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Статті в журналах з теми "Neurological soft sign"
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Dazzan, Paola, Tuhina Lloyd, Kevin D. Morgan, Jolanta Zanelli, Craig Morgan, Ken Orr, Gerard Hutchinson, et al. "Neurological abnormalities and cognitive ability in first-episode psychosis." British Journal of Psychiatry 193, no. 3 (September 2008): 197–202. http://dx.doi.org/10.1192/bjp.bp.107.045450.
Повний текст джерелаАнотація:
BackgroundIt remains unclear if the excess of neurological soft signs, or of certain types of neurological soft signs, is common to all psychoses, and whether this excess is simply an epiphenomenon of the lower general cognitive ability present in psychosis.AimsTo investigate whether an excess of neurological soft signs is independent of diagnosis (schizophrenia v. affective psychosis) and cognitive ability (IQ).MethodEvaluation of types of neurological soft signs in a prospective cohort of all individuals presenting with psychoses over 2 years (n=310), and in a control group from the general population (n=239).ResultsPrimary (P<0.001), motor coordination (P<0.001), and motor sequencing (P<0.001) sign scores were significantly higher in people with any psychosis than in the control group. However, only primary and motor coordination scores remained higher when individuals with psychosis and controls were matched for premorbid and current IQ.ConclusionsHigher rates of primary and motor coordination signs are not associated with lower cognitive ability, and are specific to the presence of psychosis.
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Thioritz, Wempy, Erlyn Limoa, J. C. Hutomo, Saidah Syamsuddin, and Sonny T. Lisal. "Differentiation in Neurological Soft Sign Scores on Schizophrenic Patients with Antipsychotic Treatment." Open Access Macedonian Journal of Medical Sciences 9, T3 (July 2, 2021): 249–53. http://dx.doi.org/10.3889/oamjms.2021.6356.
Повний текст джерелаАнотація:
Background: Schizophrenia is a chronic mental illness that affects cognitive aspect of a patient which need long term care with antipsychotics. Long term use of antipsychotic itself causes neurobiological change in the brain which results in alteration of cognitive function. The latest research had demonstrated that NSS (Neurological Soft Sign) reflect a rather wide range of cognitive impairments in schizophrenia which was not accounted for by age, education or severity of global cognitive deficits. Therefore, we examined the effects and impact of antipsychotic Haloperidol and Risperidone treatment in schizophrenic patient using NSS scores.
The Study showed that chronic schizophrenia patients had a higher NSS scores than acute patients. NSS also significantly associated with all neuropsychological domains of MMSE in both groups and were confirmed when age, education and severity of global cognitive deficits were not accounted for. This study also obtained a lower NSS score in patients who received Risperidone therapy compared to Haloperidol with p = 0.003. Out of 5 NSS domain in the Heidelberg scale, there was a significant improvement in motor coordination and motor sequencing (p = 0.004) and (p = 0.048) in patients who received Risperidone therapy compared to Haloperidol. There was an association between the chronicity of the disease and NSS, NSS also shows that it’s not influenced by age, education and severity of global cognitive deficits as a screening instrument. Finally the improvement of NSS scores in the Risperidone group was far superior compared to the Haloperidol group particularly in motor coordination and motor sequencing.
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Phillips, P. H. "Intermittent exotropia increasing with near fixation: a "soft" sign of neurological disease." British Journal of Ophthalmology 89, no. 12 (December 1, 2005): 1120–22. http://dx.doi.org/10.1136/bjo.2004.063123.
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Phillips, P. H., K. J. Fray, and M. C. Brodsky. "Intermittent Exotropia Increasing with Near Fixation: A “Soft” Sign of Neurological Disease." Journal of American Association for Pediatric Ophthalmology and Strabismus 10, no. 2 (April 2006): 188. http://dx.doi.org/10.1016/j.jaapos.2006.03.006.
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Picard, Hernàn, Anne Le Seac'h, Isabelle Amado, Raphael Gaillard, Marie-Odile Krebs, and Cécile Beauvillain. "Impaired saccadic adaptation in schizophrenic patients with high neurological soft sign scores." Psychiatry Research 199, no. 1 (August 2012): 12–18. http://dx.doi.org/10.1016/j.psychres.2012.04.039.
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GARDNER, DAVID, PETER B. LUCAS, and REX W. COWDRY. "Soft Sign Neurological Abnormalities in Borderline Personality Disorder and Normal Control Subjects." Journal of Nervous and Mental Disease 175, no. 3 (March 1987): 177–80. http://dx.doi.org/10.1097/00005053-198703000-00009.
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King, D. J., A. Wilson, S. J. Cooper, and J. L. Waddington. "The Clinical Correlates of Neurological Soft Signs in Chronic Schizophrenia." British Journal of Psychiatry 158, no. 6 (June 1991): 770–75. http://dx.doi.org/10.1192/bjp.158.6.770.
Повний текст джерелаАнотація:
Among 16 chronic schizophrenic in-patients, all had at least one neurological soft sign (NSS), and 6 (40%) had definite neurodysfunction. NSS and TD scores were highly intercorrelated, and NSS were significantly correlated with neuroleptic drug exposure. NSS correlated positively with both positive and negative symptoms and cognitive impairment but not with cerebral ventricular size on CT. Patients with neurodysfunction had more positive and negative psychopathology, cognitive impairment and TD than those without. Cerebral ventricular sizes and family histories of schizophrenia were similar in both NSS groups. The presence of NSS may be a simple but important way of identifying a subgroup of schizophrenics with neurodevelopmental predisposing abnormalities, and vulnerability to TD.
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Aronowitz, Bonnie R., Concetta Decaria, Andrea Allen, Nicola Weiss, Audrey Saunders, Lisa Margolin, Serge Mosovich, Montebuchs Baum, and Eric Hollander. "The Neuropsychiatry of Autism and Asperger's Disorder: Review of the Literature and Case Reports." CNS Spectrums 2, no. 5 (May 1997): 43–60. http://dx.doi.org/10.1017/s1092852900004892.
Повний текст джерелаАнотація:
AbstractThe literature on neuropsychiatric, neuropsychological, and neuroimaging findings in autism and Asperger's disorder is briefly reviewed. Neurological soft sign, neuropsychological, and positron-emission tomography findings in one patient with Asperger's disorder and one patient with autism are highlighted, discussed as examples of heterogeneity, and integrated with the relevant literature.
