Search PubMed⌕ Search

Biomedical subjects

F Assal

Publications and source records attributed to F Assal.

At least 19 recordsLinked to original sources
PubMed2006

[Neurodegeneration and cerebrovascular disease: causal or incidental link?].

Neurodegenerative and cerebrovascular diseases have been related for more than a century. Epidemiological data show that main vascular risk factors are also risk factors for Alzheimer disease. Experimental evidences demonstrate that some of those risk factors accelerate the progress of Alzheimer lesions, mainly by acting on the amyloid cascade. Recent advances in understanding the basic mechanisms of CADASIL and familial amyloid angiopathy reveal that these forms of vascular dementias are degenerative disease of brain vessels. Modern neuroimaging techniques will allow to better understand relations between symptomatic strokes, silent infarcts, leukoaraiosis, microbleeds and degenerative pathology before the stage of dementia.

Cerebrovascular Disorders↗
PubMed2005

[Is there a treatment for Alzheimer's disease?].

Alzheimer's disease is a frequent neurodegenerative disease, which affects more than one third of elderly persons over 80 years. No curative treatment is currently available for this disease, but symptomatic treatments have produced significant improvements in patients' condition. Cholinesterase inhibitors should be prescribed for early and moderate stages and memantine for more severe stages of the disease. These drugs have an impact on cognitive performances, may delay functional decline and improve behaviour disturbances. From a preventive perspective, evidence of benefit from early management of vascular risk factors is accumulating. In the near future, the improved comprehension of the underlying mechanisms of Alzheimer's disease will hopefully bring new treatments, thats will delay or modify its course.

Alzheimer Disease↗
PubMed2004

ADC mapping of the aging frontal lobes in mild cognitive impairment.

Normal aging, leukoaraiosis (LA) and vascular disease particularly involve the human frontal lobes. We decided to investigate a population of elderly patients referred for neuroimaging because of progressive minor cognitive deficits but no dementia. They underwent conventional Magnetic resonance imaging (MRI) using axial T1 and T2-weighted imaging as well as coronal FLAIR sequences in addition to the axial diffusion-weighted MRI. MRI allowed us to differentiate patients with leukoaraïosis (LA+) from those without it (LA-) and mapping of the apparent diffusion coefficient (ADC) to investigate local tissular water motion. We observed an increase in the ADC in all investigated patients with increasing age (r=0.326, p=0.002). This increase was observed in both patients groups (LA+ and LA-). In addition, the LA+ group had significant higher ADC values than the LA- group after controlling for age (p<0.0001).

Adult↗
PubMed2001

SPECT in periodic lateralized epileptiform discharges (PLEDs): a form of partial status epilepticus?

Periodic lateralized epileptiform discharges (PLEDs) are a well defined electroencephalographic entity but whether PLEDs represent an ictal condition or not remains debated. Much work has been done using electroencephalography (EEG) but new approaches using cerebral perfusion imaging may give more information about this question. We aimed to evaluate if PLEDs were associated with high regional cerebral blood flow (rCBF). We studied 18 patients with PLEDs and different pathologies, and performed brain single-photon-emission computed tomography (SPECT) during and, for three cases, after the disappearance of PLEDs. Qualitative variations and locations of rCBF were compared with PLEDs. Association with seizures and type of seizures were also assessed. SPECT showed high rCBF in 18/18 patients (100%). The location of PLEDs and high rCBF matched in 17/18 cases (94%). In the three cases where SPECT was performed after PLEDs disappeared, the high rCBF had cleared (100%). Eighteen cases (100%) presented seizures before recording of PLEDs, mainly motor (partial motor or generalized tonic-clonic). Where there was a decreased rCBF (related to a lesion) there was little relationship to PLEDs and all patients with decreased rCBF had an adjacent increased rCBF. These results confirm preliminary case reports. Hyperperfusion adds further to the argument that PLEDs may be related to a form of partial status epilepticus.

Aged↗
PubMed2001

Functional neuroanatomical correlates of hysterical sensorimotor loss.

Hysterical conversion disorders refer to functional neurological deficits such as paralysis, anaesthesia or blindness not caused by organic damage but associated with emotional "psychogenic" disturbances. Symptoms are not intentionally feigned by the patients whose handicap often outweighs possible short-term gains. Neural concomitants of their altered experience of sensation and volition are still not known. We assessed brain functional activation in seven patients with unilateral hysterical sensorimotor loss during passive vibratory stimulation of both hands, when their deficit was present and 2-4 months later when they had recovered. Single photon emission computerized tomography using (99m)Tc-ECD revealed a consistent decrease of regional cerebral blood flow in the thalamus and basal ganglia contralateral to the deficit. Independent parametric mapping and principal component statistical analyses converged to show that such subcortical asymmetries were present in each subject. Importantly, contralateral basal ganglia and thalamic hypoactivation resolved after recovery. Furthermore, lower activation in contralateral caudate during hysterical conversion symptoms predicted poor recovery at follow-up. These results suggest that hysterical conversion deficits may entail a functional disorder in striatothalamocortical circuits controlling sensorimotor function and voluntary motor behaviour. Basal ganglia, especially the caudate nucleus, might be particularly well situated to modulate motor processes based on emotional and situational cues from the limbic system. Remarkably, the same subcortical premotor circuits are also involved in unilateral motor neglect after organic neurological damage, where voluntary limb use may fail despite a lack of true paralysis and intact primary sensorimotor pathways. These findings provide novel constraints for a modern psychobiological theory of hysteria.

