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Biomedical subjects

G Northoff

Publications and source records attributed to G Northoff.

17 recordsLinked to original sources
PubMed1999

Impairment in visual-spatial function in catatonia: a neuropsychological investigation.

Catatonia is a psychomotor syndrome with motor and behavioral abnormalities which may be due to alterations in fronto-parietal cortical function. We therefore investigated neuropsychological tasks (attention, executive, visual-spatial, working memory) associated with frontal and parietal cortical function. Thirteen catatonic patients, diagnosed as catatonic according to criteria by Rosebush and Bush, were compared with 13 psychiatric non-catatonic controls (matched with regard to underlying psychiatric diagnosis, age, sex, and medication), and 13 age- and sex-matched healthy controls. Catatonics showed significantly poorer performances and different neuropsychological intercorrelation patterns in visual spatial object perception (VOSPobject) than psychiatric and healthy controls. In addition, we found significant correlations between catatonic symptoms, visual-spatial abilities, and attentional measures (i.e., d2, CWI). Catatonia was characterized by specific visual-spatial deficits which are related to attentional abilities and right parietal cortical function. The data suggest attentional-motor and fronto-parietal dysfunction in catatonia, a conclusion which should be considered as preliminary, however, due to the small sample size.

Adult↗
PubMed1999

Catatonia as a psychomotor syndrome: a rating scale and extrapyramidal motor symptoms.

BACKGROUND: Catatonia was first described by Kahlbaum as a psychomotor disease with motor, behavioral, and affective symptoms. In keeping with this concept, we developed a rating scale for catatonia (Northoff Catatonia Scale [NCS]) with three different categories of symptoms (i.e., motor, behavioral, affective). Furthermore, the question of the relationship among catatonic symptoms, extrapyramidal motor symptoms, and neuroleptics was addressed in the present study. METHOD: 34 acute catatonic patients and 68 age-, sex-, diagnosis-, and medication-matched psychiatric control subjects were investigated on days 0, 1, 3, 7, and 21 with the NCS, with other already validated catatonia rating scales by Rosebush, Bush (BFCRS), and Rogers (MRS), as well as with scales for hypokinetic (SEPS) and dyskinetic (AIMS) extrapyramidal motor features. Validity and reliability of the new scale, factor analysis, correlational analysis, and differences between catatonic patients and psychiatric control subjects were statistically calculated. RESULTS: NCS showed high validity (i.e., significant positive correlations [p <0.0001] with the other scales, significant differences between catatonic and control subjects), high intra-and interrater reliabilities (r = 0.80-0.96), and high affective subscores. Factor analysis revealed four factors best characterized as affective, hypoactive, hyperactive, and behavioral. Catatonic scores in NCS correlated significantly with AIMS on day 0 and SEPS on days 7 and 21. There were no significant differences in catatonic (i.e., NCS, MRS, BFCRS) and extrapyramidal (i.e., AIMS, SEPS) scores between neuroleptically treated and untreated catatonic subjects. CONCLUSIONS: The following conclusions were drawn: (1) the NCS has to be considered as a valid and reliable rating instrument for catatonia; (2) catatonia can be characterized by psychomotor symptoms encompassing motor, affective, and behavioral alterations; and (3) extrapyramidal hyperkinesias like dyskinesias are apparently closely related to catatonic symptoms which, in general, seem to be relatively independent of previous neuroleptic medication.

Acute Disease↗
PubMed1998

Schizophrenia and anteroventral thalamic nucleus: selective decrease of parvalbumin-immunoreactive thalamocortical projection neurons.

This study was designed to examine possible anatomical changes of thalamocortical circuits in schizophrenics. Previous immunocytochemical studies have shown that parvalbumin, a calcium-binding protein, occurs in thalamocortical projection neurons, but not in GABAergic interneurons in the anteroventral thalamic nucleus (AN). Using parvalbumin-immunocytochemistry we investigated the densities of thalamocortical projection neurons in the AN of schizophrenic cases (n = 12) and controls (n = 14). The densities of all neurons in the AN were estimated by Nissl-staining. The majority of thalamocortical projection neurons in AN were identified by parvalbumin-immunoreaction. Significantly reduced densities of thalamocortical projection neurons were estimated in the right (P = 0.003) and left AN (P = 0.018) in schizophrenic subjects. The densities of all neurons in right and left AN were also diminished in schizophrenics; however, these decreases did not reach statistical significance. The reductions of parvalbumin-positive thalamocortical projection neurons were not correlated with the length of disease, this finding supporting the neurodevelopmental etiology of structural abnormalities in schizophrenia.

