[Acute polyneuropathy combined with myasthenic syndrome].
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Biomedical subjects
Publications and source records attributed to J Vardi.
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Dopamine-Beta-Hydroxylase (D.B.H.)-activity was measured in the plasma of untreated Parkinsonian patients, after tretment with L-dopa and 2-Bromo-alpha-ergocriptine. The findings were compared to the D.B.H.-activity of a matched healthy control group. After L-dopa loading D.B.H.-activity decreased in the Parkinsonian patients by 27.6 +/- 3.1% compared to 16.2 +/- 3.3% (p less than 0.02) in the control group. After 2-Bromo-alpha-ergocriptine laoding the decrease in D.B.H.-activity was 32.6 +/- 4.4% in the parkinsonian patients, and 158 +/- 4.9% (p less than 0.02) in the control group. This reduced D.H.B.-activity after L-dopa loading may reflect an impairment, in the Parkinsonian patients' ability to metaoblize L-dopa. The reduced D.B.H.-activity after treatment with 2-Bromo-alpha-ergocriptine may be explained by a pronounced antagonistic influence of 2-Bromo-alpha-ergocriptine on the presynaptic dopamine receptors, suggesting that presynaptic dopaminergic receptors are involved in Parkinson's disease.
The nocturnal sleep patterns of six Parkinsonian patients treated with Bromocryptine (2-Br-L-ergocryptine CB-154), a dopamine-like agonist, were compared with those of the same patients under L-DOPA treatment. No significant differences were found between the two groups. It is suggested that Bromocryptine, acting on dopamine receptors in the sleep regulating systems at the reticular level in the midbrain has the same effect on sleep patterns of Parkinsonian patients as L-DOPA.
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Six patients with Parkinson's disease developed nocturnal myoclonic attacks after prolongued treatment with L-Dopa which were electroencephalographically recorded. These symptoms persisted after treatment with 2 bromo-alpha-ergocryptin (Bromocryptin), a dopamine receptor agonist, which was substituted for L-Dopa. Bromocryptin is known to have no pre- or postsynaptic effect on serotonin metabolism. It is proposed that these myoclonic phenomena are the expression of the hypersensitivity of denervated catecholamine receptors in the brainstem to the stimulation of L-Dopa and Bromocryptin. This thesis differs with previous suggestions that serotonin plays a major role in the genesis of myoclonic seizures in Parkinsonian patients treated with L-Dopa.
A 33 year old male, suffering from Kleine-Levine syndrome associated with periods of apnea during the hypersomnic attacks, is reported. Ventilatory studies negate the Pickwickian syndrome. The E.E.G.'s recorded during the hypersomnic attacks and the apneic periods showed a direct correlation between high-voltage delta waves paroxysmal E.E.G. activity, and apneic period. Medications known to improve Kleine-Levin syndrome, in our case, had no effect upon the clinical hypersomnic and apnea periods, nor on the correlatives E.E.G.'s pattern and spirometric studies. Theoretical considerations let us assume that these paroxysmal E.E.G. patterns associated with apnea are NRem-sleep serotonin dependent, and have an inhibitory influence on the respiratory centers, by alternating the equilibrium between the catecholamines and acetylcholine activities.
Nocturnal sleep patterns were registered from 6 parkinsonian patients treated with bromocryptine, ("-Br-L-ergocryptine, C.B.-154) a dopamine-like agonist. No significant differences in their sleep patterns were found in comparison with patients treated with L-dopa. Since bromocryptine acts direct on the dopaminergic receptor sites, it is suggested that the disturbed EEG sleep patterns in parkinsonian patients cannot be explained by altered dopaminergic or serotoninergic effects whether pre- or postsynaptic.
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In 16 patients suffering from cerebrovascular events, prostaglandin (PG) E2 was measured in their cerebrospinal fluid and correlated with their clinical status and evolution. Prostaglandin E2 ranged from 200-3000 pg (picogram)/ml of cerebrospinal fluid. A positive correlation was found between PG E2 levels and the severity and clinical outcome of the stroke.
L-tryptophan (L-T) was added at a dose of 150-450 mg daily to eight Parkinsonian patients who developed visual hallucinations with paranoidal features under L-dopa (L-D) treatment (112.5-75 mg daily) in combination with alpha-methyldopa hydrazine (12.5-75 mg daily). In six patients L-T ameliorated the symptomatology by arresting the visual paranoidal hallucinations or diminishing their frequency and relieving the psychomotor agitation. As a 'side effect', L-T produced new 'pleasurable', 'LSD-like' visual images in three patients. In two patients, in whom L-T did not affect the mental disturbances, amelioration was obtained only by phenothiazines. Theoretical considerations on the role of dopamine in the genesis of visual hallucinations and mental disturbances emphasizes the benefit of L-T administration in this 'organomental' syndrome.
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Seven aged Parkinsonian patients treated with levodopa (average dose 3-4 g daily for 1-3 years), showed a considerable weight loss. They were compared to two control groups of elderly and young volunteers after levodopa stimulation and after oral glucose tolerance tests. It was found that after levodopa administration the plasma free fatty acids, glucose, growth hormone and cortisol were significantly higher in the Parkinsonian group than in the young control group and only slightly higher than in the aged control group. It was also found that the serum insulin was significantly higher in Parkinsonian patients than in the aged control group. We think that the metabolic disturbances found in Parkinsonian patients are not solely due to levodopa administration but may be due to ageing processes. We suggest that weight loss in the older Parkinsonian patients treated over long periods with high doses of levodopa, is due to the enhancement of the lipolytic activity of the ageing fat cells caused by high levels of circulating insulin.
Seventeen placentas from term gestation complicated by toxemia of pregnancy and 17 normal controls were tested by the fluorescent antibody technic. Antisera to normal placental connective tissue and toxemic placental connective tissue were used. The antisera were obtained by the injection into rabbits of placental extracts rich in connective tissue elements from normal and toxemic placentas. The antitoxemic antisera, after absorption with soluble sonic fraction of normal placentas, stained the following elements exclusively in 14 of the 17 placentas: part of the syncytial knots, fibrillar elements in the adventitia of blood vessels, and amorphous deposition of connective tissue. In each of the remaining three placentas at least two of the lesions were observed. The observation of bright fluorescence in part of the syncytiotrophoblasts and the syncytial knots in toxemic placentas led to the suggestion that they arise late in pregnancy during the disease. The thin fibrillar elements and the amorphous deposition of connective tissue were documented in the various developmental stages in toxemic and normal placentas as well. These findings established possible characteristic lesions in the placenta of pregnancies complicated by toxemia.
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