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Biomedical subjects

F Placidi

Publications and source records attributed to F Placidi.

At least 19 recordsLinked to original sources
PubMed2006

Effect of cabergoline added to levodopa treatment on sleep-wake cycle in idiopathic Parkinson's disease: an open label 24-hour polysomnographic study.

Few studies focused on the effects of cabergoline on sleep-wake cycle in PD. Twelve patients affected by PD treated with levodopa as monotherapy underwent two 24-hour ambulatory polysomnographic (A-PSG) sessions twice: in baseline condition (levodopa as monotherapy) and after addition of cabergoline. In each condition, a subjective evaluation of sleep quality and daytime sleepiness was obtained by means of Parkinson's disease Sleep Scale (PDSS) and the Epworth Sleepiness Scale. The statistical analysis of sleep parameters revealed a significant increase of sleep efficiency and slow wave sleep under cabergoline. The PDSS total score showed a significant improvement of overall sleep quality after cabergoline. No significant changes in daytime sleepiness were observed. No patient referred and/or showed sleep attacks before and after addition of cabergoline. We hypothesize that the long-lasting effect of cabergoline may improve the objective quality of nocturnal sleep in PD patients complaining nocturnal motor disability without inducing daytime sleepiness.

Aged↗
PubMed2005

Temporal lobe epileptic activity mimicking dementia: a case report.

Epileptic activity is an underdiagnosed cause that can determine a disruption of memory and cognitive performance, leading an incorrect diagnosis of dementia. We report a 68-year-old man, referred with a 5-year history of subtle behavioral changes and a subjective memory impairment, who was admitted to our department because of recurrent episodes of confusional state lasting from 1 week. Neuropsychological evaluation demonstrated a marked impairment of all cognitive domains examined. Electroencephalogram (EEG) recording showed frequent almost continuous sharp waves localized on the bilateral posterior temporal regions with mild right side predominance. Treatment with phenytoin reversed his cognitive dysfunction and behavioral disturbances. We presume that ictal temporal lobe epileptiform activity is the cause of his confusional episodes and cognitive dysfunction, showing an electroclinical picture of complex partial status epilepticus. However, we hypothesize that the interictal discharges and ictal and postictal effects of subclinical seizures could be involved in the behavioral changes and memory impairment complained by our patient in the last years.

Aged↗
PubMed2004

Sleep episodes and daytime somnolence as result of individual susceptibility to different dopaminergic drugs in a PD patient: a polysomnographic study.

The association between excessive daytime somnolence (EDS) and idiopathic Parkinson's disease (PD) is often reported but still debated. The possible role of antiparkinsonian therapy or primarily of PD on excessive diurnal sleepiness is controversial. We describe the case of a 61-year-old patient affected by PD who experienced sleep episodes (SE) occurring during pramipexole plus L-Dopa therapy. Polysomnographic sleep studies and subjective evaluations of daytime sleepiness (Epworth Sleepiness Scale) were carried out under administration of pramipexole plus L-Dopa, L-Dopa monotherapy and cabergoline plus L-Dopa. The polysomnography revealed two sleep events during pramipexole plus L-Dopa. Moreover, the polysomnographic data showed an increase of both diurnal and nocturnal sleep under pramipexole plus L-Dopa compared with cabergoline plus L-Dopa and L-Dopa as monotherapy. In addition, while Epworth Sleepiness Scale (ESS) Score showed a mild sleepiness under pramipexole (ESS score=11), ESS scores were normal under both L-Dopa and cabergoline plus L-Dopa. Sleep episodes also disappeared under both L-Dopa and cabergoline plus L-Dopa (2- and 12-month follow-up). We hypothesize that an individual susceptibility to specific antiparkinsonian drug may play a significant role in the genesis of sleepiness in our PD patient.

Disorders of Excessive Somnolence↗
PubMed2003

Bilateral frontal polymicrogyria and epilepsy in a patient with Turner mosaicism: a case report.

