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The origin of ADHD is multifactorial and both the aetiology and pathophysiology of ADHD are as yet incompletely understood. The monoamine deficit hypothesis of ADHD postulates a dysbalance in the interaction of the neurotransmitters dopamine, noradrenaline and serotonin. Pathophysiological mechanisms involved in ADHD include alterations in fronto-striatal circuits. The currently proposed animal models of ADHD are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. Some evidence points to a genetic basis for ADHD which is likely to involve many genes of small individual effects. In summary, specific neurobiological substrates of ADHD are unknown and multiple genetic and environmental factors appear to act together to create a spectrum of neurobiological liability.

Groups of patients with Hungington's disease and probable dementia of Alzheimer type (DAT) matched for level of dementia on the basis of mini mental state examination scores were compared in several tests of visual memory and tests sensitive to frontal lobe dysfunction. Whereas recall of patients with DAT tended to be worse on the Kendrick object learning test, the two groups were equivalent on tests of sensorimotor ability and delayed matching to sample performance. By contrast, the patients with Huntington's disease were significantly worse on tests of pattern and spatial recognition, simultaneous matching to sample, visuospatial paired associates, and on three tests sensitive to frontal lobe dysfunction--namely, the Tower of London test of planning, spatial working memory, and a visual discrimination learning and reversal paradigm. The impairments in these tests, however, did not always qualitatively resemble those seen in patients with frontal lobe damage and may be more characteristic of primary neostriatal deficit. In the visual discrimination paradigm the patients with Hungtington's disease were significantly worse than the patients with DAT at the simple reversal stage, where they displayed significant preservation to the previously rewarded alternative. The results are consistent with the hypothesis that patients with Huntington's disease exhibit deficits in tests sensitive to frontostriatal dysfunction and that this form of intellectual deterioration is qualitatively distinct from that seen in Alzheimer's disease.

Purpose. To study and follow-up achromatopsia, prosopagnosia, and topographagnosia in a patient who suffered a bilateral stroke of the posterior cerebral arteries. Methods. Ophthalmological, neuropsychological and neuroradiological examinations were conducted over a span of 3 years to assess the amount of brain damage and look for signs of functional recovery. Results. After the onset of achromatopsia, perception of the color green re-appeared first, followed by red, yellow, and brown. Blue which had appeared entirely black was last to return. While reading and color naming have largely recovered, color discrimination after three years remains poor especially in dim lighting. Similarly, with prosopagnosia, while the patient has learn to identify people (including photographs) by individual features, his ability to perceive and recognize faces and facial expressions holistically remains severely impaired. Recognition of streets, houses, and topographical layouts also continues to be affected, while the perception of speed and distance has somewhat improved. Perimetry further suggests a mild improvement of the superior hemianopia in his visual fields. Conclusions. Although major deficits in color, face and place perception remain, some functions impaired by the stroke have returned par-alleling a partial recovery from the brain lesion as demonstrated by NMR.

Methylphenidate (MPH) is a centrally acting (psycho)stimulant which reversibly blocks the dopamine re-uptake transporter. At present MPH is one of the most frequently prescribed drugs for the symptomatic treatment of attention deficit hyperactivity disorder (ADHD). Although MPH has been in use for about 50 years, there is no information available concerning the long-term benefits and risks of medication. Based on experiments in rats it has been suggested that MPH treatment may affect the maturation of central dopaminergic systems and may be a risk factor for the development of Parkinson's disease (PD). The aim of the present case-control study was to gain information about (1) ADHD-like symptoms that may precede PD motor symptoms, and (2) the exposure to psychostimulants in childhood. We used a German short version of the Wender Utah Rating Scale (WURS-k, Retz-Junginger et al., 2002) which is a reliable measure for the retrospective diagnosis of childhood ADHD, and another questionnaire including a rating scale for symptoms of ADHD in childhood (Q-ADHD-Child) according to DSM-IV and ICD-10 criteria. A total of 92 patients with PD and 115 control subjects were enrolled in this study. Ninety-six percentage of PD patients (N = 88) completed the two rating scales. The data of these patients and of 88 randomly selected individuals of the controls were included for analysis. In the WURS-k, the PD group showed higher total scores compared to control subjects. In addition, we found increased scores in PD patients regarding the items attention deficit, hyperactivity and anxious and depressive symptoms, but not regarding impulsivity, oppositional behaviour and deficits in social adaptation. The results of the Q-ADHD-Child also showed increased scores in PD patients regarding attention deficit and hyperactivity. However, one cannot conclude that the PD patients enrolled in this study had suffered from childhood ADHD, since the average total WURS-k score of (14.4) was far below the cut-off score of 30 or higher which is considered to identify childhood ADHD. Finally, we found no evidence that PD patients had been exposed to psychostimulants such as MPH and amphetamine.

