Provision of child and adolescent psychiatric services in the Federal Republic of Germany.
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Biomedical subjects
Publications and source records attributed to A Rothenberger.
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A total of 11 children with attention deficit disorder (ADD) and nine control children performed a continuous performance test (CPT) of the A-X type with concurrent neuroelectric brain mapping to assess preparatory processing, purportedly mediated by the frontal lobes. This cued CPT task proved to be a highly specific task. The groups could be clearly differentiated both at the behavioral and electrophysiological level. ADD children detected fewer signals and made more false alarms. There were no major group differences in topographical distribution of the event-related potential microstates, but ADD children displayed reduced global field power (GFP) in an early CNV/P3 microstate to cues. This indicated that impaired orienting to cues, rather than impaired executive target processing, determines the initial processing stages in ADD. In comparison with data from the same task run in Utrecht, the same orienting deficit in clinically diagnosed ADHD children was demonstrated. Low resolution electromagnetic tomography (LORETA) estimated posterior sources underlying these orienting processes and the orienting deficit. This argued against frontal lobe involvement at this stage and suggested involvement of a posterior attention system.
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OBJECTIVE: For the first time in the German-speaking countries a complete evaluation of all 1236 inpatient treatment episodes within one year of investigation was carried out. METHOD: Case-related patient documentation at all of the 13 clinics for child and adolescent psychiatry in Lower Saxony and Bremen were evaluated. RESULTS: Data from all clinics agreed widely on the following: 1. the divergent family structures of the young patients compared to those of the general public, 2. a high degree of individual psychotherapy, and 3. the inclusion of the patient's social circumstances in the individual psychotherapy. Nonetheless, results for most of the variables assessed differed strongly. Inpatient child and adolescent psychiatric care thus seems to vary highly among clinics within the same epidemiological area. CONCLUSIONS: Hence, even when the reported number of episodes is high, no general conclusions on inpatient child and juvenile psychiatric treatment can be drawn on the basis of admissions data for individual clinics. Interinstitutional comparisons must be made on the assumption that there is no prototype clinic for child and adolescent psychiatry. Additional general conclusions include the lack of a disorder-specific approach to treatment. The entry of a large number of patients into foster or state homes following inpatient treatment reflects the impact upon them of abnormal psychosocial circumstances, as well as their decreased psychosocial adaption.
Visually-guided saccades of 21 offspring of schizophrenic parents and 21 individually matched controls were compared with regard to the frequency of occurrence of saccadic hypometria and hypermetria, non-fixations, and omissions of target jumps. Target steps ranged from 10 to 60 degrees, and interstimulus intervals averaged 2.5 s; subjects were promised financial reward depending on performance. Recordings were carried out at the subjects' homes. To screen for cognitive abilities and psychopathological behavior, subjects were tested by means of an intelligence scale and a behavioral checklist. With large target steps (40-60 degrees), the high-risk group made significantly more grossly hypometric saccades (gain < or = 0.8) than the control group; responses to small target steps (10-30 degrees) exhibited a similar, albeit statistically not significant, trend. There were no significant differences with regard to the occurrence of hypermetria. Non-fixations scored marginally higher in the high-risks as compared to controls, but this was again not a significant difference. The incidence of omissions of saccades was very low in both groups. The results of the study suggest that subjects at genetic risk for schizophrenia may differ from controls by an increased incidence of conspicuously hypometric saccades. Clearly, this difference is not caused by a deficit of the saccadic motor circuitry proper; comparison to control data obtained with a similar experimental protocol suggests that it probably reflects an impaired internal control of saccades in the presence of distraction and stress. The relevance of saccades as indicators of a possible schizophrenic vulnerability is discussed.
Comorbidity of tic disorder (TD) and attention-deficit hyperactivity disorder (ADHD) in children is common but not fully understood. Thus we investigated the effect of TD and ADHD on the amplitude of the postimperative negative variation (PINV) in children with combined tic + hyperactivity symptoms (TD + HA). PINV was chosen as an indicator of frontal lobe functioning that is closely related to self-regulation of behavior. PINVs of four groups of children (healthy controls, pure TD, pure ADHD, and combined TD + HA; total number 43) were elicited in an auditory warned reaction task in three conditions (control = CC, loss-of-control = LoCC, and lack-of-control = LaCC) at midfrontal (Fz) and midcentral (Cz) leads of the scalp. Effects of TD and ADHD were revealed only in the noncontrol conditions, being independent in the LaCC, but interactive in the LoCC. Thus, the additive model of psychopathological classification concerning the comorbidity of TD and ADHD was only partially supported by the observed pattern of psychophysiological results.
