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Biomedical subjects

C Ferrarese

Publications and source records attributed to C Ferrarese.

At least 37 records · Page 2Linked to original sources
PubMed2004

Optic neuritis: diagnostic criteria application in clinical practice.

Optic neuritis (ON) refers to any inflammatory optic neuropathy. In clinical practice ON is mainly diagnosed by ophthalmologists and less frequently by neurologists. ON diagnostic criteria are included in the Classification of International Headache Society (IHS) and in other classification systems, both in neurological and ophthalmologic fields. The aims of this study were to verify the application of IHS ON diagnostic criteria in clinical practice and the role of the ocular pain qualitative aspects. We performed a partially retrospective (140 cases) and prospective (43 cases) study analysing the clinical characteristics of patients with ON. We observed retro orbital pain in a huge percentage of patients; it was provoked or spontaneous and worsened by eye movements. We found that the new IHS classification criteria (IHS 2004) do not fully satisfy the requirements for ON diagnosis. Further study is necessary to validate the diagnostic criteria of ON in clinical practice.

Eye Movements↗
PubMed2004

Migrainous cerebral infarction: case reports.

Migraine is a common and chronic disorder. It is considered benign but several studies have suggested it as a rare risk factor for ischaemic stroke. The association is still conflicting and seems to be restricted to particular subgroups of patients (i.e., women under the age of 45, with migraine with aura, and particularly ones who smoke and use oral contraceptives). The pathogenetic mechanisms underlying this condition are not known. We describe 6 cases of migrainous stroke fully meeting the diagnostic criteria of the International Headache Society (IHS). For each patient, demographic and anamnestic data, clinical features, results of laboratory tests and neuroimaging findings were recorded. Five of the 6 cases were women (median age of 29, range from 23 to 40). The man was 36. All patients fulfilled the IHS criteria for migraine with aura. At the time of the event, 2 patients were taking oral contraceptives and smoked, one patient smoked and three patients had no vascular risk factors. The stroke manifested as homonymous hemianopia in 3 patients, lower homonymous quadrantopia in 1 patient and sensory symptom in 1 patient. The neurological examination was normal in 1 case. All patients underwent several tests with negative results: blood test (antithrombin III, protein C or S, autoantibodies), transthoracic and transoesophageal echocardiography, extracranial and intracranial Doppler sonography, and angiography which was not performed in 1 patient. All patients had a cerebral infarct visible on neuroimaging study (MRI): posterior cerebral artery in 4, middle cerebral artery in 1 and anterior cerebral artery in 1. We support the findings reported by others that migrainous stroke is more common in young women affected by migraine with aura. In consideration of the high prevalence of migraine in the population, further research is indicated and necessary to establish if migraine is independent from other vascular risk factors.

Adult↗
PubMed2003

Deep brain stimulation for the treatment of Parkinson's disease: the experience of the Neurosurgical Department in Monza.

deep brain stimulation is a widely accepted surgical therapy for the symptomatic treatment of advanced parkinson's disease; high frequency chronic stimulation of the subthalamic nucleus proved its efficacy to control the major motor symptoms. In the neurosurgical department of Monza we treated 72 parkinsonian patients (November 1998-January 2003). One year follow-up results are: decrease of tremor 90%, hypertonous 56%, bradykinesia 70%, voice impairment amelioration 30%, mean total daily L-dopa intake reduced 58%. Freezing and balance did not ameliorate, some voice impairment and psychic derangement have been observed. Major surgical complications were: haemorrage (1 case - transient hemiparesis), infections (2 cases), pulmonary embolisation (1 case). To optimise the surgical results, careful clinical and instrumental selection of the patients are mandatory before surgery.

Clinical Trials as Topic↗
PubMed2003

Physical anhedonia in Parkinson's disease.