The present article provides a review of a series of studies in children with attention deficit hyperactivity disorder (ADHD) concerning (1) the effects of methylphenidate on various attentional functions, (2) the stimulant-induced changes of both qualitative and quantitative (i.e. kinematic) aspects of handwriting, (3) the interaction between conscious control of handwriting and fluency of handwriting movements, and (4) possible therapeutic approaches to graphomotor disturbances. Children with ADHD showed impairments in various aspects of attentional functioning. Pharmacological treatment of ADHD children with methylphenidate resulted in marked improvements of various components of attentional functioning. In comparison to the performance following the withdrawal of methylphenidate, children with ADHD on methylphenidate displayed a significant improvement in task accuracy in the areas of vigilance, divided attention, selective attention (inhibition, focused attention and integration of sensory information) and flexibility. However, the comparison with healthy children revealed considerable deficits regarding vigilance, divided attention, flexibility and selective attention (focused attention and integration of sensory information) in children with ADHD on methylphenidate. The comparison of writing movements of children on and off methylphenidate revealed that medication resulted in a better handwriting, but a deterioration in handwriting fluency as assessed by kinematic analysis. Children with ADHD may use their increased attentional capacities to focus on skills (e.g. handwriting) that are independent of conscious control or may even be disturbed by attention. The findings summarized in this paper indicate, therefore, that administration of methylphenidate alone is insufficient in the treatment of children with ADHD. Children with ADHD may benefit from instructions on how to best use their improved attentional capacities.

The neurotoxin 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) has been reported, both in vitro and in vivo models, to produce neurodegeneration and parkinsonian symptoms after prolonged exposure in rats. The aim of the present study was to investigate the effects of TaClo on the cognitive performance of rats. We used the COGITAT hole board system where rats can find hidden pellets by exploring the board. TaClo-treated rats found as many pellets as control rats treated with saline. Furthermore, their search was as efficient as that of control animals since there were no differences between the groups regarding explorative activity, visits to non-baited holes and time needed to find the pellets. These results suggest that there is no deficit in spatial memory following the chronic administration of TaClo to rats.

Although the neurotoxicity of many anticancer therapies is well documented, the impact of cancer treatment on cognitive functioning has been studied less frequently. The present study examines deficits in cognitive functioning and their correlation with medical data as well as with psychosocial variables. A standardised neuropsychological test battery and several questionnaires were administered to a random sample of 119 patients. 24% of our patients fulfilled our criterion for cognitive impairment. There were no significant associations between the results of the neuropsychological testing and the current affective status or self-reports of attentional deficits in daily life. Cognitive impairment occurs in a clinically relevant percentage of cancer patients and cannot be explained exclusively due to depression or anxiety. Since subjective and objective cognitive impairment data showed little correlation, neuropsychological evaluation should not only be based on subjectively-reported complaints, but also on objective measurements.

We report on a patient with long standing, full-blown mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS). In contrast to earlier publications, detailed neuropsychological assessment revealed no dementia but a pattern of distinct cognitive deficits with marked impairment of visuo-constructive and executive functions. Focal lesions and progressing atrophy mainly of the basal ganglia and the temporo-parieto-occipital area with preservation of hippocampal and entorhinal structures were present. Furthermore, a 4-year follow-up assessment revealed an increasing deterioration of distinct cognitive functions, including phasic alertness, tactile functions and the discrimination of tone pitch and rhythm. This may be because of chronic regional metabolic disturbances, as there was no further stroke-like episode in that period of time.