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Toro Espinoza, P., M. E. Ceballos, D. Valenzuela, M. F. Inostroza, and J. Schröder. "Subtests of the heidelberg neurological soft sign scale that discriminate HIV patients with and without hand." Journal of the Neurological Sciences 357 (October 2015): e5. http://dx.doi.org/10.1016/j.jns.2015.08.096.
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Bajraktari, Mustafa, Majlinda Naco, Gentian Huti, Blerim Arapi, and Rudin Domi. "Fat Embolism Syndrome Without Bone Fracture: Is It Possible?" Open Access Macedonian Journal of Medical Sciences 10, no. C (December 19, 2022): 331–35. http://dx.doi.org/10.3889/oamjms.2022.11169.
Повний текст джерелаАнотація:
BACKGROUND: Fat embolism syndrome is a life challenge syndrome. Early diagnosing and treatment can significantly improve the patient’s prognosis and likelihood of success. This syndrome occurs mainly after long bones fractures or orthopedic surgery up to 95% of diagnosed cases, but in unusual situation can be faced as well. These rare situations include diabetes mellitus, video-assisted thoracoscopies, fatty liver, and fat injection in plastic and cosmetic procedures. The likelihood of this syndrome can be increased if multiplex long bones fractures occur in the same patient simultaneously. This syndrome is usually manifested with respiratory changes (hypoxemia and ARDS), neurological focal symptoms (confusion, headache, aphasia, and hemiplegia), and skin abnormalities (petechias, and rush in conjunctiva and oral mucosa). The clinical scenario begins typically after 24−72 h of injury, and mainly, respiratory changes are the first, followed by neurological abnormalities and finally petechias as the most significant sign. CASE REPORT: In this case, we report a rare case of unexpected fat embolism syndrome after soft-tissue minimal trauma. This is the first case that we faced according to literature, and the aim of reporting this case is to emphasize that fat syndrome embolism can happen perhaps in every trauma patient even in minor soft-tissue trauma in absence of bone fractures. CONCLUSION: We strongly suggest that this case should make the physicians taking in consideration fat embolism syndrome even if bone fracture missed, to early diagnosing and adequately treating the patient, and optimizing his chances to survive.
Дисертації з теми "Neurological soft sign"
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Chen, Eric Y. H. "Soft neurological signs in schizophrenia." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24331.
Повний текст джерелаАнотація:
This dissertation describes a series of studies addressing the prevalence, correlates and longitudinal changes in soft neurological signs (SNS) in schizophrenia. SNS are found to be increased in schizophrenia. The increase appeared to have both a genetic and a non-genetic component. It has been proposed that SNS could be considered as one of the biological markers expressing a mediating risk for schizophrenia. In order to clarify the role of SNS in this perspective it is important to understand factors that affect the expression of SNS in a given population. Previous studies have identified possible relationships between SNS on one hand, and age, ethnicity, intelligence as well as education levels on the other. Associations with clinical features as well as cognitive function impairment have also been suggested. Antipsychotic medication side-effects appear not to be directly related to SNS, nevertheless their impacts cannot be entirely ruled out. Inconsistencies have also emerged as a result of sampling and methodological variations. The potential change of SNS with time in different phases of the disorder is another important issue that has not been adequately addressed with longitudinal studies. This dissertation describes works that addressed some of these issues in different samples using the same assessment methodology. A relatively extensive cross-sectional study addresses the relationship of SNS with demographic, educational, clinical and cognitive factors. The level of SNS in a Chinese sample is also compared with that obtained in a Caucasian sample to investigate effects of ethnicity. Data from the cross-sectional study also allow a limited analysis addressing the contributions of age and illness duration across a wider time range. Two longitudinal studies then focus on specific phases of the disorder. The first study investigates changes in SNS amongst chronic patients approaching old age (the fifth decade). The second study addresses changes in SNS following first episode psychosis. In the first chapter a broad introduction to methodological issues is presented. Chapter 2 continues with a more detailed review of the existing data about SNS in schizophrenia. Chapter 3 presents the core methodology and assessment instruments used in the studies. In Chapter 4 the recruitment procedures and the characteristics of the samples are described. Data analysis and results are presented in Chapters 5 to 8. In Chapter 5 important correlates of SNS are explored using data from a larger crosssectional sample of Chinese patients and controls. These include age, gender, education level, intelligence, as well as symptom correlates of SNS. The potential effects of ethnicity were further explored by comparison between Chinese and Caucasian control samples. Additional analyses were carried out to attempt to address the relative importance of age and illness duration for SNS in patients. Chapter 6 describes in more detail the relationship between SNS and cognitive functions in this cross-sectional sample. Chapters 7 and 8 describe two longitudinal studies. Chapter 7 deals with a 3-year follow-up study for stable chronic patients. Chapter 8 addresses a 2-year follow-up study of SNS in first episode patients. In Chapter 9 the dissertation ends with a general discussion of the current findings and suggestions for key areas for future research.
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Oskamp, Andrea [Verfasser]. "Neurological Soft Signs in Stadien der Anorexia nervosa / Andrea Oskamp." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/103563824X/34.
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Goldhahn, Klaus [Verfasser]. "Neurological Soft Signs bei Patientinnen mit Anorexia nervosa / Klaus Goldhahn." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023956985/34.
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Dazzan, Paola. "Neurological soft signs in first episode psychoses : their clinical and neuroanatomical correlates." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430827.
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Galindo, Guarin Liliana. "Neurological soft signs, temperament and schizotypy in patients with schizophrenia and unaffected relatives: an FMRI study." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/403815.
Повний текст джерелаАнотація:
La esquizofrenia es un trastorno psiquiátrico grave, un síndrome complejo y heterogéneo originado por la alteración del desarrollo del cerebro por factor genéticos o ambientales. Las bases genéticas pueden estar presentes en individuos sin enfermedad como en hermanos de pacientes y pueden ser identificadas a través de marcadores biológicos. Los signos neurológicos menores son discretas alteraciones sensitivo-motoras asociadas con un desarrollo cerebral alterado que se han propuesto como un endofenotipo de la esquizofrenia. Un perfil específico de temperamento y carácter así como la presencia de rasgos de personalidad esquizotípicos también se han relacionado con rasgos de personalidad esquizotípicos se han propuesto como un marcador de vulnerabilidad a la esquizofrenia. La etiopatogénesis de la esquizofrenia sugiere que puede haber una “alteración progresiva del neurodesarrollo”. Esta visión aboga por una alteración en los circuitos funcionales que implican áreas de asociación heteromodal más que alteraciones específicas en un área concreta del cerebro.
