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Relevant bibliographies by topics / Hyperkinesis

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Academic literature on the topic 'Hyperkinesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 June 2025

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Journal articles on the topic "Hyperkinesis"

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Khanenko, N., N. Svyrydova, G. Chuprina, et al. "Hyperkinesis: pathogenesis, clinical features, diagnosis, treatment (clinical lecture)." East European Journal of Neurology, no. 3(21) (September 20, 2018): 13–18. http://dx.doi.org/10.33444/2411-5797.2018.3(21).13-18.

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Traditionally, the basic etiological concepts are considered in the views on the morphophysiological basis of hyperkinesis. Hyperkinesia is associated with hypotonia, a decrease in muscle tone, and hyperkinetic disorders are psychogenic and manifest in childhood. Hyperkinesia can be caused by a large number of various diseases, including metabolic disorders, endocrine disruption, hereditary disorders, vascular disorders or traumatic disorders. Other causes include intoxication of the nervous system, autoimmune diseases and infections. The classification of hyperkinesis is that hyperkinetic motions can be defined as any undesirable, excessive movements that can be distinguished from each other, based on the degree to which they are rhythmic, discrete, repetitive and random. When assessing a patient with suspected hyperkinesia, the doctor thoroughly records in the history of the disease a clear description of the movements, the medications prescribed in the past and present, the family history of the similar diseases, the history of the disease, including past infections, and any other influences. Treatment is aimed at reducing symptoms, restoring normal posture and improving the general condition of the patient.

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Yakimovskii, Аndrey F. "The influence of acizol into effects of picrotoxin, injected in rat’s neostriatum." Medical academic journal 19, no. 2 (2019): 57–62. http://dx.doi.org/10.17816/maj19257-62.

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The aim of the article. The article is devoted to investigation of of zinc donator acizol influence to rat’s behavior, broken by intrastriatal injection of GABA-A receptor antagonist picrotoxin. Materials and methods. Adult male Wistar rats with avoidance conditioning reflexes in “shuttle box” and free locomotor activity in “open field” were used. Daily microinjection of picrotoxin (2 mcg/1 mcl) bilateral into rostral neostriatum in term of 15 days were made. Zinc donator acizol was injected intraperitoneal (24 mg/kg). Results. Steady losses of avoidance conditioning and choreo-mioclonic hyperkinesis of limbs and body, similar with human Huntington’s chorea by picrotoxin were produced. Acizol is contribute to restore avoidance conditioning and to prevent the development of hyperkinesis or essentially extend latency and lover duration of it. Conclusion. With the early data obtained, there is reason to propose, that acizol, to increasing the zinc content in the body, especially in the brain, is recover damaged cognitive function and to prevent the picrotoxin-induced hyperkinesis. Acizol should be proposed as perspective drug in extrapyramidal hyperkinetic deviation treatment in human.

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Yakimovskii, A. F. "INFLUENCE OF ZINC ALIMENTARY TREATMENT ON NORMAL AND PATHOLOGICAL MOTOR BEHAVIOR OF RATS." Trace Elements in Medicine (Moscow) 21, no. 2 (2020): 34–40. http://dx.doi.org/10.19112/2413-6174-2020-21-2-34-40.

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Chronic experiments were performed on rats to study the influence of prolonged acetic zinc alimentary treatment on normal (spontaneous movement in “open field and condition active avoidance reflex in “shuttle box”) and abnormal (choreomyoclonic hyperkinesia, produced by intrastriatal microinjections GABA-A receptors antagonist picrotoxin  2 mcg) motor behavior. 4 mg acetic zinc is used by rats with food ball once a day. 12 mg zinc сonsumption by rats per week did not affected on normal behavior. While 24 mg is produced smaller negative effects on rats reflex performance to 6570% correct responses (of total present during the experiment) but to improved condition avoidance behavior, violated by picrotoxinin rats and reduce the reproducibility of picrotoxin-induced choreo-mioclonic hyperkinesis (human Huntington disease hyperkinesis analog). The influence of zinc on motor behavior depending on its dose and mode of administration is discussed.

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Millichap, J. Gordon. "Food-Induced Hyperkinesis." Pediatric Neurology Briefs 6, no. 8 (1992): 63. http://dx.doi.org/10.15844/pedneurbriefs-6-8-10.

