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Biomedical subjects

K Wessel

Publications and source records attributed to K Wessel.

At least 73 records · Page 4Linked to original sources
PubMed1993

Follow-up of neurophysiological tests and CT in late-onset cerebellar ataxia and multiple system atrophy.

The follow-up of neurophysiological tests (brain-stem auditory evoked potentials; blink reflex; sensory, motor and visual evoked potentials) and CT was investigated in 21 patients with late-onset cerebellar ataxia (CA) or multiple system atrophy. The study included an initial investigation and a follow-up examination on average 25.3 months later (minimum 8, maximum 36). Patients were divided into four groups: (1) those with pure CA after a minimum course of 5 years; (2) those with pure CA with pathological neurophysiological findings at the last examination; (3) those who at the first examination clinically presented with pure CA, but at the last examination were seen to have developed a multisystem disorder; (4) those with multiple system atrophy (mostly olivopontocerebellar atrophy) presenting additional non-cerebellar signs of involvement. Conforming to a strict interpretation of pure CA, group 1 patients invariably exhibited normal neurophysiological findings at all examinations. All patients in group 4, except for 2 only at the first examination, showed pathological changes in at least one of the neurophysiological tests. The main conclusion of this paper is that individuals who according to clinical criteria were initially classified as having CA but finally developed a multisystem disorder already had pathological neurophysiological findings at the initial examination (group 3). The increasing frequency of pathology in the several neurophysiological tests together with the progression of the disease is obviously of prognostic significance. CT revealed cerebellar atrophy without apparent involvement of brain-stem structures in all patients with CA; the majority of patients with multiple system atrophy also had atrophy of the brain-stem, pointing to olivopontocerebellar atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Long-latency reflexes, somatosensory evoked potentials and transcranial magnetic stimulation: relation of the three methods in multiple sclerosis.

Afferent and efferent central pathways were tested by electrically elicited long-latency reflexes (LLRs), somatosensory evoked potentials (SEPs), and motor potentials (MEPs) evoked by transcranial magnetic stimulation (TMS) in 37 patients with multiple sclerosis. Of these 27 (72.9%) had abnormal results, with bilateral abnormalities in 17 (45.9%). MEPs were abnormal in 21 (56.8%), LLRs in 17 (45.9%) and SEPs in 16 (43.2%). Compared with TMS (MEPs) alone, additional testing of LLRs and SEPs revealed abnormalities in 6 additional patients (2 LLRs, 3 SEPs, 1 LLR and SEP). When the hands were analysed separately 32 (47.3%) showed abnormal results with TMS, 29 (39.2%) with LLRs and 22 (29.7%) with SEPs. All hands with absent or delayed N20 components of the SEP also had abnormal LLRs, supporting the hypothesis that LLRs and SEPs share the same afferent pathways. In contrast to this, 10 hands had normal LLRs but slightly delayed central motor conduction times. Calculating the sum of the latency of the N20 component of the SEP and the latency of the MEP, we found a mean cortical relay time for the LLR of 8.5 +/- 4.7 msec, which is compatible with a polysynaptic transcortical pathway. This is supported by our finding of a linear correlation between the LLR latency and the sum of N20 and MEP latencies.

Electroencephalography↗
PubMed1993

Carotid artery disease in vascular ocular syndromes.

We prospectively investigated 83 consecutive patients with vascular ocular syndromes: 19 suffered from amaurosis fugax attacks, 23 had occlusions of the central retinal artery or a branch retinal artery occlusion, 26 had a central retinal vein occlusion or a branch retinal vein occlusion, and another 15 exhibited an anterior ischemic optic neuropathy. In 5 patients bilateral symptoms occurred; thus a total of 88 eyes were affected. All patients underwent a neurological examination and ultrasound investigations of the carotid arteries, including continuous wave (cw)-Doppler-sonography and duplex ultrasound. Stenosis of more than 50% diameter reduction and occlusion of the internal carotid artery ipsilateral to the symptomatic eye were significantly more frequent in amaurosis fugax attacks and central or branch retinal artery occlusion than in central or branch retinal vein occlusion or anterior ischemic optic neuropathy (p < .025). Additionally, the analysis of plaque surface and echogenicity of the plaques on the affected side with a high-resolution duplex scan uncovered that ulcerated plaque surfaces and plaques with a heterogeneous echogenicity were found significantly more frequent in the internal carotid arteries of patients with amaurosis fugax attacks and central or branch retinal artery occlusions than in patients with anterior ischemic optic neuropathy (p < .04) or central and branch retinal vein occlusion (p < .025). We conclude that amaurosis fugax attacks and central retinal artery or branch retinal artery occlusions are due to arterio-arterial embolization from ulcerated and heterogeneous carotid artery plaques.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Low-tension glaucoma: a comparative study with retinal ischemic syndromes and anterior ischemic optic neuropathy.