Poor handwriting in hyperactive children often contributes to academic failure. Beneficial effects of methylphenidate on the quality of handwriting have been shown. Using a digitizing tablet, the handwriting of 21 hyperactive boys was examined both during methylphenidate treatment and following withdrawal of the drug. Half of the hyperactive boys were tested first on methylphenidate and then following withdrawal of the drug and the remaining hyperactive boys were examined in the reverse order. Twenty-one control boys underwent the same examination. Velocity and acceleration of handwriting movements were measured. Furthermore, every writing specimen was independently rated by four examiners regarding the quality of handwriting. Following withdrawal of the drug, the quality of handwriting specimens of hyperactive boys was poorer than during treatment with methylphenidate. Statistical comparison of writing movements of hyperactive boys on and off methylphenidate revealed that the medication resulted in a deterioration in handwriting fluency. The results showed that following withdrawal of medication, hyperactive children did not differ from control boys in handwriting movements. The improvement in hyperactive behavior through methylphenidate was associated with increased legibility and greater accuracy of handwriting. The intention to write neatly may interfere with the fluent writing process.

Administration of botulinum neurotoxin A (BONT/A) is a common and effective treatment of blepharospasm. There is, however, no information regarding the emotional and social well-being of patients with blepharospasm and patient acceptance of BONT/A therapy. The purpose of this study was to investigate aspects of quality of life of patients with blepharospasm and level of patient satisfaction with treatment.Fifty-one patients with blepharospasm who had been treated with BONT/A for years completed a questionnaire providing information about quality of life.Results revealed reductions in social and emotional well-being of patients but, nonetheless, good acceptance of BONT/A therapy. The positive effects of BONT/A therapy were, however, accompanied by fear of a decreasing effect of BONT/A injections.Although the objective findings following BONT/A injections in the treatment of blepharospasm are appreciated by the patients, their well-being is affected by fears and depression.

We analyzed trace metals in frozen brain tissue of several subcortical nuclei from 3 patients with primary adult-onset dystonia and 10 control subjects. Copper levels were significantly increased in the globus pallidus and putamen of patients with dystonia A slight increase in manganese content was identified in the putamen and thalamus of patients with dystonia. Our findings show for the first time an accumulation of trace metals in the lentiform nuclei in patients with primary dystonia, which may play a pathogenetic role in primary dystonia and may explain recent ultrasound and magnetic resonance imaging findings.

In the treatment of patients with brain tumours, quality of life, as subjectively assessed according to the needs, stresses and circumstances of the patient and the subjectively experienced effects of the brain tumour, has recently been considered. While much has been written relating to the difficulty in defining and measuring the construct "quality of life" in the fields of clinical oncology and geriatrics, possible alterations in the quality of life following brain tumour have been largely ignored. The present article describes the targets of research on quality of life in brain tumour patients and difficulties in defining this construct. Furthermore, it discusses the limitations of the assessment of quality of life, in particular with regard to available tests and the reliability of brain damaged patients' self-assessment. In addition, a short overview is given concerning research on quality of life in meningioma patients.

Motorische Storungen wie progrediente Be-wegungsverlangsamung, erhOhter Muskeltonus, Ruhetremor und Auffalligkeiten von Haltung und Gang bestimmen das klinische Bild der Parkinsonkrankheit. Hinsichtlich mOglicher kognitiver Veranderungen stellte James Parkinson (1817) bei der Erstbeschreibung der Erkrankung fest, das die intellektuellen Fahigkeiten der Patienten nicht beeintrachtigt seien. Allerdings weist das sorgfaltige Studium von Parkinsons Monographie auf einen abnormen mentalen Status bei zumindest einem der von ihm beschriebenen sechs Patienten hin. Gegen Ende des 19. Jahrhunderts vertraten franzOsische und englische Neurologen die Auffassung, das Parkinsonkranke vor allem in den spaten Krankheitsstadien durchaus kognitive Einbusen wie z. B. GedachtnisstOrungen aufweisen (Trousseau 1886, Charcot 1872, Gowers 1899).

Parkinsonpatienten leiden haufig unter affektiven Storungen, vor allem unter Depression und Angst (Schiffer et al. 1988, Stein et al. 1990). Die in der Literatur beschriebenen Pravalenzraten fur das Vorliegen einer Depression bei der Parkinsonkrankheit reichen von vier bis 90% bei einer mittleren Haufigkeit von etwa 40–50% (Levin et al. 1988, Cummings 1992). Depressive Parkinsonpatienten haben einen verminderten Antrieb, sind wegen ihrer Gesundheit besorgt, ausern somatische Beschwerden, sind pessimistisch und betrachten ihre Lage oft als aussichtslos. Suizidgedanken kommen bei Parkinsonkranken vor, Suizide sind jedoch selten. Depression wird zuweilen bereits vor der Parkinsondiagnose beobachtet, tritt haufig etwa zum Zeitpunkt der Diagnosestellung auf und erscheint bei einer Reihe von Parkinsonpatienten erst im weiteren Verlauf der Krankheit.

