Search PubMed⌕ Search

Biomedical subjects

C Loeb

Publications and source records attributed to C Loeb.

At least 19 recordsLinked to original sources
PubMed1992

Accumulation of labeled gamma-aminobutyric acid into rat brain and brain synaptosomes after i.p. injection.

The accumulation of labeled GABA into brain and brain nerve endings was studied in the adult rat after i.p. injection of large doses of neurotransmitter (740 mg/Kg). In the first 5-30 minutes after the injection the exogenous neurotransmitter reaches a stable plasma level of around 5 mM. The accumulation of radioactive GABA into the brain presents a latency of a few minutes from the time of the injection. Thereafter, the accumulation of the neurotransmitter is almost linear with time. Once in the brain tissue labeled GABA is in part broken down. The exogenous neurotransmitter is taken up in GABA-ergic nerve endings with a steep increase between 20 and 30 minutes after the injection. From a quantitative point of view, the data show that the brain accumulation of labeled GABA at 30 minutes post injection is minimal in the respect of the steady state average concentration of the endogenous neurotransmitter (0.014%). However, the amount of radioactive GABA which accumulates in the nerve endings, at the same post injection time, is around 7% of the endogenous neurotransmitter in that compartment. The data thus show a selective enrichment of exogenous systemic GABA in a physiologically important compartment of the brain.

Animals↗
PubMed1992

MRI findings in epileptic patients on vigabatrin for more than 5 years.

Although vigabatrin is a promising new antiepileptic drug, its safety has been challenged by the report of dose-dependent central nervous system myelin vacuolation in some preclinical animal studies. Since it has been shown that vacuolation is associated with specific magnetic resonance imaging (MRI) findings in rats and dogs, MRI of the brain was performed in 11 patients with complex partial seizures who had been receiving vigabatrin for 64-78 months (mean 74.0 +/- 5.0 sd) as additional treatment for epilepsy, with a cumulative exposure ranging 4200 to 9360 g. In no case did MRI show white matter changes similar to the pathological findings of microvacuolation observed in animals. These results would appear to confirm that current doses of vigabatrin do not cause myelin vacuolation in humans, even for treatment periods of longer than 5 years.

Adult↗
PubMed1992

Dementia associated with lacunar infarction.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the number of patients with lacunar lesions who develop dementia and to evaluate in patients with and without dementia the relevance of risk factors for cerebrovascular disease, the occurrence of leukoaraiosis, the volume and location of vascular lesions, the size of ventricular and subarachnoid spaces, and stroke recurrence. METHODS: One hundred eight patients in whom computed tomograms revealed lacunar lesions that could account for their clinical neurological pictures were followed up for an average of 4 years after their first lacunar stroke. RESULTS: Twenty-five patients (23.1%) developed dementia. The prognosis regarding occurrence of dementia during the follow-up period, evaluated by the Kaplan-Meier method, was significantly worse in subjects with the greatest evidence of cerebral atrophy (p less than 0.009) and in subjects who underwent new focal cerebrovascular episodes (p less than 0.000001). No differences were seen in the frequency of vascular risk factors or the site or volume of lesions between the demented and nondemented groups. CONCLUSIONS: Patients with lacunar infarcts suffer from dementia 4-12 times more frequently than the normal population. Cerebral atrophy and recurrent stroke, as well as other as-yet unclarified factors, are involved in producing dementia.

Aged↗
PubMed1991

Amyloid beta protein deposition in brains from elderly subjects with leukoaraiosis.

We studied immunocytochemically with 2 amyloid beta protein (ABP) antisera brains from 5 non-demented elderly subjects with evidence of diffuse periventricular white matter hypodensity on computed tomography. In periventricular white matter of all brains we found ABP reactive deposits arranged around small vessels walls. Furthermore ABP reactive deposits, identical to those currently called diffuse plaques, were detected in neocortex in amount proportional to that of white matter deposits. We suggest that ABP microangiopathy and parenchymal deposition is responsible of white matter rarefaction in a subset of cases with a diffuse hypodensity on CT scan which has been called leukoaraiosis.

Aged↗
PubMed1991

Abnormal tau-reactive filaments in olfactory mucosa in biopsy specimens of patients with probable Alzheimer's disease.

We immunocytochemically analyzed pieces of olfactory mucosa removed by biopsy in 8 patients with probable Alzheimer's disease (AD) and 6 age-matched controls, with tau and ubiquitin antisera. There were tau-reactive and, partially, ubiquitin-reactive dystrophic neurites in the lamina propria of olfactory mucosa in all AD cases. The tau-reactive neurites contained abnormal straight filaments, 15 to 18 nm in diameter, morphologically identical to those found in AD cerebral brain tissue obtained at autopsy. Tau and ubiquitin immunoreactivity were absent in controls. If these neuritic alterations are confirmed in a larger number of cases, analysis of olfactory mucosa may increase the current reliability of clinical diagnosis of AD.

Alzheimer Disease↗
PubMed1991

Protective effect of cyproheptadine in a gerbil model of cerebral ischemia.

The efficacy of Cyproheptadine, a serotonin antagonist, in preventing the cerebral ischemic damage was tested on experimental model of transient global cerebral ischemia in Mongolian Gerbil. The semi-quantitative histological evaluation of the severity of ischemic damage showed a protective effect of Cyproheptadine, mainly in the anterior cortical areas.

Animals↗
PubMed1990

The excitatory amino acid antagonist amino-phosphono-valeric acid (APV) provides protection against penicillin-induced epileptic activity in the rat.