OBJECTIVE: Fluctuating motor and vocal tics are the diagnostic feature of Tourette's disorder. The pathophysiology of tics is still unclear. One major hypothesis is a deficient inhibitory control through the cortical-striatal-thalamic-cortical motor loop. The authors tested this hypothesis by investigating motor cortex excitability through use of the technique of transcranial magnetic stimulation. METHOD: Twenty patients with Tourette's disorder and a comparison group of 21 healthy subjects were studied. Focal transcranial magnetic stimulation was applied to the left motor cortex, and surface electromyography (EMG) was recorded from the right abductor digiti minimi muscle. As measures of motor cortex excitability, motor threshold, cortical silent period, and intracortical inhibition and facilitation were studied. The peripheral silent period and the maximum M wave after supramaximal electrical stimulation of the ulnar nerve at the wrist were also determined. RESULTS: Motor threshold and peripheral motor excitability were normal in the Tourette's disorder group, but the cortical silent period was shortened and the intracortical inhibition reduced. A subgroup analysis of the patients with Tourette's disorder revealed that these abnormalities were seen mainly when tics were present in the EMG target muscle or in patients without neuroleptic treatment. Age, sex, attention deficit hyperactivity disorder, obsessive-compulsive disorder, and sensory urges had no significant effect on motor excitability. CONCLUSIONS: Findings are consistent with the hypothesis that tics in Tourette's disorder originate either from a primarily subcortical disorder affecting the motor cortex through disinhibited afferent signals or from impaired inhibition directly at the level of the motor cortex or both.
This review summarizes some important principles of human brain development. Special emphasis is placed on the role of psychosocial stress during childhood on the developing brain. Depending on the degree of cognitive, behavioral and socio-emotional maturation, previous experiences and actual context, psychosocial stressors may be perceived by children as being either controllable (challenge) or uncontrollable (disaster). Controllable stress experiences are associated with a preferential activation of the central and peripheral noradrenergic system, i.e., of a system endowed with the gating of cortical information processing and the facilitation and stabilization of neuronal pathways and synaptic connections involved in behavioral responding. Uncontrollable stress responses are elicited if all previously acquired behavioral or cognitive strategies are inadequate or fail to overcome the stressor. The resulting severe and long-lasting activation of the central stress responsive systems will finally lead to a full activation of the HPA system, accompanied by adrenocortical cortisol release. The major central effect of this response is the destabilization of previously established neuronal circuits and synaptic connections. Thus, severe uncontrollable psychosocial stress may act as an important trigger of and a prerequisite for the reorganization of neuronal connectivity. It may, above a certain threshold, threaten the mental and affective stability, integrity, and the future development of a child. The long-term consequences of psychosocial stress on the structural and functional maturation of the brain are documented by findings from animal research and by results in the field of developmental psychopathology in children. The role of risk and protective factors during different phases of child development is briefly summarized and the need for a biopsychosocial model concerning the relationship between human brain development and behavior is emphasized.
Reasons for the need for a coordinated multi-centered documentation for quality safeguarding are given. Based upon experiences with patient documentation, where 13 child and youth psychiatries in the German states Lower Saxony and Bremen participated for one year, problems with a documentation system are shown and discussed. In conclusion recommendations are given for carrying out such studies, which will become more important in the framework of quality safeguarding in child and youth psychiatries.
Reported here is the therapeutic efficacy of Tiapride with 10 10- to 17-yr.-old patients afflicted with severe stuttering problems. During the 20-wk. open, controlled study (baseline, low dose of Tiapride, high dose of Tiapride, follow-up observation without medication) the stuttering in various speech situations decreased markedly. No substantial change in different parameters of acoustic analysis and psychopathological characteristics accompanied the reduction in stuttering when group data were compared although positive effects concerning these variables could be seen in some cases. Several conclusions based on these results are presented. One assumed effect of the medication is improvement of central nervous regulatory mechanisms of speech motor coordination. Further, the value of the medication Tiapride in comprehensive stuttering therapy is discussed.
Contrary to the current assumption that there are no specific correlates of dyslexia in the standard clinical EEG, we have often noted a spontaneous "intermittent left parietal alpha desynchronization" (ILPAD) when visually evaluating the standard EEGs of children with delayed speech and language development and/or dyslexia. Visual evaluations of EEGs, as well as computer-assisted frequency analysis of three pairs of matched groups (healthy and hyperkinetic children with vs. without relatively "low levels" of verbal performance, as well as children with other child psychiatric disorders with vs. without dyslexia), revealed that healthy children did not display the ILPAD phenomenon. It was seen neither in healthy children with a homogeneous performance profile ("high level" of verbal performance) nor in those with a relatively "low level" of verbal performance. However, the ILPAD phenomenon was evident mainly in children with psychiatric disorders who suffered from dyslexia. Its intermittent occurrence prevented its detection by means of the usual computer-supported analyses of EEG power spectra. Nevertheless, auditory cognitive loading was accompanied by a decrease in alpha power in both healthy and hyperkinetic children with "high" or "low" levels of verbal performance. In a further group of 8-year-old children with dyslexia, but otherwise healthy, the ILPAD phenomenon was also observed if their CNS maturation as reflected in the EEG was normal for their age. These results seemed to indicate at least a deficit-specificity of the ILPAD phenomenon, which is interpreted as an electrophysiological correlate of a "brain-electrical developmental deviation" with regard to the "functions of communication": speech, language, reading and spelling.
