Journal articles: 'Hyperkinetický syndrom'

1

Lejčarová, Alena, and Martina Skálová. "The use of canistherapy in a child with hyperkinetic syndrome." Kontakt 11, no. 2 (December 18, 2009): 413–23. http://dx.doi.org/10.32725/kont.2009.064.

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EGGER, JOSEPH. "Hyperkinetic Syndrome." Journal of Nutritional & Environmental Medicine 7, no. 4 (January 1997): 353–57. http://dx.doi.org/10.1080/13590849762484.

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Glushchenko, Vita Valentinovna. "Rational pharmacotherapy of hyperkinetic disorders." Reviews on Clinical Pharmacology and Drug Therapy 12, no. 4 (December 15, 2014): 58–63. http://dx.doi.org/10.17816/rcf12458-63.

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The data concerning hyperkinetic disorder syndrome are shortly reviewed in the paper. Principal attention is focused on the analysis of effects of metabolic activators (atomoxetine), neuroleptics (thioridazine, chlorprotixene) and different antidepressants (fluoxetine, fluvoxamine, sertraline, tianeptine, pipophesine).

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Kay, A. B., A. J. Frew, J. O. Warner, M. H. Lessof, Joseph Egger, Adelheid Stolla, and LeonardM Mcewen. "Hyposensitisation for food-induced hyperkinetic syndrome." Lancet 341, no. 8837 (January 1993): 114–15. http://dx.doi.org/10.1016/0140-6736(93)92592-h.

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Franklin, A. J. "Hyposensitisation for food-induced hyperkinetic syndrome." Lancet 341, no. 8842 (February 1993): 437. http://dx.doi.org/10.1016/0140-6736(93)93031-u.

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Haddad, P. M., and M. E. Garralda. "Hyperkinetic Syndrome and Disruptive Early Experiences." British Journal of Psychiatry 161, no. 5 (November 1992): 700–703. http://dx.doi.org/10.1192/bjp.161.5.700.

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Five children aged 8–10 years presenting to child psychiatric clinics with hyperkinetic syndrome and severe disruptive early experiences are described. At referral all had been living in stable families for a minimum of four years. Biological risk factors were absent. It is proposed that the disruption of early attachments resulted in ill-regulated search and exploratory behaviour and that this had a continuing effect on the children's ability to focus and control attention skills and motor behaviour.

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Rapoport, Judith L., and H. Bruce Ferguson. "Biological Validation of the Hyperkinetic Syndrome." Developmental Medicine & Child Neurology 23, no. 6 (November 12, 2008): 667–82. http://dx.doi.org/10.1111/j.1469-8749.1981.tb02053.x.

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Steinhausen, Hans-Christoph, and Dietmar G�bel. "The validity of the hyperkinetic syndrome." European Archives of Psychiatry and Neurological Sciences 235, no. 2 (1985): 122–28. http://dx.doi.org/10.1007/bf00633484.

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9

Cameron, Mary, and Peter Hill. "Hyperkinetic disorder: assessment and treatment." Advances in Psychiatric Treatment 2, no. 3 (May 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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TP, Borysova, Badogina LP, Allahverdieva ZS, and Samsonenko SV. "Hyperkinetic Syndrome in Adolescent with HIV-Infection." Acta Scientific Paediatrics 4, no. 5 (April 23, 2020): 09–12. http://dx.doi.org/10.31080/aspe.2020.03.0243.

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Wiśniewski, Artur. "Atomoxetine in the pharmacotherapy of hyperkinetic syndrome." Psychiatria i Psychologia Kliniczna 20, no. 1 (April 30, 2020): 71–76. http://dx.doi.org/10.15557/pipk.2020.0009.

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Dolgan, Anna, Slawomir Budrewicz, Magdalena Koszewicz, Joanna Bladowska, Krzysztof Slotwinski, Mieszko Zagrajek, Ewa Koziorowska-Gawron, and Ryszard Podemski. "Acute Hyperkinetic Syndrome Due to Ephedrone Abuse." Journal of Addiction Medicine 9, no. 3 (2015): 244–45. http://dx.doi.org/10.1097/adm.0000000000000048.

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Madias, John E. "Pre-Hypertension and Hyperkinetic Heart (Gorlin's) Syndrome." Journal of the American College of Cardiology 60, no. 22 (December 2012): 2342. http://dx.doi.org/10.1016/j.jacc.2012.07.061.

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Kolesnik, Olena. "Clinical and pathogenetic features and correction of hyperkinetic disorders in vegetative dysfunctions." Ukrains'kyi Visnyk Psykhonevrolohii, Volume 28, issue 1 (102) (March 25, 2020): 6–9. http://dx.doi.org/10.36927/20790325-v28-is1-2020-1.

