C Scoppetta

Sapienza University of Rome, Roma, Latium, Italy

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Publications (73)327.72 Total impact

  • C Scoppetta · M Scoppetta ·

    European review for medical and pharmacological sciences 03/2014; 18(6):937-8. · 1.21 Impact Factor
  • C Scoppetta · M Scoppetta ·
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    ABSTRACT: We have recently designed a new type of walker for those severely disabled patients who cannot walk with commonly used medical walkers. A drawing and the description of this new walker is reported in order to permit the worldwide companies as well as artisans to develop and produce it for the people affected from severe motor problems. This walker supposes the patient wearing either a modified climbing harness or equipped clothes and being suspended to the walking frame. It consists in two series of bands suspending the patient from the frame; the upper one suspends him for the upper part of his trunk, the lower one by his pelvis. This walker is suggested for patients belonging to three principal groups: (1) Persons who have no trunk control (e.g.: patients affected by severe stroke or ataxias). (2) Persons whose walk is allowed only if they achieve a significant reduction (up to 30-40%) of the their body weight charging on trunk, spine, and lower limbs. (3) Persons who need a differentiated reduction of the body weight either among anterior and posterior side or among their right and left part of the body (hemiparesis, Parkinson disease, scoliosis, kyphosis). Creating this walker is easy; producing costs are low; there are no maintenance costs.
    European review for medical and pharmacological sciences 10/2013; 17(19):2690-2. · 1.21 Impact Factor
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    ABSTRACT: The mRNA levels of NKCC1, an inwardly directed Na(+), K(+)-2Cl(-) cotransporter that facilitates the accumulation of intracellular Cl(-), and of KCC2, an outwardly directed K(+)-Cl(-) cotransporter that extrudes Cl(-), were studied in surgically resected brain specimens from drug-resistant temporal lobe (TL) epilepsy (TLE) patients. Quantitative RT-PCR analyses of the mRNAs extracted from the human TLE-associated brain regions revealed an up-regulation of NKCC1 mRNA and a down-regulation of KCC2 mRNA in the hippocampal subiculum, compared with the hippocampus proper or the TL neocortex, suggesting an abnormal transcription of Cl(-) transporters in the TLE subiculum. In parallel experiments, cell membranes isolated from the same TLE-associated brain regions were injected into Xenopus oocytes that rapidly incorporated human GABA(A) receptors into their surface membrane. The GABA currents elicited in oocytes injected with membranes from the subiculum had a more depolarized reversal potential (E(GABA)) compared with the hippocampus proper or the neocortex. The NKCC1 blocker bumetanide or a temperature decrease of 10 degrees C shifted the GABA-current E(GABA) more negative in oocytes injected with membranes from TLE hippocampal subiculum, matching the E(GABA) of TL neocortex-injected oocytes. We conclude that the anomalous expression of both Cl(-) transporters, NKCC1 and KCC2 [corrected] in TLE hippocampal subiculum probably causes altered Cl(-) transport in the "epileptic" neurons, as revealed in the microtransplanted Xenopus oocytes, and renders GABA aberrantly "exciting," a feature that may contribute to the precipitation of epileptic seizures.
    Proceedings of the National Academy of Sciences 06/2006; 103(22):8465-8. DOI:10.1073/pnas.0602979103 · 9.67 Impact Factor
  • C Scoppetta · F Grassi ·
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    ABSTRACT: The main action of erythropoietin (EPO) is to regulate the production of red cells. However both experimental evidence and clinical experience suggest that erythropoietin has a positive effect on skeletal and cardiac muscle. Mice lacking EPO or its receptors suffer from hearth hypoplasia and have a reduced number of proliferating cardiac myocytes. EPO receptors are expressed on mouse primary satellite cells and in cultured myoblasts, and their stimulation appears to enhance proliferation and reduce the differentiation of both cell types. Moreover EPO is capable of promoting angiogenesis in muscle cells, which provides an additional route to increase oxygen supply to active muscles. In men, the effects of EPO on muscle cells are suggested by the illegal use of EPO by agonistic and amateur athletes to enhance their performances. In some athletes EPO improved their long-duration muscular performances much more than expected on the basis of the increment of the blood hemoglobin alone. Our proposal is to investigate the effect of EPO treatment in various animal models of muscular dystrophies (MD), which are common hereditary primary muscle disorders characterized by muscle damage and wasting, to date without any effective treatment. The ability of EPO to induce the proliferation of satellite cells in the presence of differentiating conditions, typical of the damaged muscle, may represent a tool to expand the cellular population competent for muscle repair. This would lengthen the period when muscles can be efficiently repaired. In the presence of positive results, the possibility could be considered of selecting some of the human forms of MD and treating the patients with EPO.
    Medical Hypotheses 02/2004; 63(1):73-5. DOI:10.1016/j.mehy.2003.12.044 · 1.07 Impact Factor
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    C Scoppetta · P Onorati · F Eusebi · M Fini · A Evoli · A Vincent ·

