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M Onofrj

Publications and source records attributed to M Onofrj.

At least 19 recordsLinked to original sources
PubMed2006

Visual hallucinations in Parkinson's disease: clues to separate origins.

Our paper discusses two experimental studies suggesting that Visual Hallucinations (VH) in Parkinson's Disease (PD) may have separate origins. The first is a prospective 8years study evaluating the appearance of VH, visual abnormalities assessed by Visual Evoked Potentials (VEPs) and REM sleep Behaviour Disorder (RBD), in 80 PD patients treated with l-Dopa and Dopaminoagonists (DA). In chronically treated, cognitively unimpaired, PD patients VH were statistically related (p=0.001) to RBD occurrence and high DA doses. Visual abnormalities were significantly reduced by l-Dopa or DA intake, and were statistically unrelated to VH. The second study involved PD patients placed in a Virtual Reality Environment, to decontextualize visual input. When motor symptoms worsened and VEP abnormalities developed patients consistently described hallucinatory dysperceptions of the virtual environment. The two studies therefore show that VH can occur in two seemingly distinct conditions, one is related to chronic treatment and to a sleep disorder frequently observed in PD, the other is probably related to a hypodopaminergic state. Our studies support a recently proposed integrative model of VH, and show that the neural circuits purported to explain VH must include the retinal dopaminergic system and the REM sleep regulatory system.

Antiparkinson Agents↗
PubMed2005

Cortical rhythms reactivity in AD, LBD and normal subjects: a quantitative MEG study.

The present study evaluated the reactivity of cortical rhythms in 15 Alzheimer's disease (AD) patients, 7 Lewy body dementia (LBD) patients and 9 control subjects using a 165 SQUID whole-head MEG system. The absolute power values of the rhythms recorded over different areas over the brain (frontal, parietal, temporal, occipital) were analysed in the 3-47Hz frequency range. The cortical reactivity of the alpha (9-14Hz) and pre-alpha rhythms (7-9Hz) during open and closed eyes conditions differentiated the control group from the patient groups and moderate AD from severe AD and LBD groups, respectively. The cortical reactivity of the slow-band (3-7Hz) obtained by comparing a simple mental task and the rest discriminated the severe AD group from the other groups. In addition, spectral coherence analysis in the alpha band showed that the loss of coherence in AD and LBD patients mainly involved long connections. These results suggest that investigations on rhythms reactivity and spectral coherence might help on the study of the dementias with different etiology.

Aged↗
PubMed2004

Improvement of motor function in early Parkinson disease by safinamide.

A median safinamide (SAF) dose of 70 mg/day (range 40 to 90 mg/day) increased the percentage of parkinsonian patients improving their motor scores by > or =30% from baseline (responders) after 3 months from 21.4% (placebo) to 37.5% (p < 0.05, calculated by logistic regression analysis). In a subgroup of 101 patients under stable treatment with a single dopamine agonist, addition of SAF magnified the response (47.1% responders, mean 4.7-point motor score decrease; p > or = 0.05). These results suggest that doses of SAF exerting ion channel block and glutamate release inhibition add to its symptomatic effect and warrant exploration of higher doses.

Adult↗
PubMed2004

Combining entacapone with levodopa/DDCI improves clinical status and quality of life in Parkinson's Disease (PD) patients experiencing wearing-off, regardless of the dosing frequency: results of a large multicentre open-label study.

The efficacy of entacapone and its impact on patient quality of life (QOL) was investigated in an open-label study of 899 patients with idiopathic Parkinson's Disease (PD) experiencing wearing-off fluctuations. Patients were divided into 3 groups (3, 4 or 5 doses daily) based on their current levodopa dosage frequency. Patients received 200 mg entacapone with each levodopa/dopa-decarboxylase inhibitor (DDCI) dose, while continuing their same levodopa/DDCI dosage regimen for 4 weeks. Primary efficacy measure was the Investigators' Clinical Global Impression of Change (CGIC). Patient QoL was assessed using the validated 8-item Parkinson's Disease Questionnaire (PDQ-8). Investigators' CGIC revealed that 76.5% of entacapone treated patients experienced an improvement in global status after 4 weeks. Treatment with entacapone was also associated with improvement in patient QoL, with a mean reduction (improvement) in PDQ-8 score of 1.8 from baseline. This study confirms and extends the results of earlier studies demonstrating that, independent of dosing frequency, completing levodopa/DDCI therapy with entacapone provides clinically relevant improvements in global status and QoL in PD patients experiencing wearing-off on their current levodopa dosing frequency.

Aged↗
PubMed2004

Clinically evidenced unilateral dissociation of saccades and pursuit eye movements.

A patient affected by an ischaemic lesion of the right medial thalamic nucleus presented with a uniocular dissociation of upward vertical saccades and pursuit movement, with absent upward vertical saccades in the left eye. Clinical observations were confirmed by magnetic field scleral search coils analysis. During the vertical eye movement the patient denied any diplopia, thus suggesting a transient visual suppression in the left eye.

Antibodies, Antiphospholipid↗
PubMed2004

Duration of amantadine benefit on dyskinesia of severe Parkinson's disease.

