Alpha-chemokine receptors CXCR1–3 and their ligands in idiopathic inflammatory myopathies

The idiopathic inflammatory myopathies (IIM) are a heterogeneous group of neuromuscular disorders subdivided into polymyositis (PM), sporadic inclusion body myositis (sIBM) and dermatomyositis (DM). Chemokines play an essential role in sustained inflammation associated with IIM. We studied the distribution of the -chemokine receptors CXCR1, 2, 3 and their ligands interferon- (IFN-)-inducible T cell chemoattractant (I-TAC), IFN--inducible protein of 10 kDa (IP-10), monokine induced by IFN- (MIG) and growth-related oncogene (GRO) in IIM using immunohistochemistry, immunofluorescence and Western blotting. Abundant expression of IP-10 was observed on macrophages and T cells surrounding and invading non-necrotic muscle fibers in PM and sIBM and in T cells in perimysial infiltrates of DM. IP-10 was also localized to blood vessel endothelial cells in all inflammatory and normal muscle tissues. The distribution of other -chemokines was variable: Only low levels of MIG and I-TAC were detected; GRO was localized to the endomysial infiltrates of some PM and sIBM samples, but not in DM. Muscle tissues were invariably CXCR1 negative, while a subset of inflammatory cells in all IIM were CXCR2 positive. Strong CXCR3 expression was observed on the majority of T cells in each IIM. We describe the differential repertoire of -chemokines in IIM, and offer additional proof of the predominance of Th1-driven reactions in the immunopathogenesis of all three diagnostic subgroups. We suggest the Th1-mediated immunity in general, and the CXCR3/IP-10 interaction in particular, as potential targets for novel therapeutic intervention in IIM.     

Psychometric properties of the parental bonding instrument in a spanish sample

Summary The Parental Bonding Instrument was translated into Spanish and administered to a sample of 205 Spanish primiparae 3 days after childbirth. Reliability, factorial structure and predictive validity for affective disorders were evaluated. The Spanish version of the PBI has psychometric features similar to those described in other cultures. However, the results suggest that in future research the predictive power of the Control factor in affective disorders might be improved by splitting it into two subfactors: Overprotection and Restraint.     

The clinical,genetic and dystrophin characteristics of Becker muscular dystrophy

We have correlated a detailed clinical assessment of 67 patients with proven Becker muscular dystrophy with the results from genetic and protein analyses. There was an overall deletion frequency of 80%, rising to 92.6% in the large group of patients defined on clinical grounds as being of typically mild severity. The deletions in this group were all clustered in the region of the gene between exons 45 and 59; the most common deletion was of exons 45–47 and all but one started at exon 45. No similar deletions were seen in the patients with more severe disease, in whom the diverse genetic defects included a duplication and a very large deletion. Dystrophin patterns in the typical group were also very characteristic, and in both groups were as predicted from the genetic defect, the size of deletions being inversely proportional to the size of the protein produced.     

“Sporadic” prealbumin-related amyloid polyneuropathy: report of two cases

Summary Two sporadic cases of amyloid polyneuropathy are reported. There was no family history or plasma cell dyscrasia. Both showed sensorimotor and autonomic polyneuropathy with onset in the seventh decade. Amyloid deposits in both cases reacted with anti-human prealbumin sera but not with antisera to human AA and anti-human immunoglobulin light-chain amyloids, including A and A. One patient had the abnormal serum prealbumin and abnormal DNA sequence found in type I familial amyloid polyneuropathy (FAP) (Japanese type). Investigations in sporadic amyloid polyneuropathy should include immunohistochemistry, using antisera to the different amyloid proteins, and the radioimmunoassay and recombinant DNA techniques for diagnosis of FAP.     