    Journal of Neurology Neurosurgery & Psychiatry 04/2003; 74(3):392-3. DOI:10.1136/jnnp.74.3.392 · 6.81 Impact Factor
  • A Uncini · G Galluzzi · A Di Muzio · M V De Angelis · E Ricci · C Scoppetta · S Servidei ·
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    ABSTRACT: Facioscapulohumeral muscular dystrophy has a distinctive regional distribution but variable clinical expression and may be markedly asymmetrical. We report two patients presenting weakness and wasting confined to a single lower limb. Creatine kinase was slightly increased, electromyogram and muscle biopsy were myopathic. Muscle computed tomography showed normal shoulder, mid-arm, pelvic and mid-thigh scans but involvement of calf muscles. In both cases, weakness of facial and periscapular muscles was found in other family members unaware of the disease. Molecular analysis showed 4q35 deletion in one family. These cases broaden the presentation of facioscapulohumeral muscular dystrophy to include isolated monomelic atrophy of lower limb with calf muscle involvement.
    Neuromuscular Disorders 12/2002; 12(9):874-7. DOI:10.1016/S0960-8966(02)00027-5 · 2.64 Impact Factor
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    ABSTRACT: In 1995 Laing et al. (Am J Hum Genet 56(1995)422) described a single family with nine members affected by an autosomal dominant infantile onset distal myopathy. This family generated a LOD score of 2.6 for a locus on chromosome 14. We describe two families with an infantile onset distal myopathy: a new family with four affected members and the family previously described by Scoppetta et al. (Acta Neurol Scand 92(1955)122) in both of which haplotype segregation was compatible with linkage to the same chromosome 14 locus, generating LOD scores of 0.9 at a penetrance of 100% for the markers D14S283 and D14S64 (theta=0) in both families. The loci for autosomal recessive hereditary inclusion body myopathy and Nonaka myopathy on chromosome 9 and for autosomal dominant distal myopathy of Markesberry-Griggs and Udd on chromosome 2q31-33 were excluded by linkage analysis. The disease followed a uniform course with selective wasting of the anterior tibial muscles, starting in infancy and recognizable by a characteristic clinical sign of the 'hanging big toe'. This was followed by slow progression, with involvement of the finger and wrist extensor muscles in the third decade and proximal limb muscles in the fourth decade. Interestingly, we also found evidence of an accompanying mild peripheral neuropathy in the oldest individual with hypomyelination of numerous large myelinated fibres. In addition, this patient's muscle biopsy also showed autophagic vacuoles and numerous intranuclear tubulo-filamentous inclusions of 15-20 nm diameter. Given that all three families with infantile onset distal myopathy are compatible with linkage to the same locus on chromosome 14, this study supports evidence for, and enlarges the clinical and neuropathological spectrum of the distal myopathy on chromosome 14.
    Neuromuscular Disorders 02/2001; 11(1):11-9. DOI:10.1016/S0960-8966(00)00158-9 · 2.64 Impact Factor
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    C Scoppetta ·