Turner's syndrome (TS) is rarely associated with serious abnormalities of brain structure or malformations of cortical development. We report a 17-year-old girl with TS and 45,XO/46,XX mosaicism presenting bilateral frontal polymicrogyria (BFP) and epilepsy. To our knowledge, the association between TS and BFP has never been reported to date. Our observation confirms that in humans the X-chromosome plays an important role in the development and specialization of brain structure and function. We hypothesize that the absence or abnormalities of developmental genes localized on the X-chromosome could be involved in the pathogenesis of BFP observed in our patient.

Adolescent↗
PubMed2003

Cortical dysplasia, temporal atrophy, mental retardation, dysmorphic facies, and partial epilepsy: an EEG and dynamic susceptibility contrast (DSC) MRI study in a new possible genetic syndrome.

We report the case of a 24-year-old female with partial epilepsy, mental retardation, and dysmorphic facies. In EEG, a high spiking rate (HSR) was evident with abnormalities in the right frontal region. Morphological MRI showed a left temporo-mesial sclerosis and a cortical dysplasia localized in the right frontal cortex. Dynamic susceptibility contrast (DSC) MRI showed hyperperfusion in right frontal region and hypoperfusion in left fronto-temporal region. Left fronto-temporal hypoperfusion is consistent with temporo-mesial sclerosis. Right frontal hyperperfusion is related to the cortical dysplasia area with HSR. HSR may resemble both electroencephalographic and perfusional ictal pattern. DSC MRI is useful in the evaluation of regions involved in the genesis of ictal and interictal epileptiform activity. Furthermore, we hypothesize that our patient would be affected by a new possible genetic syndrome.

Adult↗
PubMed2002

Sleep organization pattern as a prognostic marker at the subacute stage of post-traumatic coma.

OBJECTIVES: The aim of this study is to identify the predictive indexes for post-traumatic coma prognosis, which is important to better direct acute and subacute treatments and rehabilitation efforts. The pattern of sleep organization is a potential prognostic marker, but its role has not been established yet in the context of modern critical care. In the present study, we used a new protocol to evaluate the prognostic value of the different levels of sleep-wake organization recorded at the subacute stage of post-traumatic coma. METHODS: Twenty-four head-injured comatose patients were monitored with 24h polysomnographic recordings. The predictivity of the different levels of sleep-wake organization on polysomnography was compared with other possible prognostic indexes (i.e. neuroradiological findings, age and Glasgow Coma Scores (GCS)). Main outcome measures were survival and the degree of disability after recovery from coma. RESULTS: The presence of organized sleep patterns, but not GCS, was highly predictive of better outcome (odds ratio=10.78, P=0.01), even after correction for potentially confounding variables with multivariate analysis. CONCLUSIONS: Our study demonstrates that the sleep-wake organization pattern based on 24h polysomnographic recordings at the subacute stages of post-traumatic coma is a reliable prognostic marker, both for survival and for functional recovery.

Adolescent↗
PubMed2001

Ketotic hyperglycemia and epilepsia partialis continua.

Epilepsia partialis continua (EPC) may occur during nonketotic hyperglycemia but has not been described with diabetic ketoacidosis. The authors report a patient with EPC associated with ketotic hyperglycemia. Brain MRI showed two areas of abnormal signal intensity in the left precentral gyrus and in the right cerebellar hemisphere. Hyperglycemia may reduce seizure threshold because of the increase in gamma-aminobutyric acid metabolism and may trigger epileptic discharges.

Adult↗
PubMed2001

Cerebrovascular reactivity and subcortical infarctions.

