised seizures and prolonged loss of consciousness. Her work-up revealed an elevated serum homocysteine level which might be a possible causative association in the etiopathogenesis of this neuromuscular condition.
{"title":"Hyper Homocysteinemia Related Cerebral Venous Sinus Thrombosis –Presenting as Generalised Tonic-Clonic Seizure –A Case Report","authors":"S. Chaudhuri, Deep Das, S. Bhattacharya, S. Chakraborty, Kingshuk Bhattacharjee","doi":"10.12691/ijcen-5-1-2","DOIUrl":"https://doi.org/10.12691/ijcen-5-1-2","url":null,"abstract":"Cerebral venous sinus thrombosis (CVST) is a neuromuscular disorder with protean manifestation requiring a high index of suspicion. Early diagnosis is sometimes lifesaving. It is particularly challenging is to establish an accurate etiology as it guides the clinician for long term thrombo-prophylaxis. We report a young female with no conventional risk factors for CVST, who presented with headache, generalised seizures and prolonged loss of consciousness. Her work-up revealed an elevated serum homocysteine level which might be a possible causative association in the etiopathogenesis of this neuromuscular condition.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"5 1","pages":"5-8"},"PeriodicalIF":0.0,"publicationDate":"2017-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44271357","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}
V. Puspitasari, S. Wahid, Amiruddin Aliah, Budhianto Suhadi
Transforming Growth Factor Beta (TGFβ) was a major regulatory molecule to suppress the immune response in the inflammatory process. TGFβ was also a growth factor that affects growth, homeostasis, angiogenesis and tissue repair. In the acute phase of stroke, astrocytes were activated and the cells were able to produce anti-inflammatory cytokines such as TGFβ. The purpose of this study was to determine whether there is a correlation between serum levels of TGFβ at acute phase of ischemic stroke and patients’ clinical outcomes. The study was conducted in patients with acute anterior system ischemic stroke who came to Siloam Hospital in Tangerang, Indonesia. Blood samples were taken to measure the levels of TGFβ-1serum at ≤ 72 hours and the 3rd day of onset. Clinical severity of stroke assessed using the National Institute of Health (NIH) Stroke Scale at 72 hours, 7th days and 30th days after stroke. The mean serum levels of TGFβ-1 at ≤ 72 hours in the group of subjects with mild NIH Stroke Scale degree was higher than in the group of subjects with moderate/severe NIH Stroke Scale degree (p = 0.046). The subjects with elevated levels of TGF-β1 in the acute phase of stroke had better clinical degrees at the 30th day after the stroke, although statistically was not significant (p = 0.241). Result of this study showed that TGFβ-1 may act as a neuroprotector against brain tissue damage after ischemic stroke.
{"title":"Correlation between Levels of Transforming Growth Factor Beta 1 (TGF-β1) serum with Clinical Outcome on Acute Anterior Circulation Ischemic Strokes","authors":"V. Puspitasari, S. Wahid, Amiruddin Aliah, Budhianto Suhadi","doi":"10.12691/IJCEN-5-1-1","DOIUrl":"https://doi.org/10.12691/IJCEN-5-1-1","url":null,"abstract":"Transforming Growth Factor Beta (TGFβ) was a major regulatory molecule to suppress the immune response in the inflammatory process. TGFβ was also a growth factor that affects growth, homeostasis, angiogenesis and tissue repair. In the acute phase of stroke, astrocytes were activated and the cells were able to produce anti-inflammatory cytokines such as TGFβ. The purpose of this study was to determine whether there is a correlation between serum levels of TGFβ at acute phase of ischemic stroke and patients’ clinical outcomes. The study was conducted in patients with acute anterior system ischemic stroke who came to Siloam Hospital in Tangerang, Indonesia. Blood samples were taken to measure the levels of TGFβ-1serum at ≤ 72 hours and the 3rd day of onset. Clinical severity of stroke assessed using the National Institute of Health (NIH) Stroke Scale at 72 hours, 7th days and 30th days after stroke. The mean serum levels of TGFβ-1 at ≤ 72 hours in the group of subjects with mild NIH Stroke Scale degree was higher than in the group of subjects with moderate/severe NIH Stroke Scale degree (p = 0.046). The subjects with elevated levels of TGF-β1 in the acute phase of stroke had better clinical degrees at the 30th day after the stroke, although statistically was not significant (p = 0.241). Result of this study showed that TGFβ-1 may act as a neuroprotector against brain tissue damage after ischemic stroke.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"5 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45364182","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}
H. Al-Jafar, R. Alroughani, T. Abdullah, Fatma Al-Qallaf
Sickle cell disease is a common inherited blood disorder that affects red blood cells. It is a hemoglobinopathy characterized by hemoglobin polymerization, erythrocyte stiffening, and subsequent vaso-occlusions. These changes can lead to microcirculation obstructions, tissue ischemia, infarction and acute stroke. In addition, chronic cerebral ischemia and cerebral vascular anomalies are considered among the most disabling problems in sickle cell disease. Neurological complications of sickle cell disease include, Ischaemic Stroke, hemorrhagic stroke, transient ischemic attack, silent cerebral infarction, headache, Moyamoya disease, neuropathic pain, and neurocognitive impairment. Early diagnosis and proper management of sickle cell disease neurological complications require specialised hematological and neurological experties. The newly used medications under ongoing research foster the hope to overcome this devastating disease and its complications.