El objetivo de este estudio es explorar las anomalías de conectividad funcional en el Default Mode Network relacionados con la asociación entre signos neurológicos menores y rasgos de personalidad en la esquizofrenia.
Para investigar esta asociación se plantea un estudio transversal comparando un grupo de pacientes con esquizofrenia, un grupo de parientes no afectos de pacientes y un grupo de sujetos sanos, para explorar la asociación de estos posibles marcadores biológicos de esquizofrenia se estudio:
a) Asociación entre signos neurológicos menores y rasgos de personalidad : Inventario de temperamento y carácter TCI, Cuestionario de personalidad esquizotípica SPQ) y una evaluación de los signos neurológicos menores.
b) Asociación entre cambios en la conectividad cerebral en el default mode network con la presencia de signos neurológicos: fMRI en estado de reposo..
El principal hallazgo de este estudio es que los pacientes con esquizofrenia y los parientes no afectos presentan un perfil específico de temperamento y carácter con más rasgos de personalidad esquizotípicos que se correlacionan con una mayor presencia se signos neurológicos menores.
Los resultados revelan que la asociación entre estos posibles biomarcadores a nivel teórico como el temperamento (especialmente la evitación del daño, la búsqueda de recompensa y la persistencia) y el carácter (especialmente la autodirección y la cooperación) que se correlaciona con la presencia de signos neurológicos menores en toda la muestra. También los rasgos esquizotípicos de personalidad mostraron una fuerte correlación con la presencia de signos neurológicos menores en toda la muestra.
Los resultados muestran la susceptibilidad a los signos neurológicos menores y a la esquizofrenia está relacionada en ambos casos con diferencias individuales en aspectos de personalidad en parientes no psicóticos de pacientes con esquizofrenia. Estos hallazgos subrayan el valor de usar ambos parámetros para el estudio de poblaciones de riesgo.
Los resultados de neuroimagen mostraron cambios en la conectividad de las redes neuronales por defecto posiblemente asociados a la presencia de signos neurológicos menores. Estos hallazgos apoyan la teoría de la dismetría cognitiva como una posible disfunción en las conexiones córtico-tálamo-cerebelares. Este modelo también podría explicar la diversidad de síntomas de la esquizofrenia y sus asociaciones (como en este estudio que incluye personalidad y funciones sensitivo-motoras).Schizophrenia is a severe psychiatric disorder that has a profound effect on both the individuals affected and society. This common mental illness is a complex, heterogeneous behavioural and cognitive syndrome that seems to originate from disruption of brain development caused by genetic or environmental factors, or both. The genetic basis may be present in individuals without disease, as in the case of relatives of patients, being detectable through biological markers. Neurological soft signs (NSS) are discrete sensorimotor impairments associated with deviant brain development that were postulate as an endophenotype of schizophrenic spectrum disorder. Also the personality traits have been proposed as a vulnerability marker in schizophrenia. A specific profile of temperament and character and the schizotypal personality traits have also been correlated with schizotypal personality traits. These traits and some neurological abnormalities have been shown to aggregate in the relatives of schizophrenia patients. The etiopathogenesis of schizophrenia suggests it may be a "progressive neurodevelopmental disorder". This view postulates a disruption in functional circuits involving hetero modal association areas rather than a specific abnormality in a single brain region. The aim of this study is to explore the abnormalities in the functional connectivity of the default mode network related to the association between neurological soft signs and personality in schizophrenia. To investigate this a cross-sectional study is proposed, comparing a group of patients with schizophrenia, a group of unaffected relatives and a group of healthy controls. In order to explore the association of these potential biomarkers of schizophrenia the study was composed of two parts: a) To explore the association between neurological soft signs and personality traits in schizophrenia, two personality examinations (Temperament and Character Inventory and the Schizotypal Personality Questionnaire) and an evaluation of Neurological Soft Signs were performed. b) To explore the association between cerebral connectivity changes in the default mode network with the presence of neurological soft signs in schizophrenia a functional magnetic resonance scan was performed on participants in a resting state. The major finding in this study was that patients with schizophrenia and non-psychotic relatives display a unique profile of temperament and character and more schizotypal traits that correlate with higher presence of NSS. Our results reveal an association between these hypothesized vulnerability markers, as temperament (especially harm avoidance, reward dependence and persistence) and character (especially self-directedness and cooperativeness) correlated with the presence of NSS in the entire sample. Also the schizotypal traits (total scores and subscores) showed a very strong correlation with the presence of NSS in the entire sample. The results showed that susceptibility to NSS and to schizophrenia are both related to individual differences in personality features in non-psychotic relatives of patients with schizophrenia. These findings highlight the value of using both assessments to study high risk populations. The neuroimaging results showed connectivity changes in the default mode network with a possible association with the presence of neurological soft signs. These findings support the theory of cognitive dysmetria as a possible dysfunction in cortical-thalamic-cerebellar connectivity. This model also could explain the diversity of symptoms in schizophrenia and their associations (like this study that includes personality and sensory and motor functions). One strength of the study is that the relatives of patients with schizophrenia had no familial ties to the patients used, thus decreasing the possibility that similar upbringing would confound the results.
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Negash, Alemayehu. "Bipolar disorder in rural Ethiopia : community-based studies in Butajira for screening, epidemiology, follow-up, and the burden of care." Doctoral thesis, Umeå universitet, Psykiatri, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-21743.