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One of the early syndromes in vascular pathology is motor disorders in the form of tremor. We examined 101 patients with cerebral dystonia on the background of chronic cerebral ischemia with compensated and subcompensated stages (n = 55) and autonomic dystonia syndrome (n = 46). Pathological mechanisms of formation of trembling hyperkinesis in cerebral angiodystonia of different etiology have been studied. Participation in these processes of the autonomic nervous system (ANS) is established. It is proved that the severity of this type of motor disorders depends on the condition of the ANS at different levels of its organization, especially on the background of sympathicotonic effects, as well as the vegetative characteristics of the patient. At the same time, signifi cant changes in electrophysiological parameters, as well as data of vegetative, emotional, psychometric testing, were obtained. For an objective evaluation of the severity of the tremor, a tremograph with the calculation of an integrative tremographic index was used. Developed a complex of cerebral angiodystonia with hyperkinetic syndrome and the use of antioxidants, nootropic drugs, which allowed to reduce or eliminate subjective experiences, to increase the adaptation capacity of the organism with the normalization of sympatho-parasympathetic relationships, to the normalization of the organism. also inhibition of the implementation of trembling hyperkinesis in both research groups. The average values of the tremographic index decreased towards an adequate distribution with sympathicolytic influence on the indices of vegetative testing and caused skin sympathetic potentials. At the same time, a greater effect was achieved when using the proposed method of treatment, with the maximum — in the syndrome of autonomic dystonia, as well as in the compensated stage of chronic brain ischemia. Keywords: cerebral angioedema, cerebral ischemia, autonomic disorders, tremor, treatment

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15

Gasanov, R. F. "Specific cognitive deficits in children with hyperkinetic disorder." V.M. BEKHTEREV REVIEW OF PSYCHIATRY AND MEDICAL PSYCHOLOGY, no. 3 (November 2, 2018): 3–9. http://dx.doi.org/10.31363/2313-7053-2018-3-3-9.

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In this review article, features of a specific cognitive deficit in children with hyperkinetic disorder are considered. The uneven development of higher mental functions observed in these cases, the hierarchical structure of the detected defects, neuropsychological features is determined, in the author’s opinion, to distinguish hyperkinetic disorder of childhood from atonic forms of mental retardation and other hyperdynamic syndromes in a wide range of child psychopathology, creating a model of a specificcognitive deficit.

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Glushchenko, Vita Valentinovna. "Atomoxetine, thioridazine, pipophezine in treatment adolescents with ADHD." Pediatrician (St. Petersburg) 6, no. 2 (June 15, 2015): 39–44. http://dx.doi.org/10.17816/ped6239-44.

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Analysis of published data on the diagnostic criteria used in the qualification of hyperkinetic syndrome found that along with the data on residual-organic failure CNS causes the development of hyperkinetic syndrome expanded range of studies on the endogenous nature of this syndrome. Thus the international “Genomics Consortium psychiatric” (Psychiatric Genomics Consortium) identify common loci in hyperkinetic disorder and schizophrenia which are located on the short arm of the 3rd chromosome (3r21) and on the long arm of chromosome 10 (10q24) and revealed single nucleotide substitutions (SNPs) in the two genes (CACNA1C and CACNB2) which encode proteins that are part of the channels regulating calcium transport into brain cells. Hyperactivity disorder (GR) as a mental disorder (F90) is multifactorial in nature, which requires consideration of clinical symptom in different planes with the release of endogenous and exogenous forms the primary etiological factor for differentiation therapy. Were studied 231 adolescents with a diagnosis of “Attention-Deficit hyperactivity Disorder” (mean age - 17,7 years). The main components of adolescents AHHD are given by BPRS: arousal (3,63 ± 0,06); cognitive (2,94 ± 0,06) and emotional (2,64 ± 0,06) disorder. Patients were split into threatment group: group 1 (n = 23) received Atomoxetine 25mg/day; group 2 (n = 20) received thioridazine 25mg/day, group 3 (n = 22) - pipophezine 50 mg/day. The positive dynamics of disregulatory-motor typeractivity, cognitive and emotional components of ADHD was observed. The aim: to evaluate the influence of Atomoxetine, Thioridazine, Pipophezine on the main psychopatological clinical-components of adolescents AHHD.

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James, A., and E. Taylor. "Sex Differences in the Hyperkinetic Syndrome of Childhood." Journal of Child Psychology and Psychiatry 31, no. 3 (March 1990): 437–46. http://dx.doi.org/10.1111/j.1469-7610.1990.tb01580.x.

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18

Uzbekov, M. "Kynurenine Involvement in Pathogenesis of Hyperkinetic Children Syndrome." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)71225-8.