{"title":"Neurological Complications in Sickle Cell Disease","authors":"H. Al-Jafar, R. Alroughani, T. Abdullah, Fatma Al-Qallaf","doi":"10.12691/IJCEN-4-1-2","DOIUrl":"https://doi.org/10.12691/IJCEN-4-1-2","url":null,"abstract":"Sickle cell disease is a common inherited blood disorder that affects red blood cells. It is a hemoglobinopathy characterized by hemoglobin polymerization, erythrocyte stiffening, and subsequent vaso-occlusions. These changes can lead to microcirculation obstructions, tissue ischemia, infarction and acute stroke. In addition, chronic cerebral ischemia and cerebral vascular anomalies are considered among the most disabling problems in sickle cell disease. Neurological complications of sickle cell disease include, Ischaemic Stroke, hemorrhagic stroke, transient ischemic attack, silent cerebral infarction, headache, Moyamoya disease, neuropathic pain, and neurocognitive impairment. Early diagnosis and proper management of sickle cell disease neurological complications require specialised hematological and neurological experties. The newly used medications under ongoing research foster the hope to overcome this devastating disease and its complications.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"4 1","pages":"9-18"},"PeriodicalIF":0.0,"publicationDate":"2016-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636461","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 : 2016-03-21DOI: 10.1016/b978-0-323-44781-2.50197-2
D. Rs, J. Harrison, M. Field, Boyle Rs
{"title":"Posterior cortical atrophy.","authors":"D. Rs, J. Harrison, M. Field, Boyle Rs","doi":"10.1016/b978-0-323-44781-2.50197-2","DOIUrl":"https://doi.org/10.1016/b978-0-323-44781-2.50197-2","url":null,"abstract":"","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"53977425","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}
M. Matsui, Chiaki Tanaka, Lisha Niu, K. Noguchi, W. Bilker, Michael R. Wierzbicki, R. Gur
Despite increasing evidence of the role of the prefrontal cortex in providing the neural substrate of higher cognitive function and neurodevelopment, little is known about neuroanatomic changes in prefrontal subregions during human development. In this prospective study, we evaluated prefrontal gray and white matter volume in healthy infants, children, adolescents, and adults. Magnetic resonance imaging was performed on 107 healthy people aged one month to 25 years. Gray and white matter volumes of the dorsolateral, dorsomedial, orbitolateral, and orbitomedial prefrontal cortex were quantified. The results indicated that both children and early adolescents had larger dorsolateral gray matter volume than infants and adults. Dorsolateral white matter volumes in children, early adolescents, and late adolescents were larger than those of infants. Dorsomedial white matter volumes of early adolescents, late adolescents, and adults were also larger than those of infants. There was no significant difference among age groups in both orbital prefrontal regions. These findings suggest that there are two important stages of structural change of the prefrontal cortex from infancy to young adulthood. First, growth spurts of both gray matter and white matter during the first 2 years of life have been shown to occur specifically in the dorsal prefrontal cortex. Second, gray matter changes have been shown to be regionally specific, with changes in the dorsal, but not orbital, prefrontal cortex peaking during late childhood or early adolescence. Thus, developmental differences within sectors of the prefrontal lobe and evidence of neural pruning and myelination may be useful in understanding the mechanisms of neurodevelopmental disorders.
