Biomedical subjects

Federica Provini

Publications and source records attributed to Federica Provini.

22 records · Page 2Linked to original sources

PubMed2001

Agrypnia excitata: clinical features and pathophysiological implications.

Fatal familial insomnia, Morvan's chorea and delirium tremens share the same clinical features: severe insomnia and mental confusion with dream enactment, associated with motor and autonomic activation. Polygraphically, they share an inability to generate slow wave sleep. Agrypnia excitata is the term which aptly defines this peculiar medical condition. In fatal familial insomnia, the syndrome is due to a functional imbalance between activating and deactivating structures within the limbic system provoked by the atrophy of the mediodorsal and anteroventral thalamic nuclei. In Morvan's chorea and delirium tremens, a functional imbalance within the thalamolimbic circuits might be explained by the accumulation of some antireceptor antibodies and by a transient prevalence of excitatory over inhibitory synapses, down-regulated by chronic alcohol abuse, respectively. The selective disappearance of slow sleep (i.e. sleep spindles and delta rhythms) characterizing the agrypnia excitata syndrome, together with other clinical and experimental findings, suggests that sleep can be divided into three types. The most archaic form of sleep corresponding to stage 1 non-REM sleep is shared by man and poikilothermic animals and generated within activating and deactivating neuronal poles located in the basal forebrain, hypothalamus and brain stem; the other two forms of sleep, slow wave sleep and paradoxical sleep, confined to homeothermic animals, are generated in the thalamus and pontine reticular formation respectively. 2001 Harcourt Publishers Ltd

Journal Article↗

PubMed2000

The wide clinical spectrum of nocturnal frontal lobe epilepsy.

Nocturnal frontal lobe epilepsy (NFLE) has become clinically relevant in recent years. NFLE represents a spectrum of clinical manifestations, ranging from brief, stereotyped, sudden arousals, often recurring several times per night, sometimes with a quasi-periodic pattern, to more complex dystonic-dyskinetic seizures and to prolonged "somnambulic" behaviour. Episodes of increasing intensity have been labelled as paroxysmal arousal (PA), nocturnal paroxysmal dystonia (NPD) and episodic nocturnal wandering (ENW). NFLE affects both sexes with a higher prevalence for men, is frequently cryptogenetic and displays a strong familial trait for parasomnias and epilepsy (NFLE). Seizures appear more frequently between 14 and 20 years of age, but can affect any age and tend to increase in frequency during life. Interictal and ictal scalp electroencephalography (EEG) are often normal, the use of sphenoidal leads may be helpful. Carbamazepine taken at night is often effective at low doses, but a third of the patients are resistant to anti-epileptic drugs (AED) treatment. A familial form, characterized by an autosomal dominant transmission, has also been described. Autosomal dominant nocturnal frontal lobe epilepsy is a genetic variant of NFLE, in itself both clinically and biologically heterogeneous. NFLE should be suspected in the presence of frequent stereotyped paroxysmal nocturnal motor events arising or persisting into adulthood. Videopolysomnography is mandatory to confirm the diagnosis.

Journal Article↗

PubMedDate not supplied

Cardiovascular disorders and obstructive sleep apnea syndrome.

The first polysomnographic recordings with concomitant monitoring of cardiocirculatory parameters demonstrated that obstructive apneas arising during sleep are accompanied by a marked increase in pulmonary and systemic arterial pressure and severe alveolar hypoventilation. Apneas also may give rise to cardiac arrhythmias, namely potentially life-threatening bradyarrhythmias. The long-term repercussions of these nocturnal cardiocirculatory changes on subsequent cardiovascular diseases and the patient's life expectancy are more controversial. There is little doubt that patients with obstructive sleep apnea syndrome (OSAS) have systemic arterial hypertension, ischemic heart disease, transient ischemic attacks, or stroke more often than control populations and have a shorter life expectancy. However, these clinical manifestations may be at least partly due to myriad other risk factors almost always present in OSAS patients (in particular obesity, diabetes, alcoholism, and cigarette smoking). Few multivariate epidemiological surveys have addressed all these confounding factors. The effectiveness of continuous positive airway pressure treatment in reducing the incidence of cardiovascular comorbidity in OSAS patients is not disputed, even though controlled epidemiological surveys on large populations are scant. This overview of cardiovascular disorders and OSAS examines the latest literature findings aimed at establishing the true impact of nocturnal apneas on cardiocirculatory disease (systemic arterial hypertension, ischemic heart disease, stroke, pulmonary hypertension and right heart failure and mortality).

Blood Pressure↗

PubMedDate not supplied

Excessive daytime sleepiness and levodopa in Parkinson's disease: polygraphic, placebo-controlled monitoring.

The authors performed 72-hour polysomnography, including a levodopa-placebo-controlled choice reaction time test with continuous monitoring of cardiovascular variables in two patients with Parkinson's disease complaining of excessive daytime sleepiness on levodopa monotherapy. The subacute levodopa challenge was accompanied by physiologic sleep episodes, worsened reaction times, and a reduction in mean blood pressure and heart rate over baseline values, linked temporally to the sleep episodes.

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