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PubMed1992

Effect of afterload and beta-adrenergic blockade on nonischemic myocardial contraction pattern.

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.

Adrenergic beta-Antagonists↗
PubMed1978

Hyperkinetic disorder in psychiatric clinic attenders.

Sixty-eight boys (age-range five to 11 years), referred to a child psychiatric clinic, were studied in order to determine the validity of a broadly-based concept of hyperkinetic syndrome, as generally employed in the USA. Hyperactivity was measured on the Conners' Teacher Questionnaire, the Conners' Parent Questionnaire and by systematic time-sampled observations of each child's behaviour during psychological testing. There were low and statistically insignificant correlations between these different measures of hyperkinesis. On the other hand, overactivity correlated highly with conduct disturbance. Psychiatrically abnormal children with and without hyperkinesis were compared on cognitive functioning, perinatal history, neurological examination, congenital anomalies and psycho-social circumstances. Few differences were found, and it was concluded that there was no evidence for the validity of a broad concept of hyperkinetic syndrome. Nevertheless, a small number of children were found who were overactive in all situations studied. These children had a variety of clinical diagnoses but differed significantly from their peers--matched for age, IQ and diagnosis--with respect to neurological anomalies, erratic responses on the Matching Familiar Figures Test, and early onset of hyperkinesis. It is suggested that this less common clinical picture of hyperkinesis may have some validity, but it remains uncertain whether it constitutes a distinct syndrome or rather a constitutional risk factor.

Attention↗
PubMed1983

Hyperkinetic disorders in seven-year-old children with perceptual, motor and attentional deficits.

One hundred and forty-one seven-year-old Swedish children took part in an extensive neuropsychiatric study involving total population samples of children who had shown perceptual, motor and attentional deficits in pre-school, and blindly examined comparison children. The present paper reports on generalized hyperkinesis, i.e. hyperactivity in the child in all of three different assessment settings. About a third of children diagnosed according to strict criteria as suffering from 'Minimal Brain Dysfunction' showed generalized hyperkinesis. In children without perceptual-motor deficits, hyperkinesis was very much rarer. A total population frequency for generalized hyperkinesis in the range of 1-3% is reported as probable. Heredity for delayed maturation, non-optimal pre-, peri- and neonatal factors and adverse psychosocial factors were found to interact in the shaping of the disorder.

Attention↗
PubMed1982

Echocardiographic assessment of left ventricular wall motion in hypertrophic cardiomyopathy.

M-mode and two-dimensional parasternal long axis view echocardiography, and left anterior oblique cineangiography were employed to assess the left ventricular wall motion in 10 normal subjects (N) and in 25 patients with hypertrophic cardiomyopathy: 7 patients with symmetric hypertrophy (SH) and 6 patients with apical cardiomyopathy (AHCM) and no intraventricular gradient; 12 patients with hypertrophic obstructive cardiomyopathy and asymmetric septal hypertrophy with resting intraventricular gradient (6 pts) (HOCM-R) or gradient occurring only after isoproterenol infusion (6 pts) (HOCM-I). The left ventricle was divided into five portions: upper and lower septum, upper and lower posterior wall and apex. The excursion and thickness of the upper and lower portions of the septum and posterior wall were measured in all patients and compared to 10 normal subjects (N). From the superimposed end-diastolic and end-systolic echo frames and angio silhouettes a chordal and a radial-chordal method were used, respectively, to measure the motion of the left ventricular wall segments. In SH the left ventricular wall motion was qualitatively similar to N but a little reduced; the thickness was increased and no pressure gradient was present. In AHCM the lower septum, posterior wall, and apex showed significantly increased thickness and motion compared to N and compared to the upper portions of the septum and posterior wall. No gradient was present. In HOCM-R the upper septum moved towards the apex, the lower septum, upper posterior wall and lower posterior wall moved towards the left ventricular cavity. The upper posterior wall was hyperkinetic compared to N and compared to the lower posterior wall, resting gradient and SAM was present in all. In HOCM-I the upper septum moved towards the apex; the posterior wall was hyperkinetic (the excursion was a little wider in the lower posterior wall than in the upper posterior wall). No gradient was recorded at rest, but it could be provoked by isoproterenol. Echocardiography provides precise information on left ventricular wall motion in hypertrophic cardiomyopathy. Hyperkinesis of the lower left ventricular wall is related to AHCM; hyperkinesis of the upper posterior wall and the motion of the upper septum towards the apex are related to HOCM-R. Hyperkinesis of the lower posterior wall is related to HOCM-I. SAM and pressure gradients may be related to the hyperkinesis of the upper posterior wall. Finally, the septum is not an immobile structure in HOCM, since it moves mainly from the base to the apex and a less (or not at all) towards the posterior wall.

