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Biomedical subjects

G Plazzi

Publications and source records attributed to G Plazzi.

54 records · Page 3Linked to original sources
PubMed1997

Motor disorders in sleep.

Sleep is normally a time of motor quiescence. Motor disorders may, however, arise during the different phases of sleep. Nocturnal myoclonus or periodic leg movements in sleep usually occur during light sleep and may be considered the motor accompaniment of the cyclic fluctuations in excitability typical of such stages. Nocturnal frontal lobe epilepsy also occurs during NREM sleep and may be misdiagnosed as parasomnia. REM behavior disorders are instead dissociated episodes of REM sleep without atonia, often associated with or even heralding Parkinson's disease or multiple system atrophy.

Basal Ganglia Diseases↗
PubMed1997

Heavy snorer disease: from snoring to the sleep apnea syndrome--an overview.

This short review discusses the clinical, pathophysiological and epidemiological aspects of heavy snorer disease. Snoring and obstructive apneas constitute the end points of the same syndrome, i.e. an enhancement in upper airway resistance during sleep. Obstructive apneas, and possibly snoring, are risk factors of chronic arterial hypertension.

Airway Resistance↗
PubMed1997

REM sleep behavior disorders in multiple system atrophy.

We report the results of clinical and polysomnographic investigations on 39 consecutive multiple system atrophy (MSA) patients. Twenty-seven patients (69%) reported nocturnal motor paroxysmal episodes related to dreams, suggesting the clinical diagnosis of REM sleep behavior disorder (RBD). In 12 of them (44%), RBD preceded the clinical onset of the disease by more than 1 year. In seven (26%), the RBD onset was concomitant with and in eight (30%) was at least 2 years after the appearance of motor or autonomic symptoms. On polysomnographic recordings, 35 of 39 MSA patients (90%) had RBD. Other polysomnographic findings included nonclinical obstructive sleep apnea in 6 patients, laryngeal stridor in 8 patients, and periodic limb movements during sleep in 10 patients. Our data show that RBD represents the most common clinical sleep manifestation and polysomnographic finding in patients with MSA. RBD can frequently herald the appearance of other MSA symptoms by years. Extended polysomnographic montages are recommended in MSA sleep studies.

Adult↗
PubMed1997

Alterations of sleep and circadian blood pressure profile.

The organization of sleep activity in stages of different depth is reflected by consistent changes in blood pressure that account for the major part of the day-night blood pressure difference. On the other hand, different mechanisms may underlie dysregulation of nocturnal blood pressure. Cyclic variations in autonomic nervous system activity play an important role in the mediation of the influences of sleep and wakefulness on blood pressure. In addition, several physiologic substances that are knoiwn to induce sleep or arousal are knoiwn to exert actions on blood pressure. Hence, derangements in autonomic nervous system activity, either primitive or secondary to alterations in the circadian rhythm of a variety of neurohumoral factors, are reflected in changes of the circadian blood pressure profile. Important additional influences of sleep on blood pressure may be exerted through respiratory variations, so that sleep-disordered breathing is bound to alter nocturnal blood pressure. Finally, insomnia has to be taken into account as a major cause of sleep-related alteration of the circadian blood pressure profile. The number of medical disorders that can cause insomnia is huge, and includes many if not all of the conditions in which a loss or reversal of the physiologic blood pressure fall at night is found to be prevalent. Unfortunately, objective sleep studies have been performed only in studies of a minority of these disorders, and further studies to assess the pathophysiologic mechanisms actually involved in causing sleep disturbances in each pathologic condition are necessary.

Journal Article↗
PubMed1996

Partial epilepsy of long duration: changing semiology with age.

There are few data on changing patterns of localization-related epileptic syndromes with time and particularly on changes in seizure semiology as patients age. We retrospectively reviewed 53 patients aged > 60 years who had had partial epileptic seizures for a mean duration of 44 years. In 29 patients, seizures became progressively less elaborate and briefer with time. In 20 patients, seizures were unchanged. In four patients, seizures worsened, with the appearance of drop attacks, secondarily generalized seizures, increasing drug resistance, and mental deterioration. These latter 4 patients had cerebrovascular disease with multiple strokes.

Adolescent↗
PubMed1996

Pontine lesions in idiopathic narcolepsy.

Three patients had longstanding (37 to 50 years), highly disabling narcolepsy, poorly controlled by treatment. The clinical histories were typical, consisting of sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations, disturbed nocturnal sleep, and HLA-DR2 tissue typing. Polygraphic findings confirmed the diagnosis. Neurologic examination, spinal fluid, and evoked potentials were normal. On MRI scanning, all three patients showed overlapping bilateral and symmetric brainstem T2 hyperintensities circumscribed to the ventrolateral aspect of the midrostral pons. The nature of the lesions remains uncertain but their location corresponded to the pontine oral reticular formation, where the neuronal network generating REM sleep is located. This is the first report of MR signal abnormalities in patients with idiopathic narcolepsy and suggests a causal relationship between the disease and the central pontine lesions.