Adult↗
PubMed1998

[Subjective experiences of patients with acute neuroleptic-induced akathisia].

Neuroleptic-induced akathisia is a clinically important neuropsychiatric syndrome with mainly subjectively experienced psychic symptoms on the one hand and well-observable motor signs on the other. There is no general consensus of opinion on the relative importance of these two aspects for diagnosing akathisia. Hence, differential diagnosis is difficult and in the absence of a biological marker it depends crucially on clinical judgement. Systematic investigation of 27 in-patients via a semistructural interview, a self-assessment scale (20 in-patients) and established akathisia rating scales (Hillside, Barnes, Prince Henry Hospital and Chouinard) revealed four characteristics of subjective experience in acute neuroleptic-induced akathisia: 1. perception of a foreign but nevertheless inner compulsion to move; 2. lack of control over motor behaviour; 3. feeling of inhibition of purposeful actions and 4. subjectively close or inseparable relationship between inner restlessness and restless movements. These features are strongly interrelated and correlate with severity of akathisia. They could be useful in differentiating akathisia from other states of restlessness. The results of this study are discussed in context of the literature on clinical phenomenology of akathisia. We propose a symptom-severity model of akathisia emphasizing psychodynamic aspects with considerable consequences for diagnosis and quantification of the disorder. The model points to the relevance of patient exploration for optimizing diagnostic reliability and should be taken into account when developing new and valid akathisia rating instruments.

Adolescent↗
PubMed1997

[The symptomology of akathisia].

The phenomenon of akathisia is characterised by a subjective feeling of inner agitation accompanied by general motoric restlessness, which particularly affects the legs. It is mainly the inner agitation from which the patients suffer, but which they often cannot describe in any detail. The psychopathology of akathisia is presented in a case report, the emphasis being on a detailed description of inner agitation. Furthermore, motor, affective and cognitive symptoms of akathisia are pointed out. Finally, differential diagnosis of akathisia and standardised scales for assessment are discussed.

Adult↗
PubMed1997

Glutamatergic dysfunction in catatonia? Successful treatment of three acute akinetic catatonic patients with the NMDA antagonist amantadine.

Therapeutic efficiacy of the NMDA antagonist amantadine is reported in three acute neuroleptic free akinetic catatonic patients. Intravenous infusion of amantadine led to the resolution of catatonic symptoms and considerable reductions of scores in various motor scales (Simpson Angus scale for extrapyramidal side effects (SEPS), the abnormal involuntary movement scale (AIMS), Rogers catatonia and schizophrenia scales). The therapeutic effect of amantadine showed a characteristic temporal pattern with most pronounced effects four to six hours after administration and recurrence of catatonic symptoms by 24 hours later, at least partially. Such a temporal pattern of therapeutic efficacy and decreasing efficacy occurred in all three patients on all days. The results suggest the central importance of glutamatergic dysfunction in catatonic syndrome.

Adult↗
PubMed1996

Plasma homovanillic acid concentrations in catatonia.

We investigated the dopamine metabolite plasma homovanillic acid (plasma HVA) levels in 37 catatonic patients on the day of admission before initial medication as well as in 17 healthy controls. In a prospective study catatonic syndrome was diagnosed according to criteria of Lohr and Wiesniwski (1987) and Rosebush et al (1990) whereas comorbid diagnosis was made by Diagnostic and Statistical Manual of Mental Disorders, 3rd ed, revised (DSM III/R) (APA 1987). On the day of admission blood samples were taken before initial medication. Compared to controls (80.1 +/- 40.1 pmol/mliter) catatonic patients showed significantly (P = 0.0286) increased plasma HVA (140.9 +/- 53.6 pmol/mliter). Catatonic patients free of neuroleptic medication (n = 21) differed significantly (p = 0.0416) from controls whereas neuroleptically treated catatonics (n = 16) did not. Our findings of increased plasma HVA in catatonia are explained by an alteration in either mesolimbic or mesocortical dopaminergic function, as is assumed in the case of schizophrenia. As an alternative, it may be due to increased nigrostriatal function, which can lead, as shown in animal experiments with the dopamine agonist amphetamine, to hypokinetic states resembling catatonia in humans.