Cardiac Catheterization↗
PubMed2001

[Electric stimulation of the brain in patients with hepatocerebral Wilson-Konovalov's degeneration (neuromorphological and neurophysiological analysis)].

36 stereotactic operations were carried out in 27 patients. Either the total lack of hyperkinesis or its significant decrease was found in 17 cases; 5 patients died. There was no correlation between manifestations of hepatocerebral degeneration and relatively normal quantitative characteristics of both cortical and subcortical biopotentials. These potentials are produced on the background of the microstructural changes in the neurons of the same regions. It is suggested that qualitative importance of such biopotentials lies in their exceeding pathologic impulsation, arising hyperkinesis. That was confirmed by the fact, that hyperkinesis eliminates after surgical destruction of the ventrolateral nucleus of the thalamus and the subthalamic structures.

Adolescent↗
PubMed1999

Actions of the D1 agonists A-77636 and A-86929 on locomotion and dyskinesia in MPTP-treated L-dopa-primed common marmosets.

Common marmosets show parkinsonian motor deficits following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration and develop dyskinesias during chronic L-dopa exposure. The D1 agonists A-77636 [(1R, 3S) 3-(1'-adamantyl)-1-aminomethyl-3, 4-dihydro-5, 6-dihydroxy-1H-2-benzopyran HCl] and A-86929 [(-)-trans 9, 10-hydroxy-2-propyl-4, 5, 5a, 6, 7, 11b-hexahydro-3-thia-5-azacyclopent-1-ena[c]phenanthrene hydrochloride] possess potent antiparkinsonian activity in the MPTP-treated marmoset and we now assess their influence on L-dopa-induced dyskinesias. MPTP-treated marmosets with stable motor deficits were treated with L-dopa plus carbidopa for 28 days to induce dyskinesias. Subsequently, they received A-86929 for 10 days, initially at 0.5 micromol/kg and then at 1.0 micromol/kg for a further 5 days. Several months later, L-dopa 12.5 mg/kg plus carbidopa 12.5 mg/kg was given orally twice daily for 7 days, followed by A-77636 1 micromol/kg for 10 days, and then both A-77636 and L-dopa plus carbidopa were given concurrently for 3 further days. In these L-dopa-primed animals, A-86929 effectively reversed akinesia and produced dose-dependent dyskinesias which were significantly less intense than those produced by L-dopa administration. A degree of behavioral tolerance was encountered, but antiparkinsonian activity was preserved and elicited behaviour was free of hyperkinesis and stereotypy and more naturalistic than that seen with L-dopa. After a week of twice-daily L-dopa dosing, administration of the long-acting D1 agonist A-77636 initially dramatically enhanced locomotion and reproduced dyskinesia with prominent dystonia, but after repeated administration of A-77636, dyskinesia and in particular chorea, gradually disappeared. Tolerance to locomotor stimulation greater than with A-86929 occurred, although activity remained significantly above baseline levels. There was a marked reduction in L-dopa-induced climbing, stereotypy and hyperkinesis and behaviour more closely resembled that of normal unlesioned marmosets. Upon reintroduction of L-dopa concurrently with continued A-77636 administration, dystonic, but virtually no choreic dyskinesias appeared and behaviour was once again free of stereotypy and hyperkinesis, contrasting dramatically with the presence of these behaviours along with abundant chorea when L-dopa is given alone. These results show a lesser liability of A-86929 and A-77636 to reproduce dyskinesia in L-dopa-primed MPTP-lesioned subjects while maintaining effective antiparkinsonian activity and producing a more naturalistic motor response. The differential effects of A-77636 on chorea and dystonia, with suppression of chorea and stereotypy on co-administration with L-dopa, may reflect an altered balance of activity in the direct and indirect striatofugal pathways. These results suggest a possible role for D1 agonists in the treatment of Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

Evolution of left ventricular function after intracoronary thrombolysis for acute myocardial infarction.