Anhedonia is the inability to experience physical or social pleasure. Its physical component is hypothesised to be due to dysfunction of a dopaminergic frontotemporal-subcortical circuit and has never been investigated as a possible affective complication of Parkinson's disease (PD). The aim of this study was to formally assess prevalence and correlates of physical anhedonia in PD patients compared with normal controls. Twenty five people with PD and 25 matched controls were administered a psychometric battery exploring mainly executive functions and mood. Hedonic tone was assessed using Chapman's Physical Anhedonia Scale. PD patients also underwent MRI linear measurement of frontal structures. Anhedonia levels were significantly higher in PD patients with respect to controls, although not extremely elevated; prevalence rate was 40% for parkinsonians, while no anhedonics were found among controls. Clinical, neuropsychological, and quantitative neuroradiological features did not show any significant correlation with physical anhedonia. Physical anhedonia appears to be a relatively frequent, although mild, affective disturbance of PD, independent from neurological, frontal, and depressive aspects.

Aged↗
PubMed2002

Cisplatin-induced peripheral neurotoxicity in rats reduces the circulating levels of nerve growth factor.

The pathogenesis of the neurotoxicity of most antineoplastic drugs is unknown. Recent reports suggest that changes in the circulating levels of nerve growth factor (NGF) might be related to the dorsal root ganglia sensory neuron damage induced by cisplatin (CDDP), the first member of a family of widely used and very effective platinum-derived anticancer agents. Using a well-characterized model of CDDP neurotoxicity, we demonstrated that the NGF circulating level decreased during chronic CDDP administration in close accordance with the clinical course and returned to normal levels after recovery from the neurotoxic damage. Moreover, these changes were restricted to NGF and did not involve other trophic factors of the same neurotrophin family. Our findings are in agreement with previous in vitro and in vivo results and further suggest that NGF plays a specific role in the course of CDDP-induced primary sensory neuron damage.

Animals↗
PubMed2002

Characterisation of adducts of the lipid peroxidation product 4-hydroxy-2-nonenal and amyloid beta-peptides by liquid chromatography/electrospray ionisation mass spectrometry.

Alzheimer's disease is characterised by brain neuritic plaques composed of a 39-44 amino acid peptide (Abeta). Lipid peroxidation is an early event induced by these amyloid beta-peptides, leading to the formation of 4-hydroxy-2-nonenal (HNE), which is one of the major end products of this process. HNE has been reported to form adducts via a stable covalent binding to proteins through a Michael addition to amino acid residues with a nucleophilic side chain. The present study reports an investigation of the conditions for formation of Abeta-HNE (Abeta 1-28 and Abeta 1-42) adducts, and their characterisation by liquid chromatography/electrospray ionisation mass spectrometry (LC/ESI-MS). The results suggest that one or more HNE moieties are localised in the 6-16 region of these adducts, while Asp-1, Lys-16 and Lys-28 are not modified under the described reaction conditions.

Aldehydes↗
PubMed2001

Increased glutamate in CSF and plasma of patients with HIV dementia.

BACKGROUND: Experimental evidence suggests that excitotoxicity might play a major role in HIV-induced neurodegeneration. However, few studies have investigated the role of endogenous glutamate in patients with HIV dementia. OBJECTIVE: To analyze CSF and plasma glutamate levels in 30 patients with AIDS with different dementia severity compared with 10 patients with other neurologic disorders, 11 healthy control subjects, and 10 patients with Alzheimer-type dementia. METHODS: CSF and plasma glutamate levels were measured by reverse-phase high-performance liquid chromatography followed by fluorometric analysis. RESULTS: Glutamate CSF levels were increased fivefold in the patients with HIV vs normal control subjects (p = 0.001), patients with Alzheimer-type dementia (p < 0.0001), and patients with other neurologic disorders (p < 0.01). CSF glutamate levels were also related to the degree of dementia (p < 0.02) and brain atrophy (p < 0.002). Plasma levels were also higher in the patients with HIV (p < 0.0001) but did not correlate with either clinical or imaging features. CONCLUSION: Increased CSF glutamate may originate within the CNS and may play a pathogenetic role in HIV dementia, thus supporting the treatment of these patients with glutamate receptor antagonists.

AIDS Dementia Complex↗
PubMed2001

Decreased platelet glutamate uptake in patients with amyotrophic lateral sclerosis.

Decreased glutamate uptake and a loss of the astrocytic glutamate transporter EAAT2 (GLT-1) have been shown in spinal cord and motor cortex of patients with ALS. Because platelets express the three major glutamate transporter subtypes, including GLT-1, and possess a high-affinity glutamate uptake, the authors investigated glutamate uptake in platelets from patients with ALS and controls. A 43% reduction of high-affinity glutamate uptake rate (p < 0.0001) was observed in patients with ALS compared with normal controls and chronic neurologic disorder patients, suggesting a systemic impairment of glutamate uptake in ALS.

