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Journal articles on the topic 'Global apraxia'
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Pineda Pérez, Christian. "Las respuestas académicas a la objeción de apraxia." Praxis Filosófica, no. 46 (February 5, 2018): 221–42. http://dx.doi.org/10.25100/pfilosofica.v0i46.6170.
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En este artículo reconstruyo y analizo las respuestas de los escépticos académicos a la objeción de apraxia. Esta objeción afirma que el escepticismo es una doctrina imposible de practicar puesto que sus tesis conducen a la apraxia, esta es, un estado de privación o imposibilidad de acción. Las respuestas a la objeción se dividen en dos clases. La primera prueba que el asentimiento no es una condición necesaria para realizar acciones, por lo que la recomendación escéptica de suspender global y permanentemente el asentimiento no conduciría a la apraxia. La segunda prueba que es posible deliberar y orientar racionalmente nuestras acciones sin impresiones aprehensivas, por lo que la tesis escéptica de que no existen impresiones aprehensivas tampoco conduciría a la apraxia. Tras unas breves consideraciones generales, en la primera parte de este artículo presento las respuestas de Arcesilao y en la segunda parte las repuestas de Carnéades.
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Baranowski, Susan L., and Scott B. Patten. "The Predictive Value of Dysgraphia and Constructional Apraxia for Delirium in Psychiatric Inpatients." Canadian Journal of Psychiatry 45, no. 1 (February 2000): 75–78. http://dx.doi.org/10.1177/070674370004500111.
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Objective: To evaluate the predictive value of dysgraphia and constructional apraxia for delirium among psychiatric inpatients. Method: Data were collected from 2 sources. First, a series of nondelirious psychiatric inpatients that had participated in a previous study was selected to determine the specificity of various indices of dysgraphia and constructional apraxia. Second, a series of 56 psychiatric inpatients with delirium as identified using electronic administrative data and clinical records was selected to evaluate sensitivity. Results: Of the various indices of dysgraphia examined, only a global rating of writing quality and evidence of jagged or angled letter loops were informative clinical signs. The predictive value of constructional apraxia resembled the predictive value of the 2 dysgraphia indices. Conclusions: Dysgraphia and constructional apraxia are useful clinical signs of delirium in the psychiatric inpatient population. Evaluation of these functions can substantially impact diagnostic decisions where diagnostic uncertainty exists. An evaluation of writing and constructional praxis can be easily incorporated into bedside mental status examinations.
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Lesourd, Mathieu, Josselin Baumard, Christophe Jarry, Frédérique Etcharry-Bouyx, Serge Belliard, Olivier Moreaud, Bernard Croisile, et al. "Rethinking the Cognitive Mechanisms Underlying Pantomime of Tool Use: Evidence from Alzheimer’s Disease and Semantic Dementia." Journal of the International Neuropsychological Society 23, no. 2 (February 2017): 128–38. http://dx.doi.org/10.1017/s1355617716000618.
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AbstractObjectives: Pantomiming the use of familiar tools is a central test in the assessment of apraxia. However, surprisingly, the nature of the underlying cognitive mechanisms remains an unresolved issue. The aim of this study is to shed a new light on this issue by exploring the role of functional, mechanical, and manipulation knowledge in patients with Alzheimer’s disease and semantic dementia and apraxia of tool use. Methods: We performed multiple regression analyses with the global performance and the nature of errors (i.e., production and conception) made during a pantomime of tool use task in patients and control participants as dependent variables and tasks investigating functional, mechanical, and manipulation knowledge as predictors. Results: We found that mechanical problem solving, assessing mechanical knowledge, was a good predictor of the global performance of pantomime of tool use. We also found that occurrence of conception errors was robustly predicted by the task assessing functional knowledge whereas that of production errors was not explained by only one predictor. Conclusions: Our results suggest that both functional and mechanical knowledge are important to pantomime the use of tools. To our knowledge, this is the first demonstration that mechanical knowledge plays a role in pantomime of tool use. Although impairment in pantomime of tool use tasks (i.e., apraxia) is widely explained by the disruption of manipulation knowledge, we propose that pantomime of tool use is a complex problem-solving task. (JINS, 2017, 23, 128–138)
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Silva, Risayane Santos da, Julyane Feitoza Coêlho, Manuela Leitão de Vasconcelos, Isabelle Cahino Delgado, and Giorvan Ânderson dos Santos Alves. "Análise da intervenção fonoaudiológica em apraxia de fala na síndrome de Down: um estudo de caso." Distúrbios da Comunicação 32, no. 4 (November 25, 2020): 658–68. http://dx.doi.org/10.23925/2176-2724.2020v32i4p658-668.
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Introdução: A síndrome de Down (SD), trissomia do cromossomo 21, é uma condição genética que se caracteriza por um déficit cognitivo e atraso global do desenvolvimento. Dentre as habilidades que podem apresentar fragilidades, merecem destaque as alterações envolvendo a linguagem expressiva, com comprometimentos na fala. Essas alterações podem interferir no planejamento e na programação motora, caracterizando a ocorrência da apraxia de fala na infância, um distúrbio de origem neurológica, no qual a precisão e a consistência dos movimentos subjacentes à fala são prejudicadas na ausência de déficits neuromusculares. Objetivo: Apresentar a intervenção fonoaudiológica voltada à apraxia de fala em uma criança com SD. Método: O participante foi um menino com 07 anos de idade, diagnosticado com apraxia de fala associada à SD. A intervenção foi individualizada, baseada nos princípios do aprendizado motor e realizada durante 10 sessões, de 30 minutos cada. Na apresentação do caso, são abordados os dados da avaliação fonoaudiológica, os objetivos e procedimentos utilizados no planejamento terapêutico proposto. Resultados: Os dados coletados durante as sessões foram descritos e os efeitos da fonoterapia foram analisados. Os dados da reavaliação apontaram que os movimentos de praxias não verbais apresentaram melhores escores após a intervenção, sendo os resultados mais expressivos. Além disso, os resultados foram positivos quanto à estimulação para o desenvolvimento da fala, com os melhores resultados obtidos nos fonemas bilabiais /p, b e m/ e no fonema glotal /h/. Conclusão: A intervenção apresentou resultados satisfatórios, disponibilizando informações relevantes para uma melhor prática clínica na área.
