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Biomedical subjects

J M Rabey

Publications and source records attributed to J M Rabey.

89 records · Page 5Linked to original sources
PubMed1979

Plasma dopamine beta hydroxylase (D.B.H.) activity in Parkinsonian patients under L-dopa, and 2-bromo-alpha-ergocriptine loading.

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.

Bromocriptine↗
PubMed1979

Detrusor hyperreflexia in multiple sclerosis. Alleviation by a combination of imipramine and propantheline, a clinico-laboratory study.

16 patients with multiple sclerosis, complaining of urgency, frequency and urge incontinence were studied urologically. They all suffered from detrusor hyperreflexia. We managed to improve this disturbance by lowering the parasympathetic tone and at the same time increasing the sympathetic tone of the urinary outlet, using a combination of imipramine and propantheline. The subjective clinical alleviation was also corroborated by cystomanometry and urethral pressure profile before and after treatment.

Adult↗
PubMed1978

Myoclonic attacks induced by L-dopa and bromocryptin in Parkinson patients: a sleep EEG study.

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.

Aged↗
PubMed1978

Kleine-Levin syndrome with periodic apnea during hypersomnic stages--E.E.G. study.

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.

Adult↗
PubMed1977

L-tryptophan administration in L-dopa-induced hallucinations in elderly Parkinsonian patients.

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.

Aged↗
PubMed1977

Ophthalmoplegic migraine: amelioration by Flufenamic acid, a prostaglandin inhibitor.

It was recently suggested that prostaglandins' release (especially PGE1 and PGF2alpha) play a key role in the development of the migrainous attack. Based on this hypothesis a therapeutic trial with flufenamic acid (a prostaglandin inhibitor of the fenamates group) was conducted during 1 year in 5 patients suffering from recurrent ophthalmoplegic migraine. We treated 25 migrainous attacks; in 22 of them the patients reported marked alleviation of the headaches and only in two occasions a partial third nerve palsy accompanied the attack.

Adolescent↗
PubMed1976

Herpes simplex encephalitis simulating systemic embolism.

A case of herpes simplex virus encephalitis is described in a patient known to suffer from chronic atrial fibrillation and whose clinical symptoms suggested cerebral embolism of cardiac origin. The final diagnosis was based on the presence of herpes simplex virus type 1 antibodies in the cerebrospinal fluid and a significant rise in antibody titers in the serum. The patient regained consciousness after craniotomy and treatment with idoxuridine. The case emphasizes that the possibility of herpetic encephalitis should be considered in patients presenting with typical signs of a cerebrovascular accident.

Adult↗
PubMedDate not supplied

Selective influence of rat genotype on age-related regional changes in forebrain muscarinic binding.

Muscarinic binding was analyzed in the hippocampus and frontal cerebral cortex of 3 (young) and 24-month-old (aged) inbred Wistar-Kyoto (WKY), Brown-Norway (BN) and Lewis rats, by the specific binding of the antagonist quinuclidinylbenzilate (QNB). While no age-related changes were detected in the hippocampus of all strains, complex changes were found in the cortex. Maximal binding capacity (Bmax) of [3H]QNB was decreased in the cortex of aged WKY rats, remained unchanged in the BN strain and was elevated in Lewis rats. We conclude that regional differences exist in age-related changes in forebrain muscarinic binding which are probably due to differences in the types and connections of cholinoceptive neurons in these regions. The results suggest that it is the rate of these changes which is affected by the rat genotype.

Aging↗
PubMedDate not supplied

Developmental regulation of the brain polyamine-stress-response.

A transient increase in brain polyamine metabolism, termed the polyamine-stress-response is a common response to stressful stimuli. Previous studies have implicated an over-reactive polyamine response as a component of the maladaptive brain response to stressful events, and as a novel molecular mechanism involved in the pathophysiology of affective disorders. Ample evidence indicates that stressful experiences during early life can alter normal developmental processes and may result in pathophysiological and behavioral changes in the adult. Additionally, an important characteristic of affective disorders is their age dependency, a phenomenon that may be correlated with a maladaptive regulation of the hypothalamic-pituitary-adrenocortical (HPA) neuroendocrine system. In the present study we measured the activities of the enzymes ornithine decarboxylase and S-adenosylmethionine decarboxylase as markers of polyamine synthesis and found that unlike adults, immature rats do not show the characteristic brain polyamine-stress-response. Instead of the characteristic increase observed in adults, ornithine decarboxylase activity in immature animals was reduced or remained unchanged (for up to 16 days of age) after a dexamethasone injection or restraint stress application. The ontogenesis of this ornithine decarboxylase response was brain region-specific, indicating its dependence on the stage of neuronal maturation. Animals treated with dexamethasone at 7 days of age, showed increased behavioral reactivity in the open-field test as adults and an attenuated increase in ornithine decarboxylase activity after a re-challenge with dexamethasone at age 60 days. The results indicate that: (1) the brain polyamine-stress-response is developmentally regulated and its ontogenesis is brain region-specific, indicating dependence on the stage of neuronal maturation; (2) the switch to a mature polyamine-stress-response pattern coincides with the cessation of the stress hyporesponsive period in the HPA system: (3) activation of the polyamine-stress-response, as in the mature brain, appears to be a constructive reaction, while its down-regulation, as in the developing brain, may be implicated in neuronal cell death; (4) an attenuated dexamethasone-induced increase in ornithine decarboxylase activity implicates an altered polyamine-stress-response in the maladaptive response of the brain to stressful events.

Adenosylmethionine Decarboxylase↗
PubMedDate not supplied

Rasagiline mesylate, a new MAO-B inhibitor for the treatment of Parkinson's disease: a double-blind study as adjunctive therapy to levodopa.

Rasagiline mesylate (TVP-1012) is a potent, selective, non-reversible MAO-B inhibitor, without the tyramine-potentiating effect and with neuroprotective activities. The benefit of rasagiline as monotherapy in patients with early Parkinson's disease (PD) has already been reported. To evaluate the safety, tolerability, and clinical effect of rasagiline as adjunctive therapy to levodopa, a multicenter, double-blind, randomized, placebo-controlled, parallel-group study (0.5, 1, and 2 mg/d) was conducted for 12 weeks in 70 patients with PD (mean age, 57.4 y; mean disease duration, 5.7 y; 32 patients had motor fluctuations). A beneficial clinical effect was observed in fluctuating patients treated with rasagiline (all doses), expressed as a decrease in total Unified Parkinson's Disease Rating Scale (UPDRS) score (23.0% vs 8.5% in the placebo group). The treatment effect was still evident 6 weeks after drug discontinuation (in all doses). The safety and tolerability of rasagiline were good. Adverse events were no different than those of patients taking placebo. Almost complete platelet MAO-B inhibition was obtained at all rasagiline doses. This study has demonstrated that rasagiline (up to 2 mg/day) has a good safety profile and a beneficial clinical effect in fluctuating patients with PD when given as an add-on to chronic levodopa therapy.

Adult↗