Adult↗
PubMed2001

Stenting of atherosclerotic stenoses of the extracranial carotid artery.

BACKGROUND: Percutaneous transluminal angioplasty (PTA) and stenting seems to be, at present, the treatment of choice for early restenosis after endarterectomy and for atherosclerotic stenoses of supra-aortic trunks near or at the ostium. In contrast, the role of PTA and stenting for treatment of symptomatic and asymptomatic atherosclerotic stenosis of carotid bifurcation is still debated. METHODS: The present study comprises 27 consecutive cases of atherosclerotic lesions of the carotid bifurcation treated with PTA and stenting. All patients were symptomatic, except for 2 suffering from asymptomatic stenosis with contralateral carotid occlusion. There were 23 stenoses occluding 70% or more of the lumen according to the NASCET criteria and 4 mild stenoses (50-60% of the lumen) with large type C ulcers. Criteria for exclusion from surgery in these cases were aged >79 years, previous neck surgery for laryngeal cancer, carotid bifurcation at C2, association with intracranial aneurysms, occlusion of the contralateral carotid artery, and heart, lung and kidney diseases. All procedures were performed under local anaesthesia associated with mild sedation in a few cases. In all cases, self-expandable stents (Wallstent) were used. Follow-up ranged from 6 to 37 months. FINDINGS: Transient neurological deficit occurred in 3 cases (11%). One case (3.7%) experienced a minor stroke at three months. Asymptomatic tight restenosis due to intimal hyperplasia occurred in one case (3.7%). In 8 cases (40%) of complex stenosis involving common and internal carotid arteries there was some loss of contact of the stent with the wall of the common carotid artery in the late follow-up. One case (3.7%) experienced severe and prolonged hypotension and bradycardia during the release of the stent. INTERPRETATION: From literature data and our results it emerges that periprocedural catastrophic embolism is unlikely to occur. The best results are undoubtedly obtained when treating stenosis limited to the internal carotid artery. Nevertheless, the ideal stent to treat vessels of different calibre, as occurs at the carotid bifurcation, is not yet available. The problem of periprocedural cerebral protection has not been resolved. Reported series are heterogeneous and retrospective, and an adequate follow-up of cases is still lacking.

Adult↗
PubMed2001

Decreased platelet glutamate uptake and genetic risk factors in patients with Parkinson's disease.

Genetic risk factors seem to play a role in sporadic Parkinson's disease (PD), maybe triggering oxidative stress and excitotoxicity within substantia nigra. However, genetic factors act at systemic level: reduced activity of mitochondrial enzymes and decreased glutamate uptake have been shown in platelets from PD patients. In this study we investigated glutamate uptake in platelets from 38 sporadic PD patients, 13 patients with parkinsonian syndromes and 28 controls and assessed polymorphisms of alpha-synuclein and ApoE genes. A 48% reduction of glutamate uptake p)<0.0001) was observed in PD patients which, with respect to control groups, correlated with the disease severity (r = -0.44, p < 0.05). Genetic studies of this population did not show differences between PD and controls, nor correlations with platelet glutamate uptake.

Apolipoproteins E↗
PubMed2001

Nerve growth factor and transforming growth factor-beta serum levels in acute stroke patients. Possible involvement of neurotrophins in cerebrovascular disease.

BACKGROUND AND PURPOSE: Experimental evidence indicates cytokine and neurotrophin production in brain tissue after stroke. Since neurotrophins may also be released from blood cells, we measured nerve growth factor (NGF) and transforming growth factor (TGF)-beta serum levels in 40 patients at various times after stroke and compared them to those in 20 healthy controls. METHODS: Venous blood was obtained 1, 4, 10, 30 and 90 days after stroke and NGF and TGF-beta serum levels were measured by commercial ELISA. Values at each time were correlated with stroke severity, assessed using the National Institute of Health Stroke Scale, and with lesion volume, calculated using Cavalieri's direct estimator on a computerized tomography scan performed 5 days after stroke. RESULTS AND CONCLUSIONS: Although no significant differences between the two groups were demonstrated, in stroke patients, serum neurotrophins were significantly associated with clinical and neuroradiological parameters of brain injury and positively correlated with each other in the acute phases of stroke, suggesting that stroke may modulate peripheral neurotrophin levels.