Повний текст джерелаАнотація:
Background: The challenges of research in economically stunted countries’ settings remains a profound concern and is linked to socioeconomic development of these countries. More research is needed regarding psychiatric morbidity in rural areas of the developing and poverty stricken countries. The present studies were undertaken within the framework of a broader ongoing community-based project on the course and outcome of major psychiatric disorders in the rural Butajira district located in Ethiopia. This thesis treats the course and outcome of bipolar I disorder in the district. Objectives: Through appraising mental health and population based research in a rural Ethiopian district, to evaluate the utility of modern research instruments, and to obtain baseline information relating to bipolar I disorder in the poverty stricken rural Butajira district of Ethiopia. The specific objectives were: 1. Evaluating and comparing two different screening methods of case detection and identification for schizophrenia and bipolar I disorder in the adult population of Butajira district. 2. Assesing the prevalence and clinical characteristics of of bipolar I disorder in Butajira at the community level. 3. Evaluating short-term outcome at follow-up of bipolar I disorder in the Butajira district. 4. Determining Neurological Soft Signs in community-identified cases of bipolar I disorder in Butajira district in comparison with healthy controls. 5. Assessing the burden of care among caregivers of those affected by bipolar I disorder identified in the Butajira Study. Methods: The district’s entire adult population aged 15-49 was identified through a double-sampling design. In the first stage of screening, door-to-door interviews were conducted by lay trained high school completed individuals who knew the culture of the people. Females interviewed females whereas males interviewed males. Additionally, the key-informants method was used to identify cases that would be missed by the CIDI or otherwise. The final confirmatory diagnostic interview was conducted by clinicians using the SCAN on door-to-door basis as well. The probable cases that fulfilled the lifetime DSM-IV diagnosis of bipolar I disorder were assigned for assessment by other baseline research instruments such as Neurological Evaluation vii Scale (NES), Young Mania Rating Scale, Hamilton Rating Scale for Depression, LCSS, PANS and SANS, BISS, BII, FIS and so on. Cases so identified with bipolar I disorder were subject to a follow-up for upto 2.5 years on the average (range 1 to 4 years). Two of the main clinical outcomes assessed were relapse to a mood episode, and remission from a mood episode. Outcomes were assessed annually by the instruments, and were further assessed monthly by trained psychiatric nurses. We also did a cross-sectional study of caregivers of bipolar I disorder cases, and assessed objective burden on the caregivers as considered from social, family strain, occupational and financial domains. Results: Information provided by the key informants was better at detecting schizophrenia or chronic psychiatric disease, whereas the CIDI was better at detecting affective disorders. Of the around 100 000 adults living in Butajira, 83.3% were found by the project’s census, of which 82% (68,378 subjects) were successfully screened by the CIDI, yielding 2,161 CIDI positive. These, together with 719 cases identified by the key informants, were invited for the SCAN interview, of which 74.7% agreed. This yielded 315 SCAN positive cases for bipolar I disorder, and complete information could be collected on 295 of these. Lifetime prevalence was estimated as 0.6% for males and 0.3% for females. The mean age of onset of the manic phase was 22.0 years and that of the depressive phase was 23.4 years. For 22.7% of the cases the illness started with a depressive episode and for the remaining 77.3% it started with a manic episode. Over half of the cases (55.9%) had never sought help from modern health care sector, and only 13.2% had ever been admitted to psychiatric hospital. At follow-up, 65.9% had exprerienced a relapse and 31.1% had persistent illness, while only 5% of the patients were in remission for most of the follow-up time. The bipolar I cases, as compared with healthy controls, performed worse on several items of NES, thus having more neurological dysfunction compared to controls. Caregives were largely (80.3%) first-degree relatives and spouses. Overall, 84% of the caregivers reported difficulties in at least one of the domains of family burden. Of these, 58.7% reported a severe degree of difficulties. Caregivers reported a high level of difficulties in intrafamilial relationships and social restrictions, disruption in earning a livelihood, and financial difficulties. Conclusions: The prevalence of bipolar I disorder is comparable to the prevalences reported from other countries, and our findings support the cross-cultural validity of the concept of bipolar I disorder. Majority of the cases are not treated in contrast to that in the developed countries. The burden of care for the caregivers is substantial in the population studied.
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Rothman, David J. "An Investigation of Neurological soft signs as a discriminating factor between Veterans with Post-traumatic Stress Disorder, mild Traumatic Brain Injury, and co-occurring Post-traumatic Stress Disorder and mild Traumatic Brain Injury." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5915.
Повний текст джерелаАнотація:
While multiple Operation Enduring Freedom/Operation Iraqi Freedom/Operation New Dawn veterans suffer from mild Traumatic Brain Injury (mTBI), Post-traumatic Stress Disorder (PTSD), and co-morbid mTBI and PTSD, there remains difficulty disentangling the specific symptoms associated with each disorder using self-report and neurocognitive assessments. We propose that neurological soft signs (NSS), which are tasks associated with general neurologic compromise, may prove useful in this regard. Based on our review of the literature we hypothesized that individuals with PTSD would present with a greater number of NSS than controls or individuals with mTBI. Further, we hypothesized a synergistic effect, such that individuals with mTBI + PTSD would present with the greatest number of NSS. To test these hypotheses, we analyzed a subset of individuals (N=238) taken from a larger study of neurocognitive functioning in veterans. Participants completed a battery of neuropsychological measures, which included the Behavioral Dyscontrol Scale (BDS), the current study’s measure of NSS. A subset of other neuropsychological measures were also included to examine the utility of NSS over and above traditional neuropsychological measures. Individuals were removed from the study if they sustained a moderate/severe TBI or did not meet validity criteria on the Green’s Word Memory Test or the Negative Impression Management subscale of the Personality Assessment Inventory. Binomial logistic and multinomial logistic regression were used to examine the ability of NSS to discriminate between the study groups, first by themselves and then after the variance explained by the traditional neuropsychological measures was accounted for. Exploratory cluster analyses were performed on neuropsychological measures and NSS to identify profiles of cognitive performance in the data set. Results indicated that individuals in the mTBI and/or PTSD group had more NSS compared to controls. Of the individual NSS items only a go/no-go task of the BDS discriminated between groups, with worse performance among individuals in the mTBI, PTSD, and mTBI + PTSD group compared to controls. In contrast, the overall BDS score and individual NSS, in general, did not discriminate between the mTBI, PTSD, and mTBI + PTSD group. Overall, the current study suggests that, when eliminating participants who do not meet validity criteria, NSS do not aid in discriminating between individuals with mTBI, PTSD, and mTBI + PTSD.
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Gay, Olivier. "Marqueurs neurodéveloppementaux en psychiatrie : intérêt dans les troubles schizophréniques." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB016/document.