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Basso, A., and E. Capitani. "Spared musical abilities in a conductor with global aphasia and ideomotor apraxia." Journal of Neurology, Neurosurgery & Psychiatry 48, no. 5 (May 1, 1985): 407–12. http://dx.doi.org/10.1136/jnnp.48.5.407.
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Usinskiene, Jurgita, Michael Mouthon, Chrisovalandou Martins Gaytanidis, Agnes Toscanelli, and Jean-Marie Annoni. "Orthographic Visualisation Induced Brain Activations in a Chronic Poststroke Global Aphasia with Dissociation between Oral and Written Expression." Case Reports in Neurological Medicine 2019 (July 2, 2019): 1–12. http://dx.doi.org/10.1155/2019/8425914.
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We propose a method of orthographic visualisation strategy in a poststroke severe aphasia person with dissociation between oral and written expression. fMRI results suggest that such strategy may induce the engagement of alternative nonlanguage networks and visual representations may help improving oral output. This choice of rehabilitation method can be based on the remaining capacities and, therefore, on written language. Most notably, no study so far addressed how orthographic visualisation strategy during speech rehabilitation might influence clinical outcomes in nonfluent aphasia and apraxia patients.
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Förstl, H., A. Burns, R. Levy, and N. Cairns. "Neuropathological basis for drawing disability (constructional apraxia) in Alzheimer's disease." Psychological Medicine 23, no. 3 (August 1993): 623–29. http://dx.doi.org/10.1017/s003329170002540x.
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SynopsisThe performance on four drawing tasks was studied in a sample of patients with verified Alzheimer's disease in order to examine the relationship of ‘constructional apraxia’ to neuropathological changes in the parietal lobe and in other brain areas. Twenty-three patients were able to attempt to copy pentagons, a spiral and a three-dimensional drawing of a house, 22 patients were able to draw a clock-face spontaneously. The results were rank-ordered by two independent raters. The values obtained in the different drawing tasks were correlated significantly with each other, with global estimates of cognitive performance (CAMCOG, Mini-Mental State), with a shorter duration of illness, higher brain weight (in the subsample of female patients), higher counts of large neurons in the parahippocampal gyrus and hippocampus, but not in the parietal lobe. This suggests that there is no specific relationship between ‘constructional apraxia’ and neuropathological changes in the parietal lobes of patients with advanced Alzheimer's disease, but that there is a correlation between widespread brain changes and several neuropsychological deficits, one of them being drawing disability.
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Cubelli, Roberto, Piera Trentini, and Carmelo G. Montagna. "Re-education of Gestural Communication in a Case ol Chronic Global Aphasia and Limb Apraxia." Cognitive Neuropsychology 8, no. 5 (September 1991): 369–80. http://dx.doi.org/10.1080/02643299108253378.
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Chenausky, Karen, Sébastien Paquette, Andrea Norton, and Gottfried Schlaug. "Apraxia of speech involves lesions of dorsal arcuate fasciculus and insula in patients with aphasia." Neurology: Clinical Practice 10, no. 2 (July 29, 2019): 162–69. http://dx.doi.org/10.1212/cpj.0000000000000699.
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ObjectiveTo determine the contributions of apraxia of speech (AOS) and anomia to conversational dysfluency.MethodsIn this observational study of 52 patients with chronic aphasia, 47 with concomitant AOS, fluency was quantified using correct information units per minute (CIUs/min) from propositional speech tasks. Videos of patients performing conversational, how-to and picture-description tasks, word and sentence repetition, and diadochokinetic tasks were used to diagnose AOS using the Apraxia of Speech Rating Scale (ASRS). Anomia was quantified by patients' scores on the 30 even-numbered items from the Boston Naming Test (BNT).ResultsTogether, ASRS and BNT scores accounted for 51.4% of the total variance in CIUs/min; the ASRS score accounted for the majority of that variance. The BNT score was associated with lesions in the left superior temporal gyrus, left inferior frontal gyrus, and large parts of the insula. The global ASRS score was associated with lesions in the left dorsal arcuate fasciculus (AF), pre- and post-central gyri, and both banks of the central sulcus of the insula. The ASRS score for the primary distinguishing features of AOS (no overlap with features of aphasia) was associated with less AF and more insular involvement. Only ∼27% of this apraxia-specific lesion overlapped with lesions associated with the BNT score. Lesions associated with AOS had minimal overlap with the frontal aslant tract (FAT) (<1%) or the extreme capsule fiber tract (1.4%). Finally, ASRS scores correlated significantly with damage to the insula but not to the AF, extreme capsule, or FAT.ConclusionsResults are consistent with previous findings identifying lesions of the insula and AF in patients with AOS, damage to both of which may create dysfluency in patients with aphasia.
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MATUTE, ESMERALDA, FERNANDO LEAL, DANIEL ZARABOZO, ANTONIA ROBLES, and CONCEPCIÓN CEDILLO. "Does literacy have an effect on stick construction tasks?" Journal of the International Neuropsychological Society 6, no. 6 (September 2000): 668–72. http://dx.doi.org/10.1017/s1355617700666043.
