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Biomedical subjects

E Melamed

Publications and source records attributed to E Melamed.

At least 271 records · Page 15Linked to original sources
PubMed1976

Reactive hyperglycaemia in patients with acute stroke.

Initial and follow-up fasting serum glucose levels following acute stroke were evaluated retrospectively in 392 selected hospitalized patients. Transitory reactive hyperglycaemia was observed in a large number of patients (28% of the total series) without a history of diabetes prior to the acute cerebrovascular event. The data from this group suggest a possible relationship between the impairment of carbohydrate metabolism and the type and location of stroke since both the frequency and severity of the hyperglycaemic response were higher in patients with haemorrhagic stroke and brainstem infarction as compared with cerebral infarction. The incidence and degree of the reactive hyperglycaemia were also related to the severity of the acute stroke. There were more comatose patients in the group showing this phenomenon. Initial serum glucose levels in the latter group were higher in unconscious patients than in alert ones. In addition, hospital mortality was significantly higher in these patients. Transitory reactive increases of serum glucose levels were also observed in the majority of patients with a history of overt diabetes prior to the acute stroke. The hyperglycaemic reaction following acute stroke may be attributed to several underlying mechanisms. These include: a non-specific reaction to acute stress and tissue injury with the associated autonomic, hormonal and metabolic alterations; uncovering of underlying latent diabetes by the acute stroke; increased secretion of growth hormone due to stroke-induced hypothalamic dysfunction; and irritation of the glucose regulatory centres in the hypothalamus and brain stem by blood-laden cerebrospinal fluid or local ischaemia.

Acute Disease↗
PubMed1976

Internal carotid arterial occlusion simulating extracerebral hematoma: relation to diagnosis of stroke.

In 2 elderly male patients, a progressive neurologic deficit and alteration of consciousness developed following substantial head trauma succeeded by an asymptomatic "lucid" interval. The sequence of events and the associated electroencephalographic, echoencephalographic and cerebrospinal fluid findings strongly suggested the presence of an extracerebral hematoma. The cerebral angiographic study, however, disclosed complete occlusion of the extracranial portion of the internal carotid artery in both patients. This report stresses the diagnostic difficulties sometimes encountered in relation to stroke patients.

Aged↗
PubMed1976

Aseptic cavernous sinus thrombosis after internal carotid arterial occlusion in polycythaemia vera.

Two patients with untreated polycythaemia vera developed intracranial internal carotid arterial occlusion followed by monocular blindness and the characteristic features of ipsilateral cavernous sinus thrombosis. Primary septic source and signs of systemic infection were absent. It is suggested that the predisposing factors in this unusual syndrome were hyperviscosity and venous sludging induced by the basic haematological disorder and progression of the thrombotic process within the internal carotid artery towards its intracavernous portion with occlusion of the ophthalmic artery and of the arterial branches which supply the walls of the sinus.

Adult↗
PubMed1976

Interictal regional cerebral blood flow in patients with partial seizures.

Interictal regional cerebral blood flow was determined in 11 adult patients with partial epilepsy and lateralized electroencephalographic abnormalities by means of the xenon 133 intracarotid injection method. A hemispheric area demonstrating significantly low regional cerebral blood flow values as compared with the hemispheric mean cerebral blood flow was observed in each of the patients. In 10 of the 11 patients the localized reduced regional cerebral blood flow levels deviated significantly from levels obtained from parallel regions and hemispheres of normal controls. In the majority of patients, the site of low regional cerebral blood flow closely correlated with the clinical type of partial seizures and/or the site of main electroencephalographic abnormality. On the basis of these data, we suggest that the epileptogenic focus responsible for the partial seizures may be localized within the hemispheric area demonstrating the abnormal regional cerebral blood flow reduction.

Adult↗
PubMed1975

Correlation between regional cerebral blood flow and EEG frequency in the contralateral hemisphere in acute cerebral infarction.

The relationship between the rCBF and the electroencephalographic (EEG) frequency was investigated in the contralateral hemisphere of 22 patients with acute cerebral infarction. Reduced rCBF was observed in all patients studied. The degree of rCBF reduction was mild, moderate, or severe and ranged between 6 and 80% from the lowest age-matched normal values obtained in our laboratory. The frequency indices remained within normal limits (mean - 10.4 Hz) in 16 patients. Slower frequencies (mean - 6.3 Hz) were recorded in 6 patients. No correlation was found between the two parameters (P = 0.89). Both the EEG frequency and the rCBF are known to be closely related to the cerebral metabolic rate. The observed rCBF depression without concomitant changes in the EEG frequency raises the question of the role of globally-reduced cerebral metabolism as the cause of rCBF reduction in the noninfarcted hemisphere in stroke patients. Our findings constitute additional evidence that the contralateral hemisphere is involved in the haemodynamic changes occurring in acute cerebral infarction.

Acute Disease↗
PubMed1975

Reversible central nervous system dysfunction in folate deficiency.

An epileptic patient on chronic anticonvulsant drug therapy is described, in whom anaemia and neurological abnormalities including progressive dementia, bilateral pyramidal tract signs, incontinence and ataxia developed. Vitamin B12 serum levels and absorption were normal, but serum folic acid levels were low. Both the neurological disturbances and anaemia resolved following oral folic acid administration. This sequence of events in our patient suggests a cause and effect relationship between the folate deficiency and the coexistent, transient neurological syndrome.