The temporal evolution of left ventricular (LV) function after intracoronary streptokinase therapy for acute myocardial infarction (AMI) was assessed from the data of 264 patients who had complete occlusion of either the left anterior descending or the right coronary artery before treatment. Angiography was performed immediately, and at 3 days and 6 months after AMI in 91%, 71% and 47% of the study group, respectively. Wall motion was measured by the centerline method. In patients with sustained reperfusion, the ejection fraction decreased at 3 days (delta = -2.0 +/- 9.9%, n = 134, p = 0.02) and recovered later (from 54 +/- 12% acutely to 57 +/- 12% at 6 months, n = 82, p less than 0.05). These changes in global function were associated with a marked regression in hyperkinesis in the noninfarcted wall by 3 days, and delayed recovery of wall motion in the infarct region (delta = 0.2 +/- 0.9 at 3 days, p = 0.055; 1.0 +/- 1.2 at 6 months, p less than 0.001). Patients without reperfusion or with reocclusion had a more severe decrease in ejection fraction at 3 days, and little or no subsequent functional recovery. The length of the hypokinetic segment increased significantly by 3 days but subsequently diminished to slightly less than the acute value. It is concluded that full recovery of ischemically impaired myocardium takes greater than 3 days, but compensatory hyperkinesis regresses earlier so that global LV function deteriorates by the third day. Variability or deterioration of LV function early after AMI need not be due to infarct extension; it can reflect regression of hyperkinesis in the noninfarcted region.

Angiography↗
PubMed2004

Plasma brain natriuretic peptide in takotsubo cardiomyopathy.

BACKGROUND: Takotsubo cardiomyopathy is a reversible left ventricular dysfunction with symptoms resembling acute myocardial infarction, but without coronary lesions. Patients have wall motion abnormalities (apical akinesis and basal hyperkinesis), and characteristic left ventricular morphology. AIM: To investigate plasma brain natriuretic peptide (BNP) concentrations in takotsubo cardiomyopathy. METHODS: Ten consecutive patients with takotsubo cardiomyopathy underwent cardiac catheterization on their first hospital day, and blood was collected to measure BNP. To evaluate acute basal hyperkinesis, the difference in diameter between systole and diastole was measured at 10 mm below the aortic valve (the deltaBase value). RESULTS: Coronary angiography revealed no significant stenosis in any patient. Initial ejection fraction was 42.2 +/- 7.3%, cardiac index was 1.90 +/- 0.39 l/min/m(2), and plasma BNP was 522.5 +/- 632.9 pg/ml. Ventricular contraction and the ejection fraction were normalized on echocardiography after 17.9 +/- 6.3 days. BNP was significantly correlated with deltaBase, but not with other cardiac parameters. DISCUSSION: Initial deltaBase value seems to be a good indicator of the severity of basal hyperkinesis in patients with takotsubo cardiomyopathy. In contrast to other diagnoses, a high BNP concentration is not associated with a poor prognosis in this condition.

Aged↗
PubMed1975

The hyperkinetic child: some misleading assumptions.

There is much controversy in the literature concerning prevalence, cause, diagnosis and treatment of hyperkinesis. The subject is complex; there is much ambiguity, and many research studies and reports of successful treatment appear to be overly simplistic in their approach to the problem. The use of the term "hyperkinesis" as synonymous with "hyperactivity" and often also with "minimal cerebral dysfunction" causes much confusion. There appear to be some common underlying beliefs about hyperkinetic children; these are critically examined. From integration of reports in the literature with clinical experience, it is contended that the term hyperkinesis should be restricted to the definition used in the British studies, and hyperactivity should be considered only a symptom. Hyperactivity has a large number of underlying causes, and management plans need to be individualized.