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Since constructional apraxia is often concomitant with brain lesions, the study of constructional tasks in the non-brain-damaged population might be useful in helping to disentangle other causal factors. This paper explores the performance of illiterate individuals (N = 29) as compared to that of semiliterates (N = 21) and literates (N = 23) in order to see the effect of reading and writing abilities on constructional tasks. Each participant was asked to construct 4 figures based upon models having varying degrees of complexity. A global criterion of lack of fidelity and several analytic criteria (related to distortion, rotation, and disarticulation errors) were used to evaluate performance. Although illiterates generally made more errors than semiliterates and semiliterates more than literates, only some of these differences were statistically significant. Significant differences were found for lack of global fidelity and disarticulation errors when all 4 figures were considered together. Subtler data emerged with respect to single figures. (JINS, 2000, 6, 668–672.)
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Reynolds, John J., Sherif F. El-Khamisy, Sachin Katyal, Paula Clements, Peter J. McKinnon, and Keith W. Caldecott. "Defective DNA Ligation during Short-Patch Single-Strand Break Repair in Ataxia Oculomotor Apraxia 1." Molecular and Cellular Biology 29, no. 5 (December 22, 2008): 1354–62. http://dx.doi.org/10.1128/mcb.01471-08.
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ABSTRACT Ataxia oculomotor apraxia 1 (AOA1) results from mutations in aprataxin, a component of DNA strand break repair that removes AMP from 5′ termini. Despite this, global rates of chromosomal strand break repair are normal in a variety of AOA1 and other aprataxin-defective cells. Here we show that short-patch single-strand break repair (SSBR) in AOA1 cell extracts bypasses the point of aprataxin action at oxidative breaks and stalls at the final step of DNA ligation, resulting in the accumulation of adenylated DNA nicks. Strikingly, this defect results from insufficient levels of nonadenylated DNA ligase, and short-patch SSBR can be restored in AOA1 extracts, independently of aprataxin, by the addition of recombinant DNA ligase. Since adenylated nicks are substrates for long-patch SSBR, we reasoned that this pathway might in part explain the apparent absence of a chromosomal SSBR defect in aprataxin-defective cells. Indeed, whereas chemical inhibition of long-patch repair did not affect SSBR rates in wild-type mouse neural astrocytes, it uncovered a significant defect in Aptx − / − neural astrocytes. These data demonstrate that aprataxin participates in chromosomal SSBR in vivo and suggest that short-patch SSBR arrests in AOA1 because of insufficient nonadenylated DNA ligase.
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Marbach, Felix, Georgi Stoyanov, Florian Erger, Constantine A. Stratakis, Nikolaos Settas, Edra London, Jill A. Rosenfeld, et al. "Variants in PRKAR1B cause a neurodevelopmental disorder with autism spectrum disorder, apraxia, and insensitivity to pain." Genetics in Medicine 23, no. 8 (April 8, 2021): 1465–73. http://dx.doi.org/10.1038/s41436-021-01152-7.
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Abstract Purpose We characterize the clinical and molecular phenotypes of six unrelated individuals with intellectual disability and autism spectrum disorder who carry heterozygous missense variants of the PRKAR1B gene, which encodes the R1β subunit of the cyclic AMP-dependent protein kinase A (PKA). Methods Variants of PRKAR1B were identified by single- or trio-exome analysis. We contacted the families and physicians of the six individuals to collect phenotypic information, performed in vitro analyses of the identified PRKAR1B-variants, and investigated PRKAR1B expression during embryonic development. Results Recent studies of large patient cohorts with neurodevelopmental disorders found significant enrichment of de novo missense variants in PRKAR1B. In our cohort, de novo origin of the PRKAR1B variants could be confirmed in five of six individuals, and four carried the same heterozygous de novo variant c.1003C>T (p.Arg335Trp; NM_001164760). Global developmental delay, autism spectrum disorder, and apraxia/dyspraxia have been reported in all six, and reduced pain sensitivity was found in three individuals carrying the c.1003C>T variant. PRKAR1B expression in the brain was demonstrated during human embryonal development. Additionally, in vitro analyses revealed altered basal PKA activity in cells transfected with variant-harboring PRKAR1B expression constructs. Conclusion Our study provides strong evidence for a PRKAR1B-related neurodevelopmental disorder.
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Hsu, Tina, Carrie C. Coughlin, Kristin G. Monaghan, Elise Fiala, Robert C. McKinstry, Alex R. Paciorkowski, and Marwan Shinawi. "CEDNIK." Child Neurology Open 4 (January 1, 2017): 2329048X1773321. http://dx.doi.org/10.1177/2329048x17733214.
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Synaptosomal-associated protein 29 (SNAP29) is a t-SNARE protein that is implicated in intracellular vesicle fusion. Mutations in the SNAP29 gene have been associated with cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma syndrome (CEDNIK). In patients with 22q11.2 deletion syndrome, mutations in SNAP29 on the nondeleted chromosome are linked to similar ichthyotic and neurological phenotypes. Here, the authors report a patient with cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma syndrome who presented with global developmental delay, polymicrogyria, dysgenesis of the corpus callosum, optic nerve dysplasia, gaze apraxia, and dysmorphic features. He has developed ichthyosis and palmoplantar keratoderma as he has grown. Exome sequencing identified a homozygous nonsense mutation in SNAP29 gene designated as c.85C>T (p.Arg29X). The authors compare the findings in the proband with previously reported cases. The previously unreported mutation in this patient and his phenotype add to the characterization of cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma syndrome and the accumulating scientific evidence that implicates synaptic protein dysfunction in various neuroectodermal conditions.