BACKGROUND: Recent short-term studies suggested that amantadine (Ama) might ameliorate dyskinesia in patients with Parkinson's disease. A double-blind study programmed over 12 months was designed to assess the duration of the antidyskinetic effect of amantadine on levodopa induced dyskinesia. METHODS: 40 patients treated for 7.5 (2.2) years with levodopa (729.3 (199.4) mg/day) and dopaminoagonists, having peak dose or dyphasic dyskinesia with or without pain, were assessed with the Unified Parkinson's Disease Rating Scale subscale IV, Items 32-34, the Dyskinesia Rating Scale and Investigator Global Assessment. Twenty patients received amantadine chloridrate (100 mg) and 20 received a placebo. The Ama or placebo could be withdrawn when scores indicated worsening of dyskinesia, after agreement with the patient. RESULTS: After 15 days of amantadine treatment there was a reduction by 45% in the total dyskinesia scores. All patients in the placebo group were withdrawn in 1-3 months and all patients in the Ama group were withdrawn in 3-8 months (p = 0.01, p<0.001). Ama withdrawal induced a rebound with increase of dyskinesia by 10-20% in 11 patients. CONCLUSION: 300 mg amantadine reduces dyskinesia in Parkinson's disease by approximately 45% but the benefit lasted less than eight months.

Aged↗
PubMed2004

Neural stem cells: an overview.

Multipotent stem cells are present in the majority of mammalian tissues where they are a renewable source of specialized cells. According to the several biological portions from which multipotent stem cells can be derived, they are characterized as a) embryonic stem cells (ESCs) isolated from the pluripotent inner-cell mass of the pre-implantation blastocyste-stage embryo; b) multipotent fetal stem cells (FSCs) from aborted fetuses; and c) adult stem cells (ASCs) localized in small zones of several organs known as "niche" where a subset of tissue cells and extracellular substrates can indefinitely house one or more stem cells and control their self-renewal and progeny production in vivo. ECSs have an high self-renewing capacity, plasticity and pluripotency over the years. Pluripotency is a property that makes a stem cell able to give rise to all cell type found in the embryo and adult animals.

Animals↗
PubMed2003

Mirtazapine induces REM sleep behavior disorder (RBD) in parkinsonism.

Shortly after initiation of mirtazapine (a noradrenergic and serotonergic antidepressant) treatment in four patients with parkinsonism, the authors observed the appearance of REM sleep behavior disorder (RBD). In the two patients with severe motor symptoms, RBD was accompanied by hallucinations and confusion. These disturbances resolved with drug discontinuation, and remained resolved by 12- to 24-month follow-up, suggesting that RBD can be triggered by a drug lacking anticholinergic activity.

Aged↗
PubMed2003

Acute akinesia or akinetic crisis in Parkinson's disease.

In 22 patients with idiopathic Parkinson's disease we observed a sudden worsening of motor symptoms and severe akinesia during hospitalization because of infectious diseases, bone fractures, surgery for gastrointestinal tract diseases, and iatrogenic causes. Of these patients, 12 recovered completely, 6 had a partial recovery, and 4 died. Treatments included subcutaneous apomorphine/lisuride infusion and dantreolene (with a creatine phosphokinase level higher than 200 IU). In all patients a definite refractoriness to therapy was shown with a transient lack of response to apomorphine.

Aged↗
PubMed2002

Incidence of RBD and hallucination in patients affected by Parkinson's disease: 8-year follow-up.

We describe the 8-years follow-up of 80 patients affected by idiopathic, L-dopa-responsive Parkinson's disease. All patients were evaluated at baseline and during the follow-up with visual evoked potential, P300 event related potentials and polysomnography. The patients and their relatives compiled sleep and hallucination questionnaires. Statistical analysis was performed to evaluate if visual abnormalities, abnormal P300 recordings or sleep disturbances were linked to the development and hallucinations. Our results show that abnormal vision and abnormal P300 did not correlate with the incidence of hallucinations. However, the presence of REM sleep behavioral disorder (RBD) was significantly related to the development of hallucinations,independently of age, gender or duration of disease but dependent on the amount of dopaminoagonist treatment.

Age Factors↗
PubMed2001

Amantadine for dyskinesia in patients affected by severe Parkinson's disease.

20 patients (12 men and 8 women, mean age 65 years) affected by severe Parkinson's disease (PD) with peak-dose and/or diphasic dyskinesias or painful dyskinesia were treated with amantadine (300 mg/day) as adjunctive therapy to current levodopa, carbidopa and dopaminoagonist. UPDRS (Unified Parkinson's disease rating scale), dyskinesias rating scale (DRS) and IGA (investigator global assessment) scale were used to evaluate the severity of PD symptoms during follow-up. After 15 days with amantadine treatment all patients improved with an average 38% reduction in dyskinesias (p<0.001). After 2-8 months. amantadine was withdrawn in all patients. After amantadine withdrawal, 2 patients experienced severe hyperthermia (39 degrees C and 40 degrees C). No difference was found between end of treatment dyskinesia scores and final withdrawal scores (p<0.5). In the two patients with hyperthemia amantadine was reintroduced; after four days hyperthermia subsided and amantadine was finally tapered over 15 days without further adverse reactions.

