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Biomedical subjects

L Gerhard

Publications and source records attributed to L Gerhard.

At least 55 records · Page 3Linked to original sources
PubMed1980

[Contribution of intracranial "traumatic aneurysm" (author's transl)].

Three clinically and histologically verified cases of "traumatic aneurysm" concerning the a. basilaris, a. communicans posterior, and a. lenticulostriata have been used to demonstrate that these acute and subacute lesions do not belong to the true aneurysms, as defined pathologically and anatomically. They can be considered as acute traumatic lesions of arteries with periarterial hematoma (aneursyma spurium) and should be designated as pseudoaneurysms. Such pseudoaneurysms must not only be differentiated from true aneurysms by radiological and clinical findings but also by histological investigation. An intracranial artery rupture with formation of an pseudoaneurysm due to a blunt injury can also exist without a fracture of the base of the skull. Since traumatic lesions of the striatum arteries are caused especially in children and young adults, the localization of an acute hemorrhage in the basal ganglia does not exclude a traumatic etiology. Early closure of the injury in the artery wall and surroundings by fibrin and thrombotic material with following repairing processes are important for latency between injury and rupture of the pseudoaneurysm.

Brain Injuries↗
PubMed1980

[Computertomographic and morphological findings in cerebral infarctions and intracerebral haematomas in identical sections (author's transl)].

The paper deals with computertomographic and morphological studies in patients who died suffering from brain ischaemia, haemorrhagical infarction and haemorrhages. These examinations were done in identical sections. Methodically computerized tomograms in living patients, postmortal tomograms, brain sections and macrosections were used. Not in all cases corresponding findings were observed, due to the following factors 1. Size of the lesion 2. Localisation 3. Time of examination 4. Premortal alterations. The different factors are discussed in detail.

Adult↗
PubMed1979

Clinical and morphological studies of pineal tumours.

This is a report of clinical, morphological, diagnostic, endocrinological and therapeutical experiences with 18 patients with tumours in the pineal region. The histological diagnosis was verified in four cases by autopsy, in seven cases by biopsy, and in one case by microscopical verification of tumour cells in the CSF. In all biopsy cases we are dealing with typical germinomas. In the other clinical cases diagnosis was made by neuroradiological and endocrinological methods. The localization was possible by encephalotomography or CT scan, according to Kageyama, Particular attention was given to the endocrinological dysfunctions which originate in the hypothalamus. Also the hypothalamic dysfunctions after irradiation were discussed. Since the results of primary surgical approach and biopsy have been unsatisfactory, we preferred a non-operative schedule for treatment of pineal tumours.

Biopsy↗
PubMed1975

[Centronuclear myopathy with autosomal dominant inheritance(author's transl)].

For the first time in Germany cases of a "centronuclear myopathy" are described in a 14-year-old boy and his 18-year-old sister. First symptoms in both patients appeared at 4 to 5 years of age with a "sleepy facial expression", clumsy gait and rapid fatigue. Within few years the disease progressed to generalized muscle weakness and atrophy, ptosis, ophthalmoplegia externa and areflexia. Weakness and atrophy were most pronounced in the distal muscles of the lower extremities. Both patients were free of epilepsy and the EEG recordings were normal. Motor and sensory nerve conduction velocities were normal. Repetitive stimulation of nerves revealed a normal transmission from nerve to muscle. Muscle biopsy showed a type I muscle fiber hypotrophy and a type II muscle fibre hypertrophy in addition to a predominance of type I fibres. Both fibre types showed central nuclei, sometimes appearing as chains in longitudinal sections. In most cells with central nuclei there persists a very small pericentral zone free of myofibrils but with increased activity of oxidative enzymes and phosphorylase. 2--3% of muscle fibres in cross sections showed a decreased of absent enzyme activity in the most peripheral fibre zone. Electron microscopy showed evidence of a centrally distinct myofibrillar disintegration. The father of both children had a ptosis at least from the 20th year of age. 5 years later generalized progressive muscle atrophy was recorded. Aged 51 years he died of pneumonia. Though not proved most probably the father suffered from the same disease as the children, pointing to an autosomal dominant inheritance in this family. The disease, according to the literature, seems to be genetically heterogeneous. The clinical picture seems to be independent of the mode of inheritance. Our patients showed a relatively rapid progression of symptoms. Pathogenetically the "centronuclear myopathy" may result from a disturbance of correlated nerve-muscle structures starting during early fetal life.

Adolescent↗