Повний текст джерелаАнотація:
Le terme de neurodéveloppement dans son acception la plus large renvoie à l'ensemble des processus permettant le développement du système nerveux depuis les étapes les plus précoces de sa formation in utero jusqu'aux étapes plus tardives de maturation à l'adolescence aboutissant au système nerveux adulte. Les travaux de ces quarante dernières années ont conduit à proposer un modèle neurodéveloppemental des troubles psychiatriques, notamment schizophréniques, sur la base d'arguments génétiques, épidémiologiques et d'imagerie. Ce modèle propose que l'apparition de la maladie soit liée à une/des anomalie(s) dans les processus de formation (neurodéveloppement précoce) et de maturation (neurodéveloppement tardif) du système nerveux, sous l'effet combiné de facteurs génétiques et environnementaux. Dans ce contexte, ce travail de thèse vise à préciser les effets des anomalies neurodéveloppementales sur les troubles psychiatriques, notamment schizophréniques à travers l'étude de différents marqueurs. La première étude a pour objectif d'étudier les corrélations entre deux marqueurs du développement cérébral précoce : un marqueur clinique (les signes neurologiques mineurs) et un marqueur en imagerie (la sulcation du cortex cérébral) dans une population de sujets atteints de schizophrénie. Une corrélation entre ces deux marqueurs est mise en évidence : l'index de sulcation est d'autant plus faible que les sujets présentent des signes neurologiques mineurs significatifs. Notre conclusion est que l'étude combinée de différents marqueurs peut permettre d'isoler des sous-groupes de patients ayant eu des atteintes neurodéveloppementales précoces plus marquées. La deuxième étude a pour objectif de caractériser l'effet de différents marqueurs d'anomalies neurodéveloppementales précoces sur le fonctionnement cognitif de sujets atteints de schizophrénie. L'effet sur le contrôle exécutif (mesuré par la tâche du Trail Making Test) de marqueurs cliniques (signes neurologiques mineurs, latéralisation manuelle) et en imagerie (sulcation du cortex cingulaire antérieur et élargissement des ventricules ventraux) est mesuré en recherchant les effets principaux et les interactions entre chaque marqueur. Nous trouvons des interactions entre différents marqueurs, avec principalement un effet de sommation non-linéaire. Notre interprétation est que les différents marqueurs reflètent des atteintes distinctes, bien que toutes précoces, du développement cérébral avec un effet final commun sur les fonctions exécutives. La troisième étude a pour objectif de préciser la spécificité de la sulcation comme marqueur d'anomalies neurodéveloppementales précoces à travers son étude dans une population de sujets adultes présentant un trouble du spectre autistique (TSA), pathologie débutant dès la petite enfance, en lien évident avec des atteintes neurodéveloppementales précoces. Des anomalies de sulcation du cortex cingulaire antérieur, similaires à celles observées chez les patients atteints de troubles schizophréniques, sont détectées chez les patients présentant un TSA. Ces résultats sont en faveur d'anomalies neurodéveloppementales précoces partagées entre différentes pathologies psychiatriques : les modifications de la sulcation corticale sont spécifiques non pas d'un trouble donné mais de la précocité des atteintes. En conclusion, nous proposons que l'étude des anomalies neurodéveloppementales soit intégrée dans une approche dimensionnelle en psychiatrieThe term neurodevelopment in its broadest sense refers to all of the processes encompassing development of the nervous system from the earliest stages of formation in utero to later stages of maturation during adolescence to produce the fully functional adult nervous system. Work over the last thirty years has led to a neurodevelopmental model of human psychiatric disorders, including schizophrenia, based on genetic, epidemiological and imaging evidence. This model asserts that disease is fundamentally linked to or develops from abnormality(s) in the formation processes (early neurodevelopment) and maturation (late neurodevelopment) of the nervous system due to a combination of genetic and environmental factors. In this context this thesis aims to clarify the effects of neurodevelopmental abnormalities on psychiatric disorders, including schizophrenia, through the study of different markers. The first study aims to investigate correlations between markers of early brain development: a clinical marker (neurological soft signs) and an imaging marker (sulcation of the cerebral cortex) in a population of subjects with schizophrenia. A correlation between these two markers is presented: the sulcation index was found to be lower in subjects that had significant neurological soft signs. We concluded that the combined study of different markers may help to isolate subgroups of patients with greater early neurodevelopmental damage. The second study aims to characterize effects of different markers of early neurodevelopmental abnormalities on cognitive functioning in patients with schizophrenia. Effects on executive control (as measured by the Trail Making Test) were correlated with clinical markers (neurological soft signs, handedness) and imaging (sulcation of the anterior cingulate cortex and enlargment of the ventricles). We found interactions between different markers with a mainly non-linear summation effect. Our interpretation is that different markers reflect separate insults, though all early, on brain development with a common final effect on executive function. The third study aims to clarify the specificity of sulcation as a marker of early neurodevelopmental abnormalities by studying a population of adult subjects with autism spectrum disorder (ASD), a patholody beginning in early childhood and linked with evidence of early neurodevelopmental damage. Sulcation abnormalities of the anterior cingulate cortex, similar to those observed in patients with schizophrenia are detected in patients with ASD. These results suggest early neurodevelopmental abnormalities are shared by different psychiatric disorders and that changes in cortical sulcation are not specific to a given disorder but the early damage. In conclusion, we suggest that the study of neurodevelopmental abnormalities should be integrated into a dimensional approach in psychiatry
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Aguirre, Pacheco Cándida Isabel. "Los signos neurológicos menores en la esquizofrenia: correlatos con las características clínicas, la función cognitiva y los cambios cerebrales estructurales." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/665695.
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Los Signos Neurológicos Menores (SNM), entendidos como alteraciones neurológicas que no tienen una localización específica a nivel cerebral, presentan una mayor prevalencia en los pacientes con esquizofrenia que en la población sana. También se ha descrito una mayor frecuencia de los mismos en los familiares de los pacientes con esquizofrenia (aunque en menor medida que en los pacientes). Algunos aspectos de la asociación de los SNM con el cuadro clínico de la esquizofrenia permanecen sin esclarecer. Otros temas de interés en la literatura se dirigen hacia la relación entre los SNM y los déficits neuropsicológicos observados en la esquizofrenia y su asociación con los cambios estructurales que caracterizan el trastorno.
El objetivo general de esta tesis fue el de estudiar la relación entre los SNM y diversos aspectos de la esquizofrenia en una muestra relativamente amplia de pacientes. El primer estudio examinó los correlatos con: a) los síntomas de la enfermedad organizados en los síntomas positivos (delirios y alucinaciones), el síndrome de desorganización (principalmente trastorno formal del pensamiento) y los síntomas negativos, y b) con el deterioro cognitivo, específicamente con dos aspectos concretos del déficit neuropsicológico observados en la esquizofrenia como son la función ejecutiva y la memoria. El segundo estudio evaluó la relación de los SNM con las estructuras cerebrales, específicamente con los cambios en la sustancia gris. Los SNM fueron valorados en ambos estudios a través de una escala detallada y estructurada, la NES de Buchanan y Heinrichs, que ofrece una puntuación total y tres subescalas: integración sensorial, coordinación motora, secuenciación de actos motores complejos.