Adolescent↗
PubMed1996

Increase of serum creatine phosphokinase in catatonia: an investigation in 32 acute catatonic patients.

We investigated serum creatine phosphokinase (CPK) and associated parkinsonic (SEPS) and dyskinetic (AIMS) movements in 32 hospital admitted acute catatonic patients. Thirty-two (N = 24 without neuroleptics on admission) catatonic patients were compared with 32 non-catatonic dyskinetic psychiatric patients, 32 non-catatonic non-dyskinetic psychiatric patients and 32 healthy controls. CPK was significantly higher (P = 0.015) in catatonics (mean 255.75, S.D. +/- 226.54) than in healthy controls (38.6, +/- 27.4) and non-catatonic non-dyskinetic psychiatric patients (57.1, +/- 120.8) whereas there was no significant difference between catatonics and non-catatonic dyskinetic psychiatric patients (453.4, +/- 128.5). There were significantly positive correlations between CPK and AIMS, as well as significantly negative correlations between CPK and SEPS, in all three groups. Our results suggest that increased serum CPK in catatonia may be related to occurrence of dyskinetic movements. Furthermore, we were able to distinguish a parkinsonic (low CPK, low AIMS, high SEPS) and a dyskinetic (high CPK, high AIMS, low SEPS) subtype in catatonia.

Acute Disease↗
PubMed1996

Do brain tissue transplants alter personal identity? Inadequacies of some "standard" arguments.

Currently, brain tissue transplantations are being developed as a clinical-therapeutic tool in neurodegenerative diseases such as Parkinson's or Alzheimer's disease. From an ethical point of view, distinguishing between the preservation and an alteration of personal identity seems to be central to determining the scope for further application of brain tissue transplantation therapy. The purpose of this article is to review "standard" arguments which are used on the one hand by proponents to prove preservation of personal identity and by opponents on the other hand to prove that brain tissue transplantation results in an altered personal identity. Proponents and opponents are shown to use the same arguments, albeit with different presuppositions. These presuppositions concern the meaning of the term "identity", either numerical or qualitative, the definition of brain identity, either structurally or functionally, and the relationship between mental states, psychological functions and neurophysiological properties as criteria for personal identity. Furthermore the respective neurophysiological, clinical and philosophical evidence for the different presuppositions are discussed. It is concluded that evaluation of personal identity in brain tissue transplantation should not only rely on the "standard" arguments but, additionally, neurophysiological, clinical and philosophical implications should be discussed.

Brain Diseases↗
PubMed1996

[The subjective experience in catatonia: systematic study of 24 catatonic patients].

Catatonic patients are often not able to communicate their subjective experiences behind their "fassade of immobility." Therefore was retrospectively (3 weeks later) investigated subjective experiences in 24 catatonic patients with a self-assessment-scale especially for catatonia developed by us. Our results showed that catatonic patients subjectively experience less their altered movements but rather cognitive, i.e. ambivalence, or affective, i.e. intense emotions which couldn't be controlled, alterations. According to our results we were able to distinguish an emotive (intense anxiety) from a non-emotive, i.e. cognitive (predominating ambivalence), subtype in catatonia with regard to subjective experience.

Adult↗
PubMed1995

Ball experiments in 32 acute akinetic catatonic patients: deficits of internal initiation and generation of movements.

We undertook ball experiments in 32 akinetic catatonic patients in order to determine specific functional deficits in the motor system in akinetic catatonia. Standardized ball experiments (catching, throwing, stopping, kicking) were conducted in 32 acute akinetic catatonic patients (23 without neuroleptics on admission), diagnosed according to Lohr, Rosebush, and the Diagnostic and Statistical Manual of Mental Disorders (3rd ed, revised) on days 0 and 21. Additionally, associated psychopathology was evaluated using different scales on days 0 and 21: the Global Assessment Scale, the Brief Psychiatric Rating Scale, the Hamilton-Anxiety Scale, the scale for the assessment of negative symptoms (SANS), and the Simpson scale for extrapyramidal side effects (SEPS). Significantly more patients were able to perform more externally guided tasks (catching, stopping) than internally guided tasks (throwing, kicking). Patients showed significantly more posturing and awkward movements on day 0 than on day 21. There was a significantly positive correlation between hypokinetic extrapyramidal features (SEPS) and negative symptoms with their cognitive alterations (SANS) on day 0. The findings suggest a deficit of internal initiation, as in parkinsonism, as well as a dysfunction in the generation of voluntary movements in akinetic catatonia. We assume an underactivity in the dorsolateral prefrontal cortex and the supplementary motor area with consecutive down-regulation of the cortical-striatal-thalamic circuit, the "motor loop," in catatonia.