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Objectives:The aim of the study was to evaluate the response of different monoaminergic systems to psychostimulant treatment in children with mild form of hyperkinetic syndrome (HKS).Methods:The levels of N-methylnicotinamide (end product of kynurenine pathway of tryptophan metabolism), 5-hydroxyindoleacetic (product of serotonin pathway of tryptophan metabolism), homovanillic and vanillylmandelic acids were measured in daily (3 days) urine samples of children (30 patients, 7-11 years old) with mild HKS with normal intellect or borderline mental insufficience. Biochemical measurements were performed before and 3 weeks after sydnocarb medication (5-15 mg sydnocarb daily). (Sydnocarb is a psychostimulant introduced into the clinical practice in the Soviet Union in the 70th of XX century).Results:After 3 weeks of sydnocarb therapy there were found the improvement of children's clinical status in both groups. It was followed by a significant decrease in the excretion of homovanillic (by 45 %), vanillylmandelic (by 35 %) and 5-hydroxyindoleacetic (by 50 %) acids but by a significant increase in N-methylnicotinamide excretion (by 30%).Conclusions:Psychostimulant medication has revealed the involvement of kynurenine and serotonin in HKS pathogenetic mechanisms. There were found a reciprocal relationship between serotonergic and kynurenine systems. It is proposed the kynurenine hypothesis of pathogenesis of HKS. It is characterized by the decreased activity of kynurenine system in HKS children. Clinical improvement of HKS children under psychostimulant medication is connected with activation of kynurenine system along with the decrease of serotonergic activity.

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19

Egger, J., P. J. Graham, C. M. Carter, D. Gumley, and J. F. Soothill. "CONTROLLED TRIAL OF OLIGOANTIGENIC TREATMENT IN THE HYPERKINETIC SYNDROME." Lancet 325, no. 8428 (March 1985): 540–45. http://dx.doi.org/10.1016/s0140-6736(85)91206-1.

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20

JURKO, A., A. JURKOJR, Z. FARSKA, and A. IPARCOVA. "370 Bisoprolol treatment in children with hyperkinetic heart syndrome." European Journal of Echocardiography 1 (December 1999): S66. http://dx.doi.org/10.1016/s1525-2167(99)80231-5.

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21

Braillon, Alain, Richard Moreau, Antoine Hadengue, Dominique Roulot, Raymond Sayegh, and Didier Lebrec. "Hyperkinetic circulatory syndrome in patients with presinusoidal portal hypertension." Journal of Hepatology 9, no. 3 (November 1989): 312–18. http://dx.doi.org/10.1016/0168-8278(89)90139-6.

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22

Paparrigopoulos, T., G. Persefonis, E. Tzavellas, D. Karaiskos, and I. Liappas. "Tourette syndrome (TS) mimicking tardive dystonia." European Psychiatry 26, S2 (March 2011): 980. http://dx.doi.org/10.1016/s0924-9338(11)72685-2.

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Tourette syndrome (TS) is a neurodevelopmental disorder characterized by early onset motor and vocal tics. Tics are brief, stereotypical, repetitive and non-rhythmic movements or phonations that typically follow a waxing and waning pattern of severity, intensity and frequency; they can be distinguished from other hyperkinetic movement disorders on the basis of their temporary voluntary suppression. TS should be differentiated from various movement disorders. We report a case of a young man who presented with torticollis, which was eventually attributed to TS.Case reportA 21-year-old man was admitted to our clinic due to treatment resistant cervical dystonia attributed to neuroleptics. During the last five years he had been treated for depressed mood, somatic delusions and aggressive behaviour. He had been given SSRIs and atypical antipsychotics at low doses; six months prior to his admission he had been switched to risperidone.Present clinical examination revealed torticollis, motor stereotypies, vocal tics (sniffing, repetition of words), mental koprolalia and obsessive-compulsive symptoms. He complained of repetitive intrusive thoughts of harming his sister and thoughts of a ‘delusional’ nature regarding somatic complaints were also present. The patient was diagnosed as TS and was successfully treated accordingly.TS can mimic many hyperkinetic states. Whether patients with TS are at higher risk of developing dystonia, or tics and dystonia share a common pathophysiological mechanism (dopamine-inhibiting processes are probably involved in both conditions) is still debatable.

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23

Wong, C. K., and Joseph T. F. Lau. "Psychiatric Morbidity in a Chinese Primary School in Hong Kong." Australian & New Zealand Journal of Psychiatry 26, no. 3 (September 1992): 459–66. http://dx.doi.org/10.3109/00048679209072071.

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The psychiatric morbidity among 718 Chinese primary school children from a lower middle social class area in Hong Kong was studied, using a two-stage design. The screening procedures included two parts, a multi-component scale and a battery of probing questions. The screening procedures achieved an overall sensitivity of 75% and a specificity of 97%. The findings on prevalence were: (i) a total prevalence of all definite psychiatric cases of 16.3%; (ii) prevalence according to diagnostic categories: emotional disorder, 8.8%; conduct disorder, 2.0%; mixed disturbance of emotion and conduct, 3.0%; hyperkinetic syndrome, 1.0%; hyperkinetic conduct disorder, 1.0%; and Gilles de la Tourette's syndrome, 0.4%; (iii) boys 2.7 times more affected than girls; (iv) emotional disorder much more common than conduct disorder, even in boys; and (v) the prevalence of borderline cases was 19.5%. The mean duration of morbidity for all definite cases was 41.7 months. About half of all definite cases were seriously impaired in one or more areas of functioning and the other half moderately impaired. These results were compared with findings obtained from studies done in other countries.