Cytoplasmic and axoplasmic density variations in relation to hyperactivity

Summary The density of the cytoplasm and axoplasm of the anterior horn cell in rats was determined by X-ray microradiography. The average density of the cytoplasm of more than 400 cells from control rats was 0.31 g/³, while that of over 600 cells from rats fed IDPN (- iminodipropionitrile) was 0.43 g/³.Hyperactivity developed during the first 5 weeks and was associated with a gradual increase in cytoplasmic density to 0.51 g/³.At 6 weeks there was a drop in density to 0.36 g/³ which coincided with the appearance of axonal balloons having a density of 0.17 g/³.During the 7–12th week on the diet, the cytoplasmic density showed a gradual increase to 0.59 g/³ and the balloons to 0.29 g/³.The volume of the nerve cells remained fairly constant. The density increases were discussed in relation to hypertrophy, dystrophy, and hyperactivity.

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Zusammenfassung Die Dichte des Cytoplasmas und Axoplasmas der Vorderhornzellen von Ratten wurde durch Röntgenmikroradiographie bestimmt. Die mittlere Dichte des Cytoplasmas von mehr als 400 Zellen der Kontrollratten war 0,31 g/³, während die mittlere Dichte von mehr als 600 Zellen der Ratten, die mit IDPN (- iminodipropionitrile) gefüttert waren, 0,43 g/³ war.Hyperaktivität entwickelte sich während der ersten 5 Wochen und war mit einer progressiven Zunahme der Cytoplasmadichte bis auf 0,51 g/³ verbunden.Nach 6 Wochen sank die Dichte auf 0,36 g/³. Diese Tatsache traf mit dem Auftreten der Axonauftreibungen zusammen, die eine Dichte von 0,17 g/³ hatten.Nach 7–12 Wochen zeigte die Cytoplasmadichte eine progressive Zunahme auf 0,59 g/³ und die der Auftreibungen eine Zunahme auf 0,29 g/³.Das Volumen der Nervenzellen blieb ziemlich konstant.Die möglichen Zusammenhänge zwischen Zunahme der Dichte, Hypertrophie, Dystrophie und Hyperaktivität werden dargestellt.

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Supported by U. S. Public Health Grant NB 1305.     

Neuroectodermal tumors of the peripheral and the central nervous system share neuroendocrine N-CAM-related antigens with small cell lung carcinomas

Summary The current study describes the presence of neuroendocrine antigens of peripheral and central neural tumors using eight monoclonal antibodies raised to small cell lung carcinoma (SCLC), which recognize neural/neuroendocrine or neural antigens, as defined by their reaction pattern in normal tissues and tumors. At least five of them recognize different epitopes of the neural cell adhesion molecule (N-CAM). It was found that all of 12 neuroblastomas, 2 ganglioneuroblastomas and 4 ganglioneuromas as well as 23 central primitive neuroectodermal tumors, 13 astrocytomas and 4 ependymomas share neural/neuroendocrine antigens (as defined by the anti-N-CAM antibodies Moc-1,-21,-32,-52 and-191) with SCLC. The neural/neuroendocrine antigen defined by Moc-171 was also found in all peripheral tumors, but only in further differentiated central tumors. Non-N-CAM related neural antigens (as defined by Moc-51 and-172) were found only in better-differentiated peripheral and central tumors, but they could be demonstrated in all three medulloblastoma cell lines studied. In addition, the antigen defined by Moc-51 was demonstrated in an immunoblot of a neuroblastoma cell line. Antibodies recognizing epithelia antigens of SCLC and other epithelia and their tumors (Moc-31 and-181) were non-reactive. It was concluded that these findings give further support for a relation between neural and neuroendocrine tumors and that some of the antibodies may be useful for the detection of differentiation in neural tumors. Antibodies with an epithelia recognition pattern may serve to distinguish neural from neuroendocrine tumors.Supported by NIH grant CA 36245 W.M.M. was a Fullbright scholar     

Selective localization of gelatinase A,an enzyme degrading β-amyloid protein,in white matter microglia and in Schwann cells