{"title":"Age-related Volumetric Changes of Prefrontal Gray and White Matter from Healthy Infancy to Adulthood","authors":"M. Matsui, Chiaki Tanaka, Lisha Niu, K. Noguchi, W. Bilker, Michael R. Wierzbicki, R. Gur","doi":"10.12691/IJCEN-4-1-1","DOIUrl":"https://doi.org/10.12691/IJCEN-4-1-1","url":null,"abstract":"Despite increasing evidence of the role of the prefrontal cortex in providing the neural substrate of higher cognitive function and neurodevelopment, little is known about neuroanatomic changes in prefrontal subregions during human development. In this prospective study, we evaluated prefrontal gray and white matter volume in healthy infants, children, adolescents, and adults. Magnetic resonance imaging was performed on 107 healthy people aged one month to 25 years. Gray and white matter volumes of the dorsolateral, dorsomedial, orbitolateral, and orbitomedial prefrontal cortex were quantified. The results indicated that both children and early adolescents had larger dorsolateral gray matter volume than infants and adults. Dorsolateral white matter volumes in children, early adolescents, and late adolescents were larger than those of infants. Dorsomedial white matter volumes of early adolescents, late adolescents, and adults were also larger than those of infants. There was no significant difference among age groups in both orbital prefrontal regions. These findings suggest that there are two important stages of structural change of the prefrontal cortex from infancy to young adulthood. First, growth spurts of both gray matter and white matter during the first 2 years of life have been shown to occur specifically in the dorsal prefrontal cortex. Second, gray matter changes have been shown to be regionally specific, with changes in the dorsal, but not orbital, prefrontal cortex peaking during late childhood or early adolescence. Thus, developmental differences within sectors of the prefrontal lobe and evidence of neural pruning and myelination may be useful in understanding the mechanisms of neurodevelopmental disorders.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"4 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2016-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635859","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}
Urbach–Wiethe (or lipoid proteinosis) disease (UWD) is a rare autosomal recessive disorder characterized by dermatological, psychiatric, and neurological symptoms. Presentation occurs during childhood, but can be observed from birth. While benign, the disease is progressive and chronic with no known cure. Treatment modalities are palliative for symptoms. The extant literature consists mainly of anecdotal reports and case studies that are limited by small sample sizes and paucity of controlled studies. Incidence and prevalence rates are unknown. There are less than 500 documented cases reported worldwide, and of those, less than 50 cases demonstrate neurological and neuropsychiatric conditions. Worldwide occurrence of the disease is documented, with the largest cohort living in a remote area of South Africa. The affected individuals are mainly Caucasian, born to consanguineous parents, and from Dutch or German heritage. Patients affected have been reported in China, Pakistan and Iran. Current and earlier studies focus primarily on the most visible signs of disease, dystonia and dermatological symptoms, while other studies have reported calcification in the amygdala, hippocampus, parahippocampal gyrus, and the striatum. While central nervous system involvement can lead to a wide range of clinical manifestations such as epilepsy and neuropsychiatric symptoms, there is not a consensus of reported cases with amygdala calcifications accompanied by neurological symptoms. Quantitative research is warranted to further identify the role and relationship between amygdala calcification and neurologic and neuropsychiatric symptoms, while qualitative research will afford insights into the lived experience of individuals and families living with UWD.