Acute Disease↗
PubMed1995

Catatonia: short-term response to lorazepam and dopaminergic metabolism.

Therapeutic response to lorazepam and dopaminergic metabolism were investigated in 18 neuroleptically naive acute catatonic patients. They were diagnosed as catatonic according to criteria by Lohr and Rosebush and treated exclusively with lorazepam (2-4 mg) during the first 24 h. Dopaminergic metabolism (plasma HVA, plasma MHPG), anxiety (HAM-A) and parkinsonic/dyskinetic movements (SEPS, AIMS) were measured under standard conditions before initial treatment with lorazepam (day 0) and 24 h after initial treatment (day 1). On day 0 responders to lorazepam treatment (complete remission of catatonic syndrome after 24 h according to Rosebush and Lohr) showed significantly higher (P = 0.004) plasma HVA (130.4 +/- 51.2 pmol/ml; means +/- SD) than non-responders (no remission of catatonic syndrome after 24 h; 73.2 +/- 40.5 pmol/ml; means +/- SD). On day 1 plasma HVA did not differ any more significantly between both groups Clinically, responders showed significantly higher HAM-A (P = 0.025) and AIMS (P = 0.022) scores as well as significantly lower SEPS (P = 0.049) scores than non-responders on day 0. Hence catatonic short-term responders and nonresponders to lorazepam can be distinguished with regard to plasma HVA, anxiety and dyskinetic/parkinsonic movements.

Acute Disease↗
PubMed1992

[Encephalitis lethargica--a neuropsychiatric disease].

Encephalitis lethargica is presented as an exemplaric neuropsychiatric illness. Its history, the symptoms and the diagnostics, as well as its pathology and therapy are illuminated. Finally, specific problems and questions with regard to encephalitis lethargica are discussed: the question of a viral genesis and of a probable reappearance of the apparently disappeared encephalitis lethargica, the problems concerning the account for the neurological and psychiatric symptoms, and the question of role and function of the basal ganglia.

Brain↗
PubMed1992

[Approaches to neuropsychiatry as a transition in the separation of neurology and psychiatry].

The focus of the article is on the separation of neurology and psychiatry and their interconnection by means of the discipline of neuropsychiatry. First, the oppositions of "Structure versus Functions" and "Localization versus Holism" are worked out as the main reasons for the separation of neurology and psychiatry. This is followed by the demonstration of the recent developments of "biological psychiatry", "behavioral neurology" and "neuropsychology" which try to bridge the gulf between neurology and psychiatry. Their inadequacies with regard to a real bridge between the two disciplines, which takes account for both sides, is shown. Consecutively, a specific neuropsychiatric conception as a functional dynamic one, is suggested, which can be distinguished from the approaches in "biological psychiatry" and "behavioral neurology". This neuropsychiatric conception is applied, in a last step, to the oppositions of "Structure versus Function" and "Localization versus Holism", by means of which these oppositions, and the one between neurology and psychiatry, can be bridged--this is exemplified by means of the Parkinson-Syndrome with its neurologic and psychiatric symptoms.

Biological Psychiatry↗
PubMed1992

[Biosocial relations as contact points in the social network. A contribution to the theoretical discussion in psychosomatic medicine].

Psychosomatic medicine needs a theoretical model for clinical tasks and for research. To start from Freud's psychoanalytic theory (conversion and anxiety neurosis) and Alexander's model of the "vegative neurosis" a system theory concept of the bio-psychosocial model (Lipowski) is presented and discussed critically. Instead of further investigation on the problem of "unity", or on monistic or dualistic views of the mind-body problem, we propose a new theoretical approach. If we focus our interest on nodal points of the bio-psychosocial network we can learn more about somatic-psychosocial interaction and can develop practical consequences for research and clinical issues.

Anxiety Disorders↗