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Salman, Michael S., and Kristin M. Ikeda. "The Syndrome of Infantile-Onset Saccade Initiation Delay." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 40, no. 2 (March 2013): 235–40. http://dx.doi.org/10.1017/s0317167100013792.
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Introduction:Infantile-onset saccade initiation delay (ISID), also known as congenital ocular motor apraxia, is characterized by the inability to initiate volitional horizontal saccades. Other abnormalities including developmental delay and ataxia have been reported. The frequency of these abnormalities is unknown. We performed a detailed review of the medical literature to quantify features of ISID.Methods:We searched the English medical literature for articles related to ISID from 1952 to 2010. Whenever possible, patients were excluded if they had acquired SID, Joubert syndrome or neurodegenerative conditions. The minimum prevalence was calculated for each abnormality.Results:Sixty-six articles with information on 288 patients were included in the analysis. Head thrusts were reported in 84.7%. Blinks without head thrusts were used to initiate saccades in 41%. The fast phases of the optokinetic response and vestibulo-ocular reflex were impaired in 69.8% and 34.4% respectively. Smooth ocular pursuit was abnormal in 33%. Global developmental delay occurred in 41.3%, speech or language delay in 36.5%, cognitive delay in 17%, hypotonia in 35.8%, motor delay in 48.6%, and ataxia/clumsiness in 49.3% of patients. Neuroimaging was performed on 197 patients and was normal in 39.1%. Abnormalities involved the cerebellum (24.9%), cerebrum (15.7%), other infratentorial structures (11.7%), and corpus callosum (6.1%).Conclusions:Infantile-onset saccade initiation delay is frequently associated with deficits in reflexive saccades and less frequently with impaired smooth ocular pursuit. Developmental delay, hypotonia, and ataxia occur frequently in ISID, suggesting more global brain impairment and not just a saccadic disorder.
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Hayata, Yuki, Kensuke Hamada, Yasuhisa Sakurai, Izumi Sugimoto, Toru Mannen, and Yukitoshi Takahashi. "Anti-Glutamate ε2 Receptor Antibody-Positive and Anti-N-Methyl-D-Aspartate Receptor Antibody-Negative Lobar Encephalitis Presenting as Global Aphasia and Swallowing Apraxia." Case Reports in Neurology 6, no. 3 (December 24, 2014): 291–96. http://dx.doi.org/10.1159/000371442.
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DeCampli, William M. "Laboratory studies regarding regional low-flow perfusion for neonatal cardiac surgery." Cardiology in the Young 15, S1 (February 2005): 134–41. http://dx.doi.org/10.1017/s1047951105001174.
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As the overall mortality declines following repair of complex congenital cardiac malformations, attention has focused on reducing the lasting morbidity of these interventions, particularly the observed neurodevelopmental deficiencies. Both cardiopulmonary bypass and deep hypothermic circulatory arrest produce transient alterations in cerebral hemodynamics and metabolism. In studies performed in animals, deep hypothermic circulatory arrest, as compared to cardiopulmonary bypass alone, has been shown to produce excess injury to, and death of, neuronal and glial cells.1 In neonates, deep hypothermic circulatory arrest of greater duration than one hour is a risk factor for early post-operative seizures, and for subsequent neurodevelopmental deficits.2 The Boston Circulatory Arrest Study suggests that, at follow-up of eight years, infants subjected to greater than 41 minutes of deep hypothermic circulatory arrest had excess deficits in full-scale, verbal and performance intelligence quotient, the Mayo apraxia test, and grooved pegboard testing.3 The independent adverse effects of deep hypothermic circulatory arrest have encouraged clinicians to develop the alternative technique of intermittent global perfusion, or continuous regional perfusion at low flow perfusion, in an attempt to reduce the degree of injury to the central nervous system.4–7
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McMillan, HJ, A. Holahan, and J. Richer. "P.129 Worster-Drought syndrome caused by LINS mutations." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, s2 (June 2018): S50. http://dx.doi.org/10.1017/cjn.2018.231.
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Background: Worster-Drought syndrome (WDS) is a congenital, pseudobulbar paresis. Patients show oromotor apraxia causing impaired speech, drooling, dysphagia and varying degrees of cognitive impairment. Familial cases are reported although causative genes have not been identified. LINS mutations have recently been reported in patients with severe cognitive and language impairment. Methods: The proband was diagnosed with WDS at 8 years old because of longstanding drooling, dysphagia and impaired tongue movement. At 14 years old, he remains aphonic, using sign language and typing on a smart-tablet to communicate. Neurological examination including facial and extraocular movement was otherwise unremarkable. MRI brain revealed no heterotopia or atrophy. Results: An expanded intellectual disability panel at GeneDx identified nonsense mutations in LINS alleles: c.1096; p.Glu366X and c.1178 T>G, p.Lys393X. Neuropsychological testing at 14 years old noted nonverbal reasoning skills at 5 year old level with relative sparing of his receptive vocabulary and visual attention. Compared to prior testing at 9 years his receptive language improved from a 6 year old to an 8.5 year old level. Conclusions: Nonsense mutations of LINS have been identified in a patient with WDS. Despite his severe and persistent aphonia, improvements in receptive language were observed with global intellectual functioning better than expected.
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Xu, Shuqin, Pei Liu, Yuanxing Chen, Yi Chen, Wei Zhang, Haixia Zhao, Yiwei Cao, et al. "Foxp2 regulates anatomical features that may be relevant for vocal behaviors and bipedal locomotion." Proceedings of the National Academy of Sciences 115, no. 35 (August 13, 2018): 8799–804. http://dx.doi.org/10.1073/pnas.1721820115.