OBJECTIVES: To investigate the association between different kinds of ischemic lesions and cerebrovascular reactivity (CR) and to evaluate their relationships with the major risk factors for stroke. SUBJECTS AND METHODS: We evaluated CR using the breath-holding index technique during bilateral transcranial Doppler monitoring of flow velocity in the middle cerebral arteries of 41 consecutive patients attending our clinic for a recent, first-ever, ischemic stroke and in 15 control subjects. Based on the location of the lesion determined by computed tomography, the following 3 types of infarctions were identified: cortical (or territorial), single subcortical, and subcortical with multiple silent subcortical infarctions. Patients with a condition of severe carotid artery stenosis or occlusion, which in itself could account for altered CR, were excluded from this study. All physiological and pathologic conditions that could possibly cause an impairment in CR were recorded. RESULTS: The breath-holding index was significantly lower in the multiple subcortical infarctions group than in the control subjects (P < .001), single subcortical infarctions group (P < .01), and cortical infarctions group (P < .01). In all of the groups male sex (P < .05) and a history of hypertension (P < .05), regardless of whether hypertension was treated, correlated with low CR. The multiple regression analysis indicated that the only significant factor able to influence the breath-holding index was the type of lesion. CONCLUSIONS: Nonstenotic patients with first-ever stroke who had a recent symptomatic subcortical infarction associated with multiple silent infarctions seem to have an impaired cerebrovascular reserve capacity. The strong association of subcortical infarctions with multiple silent infarctions with low CR indicates the role of small vessel vasculopathy and hypoperfusion as possible pathogenetic mechanisms of subcortical infarctions with multiple silent infarctions.

Adult↗
PubMed2000

Gabapentin-induced modulation of interictal epileptiform activity related to different vigilance levels.

OBJECTIVES: Gabapentin (GBP) is a novel antiepileptic drug (AED), currently used as add-on therapy in patients with partial seizures. Similar to other AEDs, little is known about its effects on nocturnal sleep, despite the strict relationship between sleep and epileptic discharges. The aim of our study was to evaluate the effects of chronic therapy with GBP on both nocturnal sleep and on interictal epileptiform abnormalities (IEA) in relation to the different sleep stages. METHODS: Eighteen patients affected by partial seizures resistant to common AEDs were submitted to nocturnal polygraphic recordings under baseline conditions and after 4 months of add-on GBP treatment. RESULTS: We observed a significant increase in unilateral/focal IEA during light NREM sleep and a significant reduction in bilateral/diffuse IEA during wakefulness after sleep onset (WASO) with respect to the baseline condition. A significant increase in REM sleep and slow wave sleep (SWS) associated with a reduction in the number of awakenings and Stage 1 was also observed after GBP chronic therapy. CONCLUSIONS: GBP therapy improves the sleep pattern of epileptic patients and it seems to modulate the expression of IEA with different effects in relation to the various vigilance levels.

Acetates↗
PubMed2000

Effect of antiepileptic drugs on sleep.

The interactions between sleep and epilepsy are well known. A nodal point of the relationship between sleep and epilepsy is represented by pharmacological treatment. Sleep disturbances such as drowsiness are among the most frequent side effects of treatment with antiepileptic drugs, since they can deeply modify both sleep architecture and the sleep-wake cycle. Severe daytime somnolence affects patients' activities and it may facilitate the occurrence of seizures. These considerations underline the importance of antiepileptic drugs having anticonvulsant properties that do not negatively influence sleep and daytime somnolence. In this paper we review some relevant aspects of the effects of antiepileptic drugs on sleep.

Anticonvulsants↗
PubMed2000

Gabapentin as add-on therapy in focal epilepsy: a computerized EEG study.

OBJECTIVES: Gabapentin (GBP) possesses a well documented clinical efficacy in those types of focal epilepsy otherwise resistant to conventional antiepileptic drugs (AEDs); on the basis of this, it appears important to investigate the drug effects on the EEG epileptiform and background activity. METHODS: Twenty-five patients with cryptogenic or symptomatic partial epilepsy resistant to conventional AED treatment were included in the study. All patients underwent long-term video-EEG recordings before and after GBP addition (900-1200 mg/day). RESULTS: Quantitative analysis of the interictal EEG paroxysms revealed that GBP had no effect on the rate of occurrence of interictal and ictal EEG abnormalities. GBP was active in delimiting the spatial extent of the interictal spiking activity in those patients who displayed a significant reduction (> or =50%) in seizure occurrence (32% of the patients). EEG background activity recorded under rest condition from 18 out of 25 epileptic patients, before GBP therapy, was characterised by a higher content of the slow spectral components (delta and theta) with respect to control subjects. After GBP addition, the increase of theta relative power was also evident during task performance. CONCLUSIONS: These findings suggest that GBP does not interfere with the generation of interictal EEG spiking while it appears to reduce the susceptibility to seizures concomitantly with a limiting effect on the spiking activity spatial extent. The utilization of GBP in controlling focal seizures is reinforced by the absence of negative influence on cognitive functioning.