Gelatinase A is an enzyme capable of cleaving soluble -amyloid protein (AP), and may function as an -secretase to produce secretory forms of amyloid precursor protein. We examined gelatinase A immunoreactivity in the brains and posterior roots of neurologically normal, lacunar stroke, Alzheimer disease (AD), amyotrophic lateral sclerosis, progressive supranuclear palsy and myasthenia gravis cases. The gelatinase A antibody stained only microglial cells in the white matter in all the brain tissues. In AD brain, the reactive microglia located in the center of classical senile plaques, as well as in other microglial cells in the gray matter, showed no immunoreactivity. Gelatinase A in white matter microglial cells may play a role in preventing local deposition of AP. In the posterior root, Schwann cells had positive immunoreactivity. As with other metalloproteases, gelatinase A in Schwann cells may play an antiproliferative role.     

Electron microscope studies of Schwann cells during the Wallerian degeneration with special reference to the cytoplasmic filaments

Summary The fine structure of Schwann cells of the sciatic nerve of adult rabbits during the several phases of Wallerian degeneration was studied. For electron microscopy buffered osmium tetroxide, Vestopal W and the lead and uranyl staining was used As a result of the axon degeneration, the Schwann cells are activated and the myelin sheaths break down. During the phase of intraplasmatic digestion of the myelin, the ribosomes increase considerably and the ER swells. Afterwards a conspicuous granular thickening of the ground plasm is to be noted (stage of dark cells). The granular ground plasm forms into filaments, which stand out clearly before the light background as tender strings about 60–80 Å in thickness (stage of light cells). During this stage, the ribosomes have disappeared almost completely and the ER has collapsed. The Schwann cell has entered into its stage of rest which is characterized by a high amount of plasmatic filaments. Schwann cell filaments differ from so-called neurofilaments in respect of their genesis and their ultrastructure. In conclusion, the differences in genesis and morphology between the two filamentous structures are discussed.

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Zusammenfassung Elektronenoptisch wurden die verschiedenen Phasen untersucht, die Schwannsche Zellen während der Wallerschen Degeneration durchlaufen. Als Untersuchungsmaterial dienten der N. ischiadicus des erwachsenen Kaninchens. Für die Elektronenmikroskopie wurden Osmium-tetroxyd, Vestopal W sowie die Bleiund Uranylkontrastierung verwendet.Als Folge der Axondegeneration werden die Schwannschen Zellen aktiviert und die Markscheiden fragmentiert. In der Phase des intraplasmatischen Myelinabbaus findet eine hochgradige Vermehrung der Ribosomen und eine Schwellung des endoplasmatischen Reticulums statt. Danach tritt eine starke granuläre Verdichtung des Grundplasmas in Erscheinung (Phase der dunklen Zellen). Aus dem granulären Grundplasma formieren sich anschließend die Filamente, die sich vor dem hellen Untergrund als zarte, etwa 60–80 Å dicke Fäden abzeichnen (Stadium der hellen Zellen). In diesem Stadium sind die Ribosomen bis auf kleine Reste verschwunden, und das ER ist abgeschwollen. Die Schwannsche Zelle hat ihr Ruhestadium eingenommen, das durch eine starke Anhäufung der Plasmafilamente charakterisiert ist. Die Schwannschen Zellfilamente unterscheiden sich von sogenannten Neurofilamenten in bezug auf die Genese und die Feinstruktur. Abschließend werden die Unterscheidungsmerkmale in der Genese und der Morphologie beider filamentärer Strukturen diskutiert.

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Supported by the Deutsche Forschungsgemeinschaft.     

Mind-Body Innovations—An Integrative Care Approach

Integration of behavioral health and medicine has gained increased support recently within the new field of complementary medicine. Providers from both disciplines are acknowledging the mind-body connection and recognizing the value of treating the whole patient through working within an integrative delivery model. This paper describes two treatment programs which were developed using the principles of the mind-body connection and implemented within an integrative setting at a large HMO. The results of research studies are presented and discussed to demonstrate the efficacy of these programs.     