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Fundamental human traits, such as language and bipedalism, are associated with a range of anatomical adaptations in craniofacial shaping and skeletal remodeling. However, it is unclear how such morphological features arose during hominin evolution. FOXP2 is a brain-expressed transcription factor implicated in a rare disorder involving speech apraxia and language impairments. Analysis of its evolutionary history suggests that this gene may have contributed to the emergence of proficient spoken language. In the present study, through analyses of skeleton-specific knockout mice, we identified roles of Foxp2 in skull shaping and bone remodeling. Selective ablation of Foxp2 in cartilage disrupted pup vocalizations in a similar way to that of global Foxp2 mutants, which may be due to pleiotropic effects on craniofacial morphogenesis. Our findings also indicate that Foxp2 helps to regulate strength and length of hind limbs and maintenance of joint cartilage and intervertebral discs, which are all anatomical features that are susceptible to adaptations for bipedal locomotion. In light of the known roles of Foxp2 in brain circuits that are important for motor skills and spoken language, we suggest that this gene may have been well placed to contribute to coevolution of neural and anatomical adaptations related to speech and bipedal locomotion.
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Beeson, Pélagie M., Kristina Higginson, and Kindle Rising. "Writing Treatment for Aphasia: A Texting Approach." Journal of Speech, Language, and Hearing Research 56, no. 3 (June 2013): 945–55. http://dx.doi.org/10.1044/1092-4388(2012/11-0360).
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Purpose Treatment studies have documented the therapeutic and functional value of lexical writing treatment for individuals with severe aphasia. The purpose of this study was to determine whether such retraining could be accomplished using the typing feature of a cellular telephone, with the ultimate goal of using text messaging for communication. Method A 31-year-old man with persistent Broca's aphasia, severe apraxia of speech, global dysgraphia, and right hemiparesis participated in this study. Using a multiple baseline design, relearning and maintenance of single-word spellings (and oral naming) of targeted items were examined in response to traditional Copy and Recall Treatment (CART) for handwriting and a new paradigm using 1-handed typing on a cell phone keyboard (i.e., a texting version of CART referred to as T-CART). Results Marked improvements were documented in spelling and spoken naming trained in either modality, with stronger maintenance for handwriting than cell phone typing. Training resulted in functional use of texting that continued for 2 years after treatment. Conclusions These results suggest that orthographic retraining using a cell phone keyboard has the potential to improve spelling knowledge and provide a means to improve functional communication skills. Combined training with both handwriting and cell phone typing should be considered in order to maximize the durability of treatment effects.
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Oliveira, S. G., S. M. Pereira, and J. Mendes. "Dementia in Parkinson's disease: Case report." European Psychiatry 26, S2 (March 2011): 846. http://dx.doi.org/10.1016/s0924-9338(11)72551-2.
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IntroductionParkinson's disease (PD) dementia is a rapidly growing global health problem. Dementia in PD is often accompanied with neuropsychiatric manifestations, such as depression, insomnia, visual hallucinations and psychomotor agitation, which need psychiatric attention.ObjectivesThe authors’ aim is to report a case of a 76-year-old female suffering from PD who was admitted to the psychiatric yard exhibiting neuropsychiatric symptoms. A literature's review about PD dementia was also made.Case reportPatient had one psychiatric hospitalization at age 41, due to depressive symptoms. PD diagnose was made at age 65 and initially responded well to levodopa. Over the subsequent years, motor fluctuations and dyskinesias as well as autonomic, cognitive and psychological symptoms gradually developed. At 75 years, patient's family stated that she had been more forgetful, impulsive, showing signs of anxiety and dysphoria. She was hospitalized exhibiting psychomotor agitation, disorientation, insomnia and mainly nocturnal visual hallucinations with persons. Diagnostic testing included: cranial tomography which showed mild generalized atrophy but no other structural cause of her symptoms; laboratory tests with B12, folic acid, thyroid function; syphilis detection test and examinations of serum and urine were normal. The MMSE scored 19. Attention deficits and constructional apraxia were present in clock drawing test. Treatment was initiated with memantine and a low dose of quetiapine. She was discharged after 20 days with improvement of neuropsychiatric symptoms.ConclusionsEarly diagnosis and treatment of dementia in PD may prevent psychiatric hospitalization and avoid patient's and family's distress.
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Chieffo, Daniela, Gianpiero Tamburrini, Massimo Caldarelli, and Concezio Di Rocco. "Preoperative neuropsychological and behavioral evaluation of children with thalamic tumors." Journal of Neurosurgery: Pediatrics 13, no. 5 (May 2014): 507–13. http://dx.doi.org/10.3171/2014.2.peds13352.
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Object Functional involvement of the thalamus in cognitive processing has been only anecdotally reported in the literature, and these cases are mostly related to thalamic hemorrhages; there is no available information on cognitive development in children with thalamic tumors. Methods All children admitted with a diagnosis of thalamic tumor at the authors' institution between January 2008 and January 2011 were considered for the present study. Exclusion criteria were age less than 18 months and the presence of severe neurological deficits, both of which prevented a reliable neuropsychological evaluation. A complete preoperative neuropsychological evaluation was performed. Results Twenty children were selected (mean age 102.4 months). Total IQ was in the normal range in all patients (mean 90.1, SD 13.87) with a significant difference between verbal IQ (mean 97.70, SD 17.77) and performance IQ (mean 84.82, SD 17.01). A significant correlation was found between global cognitive impairment and a histological finding of low-grade tumors (p < 0.001). Children with a mesial thalamic tumor had a higher working memory deficit and delayed recall disorders (p < 0.001). Naming disorders were related to the presence of a bilateral (p < 0.001) or mesial (p < 0.001) thalamic tumor, without a significant difference between left or right hemisphere involvement. A significant correlation was also found between the presence of neurolinguistic disorders and mesially located tumors (p < 0.001). Children with right-sided tumors more frequently had constructional apraxia and executive function disorders (p < 0.001). Conclusions The present study suggests that thalamic tumors in different locations might have specific neuropsychological profiles.