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Churton, Michael W. "Hyperkinesis: A Review of Literature." Adapted Physical Activity Quarterly 6, no. 4 (1989): 313–27. http://dx.doi.org/10.1123/apaq.6.4.313.

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The review of literature focuses upon a disorder that affects between 2 and 25% of school-age children. Commonly referred to as hyperkinesis, the disorder lacks definitive consensus on nomenclature, etiology, treatment, and symptomatology. The divergence in identifying hyperkinesis as a homogeneous disorder has prevented the development of data based educational strategies. The disorder is often associated with learning disabilities, and research in hyperkinesis or attentional deficit disorder relative to psychomotor skills and learning has been limited. Subsequently, motor activity programs have not had the resources to address the motor needs of these children. This paper reviews the divergency in the literature on hyperkinesis and offers research considerations in the area of motor learning and development for these children.

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Cameron, Mary, and Peter Hill. "Hyperkinetic disorder: assessment and treatment." Advances in Psychiatric Treatment 2, no. 3 (1996): 94–102. http://dx.doi.org/10.1192/apt.2.3.94.

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Hyperkinetic disorder is the generic ICD-10 (WHO, 1992) term used to describe one of the most common childhood psychiatric disorders. It is a severe form of a syndrome which is referred to in DSM–IV (APA, 1994) and the American literature as attention deficit hyperactivity disorder (ADHD). Hyperactivity or hyperkinesis can be defined as “an enduring disposition to behave in a restless, inattentive, distractible and disorganised fashion” (Taylor, 1994). It is thus more than motor overactivity. Diagnostically there are three main groups of symptomatology: overactivity, inattentiveness and impulsiveness.

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Levitina, E. V., M. U. Kolchanova, O. A. Rakhmanina, and E. B. Hramova. "Structure of comorbide disorders in ticose hyperkinesis in children." Medical Science And Education Of Ural 21, no. 4 (2020): 72–74. http://dx.doi.org/10.36361/1814-8999-2020-21-4-72-74.

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Purpose. To study the structure of comorbid disorders in children with tycotic hyperkinesis of the city of Tyumen. Materials and methods. We examined 103 children aged 5 to 14 years. Patients were divided into 2 groups: group 1 – local tics (n = 43), group 2 – common tics (n = 60). All patients received anticitotic therapy. Using various scales and questionnaires, an assessment of tic hyperkinesis, the level of anxiety, a study of the rational, emotional and behavioral components of the relationship between parents and a child, an investigation of the emotional sphere, and neuropsychological testing were carried out. Results. Manifestations of ticks contribute to various stressful situations, school adaptation stress. The tics are intensified by emotional overstrain, mental overwork, eye strain. A risk factor for the formation of tic hyperkinesis is family education by the type of symbiosis and hypersocialization. Comorbid disorders in patients with ticose hyperkinesis in most cases are represented by ADHD, anxiety, the prevalence of a combination of stress with pathological compensation, and the presence of a headache. The neuropsychological plan revealed impaired attention, auditory-speech and visual memory, and writing. Conclusion. Identified comorbid disorders in children with tic hyperkinesis significantly reduce the quality of life of patients, disrupts their social adaptation and require timely correction.

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Birkeland, S., J. Westby, K. Grong, and J. Lekven. "Effect of afterload and beta-adrenergic blockade on nonischemic myocardial contraction pattern." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 6 (1992): H1716—H1723. http://dx.doi.org/10.1152/ajpheart.1992.263.6.h1716.

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We studied how changes in afterload affect regional contraction in the anterior wall of the left ventricular after circumflex coronary arterial (CFX) occlusion and subsequent beta-adrenergic blockade in pentobarbital sodium-anesthetized cats. Regional function was determined by orthogonal sonomicrometry. CFX occlusion produced nonuniform hyperkinesis in the nonischemic anterior wall; shortening of circumferential segments increased from 10.1 to 14.1% (P < 0.001), whereas shortening of longitudinal segments increased from 3.0 to 9.6% (P < 0.001). Hyperkinesis of longitudinal segments was influenced neither by changes in afterload over a pressure range of +/- 30 mmHg nor by beta-adrenergic blockade, indicating that hyperkinesis of longitudinal segments does not rely on increased inotropic state or resistance to ventricular emptying. Hyperkinesis of longitudinal segments occurred at end-diastolic lengths equal to preocclusion conditions, whereas hyperkinesis of circumferential segments was dependent on activation of the Frank-Starling mechanism. Furthermore, shortening of circumferential segments decreased with increments in afterload, particularly after CFX occlusion and subsequent beta-adrenergic blockade. In conclusion, CFX occlusion alters the contraction pattern of the nonischemic anterior wall. The postocclusion contraction is sensitive to increased afterload in the cardiac minor axis direction. These initial alterations may well direct the following remodeling process in infarcted hearts.