En el primer estudio se examinó la prevalencia de los SNM en una muestra de 78 sujetos con esquizofrenia crónica. También se exploró un grupo de 36 sujetos controles sanos para su comparación. Los síntomas clínicos fueron evaluados utilizando la escala de síntomas positivos y negativos (PANSS) a través de la cual se calcularon las puntuaciones para los síntomas positivos, de desorganización y los síntomas negativos. La función ejecutiva y la memoria fueron evaluadas utilizando dos baterías de pruebas, la BADSy el RBMT. El Coeficiente Intelectual (CI) actual se utilizó como una medida de función intelectual general. Tal y como se esperaba, se encontró que los pacientes esquizofrénicos presentaron una mayor frecuencia de SNM que los sujetos controles. En cuanto a los síntomas clínicos de la enfermedad no se encontró relación entre los SNM y la clínica positiva ni tampoco con la clínica negativa; tan solo hubo evidencia equívoca en la correlación con el síndrome de desorganización. Las puntuaciones de los SNM correlacionaron de forma inversa y fuertemente con todas las puntuaciones de las pruebas cognitivas administradas. Las correlaciones con las puntuaciones de la memoria y de la función ejecutiva se mantuvieron significativas tras controlar la correlación con el deterioro general intelectual.
El segundo estudio se llevó a cabo con una muestra de 83 pacientes y un grupo de 60 sujetos controles sanos. Para medir el volumen de la sustancia gris se usó la resonancia magnética y se analizaron las imágenes mediante el análisis de morfometría basada en vóxeles de todo el cerebro. Los pacientes con esquizofrenia mostraron un patrón de reducción de volumen extendido por la corteza que también comprendía diversas estructuras subcorticales. Además, se observó un incremento de volumen de la sustancia gris en el tronco cerebral y mesencéfalo y una pequeña región del cerebelo izquierdo. No se pudieron encontrar clústeres de correlación significativa con la puntuación total de los SNM ni con las subescalas en el grupo de pacientes con esquizofrenia.
La discusión de los hallazgos de esta tesis se realizará haciendo particular referencia al fallo en la replicación de los hallazgos previos y la evidencia encontrada en muchos de los estudios revisados. También se discute acerca de las potenciales implicaciones: la hipótesis de la dismetría cognitiva de Andreasen y la idea de que representen un marcador de rasgo o endofenotipo para la enfermedad.Neurological soft signs (NSS), defined as minor neurological abnormalities that do not have localizing value, are established as being present at a higher frequency in patients with schizophrenia than in the healthy population. They are also present at a higher than normal frequency in the relatives of patients with schizophrenia, although at a lower rate than in the patients themselves, leading to considerable interest in their potential role as a marker of vulnerability or predisposition to the disorder. Nevertheless, some aspects of the association of NSS with the clinical features of schizophrenia remain unclear. Other relevant issues concern the relationship between NSS and the cognitive impairment and brain structural changes that also characterize the disorder. The general aim of this thesis was to examine the relationship between NSS and selected aspects of schizophrenia in a relatively large sample of patients. The first study examined a) their association with the symptoms of the disorder, as classified into positive symptoms (delusions and hallucinations), the disorganization syndrome (mainly formal thought disorder) and negative symptoms; and b) with the cognitive impairment seen in the disorder, specifically two major specific deficits, executive function and memory. The second study evaluated the relationship of NSS with brain structural abnormality, specifically changes in grey matter. NSS were assessed in both studies using a detailed scale, the Neurological Evaluation Scale (NES) of Buchanan and co-workers, which provides a total score and three subscale scores: sensory integration, motor coordination, and sequencing of complex motor acts. In the first study, the frequency of NSS was rated in a sample of 78 subjects with chronic schizophrenia. A comparison sample of 36 healthy control subjects was also employed. Clinical symptoms were rated using the Positive and Negative Symptom Scale (PANSS). The Behavioural Assessment of the Dysexecutive Syndrome (BADS) and the Rivermead Behavioral Memory Test (RBMT) were used to measure executive function and memory, respectively; current WAIS IQ was used as a measure of general intellectual function. As expected, the schizophrenic patients showed a higher frequency of NSS than the control subjects. With respect to symptoms, no relationship was found between NSS total or subscale scores and positive or negative symptoms; there was only equivocal evidence for a correlation with the disorganization syndrome. NSS scores correlated inversely and strongly with scores on all the cognitive measures. The correlations with memory and executive function scores remained significant after controlling for the correlation with general intellectual impairment. The second study was carried out on a sample of 83 patients with schizophrenia and a group of 60 healthy controls. Grey matter volume was measured using MRI, and the images were analyzed using whole-brain voxel-based morphometry. The patients with schizophrenia showed a pattern of widespread volume reduction in the cortex, and also in several subcortical structures. They also showed significantly increased grey matter volume in the brainstem and midbrain and in a small region of the left cerebellum. No clusters of significant correlation between NSS total or subscale scores were observed in the patients. The findings are discussed with particular reference to the failure to replicate previous findings of associations between NSS and negative symptoms, as well as the second study’s failure to find an association with structural cerebral changes in schizophrenia, something that has been reported in almost all previous MRI studies. The potential implications of the findings for two current theories of NSS in schizophrenia are also discussed: Andreasen’s hypothesis of cognitive dysmetria and the proposal that they represent a trait marker or endophenotype for the disorder.
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Martinez, Gilles. "Continuum autisme-schizophrénie : apport de l’étude de la cognition sociale et de marqueurs phénotypiques développementaux." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB065/document.