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24

Taylor, E. A. "Childhood Hyperactivity." British Journal of Psychiatry 149, no. 5 (November 1986): 562–73. http://dx.doi.org/10.1192/bjp.149.5.562.

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Severe degrees of inattentive and restless behaviour in childhood are a risk factor for later psychological disorders. They have many causes, but a pattern of severe and pervasive hyperactivity with poor concentration in the absence of affective or psychotic disorders should be recognised as a hyperkinetic syndrome. The syndrome is often associated with developmental delays in abilities such as language and motor control. Powerful short-term treatments are available, but long-term ways of promoting normal personality development need more research.

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Puoti, Claudio. "The use of vasoconstrictors in patients with liver cirrhosis: how, when, why." Clinical Management Issues 6, no. 3 (September 15, 2012): 105–15. http://dx.doi.org/10.7175/cmi.v6i3.442.

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Portal hypertension (PH) is a severe complication of liver cirrhosis. Patients with PH run the risk of developing gastro-esophageal varices and massive gastrointestinal bleeding, ascites, hepatorenal syndrome, and hepatic encephalopathy. Portal blood flow in its turn increases because of enhanced production of vasodilators, increased eNOS activity and NO release, systemic and splanchnic vasodilation, hyperkinetic circulation, and hyposensitivity to vasoconstrictors. Thus, it is now widely recognized that this hyperkinetic (hyperdynamic) circulation that characterizes liver cirrhosis is the main cause of the complications of the disease. This review is aimed at addressing the role of vasoconstrictor treatment in patients suffering from complications of decompensated cirrhosis, offering practical suggestions for the management of this treatment at bedside. In particular, the management of terlipressin in patients with cirrhosis, its side effects and the efficacy of this vasoconstrictor will be examined.

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Sadleir, Lynette G., Emily I. Mountier, Deepak Gill, Suzanne Davis, Charuta Joshi, Catherine DeVile, Manju A. Kurian, et al. "Not all SCN1A epileptic encephalopathies are Dravet syndrome." Neurology 89, no. 10 (August 9, 2017): 1035–42. http://dx.doi.org/10.1212/wnl.0000000000004331.

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Objective:To define a distinct SCN1A developmental and epileptic encephalopathy with early onset, profound impairment, and movement disorder.Methods:A case series of 9 children were identified with a profound developmental and epileptic encephalopathy and SCN1A mutation.Results:We identified 9 children 3 to 12 years of age; 7 were male. Seizure onset was at 6 to 12 weeks with hemiclonic seizures, bilateral tonic-clonic seizures, or spasms. All children had profound developmental impairment and were nonverbal and nonambulatory, and 7 of 9 required a gastrostomy. A hyperkinetic movement disorder occurred in all and was characterized by dystonia and choreoathetosis with prominent oral dyskinesia and onset from 2 to 20 months of age. Eight had a recurrent missense SCN1A mutation, p.Thr226Met. The remaining child had the missense mutation p.Pro1345Ser. The mutation arose de novo in 8 of 9; for the remaining case, the mother was negative and the father was unavailable.Conclusions:Here, we present a phenotype-genotype correlation for SCN1A. We describe a distinct SCN1A phenotype, early infantile SCN1A encephalopathy, which is readily distinguishable from the well-recognized entities of Dravet syndrome and genetic epilepsy with febrile seizures plus. This disorder has an earlier age at onset, profound developmental impairment, and a distinctive hyperkinetic movement disorder, setting it apart from Dravet syndrome. Remarkably, 8 of 9 children had the recurrent missense mutation p.Thr226Met.

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Geier, David, Janet Kern, Brian Hooker, Lisa Sykes, and Mark Geier. "Thimerosal-Preserved Hepatitis B Vaccine and Hyperkinetic Syndrome of Childhood." Brain Sciences 6, no. 1 (March 15, 2016): 9. http://dx.doi.org/10.3390/brainsci6010009.

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Hebb, Matthew O., Paula Gaudet, and Ivar Mendez. "Deep brain stimulation to treat hyperkinetic symptoms of cockayne syndrome." Movement Disorders 21, no. 1 (January 2006): 112–15. http://dx.doi.org/10.1002/mds.20665.

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VACHIERY, F. "Hepatopulmonary syndrome: What relationship with liver failure and hyperkinetic circulation?" Hepatology 18, no. 4 (October 1993): A141. http://dx.doi.org/10.1016/0270-9139(93)92091-d.