Aged↗
PubMed1975

Prognostic value of visual evoked potentials in occipital blindness following basilar artery occlusion.

Three patients suffering from sudden occipital blindness following basilar artery occlusion underwent electroretinography and visual evoked potential (VEP) examinations. The VEPs performed early in those blind patients and repeated later seem to be of prognostic value. Responses of normal shape and amplitude after monocular and binocular stimulation were followed by complete recovery of vision. Unequal and subnormal VEPs obtained following monocular stimulation, and even smaller responses reached after binocular stimulation, accompanied permanent unilateral occipital damage resulting in homonymous hemianopsia. Lack of VEP was proved to be a preceding sign of permanent blindness.

Aged↗
PubMed1975

Central nervous system complication in a patient with chronic gaucher's disease.

Central nervous system manifestations developed in a patient suffering from the chronic, adult form of Gaucher's disease. At autopsy, massive systemic fat embolism was found, involving mainly the brain and the lungs. As there was no evidence of bone fracture, or trauma to the adipose tissues, it is presumed that the severe skeletal involvement by the Gaucher's disease led to the development of the fat embolization.

Autopsy↗
PubMed1975

Chronic subdural hematoma simulating transient cerebral ischemic attacks. Case report.

A patient is presented in whom chronic subdural hematoma simulated transient ischemic attacks. The neurological manifestations were those of recurrent, transient episodes of expressive dysphasia preceded by focal sensory deficit. Various pathophysiological mechanisms which could have caused the unusual clinical picture are briefly considered.

Aphasia↗
PubMedDate not supplied

Rasagiline as an adjunct to levodopa in patients with Parkinson's disease and motor fluctuations (LARGO, Lasting effect in Adjunct therapy with Rasagiline Given Once daily, study): a randomised, double-blind, parallel-group trial.

BACKGROUND: Rasagiline mesylate is a novel drug for Parkinson's disease with selective, irreversible monoamine oxidase B (MAO-B) inhibitor activity, and is effective as monotherapy in early disease. This study investigated rasagiline efficacy and safety in levodopa-treated patients with Parkinson's disease and motor fluctuations. METHODS: In an 18-week, double-blind, multicentre (74 hospitals and academic centres in Israel, Argentina, and Europe) trial, 687 outpatients were randomly assigned to oral rasagiline (231 individuals; 1 mg once daily), entacapone (227; 200 mg with every levodopa dose), or placebo (229). Primary outcome was change in total daily off-time (intention-to-treat population). Other measures included the clinical global improvement (CGI) score and unified Parkinson's disease rating scale (UPDRS) scores. Analysis was by intention to treat. FINDINGS: 88 (13%) patients who were assigned treatment did not complete the study (23 rasagiline, 30 entacapone, 35 placebo), mainly because of withdrawal of consent (n=34) and adverse events (n=34). Both rasagiline and entacapone reduced mean daily off-time (-1.18 h rasagiline and -1.2 h entacapone vs placebo -0.4 h; p=0.0001, p<0.0001, respectively) and increased daily on-time without troublesome dyskinesia (0.85 h vs placebo 0.03 h; p=0.0005 for both). We recorded significant mean improvements in CGI scores (-0.86 rasagiline and -0.72 entacapone vs -0.37 placebo; p<0.0001, p=0.0002, respectively). Changes in UPDRS scores also significantly improved for activities of daily living during off-time (-1.71 and -1.38 vs placebo; p<0.0001, p=0.0006, respectively) and motor function during on-time (-2.94 and -2.73 vs placebo; both p<0.0001). Frequency of adverse events was similar for all treatments. INTERPRETATION: Once-daily rasagiline reduces mean daily off-time and improves symptoms of Parkinson's disease in levodopa-treated patients with motor fluctuations, an effect similar to that of entacapone.

Administration, Oral↗
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↗
PubMedDate not supplied

Catechol-O-methyltransferase decreases levodopa toxicity in vitro.

The purpose of this study was to examine the effects of 3-O-methylation by catechol-O-methyltransferase (COMT) on the toxicity of levodopa in neuronal cultures. High concentrations of levodopa are toxic in vitro. Therefore, there is concern that long-term treatment with levodopa in patients with Parkinson's disease might accelerate the rate of degeneration of nigrostriatal neurons. However, recent studies have suggested that, while levodopa is harmful in vitro, it may not be toxic in vivo. A possible defense mechanism is by means of metabolic shunting of levodopa excess to 3-O-methyldopa by COMT in peripheral and central nervous system tissues. In this study we examine whether the use of COMT inhibitor, which reduced the levels of 3-O-methyldopa, affect levodopa toxicity. Mice cerebellar granule neurons, PC12, and neuroblastoma cells were used, and their viability following exposure to levodopa and COMT with and without tolcapone, a COMT inhibitor, was measured by neutral red staining. Auto-oxidation of levodopa was evaluated using a spectrophotometer (690 nm). We found that 3-O-methyldopa, unlike levodopa, was not toxic to all cells examined. Addition of purified COMT to levodopa prevented its auto-oxidation and markedly attenuated its cytotoxicity in vitro. Additional tolcapone reversed the protective effect of COMT. The agent 3-O-methyldopa is not toxic to cell cultures. Catechol-O-methyltransferase attenuates toxicity of levodopa in vitro by its metabolism to nontoxic 3-O-methyldopa.

Animals↗