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Biomedical subjects

K W Pflughaupt

Publications and source records attributed to K W Pflughaupt.

At least 19 recordsLinked to original sources
PubMed1989

Meningoradiculitis and encephalomyelitis due to Borrelia burgdorferi: a follow-up study of 72 patients over 27 years.

In 1987, follow-up studies were conducted on 72 patients who had had meningoradiculitis and encephalomyelitis (8 patients) due to Borrelia burgdorferi 5-27 years previously. These patients had not been treated with antibiotics, either during the acute disease or during the interval prior to follow-up studies. The patients had exhibited the typical symptoms of Bannwarth's syndrome during the acute phase. At the follow-up studies, 33 patients showed no, and 23 only mild, clinical residual symptoms including normal CSF findings and low-positive serum IgG borrelia antibody titres (IFT; ELISA). Three patients without sequelae exhibited persistent intrathecal secretion of oligoclonal B. burgdorferi-specific CSF IgG antibodies (Immunoblot; positive borrelia CSF IgG antibody titres). Thirteen patients exhibited mild-to-medium sequelae with persistent intrathecal formation of oligoclonal B. burgdorferi-specific CSF IgG antibodies, up to 21 years after the acute illness. This persistence can be interpreted as an "immunological scar syndrome". Our follow-up studies appear to indicate that neurological manifestations of B. burgdorferi infections are generally (with few exceptions) of a benign nature. Most patients can be classified as having been cured without antibiotic therapy. No late manifestations of chronic progressive CNS borreliosis comparable to that of neurosyphilis have been seen following acute untreated neuroborreliosis.

Adolescent↗
PubMed1983

[Seizure prevention using carbamazepine following severe brain injuries].

In this article the efficacy of carbamazepine for seizure prophylaxis in severe head injuries is tested. In addition, conditions with high risk of seizures requiring prophylactic regimen, were defined. One hundred and thirty-nine patients above 15 years of age with severe head injuries were included in the study. They were randomly divided into two groups--carbamazepine versus placebo. Prophylaxis was started immediately after the accident and was continued for one and a half to two years. Carbamazepine dosage was adjusted individually to provide serum levels within therapeutic range. In case of a seizure all the necessary clinical management was initiated. Patients on carbamazepine showed a lower probability of post-traumatic seizures than those on placebo (p less than 0.05). This difference was statistically significant with regard to early seizures within the first week and with regard to the follow-up time in total, but not regarding late seizures per se. Brain lesions with a high risk of post-traumatic seizures were situated in the parietal and temporal areas and included acute subdural haematomas in all locations, temporal lobe contusions, parietal epidural haematomas accompanied by other lesions and the deep stages of coma. Brain stem contusions were accompanied by a rather low probability of seizures. The above mentioned types and locations of brain lesions with the exception of brain stem contusions justify antiepileptic prophylaxis. The regimen consists of oral carbamazepine 100 mg three times daily by gastric tube during the first two days increasing to about 200 mg three times daily on the third day corresponding to the serum level. If oral medication is not possible within the initial twelve hours, phenytoin in a dose of 750 mg Phenhydan-Infusion Konzentrate is given on the first day, followed by an intravenous dose of 250-500 mg on the second day or until oral carbamazepine administration is tolerated. Treatment should be continued for one year.

Brain Concussion↗
PubMed1981

A simplified radioimmunological method for the determination of human beta-endorphin in cerebrospinal fluid.

Human beta-endorphin-like immunoreactive substances (beta h-EI) in human cerebrospinal fluid (CSF) were determined radioimmunologically. The cross reactivity of the antibodies to human beta-endorphin (beta h-E) amounted to 40% for human beta-lipotropin (beta h-LPH) whilst it was less than 1% for leu- and metenkephalin, alpha- and gamma-endorphin, fraction I and II [5], substance P and alpha-MSH. Prior to radioimmunological determination, an adsorbtion of beta h-EI from CSF with silicic acid was carried out and followed by a desorbtion, using a mixture of aceton/hydrochloric acid. This method was chosen because of the ratio of beta h-LPH to beta h-E in the desorbate can be shifted in favour of beta h-E owing to the variation in recoveries r (r beta h-LPH = 33%, r beta h-E = 64%). On the one hand, this enables a more specific determination of beta h-E and, on the other hand, and separation of any peptidase than may be present [9]. An adsorbtion/desorbtion of 2 ml CSF surfaces to prove the presence of 20-150 pg/ml (65-48 fmol/ml) of beta h-EI. The CSF of 28 patients with various neurological diseases was examined and 24 of them had concentrations of 20-70 pg/ml beta h-EI. The remaining four which had concentrations less than 20 pg/ml, came from meningitis patients undergoing corticoid therapy. A purchasable RIA kid was tested for its determination of beta h-E and was found to be unsuitable.