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Rajan, Suraj, Bonnie Kaas, and Emile Moukheiber. "Movement Disorders Emergencies." Seminars in Neurology 39, no. 01 (February 2019): 125–36. http://dx.doi.org/10.1055/s-0038-1677050.

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AbstractMany acute and potentially life-threatening medical conditions have hyperkinetic or hypokinetic movement disorders as their hallmark. Here we review the clinical phenomenology, and diagnostic principles of neuroleptic malignant syndrome, malignant catatonia, serotonin syndrome, Parkinsonism hyperpyrexia, acute parkinsonism, acute chorea-ballism, drug-induced dystonia, and status dystonicus. In the absence of definitive lab tests and imaging, only a high index of clinical suspicion, awareness of at-risk populations, and variations in clinical presentation can help with diagnosis. We also discuss the principles of management and rationale behind treatment modalities in the light of more recent evidence.

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Szczepocka, Ewa, Radosław Magierski, Tomasz Sobów, and Adam Wysokiński. "The use of tetrabenazine for the treatment of drug-induced tardive dyskinesia – report of four cases." Aktualności Neurologiczne 16, no. 4 (December 30, 2016): 194–200. http://dx.doi.org/10.15557/an.2016.0025.

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Tardive dyskinesias are defined as a syndrome of involuntary, irregular, hyperkinetic movement disorders, including mixed movement disorders of the face and the mouth as well as choreoathetoid movements of the trunk and limbs. They are a serious and usually irreversible side effect of chronic neuroleptic treatment and affect approximately 15–20% of patients. Treatment attempts using amantadine, levetiracetam, piracetam, clonazepam, propranolol, vitamin B6, vitamin E, ondansetron, botulinum toxin and Ginkgo biloba were made. However, in many cases the treatment efficacy has not been confirmed in long-term studies in larger groups of patients. Tetrabenazine, registered in Poland for the treatment of hyperkinetic motor disorders in the Huntington’s disease, is one of the available therapeutic options. We present the course and the effects of tetrabenazine therapy in four patients with antipsychotic-induced tardive dyskinesias. Based on the experience gained during the research program using tetrabenazine, we believe that the use of this agent should be limited to patients in a stable mental condition, with no current symptoms of depression or active psychotic symptoms. In our opinion, suicidal tendencies or thoughts and a history of neuroleptic malignant syndrome are absolute contraindications. The off-label use of tetrabenazine requires a written informed consent of the patient and careful monitoring of their mental and neurological condition.

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Seideman, Mary F., and Travis A. Seideman. "A Review of the Current Treatment of Tourette Syndrome." Journal of Pediatric Pharmacology and Therapeutics 25, no. 5 (June 1, 2020): 401–12. http://dx.doi.org/10.5863/1551-6776-25.5.401.

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Tourette syndrome is a hyperkinetic movement disorder that presents before age 18 years and involves motor and phonic tics that may present with a wide range of severity. The severity and presentation of tics in an individual may fluctuate over time. Tourette syndrome may affect social relationships and school attendance, and may result in depression. Comorbidities are common, with attention-deficit/hyperactivity disorder and obsessive-compulsive disorder being most common. The literature supporting optimal treatment is limited but provides a framework for clinical decision-making. The focus of this review is to discuss the symptoms and possible causes of Tourette syndrome and current non-pharmacologic and pharmacologic treatment options, to help practitioners optimize care for pediatric patients with this disease.

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Blank, Rainer, and Helmut Remschmidt. "Hyperkinetic Syndrome: The role of allergy among psychological and neurological factors." European Child & Adolescent Psychiatry 3, no. 4 (October 1994): 220–28. http://dx.doi.org/10.1007/bf01978111.

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Egger, J., A. Stolla, and L. M. McEwen. "Controlled trial of hyposensitisation in children with food-induced hyperkinetic syndrome." Lancet 339, no. 8802 (May 1992): 1150–53. http://dx.doi.org/10.1016/0140-6736(92)90742-l.

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Guridi, J., R. González-Redondo, and J. A. Obeso. "Clinical Features, Pathophysiology, and Treatment of Levodopa-Induced Dyskinesias in Parkinson’s Disease." Parkinson's Disease 2012 (2012): 1–15. http://dx.doi.org/10.1155/2012/943159.

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Dyskinetic disorders are characterized by excess of motor activity that may interfere with normal movement control. In patients with Parkinson’s disease, the chronic levodopa treatment induces dyskinetic movements known as levodopa-induced dyskinesias (LID). This paper analyzed the pathophysiology, clinical manifestations, pharmacological treatments, and surgical procedures to treat hyperkinetic disorders. Surgery is currently the only treatment available for Parkinson’s disease that may improve both parkinsonian motor syndrome and LID. However, this paper shows the different mechanisms involved are not well understood.