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Ruziev, A. Sh. "CLINICAL AND NEUROLOGICAL CHARACTERISTICS OF TIC HYPERKINESIS IN CHILDREN." Oriental Journal of Medicine and Pharmacology 04, no. 02 (2024): 1–6. http://dx.doi.org/10.37547/supsci-ojmp-04-02-01.

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The article presents examination data of 70 children with tic hyperkinesis. Tic hyperkinesis affects the cognitive and emotional spheres, and these changes are most pronounced with common tics. Based on the Toulouse-Pieron test, which characterizes the ability to voluntarily concentrate attention, it has been proven that children with local tics have a significantly higher concentration of attention compared to common ones.

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Rosenbloom, Lewis. "LEARNING DISABILITIES AND HYPERKINESIS." Developmental Medicine & Child Neurology 14, no. 3 (2008): 394–95. http://dx.doi.org/10.1111/j.1469-8749.1972.tb02606.x.

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Dissertations / Theses on the topic "Hyperkinesis"

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Коленко, Фаіна Григорівна, Фаина Григорьевна Коленко та Faina Hryhorivna Kolenko. "Лицевые гиперкинезы: критерии диагностики". Thesis, Изд-во СумГУ, 2007. http://essuir.sumdu.edu.ua/handle/123456789/5636.

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MacDonald, Mary Ann. "Memory and metamemory in hyperactive children." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30999.

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Memory and metamemory were examined in 30 hyperactive and 30 nonhyperactive children matched on age, grade, and IQ (as measured by the Vocabulary and the Block Design subtests of the WISC-R), within the context of a broad range of tasks. The five tasks investigated in this study were: (a) a prospective memory task, (b) a feeling-of-knowing task, a visual retention task, (c) a word generation task, (d) and (e) an object span and recall task. Previous research has demonstrated considerable variability in the performance of hyperactive children on memory tasks. They have been shown to perform as well as normal children on tasks of cued recall, paired associates for meaningful words, and on tests of recognition memory. They are distinguished from normal children by their poor performance on tasks of uncued recall, paired associates learning for semantically unrelated words, and in addition, often display performance decrements when task demands increase. The results of this study suggest that hyperactive children are less efficient in metamemory knowledge and skills than normal children. These findings are consistent with the proposal that the difficulties hyperactive children demonstrate on memory tasks may result from a deficiency in their ability to efficiently engage in metamemory processes. The hyperactive children in this study generally had more difficulty than the control children with recall on all the tasks. These included tests of both verbal and nonverbal memory, short and long-term memory, and prospective remembering. Further, they did not derive a memorial benefit, as the control subjects did, when generating their own recall items, or when recalling visual stimuli that could be more easily verbally encoded than others. The hyperactive subjects demonstrated their recall abilities by performing as well as the normal subjects on the recall of read words in the word generation task, and on the recall of the low and medium level of labelability items in the visual retention task. Also, the recall performance of the hyperactive subjects differed significantly between a no-strategy and a provided strategy condition on the prospective memory task. Moreover, there were no group differences on the recognition memory test of the feeling-of-knowing task. The results of this study are consistent with the previous investigations of memory performance in hyperactive children. The present findings further extend the past research by demonstrating selective memory deficits in the hyperactive subjects that are consistent with deficits in metamemory abilities. The proposition that metamemory skills are implicated in the difficulties that the hyperactive children demonstrated in this study is further supported by the difficulty they experienced in describing how they remembered the task items. The hyperactive subjects had more difficulty than the control subjects when attempting to describe a strategy that they used to aid recall. The strategies they described, relative to the control subjects, tended to be vague and poorly defined. These findings suggest that there may be both qualitative and quantitative differences in the way in which hyperactive and normal children use strategies. In summary, the findings of this study suggest that hyperactive children, relative to normal children, seem to be deficient in both their metamemory knowledge and the ability to monitor and control their memory performance. Questions addressing whether these children cannot or do not employ these skills were introduced. The clinical implications of the findings were considered and recommendations were made for future research.<br>Arts, Faculty of<br>Psychology, Department of<br>Graduate

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Coghill, David Rockwell. "Heterogeneity in hyperkinetic disorder." Thesis, University of Dundee, 2010. https://discovery.dundee.ac.uk/en/studentTheses/afa9d9e9-eadb-49bf-8c83-db47eb0cadd9.