{"title":"Neuropsychiatric Symptoms of Urbach-Wiethe Disease","authors":"Richard P. Conti, J. Arnone","doi":"10.12691/IJCEN-3-2-3","DOIUrl":"https://doi.org/10.12691/IJCEN-3-2-3","url":null,"abstract":"Urbach–Wiethe (or lipoid proteinosis) disease (UWD) is a rare autosomal recessive disorder characterized by dermatological, psychiatric, and neurological symptoms. Presentation occurs during childhood, but can be observed from birth. While benign, the disease is progressive and chronic with no known cure. Treatment modalities are palliative for symptoms. The extant literature consists mainly of anecdotal reports and case studies that are limited by small sample sizes and paucity of controlled studies. Incidence and prevalence rates are unknown. There are less than 500 documented cases reported worldwide, and of those, less than 50 cases demonstrate neurological and neuropsychiatric conditions. Worldwide occurrence of the disease is documented, with the largest cohort living in a remote area of South Africa. The affected individuals are mainly Caucasian, born to consanguineous parents, and from Dutch or German heritage. Patients affected have been reported in China, Pakistan and Iran. Current and earlier studies focus primarily on the most visible signs of disease, dystonia and dermatological symptoms, while other studies have reported calcification in the amygdala, hippocampus, parahippocampal gyrus, and the striatum. While central nervous system involvement can lead to a wide range of clinical manifestations such as epilepsy and neuropsychiatric symptoms, there is not a consensus of reported cases with amygdala calcifications accompanied by neurological symptoms. Quantitative research is warranted to further identify the role and relationship between amygdala calcification and neurologic and neuropsychiatric symptoms, while qualitative research will afford insights into the lived experience of individuals and families living with UWD.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"24 1","pages":"45-50"},"PeriodicalIF":0.0,"publicationDate":"2015-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636296","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}
E. Fedosova, K. Sarkisova, V. Kudrin, V. Narkevich, A. Bazyan
WAG/Rij rats are genetic animal model of absence epilepsy with comorbidity of depression. The first spike-wave discharges (SWDs) in WAG/Rij rats begin to appear at the age of 2-3 months and are fully manifested by 5-6 months. Occurrence of SWDs in the EEG is the main index of absence epilepsy. Previously it has been shown that the extensive absence epilepsy in 5-6 months old WAG/Rij rats is accompanied by decrease of dopamine and its metabolites concentrations in the meso-cortico-limbic and nigro-striatal dopaminergic brain systems, resulting in the expression of depression-like behavioral symptoms, and impairments of the learning and memory processes. In 36 days old WAG/Rij rats, SWDs are not manifested, deficiency of the mesolimbic dopamine is not revealed, and symptoms of depression-like behavior are not expressed. In this study, behavior in the open field, light-dark choice, forced swimming tests, monoamines and their metabolites concentrations in 5 brain structures (prefrontal cortex, nucleus accumbens, hypothalamus, striatum, hippocampus) were investigated in two months old WAG/Rij rats in comparison with age-matched Wistar rats. Reduced concentration of the dopamine and its metabolites, and increased concentration of the serotonin was found in WAG/Rij rats compared with Wistar rats only in the prefrontal cortex, indicating that the prefrontal cortex is the brain structure where neurochemical abnormalities appear first. No substantial changes in the monoamine and their metabolites concentrations have been revealed in other brain structures. Two months old WAG/Rij rats didn’t exhibit depression-like behavior in the forced swimming test, and learning/memory deficits in the passive avoidance test, but they showed behavioral changes, indicating increase anxiety/stress-reactivity, and alterations in learning/memory in the active avoidance test. Results suggest that two month-old WAG/Rij rats are at the stage of so called “pre-pathology” (increased anxiety and stress reactivity) preceding the development of depression-like behavior and substantial cognitive impairments which are co-morbid to fully expressed absence epilepsy in 5-6 months old rats of this strain.
