[Psychoanalytical aspects regarding etiology and understanding of schizophrenic psychoses]. / Psychoanalytische Aspekte zur Atiologie und zum Verständnis schizophrener Psychosen.

The author -- specialized in Psychiatry and Neurology as well as a Psychoanalyst -- reports her experience during some decades of treating patients with schizophrenia in greatly different hospitals and institutions. Many examples demonstrate that psychoanalytical knowledge and recognizing psychodynamic connections can essentially contribute to understanding and treating psychotic patients. From the multitude of psychoanalytic theories on the etiology of schizophrenia some aspects are demonstrated, mainly those regarding their use in practical work. Some of them are: ego-disturbance, the psychotic symptom as a defence mechanism and the problem of countertransference. Regarding the ego-disturbance some examples show that usually not all ego-functions are impaired. Thus, cognitive functions may not only frequently be preserved, but may be working even better than usual. Out of numerous mechanisms of defense in schizophrenia projection, identification, projective identification, splitting, denial and regression are especially important. Moreover, psychotic patients frequently show certain symptoms that are related to very personal experiences. They can often be recognized quite easily as defence mechanisms. Countertransference is of great importance when treating such patients. Three of these numerous phenomenous are mentioned especially: anxiety, compassion, which may lead to identification, and the incapacity to accept the limit of therapeutic measures. The author is convinced that the so-called "psychodynamic" and "biological" psychiatry are not in opposition. Splitting them is not justified because according to the different stages of illness treatment with drugs as well as with different psychotherapeutic methods, even with psychoanalytical ones and social rehabilitation, are necessary. The etiology of schizophrenic psychosis cannot be explained with psychoanalysis either. Yet, the knowledge of psychodynamic processes can contribute essentially to understanding the illness and treating the patient. The compliance accomplished thereby can improve the quality of life of the patient and possibly for the therapist too.

Clinical manifestations of late onset cerebral storage disease: a case of metachromatic leukodystrophy.

Clinical symptoms, MRI of the brain and neuro pathological findings of a case with adult metochromatic leukodystrophy are presented. Clinically it is important to consider a possible late-onset manifestation of an inborn cerebral storage disease, when uncertain psychopathological symptoms are difficult to assign to well-known diseases. These cerebral storage diseases may appear as "juvenile behaviour disturbance" or "schizophrenia". The clinical suspicion may further be confirmed by simultaneous or subsequent neurological or ophthalmological symptoms. The definitive diagnosis is possible by biochemical or histopathological methods. MRI of brain and neuro pathological findings correspond well with regard to white matter lesions.

Brain neurotransmitter changes in three patients who had a fatal hyperthermia syndrome.

The authors examined the autopsied brains from three patients who had a fatal hyperthermia syndrome. There was marked hypothalamic noradrenaline depletion in all three patients, severe brain choline acetyltransferase deficiency with nucleus basalis cell loss in two patients, and mild to moderate brain choline acetyltransferase loss in one patient. Striatal dopamine metabolite/dopamine ratio was below normal in two patients and not elevated, as would be expected after short-term neuroleptic administration, in the third. This suggests that reduced capability (aggravated by the cholinergic deficit) of the nigrostriatal dopamine system to respond adequately to stress and/or neuroleptic-induced receptor blockade may be important in the development and course of fatal hyperthermia syndrome.

[Human urinary fluoride excretion at various ages (author's transl)]. / Fluordausscheidung bei Menschen verschiedener Altersgruppen

3 groups, each consisting of 5 subjects in the following age ranges (A 4 to 6 years, B 25 to 45 years, C 60 to 70 years) were given fluoride in the form of a single dose of 6 mg. Fluoride excretion in the urine was subsequently investigated over a period of 24 hours. In a second experiment a daily dose of 6 mg of F- was given to the 3 groups over a period of 10 days. The urinary excretion was determined in 24-hour urine samples. The results are presented in two figures. 1. A time drift in urinary fluoride excretion in the direction of delayed fluoride metabolism was seen in group C subjects. 2. A periodic increase in the urinary fluoride values was also seen in these elderly subjects, indicative of an altered regulatory mechanism.

[The so-called amaurotic idiocies. Clinical, morphological and biochemical findings as a basis for modern classification]. / Die sogenannten amaurotischen Idiotien Klinische, morphologische und biochemische Befunde als Grundlage einer zeitgemässen Klassifikation

First of all seven of our own thoroughly investigated cases of so-called amaurotic idiocies are presented, they are two infantile, two juvenile, two late infantile one, as well as one adult case. The two infantile cases represent the typ of a GM2-gangliosidosis: with cerebral symptoms and cherry-red spot in the macula they correspond clinically to the typical picture of Tay-Sachs disease. Lightmicroscopically they show neuronal storage, electronmicroscopically a deposition of "membranous cytoplasmic bodies" and biochemically a strong increase in ganglioside GM2. The two juvenile cases correspond in their symptoms and findings to the so-called ceroid-lipofuscinoses or "Myoclonic variant of amaurotic idiocy", respectively. Clinically most remarkable is the deterioration of vision caused by retinitis-pigmentosa-like changes of the fundus, which sets in at the beginning of the disease and precedes the cerebral symptoms by years. The extinguished electroretinogramm corresponds in the histological retina findings to a severe lesion of the layer of rods and cones in the sense of a tapeto-retinal degeneration. Neuropathologically finegranular, Sudan-Black-B- and PAS-positive material is mainly but not exclusively stored in the neurons. The electronmicroscope shows them to be lipofuscin-like inclusions, as well as "curvilinear" or "fingerprint-bodies". Depositions are also to be found in astrocytes and in the cells of the vascular walls. The ganglioside pattern is normal in the brain tissue of the biochemically investigated case. Of the two late infantile cases the first represents a GM2-gangliosidosis, the second one corresponds to the ceroid-lipofuscinosis. The adult patient, who suffered from an ill-defined psychiatric disease and died at the age of 51 presents a diagnostically problematic case, showing a relatively slight, regionally rather differently accentuated intraneuronal storage of granular material and biochemically a slight increase in ganglioside GM2. On discussing our own findings and commenting on the relevant literature various aspects of amaurotic idiocies are considered, such as genetics, neuropsychiatry, ophthalmology, pathomorphology and biochemistry. In this respect special attention is paid to the pathomorphological substrate documented, as localization, degree and kind of tissue changes determine the clinical picture. This is also the case for the correlation between the findings of the different fields, so e.g. concerning the ophthalmological findings it is shown, that in gangliosidoses with preserved ERG histologically a storage in the nerve cells of the ganglion cell-layer only is to be found, where as the ceroid-lipofuscinoses with early onset of deterioration of vision and extinguished ERG in the histological picture of the retina show an additional severe lesion of the layer of rods and cones...