    The Lancet 12/2000; 356(9241):1612. DOI:10.1016/S0140-6736(05)74464-0 · 45.22 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the clinical efficacy of clozapine, an atypical neuroleptic, on L-dopa induced dyskinesias of Parkinson's disease. In an open study, a group of 10 PD patients was treated with low dosage clozapine (mean 30 mg/day) for a 4-month period and L-dopa dyskinesias were evaluated in basal conditions and during clozapine treatment after the usual morning dose of clozapine. We utilized the AIMS for evaluation of dyskinesias and UPDRS for the assessment of motor performances. Clozapine produced a significant (P<0.05) reduction of dyskinesias 1 week after the therapy onset. This effect was more pronounced at the end of the 2nd week and remained stable through the following months. We did not observe significant variations of motor performances. A low dose of clozapine appears to be beneficial for patients with L-dopa induced dyskinesias that do not respond to other drugs and therapeutic measures.
    Acta Neurologica Scandinavica 06/1998; 97(5):295-9. DOI:10.1111/j.1600-0404.1998.tb05955.x · 2.40 Impact Factor
  • C Scoppetta · B Mercuri · R Di Lello · V S Tolli · G F Mennuni · M L Vaccario ·
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    ABSTRACT: The "distal myopathies" include autosomal dominant, autosomal recessive, and sporadic disorders. Two of the recessive disorders are considered to be definitive entities: Miyoshi's myopathy, which has an early adult onset and first involves the calf muscles, and distal myopathy with rimmed vacuoles. We here describe the cases of two sisters and compare them with previously reported cases. The disorder in our patients is characterised by: a) autosomal recessive inheritance; b) onset in early adult life; c) initial involvement of the tibialis anterior and peroneal muscles; d) subsequent involvement of the calf muscles spreading to the proximal muscles of the legs and, later, the arms; e) a moderately disabling evolution over a period of 10-12 years; f) marked and stably high serum levels of CK and other enzymes; g) EMG evidence of myopathic damage, with fibrillation at rest; and h) a histological picture of dystrophic myopathy, with atrophy of mainly type 2 fibres. We think that this syndrome is different from the two forms of autosomal recessive distal myopathy mentioned above.
    The Italian Journal of Neurological Sciences 11/1997; 18(5):271-6. DOI:10.1007/BF02083303
  • C. Casali · F. Calvosa · I. LaCesa · B. Mercuri · V. S. Tolli · C. Scoppetta ·

    Neuromuscular Disorders 03/1996; 6(2). DOI:10.1016/0960-8966(96)89053-5 · 2.64 Impact Factor
  • C Scoppetta · C Casali · I La Cesa · A Sermoni · B Mercuri · F Pierelli · M L Vaccario ·
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    ABSTRACT: Distal myopathies are currently regarded as a non-homogeneous group of disorders including different autosomal dominant, recessive and sporadic forms. The cases of a mother and her son and daughter are described and compared to previously reported cases from 4 families. Despite minor differences, the clinical picture is remarkably homogeneous, both within the same family and among different families. A distinct clinical form can be identified including: a) autosomal dominant inheritance; b) onset in infancy or childhood with peroneal muscles weakness; c) not disabling evolution in spite of possible late involvement of muscles others than tibio-peroneal; d) usually normal serum CK and other muscle enzymes; e) EMG evidence of primary myogenic damage; f) morphological findings of non-specific myopathy. Because of the benign evolution and the absence of true dystrophic changes in most biopsies we suggest the term infantile autosomal dominant distal myopathy should be preferred to infantile autosomal dominant distal muscular dystrophy.
    Acta Neurologica Scandinavica 09/1995; 92(2):122-6. DOI:10.1111/j.1600-0404.1995.tb01024.x · 2.40 Impact Factor

    Neuromuscular Disorders 09/1994; 4(5-6). DOI:10.1016/0960-8966(94)90199-6 · 2.64 Impact Factor
  • G C Deidda · S Cacurri · I La Cesa · C Scoppetta · L Felicetti ·