Sowohl tierexperimentelle Untersuchungen (Dunnet 1985, Ridley et al. 1985) als auch pharmakologische Studien beim Menschen (Drachman 1977) belegen die Bedeutung zentraler cholinerger Funktion fur Gedachtnisprozesse. Auch bei neurodegenerativen Erkrankungen, die mit Demenzsyndromen einhergehen, wurden Veranderungen cholinerger Systeme im Gehirn beschrieben. Dazu gehoren die Demenz vom Alzheimertyp, die Chorea Huntington und das idiopathische Parkinsonsyndrom. Bei der Alzheimerkrankheit und beim Parkinsonsyndrom korreliert das Ausmas der kognitiven Storungen und Demenz mit der Aktivitatsminderung der Cholinazetyltransferase (CAT) im Neokortex (Perry et al. 1985). Bei beiden Erkrankungen degenerieren die cholinergen Projektionen von der Substantia innominata zum Kortex sowie vom Septum zum Hippokampus (Candy et al. 1983). Fur die Chorea Huntington wurde eine verminderte CAT-Aktivitat in den Septumkernen beschrieben (Spokes 1980). Die vorliegende Studie untersuchte post mortem an Hirngewebe Veranderungen von CAT-Aktivitat und muskarinergen Azetylcholinrezeptoren bei Alzheimerdemenz, Parkinsonsyndrom und Chorea Huntington (Lange et al. 1989, 1992, 1993).

Zu den subkortikal gelegenen Basalganglien zahlen das Corpus striatum und der Globus pallidus sowie die Substantia nigra und der Nucleus subt-halamicus. Diese Hirngebiete wurden fruher unter der Bezeichnung extrapyramidales System von der kortikospinalen Pyramidenbahn abgegrenzt. Die Bedeutung der Basalganglien fur Bewegungsstorungen ist seit langem bekannt (Wilson 1925). In den letzten Jahren hat es vermehrt experimentelle Befunde gegeben, die die Hypothese unterstutzen, das das Striatum eine Schaltstation verschiedener parallel verlaufender Schleifensysteme ist, die vermutlich an unterschiedlichen Funktionen beteiligt sind (Alexander et al. 1986). Eine sogenannte motorische Schleife verlauft vom motorischen Kortex uber das Putamen, die Substantia nigra pars reticulata, den Globus pallidus und den ventrolateralen Thalamus zum pramotorischen Kortex. Kognitive Funktionen werden mit einer „komplexen“ Schleife in Verbindung gebracht, die zunachst vom prafrontalen Kortex zum Nucleus caudatus projiziert und von dort parallel zur motorischen Schleife uber Substantia nigra, Globus pallidus und anteroventrale Thalamuskerne zuruck zum prafrontalen Kortex verlauft. Aus der Hypothese dieser Schleifensysteme kann die Schlusfolgerung gezogen werden, das Lasionen an unterschiedlichen Stellen innerhalb einer Schleife dieselben Verhaltensanderungen hervorrufen sollte. Tierexperimentelle Studien zeigten tatsachlich, das durch Lasionen im Bereich des prafrontalen Kortex dieselben Verhaltensdefizite erzeugt werden konnen wie durch Lasionen in den Arealen des Nucleus caudatus, zu denen neuronale Bahnen vom prafrontalen Kortex projizieren (Divac et al. 1967, Divac 1972, Oberg und Divac 1975).

Patients with idiopathic Parkinson's disease and control subjects were given two types of time estimation task. In the verbal estimation task subjects were required to judge the duration of time intervals of 10, 30 and 60 seconds, signalled by the examiner. Operative estimation required subjects to indicate when intervals of 10, 30 and 60 seconds had passed. Parkinsonian patients off L-Dopa medication were less accurate than control subjects in both tasks. They underestimated the time intervals determined by the examiner in the verbal estimation task, while in the operative estimation task parkinsonian subjects overestimated the required time intervals compared with controls. The administration of L-Dopa to the parkinsonian patients led to time judgements that were similar to those of control subjects. The present findings lend support to the hypothesis of the role of dopamine in the modulation of the internal clock.