Adolescent↗
PubMed2000

[Drug resistant status epilepticus].

Refractory epileptic state (RES) is defined by severe seizures that are resistant to antiepileptic drug treatment. Diagnostic errors such as pseudo-seizures and encephalopathies with triphasic waves must be distinguished at an early stage from cases of RES. The latter are symptomatic of a focal brain lesion or severe systemic disease, most frequently metabolic in origin. The treatment of such conditions is aimed at correction of the underlying cause. A nosographic issue that is still a subject of discussion and which requires further study, i.e., PLEDS, will also be discussed in this article.

Anticonvulsants↗
PubMed2000

Severe but reversible encephalopathy associated with cefepime.

In this study, a report has been made of 19 cases of severe encephalopathy in patients with renal impairment who were treated during the last three years for various infections with cefepime, a new parenteral cephalosporin antibiotic. All patients (aged 57 to 91 years) presented a prolonged confusional state associated with diffuse rhythmic non-reactive triphasic sharp waves on the EEG. All the electroclinical symptomatology disappeared within 24-48 hours after discontinuation of drug administration. A clear relation was found between encephalopathy and cefepime intake. These observations underline the fact that the cefepime dosage should be reduced in renally impaired patients.

Aged↗
PubMed2000

Distinct behavioral and EEG topographic correlates of loss of consciousness in absences.

PURPOSE: To describe the behavioral and EEG topographic correlates of absences with 3-Hz generalized spike-waves and partitioned impairment of consciousness. METHODS: Two adult women had so-called "phantom" absences, characterized by brief and mild impairments of consciousness that were previously inconspicuous to both patient and physician. Neuropsychological examination was performed under video-EEG monitoring during absence status. EEG topographic mapping of spike-wave discharges was obtained in the two cases. RESULTS: Only mild attentional and executive disturbances were observed during absence status despite prolonged discharges. Spike-wave bursts were associated with selective impairment in the initiation of response and self-generated action, whereas short-term storage of external information during discharges was fully preserved. This is consistent with a predominant involvement of frontomesial cortex demonstrated by topographic mapping of spike-wave discharges in the two cases. By contrast, in two other patients with typical absences and a complete lack of retention for information given during the discharges, topographic mapping found a more lateral frontal involvement by spike-wave activity. CONCLUSIONS: Different types of absence seizures may impair distinct components of conscious behavior. A predominant involvement of frontomesial thalamocortical circuitry may underlie an "inconspicuous" disorder of consciousness as seen in phantom absences with selective loss of initiation and goal-oriented behavior, whereas involvement of more lateral frontal areas in typical absences may additionally disrupt working memory processes.

Adult↗
PubMed1998

Post-traumatic stimulus suppressible myoclonus of peripheral origin.

A patient is described who presented with myoclonus of the first dorsal interosseus muscle of the right foot. This myoclonus occurred 18 months after trauma of the cutaneous branch of the deep peroneal nerve on the dorsal aspect of the foot. Tactile stimulation in the dermatome of this nerve, or an anaesthetic block of the deep peroneal nerve stopped the myoclonus. The different innervation between the efferent motor activity responsible for the movements and the sensory afference suppressing it points firmly towards involvement of central connections. However, abolition of the movement by anaesthesia suggests the presence of a peripheral ectopic generator. This finding confirms that focal myoclonus can have its origin in the peripheral nervous system and may be modulated by sensory inputs.

Adult↗
PubMed1997

Low-dose clozapine improves dyskinesias in Parkinson's disease.

The severity of parkinsonian motor disability and dyskinesias was evaluated in seven levodopa-responsive patients with Parkinson's disease after an acute challenge with the mixed dopamine agonist apomorphine, before and after low-dose clozapine (50 mg) for 18 +/- 2 days. There was a significant 59% improvement (p < 0.05) of apomorphine-induced dyskinesias without aggravation of parkinsonian motor disability following clozapine treatment. The results suggest that low-dose clozapine, already shown to improve psychotic symptoms, may help to reduce severe levodopa-induced dyskinesias in parkinsonian patients.

Aged↗
PubMed1992

Emergence of callosally projecting neurons with stellate morphology in the visual cortex of the kitten.

Callosally projecting neurons in areas 17 and 18 of the adult cat can be classified into two types on the basis of their dendritic morphology: pyramidal and stellate cells. The latter are nearly exclusively of the spinous type and are predominantly located in upper layer IV. Retrograde transport of the carbocyanine dye DiI, applied to the corpus callosum, showed that, up to P6, all callosally projecting neurons resemble pyramids in the possession of an apical dendrite reaching layer I. At P10, however, callosally projecting neurons with stellate morphology were found. A study was designed to distinguish whether these neurons are late in extending their axons to the corpus callosum or, alternatively, have transient apical dendrites. To this end, callosally projecting neurons were retrogradely labeled by fluorescent beads injected in areas 17 and 18 at P1-P3 and then either relabeled with DiI applied to the corpus callosum at P10 or intracellularly injected with Lucifer Yellow at P57. Double-labeled stellate and pyramidal cells were found in similar proportions to those found for the total, single-labeled population of callosally projecting neurons. It is therefore concluded that callosally projecting spiny stellate cells initially possess an apical dendrite and a pyramidal morphology. At P6, i.e. close to the time when stellate cells appear, layer IV neurons with an atrophic apical dendrite were found, suggestive of an apical dendrite in the process of being eliminated.

Animals↗