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It is increasingly recognised that the broadly defined behavioural phenotype of attention deficit – hyperactivity disorder (ADHD) is a heterogeneous condition and that this heterogeneity is seen across all levels of analysis from the genetic and environmental causes to the associated neuropsychological deficits, the clinical presentation and response to treatment. This work investigated whether the more restrictive and clinically homogeneous hyperkinetic disorder (HKD) phenotype is associated with reduced neuropsychological heterogeneity compared with the broader ADHD phenotype. Using a well known, broad based battery of neuropsychological tasks from the Cambridge Neuropsychological Test Automated Battery (CANTAB) and a computerised Go/NoGo task in a large well described group of boys with rigorously diagnosed HKD who were stimulant medication naïve at baseline, it was demonstrated that the neuropsychological heterogeneity in the HKD boys was very similar to that seen previously in children with ADHD. Interestingly, and contrary to popular opinion, the strongest associations were with more simple recognition memory tasks with a low executive demand. Although there were significant associations between HKD and deficits on a range of tasks with high executive demands these were less strong. Could this neuropsychological heterogeneity be a function of different developmental issues or comorbidity? With respect to development there was evidence that boys with HKD lagged behind the healthy boys with respect to the development of their neuropsychological performance. However the pattern of development was similar with the performance of the HKD boys paralleling that of the healthy boys, suggesting that the neuropsychological heterogeneity seen in HKD is not accounted for by developmental issues. With respect to the relationship between neuropsychological functioning and comorbidity, the impact of comorbid oppositional defiant disorder (ODD) and conductdisorder (CD), it was found that all three clinical groups (pure HKD, HKD + ODD and HKD + CD) demonstrated deficits on several tasks compared with the healthy boys. Compared with healthy boys each of the three clinical groups was associated with at least one unique neuropsychological deficit. This suggests that comorbidity between HKD and both ODD and CD may contribute to the neuropsychological heterogeneity in the HKD boys. Is there an association between clinical and neuropsychological responses to the treatment of HKD with the stimulant drug methylphenidate (MPH)? Detailed analyses were conducted to investigate heterogeneity of clinical and neuropsychological response in these boys to MPH. As predicted in previous studies there is evidence for clinical heterogeneity in response with between 68 and 78% of boys with HKD responding to MPH treatment at either one or both of the doses. The precise proportion responding was dependent on the scale and definition of response used. Clinical response was not predicted by age but was predicted to a degree by severity of symptoms at baseline and it was generally true that better response was predicted by lower (better) scores at baseline. Baseline performance on a component reflecting recognition memory performance at baseline predicted clinical response to the lower (0.3 mg/kg/dose), but not the higher (0.6, mg/kg/dose) dose of MPH with poorer baseline neuropsychological performance predicting a better clinical response. Whilst there was improvement on some neuropsychological measures following administration of MPH there was little association between clinical and neuropsychological responses to medication. Clinical response was only associated with neuropsychological response on a single measure from a single task (Go/NoGo Block 2 Errors to Distractors), a task that did not itself discriminate between the HKD boys and healthy Controls at baseline.

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Eekhof, Job Lambert Adam. "Electrophysiological investigations in cranial hyperkinetic syndromes." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/81828.

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Rhodes, Sinead M. "The neuropsychopharmacology of hyperkinetic disorder (ADHD)." Thesis, University of Dundee, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288535.

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Tascone, Lyssandra dos Santos. "Morfometria baseada no voxel e sintomas neuropsiquiátricos na Doença de Alzheimer e no comprometimento cognitivo sem demência." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-25092013-155146/.

