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Biomedical subjects

G Neuhäuser

Publications and source records attributed to G Neuhäuser.

At least 19 recordsLinked to original sources
PubMed1979

[Sphingolipidoses].

Explore the source record for details and available documents.

Cytoplasmic Granules↗
PubMed1979

[ADAM complex--maxillofacial abnormalities and abnormalities of the extremities caused by amniotic strangulations].

The anomalies of the ADAM complex arise through amniotic strangulations, adhesions and amputations. In the face cleft formations, displacements and deformities of various structures occur. The limbs exhibit constriction grooves, secondary syndactyle or amptuations. According to observations on 8 patients and information from the literature, the presentation of Adam complexes can vary to an extraordinary degree. The anomalies result from exogenous influences. In genetic counselling phenotypically similar congenital malformations must be separated.

Abnormalities, Multiple↗
PubMed1978

Cranial computerized tomography in children with lymphoid malignancy and seizures.

Focal and generalized seizures occurred in 4 patients with acute lymphoblastic leukemia and non-Hodgkin-lymphoma. The etiology of the neurological complications could be established by cranial computerized tomography (CT): i.e., 1. localized metastasis with calcification and 2. acute intracerebral hemorrhage during induction therapy in two patients with malignant lymphomas; 3. diffuse cerebral infiltration with blast cells and 4. cerebral atrophy in two children with acute lymphoblastic leukemia who were in relapse. Accurate diagnosis of cerebral complications in hemoblastoses is essential for appropriate therapy and CT may lead to more effective treatment in patients with lymphoid malignancy and seizures.

Adolescent↗
PubMed1978

[Spongious cerebral dystrophy at an infant age (Canavan-Bogaert-Bertrand types) in three siblings of a non-Jewish family in upper Franconia (author's transl)].

A daughter and two sons of possibly consangineous parents died after motor and mental deterioration at 18, 16 and 15 months of age. Spongy degeneration of the CNS (Canavan-van-Bogaert-Bertrand type) was diagnosed on neuropathological examinationtion; the histological findings were almost identical in the patients. Own clinical experiences are compared with reports from the literature; data important in clinical and differential diagnosis are reviewed. Pathogenetical and etiological aspects are discussed; autosomal recessive inheritance has to be considered in genetic counselling.

Autopsy↗
PubMed1977

[Long-term treatment with anticonvulsants in childhood. Guidelines for the practice].

Long-term treatment with antiepileptic drugs is based on a differentiated diagnosis. Medication appropriate for a special type of seizures has to be chosen. Treatment must be controlled carefully to avoid side effects. Total blood count, urinalysis and determination of enzymes (alkaline phosphatase etc.) are necessary in regular intervals. Essential in treatment is the psychological guidance of the patient and his parents to handle various problems which arise during development. The treatment is terminated carefully after years when the seizures are controlled and the EEG has been normalized.

Age Factors↗
PubMed1977

Fatal CNS dysgenesis with severe microencephaly, mental retardation, seizures and paucity of myelin, autosomal recessive trait?

Siblings are reported with severe mental retardation, spastic cerebral palsy and seizures; in addition they had progressive or intermittent jaundice and recurrent infections; they died at 3 and 4 years respectively. Neuropathological studies in one showed a small brain with an almost complete lack of myelin in cerebral white matter, brain stem, cerebellum and anterolateral parts of the spinal cord. The condition most likely represents a dysgenesis of myelin (dysmyelination), possibly due to an inability of oligodendrocytes to form myelin and/or metabolic defects in the process of myelination. This mental retardation condition is probably inherited as an autosomal recessive trait and may represent a special type of a primary CNS developmental defect.

Brain↗