In a series of 2,353 multiple sclerosis (MS) patients, 40 subjects presented seizures, with an overall prevalence of 1.70%. The prevalence was 2.33% (34/1,459) in definite MS cases, 0.58 in probable cases (3/518), 0.79 in possible cases (3/376). Twenty-six patients were females, 14 were males. In 13 cases, epilepsy had begun before MS onset; in 4 patients, the two diseases started contemporarily; in 23 patients, epilepsy followed MS onset. No relationship was found between frequency of seizures and course of MS nor between frequency of seizures and MS severity. In 12 patients, magnetic resonance imaging was performed: plaques adjacent to the cerebral cortex were found in 3 cases. The electroencephalogram showed paroxysmal discharges in 11 patients (focal in 2, diffuse in 9). Slow theta and/or delta activity was found in 15 patients (focal in 7, diffuse in 6, both focal and diffuse in 2). The EEG was normal in 14 patients. Possible etiological factors other than MS were recognized in 4 patients only: cranial trauma in 3, meningitis in 1. Our study on a large MS population confirms that MS is associated to a risk for epilepsy higher than that of the general population.
Many inheritance models of schizophrenia have been proposed, in view of its variable age at onset, variable familial occurrence and the relevant influence of a great number of environmental factors (Gottsman and Shields, 1967; Heston, 1970; Ödegård, 1972). However, the real genetic predisposition to schizophrenia has not yet been experimentally verified, and genetic markers have to be looked for, i.e. we need some character, genetically determined, whose transmission is associated with schizophrenia transmission: the more polymorphous the character, the greater will be the probability of finding such associations.
A group of 33 schizophrenic patients were typed for HLA-SD antigens and their qualitative clinical responses to chlorpromazine therapy determined. A highly significant positive correlation was found between response to chlorpromazine and HLA-AI positive, while HLA-A2 positive subjects showed a significant negative correlation to chlorpromazine treatment. In a second group of 17 patients the clinical response to chlorpromazine were evaluated quantitatively, by WPRS, in HLA-AI positive and HLA-AI negative patients. There were no pre-treatment differences in the scores. After treatment the scores of positive patients were significantly lower, indicating that they responded to a greater degree. Since the frequency of HLA-AI in hebephrenic patients is higher than that in other schizophrenics this may explain our earlier finding that hebephrenics, as a group, respond better to chlorpromazine than do other schizophrenics.
Tryptophan has attracted attention during recent years for the possible role played by some of its metabolites in the aetiology and treatment of psychiatric disorders. Of these metabolites, serotonin has received special attention and considerable work has been carried out in order to elucidate its physiological and pharmacological actions. Studies from animal experiments are thus available on the function of serotonin in nervous activity (Marrazzi and Hart, 1955; Brodie et al., 1955; Pletscher et al., 1956; Welsh, 1957), but the results obtained thus far in psychiatric patients are uncertain. Recent researches in the affective psychoses (Burgermeister et al., 1963) did not reveal significant differences between patients and normal controls in the urinary output of 5-hydroxyindoleacetic acid (5-HIAA) before or after an oral 5-hydroxytryptophan load.
Twenty-two patients with the Lennox-Gastaut syndrome and their families were examined for HL-A antigens by the microlymphocytotoxicity test. The antigen HL-A7 belonging to the HL-A locus showed a significantly increased frequency (p less than 0.0005) both in parents and in patients. The same antigen showed a significantly altered segregation in patients but a normal one in healthy siblings. Another antigen of the second HL-A locus, HL-A12, did not display a normal segregation in our patients, in whom it was nearly not represented.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.