Einfluß der Tiefe der Barbiturat-Narkose und der sensorischen Stimulation auf die „Schlaf-Aktivierung“ des Epilepsie-EEG

Zusammenfassung 110 Kranke mit generalisieter oder fokaler Epilepsie zeigten mit zunehmender Tiefe der zur maximalen Aktivierung geeigneten Evipannarkose verschiedene EEG-Typen. Dies spricht dafür, daß die Bahnung der elektrischen epileptiformen Tätigkeit nicht durch einen in jedem Fall identischen Mechanismus entsteht, sondern von zahlreichen Faktoren abhängt.Solche epilepsiebahnenden Faktoren sind: a) die Quantität der im Wachzustand spontan, interiktal auftretenden Krampfpotentiale; b) die optimale Tiefe der Narkose; c) der klinische und elektrische Typus der Entladung; d) die Lokalisation der Entladung, d. h. die normalen anatomisch-funktionellen Eigenschaften der epileptischen Neuron-Population mit ihren Beziehungen zu den Weckstrukturen; e) die Barbiturat-Empfindlichkeit dieses Neuron-Aggregates; f) die primäre Dominanz oder der sekundäre Spiegel-Charakter des Focus; g) die aktuelle Synchronisierungstendenz des elektrischen Hintergrundes; h) der Einfluß äußerer und innerer sensorischer Stimuli; i) spezifische bahnende und hemmende Mechanismen (recruitment, rebound, Habituation, paradoxe Schlafphase).Mit Bezug auf experimentelle Erfahrungen läßt sich der Schluß ziehen, daß die Schlafaktivierung ein Enthemmungsphänomen ist. Die Manifestierung der verschiedenen aufgezählten Faktoren und Mechanismen ist abhängig vom funktionellen Zustand gewisser diffuser und regionaler (lokaler), unspezifischer (retikulärer) Systeme und Subsysteme. Die Barbiturat-Empfindlichkeit dieser Strukturen ist wahrscheinlich verschieden, so daß die zwischen ihnen bestehenden, aber im Wachzustand verdeckten Hemmwirkungen mit zunehmender Narkose sukzessiv behoben werden. Ergebnis dieser Enthemmungen ist die Aktivierung.     

Single drug therapy for intractable epilepsy

Summary Single drug therapy with either phenytoin or primidone resulted in complete seizure control in 11 of 35 patients (31%) referred to an epilepsy clinic for treatment of uncontrolled chronic epilepsy with complex-partial seizures. Complete seizure control was associated with an increase in the mean plasma concentrations from 14 g/ml to 23 g/ml phenytoin and from 34 g/ml to 40 g/ml phenobarbitone with no change in the antiepileptic drug. Insufficiently low plasma concentrations of less than 11 g/ml phenytoin or phenobarbitone were measured at the first visit in 14 patients (40%). Non-compliance was admitted by eight patients (23%). Optimum single drug therapy is of considerable clinical value in intractable epilepsy with complex-partial seizures.

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Zusammenfassung Eine Monotherapie mit Phenytoin oder Primidon führte zur Anfallsfreiheit bei 11 von 35 Patienten (31%), die wegen schwerbehandelbarer psychomotorischer Anfälle eine Epilepsieambulanz aufsuchten. Anfallsfreiheit trat auf bei einem Anstieg der mittleren Plasmakonzentration von 14 g/ml auf 23 g/ml Phenytoin und von 34 g/ml auf 40 g/ml Phenobarbital. Ein Wechsel der Medikamente war nicht notwendig. Während der ersten Untersuchung wurden bei 14 Patienten (40%) zu niedrige Plasmakonzentrationen von weniger als 11 g/ml Phenytoin oder Phenobarbital gefunden. 8 Patienten (23%) gaben eine unregelmäßige Einnahme der Medikamente (non-compliance) zu. Eine konsequente Monotherapie ist von klinischem Wert für die Behandlung von schwerbehandelbaren Epilepsien mit psychomotorischen Anfällen.