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Autisme et schizophrénie sont deux troubles psychiatriques neuro-développementaux. L’étude des formes précoces de schizophrénie, fréquemment associées aux troubles du spectre de l’autisme (TSA), a suggéré un possible continuum développemental entre ces troubles. Des arguments cliniques et épidémiologiques, et issus des études en génétique moléculaire ou en imagerie cérébrale, sont progressivement venus étayer cette hypothèse. Dans ce contexte, l’étude de la cognition sociale a fait l’objet d’un intérêt particulier, des altérations étant rapportées dans les deux troubles avec toutefois des résultats contrastés, révélant autant de points communs que de différences. Les relations entre altération de la cognition sociale et charge neuro-développementale ont par ailleurs été peu explorées. A travers nos trois études, nous avons confirmé l’existence d’altérations de la cognition sociale dans les TSA et la schizophrénie. Le MASC (Movie for the Assessment of Social Cognition), épreuve mixte et originale dont nous avons validé la version française, a permis de montrer une altération globale des capacités de mentalisation plus importante dans les TSA que dans la schizophrénie. Les Triangles Animés (épreuve d’attribution d’intention reposant sur un matériel non verbal) ont permis de révéler des différences qualitatives : tandis que l’hypomentalisation est commune aux deux troubles, l’hypermentalisation apparaît plus marquée dans la schizophrénie. Par ailleurs, à travers un continuum autisme-schizophrénie, l’altération de la cognition sociale était liée à la désorganisation de la pensée et du langage, et à l’importance des signes neurologiques mineurs (marqueur de vulnérabilité neurodéveloppementale). En outre, chez les sujets avec schizophrénie, l’hypermentalisation était corrélée à la précocité d’installation du trouble. Nos résultats soulignent l’intérêt de pouvoir repérer chez des patients adultes un trouble du développement. En ce sens, nous avons présenté les premiers éléments de validation d’un autoquestionnaire de dépistage des troubles du développement, permettant en population adulte un repérage rétrospectif des signes et symptômes d’autisme présents dans l’enfance. En conclusion, nos résultats apportent des arguments en faveur du continuum autisme-schizophrénie, en montrant l’existence d’une altération de la cognition sociale, dans ces deux troubles, corrélée à la charge neuro-développementale de façon trans-nosographique. Il existe toutefois des différences qualitatives. Un sous-groupe de sujets avec schizophrénie dont le trouble a débuté précocement semble par ailleurs se dessiner, caractérisé par une tendance à hyper-mentaliser et présentant une désorganisation plus marquéeAutism and schizophrenia are both neurodevelopmental psychiatric disorders. Research on early-onset schizophrenia, commonly associated to autism spectrum disorders (ASD), suggested a possible developmental continuum between both of these disorders. Clinical and epidemiological evidence, and research from molecular genetics or brain imaging, come to support this hypothesis. In this context, social cognition is a matter of special interest. Impairments are reported both in the two disorders, but with inconsistent results, revealing common features as well as differences. Otherwise, links between social cognition impairments and neurodevelopmental burden have been until now poorly explored. Through the contribution of our three studies, we confirmed the importance of social cognition impairment in autism and schizophrenia. The MASC test (Movie for the Assessment of Social Cognition), an original tool which was by our findings validated in a French version, revealed higher overall impairment of mentalizing capabilities in ASD than in schizophrenia. Animated Shapes (non verbal test of attribution of intentions) revealed qualitative differences: whereas hypomentalizing is common both to ASD and schizophrenia, overmentalizing seemed to be more important in schizophrenia. Furthermore, along a continuum between autism and schizophrenia, social cognition impairment was linked to thought and language disorganization, and to neurological soft signs (a marker for neurodevelopmental load). In addition, in subjects with schizophrenia, overmentalizing was correlated to the precocity of onset of the disease. Altogether, our results highlight the need to screen developmental feature in adulthood. In that way, we presented preliminary results in order to validate a developmental disorders screening self-rated questionnaire. As a conclusion, our results bring evidence in favour of a hypothesis of a continuum between autism and schizophrenia, showing a social cognition impairment in both disorders, correlated to the neurodevelopmental load existing in both of them in a transnosographic way. We contributed to emphasize the sub-group of subjects with schizophrenia with early-onset of disease, characterized by a tendency to overmentalizing and presenting a marked disorganization. Our work provides avenue to further studies, integrating neuroimaging and genetic data, that will help to advance in a deeper comprehension of the pathophysiology of autism and schizophrenia. Furthermore, we used and validated in this work promising tools to improve finely psychopathological evaluation and differential diagnosis in adults suffering from autism and from schizophrenia
Книги з теми "Neurological soft sign"
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E, Tupper David, ed. Soft neurological signs. Orlando: Grune & Stratton, 1987.
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Soft neurological signs in clumsy children: Indicators of timing and force control dysfunction. 1990.
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Ojagbemi, Akin. "Neurological Soft Signs." In Encyclopedia of Personality and Individual Differences, 3200–3204. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_782.
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Ojagbemi, Akin. "Neurological Soft Signs." In Encyclopedia of Personality and Individual Differences, 1–5. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_782-1.
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Shaffer, David, Cornelius S. Stokman, Patricia A. O’Connor, Stephen Shafer, Joseph E. Barmack, Suzanne Hess, D. Spalten, and Irvin S. Schonfeld. "Early Soft Neurological Signs and Later Psychopathology." In Life-Span Research on the Prediction of Psychopathology, 31–48. London: Routledge, 2021. http://dx.doi.org/10.4324/9781003165187-3.
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Neeper, Ronald, and Robert S. Greenwood. "On the Psychiatric Importance of Neurological Soft Signs." In Advances in Clinical Child Psychology, 217–58. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-9826-4_6.
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"Neurological Soft Signs." In Encyclopedia of Clinical Neuropsychology, 1754. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_4874.
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Schröder, Johannes, and Christina J. Herold. "Neurological Soft Signs in Schizophrenia Spectrum Disorders." In Movement Disorders in Psychiatry, edited by Antonio L. Teixeira, Erin Furr Stimming, and William G. Ondo, 169—C10.P105. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/med/9780197574317.003.0010.
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Abstract Neurological soft signs (NSS) are minor motor and sensory changes that are frequently found in schizophrenia spectrum disorders, including subjects with an increased liability to them, but can also be observed in bipolar disorder and dementia. In schizophrenia, high NSS-scores, which typically mark acute psychotic states, decrease in the course of illness with remission of acute symptoms. This process continues in patients with a favorable course but does not lead to a complete “normalization” of NSS, which remain in the range typical for subjects with an increased liability. As a transdiagnostic phenomenon, NSS are associated with similar symptoms and neurocognitive deficits across the respective disorders, such as negative symptoms, apathy or executive and declarative memory dysfunction. Neuroimaging studies in schizophrenia identified frontal cortices, including pre- and postcentral gyrus, inferior and middle frontal gyrus, and premotor area, alongside cerebellum, caudate, and thalamus as important sites for NSS. NSS can be used for early recognition and clinical diagnosis of schizophrenia and have the potential to facilitate our understanding of the cerebral mechanisms involved in its pathophysiology.
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Mehta, Gautam, and Bilal Iqbal. "Central Nervous System." In Clinical Medicine for the MRCP PACES. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780199542550.003.0011.