The paper is part of a special section on 'psychopharmacotherapy in children'. Drugs not only help to treat symptoms successfully but may also help researchers and clinicians to gain a better understanding of the pathophysiology underlying these disturbances. This is exemplified in three child psychiatric disorders that exhibit disturbances in motor activity as a prominent symptom. These are general motor restlessness (ADHD), tic-disorder (sudden circumscribed motor actions) and stuttering (non-fluent speech). There is evidence that clinically useful drugs increase the cortical-subcortical interaction and tuning mechanisms providing the patients with a better self-regulation related to the motor performance.
This article is part of a special section on 'self-injurious behaviour and autism' and is mainly based on a book edited by Luiselli, Matson and Singh (1992) addressing empirical data on self-injurious behaviour and mental retardation from a behavioural perspective. Within the overview of the book some information on autism is also presented and critically discussed. Self-injurious behaviour is a poorly understood phenomenon and problematic in many ways; its definition is not easy; little is known about the causes and neuroscientific models. Demographic data are scarce and functional analysis and interventions (behavioural techniques, medication, education) need to be further developed, under the protection of human rights committees.
This paper is part of a special section on 'self-injurious behavior and autism' and reports new data that variously support the suggested involvement of dopaminergic, serotoninergic and opiatergic neurotransmitter systems in the expression of self-injurious behaviour. Further, some notions concerning the underlying biological mechanisms of self-injurious behaviour related to brain function and brain topography are described. Finally, besides the critical evaluation of several drugs used to treat self-injurious behaviour, four cases of autism are reported where sulpiride, a benzamide derivative, clearly reduced self-injurious behaviour.
Total mutism, which is an extremely rare psychiatric disorder, was observed in an 11-year-old boy. He refused to speak a few weeks after starting school. Behavioural analysis showed that learning by model as well as positive and negative reinforcements were involved in the pathogenesis and maintenance of the disorder. The treatment followed principles of behaviour therapy by the use of operant techniques in the sense of contingency management methods. White noise, transmitted by earphones, was utilized to interrupt auditory feedback. It has been suggested that by this method anxiety would be diminished in the case of speech phobia. Within a few months of hospital admission the boy developed speaking behaviour progressing from barely audible breaths to sibilants of normal loudness. Short dialogues were possible after 18 months. The additional conduct disorder improved simultaneously with the increase in verbal and social skills. One year after hospitalization some social uncertainty persisted with tendencies to avoid demands.
Transient increases of the early cortical somatosensory evoked potentials (SSEP) were observed in 9 patients who received antidepressant and/or neuroleptic treatment. All patients developed myoclonus, and 2 had grand mal seizures. Three cases--one 20-, one 17- and one 15-year-old patient--are presented in detail. Similar observations have been reported in elderly patients. Possible underlying mechanisms and the potential value of the SSEP in identifying and monitoring patients at risk of developing psychotropic drug-induced side-effects are briefly discussed.
To date, in publications on hamartomas, precocious puberty and laughing seizures have been discussed, but behavioural and cognitive abnormalities have been neglected. Therefore, we report a 14-year-old girl with a proven hamartoma, in which abnormalities of behaviour and cognition played an important role within the somatopsychic complex. In our patient, urinary incontinence during the seizures and psychiatric symptoms, such as eating disorder with obesity, school phobia, antisocial behaviour, withdrawal and cognitive problems (e.g. general slowness, deficiency of cognitive flexibility) came to the fore. The girl had not attended school regularly for almost 2 years, had stayed at home and was overtaxed psychosocially. The seizures and the urinary incontinence improved with drug treatment, but psychiatric difficulties increased and remained untreated until the girl came to a child psychiatric inpatient clinic where drug treatment and behavioural therapy were combined. During well-coordinated neurological and psychiatric treatment the laughing seizures (spontaneous, event-related, psychogenic) decreased and a considerable improvement in psychiatric and psychosocial problems was attained. Consequently, we recommend a close and timely integration of the psychiatric aspects in the treatment of children with hamartomas.
We investigated 39 adolescent anorectic inpatients (27 cross-sectionally. 12 longitudinally) and, as controls, 12 emotionally disturbed inpatients with auditory evoked potentials (AEP) of subcortical and cortical origin. Different intensities of the stimuli were applied in an augmenting/reducing paradigm to test the ability to modulate auditory inputs. In addition, cranial CT was performed in each anorectic patient as well as in another group of 12 child psychiatric controls. Three main results were found: (1) anorectics may have difficulty in modulating auditory stimuli adequately at the subcortical level, even after gaining weight. At the cortical level, their modulation did not differ significantly from controls. (2) a systematic dissociation of the AEP amplitude response between subcortical and cortical CNS levels was seen mainly in anorectics when they had low body weight. This may suggest an uncoupling of cortical versus subcortical neuronal systems. After weight gain, anorectics had less subcortical/cortical dissociation of AEP, which was never seen in controls. Thus, to reach regular modulation of sensory information anorectics should gain normal weight and eating behavior in good time. (3) CT results showed no significant correlation with AEP findings. So far, the functional role of pseudoatrophy in anorectics remains unknown.