     

Types of authority and two problems of psychiatric wards

This paper concerns the relationship between authority structures and two problems reported in the literature as common to milieu or therapeutic community wards. Psychiatric wards with rational-legal and charismatic authority structures are found more likely to experience mood and morale swings on the part of patients and staff and to spend excessive time and energy changing ward rules.     

Quantitative analysis of “synaptic” ribbon profiles in the pineal complex of male and female Pirbright-White guinea pigs

Summary Previous studies have pointed in the direction of sex differences as well as regional differences in the pineal gland of guinea pigs. In the present investigation these aspects were studied at the electron-microscopic level by quantitating different types of synaptic bodies, intrinsic to pinealocytes. The two major types of synaptic organelles, ribbons and spherules, did not exhibit regional or sex differences. Synaptic structures intermediate in appearance to ribbons and spherules were significantly larger in number in males in the distal region of the pineal gland, compared to females. As previous studies have shown that ribbon and spherule numbers undergo characteristic changes depending on the functional state of the pineal gland, it is concluded that, as far as the synaptic organelles are concerned, no clear-cut sex or regional differences appear to exist in the guinea pig pineal gland.     

Über eine spezifische Haltungsschablone beim postencephalitischen Parkinsonismus

Zusammenfassung Es wurde an Hand eigenartiger und teilweise schon bekannter Haltungsanomalien beim postencephalitischen Parkonsonismus der Versuch unternommen, diese Phänomene im Sinne der Schablonenlehre zu interpretieren. Sie wurde als Schwimmschablone bezeichnet und als spezifische Haltungsschablone beim Parkinsonismus als phänomenologischer Ausdruck einer speziellen Desintegration gedeutet.     

Use of plasma levels for antiepileptic drug monitoring in clinical practice

A multi-center survey of antepileptic treatment was conducted in Italy on 245 previously untreated (new) patients with epilepsy and 355 patients treated for more than three months (old patients). Therapeutic drug monitoring (TDM) of antiepileptic drugs was evaluated in the context of routine clinical conditions, in relation to individual therapeutic problems and mode of treatment. Plasma levels (PL) were determined in 75% of new patients and 78% of old patients, with wide intercenter variability. TDM was done at 69% of the follow-up attendences for new patients and at 34% for old patients, but was apparently unrelated to specific therapeutic problems, such as poor disease control or adverse drug reactions. Plasma drug concentration measurements were made more often among patients on polytherapy. The age of the patient and the time elapsing since diagnosis did not seem to affect request patterns significantly. From these findings it appears that TDM is largerly influenced by factors unrelated to the common recommendations in the literature. In addition, the use of TDM in clinical practice reflects the limitations of the available techniques.

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Sommario In uno studio multicentrico condotto su 245 casi di epilessia di nuova diagnosi (trattati da meno di 3 mesi) e su 355 casi di epilessia di vecchia diagnosi (trattati da almeno 3 mesi)l'uso dei livelli plasmatici dei farmaci anticonvulsivanti è stato valutato in relazione alle modalità di trattamento e a problemi specifici indicati dai clinici. La percentuale di richieste di livelli plasmatici era del 75% e riguardava il 69% delle visite di follow-up nei pazienti di nuova diagnosi. Le percentuali erano rispettivamente del 78% e del 34% per i pazienti di vecchia diagnosi. In entrambi i casi vi era una marcata variabilità tra centri nelle percentuali di prescrizioni. Le richieste di livelli plasmatici erano più numerose nei pazienti in politerapia. Per contro, il monitoraggio dei farmaci antiepilettici non risultava influenzato dalla presenza di specifici problemi, quali il non completo controllo della crisi o la presenza di segni di tossicità farmacologica, né dall'età del paziente o dal tempo intercorso dalla formulazione della diagnosi. Da tutto ciò deriva che l'utilizzo dei livelli plasmatici dei farmaci antiepilettici nella pratica clinica è influenzato da fattori che spesso non riflettono le norme di comportamento comunemente suggerite dalla letteratura. Risultano inoltre ampiamente confermati i limiti delle metodiche attualmente in uso.