A group of twelve patients with idiopathic Parkinson's disease was assessed both on and off L-Dopa medication on a range of tests of cognitive performance. Withdrawal of L-Dopa produced impairments in tests sensitive to frontal lobe dysfunction such as verbal fluency and the Tower of London task. Another test of frontal lobe function, the Wisconsin Card Sorting Test, was not affected in the absence of L-Dopa. Memory functions such as short-term span and verbal paired associate memory were not impaired by L-Dopa withdrawal. The results suggest that some of the cognitive impairments observed in Parkinson's disease, namely frontal lobe deficits, are related to a loss of central dopaminergic function.

Research on Parkinson's disease has led to new hypotheses concerning the mechanisms of neurodegeneration and to the development of neuroprotective agents. Recent findings of impaired mitochondrial function, altered iron metabolism and increased lipid peroxidation in the substantia nigra of parkinsonian patients emphasize the significance of oxidative stress and free radical formation in the pathogenesis of Parkinson's disease. Present research is therefore focussing on improvements in neuroprotective therapy to prevent or slow the rate of progression of the disease. Possible neuroprotective strategies include free radical scavengers, monoamine oxidase-B inhibitors, iron chelators and glutamate antagonists. Recent studies point to the possibility of achieving neuroprotection in ageing and parkinsonism by the administration of dopamine agonists. In the rat, the dopamine agonist pergolide appears to preserve the integrity of nigrostriatal neurones with ageing. The prevention of age-related degeneration may be achieved as a result of a decreased dopamine turnover and reduced conversion of dopamine to toxic compounds. In our own study, bromocriptine treatment prevented the striatal dopamine reduction following MPTP administration in the mouse. These results suggest that the neurotoxic effects of MPTP can be prevented by bromocriptine. Monotherapy with the dopamine agonist lisuride in the early stages of Parkinson's disease delays the need for the initiation of levodopa treatment to a similar extent as has been reported for L-deprenyl. It remains to be shown whether this is due to neuroprotective efficacy of the dopamine agonist or to a direct symptomatic effect.

Parkinson's disease (PD) is characterised by the progressive degeneration of nigrostriatal dopamine (DA) neurons resulting in the major symptoms of akinesia and rigidity. Although the primary cause of PD is still not known some features make this disorder a model for neurodegenerative diseases in general. It has been known for some time that symptomatic PD can be attributed to insults with symptoms occurring many years later such as post-encephalitic PD or PD following manganese poisoning. More recently, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) has been identified as a neurotoxin selective for melanin-containing dopaminergic neurons in humans and non-human primates. The specificity of this neurotoxin and the striking clinical similarities to idiopathic PD, seen in primates, make MPTP-induced parkinsonism the most useful animal model of a neurological disease. There are numerous theoretical possibilities to interfere with both MPTP-induced neurotoxicity and the symptomatology of PD. In recent years excitatory amino acids have gained considerable interest since they can cause excitotoxic lesion of neurons under a number of pathological conditions (Olney et al., 1989; Choi, 1988). Here we summarise the present data and provide new experimental evidence indicating that MPTP-induced degeneration of dopaminergic neurons does involve glutamate-mediated toxicity. It is concluded that glutamate-mediated excitotoxicity results in the destruction of DAergic somata in the substantia nigra. Non-competitive or competitive NMDA antagonists protect nigral neurons from MPTP-induced degeneration whereas their striatal terminals still seem to degenerate.

Die Chorea Huntington ist klinisch durch hyperkinetische Bewegungsstorungen und progrediente kognitive Dysfunktion charakterisiert. In der vorliegenden Arbeit wurden die in verschiedenen Stadien der Huntingtonkrankheit auftretenden kognitiven Defizite untersucht.

Die Chorea Huntington ist klinisch durch choreatische Bewegungen und eine progredient verlaufende Demenz gekennzeichnet. Eine funktionelle Beeintrachtigung cholinerger Neuronensysteme im Gehirn scheint zumindest teilweise die Grundlage kognitiver Dysfunktion zu sein [2]. Die bei Morbus Alzheimer und Morbus Parkinson auftretende Demenz ist mit einer Degeneration subkortiko-kortikaler Systeme verbunden. Die cholinergen Neurone, die vom Nucleus basalis in der Substantia innominata zum Neokortex und vom Septum zum Hippocampus projizieren, degenerieren sowohl bei Morbus Alzheimer [4, 10, 14] als auch bei Morbus Parkinson [4, 9, 15]. Das Ausmas der kognitiven Storung korreliert bei beiden Erkrankungen mit der Aktivitatsverminderung der Cholinazetyltransferase (ChAT) im Neokortex [12, 13, 15].