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O estudo dos sintomas neuropsiquiátricos em Doença de Alzheimer (DA) através do agrupamento destes em síndromes tem sido cada vez mais utilizado, uma vez que permitiria detectar diferenças em sua prevalência, em sua evolução, em relação a determinantes psicossociais e a correlatos neurobiológicos. O objetivo deste estudo foi identificar regiões de redução de substância cinzenta em áreas corticais associadas com sintomas e síndromes neuropsiquiátricos específicos, provenientes da Escala Inventário Neuropsiquiátricos (NPI), em pacientes com DA e comprometimento cognitivo sem demência (CIND). O método de morfometria baseada no voxel (VBM) com DARTEL (Diffeomorphic Anatomical Registration Using Exponentiated Lie Algebra) foi utilizado para verificar a correlação entre presença de sintomas e síndromes neuropsiquiátricos específicos e redução regional de volume de substância cinzenta em análise em todo cérebro e em regiões previstas a priori. As síndromes utilizadas foram SN1/Agitação (agitação, alterações de sono e apetite), SN2/Hiperatividade (desinibição, comportamento motor aberrante e irritabilidade), SN3/Afetiva (depressão e apatia) e SN4/Psicose (delírios e alucinações). A presença de delírios foi associada a volume de substância cinzenta reduzido em giro frontal inferior direito (BA45); depressão com xvii redução de substância cinzenta em giro temporal médio e inferior direito (BA 37/22) e giro frontal inferior (BA09-DLPFC) e giro parahipocampal esquerdos; ansiedade com redução em giro frontal médio esquerdo (BA10); e alterações de apetite com redução em córtex anterior cingulado esquerdo (BA32) em pacientes com DA. A presença de SN1/Agitação foi associada a volume de substância cinzenta reduzido em giro frontal médio direito (BA09-DLPFC); SN2/Hiperatividade com redução em giro temporal superior direito (BA22) e frontal inferior bilateral (BA47); e SN4/Psicose com redução em giro pré-central (BA44), temporal superior (BA22) e ínsula direitos em DA. No grupo CIND, somente SN1/Agitação evidenciou associação com redução de substância cinzenta regional. Atrofia de áreas corticais específicas parecem relacionadas aos sintomas e síndromes neuropsiquiátricos em DA. Síndromes neuropsiquiátricas em DA mostraram-se correlacionadas à atrofia de estruturas centrais de alguns circuitos neuronais envolvidos na fisiopatologia de transtornos psiquiátricos<br>The study of neuropsychiatric symptoms in patients with Alzheimer\'s disease (AD) by grouping these symptoms into syndromes has been increasingly used because it would detect differences in its prevalence and evolution, in relation to psychosocial determinants and neurobiological correlates. The aim of this study was to identify regions of reduced gray matter in cortical areas associated with specific neuropsychiatric symptoms and syndromes from the Neuropsychiatric Inventory (NPI) in patients with AD and cognitive impairment, no dementia (CIND). Voxel-based morphometry (VBM) plus Dartel (Diffeomorphic Anatomical Registration Exponentiated Using Lie Algebra) was used to verify the correlation between the presence of specific neuropsychiatric symptoms and syndromes and regional gray matter volume reduction throughout the brain and in regions predicted a priori. The syndromes were NS1/ Agitation (agitation, sleep and eating disorders), NS2/Hyperactivity (disinhibition, aberrant motor behavior and irritability), NS3/Affective (depression and apathy) and NS4/Psychosis (delusions and hallucinations). The presence of delusions was associated with gray matter volume reduction in right inferior frontal gyrus (BA45), depression with reduced gray matter in right inferior middle temporal gyrus (BA 37/22) and left inferior frontal gyrus (BA09-DLPFC) and left parahippocampal gyrus; anxiety with reduction in left middle frontal gyrus (BA10), and eating disorders with reduction in left anterior cingulate cortex (BA32) in patients with AD. The presence of NS1/Agitation was associated with gray matter volume reduction in the right middle frontal gyrus (BA09-DLPFC); NS2/ Hyperactivity with reduction in right superior temporal gyrus (BA22) and bilateral inferior frontal (BA47) and NS4/Psychosis with a reduction in right precentral gyrus (BA44), right superior temporal (BA22) and in right insula in AD. In the CIND group, only SN1/Agitation showed association with regional gray matter reduction. Atrophies of specific cortical areas were showed to be related to symptoms and neuropsychiatric syndromes in patients with AD

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Domingos, Mauricio de Maio. ""O uso da toxina botulínica em doentes com hipercinesia muscular facial contralateral à paralisia facial"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-17082006-104941/.