     

Apolipoprotein E co-localizes with newly formed amyloid β-protein (Aβ) deposits lacking immunoreactivity against N-terminal epitopes of Aβ in a genotype-dependent manner

Different types of amyloid -protein (A)-containing plaques occur in brains of Alzheimers disease (AD) patients. Diffuse plaques seen during early stages of AD differ from neuritic plaques in later stages both with respect to the length of the A peptides and the presence of other proteins, e.g., apolipoprotein-E (apoE). Since apoE is involved in A transport and clearance, and the 4-allele of the apolipoprotein-E gene (APOE) is a major risk factor for sporadic AD, it is plausible to speculate that apoE plays a pathophysiological role in the initiation of A deposition. To address the issue of whether binding of apoE to A is involved in initial A deposition, we studied the human medial temporal lobe of 60 autopsy cases encompassing the full spectrum of AD-related pathology. In temporal lobe regions, which become involved for the first time at a given stage of -amyloidosis, all plaques represent newly formed plaques, and these were studied with immunohistochemical methods. ApoE was present in 36 cases, and was frequently co-localized with newly formed A deposits detectable with anti-A₄₂ but not with antibodies raised against N-terminal epitopes of A. In 10 additional cases, immunoreactivity against apoE was completely lacking in newly formed plaques, which, at the same time, displayed immunoreactivity against N-terminal epitopes of A. The failure of N-terminal epitopes of A to co-localize with apoE in newly formed plaques indicates that these deposits presumably contain apoE-A complexes, in which the N-terminal epitopes of A are often concealed after complexing with apoE, thus preventing subsequent binding of antibodies. Moreover, apoE-positive newly formed plaques were seen more frequently in APOE 4/4 cases than in non-APOE 4/4 individuals, thereby underlining the potentially crucial role of apoE for the development of A deposits.     

Hyperkinetic children: Early indicators of potential school failure

Hyperkinetic children are identified as a population-at risk upon admission to kindergarten. The etiology of hyperkinetic behavior is controversial. Organic driveness, hyperkinetic behavior disorder, postencephalitic behavior, brain damage with behavioral and conceptual deficit, Strauss syndrome, have all been used to label essentially similar symptom constellations. Bypassing the area of controversy, a study is reported that demonstrates that children who were identified as hyperkinetic (using behavioral criteria developed in an earlier study) were (1) absent from school more frequently, and (2) did remarkably less well on standardized tests of school readiness than their peers rated nonhyperkinetic. The implications are discussed and suggestions made for the development of intervention programs.An earlier version of this paper was presented at the Annual Meeting of the American Orthopsychiatric Association, March, 1967.     

Assessing the potential of change in institutions

The present article discusses the importance of evaluating the strengths and weaknesses of key institutional personnel prior to attempting program innovations. The importance of such individuals in making or breaking effective programs is emphasized, and various key hospital staff members are described. A simple evaluation process is discussed with the purpose of better anticipating problem areas in program development. It was concluded that in some cases, project implementations should not be attempted when assessed personnel problems appear capable of seriously limiting the effectiveness of a program.     