In low-tension glaucoma (LTG), nerve-fiber-bundle defects are assumed to result from ischemia of the choroidal branches of the posterior ciliary arteries, due either to local vascular changes or, presumably, hemodynamically occlusive carotid artery disease. To study the possible hemodynamical origin of LTG, we examined and compared, clinically and by ultrasound (continuous-wave Doppler and duplex-scanning), the extracranial carotid arteries of (1) 21 patients (34 eyes) with LTG, (2) 48 patients (49 eyes) with retinal ischemic syndromes (RIS), and (3) 15 patients (17 eyes) with anterior ischemic optic neuropathy (AION). High-grade stenoses and occlusions of the internal carotid arteries ipsilateral to the affected eyes were significantly more frequent in the RIS patients (17 of 49) than in the LTG patients (2 of 34; P < .01) and the AION patients (0 of 17; P < .01). Among our relatively small group of LTG patients, we found no striking evidence supporting a hemodynamic origin of LTG.

Aged↗
PubMed1993

[Unmasking congenital myotonia by hypothyroidism].

A case with the combination of hypothyroidism and true myotonia is reported, in which the latter first became manifest clinically together with the thyroid disorder and improved with L-thyroxine therapy. The hypothyroidism itself caused very few symptoms, and the diagnosis was not made until examination for myotonia. The effect of each disorder on muscle function seems to be additive.

Adult↗
PubMed1992

Selegiline--an overview of its role in the treatment of Parkinson's disease.

Selegiline (10 mg per day) selectively inhibits monoamine oxidase type B and thus thwarts the metabolism of dopamine by this enzyme. Selegiline has been used in the therapy of Parkinson's disease since 1986. It enhances the efficacy of levodopa, allows a reduction of the levodopa dose, and improves fluctuations in disability. It also interacts with mechanisms suspected of playing a role in the progression of the disease. Animal studies have shown that selegiline prevents the development of a Parkinson-like syndrome induced by the neurotoxin MPTP. It decreases oxidative stress resulting from the metabolism of dopamine via MAO-B. Clinical studies have shown that selegiline is effective in the therapy of untreated de novo patients: the progression of symptoms demanding the introduction of levodopa into the therapy was delayed, and the risk of needing levodopa treatment within one year was reduced by 57% with selegiline. The mode of action of this drug in the treatment of early Parkinson's disease is still under discussion. There is strong evidence that selegiline may slow the progression of the disease, but a direct symptomatic effect cannot be excluded.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1992

Different neuroleptics show common dose and time dependent effects in quantitative field potential analysis in freely moving rats.

Under the assumption that field potentials recorded from particular brain areas reflect the net balance of neurotransmitter activities, the dose- and time-dependent responses induced by intraperitoneal application of different neuroleptic drugs are quantified by spectral analysis of the electroencephalogram recorded from frontal cortex, hippocampus, striatum and reticular formation. The actions of haloperidol, chlorpromazine, clozapine, prothipendyl and thioridazine in general were characterized by increases of the spectral power in the alpha 1 and beta range, at higher dosages also in the theta range. This observed pattern of changes is in line with the neuroleptic induced spectral changes reported in the literature for other animals and man. In the light of the already known effects of other psychoactive drugs on the frequency content of field potentials in the rat, it should now be possible to classify different drugs in terms of their clinical indication. With respect to the type of neurotransmitter control underlying the changes produced by various neuroleptics, it is quite obvious from the comparisons with the respective drug effects that dopamine-D1-receptor controlled transmission is not responsible for this action. On the basis of earlier findings a possible interaction between dopamine-D2 receptor or glutamatergic transmitter control is discussed.

Animals↗
PubMed1992

[The importance of neurophysiology and computerized tomography for diagnosis of cerebellar ataxia with late onset].

Twenty patients diagnosed as suffering from autosomal dominant or idiopathic late onset cerebellar ataxia were investigated clinically, by means of neurophysiological tests (blink reflex, BAEP, SEP, MEP, VEP) and CT scan. Twelve patients presented with a pure cerebellar ataxia (CA) after a disease duration of at least five years (mean disease duration ten years). Eight patients presented with additional non-cerebellar signs of involvement; hence the disease was classified as olivo-ponto-cerebellar atrophy (OPCA). Eight of the twelve patients with CA already exhibited pathological results in at least one of the neurophysiological tests as subclinical evidence of a lesion beyond the cerebellum. Three of these patients showed an atrophy of brainstem structures in addition to the cerebellar atrophy. The ongoing prospective follow-up study will show whether these signs of subclinical involvement of non-cerebellar pathways are predictive for the development of a multi-system disorder in terms of OPCA. In cases of CA with subclinical signs of a lesion beyond the cerebellum there may be no clinical, non-cerebellar signs for a multisystem disorder even within a disease duration of up to fifteen years.