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As with all neurological patients, you will be more likely to pick up the diagnosis if you take a step back and look at the whole patient. Take some time to assess their facial expressions, speech, tremor, and posture. A common instruction at this station, with the patient seated on a chair is ‘Look at this patient, and examine as appropriate’. Candidates are often baffled, when given this instruction. Often the patients with Parkinson’s disease are given specific instructions to interlock the fingers of both hands, or place hands flat on their lap to mask the tremor. Picking up an expressionless face and low volume monotonous speech from the outset will provide useful clues to the diagnosis. If you are not sure at this stage, proceed to examining the gait. Once you are certain, that this is Parkinson’s disease, you may proceed to demonstrate the other features. 1. Patients with Parkinson’s disease have characteristic expressionless facies (hypomimia), often described as ‘mask-like’. This is a manifestation of bradykinesia. There is a reduced blink rate. The glabellar tap (Myerson’s sign) is an unreliable sign and is not recommended in the examination. This involves tapping the patient’s forehead repeatedly. Normal subjects will stop blinking, but in Parkinson’s disease, the patient will continue to blink. The patient may be drooling saliva (resulting from dysphagia and sialorrhoea-due to autonomic dysfunction) 2. Patients may have soft speech (hypophonia). This is also a manifestation of bradykinesia, and characteristically, the speech is low-volume, monotonous and tremulous (appears slurred). 3. Blepharoclonus is tremor of the eyelids. This will only be demonstrated if the eyes are gently closed, as opposed to tightly closing the eyes. 4. The classic tremor is present at rest and asymmetrical (more marked on one side). It is classically described as being 4–6Hz and is the initial symptom in 60% of cases, although 20% of patients never have a tremor. The tremor may appear as a ‘pill-rolling’ motion of the hand or a simple oscillation of the hand or arm. It is easier to spot a tremor if you ask the patient to rest their arms in their lap in the semi-prone position.
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Schröder, Johannes, and Christina J. Herold. "Neurological Soft Signs – A Transdiagnostic Phenomenon in Neuropsychiatric Conditions." In Reference Module in Neuroscience and Biobehavioral Psychology. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-809324-5.24016-9.
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Sechi, Elia, and Dean M. Wingerchuk. "Rapidly Progressive Numbness and Weakness After Soft-Tissue Abscess." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin, 7–9. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0002.
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A previously healthy 45-year-old man had development of neck pain and swelling, followed 1 week later by fevers, chills, and night sweats. Cervical computed tomography showed a left-sided cervical soft-tissue abscess. The patient was treated with oral cephalexin for 10 days, without benefit. Fine-needle aspiration biopsy of the mass showed granulomatous inflammation and a heterogeneous lymphocyte population without evidence of malignancy. Meropenem and gentamicin were started. Ten days later, he had development of acute urinary retention, numbness and weakness in the lower extremities, and numbness in the upper extremities. At symptom nadir 2 days later, he required the aid of a walker to ambulate. Lhermitte sign and erectile dysfunction were also present. The patient was admitted to the hospital. Spinal cord magnetic resonance imaging showed a longitudinally extensive, nonenhancing, T2-hyperintense lesion predominantly affecting the ventral and lateral parenchyma of the cervical and thoracic spinal cord. Cerebrospinal fluid examination showed a white blood cell count of 581 cells/µL with 42% neutrophils, 35% lymphocytes, and 22% monocytes, increased protein concentration (109 mg/dL), and normal glucose concentration. A diagnosis of postinfectious idiopathic transverse myelitis was made. The patient was treated with intravenous immunoglobulin, intravenous methylprednisolone, and broad-spectrum antibiotics, with improvement of both the abscess and his neurologic symptoms. After discharge, he was able to walk unassisted. At follow-up evaluation 6 months after the initial evaluation, neurologic examination showed only mild weakness of the left iliopsoas muscle and brisk reflexes in the lower extremities. Acute transverse myelopathies are a heterogeneous group of spinal cord disorders characterized by acute or subacute signs and symptoms of spinal cord dysfunction, typically a combination of sensory, motor, and autonomic manifestations. Underlying causes include vascular, infectious, neoplastic, postirradiation, traumatic, and inherited/metabolic, and inflammatory processes.
Тези доповідей конференцій з теми "Neurological soft sign"
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Silva, Bruno Custódio, Fernanda Silva dos Santos, Victória Porcher Simioni, Ana Luíza Kolling Konopka, Paulo Ricardo Gazzola Zen, and Rafael Fabiano Machado Rosa. "Type 1 neurofibromatosis and its relation to the occurrence of cerebral vascular accident." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.077.
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Context: Neurofibromatosis type 1 (NF1) is characterized by “café-au-lait” (CAL) spots, ephelids, cutaneous neurofibromas and iris Lisch nodules. Case report: A 63 year-old female patient came to evaluation due to NF1. She had a history of CAL spots, nodules on the skin, cognitive deficit and seizures. Chest X-ray showed several small nodules scattered in soft tissues of the thoracic wall. Magnetic resonance imaging of the skull demonstrated a possible increase in intracranial pressure. Computed tomography scan of the skull showed a hypodense area in the left hemisphere, consistent with a recent ischemic stroke. At the consultation, the patient reported episodes of headache, dizziness, nausea, vomiting, walking difficulty and pain in the thighs. On physical exam, she presented macrocephaly and diffuse nodular lesions. She also had masses in the abdominal and pelvic regions. On neurological exam, there was a pyramidal syndrome with right release pathway; ataxic gait; grade IV strength and Babinski sign. The patient was referred for surgical removal of the neurofibromas and died due to perioperative complications. Conclusions: Among patients with NF1, stroke is more common and occurs at a younger age than in the general population. The vasculopathy seen in NF1 involves the anterior and middle cerebral arteries, which can have serious or even fatal consequences. Anatomical vascular variants and intracranial aneurysms also occur more frequently in individuals with NF1.
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Schülke, Rasmus, Kyra Liepach, AnnaL Brömstrup, Thorsten Folsche, Maximilian Deest, Stefan Bleich, Alexandra Neyazi, Helge Frieling, and Hannah Maier. "Neurological soft signs are increased in major depressive disorder irrespective of antidepressant treatment." In Abstracts of the 3rd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1757665.
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Kaneko, Miki, Keiji Iramina, Takashi Ohya, Yushiro Yamashita, Yuichiro Kamei, Yoshinori Katayama, and Sachio Takashima. "A measurement of soft neurological signs by pronosupination using wireless acceleration and angular velocity sensors." In 2011 Biomedical Engineering International Conference (BMEiCON) - Conference postponed to 2012. IEEE, 2012. http://dx.doi.org/10.1109/bmeicon.2012.6172050.
Повний текст джерелаЗвіти організацій з теми "Neurological soft sign"
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Pitman, Roger K. Can Post mTBI Neurological Soft Signs Predict Postconcussive and PTSD Symptoms: A Pilot Study. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada602492.
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Pitman, Roger K. Can Post mTBI Neurological Soft Signs Predict Postconcussive and PTSD Symptoms: A Pilot Study. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada602679.
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