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Biomedical subjects

G Reichel

Publications and source records attributed to G Reichel.

At least 19 recordsLinked to original sources

[The inhalation 1 concentration test for the assessment of bronchial reactivity].

An unspecific bronchial provocation challenge with a 1-concentration test is a reliable method to distinguish between normal and hyperreactive persons. The patient inhales a bronchoconstricting substance such as methacholine. A significant change of lung function, for example an increase of airway resistance, characterizes a hyperreactive bronchial system. The continuous registration of transcutaneous oxygen pressure is helpful concerning a strong reaction or a peripheral airway obstruction. An exaggerated increase of airway resistance after provocation test can be treated rapidly by inhalation of sympathicomimetics. No complications were registered. Comparative studies showed a good reproducibility of this method. Summarizing, the 1-concentration test is simple, easy to perform and suitable especially for investigations in occupational medicine or epidemiology.

Airway Resistance

[Changes in the pleura of subjects occupationally-exposed to asbestos: radiological study technique, spectrum, etiological classification and coding according to the ILO classification].

Pleural abnormalities of 119 occupationally asbestos-exposed with prominent internal stripe of the lateral thoracic wall were radiodiagnostically analysed by plain films of the thorax in four views and by computed tomography in the course of medical expert's certification. Abnormalities were coded according to 1980 ILO international classification of pneumoconioses. Hardly half of the patients had pleural abnormalities caused by asbestos exposure: Pleural plaques, "diffuse" pleural fibrosis, pleural effusions, organized pleural effusions and pleural tumors. The other half of the patients had pleural involvement of pulmonary and chest wall abnormalities or variations of the lateral thoracic wall not related to asbestos exposure. The 1980 ILO classification of pneumoconioses proved to be inadequate for complete coding of the abnormalities, since only the postero-anterior plain film of the thorax must be used, since the normal appearance of the pleura is insufficiently defined and since the entity of organized pleural effusion is lacking.

Asbestosis

[Asbestos-induced bronchopulmonary diseases].

Asbestos is a collective term for fibrous crystalline silicate minerals, which can be used to produce technically useful fibers. The various types of asbestos, such as chrysotile, crocidolite and amosite, may induce not only fibrotic changes in the pleura and lungs, but also carcinomas and mesotheliomas. The increasing industrial use of asbestos has led to a marked increase in bronchopulmonary diseases, which can be shown to be caused by occupational exposure to fine asbestos dust. In this overview, the pathological anatomy, differential diagnosis and occupational-medical assessment of the various conditions induced by asbestos are discussed.

Asbestos

[Piriformis syndrome. A contribution to the differential diagnosis of lumbago and coccygodynia].

The piriformis syndrome is characterized by pain in the buttock radiating to the leg and to the coccydeal region. It is an isthmus syndrome of the N. ischiadicus and/or N. cutaneous femoris posterior. The most frequent causes are blunt traumas of the buttocks and spasms of the N. piriformis. More often than not the piriformis syndrome is the cause of a "postlaminectomy syndrome" or of a coccygodynia. The diagnosis can be established by a clinical examination with sufficient reliability.

Back Pain

36 months continuous subcutaneous insulin infusion (CSII) in insulin dependent diabetes (IDDM)--influence on early stages of retinopathy, nephropathy and neuropathy--psychological analysis.

UNLABELLED: In extremely unstable (brittle) IDDM patients (n = 11) the metabolic effect of long-term (36 months) CSII proved to be superior to conventional insulin treatment (CIT) (statistical twins, n = 11): HbA1 = 8.6 +/- 0.3 versus 10.4 +/- 0.4, MBG = 5.6 +/- 0.3 versus 8.5 +/- 0.8, M (80)- value = 23.6 +/- 0.6 versus 56.7 +/- 10.2, GCI) = 37.3 +/- 15.6 versus 132 +/- 24.2. In addition, in CSII patients the metabolic control was significantly better than intensified conventional insulin treatment (ICT) before. Retinal morphology improved under CSII in 1 eye, did not change in 10 eyes and deteriorated in 11 eyes. Under CIT retinal findings improved in none, did not change in 16 and deteriorated in 16 eyes. Deteriorations under CSII appeared more frequently during the first than during the second and third year of treatment and seemed to be a consequence of too strict metabolic control and/or too fast decrease of the glycemia at the beginning of CSII. During 36 months of CSII no deterioration but in one case normalization of microproteinuria was observed. Under CIT three cases changed from normal into microproteinuria. Reduced motor nerve conduction velocity (MCV) and/or sensory nerve conduction velocity (SCV) could be normalized in most cases under CSII, but respiratory heart arrhythmia (RHA) at rest could not. Most patients--if highly motivated before starting CSII--remained positively motivated for long-term pump therapy. IN CONCLUSION: Our experiences over three years demonstrate a positive effect of CSII on the metabolism as well as on the course of early stages of microangiopathy and neuropathy. A longer period of observations will be necessary to evaluate this, conclusively.

Adult

[Autonomic symptoms in diabetic polyneuropathies].