Adult↗
PubMed1992

[Neuro-Behçet's syndrome: encephalitis and cerebral venous thrombosis--clinical aspects and neuroradiology of 5 cases].

The value of brain CT-scan, magnetic resonance imaging (MRI) and angiography for diagnosis, differential diagnosis and follow up in Neuro-Behçet-Syndrome is assessed in 5 cases. Three of the patients presented with clinical signs of encephalitis. Further investigations led to the diagnosis of Behçet-Syndrome. CT-scan was negative in two of these cases, but MRI showed multiple, predominantly periventricular lesions with high signal intensity on T2-weighted spin-echo images in all three. Clinical symptoms improved with steroid and chlorambucil therapy in all three cases. In two patients the MRI-lesions resolved at least partially after 1.5 and 3 years of treatment respectively. In one patient the initial MRI-findings were still present after 7 months of treatment. The other two patients presented with headache, papilledema and increased CSF-pressure. The cause was superior sagittal sinus thrombosis, confirmed by angiography in both cases. Additional symptoms appeared later and led to the diagnosis of Behçet syndrome. One patient died of pulmonary aneurysms 28 months after the diagnosis had been established. The course of disease of the remaining patient is so far favorable.

Adult↗
PubMed1991

Transcranial magnetic brain stimulation: lack of oculomotor response.

We have investigated whether eye movements can be evoked by transcranial magnetic brain stimulation (TMS) from frontal, precentral, posterior- and inferior- parietal, occipital and temporal positions of the stimulating coil. Our findings were negative, even for structures concerned with voluntary eye movements, such as the frontal eye field (FEF) and the inferior parietal lobe (IPL). The lack of oculomotor responses after stimulation of the cortex shall be discussed in the following context: (1) Low-threshhold intracortical stimulation experiments suggest that in functional terms, the FEF is confined to small areas which are extend to the floor of sulci. TMS does not reach these structures to a sufficient extent. Furthermore efferent connections of the cortex to the paramedian pontine reticular formation (PPRF) seem to be polysynaptic. (2) The function of the cortex in rapid eye movement is to analyze and process conditions with differing functional requirements, rather than to directly generate saccades. TMS does not elicit oculomotor responses, demonstrating again that the role played by the cortex in eye movement is not analogous to the role of the somatic motor cortex in controlling skeletal movements.

Adult↗
PubMed1991

[Presenile dementia in xeroderma pigmentosum].

Neurological manifestations of xeroderma pigmentosum, a rare autosomal recessive neurocutaneous syndrome, are variable. The association with progressive mental retardation, usually with onset in childhood, is well known. We present a case of x.p. with progressive presenile dementia. This combination has, to our knowledge, not yet been reported in the literature. Although no hints on another aetiology have been found, the coincidental combination of x.p. with M. Alzheimer has to be taken into consideration. CT scan and MRI showed a marked cerebral atrophy.

Atrophy↗
PubMed1990

The ratio of macrophage prostaglandin and leukotriene synthesis is determined by the intracellular free calcium level.

The induction of eicosanoid synthesis in various cell types by different physiological stimuli is dependent on an increase in the intracellular calcium level and stimulation of the protein kinase C (PKC). In a model system this can be mimicked by using calcium ionophores and direct PKC activators. In mouse peritoneal macrophages calcium ionophores induced the formation of prostaglandin E2 (PGE2) and leukotriene C4 (LTC4). A synergistic enhancement of both eicosanoids could be achieved by simultaneous addition of the calcium ionophore A23187 together with a suboptimal dose of the direct protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate (TPA). Low concentrations of the ionophore, resulting in only marginally increased intracellular calcium levels, led to a more than additive prostaglandin E2 production in combination with TPA. Higher concentrations of A23187 together with TPA favoured LTC4 synthesis, whereas PGE2 levels at the same time were even diminished. This observed shift from prostaglandin to leukotriene formation was amplified by simultaneous addition of indomethacin. Manganese as inhibitor of the A23187-induced calcium influx decreased PGE2 synthesis. On the other hand, in the presence of manganese LTC4 production was also inhibited at high concentrations of A23187 but elevated in the absence or at low doses of A23187. Our data provide evidence that in macrophages the ratio of cyclooxygenase and lipoxygenase products caused by mediators, acting via the phospholipase C or D/PKC signal transduction pathway, is regulated by the extent of the intracellular calcium increase.

Animals↗
PubMed1990

Altered arachidonic acid metabolism during differentiation of the human monoblastoid cell line U937.