Aged↗
PubMed2001

Age-related changes of evoked potentials.

The aim of this review is to analyse the current state of our knowledge on evoked potentials (EPs) in ageing and to report some conclusions on the relation between EPs and elder age. Evoked potentials provide a measure of the function of sensory systems that change during the different stages of life. Each sensory system has its own time of maturation. The individuation of the exact period of life when brain ageing starts is difficult to define. Normally, the amplitude of EPs decreases, and their latency increases from adult to elder life. Many authors speculate that these modifications might depend on neuronal loss, changes in cell membrane, composition or senile plaques present in older patients, but there is no evidence that these changes might modify the cerebral function in healthy aged individuals. This review emphasises some incongruities present in different studies confirmed by daily neurophysiologic practice. Different techniques as event-related desynchronization (ERD), contingent negative variation (CNV) and Bereitschaftspotential, are available to study central neuronal changes in normal and pathologic ageing.

Aging↗
PubMed2001

Switch-over from tolcapone to entacapone in severe Parkinson's disease patients.

Forty patients affected by severe Parkinson's disease (PD) were treated with tolcapone as an adjunctive therapy to L-DOPA, for 3-7 months, until this drug was discontinued because of side-effects (2 diarrhoea, one of them with orthostatic hypotension, 2 increments of liver enzymes) or because of mandatory indications of the European drugs authority. All patients, after 3-6 months of L-DOPA therapy adjustments, received entacapone for 3 months again followed by withdrawal. L-DOPA daily dosage was significantly reduced by tolcapone and entacapone (p = 0.01 and 0.05). "On" time was increased by 15% during tolcapone treatment (p < 0.05), and by 8% during entacapone treatment. "Off" time was decreased by 16% during tolcapone and by 7% during entacapone treatment. Entacapone was withdrawn in the same patient who experienced diarrhoea and orthostatic hypotension during tolcapone because of recurrence of side-effects, in 6 patients because of increment of dyskinesias (with hallucinations) and in 1 patients because of rhythmic, jerking myoclonus.

Aged↗
PubMed2000

Stormy onset of benign childhood epilepsy with occipital paroxysmal discharges.

We studied six children with ages ranging from 4 to 10 years who were affected by childhood epilepsy with occipital paroxysms and presented after a stormy onset with prolonged loss of consciousness for 6-14 h. In all these patients, seizures were preceded by visual symptoms in the form of colored circular disks. A CT scan was performed immediately after the onset of symptoms and was normal in all patients. Routine laboratory and cerebrospinal fluid examinations were normal in all patients. The interictal EEG was characterized by continuous or subcontinuous occipital spike wave discharges, which disappeared after the patients' eyes opened. We carried out a 7-year follow-up of all these patients. Only two patients were treated with antiepileptic drugs. The therapy (phenobarbital, clobazam) in the two patients did not induce changes in the EEG pattern. The first did not suffer any further seizures. The second patient had two more seizures (at 8 and 18 months from the onset) with phosphenes, confusional state, and involuntary movements followed by loss of consciousness. Among the other four patients, who did not receive any treatment, only one had any other seizures. The stormy onset of the syndrome described in our six patients emphasizes the extreme variability in the presentation of this type of childhood epilepsy. Our follow-up confirms the good prognosis of this epilepsy even when it has a stormy onset.

Child↗
PubMed2000

Olanzapine in severe Gilles de la Tourette syndrome: a 52-week double-blind cross-over study vs. low-dose pimozide.

We selected four patients with severe Gilles de la Tourette syndrome, high frequency of tics (two to ten per minute), vocalizations, and lack of comorbidity. These patients (aged 19-40 years) underwent a 52-week double-blind cross-over study with olanzapine (5 and 10 mg daily) vs. low-dose pimozide (2 and 4 mg daily). The reduction in rating scale scores for the syndrome was highly significant with 10 mg olanzapine vs. basal and vs. 2 mg pimozide, and was significant for 5 mg olanzapine vs. 4 mg pimozide. Only moderate sedation was reported by one patient during olanzapine treatment while three complained of minor motor side effects and sedation during pimozide treatment. At the end of the study all patients opted for olanzapine treatment.

Adult↗
PubMed2000

Leucopenia induced by low dose clozapine in Parkinson's disease recedes shortly after drug withdrawal. Clinical case descriptions with commentary on switch-over to olanzapine.

Four patients affected by severe Parkinson's disease developed leucopenia (900-1200 WBC) during treatment of psychosis (3) or untreatable insomnia (1) with clozapine (37.5-75 mg/day). Clozapine withdrawal was followed by recovery of leucopenia (4000-6000 WBC) in two weeks with no need for the administration of leucokines. After 1-6 months olanzapine was administered (increasing the dose from 2.5 to 10 mg/day) to treat persisting disturbances, but the drug induced severe worsening of parkinsonism and also this drug had to be withdrawn.

Aged↗