Biomedical subjects

B Tettenborn

Publications and source records attributed to B Tettenborn.

24 records · Page 2Linked to original sources

PubMed1991

Prophylaxis and acute therapy of arterial embolism with special reference to cerebral embolism.

Prophylaxis and treatment of arterial embolism in high-risk patients includes therapy with antiplatelet drugs, anticoagulation, and vascular surgery. The prominent causes of cerebral ischemia are intraarterial emboli from atheromatous plaques and cardiac emboli. In patients with recent hemispheric transient ischemic attacks or minor stroke and ipsilateral high-grade internal carotid artery stenosis of 70 to 99% carotid endarterectomy has shown to be effective in prevention of major stroke or death. In the majority of patients with moderate atherosclerotic disease of the extracranial arteries as well as in patients with a cardiac source of emboli, no generally excepted therapy for primary and secondary prevention of cerebral ischemia or systemic embolism exists. The efficacy of antiplatelet drugs and anticoagulants in these patients is still investigated in a number of clinical multicenter studies. From the presently available data one can conclude that the antiplatelet agent acetylsalicylic acid in a dosage of 300 mg per day is effective in the secondary prevention of stroke and death in patients with preceding transient ischemic attacks, minor or major stroke and suspected artery-to-artery embolism from mild to moderate atherothrombotic carotid and vertebral artery disease. If there are no contraindications, we recommend anticoagulation in recurrent transient ischemic attacks not responding to antiplatelet drugs, in progressing stroke especially in the vertebrobasilar territory, in transient ischemic attacks in patients with rheumatic atrial fibrillation and left atrium thrombi, in minor stroke and proven cardiac embolism, in cerebral ischemia due to traumatic large vessel disease, and before and following elective cardioversion in patients with long-standing atrial fibrillation. A therapeutic dilemma still exists in patients with nonrheumatic atrial fibrillation; the presently available data are not sufficient to give recommendations whether aspirin or anticoagulants should be given for primary and secondary prevention of stroke and systemic embolism in these patients.

Anticoagulants↗

PubMed1990

Polyneuropathy due to acute arsenic intoxication: biopsy studies.

A 41-year-old vintner attempting suicide ingested 8-9 g of arsenic and developed a symmetric polyneuropathy with acute Wallerian degeneration of myelinated fibers. Under treatment with modified British Anti-Lewisite (BAL; "Dimaval") his polyneuropathy slowly, but incompletely, subsided over three years at which time another sural nerve biopsy specimen showed regenerative proliferation of myelinated and unmyelinated axons but no signs of Wallerian degeneration. By laser microprobe mass analysis (LAMMA) arsenic was located in the first biopsied sural nerve specimen but not in the second specimen. These findings demonstrated: 1) arsenic induced serial morphometric and electron microscopic findings of nerve fiber degeneration and regeneration, 2) documentation of arsenic within myelinated nerve fibers, and 3) the usefulness of the LAMMA technique as a diagnostic procedure in this context.

Acute Disease↗

PubMed1990

Pontine supranuclear facial palsy.

Two patients presented with a unilateral supranuclear facial palsy. Additional dysarthria was attributed to the pontine origin documented by magnetic resonance imaging on the contralateral side. The pontine disorder also was indicated by an isolated delay of the blink reflex R1 component or of the masseter reflex. We attribute the facial palsy to a lesion of a supranuclear fiber bundle supplying the facial nucleus. The location of the lesions favors these fibers taking a separate course from the main pyramidal tract at the mid- to upper pontine level.

Aged↗

PubMed1989

[Petit mal status in hyperthyroidism].

A 68-year-old woman who, for the first time, had a generalized tonic-clonic seizure and persisting confusional state was found to have nodular enlargement of the thyroid and a tachycardic arrhythmia. Electroencephalography (EEG) demonstrated a continuous irregular polyspike wave pattern. Total T4 concentration was elevated to 23 micrograms/dl. Consecutive Administration of 250 mg phenytoin, 4 mg clonazepam and 7.5 mg midazolam changed neither the clinical nor the EEG findings. But after general intensive care measures and high-dose thyrostatic treatment (40 mg thiamazole intravenously every four hours) the clinical and neurological status became normal. Serial EEGs over the subsequent weeks and months showed gradual disappearance of the abnormal changes with increasingly prolonged periods of normal activity.

Aged↗

PubMed1988

Exophthalmos and basilar impression. A contribution to differential diagnosis of endocrine orbitopathy.

We report on a male patient with exophthalmos of unclear etiology, basilar impression, syringohydromyelia and type II Arnold-Chiari malformation. Two diseases involving the orbital region were to be considered in differential diagnostic terms: endocrine orbitopathy and osseous orbit dysplasia. The typical physical appearance associated with basilar impression as well as suppurative keratitis in Lagophthalmos was striking. Tetraspasticity with pareses, bulbar symptoms, proximally pronounced muscular atrophy as well as a left hemihypesthesia was shown neurologically. Although the orbit CT was normal, sonography revealed thickened ocular muscles. There was euthyroidism in diffuse goiter with negative thyroid autoantibody findings. Because of lack of definitive detection of muscular swelling, tumor, or vascular anomaly in the various images, orbital dysplasia in the context of a malformation syndrome affecting several organs is suggested as the cause of the exophthalmos.

Arnold-Chiari Malformation↗

PubMedDate not supplied

Oxcarbazepine does not affect the anticoagulant activity of warfarin.

The possible interaction of the antiepileptic drug oxcarbazepine (OCBZ) on the anticoagulant effect of warfarin was investigated in 10 healthy male volunteers. After reaching steady-state conditions by repeated administration of warfarin, the prothrombin time (Quick value) was assessed before and after single (600 mg) and multiple dosing (450 mg twice daily in 1 week) of OCBZ. In 7 of the 10 volunteers with evaluable data, the prothrombin time was not significantly different (paired t test) from baseline either after single (p = 0.299) or repeated dosing (p = 0.333), indicating that OCBZ does not interact to any relevant extent with the hypothrombinemic effect of warfarin.

Adult↗