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Abdelmoumen, Imane, Sandra Jimenez, Ignacio Valencia, Joseph Melvin, Agustin Legido, Mayela M. Diaz-Diaz, Christopher Griffith, et al. "Boricua Founder Variant in FRRS1L Causes Epileptic Encephalopathy With Hyperkinetic Movements." Journal of Child Neurology 36, no. 2 (September 15, 2020): 93–98. http://dx.doi.org/10.1177/0883073820953001.

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Objective: To describe a founder mutation effect and the clinical phenotype of homozygous FRRS1L c.737_739delGAG (p.Gly246del) variant in 15 children of Puerto Rican (Boricua) ancestry presenting with early infantile epileptic encephalopathy (EIEE-37) with prominent movement disorder. Background: EIEE-37 is caused by biallelic loss of function variants in the FRRS1L gene, which is critical for AMPA-receptor function, resulting in intractable epilepsy and dyskinesia. Methods: A retrospective, multicenter chart review of patients sharing the same homozygous FRRS1L (p.Gly246del) pathogenic variant identified by clinical genetic testing. Clinical information was collected regarding neurodevelopmental outcomes, neuroimaging, electrographic features and clinical response to antiseizure medications. Results: Fifteen patients from 12 different families of Puerto Rican ancestry were homozygous for the FRRS1L (p.Gly246del) pathogenic variant, with ages ranging from 1 to 25 years. The onset of seizures was from 6 to 24 months. All had hypotonia, severe global developmental delay, and most had hyperkinetic involuntary movements. Developmental regression during the first year of life was common (86%). Electroencephalogram showed hypsarrhythmia in 66% (10/15), with many older children evolving into Lennox-Gastaut syndrome. Six patients demonstrated progressive volume loss and/or cerebellar atrophy on brain magnetic resonance imaging (MRI). Conclusions: We describe the largest cohort to date of patients with epileptic encephalopathy. We estimate that 0.76% of unaffected individuals of Puerto Rican ancestry carry this pathogenic variant due to a founder effect. Children homozygous for the FRRS1L (p.Gly246del) Boricua variant exhibit a very homogenous phenotype of early developmental regression and epilepsy, starting with infantile spasms and evolving into Lennox-Gastaut syndrome with hyperkinetic movement disorder.

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Moeller, S. "Normal red blood cell cardiac output in hyperkinetic syndrome of alcoholic cirrhosis." Journal of Hepatology 34 (April 2001): 68. http://dx.doi.org/10.1016/s0168-8278(01)80232-4.

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Henriksen, Jens H., Flemming Bendtsen, and Søren Møller. "Normal red cell cardiac output in the hyperkinetic syndrome of alcoholic cirrhosis." Journal of Hepatology 34, no. 5 (May 2001): 782–83. http://dx.doi.org/10.1016/s0168-8278(01)00019-8.

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Moeller, S., F. Bendtsen, and J. H. Henriksen. "Normal red blood cell cardiac output in hyperkinetic syndrome of alcoholic cirrhosis." Journal of Hepatology 34 (April 2001): 68. http://dx.doi.org/10.1016/s0168-8278(01)81107-7.

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Kompliti, Katie, and Christopher G. Goetz. "Hyperkinetic movement disorders misdiagnosed as tics in gilles de la tourette syndrome." Movement Disorders 13, no. 3 (May 1998): 477–80. http://dx.doi.org/10.1002/mds.870130317.

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TROTT, G. E., M. MENZEL, and H. J. FRIESE. "Treatment of hyperkinetic syndrome with Moclobemide - results of an open clinical study." Clinical Neuropharmacology 15 (1992): 578B. http://dx.doi.org/10.1097/00002826-199202001-01119.

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Verma, Rajesh, and Chetan Shettigar. "Isolated Lingual Dystonia as the Manifestation of Acute Extrapyramidal Syndrome Induced by Metoclopramide." Journal of Neurosciences in Rural Practice 10, no. 02 (April 2019): 346–48. http://dx.doi.org/10.4103/jnrp.jnrp_355_18.

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ABSTRACTOromandibular dystonia is characterized by persistent contractions and repetitive spasms of masticatory muscles surrounding the oral cavity and lingual muscles. The lingual dystonia is rare hyperkinetic movement disorder, often occurring secondary to drugs. The common drugs which can cause acute focal dystonia are neuroleptics, antiemetics, and antipsychotics. Isolated lingual dystonia is a rare form of disabling focal dystonias. We report a young female, who developed tongue dystonia in isolation and responding favorably to antihistaminics. The physicians are advised to make inquiry about administered drugs in isolated lingual dystonia.

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Zekeridou, Anastasia, Thomas Kryzer, Yong Guo, Anhar Hassan, Vanda Lennon, Claudia F. Lucchinetti, Sean Pittock, and Andrew McKeon. "Phosphodiesterase 10A IgG." Neurology 93, no. 8 (July 17, 2019): e815-e822. http://dx.doi.org/10.1212/wnl.0000000000007971.