Humans↗
PubMed2001

Pervasive developmental disorders and GABAergic system in patients with inverted duplicated chromosome 15.

Pervasive developmental disorders are characterized by severe, pervasive impairment in several areas of development, with distorted communication skills and stereotypical behavior. Pervasive developmental disorders have a heterogeneous etiology related to brain damage, familial affective psychopathology, chromosomal abnormalities, or dysfunction of neuromodulators. Recently, it has been suggested that the GABRB3 gene, located within chromosome 15q11-13, is a candidate for pervasive developmental disorder. In inverted duplicated chromosome 15 syndrome, in which there is a small marker chromosome derived from inversion and duplication of the chromosome 15q11-q13 region, all patients present with pervasive developmental disorder. To further investigate a possible involvement of the gamma-aminobutyric acid (GABA)ergic system in the inverted duplicated chromosome 15 syndrome, we evaluated plasma levels of GABA and diazepam binding inhibitor in 6 patients with inverted duplicated chromosome 15 and in 8 subjects not affected by neurologic disease. Our findings do not seem to support this hypothesis as no significant differences were found in the GABA and diazepam binding inhibitor plasma levels between patients with inverted duplicated chromosome 15 and controls, but we must consider the possibility that a genetic abnormality of the GABA(A) receptor could be present in patients with inverted duplicated chromosome 15 and still not be reflected in an alteration in either GABA or diazepam binding inhibitor levels in plasma.

Adolescent↗
PubMed2000

Glutamate uptake is decreased in platelets from Alzheimer's disease patients.

Because excitotoxicity may be involved in neurodegeneration in Alzheimer's disease, we investigated possible modifications of platelet glutamate uptake in AD patients. High-affinity glutamate uptake was studied in platelets from 35 Alzheimer's disease patients, 10 multi-infarct dementia patients, and 35 age-matched normal controls; it was decreased by 40% in platelets from Alzheimer's disease patients compared with controls and with multi-infarct dementia patients. Platelet glutamate uptake could be used as peripheral marker of glutamatergic involvement and as adjunctive diagnostic tool in Alzheimer's disease patients.

Aged↗
PubMed1999

Reduced platelet glutamate uptake in Parkinson's disease.

Defects in mitochondrial enzymes have been found not only in substantia nigra, but also in platelets from Parkinson's Disease (PD) patients, suggesting a systemic impairment of energy metabolism. Since platelets present an energy-dependent glutamate uptake similar to that described in central nervous system, glutamate uptake was determined in platelets from 34PD patients and 21 age-related normal controls, as Na+-dependent [3H]glutamate influx; glutamate level was also analyzed by reverse-phase HPLC. A 50% reduction of glutamate uptake (p < 0.001) was observed in idiopathic PD patients, respect to controls and secondary parkinsonian syndromes. The decrease correlated with the severity of PD, measured by the UPDRS (r = -0.54; P < 0.05). Glutamate level was increased in platelets of PD patients, but was not correlated to the uptake decrease. Both phoenomena may be explained by the modifications of mitochondrial enzymes described in platelets, which could be used as a peripheral model of glutamatergic function in PD.

Analysis of Variance↗
PubMed1999

Benzodiazepine-induced chemotaxis is impaired in monocytes from patients with generalized anxiety disorder.

Peripheral benzodiazepine receptors (PBR) modulate chemotaxis and cytokine production of monocytes and lymphocytes. Since PBR are decreased in animal models of stress and in patients with anxiety disorders, in the present study we analyze the ability of monocytes obtained from patients suffering from generalized anxiety to migrate towards chemoattracting benzodiazepines. In these patients, the benzodiazepine-induced chemotaxis is completely abolished, while the response to the control chemoattractant formyl-leu-met-phe is still maintained. The chemotaxis responses are not restored after pharmacological treatment of the pathology. The decreased chemotactic response could be linked to a decreased number of PBR receptors present on monocytes of generalized anxiety disorder patients.

Adult↗