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Chechlacz, Magdalena, Abigail Novick, Pia Rotshtein, Wai-Ling Bickerton, Glyn W. Humphreys, and Nele Demeyere. "The Neural Substrates of Drawing: A Voxel-based Morphometry Analysis of Constructional, Hierarchical, and Spatial Representation Deficits." Journal of Cognitive Neuroscience 26, no. 12 (December 2014): 2701–15. http://dx.doi.org/10.1162/jocn_a_00664.
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Deficits in the ability to draw objects, despite apparently intact perception and motor abilities, are defined as constructional apraxia. Constructional deficits, often diagnosed based on performance on copying complex figures, have been reported in a range of pathologies, perhaps reflecting the contribution of several underlying factors to poor figure drawing. The current study provides a comprehensive analysis of brain–behavior relationships in drawing disorders based on data from a large cohort of subacute stroke patients (n = 358) using whole-brain voxel-wise statistical analyses linked to behavioral measures from a complex figure copy task. We found that (i) overall poor performance on figure copying was associated with subcortical lesions (BG and thalamus), (ii) lateralized deficits with respect to the midline of the viewer were associated with lesions within the posterior parietal lobule, and (iii) spatial positioning errors across the entire figure were associated with lesions within visual processing areas (lingual gyrus and calcarine) and the insula. Furthermore, deficits in reproducing global aspects of form were associated with damage to the right middle temporal gyrus, whereas deficits in representing local features were linked to the left hemisphere lesions within calcarine cortex (extending into the cuneus and precuneus), the insula, and the TPJ. The current study provides strong evidence that impairments in separate cognitive mechanisms (e.g., spatial coding, attention, motor execution, and planning) linked to different brain lesions contribute to poor performance on complex figure copying tasks. The data support the argument that drawing depends on several cognitive processes operating via discrete neuronal networks and that constructional problems as well as hierarchical and spatial representation deficits contribute to poor figure copying.
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Morris, Claudia R., Janet Figueroa, Amanda Watt, Kirshma Khemani, Polly Kumari, Morgan Barnett, Nitya Bakshi, Peter A. Lane, and Carlton Dampier. "Safety of Intravenous Arginine Therapy in Children with Sickle Cell Disease Hospitalized for Vaso-Occlusive Pain: A Randomized Placebo-Controlled Trial in Progress." Blood 134, Supplement_1 (November 13, 2019): 995. http://dx.doi.org/10.1182/blood-2019-122983.
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Introduction: Vaso-occlusive pain episodes (VOE) are the leading cause of emergency department (ED) visits & hospitalizations in sickle cell disease (SCD). Low arginine (Arg) bioavailability has been associated with pain severity & need for pediatric hospitalization (Morris et al, 2000). Mitochondrial (mito) function is also impaired in SCD (Cardenes et al, 2014). We reported a dose-dependent impact of IV Arg on mito activity & oxidative stress in children with SCD (Morris, ASH 2018). Arg therapy was found to significantly decrease pain scores & reduced opioid use in children hospitalized with SCA-VOE compared to placebo in a phase 2 randomized placebo-controlled trial (RCT; Morris et al, 2013). IV Arg has an excellent safety profile, having received FDA approval for growth hormone stimulation testing in 1973, utilizing 500 mg/kg/dose or up to 30 grams/dose. Safety experience with its use in SCD is growing. Safety results of an ongoing phase 2 RCT at Emory/Children's Healthcare of Atlanta are reported here. Objectives: To review safety of IV arginine and enrollment in an ongoing RCT in children with SCD-VOE. Methods: A double-blind RCT of IV Arg (100 mg/kg/dose every 8 hours until discharge; up to 7 days/21 doses maximum) is underway in children age 3-21 years with SCD (any genotype) hospitalized for VOE requiring parenteral opioids. Patients with significant liver/renal dysfunction or those previously enrolled are excluded. Subjects are randomized into 1 of 3 arms: 1) 100 mg/kg/dose, standard dose (SD), 2) loading dose: 200 mg/kg followed by SD or 3) placebo. Demographics, clinical characteristics, total parenteral opioid use (morphine equivalents, mg/kg) time-to-crisis-resolution (time of initial study drug delivery to last parenteral opioid), length of hospital stay (hours), pain scores & biomarkers, including exhaled nitric oxide, global arginine bioavailability (plasma arginine & arginine/[ornithine+citrulline] ratio), mito function & patient reported outcomes (PROMIS) are obtained before & after treatment. The 1° outcome measure is total parenteral opioid use between study arms (power calculation based on Morris et al, 2013 & assuming 10% drop out); total sample size is 114 patients (38 per arm). Chi-squared/fisher exact tests were utilized as appropriate to compare development of adverse events (AEs) and serious AEs (SAEs) across randomization arms. This protocol utilizes IND#66943 (Sponsor-Morris), is registered with ClinicalTrials.gov (NCT02536170) & is funded by FDA-R01FD004814-01A2 & in part by NCCIH K24AT009893-01 (both to CRM). Results: A total of 1,129 patients have been screened, 220 were eligible with a guardian present, 87 were consented, and 83 were randomized; there were 4 screen failures. Most were enrolled in the ED (76%); guardians were often not present once transferred to the inpatient unit. Study drug was withdrawn by the PI on 4 patients (< 5%) for a variety of reasons that were reported as AEs; all patients completed the study with respect to monitoring per protocol. Demographics of subjects randomized by treatment group are provided in Table 1. There has been cumulative total of 16 SAEs in 13 unique patients, all involving re-hospitalization within 30 days or prolonged hospitalization. Six SAEs were "possibly related" (re-hospitalization within 7 days) and the rest were unlikely/probably not or not related to the study. 