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ObjectiveTo describe a novel antibody biomarker of neurologic paraneoplastic autoimmunity specific for phosphodiesterase 10A (PDE10A), a striatum-enriched phosphodiesterase, and to characterize the clinical phenotype of patients with PDE10A immunoglobulin G (IgG).MethodsWe describe 7 patients with autoantibodies specific for PDE10A identified in the Mayo Clinic Neuroimmunology Laboratory. Patient specimens (sera, 7; CSF, 4) produced identical basal ganglia‐predominant synaptic staining of murine brain tissue by indirect immunofluorescence. The autoantigen was identified by immunoprecipitation and mass spectrometry as PDE10A, and confirmed by antigen-specific recombinant Western blot and cell-based assays, and immune absorption experiments.ResultsThe median patient age was 70 years (range 66–76); 4 were men. Four patients with clinical information available had movement disorders (hyperkinetic in 3 [chorea, ballismus, dystonia] and parkinsonism in 1). All patients but one had cancer (lung [adenocarcinoma 1, squamous cell carcinoma 1, poorly differentiated mesenchymal carcinoma 1], renal adenocarcinoma 2, and pancreatic adenocarcinoma 1). Two of the 7 patients developed hyperkinetic movement disorders during treatment with immune checkpoint inhibitors (nivolumab and pembrolizumab), though none of 26 cancer control patients treated with immune checkpoint inhibitors harbored PDE10A IgG in their serum. MRIs from those 2 patients with hyperkinetic movement disorders demonstrated fluid-attenuated inversion recovery/T2 basal ganglia hyperintensities, and their CSF harbored unique oligoclonal bands. One of those 2 patients had substantial improvement after corticosteroids. One patient's renal adenocarcinoma expressed PDE10A by immunohistochemistry.ConclusionsPDE10A IgG defines a novel rare neurologic autoimmune syndrome and expands the spectrum of diagnosable paraneoplastic CNS disorders. The intracellular location of PDE10A suggests a T-cell-mediated pathology targeting cells displaying MHC1-bound PDE10A peptides.

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Teive, Hélio A. G., Adriana Moro, Mariana Moscovich, and Renato P. Munhoz. "Increased sexual arousal in patients with movement disorders." Arquivos de Neuro-Psiquiatria 74, no. 4 (April 2016): 303–6. http://dx.doi.org/10.1590/0004-282x20150217.

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ABSTRACT Increased of sexual arousal (ISA) has been described in different neurological diseases. The purpose of this study was present a case series of ISA in patients with movement disorders. Method Fifteen patients with different forms of movement disorders (Parkinson’s disease, Huntington’s disease, Tourette´s syndrome, spinocerebellar ataxia type 3), were evaluated in the Movement Disorders Unit of the Federal University of Paraná. Results Among Parkinson’s disease patients there were seven cases with different forms of ISA due to dopaminergic agonist use, levodopa abuse, and deep brain stimulation (DBS). In the group with hyperkinetic disorders, two patients with Huntington’s disease, two with Tourette’s syndrome, and four with spinocerebellar ataxia type 3 presented with ISA. Conclusions ISA in this group of patients had different etiologies, predominantly related to dopaminergic treatment or DBS in Parkinson’s disease, part of the background clinical picture in Huntington’s disease and Tourette’s syndrome, and probably associated with cultural aspects in patients with spinocerebellar ataxia type 3.

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Babanov, Sergey. "State of central hemodynamics and myocardial contractility in vibration disease." Terapevt (General Physician), no. 5 (May 1, 2020): 62–73. http://dx.doi.org/10.33920/med-12-2005-09.

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The article describes the peculiarities of Central hemodynamics and myocardial contractility in patients with vibration disease, various forms and degrees of severity with the help of echocardiography of the Department of pathology of the regional center of occupational pathology of SBME "Samara mediko-a sanitary part of № 5 of Kirov district". It was found that patients with vibration disease are characterized by the formation of a phase syndrome of myocardial hyperdynamics and a hyperkinetic variant of Central hemodynamics, while hemodynamic changes depend on the form of vibration disease, the severity of the disease, and the length of work in contact with vibration.

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Paton, D. M. "Deutetrabenazine: Treatment of hyperkinetic aspects of Huntington's disease, tardive dyskinesia and Tourette syndrome." Drugs of Today 53, no. 2 (2017): 89. http://dx.doi.org/10.1358/dot.2017.53.2.2589164.

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Thenganatt, Mary Ann, and Joseph Jankovic. "Recent Advances in Understanding and Managing Tourette Syndrome." F1000Research 5 (February 9, 2016): 152. http://dx.doi.org/10.12688/f1000research.7424.1.