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O tratamento da paralisia facial visa recuperar a simetria estática e dinâmica seriamente afetada pela hipercinesia muscular. A toxina botulínica pode ser utilizada em assimetrias faciais. Dezoito doentes foram submetidos à aplicação de 112,5U (0,9ml) de Dysport (toxina botulínica do tipo A), distribuídos nos músculos peribucais. A análise quantitativa das posições estática e dinâmica demonstrou redução significante na hipercinesia por 180 dias. Houve melhora da aparência e satisfação na maioria dos casos. Os eventos adversos foram leves e de curta duração (15 dias), relacionados à dificuldade para beber (9/18) e mastigar (3/18). Como conclusão, a aplicação de toxina botulínica reduziu a hipercinesia facial contralateral à paralisia facial e os doentes ficaram muito satisfeitos com o tratamento<br>The treatment of facial paralysis aims to recover symmetry in both static and dynamic states, seriously affected by the contralateral hyperkinesis. Botulinum toxin may be used to reduce facial asymmetries. Eighteen patients were injected with 112.5 U (0.9 ml) Dysport (Botulinum toxin type A) distributed evenly in the perioral muscles. The quantitative analysis demonstrated a significant reduction in the hyperkinesis for 180 days. Improvement in appearance and satisfaction were found in most of the cases. Adverse events were short-lived (first 15 days) and related to mild difficulty to drink (9/18) and chewing (3/18). Injection of Botulinum toxin was effective in reducing muscular hyperkinesis in the hemiface opposite that affected by facial paralysis and patients were very satisfied with the treatment

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Weeks, Robert Anthony. "Positron emission tomographic studies in hyperkinetic movement disorders." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368073.

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FORGET, ANNE-PASCALE. "Mise en jeu de la voie metabolique du monoxyde d'azote dans le syndrome hyperkinetique induit par le remplissage au cours du choc endotoxinique du rat." Lille 2, 1994. http://www.theses.fr/1994LIL2M267.

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FLODROPS, ETIENNE. "Apport de la debimetrie cerebrale aux troubles deficitaires de l'attention avec ou sans hyperkinesie." Lille 2, 1993. http://www.theses.fr/1993LIL2M283.

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Books on the topic "Hyperkinesis"

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Weiner, William J. Hyperkinetic movement disorders. Elsevier, 2011.

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A, Taylor Eric, and Spastics International Medical Publications, eds. The Overactive child: Edited by Eric A. Taylor. Blackwell Scientific Publications, 1986.

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Smith, Lendon H. Hyper kids: A workbook for parents and teachers : how to recognize and respond to hyperactivity, attention deficit disorders, learning disabilities. Shaw/Spelling Associates, 1990.

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Suchowersky, Oksana, and Cynthia Comella, eds. Hyperkinetic Movement Disorders. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60327-120-2.

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Albanese, Alberto, and Joseph Jankovic, eds. Hyperkinetic Movement Disorders. Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346183.

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Desjardins, Claude. Ces enfants qui bougent trop!: Deficit d'attention-hyperactivite chez l'enfant. Quebecor, 1992.

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Banaschewski, Tobias. ADHD and hyperkinetic disorder. Oxford University Press, 2010.

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Banaschewski, Tobias. ADHD and hyperkinetic disorder. Oxford University Press, 2010.

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C, Wells Karen, ed. Hyperkinetic children: A neuropsychosocial approach. Sage Publications, 1986.

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Cheresharov, Li͡ubomir. Morfo-funkt͡sionalni promeni v organizma pod vlii͡anie na khipo-i khiperkinezii͡a. Izd-vo na Bŭlgarskata akademii͡a na naukite, 1994.

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Book chapters on the topic "Hyperkinesis"

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Chess, Stella, and Mahin Hassibi. "Hyperkinesis and Attentional Deficiencies." In Principles and Practice of Child Psychiatry. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2145-3_17.

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Velasco, Rafael. "Basic Concepts on Hyperkinesis in Children." In Child and Adolescent Psychiatry, Mental Retardation, and Geriatric Psychiatry. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9367-6_8.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, et al. "Hyperkinesias." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4300.

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Knobel, Mauricio. "Childhood Hyperkinesis: Symptom or Syndrome, Discriminating Through the Use of L-Dopa as a Therapeutic Agent." In Child and Adolescent Psychiatry, Mental Retardation, and Geriatric Psychiatry. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9367-6_11.