{"title":"Behavioral and Neurochemical Characteristics of Two Months Old WAG/Rij Rats with Genetic Absence Epilepsy","authors":"E. Fedosova, K. Sarkisova, V. Kudrin, V. Narkevich, A. Bazyan","doi":"10.12691/IJCEN-3-2-2","DOIUrl":"https://doi.org/10.12691/IJCEN-3-2-2","url":null,"abstract":"WAG/Rij rats are genetic animal model of absence epilepsy with comorbidity of depression. The first spike-wave discharges (SWDs) in WAG/Rij rats begin to appear at the age of 2-3 months and are fully manifested by 5-6 months. Occurrence of SWDs in the EEG is the main index of absence epilepsy. Previously it has been shown that the extensive absence epilepsy in 5-6 months old WAG/Rij rats is accompanied by decrease of dopamine and its metabolites concentrations in the meso-cortico-limbic and nigro-striatal dopaminergic brain systems, resulting in the expression of depression-like behavioral symptoms, and impairments of the learning and memory processes. In 36 days old WAG/Rij rats, SWDs are not manifested, deficiency of the mesolimbic dopamine is not revealed, and symptoms of depression-like behavior are not expressed. In this study, behavior in the open field, light-dark choice, forced swimming tests, monoamines and their metabolites concentrations in 5 brain structures (prefrontal cortex, nucleus accumbens, hypothalamus, striatum, hippocampus) were investigated in two months old WAG/Rij rats in comparison with age-matched Wistar rats. Reduced concentration of the dopamine and its metabolites, and increased concentration of the serotonin was found in WAG/Rij rats compared with Wistar rats only in the prefrontal cortex, indicating that the prefrontal cortex is the brain structure where neurochemical abnormalities appear first. No substantial changes in the monoamine and their metabolites concentrations have been revealed in other brain structures. Two months old WAG/Rij rats didn’t exhibit depression-like behavior in the forced swimming test, and learning/memory deficits in the passive avoidance test, but they showed behavioral changes, indicating increase anxiety/stress-reactivity, and alterations in learning/memory in the active avoidance test. Results suggest that two month-old WAG/Rij rats are at the stage of so called “pre-pathology” (increased anxiety and stress reactivity) preceding the development of depression-like behavior and substantial cognitive impairments which are co-morbid to fully expressed absence epilepsy in 5-6 months old rats of this strain.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"3 1","pages":"32-44"},"PeriodicalIF":0.0,"publicationDate":"2015-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636232","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}
Shigeru Kobayashi, Yoshihiko Suzuki, S. Yamada, N. Al-khudairi, A. Meir
In order to investigate the mechanism of neurogenic pain, this study used a median nerve compression model in dogs. The nerve was compressed with a clip for three weeks. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve compression. In control animals, resident T cells were detected, but there were no macrophages. COX-2 was positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for COX-2. COX-2 may be deeply involved in neuritis arising from mechanical compression, and this mediator seems to be important in the manifestation of neurogenic pain.
{"title":"Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury","authors":"Shigeru Kobayashi, Yoshihiko Suzuki, S. Yamada, N. Al-khudairi, A. Meir","doi":"10.12691/IJCEN-3-2-1","DOIUrl":"https://doi.org/10.12691/IJCEN-3-2-1","url":null,"abstract":"In order to investigate the mechanism of neurogenic pain, this study used a median nerve compression model in dogs. The nerve was compressed with a clip for three weeks. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve compression. In control animals, resident T cells were detected, but there were no macrophages. COX-2 was positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for COX-2. COX-2 may be deeply involved in neuritis arising from mechanical compression, and this mediator seems to be important in the manifestation of neurogenic pain.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"3 1","pages":"26-31"},"PeriodicalIF":0.0,"publicationDate":"2015-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636149","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}
Facial Synkinesis is a clinical condition that is the sequel to facial nerve paralysis which develops during nerve repair like axon myelination and regeneration. Involuntary muscle activity is accompanied by voluntary muscle activity and may involve facial and extra ocular muscles. This article describes an uncommon variation of facial Synkinesis that manifested clinically in weak voluntary chewing and frequent cheek biting in the form of mucosal erosion on the buccal mucosa. Managing a case of facial paralysis that has associated facial Synkinesis has also been discussed.
{"title":"Synkinesis of Facial Musculature in a Patient with Facial Paralysis","authors":"K. Mattoo, M. Singh, P. Arora","doi":"10.12691/IJCEN-3-1-1","DOIUrl":"https://doi.org/10.12691/IJCEN-3-1-1","url":null,"abstract":"Facial Synkinesis is a clinical condition that is the sequel to facial nerve paralysis which develops during nerve repair like axon myelination and regeneration. Involuntary muscle activity is accompanied by voluntary muscle activity and may involve facial and extra ocular muscles. This article describes an uncommon variation of facial Synkinesis that manifested clinically in weak voluntary chewing and frequent cheek biting in the form of mucosal erosion on the buccal mucosa. Managing a case of facial paralysis that has associated facial Synkinesis has also been discussed.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"3 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2015-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635835","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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