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Tourette syndrome (TS) is a neurologic and behavioral disorder consisting of motor and phonic tics with onset in childhood or adolescence. The severity of tics can range from barely perceptible to severely impairing due to social embarrassment, discomfort, self-injury, and interference with daily functioning and school or work performance. In addition to tics, most patients with TS have a variety of behavioral comorbidities, including attention deficit hyperactivity disorder and obsessive-compulsive disorder. Studies evaluating the pathophysiology of tics have pointed towards dysfunction of the cortico-striato-thalamo-cortical circuit, but the mechanism of this hyperkinetic movement disorder is not well understood. Treatment of TS is multidisciplinary, typically involving behavioral therapy, oral medications, and botulinum toxin injections. Deep brain stimulation may be considered for “malignant” TS that is refractory to conventional therapy. In this review, we will highlight recent developments in the understanding and management strategies of TS.

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Wong, Lee-Chin, Shekhar Singh, Hsin-Pei Wang, Chia-Jui Hsu, Su-Ching Hu, and Wang-Tso Lee. "FOXG1-Related Syndrome: From Clinical to Molecular Genetics and Pathogenic Mechanisms." International Journal of Molecular Sciences 20, no. 17 (August 26, 2019): 4176. http://dx.doi.org/10.3390/ijms20174176.

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Individuals with mutations in forkhead box G1 (FOXG1) belong to a distinct clinical entity, termed “FOXG1-related encephalopathy”. There are two clinical phenotypes/syndromes identified in FOXG1-related encephalopathy, duplications and deletions/intragenic mutations. In children with deletions or intragenic mutations of FOXG1, the recognized clinical features include microcephaly, developmental delay, severe cognitive disabilities, early-onset dyskinesia and hyperkinetic movements, stereotypies, epilepsy, and cerebral malformation. In contrast, children with duplications of FOXG1 are typically normocephalic and have normal brain magnetic resonance imaging. They also have different clinical characteristics in terms of epilepsy, movement disorders, and neurodevelopment compared with children with deletions or intragenic mutations. FOXG1 is a transcriptional factor. It is expressed mainly in the telencephalon and plays a pleiotropic role in the development of the brain. It is a key player in development and territorial specification of the anterior brain. In addition, it maintains the expansion of the neural proliferating pool, and also regulates the pace of neocortical neuronogenic progression. It also facilitates cortical layer and corpus callosum formation. Furthermore, it promotes dendrite elongation and maintains neural plasticity, including dendritic arborization and spine densities in mature neurons. In this review, we summarize the clinical features, molecular genetics, and possible pathogenesis of FOXG1-related syndrome.

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Vegas, Nancy, Mara Cavallin, Camille Maillard, Nathalie Boddaert, Joseph Toulouse, Elise Schaefer, Tally Lerman-Sagie, et al. "Delineating FOXG1 syndrome." Neurology Genetics 4, no. 6 (November 7, 2018): e281. http://dx.doi.org/10.1212/nxg.0000000000000281.

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ObjectiveTo provide new insights into the FOXG1-related clinical and imaging phenotypes and refine the phenotype-genotype correlation in FOXG1 syndrome.MethodsWe analyzed the clinical and imaging phenotypes of a cohort of 45 patients with a pathogenic or likely pathogenic FOXG1 variant and performed phenotype-genotype correlations.ResultsA total of 37 FOXG1 different heterozygous mutations were identified, of which 18 are novel. We described a broad spectrum of neurodevelopmental phenotypes, characterized by severe postnatal microcephaly and developmental delay accompanied by a hyperkinetic movement disorder, stereotypes and sleep disorders, and epileptic seizures. Our data highlighted 3 patterns of gyration, including frontal pachygyria in younger patients (26.7%), moderate simplified gyration (24.4%) and mildly simplified or normal gyration (48.9%), corpus callosum hypogenesis mostly in its frontal part, combined with moderate-to-severe myelination delay that improved and normalized with age. Frameshift and nonsense mutations in the N-terminus of FOXG1, which are the most common mutation types, show the most severe clinical features and MRI anomalies. However, patients with recurrent frameshift mutations c.460dupG and c.256dupC had variable clinical and imaging presentations.ConclusionsThese findings have implications for genetic counseling, providing evidence that N-terminal mutations and large deletions lead to more severe FOXG1 syndrome, although genotype-phenotype correlations are not necessarily straightforward in recurrent mutations. Together, these analyses support the view that FOXG1 syndrome is a specific disorder characterized by frontal pachygyria and delayed myelination in its most severe form and hypogenetic corpus callosum in its milder form.

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Yao-chi, Wu. "Clinical research on treatment of hyperkinetic syndrome of childhood by electroacupuncture plus acupoint application." Journal of Acupuncture and Tuina Science 1, no. 4 (August 2003): 35–37. http://dx.doi.org/10.1007/bf02874742.

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Journal articles on the topic 'Hyperkinetický syndrom'

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