The human cell line U937 was used as a model for differentiation along the mononuclear phagocyte lineage. Following treatment with the phorbol ester TPA, PGE2 and TxB2 secretion was induced 50-100-fold, and both PGF2 alpha and PGI2 levels became detectable in the supernatant of TPA-differentiated U937 cells. The content of the prostaglandin precursor, arachidonic acid, remained unchanged in the cellular phospholipids of undifferentiated and TPA-differentiated U937 cells. Of the enzymes involved in the availability and metabolism of arachidonic acid, phospholipase A2 activity was increased 2-fold in the membranes of TPA-differentiated U937 cells, whereas lysophosphatide acyltransferase activity remained unaltered. Cyclooxygenase activity, however, was enhanced 5-10-fold, which was due to enhanced expression of the enzyme as demonstrated by dot-blot analysis. The data suggest that the capacity to secrete prostaglandins is acquired during differentiation with TPA and results mainly from an increased cyclooxygenase activity. Despite the capacity of TPA-differentiated U937 cells to synthesize prostaglandins, none of the known monocytic stimuli further stimulated prostaglandin secretion in TPA-differentiated U937 cells. Generation of leukotrienes appears to represent a later state in the differentiation along the monocyte-macrophage lineage, since neither LTB4 nor cysteinyl-leukotrienes were detectable in the supernatants of either undifferentiated or TPA-differentiated U937 cells.

Arachidonic Acid↗
PubMed1990

Human glomerular mesangial cells inactivate leukotriene B4 by reduction into dihydro-leukotriene B4 metabolites.

Due to its potent chemotactic properties leukotriene B4 is an important mediator of inflammatory reactions. Cultured human kidney mesangial cells converted exogenously added leukotriene B4 efficiently into three different more lipophilic metabolites, two of them probably representing dihydro-leukotriene B4 isomers. This represents an alternative metabolic pathway, in contrast to leukotriene B4 omega-oxidation found in human polymorphonuclear leukocytes. Both dihydro-leukotriene B4 isomers had nearly completely lost their ability to induce leukocyte chemotaxis as compared to leukotriene B4.

Cells, Cultured↗
PubMed1990

Monokines and platelet-derived growth factor modulate prostanoid production in growth arrested, human mesangial cells.

Previous studies have demonstrated considerable prostanoid production by cultured proliferating rat mesangial cells (MC). In this study, human mesangial cells (HMC) were examined during serum-free culture in which the cells were reversibly growth arrested and did not suffer obvious irreversible functional changes. Non-stimulated cells released 2 to 10 pg/24 hr/micrograms cellular protein of PGE2, PGF2 alpha, 6-keto-PGF1 alpha, while TXB2 was not detectable. Stimulation with interleukin-1 beta (IL-1 beta) or tumor necrosis factor alpha (TNF alpha) induced up to 18-fold (IL-1 beta) or up to fourfold (TNF alpha) increases of prostanoid release. Combinations of the two monokines resulted in significant synergistic induction of PGE2 and 6-keto-PGF1 alpha up to 38 times that of control cells. Interleukin-6 (IL-6) and the HMC-mitogen, platelet-derived growth factor-BB (PDGF-BB) only induced marginal increases in HMC prostanoid generation. However, when PDGF-BB or -AB was combined with IL-1 beta or IL-6, prostanoid generation by HMC was synergistically increased up to 222-fold (IL-1 beta) or 12-fold (IL-6) above the control values, with the induction of PGE2 greater than 6-keto-PGF1 alpha greater than PGF2 alpha much greater than TXB2. In the case of IL-1 beta + PDGF-BB the induction of PGE2 release was at least partly due to the synergistic induction of cyclooxygenase activity. These findings demonstrate that both proliferating and reversibly growth arrested HMCs release prostaglandins in response to various inflammatory stimulators and combinations thereof. The findings support the important role of HMC in the regulation of glomerular hemodynamics during inflammatory processes.

Cell Division↗
PubMed1990

Inhibition of growth of Chlamydia trachomatis by tumor necrosis factor is accompanied by increased prostaglandin synthesis.

Development of Chlamydia trachomatis (L2/434/Bu) in HEp-2 cells was inhibited by treatment of the cells with recombinant human alpha tumor necrosis factor (TNF). In the infected cultures that were treated with TNF, high concentrations of prostaglandin E2(PGE2) were detected, exceeding by far the concentrations found in TNF-treated but uninfected cells or in infected cells that were not treated with TNF. PGE2 levels increased gradually for 2 days after infection. Raising the tryptophan concentration in the culture medium, which reversed the inhibition of chlamydial replication by TNF, also blocked the increase in PGE2 formation. However, neutralizing antibodies to beta interferon, which also interfered with the antichlamydial effect of TNF, did not decrease PGE2 formation. Excessive formation of PGE2 by cells infected with chlamydiae and treated by TNF might be related to some of the complications associated with chlamydial infection.

Chlamydia trachomatis↗