72-hour re-hospitalization rate is currently 6%. Table 2 includes a summary of the cumulative 309 AEs in 75 unique patients by system per treatment arm. Headache (33%), nausea (45%) & vomiting (25%) were common, but there were no significant differences across treatment arms. No difference in the seriousness, severity or relatedness for all events (SAEs & AEs) was identified across treatment arms. The 1st patient was enrolled in March 2016; enrollment is 76.3% completed through July 2019. Conclusion: All SAEs were expected events related to SCD. Additionally, SAE/AE rates were similar across study arms, providing further support for the safety of arginine therapy in children with SCD. Re-hospitalization rates within 72-hours are less than the ~20% previously reported in the literature. The availability of study team members to obtain consent in the ED prior to admission is essential for successful enrollment into acute VOE studies, since guardians are often not available once the child is transferred to the inpatient unit. Recruitment is ongoing. Disclosures Morris: Pfizer: Consultancy; UCSF-Benioff Oakland: Patents & Royalties: Patents owned by UCSF-Benioff Children's Hospital Oakland regarding biomarkers and therapies that target arginine bioavailability; none are licensed and there is no royalties generated; UCSF-Benioff Children's Hospital Oakland: Patents & Royalties: Patents owned by UCSF-Benioff Children's Hospital Oakland, licensed by Lifetrients, generating royalties for nutritional supplement for autism/apraxia. Lane:NHLBI: Research Funding; CDC: Research Funding; GA Dept: Other: Contract for newborn screeninjg follow-up services services; Bio Products Laboratory: Other: Sickle Cell Advisory Board; FORMA Therapeutics: Other: Clinical Advisory Board. Dampier:Ironwood: Consultancy; Global Blood Therapeutics: Consultancy; Hudson Publishing Company: Consultancy; Merck: Research Funding; Micelle Biopharma: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Epizyme: Consultancy; Modus Therapeutics: Consultancy. OffLabel Disclosure: Intravenous L-arginine for the treatment of SCD-related pain
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Onalo, Richard, Peter Cooper, Antoinette Cilliers, Uche Nnebe-Agumadu, Oluseyi Oniyangi, Damilare Oladimeji, and Claudia R. Morris. "Oral Arginine Therapy As a Novel Adjuvant in the Management of Acute Pain in Children with Sickle Cell Anemia in Nigeria: A Randomized Placebo-Controlled Trial." Blood 134, Supplement_1 (November 13, 2019): 613. http://dx.doi.org/10.1182/blood-2019-122510.
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Introduction: Severe vaso-occlusive pain episodes (VOE) are a major cause of morbidityand mortality in sickle cell anemia (SCA). Low arginine bioavailability is associated with pain severity and predicts need for pediatric hospitalization (Morris et al, 2000). Arginine supplementation has opioid-sparing effects and was found to significantly decrease pain scores in children hospitalized with SCA-VOE compared to placebo in a phase-2 randomized placebo-controlled trial (RCT) performed in the United States (US, Morris et al, 2013). Its role to treat acute SCA-related pain in a Sub-Saharan African country is unknown. Objectives: To determine the role of oral arginine as adjuvant in the management of SCA-VOE. Methods: A double-blind RCT of oral L-arginine (100 mg/kg/dose every 8 hours until discharge; up to 5 days/15 doses maximum) was performed in children with SCA hospitalized with severe VOE defined as a Numerical Pain Scale Score (PS) of at least 7 on a scale of 0-10, at one of two hospitals in Abuja, Nigeria. All patients received pain management (both opioids and non-opioid analgesics) per institutional practice. Demographics, clinical characteristics, length of hospital stay (LOS), pain scores, time-to-crisis-resolution (time-to-PS<4), analgesia medications required, and plasma amino acids levels were obtained before and after supplementation. Mean total analgesic medication quantification scale score (MQS), a sensitive measure to quantify analgesic use in patients with SCA, was utilized as previously described (Jacob et al, 2007). Opioid doses were calculated based on morphine equivalents in milligrams (mg). The study was performed after obtaining the National Agency for Food & Drug Administration & Control (NAFDAC) approval, Ref No. NAF/DER/CT/LAG/2017. The protocol was approved by the Human Research Ethics Committees of the University of the Witwatersrand, University of Abuja Teaching Hospital, Abuja & the National Hospital. The study was registered at the Pan African Clinical Trial Registry (PACTR 201611001864290). Results: Sixty-eight children with SCA were recruited, aged 5-17 years (mean: 10.6±0.4 years; 35 children randomized into the arginine arm & 33 into the placebo arm). Baseline characteristics were similar between arms (Table 1). MQS was significantly lower in the arginine group vs. placebo (73 [95% CI: 62-84] vs. 120 [97-143]; p<0.001). By day 5, 54% of children treated with arginine had been discharged compared to 24% in the placebo arm. Although PS were similar in both groups prior to study drug delivery (8.7±1.1 vs. 8.4±1.2, arginine vs placebo; p=0.30), worst reported PS on day 5 were lower in children treated with arginine compared to placebo (1.2±0.4 vs. 3.0±0.5; p<0.0001). The mean rate of PS decline was also greater in the arginine arm vs. placebo (1.5 [1.2-1.8) vs. 1.1 [0.9-1.2] cm/day; p=0.009). Plasma arginine levels increased by 