The discovery of a selective striatal dopamine deficiency in Parkinson's disease has led to dopamine replacement therapies including L-DOPA, dopamine full and partial agonists, and MAO-B inhibitors. The development of new compounds and alternative methods of drug delivery may be able to overcome the long-term side effects of the established therapies. Overactivity of central glutamatergic systems appears to be important in the pathophysiology of the disorder and provides the rationale for the use of glutamate antagonists. Recent studies emphasize the significance of oxidative stress and free radical formation in the pathogenesis of Parkinson's disease. Future research will focus on improvements in neuroprotective therapy to prevent or slow the rate of progression of the disease. Possible neuroprotective strategies include selective MAO-B inhibitors, iron chelators, and free radical scavengers.

The sophisticated analysis of and growing information on the human brain requires that acquisition, dissection, storage and distribution of rare material are managed in a professional way. In this publication we present the concept and practice of our brain bank. Both brain tissue and information are handled by standardized procedures and flow in parallel from pathology to neuropathology and neurochemistry. Data concerning brain material are updated with clinical information gained by standardized procedures.

The importance of genetic aspects, ageing, environmental factors, head trauma, defective mitochondrial respiration, altered iron metabolism, oxidative stress and glutamatergic overactivity of the basal ganglia in the pathogenesis of Parkinson's disease (PD) are considered in this review.

Dopamine appears to be of less importance in the regulation of psychomotor functions than was previously thought. A central dopaminergic-glutamatergic balance may be important for both akinetic motor disorders and psychosis. In Parkinson's disease glutamate antagonists may counteract central glutamatergic hyperactivity and may be of value as anti-parkinsonian drugs. An increase of dopaminergic activity and/or a reduction of glutamatergic activity may contribute to the development of paranoid hallucinatory psychosis in schizophrenic patients and of pharmacotoxic psychosis in Parkinson's disease. Because of possibly severe side-effects of glutamatergic antagonists and agonists in the treatment of akinesia and psychosis, the development of partial glutamate agonists/antagonists could be an alternative strategy capable of producing antipsychotic or anti-kinetic effects with only mild adverse reaction.

Bei der Alzheimer-Krankheit wie auch bei der idiopathischen Parkinson-Krankheit degenerieren die subkortiko-kortikalen cholinergen Systeme von der Substantia innominata (vor allem vom Nucleus basalis nach Meynert) zum Neokortex und vom Septum zum Hippokampus (Candy et al. 1983; Dubois et al. 1983; Rossor et al. 1982; Ruberg et al. 1982). Bei beiden Erkrankungen besteht eine Korrelation zwischen der Reduktion der Cholinazetyltransferase-Aktivitat (ChAT) im Kortex und dem Grad der kognitiven Beeintrachtigung (Perry et al. 1978; Perry et al. 1985; Ruberg et al. 1982). Fur pharmakologische Ansatze zur Therapie der kognitiven Storungen und Demenz bei diesen Krankheiten ist es wichtig, die als Folge der neuronalen Degeneration auftretenden Rezeptorveranderungen zu bestimmen. Die vorhegende Studie untersuchte die Veranderungen der ChAT-Aktivitat sowie der muskarinartigen Azetylcholinrezeptoren im Neokortex und Hippokampus bei Alzheimer- und Parkinson-Krankheit (Lange et al. 1989).

Die Alzheimer-Demenz ist durch eine globale Beeintrachtigung verschiedener kogniti-ver Funktionen gekennzeichnet (Rossor 1982). Auch ein betrachtlicher Teil der Patien-ten mit Parkinson-Krankheit zeigt kognitive Defizite in unterschiedlichem Ausmas und Demenz (Brown u. Marsden 1984). Es besteht eine bemerkenswerte Uberlappung hinsichtlich der neuropathologischen und neurochemischen Veranderungen bei Alzheimer- und Parkinson-Krankheit (Whitehouse 1986). Das legt einen systemati-schen Vergleich der kognitiven Veranderungen bei diesen Erkrankungen nahe. In der vorliegenden Studie wurden visuell-raumliche Gedachtnisdefizite bei Alzheimer- und Parkinson-Patienten untersucht.