Attention Deficit Disorder with Hyperactivity↗
PubMed1978

A pyridoxine-dependent behavioral disorder unmasked by isoniazid.

A 3-year-old girl had behavioral deterioration, with hyperkinesis, irritability, and sleeping difficulties after the therapeutic administration of isoniazid. The administration of pharmacologic doses of pyridoxine hydrochloride led to a disappearance of symptoms. After discontinuing isoniazid therapy a similar pattern of behavior was noted that was controlled by pyridoxine. A placebo had no effect, but niacinamide was as effective as pyridoxine. Periodic withdrawal of pyridoxine was associated with return of the hyperkinesis. The level of pyridoxal in the blood was normal during the periods of relapse. Metabolic studies suggested a block in the kynurenine pathway of tryptophan metabolism. The patient has been followed for six years and has required pharmacologic doses of pyridoxine to control her behavior.

Child Behavior Disorders↗
PubMed1979

Diagnostic implications of parental ratings of children.

Evaluated parental ratings on aggressiveness and social responsibility for 120 school-age children and a cross-validation sample of 67 children referred to a university-sponsored developmental evaluation center in association with 10 commonly used interdisciplinary diagnoses . Parental ratings consistently and significantly related to staff diagnoses of behavior disorder and to hyperkinesis. A number of "expected " relationships, e.g., between learning disability and social irresponsibility, did not occur. In general, the results indicate: (1) that parental ratings show consistent relationships to selected interdisciplinary staff diagnoses; (2) that hyperkinesis may be related more strongly to aggressiveness than to the lack of socially responsible behavior; and (3) that parental ratings are potentially valuable in the diagnostic process.

Aggression↗
PubMed2002

Levetiracetam in autistic children: an open-label study.

The objectives of this study were to determine whether autistic children taking levetiracetam (1) showed improvement in the areas of aggression, impulsivity, hyperkinesis, and mood instability, and (2) showed a nootropic response. Ten white autistic boys ranging from 4 to 10 years were compared pretreatment and while taking levetiracetam for an average of 4.1 weeks. Inattention, hyperkinesis, and impulsivity were evaluated using the Achenbach Attention Problems scale, Conners DSM-IV Total scale, and the Conners Attention-Deficit Hyperactivity Disorder Index scale, all of which showed statistically significant improvements. Mood instability was measured with the Conners Global Index (CGI) Emotional Lability and CGI Total scales, both of which showed statistically significant improvements. Aggressive behavior, as measured with the Achenbach Aggression scale, showed statistically significant improvement only for subjects who were not recently weaned from medications that reduce aggression (e.g., risperidone, carbamazepine, desipramine). Levetiracetam may reduce hyperactivity, impulsivity, mood instability, and aggression in autistic children with these problems. No nootropic effect was observed.

Aggression↗
PubMed1987

Fragile (X) syndrome: a study of the psychological profile in 23 prepubertal patients.

In this study a further analysis of the psychological profile in the prepubertal fragile (X) (fra(X] male was performed. The results of the psycho-diagnostic examination of 23 fra(X) boys were compared to a control group of 17 males of the same age with 'non-specific' mental retardation. A number of important quantitative and qualitative differences were observed between the two groups. In the preschool age group the majority of fra(X) boys was mildly mentally retarded. In the school-age group, however, most boys were moderately to severely mentally retarded. This indication of a decline in intellectual performance with age in the fra(X) syndrome was confirmed by a longitudinal individual follow-up of seven fra(X) boys in this age group. In contrast to intellectual performance, appearance of the attention deficit disorder (or hyperkinesis), with its attendent overactivity and impulsiveness, decreases with age, and is independent of the intellectual level. Autistic behaviour was more frequently observed in the youngest fra(X) males, and was more pronounced in the moderately mentally retarded. In more than 50% of the boys of preschool age the association of hyperkinesis and autistic features was found. Language and speech development in the fra(X) syndrome is both symptomatic and specific. Beside a severe, global speech retardation, there are some distinct speech characteristics in the young fra(X) males such as rapid speech rhythm, speech impulsiveness and perseverative speech.