Antibody Specificity↗
PubMed1981

Demonstration of oligoclonal immunoglobulin G in Guillain-Barré syndrome and lymphocytic meningoradiculitis by isoelectric focusing.

Isoelectric focusing (IEF) of serum and CSF revealed oligoclonal IgG in 13 out of 16 patients with the Guillain-Barré syndrome (GBS), in 10 of them in serum only and in 3 in serum and CSF. Seventeen out of 19 patients with lymphocytic meningoradiculitis (LMR) showed oligoclonal IgG, 12 of them in CSF only. These findings, together with additional results, mean that in GBS oligoclonal IgG is synthesized mainly outside the CNS and in LMR within the CNS. Follow-up studies revealed changes in the oligoclonal IgG during the course of GBS and LMR. After treatment by plasma exchange the disappearance of oligoclonal IgG bands was followed by an improvement of GBS symptoms. The oligoclonal IgG bands returned in correlation with worsening of the disease. We were not able to elucidate the antibody character of oligoclonal IgG in GBS or LMR. No antibodies against the myelin basic protein (fragment 89-169) were detectable in the sera and CSF in any of the patients tested.

Adolescent↗
PubMed1981

Thyroid function and circulating antithyroid antibodies in myasthenia gravis.

Evaluation of thyroid function in 104 patients with myasthenia gravis by T3, T4, TBG, and TSH radioimmunoassays and the TRH-stimulation test in 47 patients disclosed thyrotoxicosis in 5.7%, preclinical hyperthyroidism probably due to autonomously functioning thyroid tissue in about 10% of patients stimulated with TRH, hypothyroidism in 1.9%, and preclinical hypothyroidism in 3.4%. Eighty-four percent were euthyroid. Antithyroid antibody activity was detected by hemagglutination tests. Twelve patients had antithyroglobulin antibodies (Tab), and 28 had antimicrosomal antibodies (Mab). Among the euthyroid myasthenic patients, 7 were Tab-positive and 20 were Mab-positive. Euthyroid antibody-positive patients had a significantly higher TSH response in the TRH stimulation test and may be at high risk for hypothyroidism.

Adolescent↗
PubMed1981

[T3, T4, TSH and circulating antithyroglobulin antibodies in myasthenia gravis].

Myasthenia gravis (MG) is a rare neuromuscular disease which is known to be associated with hyperthyroidism at high frequency (3-10%). These investigations, however, are basing on studies of the basal metabolic rate, protein bound iodine (PBI) and the thyroidal radioiodine uptake. In our study (104 MG patients, 104 control subjects) we wanted to evaluate thyroid function on the basis of T3, T4, TBG and TSH radioimmunoassays and in addition we looked for the presence of circulating antithyroglobulin antibodies (Tab) and antimicrosomal antibodies (Mab). The following thyroidal states were disclosed: Thyrotoxicosis (5.8%), hypothyroidism (1.9%), preclinical hypothyroidism (3.8%) and euthyroidism (88.5%). Twenty-eight myasthenic patients were Mab-positive and twelve in addition Tab-positive. Comparing the twenty euthyroid antibody-positive MG-patients with euthyroid antibody-negatives no statistically significant differences were found in thyroid function parameters. It is discussed that part of the thyroid antibody-positive patients may have a symptomless autoimmune thyroiditis which is finally resulting in hypothyroidism via a preclinical hypothyroid status.

Adolescent↗
PubMed1980

Thyroid function in multiple sclerosis.

Thyroid function was studied in 112 MS patients and 175 controls on the basis of T3, T4, T.B.G. and T.S.H. radioimmunoassays. In 33 MS patients with T.R.H. stimulation test was employed additionally. The MS patients had significantly increased T4 levels whereas T3 and T.S.H. were found to be significantly lower. No differences were found in the T.R.H.- stimulated T.S.H. response. The changes in thyroid function parameters were similar in different courses of MS and did not correlate with the degree of clinical disability. The results suggest that in MS the T4/T3 conversion might be reduced as seen in acute or chronic diseases. X

Adolescent↗
PubMed1979

Effect of furosemide (lasix) on acute severe experimental cerebral edema.