There is evidence to suggest that glutamate and other excitatory amino acids play an important role in the regulation of neuronal excitation. Glutamate receptor stimulation leads to a non-physiological increase of intracellular free Ca2+. Disturbed Ca2+ homeostasis and subsequent radical formation may be decisive factors in the pathogenesis of neurodegenerative diseases. Decreased glutamatergic activity appears to contribute to paranoid hallucinatory psychosis in schizophrenia and pharmacotoxic psychosis in Parkinson's disease. It has been suggested that a loss of glutamatergic function causes dopaminergic over-activity. Imbalances of glutamatergic and dopaminergic systems in different brain regions may result in anti-akinetic effects or the occurrence of psychosis. The simplified hypothesis of a glutamatergic-dopaminergic (im)-balance may lead to a better understanding of motor behaviour and psychosis.

In order to understand the particle formation processes during the precipitation deoxidation of steel melts with aluminium, in the present work a relationship for the rate of the concentration excess buildup is derived according to Slezov from the differential equations for convective diffusion and simultaneous reaction and from the mass action law for the system Fe-Al-O, using the one-dimensional circulation flow field proposed by Nakanishi and coworkers because of computation expense.

The introduction of secondary steelmaking has been one of the most significant developments in steelmaking in recent decades. In this review the operations, reactions, and reactors of secondary steelmaking are discussed in an attempt to explain the objectives, mechanisms, benefits, and potentialities of the processes by rigorous application of thermodynamic and kinetic principles. It is thought that by this means a deeper understanding might develop on what occurs in the reactors and how steelmaking can be achieved at the lowest cost. Constraints are obvious because it is not yet possible to produce steel in large quantities, and economically, in a completely closed system with controlled oxygen chemical potential.

Der Ubergang eines Stoffes zwischen zwei fluiden Phasen wird betrachtet, von denen sich einer als Strahl in der anderen bewegt. Die Geschwindigkeit der laminar stromenden Phase wird durch eine Gleichung ausgedruckt, die Geschwindigkeitsprofile zwischen der Kolben- und der Rohrstromung kontinuierlich beschreibt. Der Transport des Stoffes im Strahl durch Diffusion in radialer und durch Konvektion in axialer Richtung wird fur den isothermen, stationaren Fall untersucht. Die das Problem beschreibende Differentialgleichung wird anscheinend erstmals geschlossen gelost. Die Losungen beinhalten konfluente hypergeometrische Funktionen. Berechnet werden Eigenwerte, Koeffizienten, ortliche und mittlere Konzentrationsfelder sowie Stoffubergangszahlen.

Unilateral injection of MPP+ (4 micrograms/1 microliter) into the pars compacta of the substantia nigra in rats induced ipsiversive circling immediately after the injection. Ipsiversive circling was still present 7 days after the injection. Systemic injection of the dopamine agonist apomorphine induced contraversive circling. These results show that MPP+ exerts a powerful neurotoxic action on the nigrostriatal dopaminergic system of the rat. Furthermore, the results suggest that unilateral intranigral administration of MPP+ in the rat may induce supersensitive dopamine receptors in the ipsilateral denervated striatum.

Exposure of drug addicts to MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) has caused a Parkinsonian syndrome accompanied by a selective destruction of dopamine containing neurones in the pars compacta of the substantia nigra. MPTP in the human causes a severe irreversible state that very closely resembles idiopathic Parkinson's disease both in its clinical features and response to pharmacological treatment. Interest in potential environmental agents that might play a role in the aetiology of idiopathic Parkinson's disease is likely to increase as the result of the discovery of the relatively simple molecule MPTP which is highly toxic to the substantia nigra. Until the discovery of the neurotoxicity of MPTP there was no effective animal model of Parkinson's disease. Administration of PTP to monkeys induces persistent parkinsonism which responds to classical antiparkinsonian therapy. The morphological and biochemical changes in the brains of the animals are more limited and selective than those seen in idiopathic Parkinson's disease. The model of MPTP-treated monkeys appears to provide a useful testbed for the evaluation of future treatments for the disease. The precise mechanism of MPTP toxicity has yet to be determined and may provide the clue to the mechanism of neuronal death in Parkinson's disease. After entering the brain MPTP is oxidized to MPP+ (1-methyl-4-phenylpyridine) at an extraneuronal site.(ABSTRACT TRUNCATED AT 250 WORDS)