Aged↗
PubMed1995

Epileptic nocturnal wanderings.

Video-polysomnographic monitoring in four patients complaining of stereotyped paroxysmal ambulation and other complex motor activities during sleep demonstrated ictal epileptic discharges at the onset of the sleepwalking episodes. In addition, all patients displayed minor motor episodes resembling short-lasting nocturnal paroxysmal dystonia (NPD) attacks and paroxysmal arousals (PAs). NPD with short-lasting attacks, PAs and episodic nocturnal wanderings represent the same epileptic syndrome with variable presentations.

Adult↗
PubMed1994

Idiopathic recurring stupor.

Idiopathic recurring stupor (IRS) is a disease of unknown pathogenesis presenting with recurrent stuporous states. We describe three IRS patients in whom there were no metabolic, toxic, or structural brain dysfunctions. Ictal EEGs were characterized by fast (14- to 16-Hz), unreactive background activity. Flumazenil, a benzodiazepine receptor antagonist, promptly resolved the clinical and EEG picture. In all patients, ictal plasma determination showed a marked increase in benzodiazepine-like activity identified as endozepine-4. IRS may be due to an unexplained excess of endozepine-4.

Adult↗
PubMed1992

Endogenous benzodiazepine receptor ligands in idiopathic recurring stupor.

"Endozepines" are endogenous ligands for the benzodiazepine recognition sites on gamma-aminobutyric acid A receptors in the nervous system. Idiopathic recurring stupor (IRS) is a syndrome of spontaneous stupor or coma that is not associated with known metabolic, toxic, or structural abnormalities but can be reversed by flumazenil, a pure benzodiazepine antagonist. We measured endozepine-2 and endozepine-4 by high-performance liquid chromatography and radioreceptor assay in serum and cerebrospinal fluid from three patients with IRS. During episodes of stupor there was a large (up to 300-fold compared with control patients) increase of endozepine-4 content in cerebrospinal fluid and serum, but a return to normal concentrations between attacks. Endozepine-4 may contribute to, or be the cause of, IRS. The reasons for abnormal concentrations of endozepine in blood and brain are unknown.

Adult↗
PubMedDate not supplied

Facial asymmetry in partial epilepsies.

Fifty-six consecutive epileptic patients with partial seizures (30 temporal, 26 extratemporal) and facial asymmetry were studied. Facial asymmetry was compared with EEG, radiologic, and other clinical findings. Thirty patients had a lesional epilepsy whereas 26 were considered cryptogenic. In lesional epilepsies, 60% of patients had EEG foci ipsilateral to the smaller hemiface and only 20% had EEG foci contralaterally. In the cryptogenic group, the EEG focus was ipsilateral in 50% and contralateral to the facial smallness in 46%. No differences were noted between temporal and extratemporal epilepsies. Early acquired cerebral lesions may modify development of the hemisphere involved, leading to a small ipsilateral hemiface and seizures originating from the same side.

Adult↗
PubMedDate not supplied

Arylsulfatase A pseudodeficiency and Lafora bodies in a patient with progressive myoclonic epilepsy.

Since age 12 years, a 25-year-old woman had a syndrome with myoclonic epilepsy, cerebellar signs, and spontaneous myoclonus. Skin biopsy showed typical Lafora bodies (LB), but she lacked a progressive course and mental impairment, hallmarks of Lafora disease. Lysosomal enzyme assays showed low level arylsulfatase A (ASA) activity. DNA study disclosed a homozygous ASA Pd genotype. Both parents carried one Pd allele. The still-unknown relationship between the pathologic level of ASA activity and myoclonic epilepsies suggests introduction of ASA assays in patients with PME.

Adult↗
PubMedDate not supplied

Occipital lobe epilepsy: a chronic condition related to transient occipital lobe involvement in eclampsia.

Eleven hours and 6 days, respectively, after childbirth 2 women exhibited hypertension and paroxysmal visual disturbances followed by tonic-clonic seizures and no other preeclamptic signs. Both developed partial epilepsy with occipital lobe seizures with no other neurologic defects. Neuroimaging showed no lesion during either the acute episode or 3-5 year follow-up. Selective vulnerability of the occipital lobes during eclamptic hypertensive encephalopathy was the probable pathophysiologic mechanism. Aggressive antihypertensive treatment during the acute phase may have exacerbated the risk of permanent cerebral damage.

Adult↗