Chronic mental hospital dependency as a character defense

Summary Prolonged hospitalization may cause atrophy of the patient's self-confidence, through excessive dependent gratifications of an oral-receptive nature. Hospital dependency results, and the possibility of discharge arouses such anxiety that the patient exhibits increased psychotic behavior with the effect of maintaining the hospital adjustment. Certain persons are excessively predisposed by previous experience to develop this dependency. The basic predisposition, however, is rooted in the normal course of childhood development.Hospitalization results in three major gains for the mentally disturbed patient: (1) primary relief from anxiety caused by instinctual impulses overwhelming the ego defenses; (2) secondary gains resulting from the socially-recognized sick role; and (3) the satisfactions of becoming an accepted member of a stable social system. If a mental patient is hospitalized, the danger of chronic dependency must be recognized and guarded against. Limited hospitalization is an important therapeutic modality, but as with other therapies, excess may cause secondary complications.Therapy of the chronic patient seeks first to convert dependence on the hospital as an ego-fortifying agent into a general confidence that help will be available if needed. Subsequently, the therapy aims to work through the secondary gains of illness byh viewing psychotic behavior as resistance to giving up the hospital. For the purpose of therapy, the chronic patient is viewed as environmentally-oriented, his behavior as based in present reality; and his active co-operation as essential to any change.The author, now program chief, mental health section, County Department of Public Health and Welfare, San Mateo, Calif., takes full responsibility for the contents of this paper, but wishes to acknowledge his intellectual debt to the staff of the Winter Veterans Administration Hospital, Topeka, Kansas.     

Untersuchungen zum Aktivierungs- und Habituationsverhalten hirntraumatisch geschädigter Kinder und Jugendlicher unterschiedlichen Schweregrades

Zusammenfassung Das Ziel dieser Studie bestand in der Analyse des Aktivierungs- und Habituationsverhaltens hirntraumatisch geschädigter Jugendlicher in Abhängigkeit vom Schweregrad der Schädigung. Untersuchungsgruppen waren die i.S. einer Decerebration schwer hirngeschädigten Patienten mit Zustand nach apallischem Syndrom (N=9) sowie als Kontrollgruppe ein klinisches Klientel von N=10 Patienten mit Zustand nach leichter Hirnkontusion.Der Versuchreiz einer komplexen Reizdarbietung (optische und akustische Stimulation mit Reaktionserfordernis) bestand in einer täglich 4minütigen Dauerbelastungsphase am Wiener Determinationsgerät (n. Schuhfried). Dabei erfolgte eine kontinuierliche Registrierung der Herzfrequenz über 4 bzw. 8 Tage, wobei neben der physiologischen auch die psychisch-subjektive (Einschätzung der subjektiv erlebten Aktiviertheit) sowie die psychophysische (Leistungsquotient) Meßebene analysiert wurden, um aus der möglichen Wechselwirkung konkrete Rehabilitationsmaßnahmen ableiten zu können.Die Befunde zeigten bei allen Variablen eine klare Differenzierung zwischen den Patientengruppen: die Analyse der Herzfrequenz ergab, daß trotz gleichen Ausgangsniveaus der Aktiviertheit nur bei der Kontrollgruppe eine initiale Sensibilisierungsreaktion auftrat, die sich im Laufe der Reizwiederholung i. S. einer Habituation verminderte.Bei einer deskriptiven Analyse der HR-Verläufe in Form von mathematischen Exponentialfunktionen zeigte es sich, daß sich im wesentlichen drei relativ stabile Reaktionstypen abzeichneten, nämlich sog. Sensibilisierer, Habituierer sowie Indifferenztypen, wobei die Habituierer nur bei der Kontrollgruppe, die Indifferenztypen hingegen nur bei den apallisch geschädigten Patienten auftraten.Die Untersuchung der Wechselwirkung verschiedener Meßebenen legt eine gewisse Entkoppelung funktioneller Systeme, wie sie u.a. von Luria (1976) beschrieben werden, bei apallisch geschädigten Patienten nahe, wobei unter dem Versuchsreiz sensomotorische und physiologische Systeme offensichtlich nicht in einer optimal aufeinander abgestimmten Weise ablaufen, wie dies überwiegend bei den nur leicht hirngeschädigten Vergleichspatienten gefunden wurde.Hieraus resultierende Rehabilitationsmaßnahmen werden erörtert.Die hier zitierten experimentellen Untersuchungen stammen aus dem Teilprojekt D7 des SFB 122 an der Universität Marburg/Lahn unter Leitung von Prof. Dr. Dr. H. Remschmidt