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The role of organic factors in childhood hyperkinesis is evaluated, with a focus on electroencephalographic, neurological, biochemical, pregnancy and birth, and genetic research. Evidence that the majority of hyperkinetic children suffer from organic dysfunction is found to be minimal. This conclusion is discussed, and guidelines for future research are offered.
The first heuristic description of the hyperkinetic impulse disorder made its appearance in the literature just over twenty years ago. Although there are many who are made restless and irritable by continuing ambiguities and controversies surrounding the hyperkinetic syndrome, the past two decades have brought considerable maturation in our knowledge of this concept. The present paper sketches the state of the art in regard to hyperkinesis, and draws conclusions about directions for both research and clinical work.
A 5-year-old Japanese boy showed nephritis similar to, but distinct from, that in Alport syndrome. Nephrotic syndrome without hematuria was noticed at age 2, although renal biopsy at age 4 revealed widespread irregular thickening of the glomerular basement membrane with splitting of the lamina densa on electron microscopy, characteristic of nephritis in Alport syndrome. Sensorineural deafness was noticed at age 4 weeks by no auditory brain stem response, unusually early for Alport syndrome. Goodpasture antigen and amyloid P component were found in the glomerular basement membrane. Thus, the antigenicity of the glomerular basement membrane was different from that in male patients with X-linked Alport syndrome. In addition, growth and developmental retardation, hyperkinesis, and cleft soft palate were seen. These features are a hitherto undescribed combination. The family history was negative for any of the features of the boy.
This study results from observations, for 10 years, of children with psychomotor instability, also called hyperkinesis, generally due to "minimal brain dysfunction". A clinical summary emphasizes instability and difficult coordination of all aspects of personality. A pathogenic hypothesis concerns one of the stimulation function which may be abnormal, as the control and regulation of personality, partly located, at the subcortical level, and creating secondary symptoms and reactional ones. The results of therapy are interpreted according to a clinical research protocol. It proposes a global appreciation, an appreciation of the duration of therapeutic effect through the study of variation of specific criteria, and a general appreciation correlating both aspects. Through this stern methodology and the mean duration of treatment of 2 years, the results are significant in 55% of the cases. Compared to other drugs, Depamide seems more valid. Furthermore, this drug is without secondary clinical and psychological effects.
Insufficient effectiveness of medicamentous therapy of local hyperkineses necessitated quest for other treatment options. In view of pathogenetic features of this pathological process we have chosen reflexotherapy to be instituted in our patients: auriculopuncture, electro-corporal- and acupuncture which have been shown to be expedient and effective in treating 65 patients with local hyperkinesis (blepharospasm, facial paraspasm, writer's spasm, spasmodic torticollis). Positive findings from clinical and paraclinical methods of investigation corroborate the results of the treatments administered.
Proceeding from the standpoint of a systemic organization of nervous processes which determine the central mechanism of hyperkinesis, the authors modeled hyperkineses by a simultaneous or successional electric stimulation of the brain limbic system in dogs. It was established that there was a correlation between the external expression of hyperkineses, their stability and reproduction and the ordinal succession in which the structures are irritated. In such conditions it is possible to create a functional system where the activation of separate structures appears to be a link in the system while the separate links are inter-related on the basis of inborn and developed mechanisms.
A 3-year-old boy with mixed glomerular/tubular proteinuria, mental retardation, and hyperkinesis is described. The proteinuria was discovered at the age of 3 years on urinary mass screening. Most of the urinary protein consisted of albumin, accompanied by increases in low molecular weight proteins, including beta 2-microglobulin and alpha 1-microglobulin. Mixed glomerular/tubular proteinuria is known to be caused by the following conditions: chronic renal failure, chronic pyelonephritis, cadmium poisoning, tubulointerstitial nephritis of various etiologies, and after strenuous, short-term, exhaustive exercise. The present patient did not display any of these disorders or conditions.
The effect of bilateral intrastriatal daily microinjection of 5 and 15 micrograms of ley-enkephalin and its synthetic analog tetrapeptide during 3 weeks on behaviour, was investigated. No obvious effect was obtained after ley-enkephalin microinjections. The tetrapeptide produced obvious cataleptic status with plastic rigidity of skeletal muscles. Starting from the 2nd week of tetrapeptide microinjections, the upper arms developed a stereotyped hyperkinesis. No avoidance conditioning was possible. The findings suggest an involvement of the enkephalin neostriatal system in pathological behaviour as an analog of psychopathological disorders in humans.
A case of opsoclonus, myoclonic hyperkinesis of the eyes, is described. The causes of the occurrence of such a rare phenomenon are analyzed. A hypothesis is advanced, according to which in the mechanism of oculomotor abnormalities, of great importance are anatomic formations in the oral parts of the brain stem.
Ten years ago, Dr. Feingold proposed that hyperactivity and learning disabilities in children are commonly caused by the ingestion of food additives and claimed that elimination of foods with additives from the diet resulted in major improvements in three-quarters of hyperactive children. In the last five years, controlled double-blind studies have been conducted by many investigators to test this hypothesis. The results, which are mainly negative, are summarized. The authors conclude that 2% (contrasted with Feingold's claims of 75%) of hyperactive children respond adversely to dye additives. Even the 2% are questionable. There is no need for high-priority research or for changes in public policy regarding the use and labeling of foods containing additives. Hyperkinesis has multiple etiologies, which require other types of biological and psychological research.