The effects of intraperitoneal injection of 2-amino-5-phosphono-valeric acid (APV) on EEG-monitored penicillin-induced epileptic activity in rats were evaluated. A significant decrease in the frequency of spikes occurred with low APV dosages (10 and 20 mg/kg), while an almost complete disappearance of spike activity was observed at higher APV doses (40 and 160 mg/kg). Our data suggest that excitatory amino acids play a relevant role in penicillin-induced epileptic activity in rats.

2-Amino-5-phosphonovalerate↗
PubMed1990

Methodological problems of clinical trials in multi-infarct dementia.

In about 30% of the cases suffering from MID an unequivocal diagnosis can be made only on the basis of histopathological evidence. The imperfect diagnosis has a relevant impact on the methodology to be followed in therapeutic trial. The following points have to be considered in a therapeutic trial: (1) distribution of the patients expected to come to the observation, (2) the expected effectiveness of the treatment, (3) the likelihood of obtaining statistical significant results and (4) the required size of the study. The diagnostic inaccuracy gives rise to a decrease in the chance of yielding a statistically significant result and on the other hand produces an increase in the required number of subjects to be submitted to the trial.

Clinical Trials as Topic↗
PubMed1990

Pseudobulbar palsy: a clinical computed tomography study.

61 of 1,590 (3.8%) patients with cerebrovascular disease showed suprabulbar palsy of the pure form (42 patients; 2 had autopsy) and striate form (19 patients; 3 had autopsy). 25 patients with the pallidopyramidal syndrome were included since the clinical picture bordered on the striate form. The pure variety was characterized by dysarthria, dysphagia and automatic voluntary dissociation of facial movements. Half of the patients also had hemiparesis, primitive reflexes and short-step gait. In the striate form, the main signs were dysarthria, dysphagia, automatic voluntary dissociation, rigidity and hypokinesia. Brisk tendon reflexes, primitive reflexes, short-step gait and mental deterioration were also present in half of the patients. The pure variety was caused by multiple infarcts and/or lacunae (85.7%), while the striate form had vascular lesions by computed tomography in only 36.8% of the cases. Histological findings, showing lipohyalinosis of the arterial wall leading to stenosis and occlusion of the lumen and tissue rarefaction and disintegration, support the assumption that microinfarctions, sometimes found only by histopathological examination, are the leading pathogenetic factor in this form. Hypertension, cardiopathy, smoking habit, dyslipemia and diabetes are the most frequent risk factors in both forms.

Aged↗
PubMed1989

Focal epilepsy as a possible sign of transient subclinical ischemia.

Late-onset partial epileptic seizures occurred in 10 patients with symptoms and/or signs of ischemic cerebrovascular disease (ICVD) and were associated with transient ischemic attacks in 7 of them. History, somatic and neurological examinations, laboratory and ancillary investigations and follow-up revealed no other disease which might be responsible for the seizures. The anatomical and temporal proximity of signs of ICVD indicate the latter as the most likely cause of seizures. Although the available neuroimaging did not allow us to rule out the presence of silent cerebral infarctions in all patients, it is conceivable that jacksonian seizures, and more rarely complex partial seizures, might occasionally represent a clinical sign due to transient cerebral ischemia and thus herald major cerebrovascular events.

Adult↗
PubMed1989

The lacunar syndromes.

The term lacuna or lacunar cavity defines the pathological lesion while the clinical pictures due to lacuna or lacunes are referred to as 'lacunar syndromes'. The lacunar syndromes include: (1) the typical lacunar syndromes or lacunar syndromes proper--pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis including dysarthria and clumsy hand, sensorimotor stroke and abnormal movement syndromes, (2) reversible ischemic attacks (TIA and/or PTIA or RIND), (3) other clinical syndromes which may be due to lacunar lesions such as suprabulbar palsy; lacunar dementia, or subacute arteriosclerotic encephalopathy (or Binswanger's disease). The different clinical pictures are reviewed, some mechanisms underlying the lacunar lesion are briefly discussed and the old label 'small vessel diseases' in cases with lacunes is reconsidered.

Cerebral Infarction↗
PubMed1988

Preliminary note on the effect of denzimol in partial epilepsy.

The antiepileptic activity of the imidazole derivative denzimol has been evaluated in 10 patients with poorly controlled partial epilepsy by adding on the drug to the current therapy, in an open preliminary trial. A sustained drop in seizure frequency greater than 50% occurred in 5 patients. Although denzimol increased blood concentrations of carbamazepine, correlation analysis indicated that the improvement was more likely due to intrinsic properties of denzimol. No severe side effects were reported, although several patients experienced nausea and vomiting, which caused 2 patients to drop out.

Adult↗
PubMed1988

Phosphatidylserine increases in vivo the synaptosomal uptake of exogenous GABA in rats.

A sonicated liposome suspension of gamma-aminobutyric acid (GABA) and phosphatidylserine (liposome-entrapped GABA), intraperitoneally administered in rats, inhibited EEG epileptic activity induced by penicillin, whereas GABA did not. A significant increase (20.4%) in brain radioactivity accumulation occurred at 5 min after i.p. administration of [14C]GABA associated with phosphatidylserine in comparison with the administration of [14C]GABA; such an increase persisted after 20 min. However, the accumulation of radioactivity into brain synaptosomes demonstrated a 24.1% increase at 5 min and subsequently showed a 43.3% increase at 20 min after injection of liposome-entrapped GABA. The above findings suggest that phosphatidylserine stimulates exogenous GABA uptake into brain GABAergic nerve terminals.

Animals↗