The effect of furosemide (Lasix) therapy on a standardized experimental cerebral edema, induced in rats by applying a cooling stamp to the right side of the skull over the right coronal suture by means of a stereotactic instrument, was examined. The hemispherically separated water and electrolyte contents of the brain were analyzed after 24 h. Following furosemide therapy, the behavior of these edema parameters was compared statistically with dexamethasone, glycerol and albumin. An increase of the water and sodium content, and a decrease of potassium was observed 24 h after the trauma, especially in the right hemisphere. Furosemide did not improve either the water content or the electrolyte balance. By contrast, the administration of dexamethasone, glycerol and albumin was followed by a significant improvement of the edema. In experiments with cats, the course of the edema and the effect of furosemide on the cold brain injury of the right hemisphere were observed by measuring the intracranial pressure (ICP) values, and by continuous monitoring of the EEG. The ventricular CSF pressure and epidural pressures were also recorded. The electrical brain activity was continuously compared with the course of the ICP by means of computer analysis. In addition, the blood osmolality and diuresis were monitored. The ICP increased rapidly after the trauma, establishing considerable pressure gradients, and the EEG power intensities decreased markedly on the right side. Histologically, there was an extended edema of the white matter of both hemispheres. The ICP was not lowered by single injections or high dose infusions of furosemide, and the EEG power intensities also did not improve. Infusions of large volumes of furosemide even resulted in an increase of ICP, but infusion of 40% sorbitol effected a rapid decrease of ICP and EEG recovery over the left hemisphere. Sorbitol infusion also caused a marked rise in the blood osmolality, whereas furosemide had no such effect. The results raise considerable doubts as to the propriety of the exclusive use of furosemide for cases of acute cerebral edema with raised ICP. The diuretic effect is insufficient to establish an osmotic gradient, and its general dehydrating effect does not acutely influence the ICP. The absence of effect on the experimental tissue edema would not appear to commend furosemide as basic therapy for cases of traumatic cerebral edema.

Albumins↗
PubMed1979

Comparison of the effects of surgical decompression and resection of local edema in the therapy of experimental brain trauma. Investigation of ICP, EEG and cerebral metabolism in cats.

The effect of decompressive trepanation was compared to that of surgical resection of the traumatized tissue in the course of traumatic brain edema in standardized experimental brain trauma. Following a right parietal cold injury, the following parameters were monitored continuously in 12 cats: ventricular pressure, epidural pressure over both hemispheres, arterial and central venous pressure and heart rate. The EEG was evaluated continuously, using a computer (power spectra). After catheterization of the superior sagittal sinus, cerebral arteriovenous differences of glucose, lactate, O2 and CO2 were calculated. 6 animals were treated surgically when showing elevated intracranial pressure ICP and markedly altered EEG. In 3 animals, the right hemisphere was decompressed by extensive resection of bone and dura. In 3 further animals, the softened brain tissue of the cold lesion was resected and the skull defect closed. 6 untreated animals were used in controls. A decompression by skull hemiresection for ablation of the injured cortex abolished the high intracranial pressure, but only the latter method seemed to prevent further damage. This could be demonstrated by the EEG registration, and by the normalization of arteriovenous metabolite differences. Only animals treated with edema resection had a normal arousal reaction and survived the trauma. The results indicate, that only an ablation of the local injury will prevent further damage to the brain. After decompressive trepanation alone, the progression of tissue edema is not interrupted. As can be seen from the literature, the poor results obtained even from extensive decompressive operations in traumatic brain edema, indicate that the further development of edema is independent of the intracranial pressure, whereas the favorable results of resection of lobar contusions show an interruption of the spread of dysbolism.

Animals↗
PubMed1975

Tryptophan metabolism in nervous disease.

The paper describes effects of tryptophan loading on tryptophan metabolism in healthy persons as well as alterations of tryptophan metabolism observed in varians diseases associated with nervous symptoms, i.e. Wilson's disease, Hartnup disease, phenylketonuria and acute intermittent porphyria. The results are discussed.

Acute Disease↗