Immune complexes and complement components in Bell's palsy

The serum levels of circulating immune complexes were studied in 63 patients and the complement system in 36 patients with Bell's palsy. The IgG-C1q and IgG-C3 containing immune complexes were analyzed by an enzyme-linked immunosorbent assay. The levels were found to be significantly elevated in the acute and convalescent stages of the palsy compared with controls. The total complement activity as determined by a CH50 assay and complement component C3 titrations also showed elevated values. The levels of C2 were not altered. The results indicate in Bell's palsy an inflammatory process and an antigen-antibody response which may be triggered by a viral antigen.     

Assessment of Langerhans' cells in oral lichen planus using monoclonal antibodies

In order to demonstrate Langerhans' cells in epithelium of oral lichen planus, monoclonal antibodies were used as immunological markers in combination with immunohistochemistry. By the use of anti-Ia antibodies the Langerhans' cells were shown to express an increased number of Ia-like antigens in comparison to the amounts found in healthy oral mucosa. The subepithelial infiltrate of mononuclear cells expressed identical Ia-like antigens on their surfaces. With anti-T6 antibodies as immunological markers, the number of Langerhans' cells was found to be virtually identical in diseased and healthy epithelium. Treatment of oral lichen planus with tretinoin resulted in a decrease of epithelial Ia-like antigens compared with the number found in untreated lesions. However, treatment with tretinoin did not alter the frequency of Langerhans' cell marked with anti-T6 antibodies. The present data demonstrate an increased amount of la-like antigens per number of T6-positive Langerhans' cells in diseased oral mucosa compared to healthy conditions. The increased expression of Ia-like antigens on Langerhans' cells and the contemporary finding of Ia-like antigens on the subepithelial T-cells support the opinion that the pathogenesis of oral lichen planus is mainly a cell-mediated type of immunological reaction.     

Effects of GM1 ganglioside on developing and mature serotonin and noradrenaline neurons lesioned by selective neurotoxins

The effect of exogenous GM1 ganglioside on selective neurotoxin-induced lesions of serotonin (5-HT) and noradrenaline (NA) neurons in both the central and peripheral nervous systems has been investigated in developing and adult rats and mice by employing neuro- and histochemical techniques. 5,7-Dihydroxytryptamine (5,7-HT) was used to lesion 5-HT neurons, and 6-hydroxydopamine (6-OH-DA) was used to lesion NA neurons. In most lesion models investigated the neurotoxin causes primarily an axonal nerve terminal damage without notably affecting the perikarya. There was no evidence indicating that GM1 interferes with the primary and direct neurodegenerative actions of 5,7-HT or 6-OH-DA on 5-HT and NA nerve terminals, respectively. In all lesion models GM1 had in the chronic stage a counteracting effect on the neurotoxin-induced nerve terminal lesion or enhanced regrowth. The present results are compatible with the view that GM1 has a regrowth-stimulating effect and/or protective actions against secondary retrograde degeneration following the initial nerve terminal lesion induced by the neurotoxin.     

Abnormalities in the orienting response in senile dementia

Forty-five female patients with the diagnosis of senile dementia and subdivided according to degree of mental deterioration were paged over a loudspeaker placed directly to the right or to the left of the patient. In the most demented subgroup, motor and/or verbal orienting responses often failed to appear. A turn towards the loudspeaker used was more often evoked in the least deteriorated subgroups. Turing in inadequate directions is tentatively explained in terms of dysfunctions within the auditory system and with reference to the disorientation of the patients. Twenty of the senile dementia patients were also compared with 20 healthy aged persons concerning habituation of orienting responses when exposed to 15 stimulations with intermittent light. The demented patients did not habituate significantly whereas control subjects did. The defective habituation of the patients is tentatively explained in terms of their memory disturbances and low capacity to interpret sensory data.