    Annals of Neurology 08/1994; 36(1):117-8. DOI:10.1002/ana.410360127 · 9.98 Impact Factor
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    ABSTRACT: On the long term Parkinson Disease (PD) treatment is often complicated by the occurrence of motor fluctuations. To find out whether early treatment of PD with levodopa, dopaminoagonists or 1-deprenyl is associated with any difference in motor fluctuations occurrence, the Italian Parkinson Study Groups initiated a multicenter, randomized study. Since November 1988, 475 patients cequiring effective treatment for idiopathic PD have been randomized to receive levodopa, dopoamine agonists or deprenyl. After 2 months of therapy, all patients evaluated with the Unified Parkinson Disease Rating Scale showed a significant amelioration. Daily living activities were more impaired in patients treated with deprenyl. Study design is presented and first resuts are discussed.It trattamento a lungo termine del Morbo di Parkinson spesso complicato dalle fluttuazioni motorie. Per valutare se il trattamento precoce della malattia di Parkinson con levodopa, dopaminoagonisti e l-deprenil sia associato a un diverso rischio di comparasa della fluttuazione, l'Italian Parkinson Study Group ha organizzato uno studio multicentrico e randomizzato. Dal novembre 1988, 475 pazienti affetti da parkinson idiopatico sono stati randomizzati alle diverse terapie. A 2 mesi dall'inclusione tutti i pazienti valutati con la Unified Parkinson Disease Rating Scale mostravano un significaativo miglioramento clinico. Non stata osservata una differenza significativa di efficacia fra le diverse terapie sui punteggi a eccezione del punteggio relativo alle attivit quotidiane significativamente meno influenzate dal deprenyl.
    The Italian Journal of Neurological Sciences 11/1992; 13(9):735-739. DOI:10.1007/BF02229158

    Journal of Neuroimmunology 11/1991; 34(2-3):244-245. DOI:10.1016/0165-5728(91)90142-T · 2.47 Impact Factor
  • A Peppe · D De Angelis · V S Tolli · P A Rizzo · C Scoppetta ·
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    ABSTRACT: Most of Parkinson's disease patients treated with Levodopa develop the Long Treatment Levodopa Syndrome. Many authors showed a correlation between clinical features and plasma level of Levodopa. In our study, five parkinsonian patients with severe clinical response fluctuations, oral levodopa treatment was replaced by repeated continuous infusions of Levodopa (with oral carbidopa). Our results confirm that repeated intravenous infusion are very effective in PD patients with LTS.
    Rivista di neurologia 01/1991; 61(5):197-200.
  • C Scoppetta · C Casali · S D'Agostini · I La Cesa · L Parisi ·
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    ABSTRACT: In myasthenia gravis (MG) a typical decrementing response is frequently revealed with repetitive stimulation (RS) in clinically unaffected muscles. However, RS is unlikely to give normal results in weak muscles. In two of our patients we found a normal response in clinically affected muscles. However, a decrementing response surprisingly appeared after the administration of anticholinesterase drugs. A possible explanation for this apparently paradoxical effect is as follows: some junctions are already blocked at rest, whereas others function normally both at rest and during RS. As a consequence, the initial compound muscle action potential (CMAP) is reduced in amplitude and shows no further decrement on RS. Anticholinesterase drugs reverse some blocks, therefore causing the CMAP increase in amplitude. However, these labile junctions are more prone than normal to synaptic fatigue, so a decrementing response is produced on RS. This behavior, though not frequently encountered, can account for some negative results of RS in MG.
    Electroencephalography and Clinical Neurophysiology 03/1990; 75(2):122-4. DOI:10.1016/0013-4694(90)90160-L
  • N Scuderi · F D'Andrea · C Rubino · M Greco · C Scoppetta ·
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    ABSTRACT: The authors briefly describe the commonest forms of mitochondrial myopathies particularly those associated with disorders of ocular motility. They report their series of four patients suffering from ptosis of the eyelid caused by mitochondrial myopathies. The ptosis was corrected surgically in all cases by means of Müller's muscle adaptation technique. The authors discuss their results and the indication for this technique.
    Annales de Chirurgie Plastique Esthétique 02/1990; 35(5):405-9. · 0.31 Impact Factor

  • Progress in clinical and biological research 02/1990; 337:285-8.

Publication Stats

805 Citations
327.72 Total Impact Points


  • 1990-2014
    • Sapienza University of Rome
      • Department of Physiology and Pharmacology "Vittorio Erspamer"
      Roma, Latium, Italy
  • 2001
    • University Hospital Essen
      Essen, North Rhine-Westphalia, Germany
  • 1989-1994
    • The American University of Rome
      Roma, Latium, Italy
  • 1979-1984
    • The Catholic University of America
      Washington, Washington, D.C., United States
  • 1975
    • Università Cattolica del Sacro Cuore
      Milano, Lombardy, Italy