Acetates↗
PubMed2000

Effects of lamotrigine on nocturnal sleep, daytime somnolence and cognitive functions in focal epilepsy.

OBJECTIVES: The aim of our study was to evaluate possible changes in nocturnal sleep, daytime somnolence and cognitive functions induced by add-on therapy with lamotrigine (LTG). MATERIAL AND METHODS: Thirteen patients affected by seizures resistant to common antiepileptic drugs (AEDs) underwent nocturnal polysomnographic monitorings, daytime somnolence evaluations and a neuropsychological battery before and after 3 months of treatment with LTG. RESULTS: With LTG therapy we observed a significant increase in REM sleep and a significant reduction in the number of entries into REM and stage shifts. No significant correlation was observed between the decrease in nocturnal epileptiform activity and the increase in REM sleep. Other sleep parameters were unmodified. No significant changes were observed in daytime somnolence and in cognitive performances. CONCLUSION: LTG may produce positive effects on epileptic seizures and interictal abnormalities without interfering negatively on REM sleep, with improvement of sleep stability and without changes in daytime somnolence and neuropsychological performances. For these reasons it could be an important drug for improving epileptic patients' quality of life.

Adolescent↗
PubMed2000

Effect of anticonvulsants on nocturnal sleep in epilepsy.

Our objective was to determine, in three separate studies, the effects of controlled-release carbamazepine (CBZ-CR), lamotrigine (LTG), and gabapentin (GBP) on nocturnal sleep in epilepsy. Antiepileptic drugs (AEDs) control seizures and also modify hypnic structure. Despite widespread clinical use, their effects on sleep are not well known. PSG was performed in all three studies as follows: CBZ-CR: at baseline, after initial administration of CBZ-CR 400 mg, and after 1 month of CBZ-CR treatment (400 mg BID) in a sample of seven temporal lobe epileptic (TLE) patients. Results were compared with those of nine healthy volunteers; LTG: at baseline, after 3 months of stable treatment with LTG (300 mg/day); GBP: at baseline, after 3 months of stable treatment with GBP (1800 mg/day). Significant findings are as follows for each study. The acute administration of CBZ-CR increased number of stage shifts, reduced REM sleep, and increased REM sleep fragmentation. In the TLE group, these effects were almost completely reversed after chronic treatment. LTG increased REM sleep, reduced number of entries into REM sleep, decreased number of phase shifts, and decreased percentage of slow-wave sleep. GBP increased REM sleep percentage, increased mean duration of REM periods, reduced number of awakenings, and reduced stage 1 sleep percentage. We conclude that CBZ-CR disrupts REM sleep, but only during acute administration. LTG and GBP improve sleep stability while reducing seizures.

Acetates↗
PubMed1999

Sleep abnormalities in mentally retarded autistic subjects: Down's syndrome with mental retardation and normal subjects.