200 years have gone by since the autonomic disturbance in diabetes mellitus has been described for the first time ever. There is a great deal of information on the close relationship between somatic and visceral symptoms in diabetic polyneuropathy (PNP), so that there should be talked about only of one form of manifestations within the meaning of a distal symmetric somatovisceral PNP. The longer fibres such as the vagal fibres of the viscus, sympathetic fibres of the eye are affected at first and more intensively in the autonomic region same as in the sensory and motor region. Due to the fact that for reasons of fragmentary knowledge pathogenetically substantiated classification of the autonomic disturbances in diabetic PNP is not at hand, such a classification is being made from organotopic and phenomenologic aspects. Frequently, afferent denervation of an organ results in enhancing the effects of an autonomic innervation dysfunction, as for instance in unnoticed hypoglycaemia, in order to modify the symptoms, as for instance in rectal incontinence with unnoticed defecation, or rather to let new symptoms appear, for instance loss of testicular pain. In recent years, appropriate methods of examinations were tested for the clinical routine, permitting to give evidence of autonomic dysfunctions before clinical manifestation. It is still unclear to what extent such subclinical abnormalities are reversible with a more favourable regulation of the metabolic process, for instance with the aid of continuous subcutaneous insulin injections. An impressive symptom of innervation dysfunctions of the cardiovascular system is orthostatic hypertension that may, in exceptional cases, even lead to confinement to bed. The most important pathogenic factor seems to be vascular denervation. A pronounced tachycardia at rest, frequently found in diabetics, is the result of the failure of the vagal autonomic system, and, after additional destruction of the sympathetic fibres, it adjusts itself to a lower level that cannot be changed by reflex mechanisms. Cardialgia absent in the case of myocardial ischemia is a factor of an increased mortality of long-term diabetics. The correlation between vascular denervation and arteriosclerosis or mediasclerosis, respectively, is being under discussion. Denervation on the gastrointestinal tract has an effect on the motility and excretory functions. The innvervation dysfunctions lead to sialadenosis by changing the composition of saliva. In most cases esophageal dysfunction is not perceived by the patient.(ABSTRACT TRUNCATED AT 400 WORDS)

Autonomic Nervous System Diseases

[Sweat glands in pseudohypoaldosteronism].

Pseudohypoaldosteronism is a rare syndrome occurring during early infancy, which is mainly characterized by salt-depletion crises. Sodium chloride is lost via the kidneys resulting in a reduced sodium level and raised potassium level in the serum, leading to life-threatening disturbances of water and acid-base concentration. The excessive sodium loss seems to be caused by an unresponsiveness of the renal tubules to endogenous and exogenous mineralocorticoids. The colon, salivary and sweat glands, which are also involved in sodium reabsorption, may likewise be affected by the disease. We describe skin changes in two siblings suffering from pseudohypoaldosteronism, who developed seborrheic dermatitis, folliculitis or miliaria rubra-like lesions during salt-depletion crises. Biochemical analysis revealed a highly increased sodium-chloride concentration in the sweat, saliva, urine and stool of both patients. Destructive inflammatory reactions could be demonstrated histologically within and around the dermal sweat glands, thus indicating the important role of the sweat system in the pathogenesis of skin lesions in pseudohypoaldosteronism.

Child, Preschool

[Polyneuropathy and residual insulin secretion in diabetes mellitus type I].

In 145 patients suffering from type-I-diabetes with or without signs or symptoms of polyneuropathy basal and glucose-glucagon-induced secretion of insulin was determined. Patients without remaining insulin secretion exhibited somewhat more often polyneuropathies, slowing of nerve conduction, or reduced respiratory heart arrhythmia. If diabetes lasts for more than 10 years, insulin secretion ist reduced to such a low level that its may not have any significant preventive capability with respect to polyneuropathy.

Blood Glucose

[Diabetic polyneuropathy. 4. Synopsis of electroneurographic findings in diabetics].

Sensory conduction velocity of the median nerve, motor conduction velocity of both median and tibial nerves, and corresponding distal laterncies are sufficient parameters to establish the diagnosis of polyneuropathy almost with certainty. Considering these six parameters yielded in detection of peripheral nerve dysfunction in 22% of diabetic patients who were free from clinical signs of polyneuropathy. Electroneurographical findings in 340 out of 677 patients with diabetes mellitus were interpreted as evidence of segmental demyelination. Within this group there was the majority of patients with clinical signs of polyneuropathy and with subclinical signs of peripheral nerve dysfunction. There existed a positive correlation between signs of nerve dysfunction with angiopathy, age and duration of the disease. A second group consisting of 243 diabetics with signs of incipient segmental demyelination with or without signs of axonaal degeneration mainly included juvenile patients with a short duration of the disease and with a low frequency of angiopathy.

Adolescent

[Method for studying spinal evoked potentials].

The authors describe a new method of examing evoked spinal potentials. Derivation is by means of unipolar needle electrodes which are ventrolaterally introduced into the cervical disk space as far as the posterior longitudinal ligament. Detection of a spinal potential following the stimulation of brachial and crural nerves allows to exclude the possibility of complete transverse lesion of the spinal cord or severing of the peripheral nerve or plexus.

Brachial Plexus

[The diabetic polyneuropathy. I. Relation between impaired function in peripheral nerves and clinical findings].

789 patients with diabetes mellitus were studied by clinical and electroneurographical investigation. Motor and sensory conduction velocities of the median nerve and motor conduction velocity of the tibial nerve were determined. 86.1% of the patients suffered from juvenile diabetes, and 13.9% from maturity onset diabetes. Average duration of the disease was 9.5 years, average age of the patients was 26.7 years. Clinical signs of polyneuropathy were found in 19.1%. In 40.9% of the patients at least one of 3 conduction velocities was found to be delayed. Patients with clinical signs of polyneuropathy exhibited delayed nerve conduction velocities and delayed distal latencies. Diagnosis of polyneuropathy almost with certainty is possible by determining the three nerve conduction velocities and the three corresponding distal latencies. 22% of patients without clinical signs of polyneuropathy exhibited electroneurographical signs of impaired peripheral nerve function. Heredity, body weight, lipid metabolism, actual metabolic balance, and treatment were found to be without any significant influence on nerve conduction velocity.

Adult