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F Stögbauer

Publications and source records attributed to F Stögbauer.

65 records · Page 4Linked to original sources

[Meralgia paresthetica. A rare differential diagnosis of circumscribed alopecia].

HISTORY AND CLINICAL FINDINGS: Two patients with circumscribed alopecia on the lateral aspect of the thigh underwent a neurological investigation after medical and dermatological examinations had failed to establish the cause. Patient 1 also had neuralgia of the genitofemoral nerve after osteotomy of the iliac crest; patient 2 had insulin-dependent diabetes mellitus. Within the affected part of the skin both patients had sensory dysfunctions over the area of distribution of the cutaneous lateral femoral nerve. Patient 2 additionally had sensory dysfunctions in other areas of innervation. INVESTIGATIONS: Neurogram and recordings of sensory evoked potentials revealed decreased amplitudes on the affected side, establishing the diagnosis of meralgia paresthetica. TREATMENT AND COURSE: The painful neuropathy was successfully treated in both patients with carbamazepine (patient 1: 1.600 mg daily; patient 2: 900 mg daily). CONCLUSION: Circumscribed alopecia can be caused by peripheral nerve lesions. It should be considered in the differential diagnosis, particularly as the cause can be easily established.

Adult↗

[Molecular biology and genetics of hereditary motor and sensory neuropathies].

Hereditary neuropathies (HMSN) are among the most common genetic diseases in neurology. Various mutations in different genes are known which lead to the most frequent hereditary neuropathies. These mutations concern proteins of the myelin of the peripheral nervous system, as well as a gap-junction protein expressed in peripheral nerves. The molecular mechanisms leading from gene mutation to disease phenotypes are not fully understood. Nowadays, we are able to use DNA analysis for symptomatic, presymptomatic, and prenatal screening. The latter is of questionable value because of the variability in disease severity and outcome. Deeper insights into the molecular pathophysiology will, however, yield new therapeutic strategies in individual patients.

Connexins↗

A novel technique for identification of doppler microembolic signals based on the coincidence method: in vitro and in vivo evaluation.

BACKGROUND AND PURPOSE: The applicability of a novel differentiation technique in embolus detection based on the coincidence principle and using a multigate probe was evaluated in this study. METHODS: According to the coincidence method, high-intensity transients should only be classified as microembolic signals if they appear sequentially in the two sample volumes monitored and within a defined time window calculated from the blood velocity and the spatial distance between the insonation depths. Part A: microbubbles were introduced in a continuous flow bench model of the middle cerebral artery to evaluate the accuracy of the multigate probe in embolus detection. Part B: in the subjects and patients, the minimal and maximum time delays in the appearance of microembolic signals in the two middle cerebral artery sample volumes were calculated as 0.01 second and set at 0.1 second, respectively. The multigate probe was used to monitor (1) 5 normal volunteers in whom 1008 artifact signals were produced,(2) 2 patients undergoing aortic valve replacement surgery, and (3) 12 patients with potential cardiac or carotid embolic sources. RESULTS: In the bench model, 95.5% of microembolic signals produced by microbubbles appeared in the two sample volumes with a time delay between 0.02 and 0.05 second, while in the remaining 4.5% a shorter passage time of 0.01 second was measured. A total of 1968 high-intensity signals were recorded in subjects and patients. All but 20 of these (99%) appeared in both monitoring channels within the above time frame. To summarize, 996 (98.8%) of the 1004 artifact signals and 943 (98.1%) of the 961 microembolic signals were correctly classified. CONCLUSIONS: Application of the coincidence theory to distinguish microembolic signals from artifacts provides a promising new technique with high sensitivity and specificity that could decisively improve the validity of embolus detection.

Adult↗

Screening of adrenal medullary neuropeptides for putative neurotrophic effects.

Chromaffin granules, the secretory organelles of the neuron-like adrenal medullary chromaffin cells, have previously been shown to store and liberate neurotrophic activities that support in vitro survival of several neuron populations including those innervating the adrenal medulla. Molecules resembling fibroblast growth factor and ciliary neurotrophic factor have been identified among these activities. Since chromaffin granules store a variety of neuropeptides and many neuropeptides can have pleiotropic effects on neuronal growth and maintenance we have tested 24 different neuropeptides for their capacities to promote survival of embryonic chick ciliary, dorsal root and sympathetic ganglionic neurons. Peptides tested included several derivatives of proenkephalin (Leu- and met-enkephalin, fragments BAM 22, B, F and E), somatostatin, substance P, neuropeptide Y, neurotensin, VIP, bombesin, secretin, pancreastatin, dynorphin B, dynorphin 1-13, beta-endorphin, alpha-, beta-, and gamma-MSH. Control cultures received saturating concentrations of ciliary neurotrophic or nerve growth factor (CNTF; NGF), or no trophic supplements. At 1 x 10(-5) M leu- and met-enkephalin as well as somatostatin supported sympathetic neurons to the same extent as NGF. At the same concentrations, leu-enkephalin, the proenkephalin fragments BAM 22 and E, and somatostatin maintained about half of the dorsal root ganglionic neurons supported by NGF, but were not effective on ciliary neurons. VIP promoted the survival of approximately 50% of the ciliary and embryonic day 10 dorsal root ganglionic neurons as compared to saturating amounts of CNTF, but required the presence of non-neuronal cells in the cultures to be effective. Neurotensin (1 x 10(-5) M had a small effect on ciliary neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

Calcium-dependence of chromogranin A-catecholamine interaction.

Major components of the secretory organelle of bovine adrenal medullary cells, the chromaffin vesicles, are the acidic protein chromogranin A, catecholamines and Ca2+. The binding of Ca2+ to chromogranin A has been established. To study the interaction between chromogranin A and catecholamines and its dependence on Ca2+ we immobilized chromogranin A to a newly raised monoclonal antibody. It is shown that chromogranin A can bind (i) about 0.5 mol catecholamines per mol in a non-calcium-dependent manner and (ii) about 5 mol per mol in the presence of calcium. These results further support the notion that chromogranin A may act as a secretory granule-condensing protein.

Adrenal Medulla↗

Lumbar spinal neurinoma presenting with nocturnal pain. A case report.

Neurinomas are the most common intradural extramedullary tumors of the spine. Together with meningeoma they account for 80% to 90% of all tumors in this compartment. Radicular pain is the initial symptom in the majority of cases while motor disorders are less common and occur later in the course of the disease. We report a patient with spinal neurinoma and calf pain as the only presenting complaint. The differential diagnosis in this case required an interdisciplinary approach.

Aged↗

[Molecular genetics of hereditary neuropathies].

INTRODUCTION: Significant progress in the understanding of the molecular genetics and pathophysiology of inherited neuropathies has been achieved during the last years. DEVELOPMENT: The causative genetic defects of most of the demyelinating forms are known and different chromosomal loci have been identified for the rarer axonal forms. Mutations in genes encoding the myelin proteins peripheral myelin protein 22, myelin protein zero and connection 32 are associated with hereditary motor and sensory neuropathy type I and II and hereditary neuropathy with liability to pressure palsies. Transgenic animals have been generated allowing new insights in the pathophysiology of the diseases. CONCLUSION: The understanding of the cellular mechanisms leading to hereditary neuropathies will contribute to the development of effective therapeutic strategies.

Genotype↗