The effects of three-week daily intrastriatal 45 mcg GABA, 5 and 15 mcg picrotoxin and 5 bicuculline microinjections in rats were investigated. The inhibition of avoidance conditioning in shuttle box was registered in first days of GABA microinjection; stereotyped behaviour and paradoxal freezing in further GABA effects were developed. After the short orofacial dyskinesia as the acute picrotoxin effects, the choreo-myoclonic limb jerks, with the distinct generalization stage were observed. Picrotoxin dose increasing in toxic convulsive status results. No any dystonia, but strong avoidance conditioning inhibition in all three weeks of bicuculline treatment were observed only. The novel functional and controlled model of choreo-myoclonic hyperkinesis is proposed. The role of the striatal GABA system in human neuro-motor dyskinesias were discussed.
Transcranial micropolarization was used in the treatment of children with hyperkinetic form of infantile cerebral paralysis. The method was found to be more effective than various stereotaxic interventions on the brain or routine physiotherapy. Transcranial micropolarization exposure resulted in alleviation of hyperkinesis, posture-tonic reflexes, in improvement of active movements of the joints, supporting system, etc. Clinical status of patients exposed to this treatment modality improved by six times as against those treated traditionally. Clinical data and data of stimulation electromyography permit us to suggest a possible effect of transcranial micropolarization on the function of cerebral subcortical structures in patients with hyperkinetic form of infantile cerebral paralysis.
Although hyperkinesis is expressed in several neurological disorders, the biological basis of this phenotype is unknown. The mouse mutant coloboma (Cml+) exhibits profound spontaneous locomotor hyperactivity resulting from a deletion mutation. This deletion encompasses several genes including Snap, which encodes SNAP-25, a nerve terminal protein involved in neurotransmitter release. Administration of amphetamine, a drug that acts presynaptically, markedly reduced the locomotor activity in coloboma mice but increased the activity of control mice implicating presynaptic function in the behavioral abnormality. In contrast, the psychostimulant methylphenidate increased locomotor activity in both coloboma and control mice. When a transgene encoding SNAP-25 was bred into the coloboma strain to complement the Snap deletion, the hyperactivity expressed by these mice was rescued, returning these corrected mice to normal levels of locomotor activity. These results demonstrate that the hyperactivity exhibited by these mice is the result of abnormalities in presynaptic function specifically attributable to deficits in SNAP-25 expression.
The author examined 90 children with ticose hyperkinesis. On the basis of a thorough study of the clinical picture, course of the disease and the use of laboratory methods all the patients were divided into 3 groups: with regressive, remittent and progradient development and characteristic clinical signs. For each group a corresponding treatment with a good effect was selected.
Reviewed research related to prevailing hypotheses with regard to the influence of genetic and biochemical factors in childhood hyperkinesis. Studies focused on establishing the influence of genetic factors are methodologically weak but consistently suggest that genetic transmission is a plausible, if incomplete, explanation in some cases. Studies that involve attempts to understand the underlying biochemical mechanisms of hyperactivity by studying the relationships among behavior patterns, psychophysiological measures, and variations in monamine levels have been disappointing.
Administration of dizocilpine (MK-801, noncompetitive antagonist of NMDA glutamate receptors) into the neostriatum decreased the reproducibility and duration of hyperkinesis in rats induced by repeated microinjections of GABA(A) receptor antagonist picrotoxin. By contrast, glutamate potentiated the hyperkinetic and convulsive effect of picrotoxin and promoted the inhibition of conditioned avoidance response. Our results indicate that the striatal glutamatergic system is involved in the development of locomotor and cognitive disorders associated with deficiency of the neostriatal GABAergic system and playing a role in the pathogenesis of Huntington's chorea.
Childhood hyperkinesis or attention-deficit hyperactivity disorder (ADHD) is a behavior disorder of which the main symptoms are attention problems and hyperactivity. The main objective of the present study was to investigate whether the spontaneously hypertensive rat (SHR) strain is a useful animal model of ADHD. Five different rat strains were tested: SHR, Wistar-Kyoto (WKY), Wistar, Sprague-Dawley (SPRD), and PVG (hooded) rats. The protocol consisted of three different test procedures: 1) A 7.5-min free-exploration open-field test (home cage accessible), where the SHR was less active than Wistar and SPRD but more active than WKY; SHR showed longer latencies to leave the home cage than both Wistar and SPRD rats, spending less time in the field, ambulating and rearing less than Wistar and SPRD but more than WKY. Within session, the SHR tended to be more active at the end of the session than at the start, while the opposite tended to be the case in the other groups. 2) A 7.5-min forced exploration open-field test (home cage not accessible), where the results showed that the SHR is less active than both the Wistar and Sprague-Dawley strains, but more active than PVG and WKY. 3) A two-component multiple schedule of reinforcement with a fixed interval 2 min signalled by houselight on and a 5-min extinction signalled by houselight off. Lever pressing by SHR was markedly different from that of the other four strains, which were quite Except early in the interval, SHR pressed the lever more than any of the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)
We assessed the contractility of the contralateral wall on 2-dimensional echocardiography in 50 patients with an initial ST-elevation acute myocardial infarction who underwent coronary angiography. Compensatory hyperkinesis, which we defined as a fractional thickening of >/=60% in the contralateral wall, was a strong predictor of single-vessel coronary artery disease, with a positive predictive value of 85%.