125% vs 29% in the arginine arm vs. placebo; percent increase in arginine bioavailable inversely correlated with MSQ (r=-0.35;p=0.02). There was a non-statistically significant decrease in mean total opioid dose used in the arginine group vs. placebo (3.8 [2.7-4.9] vs 5.1 [3.8-6.5) mg/kg, p = 0.11). Patients receiving arginine had shorter time-to-crisis-resolution (p=0.0216, Fig1A), shorter LOS (p=0.015; Fig1B) and had no serious adverse events. There was 1 death in the placebo group on the second day of admission. There were no differences between groups in development of adverse events, however there was a trend towards more vomiting in the arginine arm compared to placebo (20% vs. 3%, p=0.07). Conclusion: Arginine deficiency plays a role in acute pain requiring hospitalization in Nigerian children with SCA, similar to what has been reported in the US. Plasma arginine levels significantly increased with arginine supplementation, and improved global arginine bioavailability was inversely associated with total analgesia and opioids used in VOE management. Total mean analgesia use and pain scores were lower, while time-to-crisis-resolution and LOS were shorter in children treated with arginine compared to placebo. No serious adverse events occurred in the arginine arm, while rates of adverse events were similar to placebo, providing further support for the safety of arginine therapy in children with SCA. Oral arginine is a promising adjuvant therapy for SCA-VOE management. Disclosures Morris: Pfizer: Consultancy; UCSF-Benioff Oakland: Patents & Royalties: Patents owned by UCSF-Benioff Children's Hospital Oakland regarding biomarkers and therapies that target arginine bioavailability; none are licensed and there is no royalties generated; UCSF-Benioff Children's Hospital Oakland: Patents & Royalties: Patents owned by UCSF-Benioff Children's Hospital Oakland, licensed by Lifetrients, generating royalties for nutritional supplement for autism/apraxia. OffLabel Disclosure: Oral L-arginine for treatment of acute sickle cell disease vaso-occlusive pain
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"Re-education of gestural communication in a case of chronic global aphasia and limb apraxia." Neuropsychological Rehabilitation 1, no. 3 (July 1991): 223. http://dx.doi.org/10.1080/09602019108520170.
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Peter, Beate, Laurel Bruce, Caitlin Raaz, Emma Williams, Allie Pfeiffer, and Corianne Rogalsky. "Comparing global motor characteristics in children and adults with childhood apraxia of speech to a cerebellar stroke patient: evidence for the cerebellar hypothesis in a developmental motor speech disorder." Clinical Linguistics & Phonetics, December 16, 2020, 1–25. http://dx.doi.org/10.1080/02699206.2020.1861103.
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Townley, Ryan A., Hugo Botha, Jonathan Graff-Radford, Jennifer Whitwell, Bradley F. Boeve, Mary M. Machulda, Julie A. Fields, et al. "Posterior cortical atrophy phenotypic heterogeneity revealed by decoding 18F-FDG-PET." Brain Communications, August 19, 2021. http://dx.doi.org/10.1093/braincomms/fcab182.
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Abstract Posterior cortical atrophy is a neurodegenerative syndrome with a heterogeneous clinical presentation due to variable involvement of the left, right, dorsal, and ventral parts of the visual system, as well as inconsistent involvement of other cognitive domains and systems. 18F-fluorodeoxyglucose (FDG)-PET is a sensitive marker for regional brain damage or dysfunction, capable of capturing the pattern of neurodegeneration at the single-participant level. We aimed to leverage these inter-individual differences on FDG-PET imaging to better understand the associations of heterogeneity of posterior cortical atrophy. We identified 91 posterior cortical atrophy participants with FDG-PET data and abstracted demographic, neurologic, neuropsychological, and Alzheimer’s disease biomarker data. The mean age at reported symptom onset was 59.3 (range: 45–72 years old), with an average disease duration of 4.2 years prior to FDG-PET scan, and a mean education of 15.0 years. Females were more common than males at 1.6:1. After standard preprocessing steps, the FDG-PET scans for the cohort were entered into an unsupervised machine learning algorithm which first creates a high dimensional space of inter-individual covariance before performing an eigen-decomposition to arrive at a low dimensional representation. Participant values (‘eigenbrains’ or latent vectors which represent principle axes of inter-individual variation) were then compared to the clinical and biomarker data. Eight eigenbrains explained over 90% of the inter-individual differences in FDG-PET uptake with left (eigenbrain 1) and right (eigenbrain 2) hemispheric lateralization representing 60% of the variance. Furthermore, eigenbrain-loads mapped onto clinical and neuropsychological data (i.e. aphasia, apraxia, and global cognition were associated with the left hemispheric eigenbrain 1 and environmental agnosia and apperceptive prosopagnosia were associated with the right hemispheric eigenbrain 2), suggesting that they captured important axes of normal and abnormal brain function. We used NeuroSynth to characterize the eigenbrains through topic-based decoding, which supported the idea that the eigenbrains map onto a diverse set of cognitive functions. These eigenbrains captured important biological and pathophysiologic data (i.e. limbic predominant eigenbrain 4 patterns being associated with older age of onset compared to frontoparietal eigenbrain 7 patterns being associated with younger age of onset), suggesting that approaches that focus on inter-individual differences may be important to better understand the variability observed within a neurodegenerative syndrome like posterior cortical atrophy.