Age Factors↗
PubMed1972

Paediatric neurology in Africa: a Ugandan report.

The findings in 138 children attending a neurology clinic in Uganda are presented. In contrast with findings in developed countries, only 25 had an abnormal birth and history dating from birth compared with 63 who had a normal birth and early development with symptoms of postnatal onset. The commonest mode of onset in the postnatal period was a catastrophic, feverish illness. Effective and usually easily achieved drug control of epilepsy and hyperkinesis enabled most parents to cope with disabled children. Simple explanation to parents and teachers can reduce the rejection and educational retardation associated with epilepsy.Primary prevention lies in earlier diagnosis and treatment of cerebral malaria, meningitis, and encephalitis and improved obstetric services. Secondary prevention requires closer follow-up of potentially brain-damaged children and the education of doctors in neurological and behavioural assessment and the more efficient treatment of epilepsy and hyperkinesis.

Brain Damage, Chronic↗
PubMed1975

The effect of methylphenidate on sensory perception in varying degrees of hyperkinetic behaviour.

In a double-blind study of methylphenidate, hyperkinetic children of varying levels of age and degree of hyperactivity were assessed on subtests of the Illinois Test of Psycholinguistic Ability (ITPA). The ITPA was supplemented with a combination of monosensory, bisensory, and trisensory stimuli presentations. Methylphenidate improved the ITPA's visual, auditory and tactile age scores of children who exhibited a more marked degree of hyperkinetic behaviour. That improvement was also observed in the recognition of sensory stimuli presented in a monosensory fashion. Similarly, the children with a more marked degree of hyperkinesis improved their stimuli recognition rate significantly on methylphenidate when stimuli were presented to bisensory and trisensory perceptual modalities simultaneously. It was concluded that drug improvement on sensory perception seemed to be more related to the degree of hyperkinetic behavior manifested than to chronological age. Further research of degree of hyperkinesis, age-level, sensory modality and drug administration was suggested.

Adolescent↗
PubMed1979

The management of the hyperactive child: an overview.

Hyperkinesis has been increasingly recognized as a medical problem of great significance in everyday practice. Not infrequently, a child has been labeled hyperkinetic at an early age, with a battery of tests, psychological evaluations and multiple medications, in addition to the family frustration and anxiety that follow the diagnosis of hyperkinesis of the offspring.

Behavior Therapy↗
PubMed1994

[The role of lipid peroxidation in the pathogenesis of neuropathological syndromes and in experimental therapy].

Activated lipid peroxidation observed in brain homogenates in experimental choreoid hyperkinesis and bemegride epilepsy can be arrested by antioxidant pretreatment. The same is true for parkinsonian and "malignant locomotion" syndromes provoked by intrastriatal pro-oxidant (oxidized oleinic acid) microinjection and systemic administration of haloperidol. Experimental therapy of choreoid hyperkinesis with GABA-positive and dopamine-blocking drugs alone proved ineffective. The effect was achieved at combined application of antioxidant and GABA-positive drugs.

Animals↗
PubMed1993

[The differential diagnosis of Kozhevnikov's epilepsy].

Based on the data of a comprehensive examination of 40 patients with Kozhevnikov's epilepsy, 24 with hyperkinesis epilepsy (Sokolianskiĭ-Kliuchikov syndrome), 10 with myoclonus epilepsy (Unverricht-Lundborg syndrome) and 6 with cerebellar myoclonic dyssynergy, the most informative differential diagnostic criteria were distinguished. Their use will make it possible to determine one or another above-indicated disease entity more reliably. The structure of the paroxysmal syndrome and the character of myoclonic hyperkinesis are determined by dissimilar involvement into the pathological process of the cortical, subcortical, stem and cerebellar structures.

Adolescent↗