We compared sleep parameters in mentally retarded infantile autism (MRIA) and mentally retarded Down's syndrome (MRDS) by means of polysomnography, evaluating traditional analysis with particular attention to the phasic components in each disorder. Data were compared with those obtained in normal subjects matched for age and sex. Mental age, Intellectual Quotient and the Childhood Autism Rating Scale were performed to obtain an estimation of the neuropsychological deficit. Abnormalities of phasic components of sleep and the presence of REM sleep components into non-REM sleep were observed in both MRIA and MRDS even if in different ways. In fact, MRDS subjects presented a reduction of REM sleep percentage and R index (number of high frequency REMs against number of low frequency REMs) and this was positively correlated to a low IQ. Unlike MRDS subjects, MRIA subjects did not show any parallelism between intellectual abilities and REM sleep deficit. In addition, the presence of undifferentiated sleep in autistic subjects implies a maturational deficit that is still present in adulthood. Finally, a high R index in MRIA was observed. This finding, which is not present in MRDS, could represent an estimation of the disorganized arrival of information caused by a dyscontrol or a reduction of inhibitor pathway. With reference to sleep mechanisms, our results suggest that the cognitive deficit in MRIA may differ from that of MRDS subjects. A maturational deficit of CNS with a dysfunction of brainstem monoaminergic neurons could represent the underlying mechanism.

Adolescent↗
PubMed1999

Does the antimigraine action of flunarizine involve the dopaminergic system? A clinical-neuroendocrinological study.

We have investigated the prolactin response to bromocriptine (BRC), a D2 dopamine receptor agonist in migrainous women before and after treatment with flunarizine. We evaluated whether this test was predictive of therapeutic efficacy of flunarizine treatment and whether the therapeutic response to flunarizine treatment was related to its effect on dopaminergic system at tuberoinfundibular level. Ten migrainous women underwent a BRC test in the late follicular phase before and after 1 and 3 months of treatment with flunarizine 10 mg at bedtime. Blood samples of prolactin (PRL), growth hormone, follicle-stimulating hormone, luteinizing hormone, estradiol and progesterone were taken at basal condition. PRL was also evaluated 1 and 2 h after BRC (2.5 mg) administration. Each patient kept a daily headache diary for 1 month prior to the test and throughout the study. The level of PRL inhibition after BRC administration, observed before flunarizine treatment, was not predictive of the therapeutic response observed after 1 and 3 months of treatment. The effect of flunarizine on PRL level was not related to the therapeutic efficacy of the drug. These data suggest that flunarizine does not attenuate the activity of dopaminergic neurons in migrainous patients, and that the antimigraine effect of flunarizine does not seem related to its action on dopaminergic system at least at tuberoinfundibular level.

Adult↗
PubMed1998

Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome.

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.

Adult↗
PubMed1998

Bilateral hemispheric activation in the early recovery of motor function after stroke.

BACKGROUND AND PURPOSE: Functional recovery after cerebral infarction is a complex phenomenon that depends on various factors. The aim of this study was to investigate changes in cerebral perfusion during motor activity in stroke patients with very early recovery of motor function. METHODS: We included 9 consecutive patients hospitalized for acute-onset hemiparesis who showed complete functional recovery within 24 hours. CT of the brain showed an ischemic or hemorrhagic cerebral lesion in areas compatible with the symptomatology. Within 36 hours (range, 28 to 36) all patients were examined for the effects of a thumb-to-finger opposition task on cerebral blood flow in the middle cerebral arteries, evaluated by means of bilateral transcranial Doppler ultrasonography. Data were compared with those of 9 healthy subjects matched for age and sex. In patients, the evaluation was repeated 2 to 4 months later. RESULTS: A comparable increase in flow velocity (% mean+/-SD) was observed with respect to baseline in the contralateral middle cerebral artery during motor activity with patients' normal (8.8+/-2.0%) and recovered hand (9.7+/-4.1%) and with both hands of control subjects (10.6+/-1.4%). In the middle cerebral artery ipsilateral to the hand performing the motor task, the increase in flow velocity was significantly higher (P<0.0001) during movement of the recovered hand in patients (8.6+/-2.7%) than during movement of the normal hand in both patients (2.6+/-1.6%) and control subjects (1.4+/-0.7%). In patients, pattern of changes in flow velocity during motor performance remained the same in the second evaluation. CONCLUSIONS: These observations suggest that areas of the healthy hemisphere can be activated soon after a focal injury and contribute to the positive evolution of a functional deficit in some patients. This phenomenon of ipsilateral activation cannot be considered transient because it is evident months after stroke onset.

Aged↗