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von Albert, Hans-Henning. "Hyperkinese." In Vom neurologischen Symptom zur Diagnose. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56278-5_42.

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von Albert, Hans-Henning. "Hyperkinese." In Vom neurologischen Symptom zur Diagnose. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-96923-2_42.

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von Albert, Hans-Henning. "Hyperkinese." In Vom neurologischen Symptom zur Diagnose. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-97360-4_42.

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Woods, Douglas W., Matthew R. Capriotti, Madison Pilato, et al. "Hyperkinetic Disorders." In Encyclopedia of Autism Spectrum Disorders. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_100681.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, et al. "Hyperkinetic Syndrome." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7558.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, et al. "Hyperkinetic Child Syndrome." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3308.

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Conference papers on the topic "Hyperkinesis"

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Antor, Mahamudul Hashan, Nikolai Alexandrovich Khlebnikov, and Boris Andreevich Bredikhin. "Developing a Hyperkinetic Dysarthria Speech Classification System using Residual Learning." In 2024 IEEE 3rd International Conference on Problems of Informatics, Electronics and Radio Engineering (PIERE). IEEE, 2024. https://doi.org/10.1109/piere62470.2024.10805075.

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van den Brandhof, Elina, Jan W. J. Elting, Inge Tuitert, et al. "Interpretable machine learning for the diagnosis of hyperkinetic movement disorders." In ESANN 2025. Ciaco - i6doc.com, 2025. https://doi.org/10.14428/esann/2025.es2025-73.

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Albani, Carlo, and Manuel Meyer. "Classification of hyperkinetic movements with 3D kinematic measurements." In Close-Range Photogrammetry Meets Machine Vision. SPIE, 1990. http://dx.doi.org/10.1117/12.2294344.

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Schmidt, M. H., P. Möcks, B. Lay, et al. "THE ROLE OF OLIGOANTIGENIC DIET IN HYPERKINETIC CHILDREN." In IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0162.

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Shukla, V., G. Elliott, and B. Kear. "Hyperkinetic deposition of nanopowders by supersonic rectangular jet impingement." In 37th Aerospace Sciences Meeting and Exhibit. American Institute of Aeronautics and Astronautics, 1999. http://dx.doi.org/10.2514/6.1999-679.

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Hashan, Antor Mahamudul, Chaganov Roman Dmitrievich, Melnikov Alexander Valerievich, Dorokh Danila Vasilyevich, Khlebnikov Nikolai Alexandrovich, and Bredikhin Boris Andreevich. "Deep Learning Based Speech Recognition for Hyperkinetic Dysarthria Disorder." In 2024 IEEE Ural-Siberian Conference on Biomedical Engineering, Radioelectronics and Information Technology (USBEREIT). IEEE, 2024. http://dx.doi.org/10.1109/usbereit61901.2024.10584052.

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Sharghi, Hesam, Jean-François Daneault, and Onur Bilgen. "A Wearable Biomedical Motion Sensor Employing a Vibration Energy Harvester." In ASME 2019 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/smasis2019-5634.

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Abstract Wearable motion sensors find a great number of applications in the biomedical field by recording real-time movements and transferring data to mobile electronics. Patients with hyperkinetic movements is a group of interest for such sensors to survey their conditions for long periods. Longer and more frequent recording intervals are necessary to diagnose and treat patients’ disease. Mobile battery-operated motion sensors have a limited recording span, and they need to be charged frequently, which is inconvenient for most of the patients. In this study, vibration energy harvesters are employed to extend the battery life of motion sensors: one step closer to make autonomous sensors without chargers. A vibration energy harvester is designed for a motion sensor to harvest energy from involuntary movements of patients with hyperkinetic movements. An analytical model for charging and discharging cycles is developed to predict the battery life based on the amount of harvested power. Preliminary data from commercial devices are used as a foundation for the design and the current feasibility study.

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Barišić, N., I. Lehman, B. Bunoza, et al. "408 Hyperkinetic and hypokinetic movement disorders – in pediatric clinical practice." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.408.

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Vochteloo, M., M. A. J. Tijssen, and M. Beudel. "A Clinical Applicable Smartwatch Application for Measuring Hyperkinetic Movement Disorder Severity." In 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857869.

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Schuldt, T., W. Großmann, and R. Mlynski. "Foreign bodies during childhood – epidemiology and correlation analysis with hyperkinetic disorders." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640733.

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